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    "For many of the 70 million Americans who live in highly concentrated health insurance markets, a lack of competition is a problem that keeps getting worse as consumers have more limited health insurance options to choose," AMA President Dr. Susan Bailey said in a statement. The report used a measure called the buy voltaren Herfindahl-Hirschman Index to determine market concentration.

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    Between 2014 and 2019, the report found an average HHI increase of 151 points. Seventeen percent of markets experienced HHI increases of at least 500 points buy voltaren. Of markets that were not highly concentrated in 2014, one-quarter experienced HHI upticks large enough to deem them highly concentrated by 2019.

    The study broke down its results by the buy voltaren type of insurance product, including health insurance exchanges created by the Affordable Care Act. Leemore Dafny, a Harvard Business School professor of business administration, said those findings square with those in her own research finding less competition in health insurance marketplaces, which are subsidized by the federal government. The average HHI in the exchanges was 6,623, and 99% of them are considered highly concentrated, according to the report."The exchange markets look especially concentrated," Dafny said, "and when they're less competitive, premiums go up." The AMA did not comment beyond its report, which encouraged a dialogue among regulators, policymakers, lawmakers and others about the need for a "better, more open and competitive marketplace." "These markets are ripe for the exercise of health insurer market power, which harms consumers and providers of care," the report said.

    "Our findings should prompt federal and state antitrust authorities to vigorously examine the competitive effects of proposed mergers between health insurers." The report said that buy voltaren 57% of physicians providing patient care are in practices with 10 or fewer physicians. Under antitrust law, independent physicians can't negotiate collectively with insurers, an imbalance that leaves most physicians with weak bargaining positions relative to commercial insurers, the report said. The report cited Elizabethtown-Fort Knox, Ky buy voltaren.

    As an example of an already highly concentrated market that has gotten even more concentrated over the past five years. In 2014, the market had an HHI of 3,534. By 2019, that had buy voltaren grown to 5,159.

    That's because Anthem's market share went from 45% to 70% in that time. Anthem did not return a request buy voltaren for comment. The report pointed out that health insurance mergers went largely unchallenged before the proposed 2007 merger of Independence Blue Cross and Highmark.

    That deal was ultimately called off because the Pennsylvania Insurance Department added a condition that one of them drop its Blues brand. Three years later, Blue Cross and Blue Shield of Michigan buy voltaren called off its acquisition of Physicians Health Plan of Mid-Michigan after the Department of Justice said it would sue to block it. In 2015, Anthem attempted to acquire Cigna and Aetna sought to acquire Humana.

    Both deals were ultimately abandoned after lawsuits from buy voltaren the DOJ and multiple attorneys general. America's Health Insurance Plans, a prominent industry trade group, did not respond to a request for comment on the report. AHIP has for years highlighted reports on rising healthcare costs that result from vertical provider consolidation.

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    September 11, 2020 Ottawa, ON Health Canada Today, the does voltaren gel really work Honourable Patty Hajdu issued the following statement. Yesterday’s Supreme Court of British Columbia’s decision in Cambie, which dismissed the constitutional challenge to provisions of British Columbia’s Medicare Protection Act and upheld the ban on patient charges and private insurance, validates our belief that all Canadians deserve universally accessible health care. Access to medically necessary services should be uniformly available to all, based on need rather than ability or willingness to pay.

    Patient charges—whether they take the form of charges at the point of service or payment for private insurance—undermine equity. The Government of Canada fully welcomes the Court’s decision and commends the Government of British Columbia for its successful defence of universally accessible health care. This decision validates Canada’s single-payer public health care system and the fundamental principle that access to medically necessary health services should be based on health need and not on the ability or willingness to pay.

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    September 11, buy voltaren 2020 Ottawa, ON Health Canada Today, the Honourable Patty Hajdu issued the following statement. Yesterday’s Supreme Court of British Columbia’s decision in Cambie, which dismissed the constitutional challenge to provisions of British Columbia’s Medicare Protection Act and upheld the ban on patient charges and private insurance, validates our belief that all Canadians deserve universally accessible health care. Access to medically necessary services should be uniformly available to all, based on need rather than ability buy voltaren or willingness to pay. Patient charges—whether they take the form of charges at the point of service or payment for private insurance—undermine equity.

    The Government of Canada fully welcomes the Court’s decision and commends the Government of British Columbia for its successful defence of universally accessible health care. This decision validates Canada’s single-payer public health care system and the fundamental principle that access to medically necessary health services should be based on health need and not on the ability or willingness to pay. We believe that these values are more important than ever as we continue to respond to the unprecedented challenges presented by the COVID-19 outbreak, and the Government of Canada will continue to defend universally accessible health care for all Canadians. The Honourable Patty Hajdu, P.C., M.P..

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    Serum levels voltaren dosing card of lipoprotein-associated phospholipase A2 (Lp-PLA2) activity are associated with the presence of CAVS. However, it has been unclear whether this association is due to a cause–effect relationship. In this issue of Heart, Perrot and colleagues1 used genetic association studies from eight cohorts to show that CAVS was not associated with any of four single nucleotide polymorphisms that are associated with Lp-PLA2 activity or mass. These findings voltaren dosing card suggest that although Lp-PLA2 activity is a biomarker for CAVS unfortunately, it is unlikely to be a therapeutic target (figure 1).Higher Lp-PLA2 activity is significantly associated with the presence of CAVS in patients with heart disease, but variants influencing Lp-PLA2 mass or activity are not associated with CAVS in this large genetic association study.

    CAVS, calcific aortic valve stenosis. Lp-PLA2, lipoprotein-associated phospholipase A2." data-icon-position data-hide-link-title="0">Figure 1 Higher Lp-PLA2 activity is significantly associated with the presence of CAVS in patients with heart disease, but variants influencing Lp-PLA2 mass or activity are not associated with CAVS in this large genetic association study. CAVS, calcific aortic voltaren dosing card valve stenosis. Lp-PLA2, lipoprotein-associated phospholipase A2.In an editorial, Zheng and Dweck2 discuss this article, summarise current ongoing trials of medical therapy for CAVS (table 1) and comment.

    €˜Strong evidence points towards elevated Lp(a) levels and its associated oxidised phospholipids (OxPL) as causal risk factors for CAVS, suggesting that targeting this lipid-driven, inflammatory pathway has a real chance to translate into therapy capable of mitigating disease. The current study suggests that this association is not mediated by Lp-PLA2 and underlines the importance of scrutinising whether biological factors within pathophysiological pathways are merely biomarkers or actually represent a feasible and causal target.’View this table:Table 1 Ongoing randomised clinical trials of medical therapies in aortic stenosisRheumatic heart disease (RHD) remains the primary cause of valve disease worldwide and contributes significantly voltaren dosing card to maternal and fetal morbidity and mortality. In a study by Baghel and colleagues3 of 681 pregnant women with RHD, adverse cardiovascular evens occurred in about 15% of pregnancies. Multivariable predictors of adverse outcomes during pregnancy were prior adverse cardiovascular events, lack of appropriate medical therapy, severity of mitral stenosis, valve replacement and pulmonary hypertension.

    Based on this analysis, the authors propose a risk score from pregnant women with RHD (table 2).View this table:Table 2 New prognostic score (DEVI’s score) to predict composite adverse cardiac outcome in pregnant women with rheumatic valvular heart diseaseCommenting on this paper, Elkayam and Shmueli4 point out that in about one-fourth of women, the diagnosis of RHD was not known prior to pregnancy voltaren dosing card and that a late diagnosis often was associated with adverse outcomes. Their editorial provides a concise summary of optimal management of pregnant women with RHD. They conclude ‘With proper evaluation and risk stratification prior to pregnancy, a close multidisciplinary follow-up during pregnancy, and close monitoring during labour and delivery as well as the early postpartum period most complications can be prevented.’The importance of psychosocial factors in cardiovascular disease (CVD) prevalence and outcomes is increasingly recognised. Using data from the English Longitudinal Study of Ageing, Bu and colleagues5 found that loneliness was associated with CVD, independent of possible confounders and other risk factors, with a 30% higher risk voltaren dosing card of a new CVD diagnosis in the most lonely people compared with the least lonely people.

    As O’Keefe and colleagues6 point out, this data is especially important now in the context of social distancing and stay-at-home recommendations and they offer several approaches to mitigating loneliness during the COVID-19 pandemic.The Education in Heart article7 in this issue focuses on the clinical use and prognostic implications of echocardiographic speckle tracking measurements of global longitudinal strain to detect and quantify early systolic dysfunction of the left ventricle (figure 2).Left ventricular global longitudinal strain to differentiate between mutation-positive sarcomeric hypertrophic cardiomyopathy and cardiac amyloidosis. (A) Apical four-chamber view of a 66-year-old patient known with mutation-positive hypertrophic cardiomyopathy. The thickness of the septum was 28 mm and the left ventricular ejection voltaren dosing card fraction was 55%. (B) The polar map shows markedly impaired longitudinal strain in the septal mid and basal areas and the global longitudinal strain is impaired (−13.6%).

    (C) Apical four-chamber view of a 75-year-old patient diagnosed with light chain amyloidosis. There is concentric hypertrophy of the left ventricle and voltaren dosing card the ejection fraction is 56%. Based on speckle tracking echocardiography analysis, the left ventricular global longitudinal strain is impaired (−12.2%), with typical sparing of the longitudinal strain values in the apical segments (D). ANT, anterior.

    ANT SEPT, voltaren dosing card anteroseptal. GS, global strain. INF, inferior. LAT, lateral voltaren dosing card.

    POST, posterior. SEPT, septal." data-icon-position data-hide-link-title="0">Figure 2 Left ventricular global longitudinal strain to differentiate between mutation-positive sarcomeric hypertrophic cardiomyopathy and cardiac amyloidosis. (A) Apical four-chamber view of a 66-year-old patient known with mutation-positive hypertrophic cardiomyopathy voltaren dosing card. The thickness of the septum was 28 mm and the left ventricular ejection fraction was 55%.

    (B) The polar map shows markedly impaired longitudinal strain in the septal mid and basal areas and the global longitudinal strain is impaired (−13.6%). (C) Apical four-chamber voltaren dosing card view of a 75-year-old patient diagnosed with light chain amyloidosis. There is concentric hypertrophy of the left ventricle and the ejection fraction is 56%. Based on speckle tracking echocardiography analysis, the left ventricular global longitudinal strain is impaired (−12.2%), with typical sparing of the longitudinal strain values in the apical segments (D).

    ANT, anterior voltaren dosing card. ANT SEPT, anteroseptal. GS, global strain. INF, inferior voltaren dosing card.

    LAT, lateral. POST, posterior. SEPT, septal.Our Cardiology-in-Focus article by Hudson and Pettit8 provides a clear-eyed but brief discussion and voltaren dosing card outstanding graphic of the challenges in reconciling the varying definitions of the ‘normal’ values for left ventricular ejection fraction, as stated in different guidelines (figure 3).Categories of left ventricular ejection fraction. EF, ejection fraction.

    HF, heart failure. LVEF, left ventricular ejection voltaren dosing card fraction." data-icon-position data-hide-link-title="0">Figure 3 Categories of left ventricular ejection fraction. EF, ejection fraction. HF, heart failure.

    However, it has been unclear whether this association buy voltaren is due to a cause–effect relationship. In this issue of Heart, Perrot and colleagues1 used genetic association studies from eight cohorts to show that CAVS was not associated with any of four single nucleotide polymorphisms that are associated with Lp-PLA2 activity or mass. These findings suggest that although Lp-PLA2 activity is a biomarker for CAVS unfortunately, it is unlikely to be a therapeutic target (figure 1).Higher Lp-PLA2 activity is significantly associated with the presence of CAVS in patients with heart disease, but variants influencing Lp-PLA2 mass or activity are not associated with CAVS in this large genetic association study. CAVS, calcific aortic valve buy voltaren stenosis. Lp-PLA2, lipoprotein-associated phospholipase A2." data-icon-position data-hide-link-title="0">Figure 1 Higher Lp-PLA2 activity is significantly associated with the presence of CAVS in patients with heart disease, but variants influencing Lp-PLA2 mass or activity are not associated with CAVS in this large genetic association study.

    CAVS, calcific aortic valve stenosis. Lp-PLA2, lipoprotein-associated phospholipase A2.In an editorial, Zheng and Dweck2 discuss this article, buy voltaren summarise current ongoing trials of medical therapy for CAVS (table 1) and comment. €˜Strong evidence points towards elevated Lp(a) levels and its associated oxidised phospholipids (OxPL) as causal risk factors for CAVS, suggesting that targeting this lipid-driven, inflammatory pathway has a real chance to translate into therapy capable of mitigating disease. The current study suggests that this association is not mediated by Lp-PLA2 and underlines the importance of scrutinising whether biological factors within pathophysiological pathways are merely biomarkers or actually represent a feasible and causal target.’View this table:Table 1 Ongoing randomised clinical trials of medical therapies in aortic stenosisRheumatic heart disease (RHD) remains the primary cause of valve disease worldwide and contributes significantly to maternal and fetal morbidity and mortality. In a buy voltaren study by Baghel and colleagues3 of 681 pregnant women with RHD, adverse cardiovascular evens occurred in about 15% of pregnancies.

    Multivariable predictors of adverse outcomes during pregnancy were prior adverse cardiovascular events, lack of appropriate medical therapy, severity of mitral stenosis, valve replacement and pulmonary hypertension. Based on this analysis, the authors propose a risk score from pregnant women with RHD (table 2).View this table:Table 2 New prognostic score (DEVI’s score) to predict composite adverse cardiac outcome in pregnant women with rheumatic valvular heart diseaseCommenting on this paper, Elkayam and Shmueli4 point out that in about one-fourth of women, the diagnosis of RHD was not known prior to pregnancy and that a late diagnosis often was associated with adverse outcomes. Their editorial provides a concise summary of optimal management of pregnant women buy voltaren with RHD. They conclude ‘With proper evaluation and risk stratification prior to pregnancy, a close multidisciplinary follow-up during pregnancy, and close monitoring during labour and delivery as well as the early postpartum period most complications can be prevented.’The importance of psychosocial factors in cardiovascular disease (CVD) prevalence and outcomes is increasingly recognised. Using data from the English Longitudinal Study of Ageing, Bu and colleagues5 found that loneliness was associated with CVD, independent of possible confounders and other risk factors, with a 30% higher risk of a new CVD diagnosis in the most lonely people compared with the least lonely people.

    As O’Keefe and colleagues6 buy voltaren point out, this data is especially important now in the context of social distancing and stay-at-home recommendations and they offer several approaches to mitigating loneliness during the COVID-19 pandemic.The Education in Heart article7 in this issue focuses on the clinical use and prognostic implications of echocardiographic speckle tracking measurements of global longitudinal strain to detect and quantify early systolic dysfunction of the left ventricle (figure 2).Left ventricular global longitudinal strain to differentiate between mutation-positive sarcomeric hypertrophic cardiomyopathy and cardiac amyloidosis. (A) Apical four-chamber view of a 66-year-old patient known with mutation-positive hypertrophic cardiomyopathy. The thickness of the septum was 28 mm and the left ventricular ejection fraction was 55%. (B) The polar map shows markedly impaired longitudinal strain in the septal mid and basal areas buy voltaren and the global longitudinal strain is impaired (−13.6%). (C) Apical four-chamber view of a 75-year-old patient diagnosed with light chain amyloidosis.

    There is concentric hypertrophy of the left ventricle and the ejection fraction is 56%. Based on speckle tracking echocardiography analysis, the left ventricular global longitudinal strain is impaired (−12.2%), with typical sparing of the longitudinal strain values buy voltaren in the apical segments (D). ANT, anterior. ANT SEPT, anteroseptal. GS, global strain buy voltaren.

    INF, inferior. LAT, lateral. POST, posterior buy voltaren. SEPT, septal." data-icon-position data-hide-link-title="0">Figure 2 Left ventricular global longitudinal strain to differentiate between mutation-positive sarcomeric hypertrophic cardiomyopathy and cardiac amyloidosis. (A) Apical four-chamber view of a 66-year-old patient known with mutation-positive hypertrophic cardiomyopathy.

    The thickness of buy voltaren the septum was 28 mm and the left ventricular ejection fraction was 55%. (B) The polar map shows markedly impaired longitudinal strain in the septal mid and basal areas and the global longitudinal strain is impaired (−13.6%). (C) Apical four-chamber view of a 75-year-old patient diagnosed with light chain amyloidosis. There is buy voltaren concentric hypertrophy of the left ventricle and the ejection fraction is 56%. Based on speckle tracking echocardiography analysis, the left ventricular global longitudinal strain is impaired (−12.2%), with typical sparing of the longitudinal strain values in the apical segments (D).

    ANT, anterior. ANT SEPT, buy voltaren anteroseptal. GS, global strain. INF, inferior. LAT, lateral buy voltaren.

    POST, posterior. SEPT, septal.Our Cardiology-in-Focus article by Hudson and Pettit8 provides a clear-eyed but brief discussion and outstanding graphic of the challenges in reconciling the varying definitions of the ‘normal’ values for left ventricular ejection fraction, as stated in different guidelines (figure 3).Categories of left ventricular ejection fraction. EF, ejection buy voltaren fraction. HF, heart failure. LVEF, left ventricular ejection fraction." data-icon-position data-hide-link-title="0">Figure 3 Categories of left ventricular ejection fraction.

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    As someone who had previously investigated other pandemics such as the Great Flu Pandemic of 1918-19 and AIDS, and who has worked with vaccines, I had a strong background for tracking down the relevant data to test my hypothesis.Pneumococcal Vaccination Rates Correlate With Lower COVID-19 Cases and DeathsI gathered national and some local data on vaccination rates against influenza, polio, measles-mumps-rubella (MMR), diphtheria-tetanus-pertussis (DTP), tuberculosis (BCG), pneumococci and Haemophilus influenzae type B (Hib). I correlated them with COVID-19 case rates and death rates for 24 nations that had experienced their COVID-19 outbreaks at about the same time. I controlled for factors such as percentage of the population who were obese, diabetic or elderly.I found that only pneumococcal vaccines afforded statistically knee pain cream voltaren significant protection against COVID-19. Nations such as Spain, Italy, Belgium, Brazil, Peru and Chile that have the highest COVID-19 rates per million have the poorest pneumococcal vaccination rates among both infants and adults.

    Nations with the lowest rates of COVID-19 – Japan, Korea, Denmark, Australia and New Zealand – have the knee pain cream voltaren highest rates of pneumococcal vaccination among both infants and adults.A recent preprint study (not yet peer-reviewed) from researchers at the Mayo Clinic has also reported very strong associations between pneumococcal vaccination and protection against COVID-19. This is especially true among minority patients who are bearing the brunt of the coronavirus pandemic. The report also suggests that other vaccines, or combinations of vaccines, such as Hib and MMR may also provide protection.These results are important because in the U.S., childhood vaccination against pneumococci – which protects against Streptococcus pneumoniae bacteria knee pain cream voltaren – varies by state from 74% to 92%. Although the CDC recommends that all adults 18-64 in high risk groups for COVID-19 and all adults over the age of 65 get a pneumococcal vaccination, only 23% of high-risk adults and 64% of those over the age of 65 do so.Similarly, although the CDC recommends at all infants and some high-risk adults be vaccinated against Haemophilus influenzae type B (Hib), only 80.7% of children in the U.S.

    And a handful of immunologically compromised adults have been. Pneumococcal and Hib vaccination rates are significantly lower in minority knee pain cream voltaren populations in the U.S. And in countries that have been hit harder by COVID-19 than the U.S.Based on these data, I advocate universal pneumococcal and Hib vaccination among children, at-risk adults and all adults over 65 to prevent serious COVID-19 disease.Left. Combined rates of childhood and adult (over 65) pneumococcal vaccination knee pain cream voltaren (out of a possible 200).

    Right. Cases (per knee pain cream voltaren million) population of COVID-19 at about 90 days into the pandemic for 24 nations. Nations with high pneumococcal vaccination rates have low COVID-19 case rates. (Credit.

    CC BY-SA)How knee pain cream voltaren Pneumococcal Vaccination Protects Against COVID-19Protection against serious COVID-19 disease by pneumococcal and Hib vaccines makes sense for several reasons. First, recent studies reveal that the majority of hospitalized COVID-19 patients, and in some studies nearly all, are infected with streptococci, which causes pneumococcal pneumonias, Hib or other pneumonia-causing bacteria. Pneumococcal and Hib vaccinations should protect coronavirus patients from these infections and thus significantly cut the risk of serious pneumonia.I also found that pneumococcal, Hib and possibly rubella vaccines may confer specific knee pain cream voltaren protection against the SARS-CoV-2 virus that causes COVID-19 by means of “molecular mimicry.”Molecular mimicry occurs when the immune system thinks one microbe looks like another. In this case, proteins found in pneumococcal vaccines and, to a lesser degree, ones found in Hib and rubella vaccines as well look like several proteins produced by the SARS-CoV-2 virus.Two of these proteins found in pneumococcal vaccines mimic the spike and membrane proteins that permit the virus to infect cells.

    This suggests knee pain cream voltaren pneumococcal vaccination may prevent SARS-CoV-2 infection. Two other mimics are the nucleoprotein and replicase that control virus replication. These proteins are made after viral infection, in which case pneumococcal vaccination may control, but not prevent, SARS-CoV-2 replication.Either way, these vaccines may provide proxy protection against SARS-CoV-2 infection that we can implement right now, even before we have a specific virus vaccine. Such protection may not be complete knee pain cream voltaren.

    People might still suffer a weakened version of COVID-19 but, like most infants and children, be protected against the worst effects of the infection.Fighting Influenza-related Pneumonias During the COVID-19 PandemicWhile the specific protection these other vaccines confer against COVID-19 has not yet been tested in a clinical trial, I advocate broader implementation of pneumococcal and Hib vaccination for one additional, well-validated reason.Pneumococcal and Hib pneumonias – both caused by bacteria – are the major causes of death following viral influenza. The influenza virus knee pain cream voltaren rarely causes death directly. Most often, the virus makes the lungs more susceptible to bacterial pneumonias, which are deadly. Dozens of studies around the world have demonstrated that knee pain cream voltaren increasing rates of pneumococcal and Hib vaccination dramatically lowers influenza-related pneumonias.Similar studies demonstrate that the price of using these vaccines is balanced by savings due to lower rates of influenza-related hospitalizations, intensive care unit admissions and deaths.

    In the context of COVID-19, lowering rates of influenza-related hospitalizations and ICU admissions would free up resources to fight the coronavirus, independent of any effect these vaccines might have on SARS-CoV-2 itself. In my opinion, that is a winning scenario.In short, we need not wait for a SARS-CoV-2 vaccine to slow down COVID-19.I believe that we can and should act now by fighting the coronavirus with all the tools at our disposal, including influenza, Hib, pneumococcal and perhaps rubella vaccinations.Preventing pneumococcal and Hib complications of influenza and COVID-19, and perhaps proxy-vaccinating against SARS-CoV-2 itself, helps everyone. Administering these already available and well-tested pneumococcal and Hib vaccines to people will save knee pain cream voltaren money by freeing up hospital beds and ICUs. It will also improve public health by reducing the spread of multiple infections and boost the economy by nurturing a healthier population.Robert Root-Bernstein is a Professor of Physiology at Michigan State University.

    This article was originally published on The Conversation under a Creative Commons liscense Read the original here.This story appeared in the November 2020 issue as "Bacteria and the Brain." Subscribe to Discover magazine for more stories like this.It’s not always knee pain cream voltaren easy to convince people that the human gut is a sublime and wondrous place worthy of special attention. Sarkis Mazmanian discovered that soon after arriving at Caltech for his first faculty job 14 years ago, when he explained to a local artist what he had in mind for the walls outside his new office.The resulting mural greets visitors to the Mazmanian Lab today. A vaguely knee pain cream voltaren psychedelic, 40-foot-long, tube-shaped colon that’s pink, purple and red snakes down the hallway. In a panel next to it, fluorescent yellow and green bacteria explode out of a deeply inflamed section of the intestinal tract, like radioactive lava from outer space.The mural is modest compared with what the scientist has been working on since.

    Over the last decade or so, Mazmanian has been a leading proponent of the idea that the flora of the human digestive tract has a far more powerful effect on the human body and mind than we thought — a scientific effort that earned him a $500,000 MacArthur Fellowship “Genius Grant” in 2012. Since then, Mazmanian and a small but growing cadre of knee pain cream voltaren fellow microbiologists have amassed a tantalizing body of evidence on the microbiome’s role in all kinds of brain disorders, including schizophrenia, Alzheimer’s disease, Parkinson’s disease and depression.But the results they’ve seen in autism could, in the end, prove the most transformative. Autism affects about 1 in 59 children in the U.S., and involves profound social withdrawal, communication problems, and sometimes anxiety and aggression. The causes of the knee pain cream voltaren brain disorder have remained speculative.

    Now, Mazmanian and other researchers are finding that autism may be inextricably linked to — or even caused by — irregularities in the gut microbiome.A Biology StoryAt 47, Mazmanian — with his shaved head, flannel shirt and skinny jeans — resembles a young, urban hipster on his way to write at the local café. Originally, literary life was his plan knee pain cream voltaren. Born in Lebanon to two Armenian refugees, neither of whom had more than a first-grade education, Mazmanian landed in the class of an energetic high school English teacher in California’s San Fernando Valley, where his family first settled. The teacher recognized his gift for language and encouraged him to pursue a career in literature.

    Mazmanian enrolled at UCLA in 1990, planning to major in knee pain cream voltaren English.Everything changed when he took his first biology class. Hunched over his new, thick textbook in the library, reading about basic biological concepts like photosynthesis, Mazmanian felt a vast new world opening up to him.Sarkis Mazmanian, shown in front of a mural that celebrates the human gut, is part of a group of microbiologists researching the effects of the digestive tract on a range of disorders. (Credit. Caltech)“For the first time in my life, I wanted to turn the page and see where the story was going to go,” he says.

    €œI think I decided that minute to become a scientist.”Mazmanian was most fascinated by the idea that tiny organisms, invisible to the naked eye, could function as powerful, self-contained machines — powerful enough to take over and destroy the human body. After graduating with a degree in microbiology, Mazmanian joined a UCLA infectious diseases lab and began studying bacteria that cause staph infections.As his dissertation defense approached, Mazmanian read a one-page commentary penned by a prominent microbiologist, highlighting the fact that our intestines are teeming with hundreds, if not thousands, of different species of bacteria. But it was still largely unknown what they are and how they affect the human body.When Mazmanian dug further, he found that no one had yet answered what seemed to him to be the most obvious question. Why would the human immune system, designed to attack and destroy foreign invaders, allow hundreds of species of bacteria to live and thrive in our guts unmolested?.

    To him, the bacteria’s survival implied that we had evolved to coexist with them. And if that were so, he reasoned, there must be some benefit to both the microbes and the human body — a symbiotic relationship. But what was it?. Gut InvadersMazmanian set out to study the link between gut microbes and the immune system.

    As a postdoctoral researcher, he joined the lab of Harvard University infectious disease specialist Dennis Kasper.To start, Mazmanian examined how the immune systems of germ-free mice — lab mice completely protected, starting at birth, from all microbes — differed from those of mice with either few or normal levels of microbes. He expected this initial census would be just a first step in a long and arduous quest for scientific pay dirt. But when he went to examine a printout of his results in the lab, he realized immediately he might already be onto something big. The germ-free mice had a 30 to 40 percent reduction in a specific type of immune cell known as helper T-cells.This colorized close-up of a mouse’s gut reveals the tight relationship between the gut microbe Bacteroides fragilis (red) and the epithelial surface of the colon (blue).

    (Credit. Caltech)Since helper T-cells play a key role in coordinating attacks against invading pathogens, the finding suggested that the immune systems of the germ-free mice were far less robust than those found in peers with normal levels of microbes.“That was exciting, right?. € Mazmanian recalls. €œObviously I repeated it and tested it in a number of different ways.

    Then I asked the next question. €˜Can I restore the [immune] function in an adult animal?. €™â€‰â€Mazmanian colonized the guts of the immunocompromised, germ-free mice with microbes from standard lab mice. After receiving the fecal transplant, their T-cell counts shot up.

    Within a month, their numbers were identical to mice raised outside the germ-free bubble.Resolving to identify the microorganisms causing this transformation, Mazmanian resorted to trial and error. One by one, he added strains of bacteria found in the guts of mice to the guts of germ-free mice.He got nowhere with the first five or six species he examined. Then, simply because it was convenient, he decided to test one more that was readily available in his lab. Mazmanian’s adviser, Kasper, had been studying a gut microbe called Bacteroides fragilis.

    When Mazmanian implanted one of Kasper’s specimens into the gut of his germ-free mice, the results were dramatic. The T-cell numbers spiked to normal. Eventually, Mazmanian demonstrated he could reproduce this effect simply by adding a single molecule that these bacteria produce, called polysaccharide A, to their guts.“There was no logic in the choice whatsoever,” Mazmanian recalls. €œ[B.

    Fragilis] was available, it came from the gut.” In other words, he got lucky.Mazmanian dug deeper and discovered that the biggest impact B. Fragilis had was on the population of a subtype of helper T-cells called regulatory, or suppressor, T-cells. These cells play a key role in preventing the immune system from attacking its host body, protecting against autoimmune or inflammatory diseases. It was the first time any scientist had demonstrated that a single compound from a single microbe could reverse a specific problem with the immune system.To Mazmanian, the finding, published in 2005 in the journal Cell, alluded to new approaches to treating a wide array of autoimmune, inflammatory and allergic disorders.

    What if it were possible to help a faulty immune system by tweaking a patient’s microbiome?. It was with this exploration in mind that he arrived in Pasadena in 2006 to set up his lab at Caltech.A Convenient CollaborationA few years later, Mazmanian was having lunch on campus with neuroscientist and colleague Paul Patterson. Patterson had been preoccupied with a mystery that had, for years, confounded those studying autism in humans. When pregnant mothers have a severe infection in the second trimester, their babies are much more likely to develop autism.As Mazmanian tells it, Patterson was a man of few words, and at lunch Mazmanian was “going on and on” about his own work.“You know,” Patterson interjected thoughtfully, “I think kids with autism have GI issues.”Patterson recalled reading that something like 60 percent of children with autism had some form of clinical GI problem, such as bloating, constipation, flatulence or diarrhea.

    Was it possible, he wondered, that there was a microbiome connection?. As they talked, Mazmanian’s excitement grew.A few years earlier, Patterson had discovered that when he exposed pregnant mice to pathogens like the influenza virus, they gave birth to pups that grew up more likely to be startled by loud noises, to shy away from social contact and to groom themselves repetitively — symptoms that resemble those of autism. Patterson was in the process of comparing the brains of these autism-mimicking mice with their neurotypical cousins to see if he could detect any differences that might explain how the maternal immune system was somehow interfering with the pups’ brain development.Mazmanian had a suggestion. The next time Patterson sacrificed one of his autistic mice to study their brains, what if he set the intestines aside for his colleague down the hall?.

    When the guts arrived in Mazmanian’s lab, he found that the intestines of the neurotypical mice looked normal. But the guts of the autism-mimicking offspring were almost uniformly inflamed. Could it be that the microbiome was the cause of this inflammation?. And could that, in turn, be somehow connected to the behavioral symptoms?.

    Throughout the winter and spring of 2012, Mazmanian and Patterson continued their conversation. Mazmanian found distinct differences in the microbiomes of the mice. And, they noticed, the mice with the features of autism had leaky gut syndrome, an increased permeability of the gut lining that can allow pathogens and allergens to leach out. This condition had also been reported in children with autism.So Mazmanian and Patterson turned their attention outside the gut.

    They took blood samples to see if any gut microbes, or the compounds they produce, were circulating in the rest of the body. They homed in on one molecule in particular, called 4-ethylphenyl sulfate, which was roughly 45 times as abundant in the mice that had symptoms of autism. And it looked familiar. Structurally, it was almost identical to a molecule recently found to be significantly elevated in human children with autism.It was enough to take the next step.

    Every day for three weeks, Mazmanian injected the molecule, harvested from the mice with autism-like symptoms, directly into the bloodstream of 5-week-old normal lab mice (the age at which the autistic mice normally developed leaky gut). Then Mazmanian and his team gave them a series of behavioral tests. The mice were far more easily startled and were less comfortable in large empty spaces than their untreated peers, indications of an increase in anxiety-related behaviors commonly seen in the mice with autism-like symptoms. The researchers published their results in Cell in 2013.Though surprising, the data made sense in some ways.

    Many drug companies rely on small-molecule drugs that can be taken orally, but still manage to cross the blood-brain barrier and affect behavior. It seemed entirely possible that small molecules, created by bacteria in the gut, could enter the bloodstream and reach the brain. And they don’t even have to leak out of the gut to do so.Of Mice and MenPatterson died in 2014, at age 70, just six months after the publication of the duo’s groundbreaking Cell paper. Around the same time, a series of parallel experiments in a clinic hundreds of miles away was already paving the way forward.

    While Patterson and Mazmanian had been working in mice, Rosa Krajmalnik-Brown, a microbiologist at Arizona State University, had teamed up with Jim Adams, who directs the university’s autism and Asperger’s research program, to study humans.The researchers were conducting a detailed analysis of the microbiome of human autism patients and found that the bacteria were far less diverse in the children with autism. Notably, several important species involved in the digestion of carbohydrates were severely depleted.Krajmalnik-Brown and Adams launched a preliminary trial to test the effects of fecal transplants on 18 children between the ages of 7 and 16 with severe autism, who also had severe GI issues. The researchers administered powerful antibiotics to kill off the microbiomes of the children and followed them with a bowel cleanse. They then replaced the microbes with transplanted flora taken from the guts of healthy neurotypical adult volunteers.The results were better than anyone could have expected.

    The procedure resulted in a large reduction in GI symptoms and increased the diversity of bacteria in the children’s guts. But more significantly, their neurological symptoms were reduced. At the onset of the study in 2017, an independent evaluator found 83 percent of participants had severe autism. Two years after the initial trial, only 17 percent were rated as severely autistic.

    And 44 percent were no longer on the autism scale.“[My child] did a complete 180,” says Dana Woods, whose then-7-year-old son Ethan enrolled in the initial study five years ago. €œHis ability to communicate is so much different now. He’s just so much more present. He’s so much more aware.

    He’s no longer in occupational therapy. He’s no longer in speech therapy. After the study, he tested two points away from a neurotypical child.”In their first report on the trial in 2017, the team highlighted a number of distinct changes in the microbiome after the transplants, in particular a surge in the populations of three types of bacteria. Among them was a four-fold increase in Bifidobacterium, a probiotic organism that seems to play a key role in the maintenance of a healthy gut.But figuring out what was happening on a cellular level — to really look inside some guts — would require another vehicle.

    The ASU team needed Mazmanian’s mice.“At the end of the day, what we care about is healing people and how the microbiome affects people,” explains Krajmalnik-Brown. €œThat’s why we work with people. But with mice you can do things that are more mechanistic.”The Great Mouse Detective(Credit. Caltech)Together, Krajmalnik-Brown, Mazmanian and their collaborators would uncover some tantalizing new insights that go a long way to solving the mystery.

    In May 2019, the team published another high-profile paper in Cell, after they transplanted stool samples from Krajmalnik-Brown’s severely autistic patients into the guts of Mazmanian’s germ-free mice. The offspring of these mice showed the autism-like symptoms, such as repetitive and compulsive behavior.This time, the team dug even deeper into the biochemical processes playing out in the brain, looking not just at behavior but at the chemicals involved in creating it. The mice that developed autism-like behaviors had measurably lower levels of two substances called taurine and 5-aminovaleric acid (5AV). When they dug into the literature, the team learned that these two substances are known to mimic activity of a key signaling agent in the brain called gamma-aminobutyric acid (GABA) — a neurotransmitter that other studies have found is deficient in the brains of children with autism.What’s more, some have speculated that the tendency of children with autism to experience sensory overstimulation may stem from the inability to tamp down overexcited neurons.

    A lack of GABA could lead to just that.The scientists next orally administered high levels of taurine and 5AV to pregnant mice with the autistic children’s microbiomes. When their pups were born, the researchers continued to feed the young the substances until they reached adulthood. Compared with untreated animals, the second-generation mice had significantly fewer behavioral symptoms. Taurine reduced repetitive behavior, as measured by marble burying, increased the level of social interaction, and relieved anxiety.

    Mice administered 5AV were more active and social.“We healed humans with behavioral problems,” says Krajmalnik-Brown. €œ[And we] transferred some of those deficits and behaviors to mice — basically the opposite. It’s huge.”Mazmanian hopes to take the next step in the months ahead.“I can flip a switch, turn on a light, I know that switch turns on that light. I don’t know the circuit, I don’t know where the wire is,” Mazmanian says.

    €œExactly how that’s happening … we just don’t understand that.”This most recent study, by itself, hardly proves that dysregulated microbiomes cause the brain disorder — a point that plenty of other scientists skeptical of Mazmanian’s work are happy to make.“The paper made a big splash, but trying to model psychiatric-related human conditions in mice, in my view, is a little bit of a stretch,” says Sangram Sisodia, a neurobiologist at the University of Chicago who studies the microbiome. €œA mouse with autism?. €Nor was that the only criticism. Several researchers have suggested that the group didn’t give proper attention to one of their tests ­— one whose results conflicted with their thesis ­— while others found flaws in the statistical methods they used to assess their results.

    Mazmanian downplays these criticisms, but agrees the work is not yet conclusive.Meanwhile, the ASU trial has also engendered skepticism, mainly due to its tiny sample size, the lack of a control group and the methods by which the children were assessed for autism severity. Krajmalnik-Brown and Adams say they stand by their results, but agree more research is needed. In recent months, they have launched two new studies that will address these issues.Adams insists the work is already changing lives. €œWe followed up with every one of our 18 participants,” he says, referring to the children who received fecal transplants.

    €œSure enough, we found that most of the GI benefits had remained. And family after family said their child just slowly, steadily continued making more improvement.” They published the update in Scientific Reports in spring 2019.“I’m not ready to say the case is closed,” says Mazmanian. €œHealthy skepticism is a good thing. I believe the preclinical data, I believe the mouse data.

    But there’s a lot of studies that still need to be done.” A Healthy Gut, A New OutlookEthan Woods had GI issues and symptoms of autism until researchers introduced new microbes to his gut. His mother says the treatment changed everything. (Credit. Dana Woods)Prior to his fecal transplant at age 7, Ethan Woods suffered from chronic and severe diarrhea, constipation and cramping, symptoms so extreme that to his mother, Dana, he sounded like “a bit like a woman in labor when he was trying to have a bowel movement.” “It was just awful watching your child go through this,” she says, explaining that when she enrolled her autistic son in the Arizona State study, her “only goal was to fix his gut.”Remarkably, Ethan’s agony began to disappear just a few weeks into the trial.

    But that was not the most dramatic difference. Before the transplant, Ethan’s speech was drawn out and slow, his language skills rudimentary. He seemed to live in his own bubble. He had frequent outbursts.

    For as long as Dana could remember, her mornings with Ethan had been marked by arguing, fighting, pushing and anger. But then one morning, something shocking happened.“He woke me up one morning with his face right in my face with this big smile and he said, ‘Morning, Mom!. €™â€‰â€ she recalls. €œAnd he was just excited and happy and ready to go about his day with this big smile.

    It choked me up to the point where I teared up because I had never experienced a happy kid in the morning.”Later, Ethan carried over an iPad and opened an app with a talking cat that repeats back the words children speak aloud. He played back a video recording of himself from just a few weeks earlier.“[He] looks me in the eye and says, ‘Mom, why did I talk like that?. What is wrong with me?. €™ And as soon as he did that, I caught my breath.

    I had to compose myself and say, ‘I don’t know. But do you feel better?. Do you feel different?. Why do you think?.

    €™â€‰â€Ethan’s communication skills had already begun to improve. Within a year of the study, his speech therapist graduated him from speech therapy because he had met all his goals.“He went from one end of the rainbow all the way to the other end of the rainbow,” she says. €œPrior to the study, I was very afraid. My biggest fear was ‘how is he going to navigate the world when I’m not here?.

    €™ And I think I have a lot of hope now that he is going to be OK now on his own.”There’s something strange about the female orgasm, something that scientists have been unable to explain. Biological functions are normally discussed in terms of evolutionary pressure, or reproductive advantage. If a biological trait improves your chances of having more offspring, then it’s more likely to stick around in your species. The male orgasm makes perfect sense — ejaculate contains the genetic material that’s necessary for making babies.

    But the female orgasm has been harder to nail down. Fertilization doesn’t depend on it, and “fun” isn’t exactly in the pantheon of evolutionary explanations.Researchers that study how the female orgasm relates to reproductive success have two main options — either ask people invasive questions about their most personal moments, or to find a way to stick probes in or on them during said moments. Neither of these approaches have resulted in the kind of “wet lab” research that’s the gold standard for biological understanding.What we do know, despite widespread cultural discomfort with talking openly about sex and pleasure, is that there appears to be significant sexual dysfunction in American society. Back in 2014, researchers from the Kinsey Institute, the preeminent U.S.

    Academy for the study of sex and relationships, said as much. In a survey of nearly 3,000 people, they found that men, straight or gay, orgasmed 85 percent of the time during consensual sexual encounters. Lesbian women orgasmed less often, 75 percent of the time, while straight women fared worst with just a 60 percent chance of orgasm. Other studies have shown that something like 10-15 percent of women experience lifelong anorgasmia, meaning they’ve never experienced orgasm.

    A further 40 percent of women report some kind of inability to reach orgasm in the past year.The orgasm gap is hard to explain. Some think that it comes down to straight men’s finesse, or lack thereof, citing the difference between straight and lesbian satisfaction. Indeed, it makes sense that knowing your way around the territory would help. But for many couples this isn’t a helpful revelation, since the emotional maturity necessary to teach sexual dexterity is often out of reach.

    Shortcut to SatisfactionLuckily, we live in an era of Silicon Valley disruption, which has even started lapping at the shores of sex research. Technologist Liz Klinger is at the forefront of this transition. She and her team have built a platform that lets people become citizen scientists of sex —without ever having to get out from between the sheets.About a decade ago, Klinger’s company, Lioness, released what they billed as the first “smart vibrator,” a sex toy that could actually learn about you. The final product was a far cry from the first prototype, which was much more laboratory object than sex toy.The “test device was this whole mess of wires, with a hard connection.

    We had to physically send it to our beta testers, who used it and sent it back,” recalls Klinger. The researchers would download the data collected by the toy’s four sensors — temperature, motion, acceleration and pressure — and compile it into a chart that represented arousal and orgasm, as told through the story of pelvic-floor muscle contractions.It was an immediate success for sex partners who needed ways to talk about pleasure in a more objective way. Klinger recalled that when she got the first beta-test couple on the phone, “the wife was like ‘holy crap, we finally were able to talk about these things that I’ve had a lot of trouble talking about.’ It turned out that she wanted more foreplay, and he didn’t know quite that that meant. He’d spend more time, but it just didn’t match up, you know?.

    € With the company’s signature offering in hand — a chart of sexual arousal over time — Klinger found that couples could have a conversation “without the subtext of ‘oh, you’re not good enough, or I don’t like you enough,’ on the husband’s part and ‘I’m so tired of talking about this’ on the wife’s part,” she says. The chart “can change people’s perceptions of their own experiences, and how they talk about them with others.”Doing the Deed — For ScienceThis spring, the company has launched a research platform dubbed Lioness 2.0 — a new optional service that, unsurprisingly, their data-obsessed users have greeted with open arms. Now, instead of simply using the toy to understand themselves better, Lioness owners can opt in to the kinds of hands-on studies that are necessary for a deeper understanding of sex and pleasure. So far, the company is working with Nigeria’s Society for Family Health to study how pleasure changes with menopause across age, race and orientation, as well as with the U.S.’s Center for Genital Health and Education to explore the role of pelvic floor muscles in orgasm.Pani Farvid, a professor of applied psychology at The New School in New York City, has some reservations about the platform.

    €œI really like what they’re trying to do, but there could be more added to make it a bit more comprehensive. My concern is that there's a misconception that sex is just about the orgasm, that it’s just physiological and that pleasure just has to do with the genitals.” From where she’s sitting, “that’s a very mechanical view of sexuality.” If the Lioness is helping to equalize the orgasm gap, or helping people understand their bodies better, “I think that's great,” says Farvid. €œBut as a critical sexologist, I'm interested in delving deeper into what these practices mean.” If sex is hyper-focused on orgasm, to exclusion of everything else, she cautions that these norms “have real-life negative impacts on people's sex lives and their sense of themselves.”At this point, knee-deep in an era of data collection that was once the sole purview of white-coat-wearing scientists, it’s old news that we need to be careful with what our technology is doing to us. No tool can serve as a cure-all, even if it comes loaded with a neat app and some space-age sensors.

    What it can offer, though, is the opportunity to start a conversation, and the chance to take a long, honest look at something about yourself — whether it’s the number of steps you take every day, or the way you want to be touched.Wondering how to keep your glasses from fogging up when your mask is on?. Look no further. If we've learned one thing throughout the COVID-19 pandemic, it's the importance of wearing a mask. Countless studies have shown over the past eight months that wearing a protective barrier over your nose and mouth — whether it's a standard-issue surgical mask or an N95 respirator — can significantly decrease the odds of catching and transmitting disease.

    What's more, some research shows that masking up can reduce the severity of an infection if a masked person does contract COVID-19. But while masks are potentially lifesaving, they can be uncomfortable, often changing your breathing patterns and fogging up your glasses when breath escapes through the top of the mask. Among people who choose not to wear a mask to prevent the spread of COVID-19, many cite discomfort as a key reason why.Wesley Wilson, a tumor immunologist in Pennsylvania, knows how annoying it can be when your glasses are fogging up. He says fogging is “definitely a problem” among his hospital colleagues, who need to wear protective goggles and surgical masks while on the job.

    Fortunately, they've also picked up a few helpful hacks for keeping their vision clear while wearing a mask with glasses.#1. Use Tape“If you have to keep your mask on for hours, tape works like a charm,” Wilson says. This especially applies to healthcare professionals in his practice who are required to keep their masks on at all times, except during lunch. €œIf you're putting on your mask and taking it off a lot, tape probably isn't practical — but two small pieces of tape on the cheeks keep the mask fitted closer to your face, and the hot air out of your glasses,” he says.#2.

    Fit the Mask to Your FaceWhile some air leakage is to be expected, wearing a mask that fits securely to your face will prevent glass fogging and filter the virus more effectively since less air is coming in or out. Find surgical masks or N95s that come with a nose bridge, a small, flexible piece of metal or plastic that allows the mask to more closely fit the contours of your face. Nose bridges can be sewn inside masks or affixed to the front.Read More. Why It Feels Like You Can't Breathe Inside Your Face Mask#3.

    Adjust Your MaskAccording to the American Academy of Ophthalmology, a minor adjustment in how you wear your mask could be enough to prevent fog as well. Simply pull the mask over your nose and rest your glasses on top of your face mask. As long as the mask is fitted close to your face, this should prevent hot air from slipping out.#4. Spray Your GlassesA former ice hockey player, Wilson says the protective visor under his helmet would often fog with hot air while he was on the ice during games.

    Like an ocean diver, he would use de-misting solution or a defogging spray (such as this one) to keep his visor free of fog. The same concept applies to eyeglass fog caused by masking, he says. €œYou can either buy a spray or you can make your own with either shaving cream or soap and water,” says Wilson. €œWiping some shaving cream on your glasses and then wiping it off will coat them with a similar surface-tension altering compound that prevents fog.”.

    The yearly influenza season threatens to make the COVID-19 pandemic doubly deadly, but I believe that this isn’t inevitable.There are two commonly given vaccines – the pneumococcal vaccine and buy voltaren the Hib vaccine – that protect against bacterial pneumonias. These bacteria complicate both influenza and COVID-19, often leading to death. My examination of disease trends and vaccination rates leads me to believe that broader use of the pneumococcal and Hib vaccines could guard against the worst effects of a COVID-19 illness.I am an immunologist and physiologist interested in the effects of combined buy voltaren infections on immunity. I have reached my insight by juxtaposing two seemingly unrelated puzzles.

    Infants and children buy voltaren get SARS-CoV-2, the virus that causes COVID-19, but very rarely become hospitalized or die. And case numbers and death rates from COVID-19 began varying greatly from nation to nation and city to city even before lockdowns began. I wondered why.One night I woke up with a possible answer. Vaccination rates buy voltaren.

    Most children, beginning at age two months, are vaccinated against numerous diseases. Adults less buy voltaren so. And, both infant and adult vaccination rates vary widely across the world. Could differences in the rates of vaccination against one or more diseases account buy voltaren for differences in COVID-19 risks?.

    As someone who had previously investigated other pandemics such as the Great Flu Pandemic of 1918-19 and AIDS, and who has worked with vaccines, I had a strong background for tracking down the relevant data to test my hypothesis.Pneumococcal Vaccination Rates Correlate With Lower COVID-19 Cases and DeathsI gathered national and some local data on vaccination rates against influenza, polio, measles-mumps-rubella (MMR), diphtheria-tetanus-pertussis (DTP), tuberculosis (BCG), pneumococci and Haemophilus influenzae type B (Hib). I correlated them with COVID-19 case rates and death rates for 24 nations that had experienced their COVID-19 outbreaks at about the same time. I controlled for factors such as percentage of the population who were obese, diabetic or elderly.I found that buy voltaren only pneumococcal vaccines afforded statistically significant protection against COVID-19. Nations such as Spain, Italy, Belgium, Brazil, Peru and Chile that have the highest COVID-19 rates per million have the poorest pneumococcal vaccination rates among both infants and adults.

    Nations with the buy voltaren lowest rates of COVID-19 – Japan, Korea, Denmark, Australia and New Zealand – have the highest rates of pneumococcal vaccination among both infants and adults.A recent preprint study (not yet peer-reviewed) from researchers at the Mayo Clinic has also reported very strong associations between pneumococcal vaccination and protection against COVID-19. This is especially true among minority patients who are bearing the brunt of the coronavirus pandemic. The report also suggests that other vaccines, or combinations of vaccines, such as Hib and MMR may also provide protection.These results are important because in the U.S., childhood vaccination against pneumococci – which protects against Streptococcus pneumoniae bacteria – varies by state from 74% to 92% buy voltaren. Although the CDC recommends that all adults 18-64 in high risk groups for COVID-19 and all adults over the age of 65 get a pneumococcal vaccination, only 23% of high-risk adults and 64% of those over the age of 65 do so.Similarly, although the CDC recommends at all infants and some high-risk adults be vaccinated against Haemophilus influenzae type B (Hib), only 80.7% of children in the U.S.

    And a handful of immunologically compromised adults have been. Pneumococcal and buy voltaren Hib vaccination rates are significantly lower in minority populations in the U.S. And in countries that have been hit harder by COVID-19 than the U.S.Based on these data, I advocate universal pneumococcal and Hib vaccination among children, at-risk adults and all adults over 65 to prevent serious COVID-19 disease.Left. Combined rates buy voltaren of childhood and adult (over 65) pneumococcal vaccination (out of a possible 200).

    Right. Cases (per buy voltaren million) population of COVID-19 at about 90 days into the pandemic for 24 nations. Nations with high pneumococcal vaccination rates have low COVID-19 case rates. (Credit.

    CC BY-SA)How Pneumococcal Vaccination Protects Against COVID-19Protection against serious COVID-19 disease buy voltaren by pneumococcal and Hib vaccines makes sense for several reasons. First, recent studies reveal that the majority of hospitalized COVID-19 patients, and in some studies nearly all, are infected with streptococci, which causes pneumococcal pneumonias, Hib or other pneumonia-causing bacteria. Pneumococcal and Hib vaccinations should protect coronavirus patients from these infections and thus significantly cut the buy voltaren risk of serious pneumonia.I also found that pneumococcal, Hib and possibly rubella vaccines may confer specific protection against the SARS-CoV-2 virus that causes COVID-19 by means of “molecular mimicry.”Molecular mimicry occurs when the immune system thinks one microbe looks like another. In this case, proteins found in pneumococcal vaccines and, to a lesser degree, ones found in Hib and rubella vaccines as well look like several proteins produced by the SARS-CoV-2 virus.Two of these proteins found in pneumococcal vaccines mimic the spike and membrane proteins that permit the virus to infect cells.

    This suggests pneumococcal vaccination may prevent SARS-CoV-2 buy voltaren infection. Two other mimics are the nucleoprotein and replicase that control virus replication. These proteins are made after viral infection, in which case pneumococcal vaccination may control, but not prevent, SARS-CoV-2 replication.Either way, these vaccines may provide proxy protection against SARS-CoV-2 infection that we can implement right now, even before we have a specific virus vaccine. Such protection may not be complete buy voltaren.

    People might still suffer a weakened version of COVID-19 but, like most infants and children, be protected against the worst effects of the infection.Fighting Influenza-related Pneumonias During the COVID-19 PandemicWhile the specific protection these other vaccines confer against COVID-19 has not yet been tested in a clinical trial, I advocate broader implementation of pneumococcal and Hib vaccination for one additional, well-validated reason.Pneumococcal and Hib pneumonias – both caused by bacteria – are the major causes of death following viral influenza. The influenza buy voltaren virus rarely causes death directly. Most often, the virus makes the lungs more susceptible to bacterial pneumonias, which are deadly. Dozens of studies around the world have demonstrated that increasing rates of buy voltaren pneumococcal and Hib vaccination dramatically lowers influenza-related pneumonias.Similar studies demonstrate that the price of using these vaccines is balanced by savings due to lower rates of influenza-related hospitalizations, intensive care unit admissions and deaths.

    In the context of COVID-19, lowering rates of influenza-related hospitalizations and ICU admissions would free up resources to fight the coronavirus, independent of any effect these vaccines might have on SARS-CoV-2 itself. In my opinion, that is a winning scenario.In short, we need not wait for a SARS-CoV-2 vaccine to slow down COVID-19.I believe that we can and should act now by fighting the coronavirus with all the tools at our disposal, including influenza, Hib, pneumococcal and perhaps rubella vaccinations.Preventing pneumococcal and Hib complications of influenza and COVID-19, and perhaps proxy-vaccinating against SARS-CoV-2 itself, helps everyone. Administering these buy voltaren already available and well-tested pneumococcal and Hib vaccines to people will save money by freeing up hospital beds and ICUs. It will also improve public health by reducing the spread of multiple infections and boost the economy by nurturing a healthier population.Robert Root-Bernstein is a Professor of Physiology at Michigan State University.

    This article was originally published on The Conversation under buy voltaren a Creative Commons liscense Read the original here.This story appeared in the November 2020 issue as "Bacteria and the Brain." Subscribe to Discover magazine for more stories like this.It’s not always easy to convince people that the human gut is a sublime and wondrous place worthy of special attention. Sarkis Mazmanian discovered that soon after arriving at Caltech for his first faculty job 14 years ago, when he explained to a local artist what he had in mind for the walls outside his new office.The resulting mural greets visitors to the Mazmanian Lab today. A vaguely psychedelic, 40-foot-long, tube-shaped colon that’s pink, purple and red snakes buy voltaren down the hallway. In a panel next to it, fluorescent yellow and green bacteria explode out of a deeply inflamed section of the intestinal tract, like radioactive lava from outer space.The mural is modest compared with what the scientist has been working on since.

    Over the last decade or so, Mazmanian has been a leading proponent of the idea that the flora of the human digestive tract has a far more powerful effect on the human body and mind than we thought — a scientific effort that earned him a $500,000 MacArthur Fellowship “Genius Grant” in 2012. Since then, Mazmanian and a small but growing cadre of fellow microbiologists have amassed a tantalizing body of evidence on the microbiome’s role in all kinds of brain disorders, including schizophrenia, Alzheimer’s disease, Parkinson’s disease and depression.But the results they’ve seen in autism buy voltaren could, in the end, prove the most transformative. Autism affects about 1 in 59 children in the U.S., and involves profound social withdrawal, communication problems, and sometimes anxiety and aggression. The causes of the buy voltaren brain disorder have remained speculative.

    Now, Mazmanian and other researchers are finding that autism may be inextricably linked to — or even caused by — irregularities in the gut microbiome.A Biology StoryAt 47, Mazmanian — with his shaved head, flannel shirt and skinny jeans — resembles a young, urban hipster on his way to write at the local café. Originally, literary life buy voltaren was his plan. Born in Lebanon to two Armenian refugees, neither of whom had more than a first-grade education, Mazmanian landed in the class of an energetic high school English teacher in California’s San Fernando Valley, where his family first settled. The teacher recognized his gift for language and encouraged him to pursue a career in literature.

    Mazmanian enrolled at UCLA in 1990, planning to major in English.Everything buy voltaren changed when he took his first biology class. Hunched over his new, thick textbook in the library, reading about basic biological concepts like photosynthesis, Mazmanian felt a vast new world opening up to him.Sarkis Mazmanian, shown in front of a mural that celebrates the human gut, is part of a group of microbiologists researching the effects of the digestive tract on a range of disorders. (Credit. Caltech)“For the first time in my life, I wanted to turn the page and see where the story was going to go,” he says.

    €œI think I decided that minute to become a scientist.”Mazmanian was most fascinated by the idea that tiny organisms, invisible to the naked eye, could function as powerful, self-contained machines — powerful enough to take over and destroy the human body. After graduating with a degree in microbiology, Mazmanian joined a UCLA infectious diseases lab and began studying bacteria that cause staph infections.As his dissertation defense approached, Mazmanian read a one-page commentary penned by a prominent microbiologist, highlighting the fact that our intestines are teeming with hundreds, if not thousands, of different species of bacteria. But it was still largely unknown what they are and how they affect the human body.When Mazmanian dug further, he found that no one had yet answered what seemed to him to be the most obvious question. Why would the human immune system, designed to attack and destroy foreign invaders, allow hundreds of species of bacteria to live and thrive in our guts unmolested?.

    To him, the bacteria’s survival implied that we had evolved to coexist with them. And if that were so, he reasoned, there must be some benefit to both the microbes and the human body — a symbiotic relationship. But what was it?. Gut InvadersMazmanian set out to study the link between gut microbes and the immune system.

    As a postdoctoral researcher, he joined the lab of Harvard University infectious disease specialist Dennis Kasper.To start, Mazmanian examined how the immune systems of germ-free mice — lab mice completely protected, starting at birth, from all microbes — differed from those of mice with either few or normal levels of microbes. He expected this initial census would be just a first step in a long and arduous quest for scientific pay dirt. But when he went to examine a printout of his results in the lab, he realized immediately he might already be onto something big. The germ-free mice had a 30 to 40 percent reduction in a specific type of immune cell known as helper T-cells.This colorized close-up of a mouse’s gut reveals the tight relationship between the gut microbe Bacteroides fragilis (red) and the epithelial surface of the colon (blue).

    (Credit. Caltech)Since helper T-cells play a key role in coordinating attacks against invading pathogens, the finding suggested that the immune systems of the germ-free mice were far less robust than those found in peers with normal levels of microbes.“That was exciting, right?. € Mazmanian recalls. €œObviously I repeated it and tested it in a number of different ways.

    Then I asked the next question. €˜Can I restore the [immune] function in an adult animal?. €™â€‰â€Mazmanian colonized the guts of the immunocompromised, germ-free mice with microbes from standard lab mice. After receiving the fecal transplant, their T-cell counts shot up.

    Within a month, their numbers were identical to mice raised outside the germ-free bubble.Resolving to identify the microorganisms causing this transformation, Mazmanian resorted to trial and error. One by one, he added strains of bacteria found in the guts of mice to the guts of germ-free mice.He got nowhere with the first five or six species he examined. Then, simply because it was convenient, he decided to test one more that was readily available in his lab. Mazmanian’s adviser, Kasper, had been studying a gut microbe called Bacteroides fragilis.

    When Mazmanian implanted one of Kasper’s specimens into the gut of his germ-free mice, the results were dramatic. The T-cell numbers spiked to normal. Eventually, Mazmanian demonstrated he could reproduce this effect simply by adding a single molecule that these bacteria produce, called polysaccharide A, to their guts.“There was no logic in the choice whatsoever,” Mazmanian recalls. €œ[B.

    Fragilis] was available, it came from the gut.” In other words, he got lucky.Mazmanian dug deeper and discovered that the biggest impact B. Fragilis had was on the population of a subtype of helper T-cells called regulatory, or suppressor, T-cells. These cells play a key role in preventing the immune system from attacking its host body, protecting against autoimmune or inflammatory diseases. It was the first time any scientist had demonstrated that a single compound from a single microbe could reverse a specific problem with the immune system.To Mazmanian, the finding, published in 2005 in the journal Cell, alluded to new approaches to treating a wide array of autoimmune, inflammatory and allergic disorders.

    What if it were possible to help a faulty immune system by tweaking a patient’s microbiome?. It was with this exploration in mind that he arrived in Pasadena in 2006 to set up his lab at Caltech.A Convenient CollaborationA few years later, Mazmanian was having lunch on campus with neuroscientist and colleague Paul Patterson. Patterson had been preoccupied with a mystery that had, for years, confounded those studying autism in humans. When pregnant mothers have a severe infection in the second trimester, their babies are much more likely to develop autism.As Mazmanian tells it, Patterson was a man of few words, and at lunch Mazmanian was “going on and on” about his own work.“You know,” Patterson interjected thoughtfully, “I think kids with autism have GI issues.”Patterson recalled reading that something like 60 percent of children with autism had some form of clinical GI problem, such as bloating, constipation, flatulence or diarrhea.

    Was it possible, he wondered, that there was a microbiome connection?. As they talked, Mazmanian’s excitement grew.A few years earlier, Patterson had discovered that when he exposed pregnant mice to pathogens like the influenza virus, they gave birth to pups that grew up more likely to be startled by loud noises, to shy away from social contact and to groom themselves repetitively — symptoms that resemble those of autism. Patterson was in the process of comparing the brains of these autism-mimicking mice with their neurotypical cousins to see if he could detect any differences that might explain how the maternal immune system was somehow interfering with the pups’ brain development.Mazmanian had a suggestion. The next time Patterson sacrificed one of his autistic mice to study their brains, what if he set the intestines aside for his colleague down the hall?.

    When the guts arrived in Mazmanian’s lab, he found that the intestines of the neurotypical mice looked normal. But the guts of the autism-mimicking offspring were almost uniformly inflamed. Could it be that the microbiome was the cause of this inflammation?. And could that, in turn, be somehow connected to the behavioral symptoms?.

    Throughout the winter and spring of 2012, Mazmanian and Patterson continued their conversation. Mazmanian found distinct differences in the microbiomes of the mice. And, they noticed, the mice with the features of autism had leaky gut syndrome, an increased permeability of the gut lining that can allow pathogens and allergens to leach out. This condition had also been reported in children with autism.So Mazmanian and Patterson turned their attention outside the gut.

    They took blood samples to see if any gut microbes, or the compounds they produce, were circulating in the rest of the body. They homed in on one molecule in particular, called 4-ethylphenyl sulfate, which was roughly 45 times as abundant in the mice that had symptoms of autism. And it looked familiar. Structurally, it was almost identical to a molecule recently found to be significantly elevated in human children with autism.It was enough to take the next step.

    Every day for three weeks, Mazmanian injected the molecule, harvested from the mice with autism-like symptoms, directly into the bloodstream of 5-week-old normal lab mice (the age at which the autistic mice normally developed leaky gut). Then Mazmanian and his team gave them a series of behavioral tests. The mice were far more easily startled and were less comfortable in large empty spaces than their untreated peers, indications of an increase in anxiety-related behaviors commonly seen in the mice with autism-like symptoms. The researchers published their results in Cell in 2013.Though surprising, the data made sense in some ways.

    Many drug companies rely on small-molecule drugs that can be taken orally, but still manage to cross the blood-brain barrier and affect behavior. It seemed entirely possible that small molecules, created by bacteria in the gut, could enter the bloodstream and reach the brain. And they don’t even have to leak out of the gut to do so.Of Mice and MenPatterson died in 2014, at age 70, just six months after the publication of the duo’s groundbreaking Cell paper. Around the same time, a series of parallel experiments in a clinic hundreds of miles away was already paving the way forward.

    While Patterson and Mazmanian had been working in mice, Rosa Krajmalnik-Brown, a microbiologist at Arizona State University, had teamed up with Jim Adams, who directs the university’s autism and Asperger’s research program, to study humans.The researchers were conducting a detailed analysis of the microbiome of human autism patients and found that the bacteria were far less diverse in the children with autism. Notably, several important species involved in the digestion of carbohydrates were severely depleted.Krajmalnik-Brown and Adams launched a preliminary trial to test the effects of fecal transplants on 18 children between the ages of 7 and 16 with severe autism, who also had severe GI issues. The researchers administered powerful antibiotics to kill off the microbiomes of the children and followed them with a bowel cleanse. They then replaced the microbes with transplanted flora taken from the guts of healthy neurotypical adult volunteers.The results were better than anyone could have expected.

    The procedure resulted in a large reduction in GI symptoms and increased the diversity of bacteria in the children’s guts. But more significantly, their neurological symptoms were reduced. At the onset of the study in 2017, an independent evaluator found 83 percent of participants had severe autism. Two years after the initial trial, only 17 percent were rated as severely autistic.

    And 44 percent were no longer on the autism scale.“[My child] did a complete 180,” says Dana Woods, whose then-7-year-old son Ethan enrolled in the initial study five years ago. €œHis ability to communicate is so much different now. He’s just so much more present. He’s so much more aware.

    He’s no longer in occupational therapy. He’s no longer in speech therapy. After the study, he tested two points away from a neurotypical child.”In their first report on the trial in 2017, the team highlighted a number of distinct changes in the microbiome after the transplants, in particular a surge in the populations of three types of bacteria. Among them was a four-fold increase in Bifidobacterium, a probiotic organism that seems to play a key role in the maintenance of a healthy gut.But figuring out what was happening on a cellular level — to really look inside some guts — would require another vehicle.

    The ASU team needed Mazmanian’s mice.“At the end of the day, what we care about is healing people and how the microbiome affects people,” explains Krajmalnik-Brown. €œThat’s why we work with people. But with mice you can do things that are more mechanistic.”The Great Mouse Detective(Credit. Caltech)Together, Krajmalnik-Brown, Mazmanian and their collaborators would uncover some tantalizing new insights that go a long way to solving the mystery.

    In May 2019, the team published another high-profile paper in Cell, after they transplanted stool samples from Krajmalnik-Brown’s severely autistic patients into the guts of Mazmanian’s germ-free mice. The offspring of these mice showed the autism-like symptoms, such as repetitive and compulsive behavior.This time, the team dug even deeper into the biochemical processes playing out in the brain, looking not just at behavior but at the chemicals involved in creating it. The mice that developed autism-like behaviors had measurably lower levels of two substances called taurine and 5-aminovaleric acid (5AV). When they dug into the literature, the team learned that these two substances are known to mimic activity of a key signaling agent in the brain called gamma-aminobutyric acid (GABA) — a neurotransmitter that other studies have found is deficient in the brains of children with autism.What’s more, some have speculated that the tendency of children with autism to experience sensory overstimulation may stem from the inability to tamp down overexcited neurons.

    A lack of GABA could lead to just that.The scientists next orally administered high levels of taurine and 5AV to pregnant mice with the autistic children’s microbiomes. When their pups were born, the researchers continued to feed the young the substances until they reached adulthood. Compared with untreated animals, the second-generation mice had significantly fewer behavioral symptoms. Taurine reduced repetitive behavior, as measured by marble burying, increased the level of social interaction, and relieved anxiety.

    Mice administered 5AV were more active and social.“We healed humans with behavioral problems,” says Krajmalnik-Brown. €œ[And we] transferred some of those deficits and behaviors to mice — basically the opposite. It’s huge.”Mazmanian hopes to take the next step in the months ahead.“I can flip a switch, turn on a light, I know that switch turns on that light. I don’t know the circuit, I don’t know where the wire is,” Mazmanian says.

    €œExactly how that’s happening … we just don’t understand that.”This most recent study, by itself, hardly proves that dysregulated microbiomes cause the brain disorder — a point that plenty of other scientists skeptical of Mazmanian’s work are happy to make.“The paper made a big splash, but trying to model psychiatric-related human conditions in mice, in my view, is a little bit of a stretch,” says Sangram Sisodia, a neurobiologist at the University of Chicago who studies the microbiome. €œA mouse with autism?. €Nor was that the only criticism. Several researchers have suggested that the group didn’t give proper attention to one of their tests ­— one whose results conflicted with their thesis ­— while others found flaws in the statistical methods they used to assess their results.

    Mazmanian downplays these criticisms, but agrees the work is not yet conclusive.Meanwhile, the ASU trial has also engendered skepticism, mainly due to its tiny sample size, the lack of a control group and the methods by which the children were assessed for autism severity. Krajmalnik-Brown and Adams say they stand by their results, but agree more research is needed. In recent months, they have launched two new studies that will address these issues.Adams insists the work is already changing lives. €œWe followed up with every one of our 18 participants,” he says, referring to the children who received fecal transplants.

    €œSure enough, we found that most of the GI benefits had remained. And family after family said their child just slowly, steadily continued making more improvement.” They published the update in Scientific Reports in spring 2019.“I’m not ready to say the case is closed,” says Mazmanian. €œHealthy skepticism is a good thing. I believe the preclinical data, I believe the mouse data.

    But there’s a lot of studies that still need to be done.” A Healthy Gut, A New OutlookEthan Woods had GI issues and symptoms of autism until researchers introduced new microbes to his gut. His mother says the treatment changed everything. (Credit. Dana Woods)Prior to his fecal transplant at age 7, Ethan Woods suffered from chronic and severe diarrhea, constipation and cramping, symptoms so extreme that to his mother, Dana, he sounded like “a bit like a woman in labor when he was trying to have a bowel movement.” “It was just awful watching your child go through this,” she says, explaining that when she enrolled her autistic son in the Arizona State study, her “only goal was to fix his gut.”Remarkably, Ethan’s agony began to disappear just a few weeks into the trial.

    But that was not the most dramatic difference. Before the transplant, Ethan’s speech was drawn out and slow, his language skills rudimentary. He seemed to live in his own bubble. He had frequent outbursts.

    For as long as Dana could remember, her mornings with Ethan had been marked by arguing, fighting, pushing and anger. But then one morning, something shocking happened.“He woke me up one morning with his face right in my face with this big smile and he said, ‘Morning, Mom!. €™â€‰â€ she recalls. €œAnd he was just excited and happy and ready to go about his day with this big smile.

    It choked me up to the point where I teared up because I had never experienced a happy kid in the morning.”Later, Ethan carried over an iPad and opened an app with a talking cat that repeats back the words children speak aloud. He played back a video recording of himself from just a few weeks earlier.“[He] looks me in the eye and says, ‘Mom, why did I talk like that?. What is wrong with me?. €™ And as soon as he did that, I caught my breath.

    I had to compose myself and say, ‘I don’t know. But do you feel better?. Do you feel different?. Why do you think?.

    €™â€‰â€Ethan’s communication skills had already begun to improve. Within a year of the study, his speech therapist graduated him from speech therapy because he had met all his goals.“He went from one end of the rainbow all the way to the other end of the rainbow,” she says. €œPrior to the study, I was very afraid. My biggest fear was ‘how is he going to navigate the world when I’m not here?.

    €™ And I think I have a lot of hope now that he is going to be OK now on his own.”There’s something strange about the female orgasm, something that scientists have been unable to explain. Biological functions are normally discussed in terms of evolutionary pressure, or reproductive advantage. If a biological trait improves your chances of having more offspring, then it’s more likely to stick around in your species. The male orgasm makes perfect sense — ejaculate contains the genetic material that’s necessary for making babies.

    But the female orgasm has been harder to nail down. Fertilization doesn’t depend on it, and “fun” isn’t exactly in the pantheon of evolutionary explanations.Researchers that study how the female orgasm relates to reproductive success have two main options — either ask people invasive questions about their most personal moments, or to find a way to stick probes in or on them during said moments. Neither of these approaches have resulted in the kind of “wet lab” research that’s the gold standard for biological understanding.What we do know, despite widespread cultural discomfort with talking openly about sex and pleasure, is that there appears to be significant sexual dysfunction in American society. Back in 2014, researchers from the Kinsey Institute, the preeminent U.S.

    Academy for the study of sex and relationships, said as much. In a survey of nearly 3,000 people, they found that men, straight or gay, orgasmed 85 percent of the time during consensual sexual encounters. Lesbian women orgasmed less often, 75 percent of the time, while straight women fared worst with just a 60 percent chance of orgasm. Other studies have shown that something like 10-15 percent of women experience lifelong anorgasmia, meaning they’ve never experienced orgasm.

    A further 40 percent of women report some kind of inability to reach orgasm in the past year.The orgasm gap is hard to explain. Some think that it comes down to straight men’s finesse, or lack thereof, citing the difference between straight and lesbian satisfaction. Indeed, it makes sense that knowing your way around the territory would help. But for many couples this isn’t a helpful revelation, since the emotional maturity necessary to teach sexual dexterity is often out of reach.

    Shortcut to SatisfactionLuckily, we live in an era of Silicon Valley disruption, which has even started lapping at the shores of sex research. Technologist Liz Klinger is at the forefront of this transition. She and her team have built a platform that lets people become citizen scientists of sex —without ever having to get out from between the sheets.About a decade ago, Klinger’s company, Lioness, released what they billed as the first “smart vibrator,” a sex toy that could actually learn about you. The final product was a far cry from the first prototype, which was much more laboratory object than sex toy.The “test device was this whole mess of wires, with a hard connection.

    We had to physically send it to our beta testers, who used it and sent it back,” recalls Klinger. The researchers would download the data collected by the toy’s four sensors — temperature, motion, acceleration and pressure — and compile it into a chart that represented arousal and orgasm, as told through the story of pelvic-floor muscle contractions.It was an immediate success for sex partners who needed ways to talk about pleasure in a more objective way. Klinger recalled that when she got the first beta-test couple on the phone, “the wife was like ‘holy crap, we finally were able to talk about these things that I’ve had a lot of trouble talking about.’ It turned out that she wanted more foreplay, and he didn’t know quite that that meant. He’d spend more time, but it just didn’t match up, you know?.

    € With the company’s signature offering in hand — a chart of sexual arousal over time — Klinger found that couples could have a conversation “without the subtext of ‘oh, you’re not good enough, or I don’t like you enough,’ on the husband’s part and ‘I’m so tired of talking about this’ on the wife’s part,” she says. The chart “can change people’s perceptions of their own experiences, and how they talk about them with others.”Doing the Deed — For ScienceThis spring, the company has launched a research platform dubbed Lioness 2.0 — a new optional service that, unsurprisingly, their data-obsessed users have greeted with open arms. Now, instead of simply using the toy to understand themselves better, Lioness owners can opt in to the kinds of hands-on studies that are necessary for a deeper understanding of sex and pleasure. So far, the company is working with Nigeria’s Society for Family Health to study how pleasure changes with menopause across age, race and orientation, as well as with the U.S.’s Center for Genital Health and Education to explore the role of pelvic floor muscles in orgasm.Pani Farvid, a professor of applied psychology at The New School in New York City, has some reservations about the platform.

    €œI really like what they’re trying to do, but there could be more added to make it a bit more comprehensive. My concern is that there's a misconception that sex is just about the orgasm, that it’s just physiological and that pleasure just has to do with the genitals.” From where she’s sitting, “that’s a very mechanical view of sexuality.” If the Lioness is helping to equalize the orgasm gap, or helping people understand their bodies better, “I think that's great,” says Farvid. €œBut as a critical sexologist, I'm interested in delving deeper into what these practices mean.” If sex is hyper-focused on orgasm, to exclusion of everything else, she cautions that these norms “have real-life negative impacts on people's sex lives and their sense of themselves.”At this point, knee-deep in an era of data collection that was once the sole purview of white-coat-wearing scientists, it’s old news that we need to be careful with what our technology is doing to us. No tool can serve as a cure-all, even if it comes loaded with a neat app and some space-age sensors.

    What it can offer, though, is the opportunity to start a conversation, and the chance to take a long, honest look at something about yourself — whether it’s the number of steps you take every day, or the way you want to be touched.Wondering how to keep your glasses from fogging up when your mask is on?. Look no further. If we've learned one thing throughout the COVID-19 pandemic, it's the importance of wearing a mask. Countless studies have shown over the past eight months that wearing a protective barrier over your nose and mouth — whether it's a standard-issue surgical mask or an N95 respirator — can significantly decrease the odds of catching and transmitting disease.

    What's more, some research shows that masking up can reduce the severity of an infection if a masked person does contract COVID-19. But while masks are potentially lifesaving, they can be uncomfortable, often changing your breathing patterns and fogging up your glasses when breath escapes through the top of the mask. Among people who choose not to wear a mask to prevent the spread of COVID-19, many cite discomfort as a key reason why.Wesley Wilson, a tumor immunologist in Pennsylvania, knows how annoying it can be when your glasses are fogging up. He says fogging is “definitely a problem” among his hospital colleagues, who need to wear protective goggles and surgical masks while on the job.

    Fortunately, they've also picked up a few helpful hacks for keeping their vision clear while wearing a mask with glasses.#1. Use Tape“If you have to keep your mask on for hours, tape works like a charm,” Wilson says. This especially applies to healthcare professionals in his practice who are required to keep their masks on at all times, except during lunch. €œIf you're putting on your mask and taking it off a lot, tape probably isn't practical — but two small pieces of tape on the cheeks keep the mask fitted closer to your face, and the hot air out of your glasses,” he says.#2.

    Fit the Mask to Your FaceWhile some air leakage is to be expected, wearing a mask that fits securely to your face will prevent glass fogging and filter the virus more effectively since less air is coming in or out. Find surgical masks or N95s that come with a nose bridge, a small, flexible piece of metal or plastic that allows the mask to more closely fit the contours of your face. Nose bridges can be sewn inside masks or affixed to the front.Read More. Why It Feels Like You Can't Breathe Inside Your Face Mask#3.

    Adjust Your MaskAccording to the American Academy of Ophthalmology, a minor adjustment in how you wear your mask could be enough to prevent fog as well. Simply pull the mask over your nose and rest your glasses on top of your face mask. As long as the mask is fitted close to your face, this should prevent hot air from slipping out.#4. Spray Your GlassesA former ice hockey player, Wilson says the protective visor under his helmet would often fog with hot air while he was on the ice during games.

    Like an ocean diver, he would use de-misting solution or a defogging spray (such as this one) to keep his visor free of fog. The same concept applies to eyeglass fog caused by masking, he says. €œYou can either buy a spray or you can make your own with either shaving cream or soap and water,” says Wilson. €œWiping some shaving cream on your glasses and then wiping it off will coat them with a similar surface-tension altering compound that prevents fog.”.

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