Where to get cipro

Early in this century, post-SARS, and in a period where to get cipro when China started allowing more students description and scientists to study abroad, collaboration and exchange between American and Chinese scientists blossomed. Many of China’s top scientists today were educated in the West. These include George Gao, the head of China’s Center for Disease Control and Prevention, who trained and taught at Oxford and Harvard, and Shi Zhengli, who directs the Center for Emerging Infectious Diseases at the Wuhan Institute of Virology and received her where to get cipro Ph.D. In France.

Many, like Gao, spent more than a decade abroad before returning to China for top jobs and, often, prestigious positions and big salaries. They were great at their bench work, their science was where to get cipro well respected, and top American scientists got to know them well. They became friends with their American counterparts, as is clear from Anthony Fauci’s email correspondence with Gao as the cipro emerged, recently released through a Freedom of Information Act request. But early on in what became a global crisis, when limited and reassuring information was coming out of China about the transmissibility of the novel antibiotics and the extent of its domestic outbreak, misplaced trust among America’s top scientists led some to think the spread of the cipro probably wouldn’t be so bad.

Here’s the problem where to get cipro. Chinese scientists are great scientists, but they work for an authoritarian government where politics, not facts, always comes first. If information where to get cipro they know or discover makes China look bad, it is dangerous to say it — especially to foreign colleagues, especially publicly, and, often, even to their friends or family. That may sound familiar after the presidency of Donald Trump, during which he often mocked and sidelined experts like Fauci.

But the risk for scientists in China is far worse. Loss of your job where to get cipro and your kids’ career prospects, visits by the police, false accusations, even prison. As the country’s leader, Xi Jinping, reminded his scientists in a speech last year. €œScience has no borders, but scientists have a motherland.” Every Chinese citizen knows how to interpret that statement, and I learned, too.

When I was a reporter where to get cipro in Beijing, I got to know Dr. Gao Yaojie, who exposed an epidemic of HIV/AIDS in rural China that had resulted from unsanitary blood collection practices, some state-run. She was a valued source for a series of articles I wrote on the unfolding tragedy, in which nearly the entire adult population of poor farming villages was dying, without any treatment and leaving AIDS orphans behind. Dr.

Gao (no relation to George Gao) was feted by Bill and Hillary Clinton and won international human rights awards for saving perhaps tens of thousands of lives and ending dangerous practices. But in China, that very same work meant Gao spent her retirement under house arrest, often followed and threatened by local officials for embarrassing China. She fled China in 2009 and obtained political asylum in the U.S. And that was at a time when China was less autocratic and more open than it is today.

President Joe Biden had instructed security agencies to investigate the lab leak theory — to figure out whether antibiotics, the cipro that causes buy antibiotics, emerged from the Wuhan lab or from nature. But if international scientific sleuths are hoping to see a lab log or find a whistleblower, that very likely won’t happen. That kind of information won’t be revealed, even to Chinese scientists’ many American friends and scientific partners, which include the U.S. The Wuhan lab has received more than half a million dollars of funding that originated from the National Institutes of Healthand has worked with many American scientists.

Mistakes happen in science. Pathogens leak out of good containment labs, and not because people are evil. It’s because, for example, the technician performing the bench work forgets an important step or, in a rush to go home, gets sloppy — it takes only a second. Or, for example, if scientists gathering bat samples in remote caves get a bit too comfortable in a dangerous environment — because they’ve been there dozens of times before with no problem and the biohazard suits and masks are suffocating.

So, they pull off the face mask a bit too early as they exit. When that happens, you have to acknowledge the error right away to contain the damage. But Chinese scientists can’t do that, at least publicly. When, in late December 2019, Dr.

Li Wenliang, an ophthalmologist working at one of Wuhan’s major hospitals, raised his concerns to colleagues about patients dying from a strange new cipro, he was punished and told by police to “stop making false comments” and investigated for “spreading rumours.” He died of buy antibiotics just a few weeks later. In China today, it is dangerous to say what you know if it challenges the official government narrative. People who participated in the protests on June 4, 1989, in Tiananmen Square, which were violently put down by the Chinese army, don’t even tell their children about that bloody day when many hundreds, and possibly thousands, were killed. Kai Strittmatter, a longtime China correspondent for one of Germany’s largest newspapers, told NPR’s Terry Gross.

€œOf course, this generation, they all know, but they were afraid to tell their children. Because, you know, what do you do when your child in school suddenly tells the teacher and asks the teacher about Tiananmen massacre?. € We may never know if the novel antibiotics leaked from a lab or from animal-to-human transmission from a wild animal at one of Wuhan’s live animal markets, as the Chinese first suggested. And that’s exactly the knowledge we desperately need to prevent the next cipro, because the solutions are so different.

If the former hypothesis proved true, U.S. Scientists would need to ensure that collaborations with their Chinese partners involve full transparency — access to log books, internal reports, and all. If the latter, China must fully enforce its ban on the sale of exotic animals (the “intermediate hosts” that carry the cipro) at its wet markets, a ban it promised after the original SARS cipro emerged there from a civet cat nearly two decades ago. But the Chinese government’s control over its scientists makes it unlikely we will learn the truth now — or ever.

Elisabeth Rosenthal. erosenthal@kff.org, @rosenthalhealth Related Topics Contact Us Submit a Story TipSACRAMENTO — Gov. Gavin Newsom routinely boasts that California has “one of the highest vaccination rates in the United States of America.” But Newsom, facing a recall election this fall, rarely mentions that the state’s buy antibiotics treatment uptake has largely stagnated in Black and Latino neighborhoods hardest hit by the antibiotics, and in rural outposts where opposition to treatments runs rampant. In these communities, deep distrust of government and the U.S.

Health care system has collided with the state’s high-stakes effort to finish vaccinating its 34 million treatment-eligible residents. These are places where state health officials believe they can change a significant number of minds. But the Newsom administration is struggling to do so, public health experts say, hampered by its inconsistent and hastily developed public messaging and outreach campaign that relies too heavily on private advertising firms and companies such as Google and Blue Shield of California. €œMany people don’t trust information being put out about treatments because it’s coming from private companies that have profit-seeking motives,” said Dr.

Tony Iton, a senior vice president at the California Endowment, which focuses on expanding health care access for Californians. Iton served as Alameda County’s public health officer from 2003 to 2009. What actually works, Iton and other public health experts say, are well-funded, locally designed operations led by organizations that have built trust with residents and are capable of going door to door to dispel treatment mythology, such as local nonprofits, county health departments and community clinics. But California’s 61 local public health departments have been stunted by years of declining revenue, budget cuts and staff reductions that have stymied their ability to conduct the expensive and time-consuming public health outreach campaigns necessary to combat treatment skepticism and hesitancy.

€œWhen something like buy antibiotics comes along, local knowledge is absolutely invaluable in reaching every pocket of that community, particularly in building trust in vulnerable populations,” Iton said. €œThe state doesn’t have that, Google doesn’t have that, and certainly Blue Shield doesn’t have that.” Even the Newsom administration’s internal polling shows its efforts are faltering. €œThe resounding barrier to vaccination,” state officials wrote in the latest survey published in June, “has been confusion as a result of inconsistent, contradictory or insufficient messaging from government and public health officials.” Statewide, nearly 60% of Californians are fully vaccinated, but progress is uneven. Just 39% of eligible Black residents and 40% of Latinos had been vaccinated as of Friday, and local public health officials are intensely worried about regions like the Central Valley, where vaccination rates have stalled, especially given the threat of buy antibiotics’s dangerous delta variant.

Similar disparities exist by geography, across regions and even among neighborhoods. The state’s treatment holdouts make up a cohort that cuts across political and geographic ideologies and is dominated by Latinos, African Americans, rural residents and young people. Unlike outright treatment “rejecters,” who lean Republican, undecideds align with Democrats, according to state polling. State officials are trying to change the minds of both “undecideds” and “rejecters,” and are relying primarily on treatment lotteries with giveaways totaling $116.5 million or vacation packages, and glitzy advertising campaigns featuring paid social media influencers.

The state has awarded two $40 million contracts to high-dollar ad agencies for treatment outreach and education. Companies including Facebook, Google, Comcast and TikTok are providing free advertising on social media, radio and TV, and making charitable contributions to help the state fund its public education campaigns, state records show. Lackluster vaccination uptake drove the Newsom administration to pursue the more personal approach that public health experts favor, but the still-nascent campaign leaves out large swaths of the state. The administration launched its “Get Out the Vax” campaign in April, enlisting 70 community-based organizations and 2,000 community canvassers, now focused on Los Angeles and Central Valley neighborhoods where vaccinations have plateaued or declined.

But county public health officials say the campaign isn’t big enough to combat the treatment misinformation that has infiated regions such as California’s rural north. €œIt’s terrible,” said Placer County’s health officer, Dr. Rob Oldham, who said misinformation is driving treatments down. €œUnfortunately, the lottery didn’t really help us.

We’re working so much harder to get a dozen people vaccinated, whereas before we were doing close to 1,500 shots a day.” State Health and Human Services Secretary Mark Ghaly acknowledged that the state must boost its presence on the ground and said it “needs to do better and more.” At the same time, he and other state officials argue that the treatment lottery is working and that they are seeing progress in hard-hit neighborhoods. This month the state debuted pop-up treatment clinics at McDonald’s restaurants in 11 counties, and state-funded outreach workers have fanned out in neighborhoods such as South Los Angeles to sign people up for appointments or vaccinate takers from a roving van. treatment canvassers report that the people who don’t want the treatments say they’re concerned about safety or repeat sometimes outrageous rumors, such as the false assertion that treatments turn people into zombies. €œWe’re seeing lots of disinformation and lack of a sense of urgency,” said Yolanda Richardson, secretary of the California Government Operations Agency and Newsom’s “vaccination czar.” “The work that we have left to do is really finding out what each individual person needs to make that jump.” Carnella Marks of Oroville, in Butte County, offers a telling case of how hard public health officials must work to cut through the thick swamp of misinformation and confusion.

Carnella Marks of Oroville, California, pictured with Albert Smith, her late father-in-law, doesn’t believe buy antibiotics treatments are safe. She says she wants someone to explain how the treatments work but “nobody’s knocking on my door to talk to me or answer my questions.” (Carnella Marks) Marks, 51, who is Black, has deep misgivings about the safety of the treatments that are rooted in the country’s racist history and her personal experience. When she was pregnant with her second child, her doctor suggested she get a hysterectomy even though she wasn’t ready to stop having kids and had no health complications. She wonders if the U.S.

Government is experimenting on Black people, as it did on African American men in the Tuskegee syphilis study from the 1930s into the 1970s. €œWhy do they want us to take the treatment so bad?. € Marks asked. €œWe’ve never been first in line for anything, but now all of a sudden you want to make sure that the African American community gets the treatment?.

€ She had considered getting vaccinated because she thought it might be required for work — until government officials paused the single-dose Johnson &. Johnson shot over concerns it caused blood clots. €œI don’t care what kind of money the governor is shelling out to get me to take the treatment,” said Marks, who wants to discuss the safety of the treatments with someone who knows. But “nobody’s knocking on my door to talk to me or answer my questions.” Public health experts say it could be possible to change the minds of people like Marks with targeted and relentless outreach by trusted members of the community who acknowledge their fears and mistrust of the medical system.

A knock on the door or phone call from an epidemiologist who can explain the science behind vaccinations couldn’t hurt, they added. €œSo many of these people really aren’t treatment hesitant. They’re just trying to figure out the facts for themselves and get their questions answered,” said Oldham of Placer County. But the county can’t afford its own campaign, so Oldham said it “Placerizes” state material, adapting messaging for its residents.

€œWhat we’ve seen from the state, frankly, is a lack of investment and interest in public health,” he said. €œI think it builds trust when you have the resources to call people back and tailor a message, but honestly we don’t really have that capacity.” Santa Clara County has created advertising to persuade residents to get vaccinated.(Santa Clara County Public Health) Some counties have committed scarce funds to develop ads targeting populations among whom distrust runs rampant, an effort they say has helped boost vaccination rates. Santa Clara County, for instance, has plowed at least $8.6 million into an outreach campaign and public service announcements related to buy antibiotics since March 2020, including Spanish-language ads targeting the county’s large Latino population. Health officer Dr.

Sara Cody said the county has also enlisted the help of local health clinics, nonprofit groups and county employees of various ethnicities to develop messages that might persuade people to get vaccinated. €œWe are extraordinarily fortunate,” Cody said. €œThat investment turned out to be one of the most useful. People do have fears, and we want to hear them.” About 73% of the county’s population is fully vaccinated, while other counties with fewer public health resources, like Placer, have struggled to mount effective campaigns.

There, about 48% of residents are fully vaccinated. treatment canvassers say they are making progress by using personal stories and discussing the science behind the treatments. Ricardo Márquez, a state-funded treatment outreach worker in South Los Angeles, said he has changed minds. €œSometimes facts and science work, but sometimes people who don’t believe change their minds when I tell them people are dying, like my sweet grandma,” Márquez said.

This story was produced by KHN, which publishes California Healthline, an editorially independent service of the California Health Care Foundation. Angela Hart. ahart@kff.org, @ahartreports Related Topics Contact Us Submit a Story TipThe week before Brian Colvin was scheduled for shoulder surgery in November, he tested positive for buy antibiotics. What he thought at first was a head cold had morphed into shortness of breath and chest congestion coupled with profound fatigue and loss of balance.

Now, seven months have passed and Colvin, 44, is still waiting to feel well enough for surgery. His surgeon is concerned about risking anesthesia with his ongoing respiratory problems, while Colvin worries he’ll lose his balance and fall on his shoulder before it heals. €œWhen I last spoke with the surgeon, he said to let him know when I’m ready,” Colvin said. €œBut with all the symptoms, I’ve never felt ready for surgery.” As the number of people who have had buy antibiotics grows, medical experts are trying to determine when it’s safe for them to have elective surgery.

In addition to concerns about respiratory complications from anesthesia, buy antibiotics may affect multiple organs and systems, and clinicians are still learning the implications for surgery. A recent study compared the mortality rate in the 30 days following surgery in patients who had a buy antibiotics and in those who did not. It found that waiting to undergo surgery for at least seven weeks after a buy antibiotics reduced the risk of death to that of people who hadn’t been infected in the first place. Patients with lingering buy antibiotics symptoms should wait even longer, the study suggested.

But, as Colvin’s experience illustrates, such guideposts may be of limited use with a cipro whose effect on individual patients is so unpredictable. €œWe know that buy antibiotics has lingering effects even in people who had relatively mild disease,” said Dr. Don Goldmann, a professor at Harvard Medical School who is a senior fellow and chief scientific officer emeritus at the Institute for Healthcare Improvement. €œWe don’t know why that is.

But it’s reasonable to assume, when we decide how long we should wait before performing elective surgery, that someone’s respiratory or other systems may still be affected.” The study, published in the journal Anaesthesia in March, examined the 30-day postoperative mortality rate of more than 140,000 patients in 116 countries who had elective or emergency surgery in October. Researchers found that patients who had surgery within two weeks of their buy antibiotics diagnosis had a 4.1% adjusted mortality rate at 30 days. The rate decreased to 3.9% in those diagnosed three to four weeks before surgery, and dropped again, to 3.6%, in those who had surgery five to six weeks after their diagnosis. Patients whose surgery occurred at least seven weeks after their buy antibiotics diagnosis had a mortality rate of 1.5% 30 days after surgery, the same as for patients who were never diagnosed with the cipro.

Even after seven weeks, however, patients who still had buy antibiotics symptoms were more than twice as likely to die after surgery than people whose symptoms had resolved or who never had symptoms. Some experts said seven weeks is too arbitrary a threshold for scheduling surgery for patients who have had buy antibiotics. In addition to patients’ recovery status from the cipro, the calculus will be different for an older patient with chronic conditions who needs major heart surgery, for example, than for a generally healthy person in their 20s who needs a straightforward hernia repair. €œbuy antibiotics is just one of the things to be taken into account,” said Dr.

Kenneth Sharp, a member of the Board of Regents of the American College of Surgeons and vice chair of the Department of Surgery at Vanderbilt University Medical Center. In December, the American Society of Anesthesiologists and the Anesthesia Patient Safety Foundation issued these guidelines for timing surgery for former buy antibiotics patients. €¢ Four weeks if a patient was asymptomatic or had mild, non-respiratory symptoms. €¢ Six weeks for a symptomatic patient who wasn’t hospitalized.

€¢ Eight to 10 weeks for a symptomatic patient who has diabetes, is immunocompromised or was hospitalized. €¢ Twelve weeks for a patient who spent time in an intensive care unit. Those guidelines are not definitive, according to the groups. The operation to be performed, patients’ medical conditions and the risk of delaying surgery should all be factored in.

€œLong buy antibiotics” patients like Colvin who continue to have debilitating symptoms months after 12 weeks have passed require a more thorough evaluation before surgery, said Dr. Beverly Philip, president of the society. Now that buy antibiotics has been brought to heel in many areas and treatments are widely available, hospital operating rooms are bustling again. €œIn talking to surgical colleagues, hospitals are really busy now,” said Dr.

Avital O’Glasser, medical director of the outpatient preoperative clinic at Oregon Health and Sciences University in Portland. €œI’ve seen patients with delayed knee replacements, bariatric surgery, more advanced cancer.” At the beginning of the cipro, surgical volumes dropped dramatically as many hospitals canceled nonessential procedures and patients avoided facilities packed with buy antibiotics patients. From March to June 2020, the number of inpatient and outpatient surgeries at U.S. Hospitals was 30% lower than in the same period the year before, according to McKinsey &.

Company’s quarterly Health System Volumes Survey. By May 2021, surgical volumes had mostly rebounded, and were just 2% lower than their May 2019 totals, according to the May survey. Oregon Health and Sciences University clinicians developed a protocol a year ago for clearing any patient who had buy antibiotics for elective surgery. When obtaining patients’ medical history and conducting physical exams, clinicians look for signs of buy antibiotics complications that aren’t readily identifiable and determine whether patients have returned to their pre-buy antibiotics level of health.

The pre-op exam also includes lab and other tests that evaluate cardiopulmonary function, coagulation status, inflammation markers and nutrition, all of which can be disrupted by buy antibiotics. If the assessment raises no red flags, patients can be cleared for surgery once they have waited the minimum seven weeks since their buy antibiotics diagnosis. Originally, the minimum wait for surgery was four weeks, but clinicians pushed it back to seven after the international study was published, O’Glasser said. €œWe are still learning about buy antibiotics, and uncertainty in medicine is one of the biggest challenges we face,” said O’Glasser.

€œRight now, our team is erring on the side of caution.” At Memorial Sloan Kettering Cancer Center in New York, doctors don’t follow a specific protocol. €œWe’re taking every patient one at a time. There are no hard-and-fast rules at this institution,” said Dr. Jeffrey Drebin, chair of surgery.

Clinicians work to find a balance between the urgency of the cancer surgery and the need to allow enough time to ensure buy antibiotics recovery, he said. For Brian Colvin, whose right rotator cuff is torn, delaying surgery is painful and may worsen the tear. But the rest of his life is on hold, too. A sales representative for an auto parts company, he hasn’t been able to work since he got sick.

His balance problems make him reluctant to stray far from his home in Crest Hill, Illinois, the Chicago suburb where he lives with his wife and 15-year-old son. Some days he has more energy and isn’t as short of breath as others. Colvin hopes it’s a sign he’s slowly improving. But at this point, it’s hard to be optimistic about the cipro.

€œIt’s always something,” he said. Michelle Andrews. andrews.khn@gmail.com, @mandrews110 Related Topics Contact Us Submit a Story Tip.

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Start Preamble Food and Drug Administration, Health and Human farmacia cipro Services (HHS). Notice. The Food and Drug Administration (FDA) is announcing the issuance of four Emergency farmacia cipro Use Authorizations (EUAs) (the Authorizations) for drugs for use during the buy antibiotics cipro. FDA issued four Authorizations under the Federal Food, Drug, and Cosmetic Act (FD&C Act), as requested by the Department of Health and Human Services (HHS) Biomedical Advanced Research and Development Authority (BARDA), Fresenius Medical Care, Gilead Sciences, Inc., and Fresenius Kabi USA, LLC. The Authorizations contain, among other things, conditions on the emergency use of the authorized drugs.

The Authorizations follow the February farmacia cipro 4, 2020, determination by the Secretary of HHS that there is a public health emergency that has a significant potential to affect national security or the health and security of U.S. Citizens living abroad and that involves a novel (new) antibiotics. The cipro is now named antibiotics, which causes the illness buy antibiotics. On the basis of such determination, the Secretary of HHS declared on March 27, 2020, that circumstances exist justifying the authorization of emergency use of drugs and biological products during the buy antibiotics cipro, pursuant to the FD&C Act, subject to the terms farmacia cipro of any authorization issued under that section. FDA is also announcing the subsequent revocation of the Authorization issued to BARDA for oral formulations of chloroquine phosphate and hydroxychloroquine sulfate.

FDA revoked this authorization on June 15, 2020. The Authorizations, and the farmacia cipro revocation, which include an explanation of the reasons for issuance or revocation, are reprinted in this document. The Authorization for BARDA was effective as of March 28, 2020, and the revocation of this Authorization is effective as of June 15, 2020. The Authorization for Fresenius Medical Care is effective as of April 30, 2020. The Authorization farmacia cipro for Gilead Sciences, Inc.

Is effective as of May 1, 2020. The Authorization for Fresenius Kabi USA, LLC is effective as of May 8, 2020. Submit written requests for single copies of the EUAs to the Office of Counterterrorism and Emerging Threats, Food and Drug Administration, 10903 New Hampshire farmacia cipro Ave., Bldg. 1, Rm. 4338, Silver Spring, MD 20993-0002.

Send one self-addressed adhesive farmacia cipro label to assist that office in processing your request or include a Fax number to which the Authorizations may be sent. See the SUPPLEMENTARY INFORMATION section for electronic access to the Authorizations. Start Further Info Michael Mair, Office of Counterterrorism and Emerging Threats, Food and Drug Administration, 10903 New Hampshire Ave., Bldg. 1, Rm farmacia cipro. 4332, Silver Spring, MD 20993-0002, 301-796-8510 (this is not a toll free number).

End Further Info End Preamble Start Supplemental Information I. Background Section farmacia cipro 564 of the FD&C Act (21 U.S.C. 360bbb-3) allows FDA to strengthen the public health protections against biological, chemical, nuclear, and radiological agents. Among other things, section 564 of the FD&C Act allows FDA to authorize the use of an unapproved medical product or an unapproved use of an farmacia cipro approved medical product in certain situations. With this EUA authority, FDA can help ensure that medical countermeasures may be used in emergencies to diagnose, treat, or prevent serious or life-threatening diseases or conditions caused by biological, chemical, nuclear, or radiological agents when there are no adequate, approved, and available alternatives.

II. Criteria for EUA Authorization Section 564(b)(1) of the FD&C Act provides farmacia cipro that, before an EUA may be issued, the Secretary of HHS must declare that circumstances exist justifying the authorization based on one of the following grounds. (1) A determination by the Secretary of Homeland Security that there is a domestic emergency, or a significant potential for a domestic emergency, involving a heightened risk of attack with a biological, chemical, radiological, or nuclear agent or agents. (2) a determination by the Secretary of Defense that there is a military emergency, or a significant potential for a military emergency, involving a heightened risk to U.S. Military forces, including personnel operating under the authority of title 10 or title 50, United States Code, of attack with farmacia cipro (i) a biological, chemical, radiological, or nuclear agent or agents.

Or (ii) an agent or agents that may cause, or are otherwise associated with, an imminently life-threatening and specific risk to U.S. Military forces; [] (3) a determination by the Secretary of HHS that there is a public health emergency, or a significant potential for a public health emergency, that affects, or has a significant potential to affect, national security or the health and security of U.S. Citizens living farmacia cipro abroad, and that involves a biological, chemical, radiological, or nuclear agent or agents, or a disease or condition that may be attributable to such agent or agents. Or (4) the identification of a material threat by the Secretary of Homeland Security pursuant to section 319F-2 of the Public Health Service (PHS) Act (42 U.S.C. 247d-6b) sufficient to affect national security or the health and security of U.S.

Citizens living farmacia cipro abroad. Once the Secretary of HHS has declared that circumstances exist justifying an authorization under section 564 of the FD&C Act, FDA may authorize the emergency use of a drug, device, or biological product if the Agency concludes that the statutory criteria are satisfied. Under section 564(h)(1) of the FD&C Act, FDA is required to publish in the Federal Register a notice of each authorization, and each termination or revocation of an authorization, and an explanation of the reasons for the action. Section 564 of the FD&C Act permits FDA to authorize the introduction into interstate commerce of Start Printed Page 56232a drug, device, or biological product intended for use when the farmacia cipro Secretary of HHS has declared that circumstances exist justifying the authorization of emergency use. Products appropriate for emergency use may include products and uses that are not approved, cleared, or licensed under sections 505, 510(k), 512, or 515 of the FD&C Act (21 U.S.C.

355, 360(k), 360b, and 360e) or section 351 of the PHS Act (42 U.S.C. 262), or conditionally farmacia cipro approved under section 571 of the FD&C Act (21 U.S.C. 360ccc). FDA may issue an EUA only if, after consultation with the HHS Assistant Secretary for Preparedness and Response, the Director of the National Institutes of Health, and the Director of the Centers for Disease Control and Prevention (to the extent feasible and appropriate given the applicable circumstances), FDA [] concludes. (1) That an agent farmacia cipro referred to in a declaration of emergency or threat can cause a serious or life-threatening disease or condition.

(2) that, based on the totality of scientific evidence available to FDA, including data from adequate and well-controlled clinical trials, if available, it is reasonable to believe that. (A) The product may be effective in diagnosing, treating, or preventing (i) such disease or farmacia cipro condition. Or (ii) a serious or life-threatening disease or condition caused by a product authorized under section 564, approved or cleared under the FD&C Act, or licensed under section 351 of the PHS Act, for diagnosing, treating, or preventing such a disease or condition caused by such an agent. And (B) the known and potential benefits of the product, when used to diagnose, prevent, or treat such disease or condition, outweigh the known and potential risks of the product, taking into consideration the material threat posed by the agent or agents identified in a declaration under section 564(b)(1)(D) of the FD&C Act, if applicable. (3) that there farmacia cipro is no adequate, approved, and available alternative to the product for diagnosing, preventing, or treating such disease or condition.

(4) in the case of a determination described in section 564(b)(1)(B)(ii), that the request for emergency use is made by the Secretary of Defense. And (5) that such other criteria as may be prescribed by regulation are satisfied. No other farmacia cipro criteria for issuance have been prescribed by regulation under section 564(c)(4) of the FD&C Act. III. The Authorizations The Authorizations follow the February 4, 2020, determination by the Secretary of HHS that there is a public health emergency that has a significant potential to affect national security or the health and security of U.S.

Citizens living abroad and that farmacia cipro involves a novel (new) antibiotics. The cipro is now named antibiotics, which causes the illness buy antibiotics. Notice of the Secretary's determination was provided in the Federal Register on February 7, 2020 (85 FR 7316). On the basis of such determination, the Secretary of HHS declared on March 27, 2020, that circumstances exist farmacia cipro justifying the authorization of emergency use of drugs and biological products during the buy antibiotics cipro, pursuant to section 564 of the FD&C Act, subject to the terms of any authorization issued under that section. Notice of the Secretary's declaration was provided in the Federal Register on April 1, 2020 (85 FR 18250).

Having concluded that the criteria for issuance of the Authorizations under section 564(c) of the FD&C Act are met, FDA has issued four authorizations for the emergency use of drugs during the buy antibiotics cipro. On March 28, 2020, FDA issued an EUA to BARDA for oral formulations of chloroquine phosphate and hydroxychloroquine sulfate, subject to the farmacia cipro terms of the Authorization. On April 30, 2020, FDA issued an EUA to Fresenius Medical Care for multiFiltrate PRO System and multiBic/multiPlus Solutions, subject to the terms of the Authorization. On May 1, 2020, FDA issued an EUA to Gilead Sciences, Inc. For remdesivir, subject to the terms of the farmacia cipro Authorization.

On May 8, 2020, FDA issued an EUA to Fresenius Kabi USA, LLC for Fresenius Propoven 2% Emulsion, subject to the terms of the Authorization. The Authorizations in their entirety (not including the authorized versions of the fact sheets and other written materials) follow, below section VI Electronic Access, and provide an explanation of the reasons for issuance, as required by section 564(h)(1) of the FD&C Act. IV. EUA Criteria for Issuance No Longer Met Under section 564(g)(2) of the FD&C Act, the Secretary of HHS may revoke an EUA if, among other things, the criteria for issuance are no longer met. On June 15, 2020, FDA revoked the EUA for BARDA for oral formulations of chloroquine phosphate and hydroxychloroquine sulfate because the criteria for issuance were no longer met.

Under section 564(c)(2) of the FD&C Act, an EUA may be issued only if FDA concludes that, based on the totality of scientific evidence available to the Secretary, including data from adequate and well-controlled clinical trials, if available, it is reasonable to believe that. (1) The product may be effective in diagnosing, treating, or preventing such disease or condition and (2) the known and potential benefits of the product, when used to diagnose, prevent, or treat such disease or condition, outweigh the known and potential risks of the product. Based on a review of new information and a reevaluation of information available at the time the EUA was issued, FDA now concludes it is no longer reasonable to believe that (1) oral formulations of chloroquine phosphate and hydroxychloroquine sulfate may be effective in treating buy antibiotics for the uses authorized in the EUA, or (2) the known and potential benefits of these products outweigh their known and potential risks for those uses. Accordingly, FDA revokes the EUA for emergency use of chloroquine phosphate and hydroxychloroquine sulfate to treat buy antibiotics, pursuant to section 564(g)(2) of the FD&C Act. V.

The Revocation Having concluded that the criteria for revocation of the Authorization under section 564(g) of the FD&C Act are met, FDA has revoked the EUA for BARDA's oral formulations of chloroquine phosphate and hydroxychloroquine sulfate. The revocation in its entirety follows, below section VI. Electronic Access, and provides an explanation of the reasons for revocation, as required by section 564(h)(1) of the FD&C Act. VI. Electronic Access An electronic version of this document and the full text of the Authorizations and revocation are available on the internet at https://www.fda.gov/​emergency-preparedness-and-response/​mcm-legal-regulatory-and-policy-framework/​emergency-use-authorization.

Start Printed Page 56233 Start Printed Page 56234 Start Printed Page 56235 Start Printed Page 56236 Start Printed Page 56237 Start Printed Page 56238 Start Printed Page 56239 Start Printed Page 56240 Start Printed Page 56241 Start Printed Page 56242 Start Printed Page 56243 Start Printed Page 56244 Start Printed Page 56245 Start Printed Page 56246 Start Printed Page 56247 Start Printed Page 56248 Start Printed Page 56249 Start Printed Page 56250 Start Printed Page 56251 Start Printed Page 56252 Start Printed Page 56253 Start Printed Page 56254 Start Printed Page 56255 Start Printed Page 56256 Start Printed Page 56257 Start Printed Page 56258 Start Printed Page 56259 Start Printed Page 56260 Start Printed Page 56261 Start Printed Page 56262 Start Printed Page 56263 Start Printed Page 56264 Start Signature Dated. September 3, 2020. Lowell J. Schiller, Principal Associate Commissioner for Policy. End Signature End Supplemental Information BILLING CODE 4164-01-P[FR Doc.

2020-20041 Filed 9-10-20. 8:45 am]BILLING CODE 4164-01-CAlmost one-third of households report difficulty paying their energy bills or adequately heating and cooling their homes. And more than 20 percent—roughly 25 million households—report reducing or forgoing necessities such as food and medicine to pay an energy bill. African-American families and rural households are more likely than other groups to spend a high percentage of household income on energy. It’s time for states and communities to put policies in place that will improve energy affordability and access and advance energy equity.On the Pine Ridge Indian Reservation in remote South Dakota, where many tribal residents live without electricity in their homes, community members are tackling this problem head on.

Pine Ridge received its first transmission line in 2018, but the cost of installing lines and meters has been prohibitive for many households, given that more than half the reservation lives below the poverty line. In the late 1990s, community member and entrepreneur Henry Red Cloud partnered with the Colorado nonprofit Trees, Water &. People, which had foundation funding to install portable solar heating systems in Pine Ridge at no cost to homeowners. As of November 2019, 500 homes had Red Cloud’s off-grid solar furnaces and they have reduced their heating costs by up to 30 percent.In the face of buy antibiotics, municipalities, corporations and community organizations have stepped up to address inequities in utility services—from free internet access for K-12 and college students, to bans on water and energy shut offs for people unable to pay their bills. Yet many of these protections are set to expire on arbitrary dates even though the need for them will surely continue.

While the imperative to make access to utility services more equitable became more urgent during the cipro, the real challenge is making them affordable and accessible over the long term. As the nation begins building toward an equitable and lasting recovery, we must ensure everyone’s basic needs for water, energy, and Internet are met, and that investments in infrastructure are advanced with an equity frame. Returning to the way things were is not acceptable.To build healthier communities, we must advance equitable public infrastructure. Learn more about the connection between public infrastructure and health equity..

Start Preamble Food buying cipro in usa and Drug Administration, Health and Human Services where to get cipro (HHS). Notice. The Food and Drug Administration (FDA) where to get cipro is announcing the issuance of four Emergency Use Authorizations (EUAs) (the Authorizations) for drugs for use during the buy antibiotics cipro.

FDA issued four Authorizations under the Federal Food, Drug, and Cosmetic Act (FD&C Act), as requested by the Department of Health and Human Services (HHS) Biomedical Advanced Research and Development Authority (BARDA), Fresenius Medical Care, Gilead Sciences, Inc., and Fresenius Kabi USA, LLC. The Authorizations contain, among other things, conditions on the emergency use of the authorized drugs. The Authorizations follow the February 4, 2020, determination by the Secretary where to get cipro of HHS that there is a public health emergency that has a significant potential to affect national security or the health and security of U.S.

Citizens living abroad and that involves a novel (new) antibiotics. The cipro is now named antibiotics, which causes the illness buy antibiotics. On the basis of such determination, the Secretary where to get cipro of HHS declared on March 27, 2020, that circumstances exist justifying the authorization of emergency use of drugs and biological products during the buy antibiotics cipro, pursuant to the FD&C Act, subject to the terms of any authorization issued under that section.

FDA is also announcing the subsequent revocation of the Authorization issued to BARDA for oral formulations of chloroquine phosphate and hydroxychloroquine sulfate. FDA revoked this authorization on June 15, 2020. The Authorizations, and the revocation, which include an explanation of the reasons for issuance or revocation, are where to get cipro reprinted in this document.

The Authorization for BARDA was effective as of March 28, 2020, and the revocation of this Authorization is effective as of June 15, 2020. The Authorization for Fresenius Medical Care is effective as of April 30, 2020. The Authorization for Gilead where to get cipro Sciences, Inc.

Is effective as of May 1, 2020. The Authorization for Fresenius Kabi USA, LLC is effective as of May 8, 2020. Submit written where to get cipro requests for single copies of the EUAs to the Office of Counterterrorism and Emerging Threats, Food and Drug Administration, 10903 New Hampshire Ave., Bldg.

1, Rm. 4338, Silver Spring, MD 20993-0002. Send one self-addressed adhesive label to assist that office in processing your request or include a where to get cipro Fax number to which the Authorizations may be sent.

See the SUPPLEMENTARY INFORMATION section for electronic access to the Authorizations. Start Further Info Michael Mair, Office of Counterterrorism and Emerging Threats, Food and Drug Administration, 10903 New Hampshire Ave., Bldg. 1, Rm where to get cipro.

4332, Silver Spring, MD 20993-0002, 301-796-8510 (this is not a toll free number). End Further Info End Preamble Start Supplemental Information I. Background Section 564 of the FD&C where to get cipro Act (21 U.S.C.

360bbb-3) allows FDA to strengthen the public health protections against biological, chemical, nuclear, and radiological agents. Among other things, section 564 of the FD&C Act allows FDA to authorize the use of an unapproved medical product or an where to get cipro unapproved use of an approved medical product in certain situations. With this EUA authority, FDA can help ensure that medical countermeasures may be used in emergencies to diagnose, treat, or prevent serious or life-threatening diseases or conditions caused by biological, chemical, nuclear, or radiological agents when there are no adequate, approved, and available alternatives.

II. Criteria for EUA Authorization Section 564(b)(1) of the FD&C Act provides that, before an EUA may be issued, the Secretary of HHS must declare that circumstances exist justifying the authorization based on one of the following where to get cipro grounds. (1) A determination by the Secretary of Homeland Security that there is a domestic emergency, or a significant potential for a domestic emergency, involving a heightened risk of attack with a biological, chemical, radiological, or nuclear agent or agents.

(2) a determination by the Secretary of Defense that there is a military emergency, or a significant potential for a military emergency, involving a heightened risk to U.S. Military forces, including personnel operating under the authority of title 10 or title 50, United States where to get cipro Code, of attack with (i) a biological, chemical, radiological, or nuclear agent or agents. Or (ii) an agent or agents that may cause, or are otherwise associated with, an imminently life-threatening and specific risk to U.S.

Military forces; [] (3) a determination by the Secretary of HHS that there is a public health emergency, or a significant potential for a public health emergency, that affects, or has a significant potential to affect, national security or the health and security of U.S. Citizens living abroad, and that involves a biological, chemical, radiological, or nuclear where to get cipro agent or agents, or a disease or condition that may be attributable to such agent or agents. Or (4) the identification of a material threat by the Secretary of Homeland Security pursuant to section 319F-2 of the Public Health Service (PHS) Act (42 U.S.C.

247d-6b) sufficient to affect national security or the health and security of U.S. Citizens living abroad where to get cipro. Once the Secretary of HHS has declared that circumstances exist justifying an authorization under section 564 of the FD&C Act, FDA may authorize the emergency use of a drug, device, or biological product if the Agency concludes that the statutory criteria are satisfied.

Under section 564(h)(1) of the FD&C Act, FDA is required to publish in the Federal Register a notice of each authorization, and each termination or revocation of an authorization, and an explanation of the reasons for the action. Section 564 of the FD&C Act permits FDA to authorize the introduction into interstate commerce of Start Printed Page 56232a drug, device, or biological product intended where to get cipro for use when the Secretary of HHS has declared that circumstances exist justifying the authorization of emergency use. Products appropriate for emergency use may include products and uses that are not approved, cleared, or licensed under sections 505, 510(k), 512, or 515 of the FD&C Act (21 U.S.C.

355, 360(k), 360b, and 360e) or section 351 of the PHS Act (42 U.S.C. 262), or conditionally approved under section 571 of where to get cipro the FD&C Act (21 U.S.C. 360ccc).

FDA may issue an EUA only if, after consultation with the HHS Assistant Secretary for Preparedness and Response, the Director of the National Institutes of Health, and the Director of the Centers for Disease Control and Prevention (to the extent feasible and appropriate given the applicable circumstances), FDA [] concludes. (1) That an agent referred where to get cipro to in a declaration of emergency or threat can cause a serious or life-threatening disease or condition. (2) that, based on the totality of scientific evidence available to FDA, including data from adequate and well-controlled clinical trials, if available, it is reasonable to believe that.

(A) The product may be effective in where to get cipro diagnosing, treating, or preventing (i) such disease or condition. Or (ii) a serious or life-threatening disease or condition caused by a product authorized under section 564, approved or cleared under the FD&C Act, or licensed under section 351 of the PHS Act, for diagnosing, treating, or preventing such a disease or condition caused by such an agent. And (B) the known and potential benefits of the product, when used to diagnose, prevent, or treat such disease or condition, outweigh the known and potential risks of the product, taking into consideration the material threat posed by the agent or agents identified in a declaration under section 564(b)(1)(D) of the FD&C Act, if applicable.

(3) that where to get cipro there is no adequate, approved, and available alternative to the product for diagnosing, preventing, or treating such disease or condition. (4) in the case of a determination described in section 564(b)(1)(B)(ii), that the request for emergency use is made by the Secretary of Defense. And (5) that such other criteria as may be prescribed by regulation are satisfied.

No other criteria for issuance have been where to get cipro prescribed by regulation under section 564(c)(4) of the FD&C Act. III. The Authorizations The Authorizations follow the February 4, 2020, determination by the Secretary of HHS that there is a public health emergency that has a significant potential to affect national security or the health and security of U.S.

Citizens living abroad and where to get cipro that involves a novel (new) antibiotics. The cipro is now named antibiotics, which causes the illness buy antibiotics. Notice of the Secretary's determination was provided in the Federal Register on February 7, 2020 (85 FR 7316).

On the basis of such determination, the Secretary of HHS declared on March 27, 2020, that circumstances exist justifying the authorization of emergency use of drugs and biological products during the buy antibiotics cipro, pursuant to section 564 of the FD&C Act, subject to the terms of any where to get cipro authorization issued under that section. Notice of the Secretary's declaration was provided in the Federal Register on April 1, 2020 (85 FR 18250). Having concluded that the criteria for issuance of the Authorizations under section 564(c) of the FD&C Act are met, FDA has issued four authorizations for the emergency use of drugs during the buy antibiotics cipro.

On March 28, 2020, where to get cipro FDA issued an EUA to BARDA for oral formulations of chloroquine phosphate and hydroxychloroquine sulfate, subject to the terms of the Authorization. On April 30, 2020, FDA issued an EUA to Fresenius Medical Care for multiFiltrate PRO System and multiBic/multiPlus Solutions, subject to the terms of the Authorization. On May 1, 2020, FDA issued an EUA to Gilead Sciences, Inc.

For remdesivir, subject to the where to get cipro terms of the Authorization. On May 8, 2020, FDA issued an EUA to Fresenius Kabi USA, LLC for Fresenius Propoven 2% Emulsion, subject to the terms of the Authorization. The Authorizations in their entirety (not including the authorized versions of the fact sheets and other written materials) follow, below section VI Electronic Access, and provide an explanation of the reasons for issuance, as required by section 564(h)(1) of the FD&C Act.

IV. EUA Criteria for Issuance No Longer Met Under section 564(g)(2) of the FD&C Act, the Secretary of HHS may revoke an EUA if, among other things, the criteria for issuance are no longer met. On June 15, 2020, FDA revoked the EUA for BARDA for oral formulations of chloroquine phosphate and hydroxychloroquine sulfate because the criteria for issuance were no longer met.

Under section 564(c)(2) of the FD&C Act, an EUA may be issued only if FDA concludes that, based on the totality of scientific evidence available to the Secretary, including data from adequate and well-controlled clinical trials, if available, it is reasonable to believe that. (1) The product may be effective in diagnosing, treating, or preventing such disease or condition and (2) the known and potential benefits of the product, when used to diagnose, prevent, or treat such disease or condition, outweigh the known and potential risks of the product. Based on a review of new information and a reevaluation of information available at the time the EUA was issued, FDA now concludes it is no longer reasonable to believe that (1) oral formulations of chloroquine phosphate and hydroxychloroquine sulfate may be effective in treating buy antibiotics for the uses authorized in the EUA, or (2) the known and potential benefits of these products outweigh their known and potential risks for those uses.

Accordingly, FDA revokes the EUA for emergency use of chloroquine phosphate and hydroxychloroquine sulfate to treat buy antibiotics, pursuant to section 564(g)(2) of the FD&C Act. V. The Revocation Having concluded that the criteria for revocation of the Authorization under section 564(g) of the FD&C Act are met, FDA has revoked the EUA for BARDA's oral formulations of chloroquine phosphate and hydroxychloroquine sulfate.

The revocation in its entirety follows, below section VI. Electronic Access, and provides an explanation of the reasons for revocation, as required by section 564(h)(1) of the FD&C Act. VI.

Electronic Access An electronic version of this document and the full text of the Authorizations and revocation are available on the internet at https://www.fda.gov/​emergency-preparedness-and-response/​mcm-legal-regulatory-and-policy-framework/​emergency-use-authorization. Start Printed Page 56233 Start Printed Page 56234 Start Printed Page 56235 Start Printed Page 56236 Start Printed Page 56237 Start Printed Page 56238 Start Printed Page 56239 Start Printed Page 56240 Start Printed Page 56241 Start Printed Page 56242 Start Printed Page 56243 Start Printed Page 56244 Start Printed Page 56245 Start Printed Page 56246 Start Printed Page 56247 Start Printed Page 56248 Start Printed Page 56249 Start Printed Page 56250 Start Printed Page 56251 Start Printed Page 56252 Start Printed Page 56253 Start Printed Page 56254 Start Printed Page 56255 Start Printed Page 56256 Start Printed Page 56257 Start Printed Page 56258 Start Printed Page 56259 Start Printed Page 56260 Start Printed Page 56261 Start Printed Page 56262 Start Printed Page 56263 Start Printed Page 56264 Start Signature Dated. September 3, 2020.

Lowell J. Schiller, Principal Associate Commissioner for Policy. End Signature End Supplemental Information BILLING CODE 4164-01-P[FR Doc.

2020-20041 Filed 9-10-20. 8:45 am]BILLING CODE 4164-01-CAlmost one-third of households report difficulty paying their energy bills or adequately heating and cooling their homes. And more than 20 percent—roughly 25 million households—report reducing or forgoing necessities such as food and medicine to pay an energy bill.

African-American families and rural households are more likely than other groups to spend a high percentage of household income on energy. It’s time for states and communities to put policies in place that will improve energy affordability and access and advance energy equity.On the Pine Ridge Indian Reservation in remote South Dakota, where many tribal residents live without electricity in their homes, community members are tackling this problem head on. Pine Ridge received its first transmission line in 2018, but the cost of installing lines and meters has been prohibitive for many households, given that more than half the reservation lives below the poverty line.

In the late 1990s, community member and entrepreneur Henry Red Cloud partnered with the Colorado nonprofit Trees, Water &. People, which had foundation funding to install portable solar heating systems in Pine Ridge at no cost to homeowners. As of November 2019, 500 homes had Red Cloud’s off-grid solar furnaces and they have reduced their heating costs by up to 30 percent.In the face of buy antibiotics, municipalities, corporations and community organizations have stepped up to address inequities in utility services—from free internet access for K-12 and college students, to bans on water and energy shut offs for people unable to pay their bills.

Yet many of these protections are set to expire on arbitrary dates even though the need for them will surely continue. While the imperative to make access to utility services more equitable became more urgent during the cipro, the real challenge is making them affordable and accessible over the long term. As the nation begins building toward an equitable and lasting recovery, we must ensure everyone’s basic needs for water, energy, and Internet are met, and that investments in infrastructure are advanced with an equity frame.

Returning to the way things were is not acceptable.To build healthier communities, we must advance equitable public infrastructure. Learn more about the connection between public infrastructure and health equity..

What should my health care professional know before I take Cipro?

They need to know if you have any of these conditions:

  • child with joint problems
  • heart condition
  • kidney disease
  • liver disease
  • seizures disorder
  • an unusual or allergic reaction to ciprofloxacin, other antibiotics or medicines, foods, dyes, or preservatives
  • pregnant or trying to get pregnant
  • breast-feeding

Can cipro cause yeast

How to cite can cipro cause yeast this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly can cipro cause yeast publicized events in our country.

Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went can cipro cause yeast into a frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private can cipro cause yeast and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly started getting distress calls from their patients in despair with can cipro cause yeast increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication can cipro cause yeast of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and also can cipro cause yeast his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding can cipro cause yeast the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists and mental health professionals were called can cipro cause yeast by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and can cipro cause yeast “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, can cipro cause yeast but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for can cipro cause yeast interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” can cipro cause yeast as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 can cipro cause yeast 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically.

Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods. These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies.

And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies.

The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness.

However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT.

Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past.

In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain.

The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al.

Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies.

In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al. In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala.

In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al.

In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al.

Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al.

In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered. Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT.

In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable.

The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite.

However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis.

Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT.

Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique.

In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al.

In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied.

In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus. This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT.

However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT.

Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests.

Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al.

In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail. And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this.

These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood.

Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J.

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Objective cognitive performance associated with electroconvulsive therapy for depression. A systematic review and meta-analysis. Biol Psychiatry 2010;68:568-77.

58.Tulving E, Madigan SA. Memory and verbal learning. Annu Rev Psychol 1970;21:437-84.

59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy. Systematic review.

BMJ 2003;326:1363. 60.Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy.

Historical perspective and current issues. J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP.

The effect of electroconvulsive therapy on autobiographical memory. A systematic review. J ECT 2008;24:10-7.

62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 1975;32:1557-64.

63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction. A prospective three-year follow-up study.

Br J Psychiatry 1983;142:1-8. 64.Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy.

Long-term follow-up. Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC.

Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument. Biol Psychiatry 1979;14:791-801.

66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33.

67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000;57:425-34.

68.Abrams R. Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3.

69.Peretti CS, Danion JM, Grangé D, Mobarek N. Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study.

J Affect Disord 1996;41:9-15. 70.Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects.

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints.

A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32. 72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al.

Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46. 73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ.

Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ.

Subjective memory complaints prior to and following electroconvulsive therapy. Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A.

A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24. 77.Brodaty H, Hickie I, Mason C, Prenter L.

A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB.

Electroconvulsive therapy and risk of dementia in patients with affective disorders. A cohort study. Lancet Psychiatry 2018;5:348-56.

Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

How to where to get cipro cite this article:Singh O P http://theorganicrabbit.com/paleo-spicy-cashew-chicken/. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J where to get cipro Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, news channels, and social media were full of stories providing where to get cipro minute details of the suicidal act.

Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the where to get cipro process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly where to get cipro started getting distress calls from their patients in despair with increased suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health where to get cipro Organization report on Preventing Suicide. A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and also where to get cipro his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure where to get cipro ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists where to get cipro and mental health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading where to get cipro concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the where to get cipro American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions. Methods and principles of interaction with media should form a part of our training curriculum.

Many professional societies have guidelines and resource books for interacting with where to get cipro media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the where to get cipro media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, where to get cipro Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage. This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update. Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al.

In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question.

Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today.

The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h.

This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies. Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms. Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms.

Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population.

It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder. The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower. However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover.

Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies.

It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results.

The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al.

Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity. A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development. The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect.

It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia.

It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT. One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect. This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT.

However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy.

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A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

Cipro tendon rupture incidence

AdvertisementContinue reading the main storySupported byContinue reading the main storyThe Other Side of Languishing Is Flourishing cipro tendon rupture incidence. Here’s How to Get There.Research shows that the cipro took a toll on our overall well-being and left many of us drained. Here are seven simple steps to cipro tendon rupture incidence get you thriving again.Credit...Cristina SpanòMay 4, 2021With vaccination rates on the rise, hope is in the air. But after a year of trauma, isolation and grief, how long will it take before life finally — finally — feels good?.

Post-cipro, the answer to that question may be in your own cipro tendon rupture incidence hands. A growing body of research shows that there are simple steps you can take to recharge your emotional batteries and spark a sense of fulfillment, purpose and happiness. The psychology community cipro tendon rupture incidence calls this lofty combination of physical, mental and emotional fitness “flourishing.” It is the exact opposite of languishing, that sense of stagnation Adam Grant wrote about recently for The Times.“Flourishing really is what people are ultimately after,” said Tyler J. VanderWeele, an epidemiology and biostatistics professor and director of Harvard’s Human Flourishing Program.

€œIt’s living cipro tendon rupture incidence the good life. We usually think about flourishing as living in a state in which all aspects of a person’s life are good — it’s really an all-encompassing notion.”The good news is that the scientific evidence related to flourishing is robust, and numerous studies show simple activities can lead to marked improvement in overall well-being. Here are some practical activities, backed cipro tendon rupture incidence by science, that can help you get started.Assess yourself.First, how do you know if you’re languishing, flourishing or somewhere in between?. Simply asking someone is an effective diagnostic tool, said Laurie Santos, a psychology professor at Yale who teaches a free 10-week course called “The Science of Well-Being.” Do you wake up ready to start your day or would you rather go back to sleep?.

Do you have a sense of purpose or do you find how you spend much of your day to be meaningless? cipro tendon rupture incidence. “You are kind of the expert on your own sense of flourishing,” she said.Dr. VanderWeele uses a 10-question cipro tendon rupture incidence assessment in his program at Harvard, which you can try here. Participants rate five areas of their lives on a scale of one to 10, with questions focusing on happiness and life satisfaction, physical and mental health, meaning and purpose, character and virtue and close social relationships.

Just taking the quiz and reflecting on the questions it asks cipro tendon rupture incidence can put you on a path to making positive changes, Dr. VanderWeele said.Savor and celebrate small things.After a year of Zoom birthday parties and virtual graduations, many of us want to revel in gathering together again. Celebrations help to create cipro tendon rupture incidence and cement relationships. €œIt’s really important that post-cipro we embrace more and more celebrating,” Dr.

VanderWeele said.But it’s not just the big occasions that should be cipro tendon rupture incidence marked. Acknowledging small moments is also important for well-being, research shows. Psychologists call it “savoring.” Savoring is about appreciating an event or activity in the moment, sharing tiny victories and noticing the good things around you.A 2012 study of college students found that taking part in a savoring activity called “mindful photography” resulted in overall improvements in mood and cipro tendon rupture incidence a significantly greater sense of appreciation for college life. The students were instructed to take at least five photos of their everyday lives — friends, their favorite view on campus, books they enjoyed — twice a week for two weeks.

Reflecting on the photos, and the small moments that brought them joy, helped the students focus on the good in their lives.If snapping photos of your favorite things sounds like too much work, research shows you also benefit when you savor enjoyable experiences like luxuriating in a warm bath, spending the day with your best friend or cipro tendon rupture incidence taking an “awe” walk.Try “Sunday dinner gratitude.”Some people expressed gratitude more during the cipro, whether it was clapping for health care workers or thanking a grocery checkout person. But creating a weekly gratitude ritual can cement the habit. Numerous studies show that taking time to reflect on what we’re grateful for improves our quality of life.In a 2003 cipro tendon rupture incidence study, researchers instructed college students to list, once a week, five things they were grateful for, both big and small. (Some wrote that they were grateful for waking up that morning.

One included gratitude for the Rolling Stones.) Compared to a control group, the students cipro tendon rupture incidence assigned to the gratitude intervention for 10 weeks had better feelings about life as a whole and fewer physical complaints.A gratitude practice should not be a burden. Try to stack a new gratitude habit on a weekly ritual — like Sunday dinner with family. Taking out the trash, cipro tendon rupture incidence or your weekly grocery run.Do five good deeds.Acts of kindness not only help others, they also can help you flourish. Research shows that performing five acts of kindness in a single day, once a week, can have a powerful effect.

A 2004 study showed that when college students spent a day doing five acts of kindness — like cipro tendon rupture incidence donating blood, helping a friend with a paper or writing a thank you note to a former professor — they experienced more significant increases in well-being than those who spread out five kind things over the course of a week.Volunteer work can also improve well being. Dr. VanderWeele and other researchers looked at data from a cohort of nearly 13,000 older adults and found that participants who volunteered at least two hours cipro tendon rupture incidence a week during the study period experienced higher levels of happiness, optimism and purpose in life, compared to those who did not volunteer at all.To make it easy, Dr. Grant recommends starting off with a daily “five-minute favor,” like introducing two people who could benefit from knowing each other, or sending an article or podcast link to a friend, saying you were thinking of them.Look for communities and connection.Even a quick chat with a stranger or a momentary bond with someone new can foster a sense of fulfillment, particularly when what researchers call a high quality connection occurs.

€œThey don’t cipro tendon rupture incidence have to be lasting relationships or long interactions,” Dr. Grant said. €œSometimes people feel an extra spring in their step when they talk to a stranger on a plane or a subway, or when somebody greets them at a restaurant.”Moments of being seen by other people, and being met with respect or even enthusiasm, can energize and invigorate us and help create bonds within cipro tendon rupture incidence our neighborhood or community.As you emerge from cipro life, try to reconnect with a community you’ve missed. It might be going back to church or choir practice, a running group or yoga class or even just hanging out at your local coffee shop.

And don’t be afraid to chat with a stranger, reconnect with your barista or strike up a conversation at the cipro tendon rupture incidence dog park.Find purpose in everyday routines.What things do you look forward to each day?. What gives your life meaning?. Research has found that flourishing comes from cipro tendon rupture incidence daily routines, like working on a new skill or reaching out to thank the people you value in your life, and small moments of mastery, connection and meaning.“There are lots of American adults that would meet the qualifications of feeling happy, but they don’t feel sense of purpose,” said Corey Keyes, a professor of sociology at Emory University. €œFeeling good about life is not enough.”While work doesn’t have to be the main driver behind your sense of purpose, studies show that reframing how you think about your job can improve your sense of satisfaction.

Deepening relationships cipro tendon rupture incidence with co-workers and reminding yourself how your job contributes to a greater good can change how you think about work. If you’re an insurance agent, for example, perceiving your job as a means of helping people get back on their feet after an accident, rather than focusing on a rote task like processing claims, can make your work more fulfilling.“People think that in order to flourish, they need to do whatever their version of winning the Olympics is, or climbing a mountain, or having some epic experience,” Dr. Grant said.If you’re feeling down, choose a cipro tendon rupture incidence small project. It could be as simple as cleaning the kitchen or doing yard work, or even washing your pillow cases.

Maybe you set a 10-minute timer and go for a short jog, or try a cipro tendon rupture incidence one-minute meditation. Completing a simple, impactful task can build toward a sense of accomplishment.Try something new.“Many of us think we need to change our circumstances, get a job where we earn tons more money, or switch our relationships, buy something new,” said Dr. Santos. €œBut what the research really shows is that flourishing comes from a different set of behaviors and habits.”And now that life is getting back closer to normal, there are more opportunities to branch out.

You can join a book club or running group, take a pottery class, visit a museum or outdoor art exhibit, try a new recipe, explore a nearby trail or neighborhood or test out a free language learning app like Duolingo.Most important for overall well being, Dr. Keyes said, is being interested in life. A sense of satisfaction or happiness tends to follow that. The cipro has challenged us because we haven’t been able to pursue many of our previous interests, he said.

€œThe first key to feeling good about life is to seek out new interests,” he said.Dr. Grant also said learning a skill and then teaching it to someone, or taking on passion projects as hobbies, can lead to fulfillment. The end of the cipro offers a new opportunity to reflect, he said, and to ask a new question. €œHow do I want to spend my time?.

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AdvertisementContinue reading the main storySupported byContinue reading the main http://kcuei.com/can-i-buy-seroquel-online/ storyThe Other Side of where to get cipro Languishing Is Flourishing. Here’s How to Get There.Research shows that the cipro took a toll on our overall well-being and left many of us drained. Here are seven simple where to get cipro steps to get you thriving again.Credit...Cristina SpanòMay 4, 2021With vaccination rates on the rise, hope is in the air.

But after a year of trauma, isolation and grief, how long will it take before life finally — finally — feels good?. Post-cipro, the answer to that question may be where to get cipro in your own hands. A growing body of research shows that there are simple steps you can take to recharge your emotional batteries and spark a sense of fulfillment, purpose and happiness.

The psychology community calls this lofty combination where to get cipro of physical, mental and emotional fitness “flourishing.” It is the exact opposite of languishing, that sense of stagnation Adam Grant wrote about recently for The Times.“Flourishing really is what people are ultimately after,” said Tyler J. VanderWeele, an epidemiology and biostatistics professor and director of Harvard’s Human Flourishing Program. €œIt’s living the where to get cipro good life.

We usually think about flourishing as living in a state in which all aspects of a person’s life are good — it’s really an all-encompassing notion.”The good news is that the scientific evidence related to flourishing is robust, and numerous studies show simple activities can lead to marked improvement in overall well-being. Here are some practical activities, backed by science, that where to get cipro can help you get started.Assess yourself.First, how do you know if you’re languishing, flourishing or somewhere in between?. Simply asking someone is an effective diagnostic tool, said Laurie Santos, a psychology professor at Yale who teaches a free 10-week course called “The Science of Well-Being.” Do you wake up ready to start your day or would you rather go back to sleep?.

Do you have a sense of purpose or do you where to get cipro find how you spend much of your day to be meaningless?. “You are kind of the expert on your own sense of flourishing,” she said.Dr. VanderWeele uses a 10-question assessment where to get cipro in his program at Harvard, which you can try here.

Participants rate five areas of their lives on a scale of one to 10, with questions focusing on happiness and life satisfaction, physical and mental health, meaning and purpose, character and virtue and close social relationships. Just taking the quiz and reflecting on the questions it where to get cipro asks can put you on a path to making positive changes, Dr. VanderWeele said.Savor and celebrate small things.After a year of Zoom birthday parties and virtual graduations, many of us want to revel in gathering together again.

Celebrations help to where to get cipro create and cement relationships. €œIt’s really important that post-cipro we embrace more and more celebrating,” Dr. VanderWeele said.But it’s not just the big occasions where to get cipro that should be marked.

Acknowledging small moments is also important for well-being, research shows. Psychologists call it “savoring.” Savoring is about appreciating an event or activity in the moment, sharing tiny victories and noticing the good things around you.A 2012 study of college students found that taking part in a savoring activity called “mindful photography” resulted in overall where to get cipro improvements in mood and a significantly greater sense of appreciation for college life. The students were instructed to take at least five photos of their everyday lives — friends, their favorite view on campus, books they enjoyed — twice a week for two weeks.

Reflecting on the photos, and the small moments that brought them joy, helped the students focus on the good in their lives.If snapping photos of your favorite things sounds like too much work, research shows you also benefit when you savor enjoyable experiences like luxuriating in a warm bath, spending the day with your best friend or taking an “awe” walk.Try “Sunday dinner gratitude.”Some people expressed gratitude more during the cipro, whether it was clapping for health care workers or thanking a grocery where to get cipro checkout person. But creating a weekly gratitude ritual can cement the habit. Numerous studies show that taking time to reflect on what we’re grateful for improves our quality of life.In a 2003 study, where to get cipro researchers instructed college students to list, once a week, five things they were grateful for, both big and small.

(Some wrote that they were grateful for waking up that morning. One included where to get cipro gratitude for the Rolling Stones.) Compared to a control group, the students assigned to the gratitude intervention for 10 weeks had better feelings about life as a whole and fewer physical complaints.A gratitude practice should not be a burden. Try to stack a new gratitude habit on a weekly ritual — like Sunday dinner with family.

Taking out the trash, or your weekly grocery where to get cipro run.Do five good deeds.Acts of kindness not only help others, they also can help you flourish. Research shows that performing five acts of kindness in a single day, once a week, can have a powerful effect. A 2004 study showed that when college students spent a day doing five acts of kindness — like donating blood, helping a friend with a paper or writing a thank you note to where to get cipro a former professor — they experienced more significant increases in well-being than those who spread out five kind things over the course of a week.Volunteer work can also improve well being.

Dr. VanderWeele and other researchers looked at data from a cohort of nearly 13,000 older adults and found that participants who volunteered at least two hours a week during the study period experienced higher levels of happiness, optimism and purpose in life, compared to those who did where to get cipro not volunteer at all.To make it easy, Dr. Grant recommends starting off with a daily “five-minute favor,” like introducing two people who could benefit from knowing each other, or sending an article or podcast link to a friend, saying you were thinking of them.Look for communities and connection.Even a quick chat with a stranger or a momentary bond with someone new can foster a sense of fulfillment, particularly when what researchers call a high quality connection occurs.

€œThey don’t have to be lasting where to get cipro relationships or long interactions,” Dr. Grant said. €œSometimes people feel an extra spring in their step when they talk to a stranger on a plane or a subway, where to get cipro or when somebody greets them at a restaurant.”Moments of being seen by other people, and being met with respect or even enthusiasm, can energize and invigorate us and help create bonds within our neighborhood or community.As you emerge from cipro life, try to reconnect with a community you’ve missed.

It might be going back to church or choir practice, a running group or yoga class or even just hanging out at your local coffee shop. And don’t be afraid to chat with a stranger, reconnect with your barista or strike up a conversation at the dog park.Find purpose where to get cipro in everyday routines.What things do you look forward to each day?. What gives your life meaning?.

Research has found that where to get cipro flourishing comes from daily routines, like working on a new skill or reaching out to thank the people you value in your life, and small moments of mastery, connection and meaning.“There are lots of American adults that would meet the qualifications of feeling happy, but they don’t feel sense of purpose,” said Corey Keyes, a professor of sociology at Emory University. €œFeeling good about life is not enough.”While work doesn’t have to be the main driver behind your sense of purpose, studies show that reframing how you think about your job can improve your sense of satisfaction. Deepening relationships with co-workers and reminding yourself how your job contributes to a greater good where to get cipro can change how you think about work.

If you’re an insurance agent, for example, perceiving your job as a means of helping people get back on their feet after an accident, rather than focusing on a rote task like processing claims, can make your work more fulfilling.“People think that in order to flourish, they need to do whatever their version of winning the Olympics is, or climbing a mountain, or having some epic experience,” Dr. Grant said.If you’re feeling down, choose where to get cipro a small project. It could be as simple as cleaning the kitchen or doing yard work, or even washing your pillow cases.

Maybe you set a where to get cipro 10-minute timer and go for a short jog, or try a one-minute meditation. Completing a simple, impactful task can build toward a sense of accomplishment.Try something new.“Many of us think we need to change our circumstances, get a job where we earn tons more money, or switch our relationships, buy something new,” said Dr. Santos.

€œBut what the research really shows is that flourishing comes from a different set of behaviors and habits.”And now that life is getting back closer to normal, there are more opportunities to branch out. You can join a book club or running group, take a pottery class, visit a museum or outdoor art exhibit, try a new recipe, explore a nearby trail or neighborhood or test out a free language learning app like Duolingo.Most important for overall well being, Dr. Keyes said, is being interested in life.

A sense of satisfaction or happiness tends to follow that. The cipro has challenged us because we haven’t been able to pursue many of our previous interests, he said. €œThe first key to feeling good about life is to seek out new interests,” he said.Dr.

Grant also said learning a skill and then teaching it to someone, or taking on passion projects as hobbies, can lead to fulfillment. The end of the cipro offers a new opportunity to reflect, he said, and to ask a new question. €œHow do I want to spend my time?.

€AdvertisementContinue reading the main story.