Hormonal Contraceptive Use May Delay Return of Fecundability

WEDNESDAY, Nov. 18, 2020 — Pregravid use of some hormonal contraceptives is associated with delays in return of fertility, according to a study published online Nov. 11 in The BMJ.

Jennifer J. Yland, from the Boston University School of Public Health, and colleagues examined the correlation between pregravid use of a variety of contraceptive methods and subsequent fecundability in a prospective cohort study. Data were included for 17,954 women who had tried to conceive for up to six menstrual cycles at study entry. Contraceptive histories and personal, medical, and lifestyle characteristics were reported at baseline.

The researchers found that about 38, 13, and 31 percent of participants had recently used oral contraceptives, long-acting reversible contraceptive methods, and barrier methods, respectively. Compared with users of barrier methods, women who had recently stopped using oral contraceptives, the contraceptive ring, and some long-acting reversible contraceptive methods experienced short-term delays in return of fertility. There was a correlation seen for use of injectable contraceptives with decreased fecundability compared with barrier method use (fecundability ratio, 0.65). The longest delay in return of normal fertility was seen for users of injectable contraceptives, followed by users of patch contraceptives, users of oral and ring contraceptives, and users of hormonal and copper intrauterine devices and implant contraceptives (five to eight, four, three, and two cycles, respectively).

“Our results, although imprecise, indicate little or no lasting effect of long-term use of these methods on fecundability,” the authors write.

Several authors disclosed financial ties to the pharmaceutical industry.

Abstract/Full Text

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Having a baby later in life may increase longevity, study suggests

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Women who have kids later on in life may live longer, according to the findings of a recent study.

Following the birth of a woman’s last child, certain measurements may be linked with her projected lifespan, according to a study published Wednesday in Menopause, the journal of The North American Menopause Society (NAMS).

More specifically, leukocyte telomere length – telomeres “are repeating DNA-protein complexes that protect the ends of chromosomes and have proven to be critical for maintaining genomic stability,” per a news release on the findings – may play a role in a woman’s longevity. A woman’s age at the birth of her last child may affect telomere length, ultimately impacting long-term health, the researchers said.

Longer telomeres are thought to be beneficial for long-term health, while shorter ones can signify “various chronic conditions such as cardiovascular disease, type 2 diabetes, some neurologic conditions, and various cancers,” past studies have suggested, according to the news release.

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At least one previous study has suggested that a woman’s age at the birth of her last child affected telomere length, said researchers. The study published Wednesday was larger, including more than 1,200 perimenopausal and postmenopausal women of “various ethnicities and backgrounds.”

“In addition, unlike previous studies, this study took into consideration sociodemographic factors related to childbearing patterns and health decisions,” per the release.

The researchers who conducted the new study found that a woman’s age at the birth of her final child “is positively associated with telomere length, meaning that women who delivered their last child later in life were likely to have longer telomeres, a biomarker of long-term health and longevity.”

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However, “more research is needed to determine whether older maternal age at last birth causes telomeres to lengthen or whether telomere length serves as a proxy for general health and corresponds with a woman’s ability to have a child at a later age,” said Dr. Stephanie Faubion, NAMS medical director, in a statement.

The findings were also limited to women who had one or two live births or those who had used birth control orally, they said.

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Antibiotics May Be Best First Treatment for Appendicitis

TUESDAY, Oct. 6, 2020 — For some patients suffering from appendicitis, antibiotics may do the trick, a large U.S. trial suggests.

More than 70% of patients who received antibiotics avoided surgery for at least 90 days, according to the new report.

“When we compared the outcomes of people treated with antibiotics alone or surgery to remove the appendix, we found that people receiving either treatment felt well at 30 days,” said co-principal investigator Dr. David Talan. “In terms of overall health status, antibiotics were no worse than surgery and allowed most people to avoid an operation in the short term.”

Talan is a professor of emergency medicine and infectious diseases at the David Geffen School of Medicine at UCLA.

In the trial, more than 1,500 patients in 14 U.S. states randomly received antibiotics first or an appendectomy. The trial is the largest ever clinical randomized look at appendicitis treatment, the study authors said.

According to Bonnie Bizzell, chairwoman of the trial’s patient advisory board, “People treated with antibiotics more often returned to the emergency department, but missed less time from work and school. Information like this can be important for individuals as they consider the best treatment option for their unique circumstance.”

About three in 10 patients given antibiotics had surgery within 90 days, according to researcher Dr. David Flum, associate chairman of surgery at the University of Washington School of Medicine, in Seattle. “There were advantages and disadvantages to each treatment, and patients will value these differently based on their unique characteristics, concerns and perspectives.”

Initial treatment with antibiotics created a higher risk for patients with an appendicolith — a calcified deposit within the appendix that occurs in roughly one-quarter of patients. It is associated with more complications and a 40% chance of surgery within 90 days, the researchers said.

The findings were published online Oct. 5 in the New England Journal of Medicine.

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Those who send photos more often during the coronavirus pandemic may be at higher risk of depression

The COVID-19 pandemic has rewritten social media usage habits: People spend more time on Facebook, Instagram and YouTube, and more often, they post pictures and videos of themselves and their loved ones. However, all of this can lead to an increased risk of depression, according to a recent study.

“In order to get a snapshot of the change in social media usage patterns and its mental health implications, we examined the responses of 170 participants using a 20-question online questionnaire during the peak period of the first wave of the coronavirus pandemic in Hungary. The data collection took place between 22 April and 11 May 2020, during the strict lockdown measures, so that the participants could perceive the changes more realistically compared to the pre-epidemic period,” said communication and media expert Alexandra Valéria Sándor, a Ph.D. student at the Doctoral School of Sociology of Eötvös Loránd University, Budapest.

The popularity of social media platforms is shown by the fact that all the respondents were Facebook and Messenger users, followed by YouTube (76%) and Instagram (59%). When asked how their own time spent on social media changed during the pandemic, 19% of respondents said it “greatly increased” and 36% said it “somewhat increased.” As one respondent put it in an open question about changes due to COVID-19, “I had no choice but to use social media much more often because my child’s school requires teachers to keep in touch with parents through Facebook groups.” Another user stressed that they engage in “one hour of video chat every day with family and friends. I haven’t done this before.”

The study also revealed that the participants perceived the change in their own habits significantly differently from what they experienced in their environment during the lockdown period. 42% thought that others’ social media activity had “greatly increased,” and 46% said it had “increased somewhat.” There was a 36% rate of those who said their own social media activity “didn’t change,” while only 6% perceived others as unchanged.

The time spent using social media also increased significantly among participants during the restrictive measures during the first wave of the COVID-19 pandemic. The most significant change was observed for Facebook: The most common response was that the participants spent “more than two hours” per day there, compared to only 9% before the epidemic.

To monitor the intensity of self-representation, respondents also stated the frequency with which they posted or sent pictures and videos of themselves or their loved ones (including their pets) on each social media platform before and during the lockdown. Nearly 18% of them shared such content on Messenger multiple times a day, while 8% said they had done the same before the epidemic.

In terms of self-representation, selfies were the most common on all the platforms examined, but interestingly, users also posted photographs and videos taken in the company of others and on trips. The latter may be explained by the answer of one of the respondents to the related open question who said that they share nice memories during the lockdown.

To obtain a basic assessment of the mental health of participants, the Patient Health Questionnaire-2 (PHQ-2) was administered through the question “Over the last two weeks, how often have you been bothered by the following problems?” These problems included “little interest or pleasure in doing things” and “feeling down, depressed or hopeless.” The possible responses were “not at all” (0 points), “several days” (1 point), “more than half the days” (2 points), and “nearly every day” (3 points). Final PHQ-2 scores ranged from 0-6. A score of at least 3 indicates the possibility of major depressive disorder and suggests that further examinations are necessary; 16% of participants scored a 3 or higher. However, the likelihood of major depression was higher (19%) among those who shared photos of themselves or their close relations “multiple times a day” or “daily” on Messenger, the platform where the frequency of photo sharing increased the most.

“The results show that during the COVID-19 pandemic lockdown, the use of social media has increased, which has also made the sharing of self-representative content more common. The responses also suggest that there may be a link between mental health and the increase in social media usage, which is certainly worth examining in the future with a larger sample. The most important thing was to be able to shed light on the changes in the use of social media for self-representation, their nature, and possible mental hygiene consequences, even with the methodological challenges and time constraints of the pandemic,” concluded Alexandra Valéria Sándor.

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Bacteria virus combo may be cause of neonatal brain infections in Uganda

A newly identified bacteria and a common virus may be the underlying cause of infection-induced hydrocephalus in Uganda, according to an international team of researchers.

“Thirteen years ago, while visiting Uganda and seeing a stream of kids with hydrocephalus after infection I asked the doctors, ‘What is the biggest problem you have that you can’t solve?'” said Steven J. Schiff, Brush Chair Professor of Engineering and professor of engineering science and mechanics, neurosurgery and physics, Penn State. “‘Why don’t you figure out what makes these kids sick?’ was the reply.”

By that time, the doctors at CURE Children’s Hospital of Uganda, had seen more than a thousand infants with infection-caused hydrocephalus and were unable to culture a single thing in the laboratory. They have now seen over 8,000 similar children in this one, small Ugandan hospital.

“Hydrocephalus is the most common childhood neurosurgical condition that we see in the population that we serve,” said Edith Mbabazi-Kabachelor, director of research, CURE Children’s Hospital of Uganda. “If hydrocephalus is left untreated in children less than two years old, the progressive increase in head size will lead to further brain damage, resulting in the majority of these children dying, and those that survive being left with severe cognitive and physical disability.”

Severe systemic bacterial infection during the first four weeks of life accounts for an estimated 680,000 to 750,000 yearly neonatal deaths worldwide. Hydrocephalus is the most common brain disorder in childhood and the largest single cause of childhood hydrocephalus is neonatal infection, accounting for an estimated 160,000 yearly cases, said Schiff.

Over a 5-year study in Uganda, supported by the U.S. National Institutes of Health, using advanced genomic techniques the team uncovered the major bacterial and viral underpinnings of these infections, the researchers report today (Sept. 30) in Science Translational Medicine.

Schiff and his team have studied this problem for more than 10 years, but in the last five years, they took a different approach, using DNA and RNA sequencing techniques to identify the causative agents. The researchers looked at blood and cerebrospinal fluid drawn from 100 cases of post-infectious hydrocephalus and control patients without infection in Uganda. There were 64 infants with post-infectious hydrocephalus and 36 with non-post-infectious hydrocephalus. All infants were under three months old. The researchers prepared the samples in two ways—fresh-frozen and preserved—and they sent samples to two different laboratories in the U.S., where samples were analyzed with different techniques. This was to ensure valid and reproducible results.

“We found this weird bacteria dominating,” said Schiff.

The bacteria was a previously unidentified strain of Paenibacillus thiaminolyticus, now named Mbale after the city where the CURE Children’s Hospital is located.

“The initial link between hydrocephalus and Paenibacillus was made through high-throughput sequencing and PCR analyses at the Center for Infection and Immunity in the Mailman School of Public Health at Columbia University, a renowned center led by W. Ian Lipkin,” said Schiff.

High-throughput sequencing allows sequencing of more than one DNA molecule at the same time, and PCR analysis multiplies existing DNA samples so that they are easier to analyze and identify.

“You build a field of dreams—in this case a platform for pathogen discovery—and wait for the right partner and the right project,” said W. Ian Lipkin, John Snow Professor of Epidemiology and director, Center for Infection and Immunity, Mailman School of Public Health, and professor of pathology and neurology, College of Physicians & Surgeons, Columbia University. “Steven Schiff is a remarkable investigator and this is such a project. It stands out for impact amongst hundreds we’ve done over a period of more than 30 years. Our team is delighted to have had an opportunity to help implicate an agent and contribute to control of this devastating disorder.”

The researchers managed to grow the difficult-to-culture new bacterial strain at Penn State, and tested it on mice. While the common variants of Paenibacillus are harmless, the Mbale strain was lethal to the mice.

The researchers found the new bacterial strain in the cerebrospinal fluid of the infection-induced hydrocephalic children and then only in the youngest patients.

“While we tested infants up to three months old, we mostly identified the cause of infections in those less than six weeks of age,” said Schiff. “If we didn’t study them really early in life, then the infection had already burned out. Between 6 and 12 weeks there were very few positive results.”

Schiff was not satisfied with finding the proposed bacterial cause of the problem, he said. He reasoned that other diseases had both a bacterial and viral component and so the team looked for viral, fungal and parasitic genetic material. They found cytomegalovirus (CMV) in the cerebrospinal fluid of the infection-caused hydrocephalic infants, but not in that of the other hydrocephalus patients.

CMV is a common virus found around the world. The virus causes minor symptoms, if any, in most adults, although babies may be born with congenital CMV or acquire it early in life and be significantly harmed by neurological damage. The researchers only found CMV in the cerebrospinal fluid of babies with post-infection hydrocephalus.

While the researchers believe they have found the source of the infections that cause the high prevalence of hydrocephalus, they do not know where the babies encounter the new bacteria. According to Schiff, the bacteria may be soil- or water-born and more work is necessary to find the bacterial source.

The researchers are creating predictive models that, coupled with data they are now analyzing from thousands of infants and satellite-acquired rainfall to predict optimal treatment for individual locations. The researchers said they do not know if this particular bacterial virus combination exists outside this area of Uganda. However, the same strategy of using DNA and RNA to diagnose previously unknown causes of similar infections can be used in many other regions in the developing world where similar cases are seen.

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Insomnia, sleeping less than six hours may increase risk of cognitive impairment

Middle-aged adults who report symptoms of insomnia and are sleeping less than six hours a night may be at increased risk of cognitive impairment, according to a study by Penn State College of Medicine researchers. The results may help health care professionals understand which patients who report insomnia are at increased risk for developing dementia.

Insomnia is characterized by reports of difficulty falling asleep, difficulty staying asleep, or waking up too early and not being able to get back to sleep. When these symptoms occur at least three nights a week and for at least three months, it is considered a chronic disorder. Researchers found that adults who reported insomnia and obtained less than six hours of measured sleep in the laboratory were two times more likely to have cognitive impairment than people with the same insomnia complaints who got six or more hours of sleep in the lab. The study results were published in the journal Sleep on Sept. 24.

According to Julio Fernandez-Mendoza, associate professor of psychiatry and behavioral health and sleep specialist at Penn State Health Sleep Research and Treatment Center, about 25% of the adult general population reports insomnia symptoms and another 10% suffers from chronic insomnia. He said that being able to distinguish which of these individuals are at risk for further adverse health conditions is critical.

“This study reinforces the need to objectively measure the sleep of adults who complain of insomnia,” Fernandez-Mendoza said. In previous research, the team found that adults with insomnia who obtained less than six hours of sleep were at risk for various cardiometabolic conditions, including hypertension, diabetes, heart disease or stroke and mental health problems, such as depression.

“These new results demonstrate that these middle-aged adults also have an increased risk of cognitive impairment, which can be an early indicator of future dementia in a significant proportion of them,” Fernandez-Mendoza said.

Researchers examined data from the Penn State Adult Cohort, a randomly-selected, population-based sample of 1,741 adults who had one measured night of sleep. Before having their sleep measured in a sound, light and temperature-controlled room, participants completed a clinical history, physical exam and questionnaire to identify self-reported sleep disorders, physical health conditions, mental health problems and substance use. They also were evaluated for cognitive impairment before sleeping in the laboratory, including receiving tests that assessed attention, memory, language and other measures.

Fernandez-Mendoza and colleagues found that adults who reported insomnia symptoms or chronic insomnia and slept less than six hours in the lab were two times more likely to have cognitive impairment when compared to good sleepers. They also found that this association was particularly strong for adults with coexisting cardiometabolic conditions and cognitive impairment, which may be an indicator of vascular cognitive impairment—a condition where poor cardiovascular health results in impaired brain function.

Adults who reported insomnia but who slept six or more hours in the lab were not at risk of cognitive impairment when compared to good sleepers. The research team accounted for potential differences in sociodemographic factors—including age, sex, race, ethnicity, years of education—and the presence of physical and mental health problems, including sleep apnea, as well as substance use, such as smoking and alcohol intake.

Fernandez-Mendoza said that only having one measured night of sleep limited the study’s conclusion to in-lab sleep studies and cautioned that these data do not prove causality. Nevertheless, they further show that insomnia, cognitive impairment and cardiometabolic conditions, like high blood pressure, diabetes and heart disease, often tend to co-occur in adults who get less than six hours of sleep in the lab but not in those who can sleep six hours or more, he highlighted.

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Scientists track down a protein that may add to lung damage in asthma and related diseases

Your lungs and airways need to be stretchy, sort of like balloons. Take a big breath, and they’ll open right up.

Damaged lungs can’t open properly. Patients with asthma, idiopathic pulmonary fibrosis and systemic sclerosis suffer from fibrosis and tissue remodeling, where a build-up of tissue and immune cells, and proteins that form a glue-like substance, keep the airways from expanding. As fibrosis gets worse, taking a breath feels like blowing up a balloon filled with concrete.

In a new study, researchers at La Jolla Institute for Immunology (LJI) report that a protein called TL1A drives fibrosis in several mouse models, triggering tissue remodeling, and making it harder for lungs and airways to function normally.

“Our new study suggests that TL1A and its receptor on cells could be targets for therapeutics aimed at reducing fibrosis and tissue remodeling in patients with severe lung disease,” says LJI Professor Michael Croft, Ph.D., director of scientific affairs at LJI and senior author of the new study in The Journal of Immunology.

Croft’s laboratory is focused on understanding the importance of a family of proteins, called tumor necrosis factors (TNF) and tumor necrosis factor receptors (TNFR), in inflammatory and autoimmune diseases. By investigating these molecules, researchers hope to track down the root causes of inflammation and stop tissue damage before it’s too late.

Previous research had shown that a TNF protein called TL1A can act on immune cells involved in allergic reactions and drive those immune cells to make inflammatory molecules. The Croft Lab wondered—if TL1A leads to inflammation, could it contribute to fibrosis in the lungs?

For the new study, Croft and his colleagues used genetic and therapeutic interventions, tissue staining, and fluorescence imaging techniques to study protein interactions in mouse models of severe asthma, idiopathic pulmonary fibrosis and systemic sclerosis. They first discovered that TL1A acts directly on a receptor on cells in the lungs and bronchial tubes, which leads to fibrosis and tissue remodeling.

We’re all familiar with the idea of tissue remodeling. When a wound on the skin heals, the new area of skin is sometimes shiner, darker or tougher than the skin around it. The tissue has been remodeled. When lungs and airways try to heal—in response to an asthma attack, for example— the cells in the area also change. The damaged area accumulates cells called fibroblasts, which make several glue-like proteins, including collagen. Too much collagen makes the lungs and airways less elastic—and less functional.

As Croft describes it, tissue remodeling is like wound healing, “but wound healing that goes wrong and becomes so exaggerated that it blocks tissue from behaving in its normal way.” With the new study, scientists now know that TL1A is driving this harmful remodeling in the lungs.

In addition to causing fibroblasts to make collagen, the researchers found that TL1A also helps fibroblasts to behave like smooth muscle cells. A thin layer of smooth muscle cells naturally lines the bronchial tubes allowing them to dilate and constrict, but a thick layer of these smooth muscle cells—that includes fibroblasts—will keep the airways from expanding and contracting normally, making it even hard for a patient to breathe.

The scientists then studied lung tissue remodeling in mice that lacked the receptor for TL1A, called DR3, or were given a reagent that blocked TL1A activity. These mice showed less lung remodeling, less collagen deposition and reduced smooth muscle mass in the lungs.

These animal model data may support recent research in humans. Researchers have found that patients with severe asthma have excessive production of TL1A. This could explain why these patients are more vulnerable to lung fibrosis and remodeling.

“This type of research needs to be expanded to really understand if there are subsets of patients with asthma or other inflammatory lung diseases who might express TL1A at higher levels than other patients—which could potentially guide future therapies for targeting TL1A to reduce remodeling and fibrosis,” says Croft.

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Winter may bring a lot more coronavirus cases, new research finds

Early in the coronavirus pandemic, scientists speculated that warm summer air would dampen its spread.

Then as the virus spread rapidly around the world, racking up more than 27 million cases in the spring and summer, the seasonal impact largely fell out of the public conversation.

But researchers at Johns Hopkins University are coming out with new research that suggests rising temperatures do moderate the spread of the virus—and a big new wave of cases could be coming with the cooler fall air.

“We have made significant inroads in this pandemic, and we can say a lot of that is because of social interventions,” said Dr. Adam Kaplin, assistant Hopkins professor of psychiatry and behavioral sciences and the lead researcher.

The warm weather served as a tail wind for those efforts, he said.

“In the fall and colder months we are going to hit a head wind in the other direction and that will make control much more difficult,” Kaplin said.

The findings were so striking that Kaplin took the unusual step of discussing the work while the research still was under review for publication in a scientific journal.

Maryland and other states, as well as other countries, have been easing restrictions with a drop in cases of COVID-19, the disease caused by the coronavirus. But Kaplin said cases could spike with more virus-friendly cool air even with the same restrictions.

The findings of seasonal variation are not new. The flu, the common cold and other coronaviruses typically moderate during warmer months. This could be due to the direct effects of heat on viruses and because fewer people congregate indoors.

Other recent studies or models on the pandemic coronavirus, from the University of Maryland to Harvard and Princeton universities, have found at least some impact from temperature changes or projected that there would be effects even if they weren’t obvious yet.

A paper published in the Journal of the American Medical Association by the Maryland researchers found, for example, the virus acted in a way “consistent with the behavior of a seasonal respiratory virus,” spreading along with temperature and humidity levels. The College Park researchers said it would be possible to develop a weather model to predict places most likely at higher risk for spread.

Rachel Baker from the Princeton Environmental Institute downplayed how much the weather was a factor, instead pointing to the importance of other measures such as wearing masks and physical distancing.

“I think it is possible that upcoming wintertime conditions could increase transmission, particularly in locations with more severe winters,” she said. “However, if we have effective control measures in place, we should be able to limit large secondary outbreaks.”

Baker said studies suggest the effects would be more clear over time. For now, a lot of the studies face challenges, such as differences in how cases are reported around the world.

Dr. Michael Ryan, executive director of the World Health Organization’s Health Emergencies Programme, was even less sure there would be a visible impact from temperature changes.

“This virus has demonstrated no seasonal pattern as such so far,” he said during an Aug. 10 news conference.

But other studies have raised concerns that a cold winter will lead to more cases if steps aren’t taken now to tamp down cases and keep them low.

That includes Dr. David Rubin at the Children’s Hospital of Philadelphia’s PolicyLab, which has incorporated weather into models it regularly produces. (The model suggests a slight uptick in Baltimore in the fall due to various factors including students returning to college campuses.)

The PolicyLab’s own weather study found a narrow range of springlike temperatures were the safest, 60-65 degrees. The researchers hypothesize that colder weather may facilitate more virus transmission but warmer weather may encourage more social gatherings conducive to spread.

The study, published in July in JAMA Network Open, also found distancing measures were the most effective means of controlling the virus no matter the temperature.

“There is a reason the meatpacking industry was hit so hard by this pandemic,” Rubin said. “They do live in congregate housing, but they also work in freezers. … We need to start now and get a good control of the virus so we don’t go into winter already in a surge.”

Kaplin at Hopkins agreed that measures taken now will matter.

A psychiatrist, Kaplin doesn’t normally do weather-related research, but wanted to sound early alarms to get the public’s attention while there is still time.

The issue became clear to him while in Brazil for his wedding in February, a summer month. He noticed a lower rate of viral transmission compared with the infection rate in the United States during a winter month.

Kaplin enlisted statistician colleagues and used data collected by other Hopkins researchers for their public coronavirus dashboard as well as available government weather data. The researchers got information from 50 countries that had reporting early in their outbreaks, before controls such as mask-wearing and physical distancing. The researchers accounted for population and land area in their calculations and looked for a pattern.

They found from January to April, places such as Singapore with average temperatures in the 80s had much lower rates of viral spread than places such as Turkey with average temperatures in the 20s.

Kaplin didn’t want to weigh in on specific actions to get ahead of another big wave of cases. But he said policymakers likely would have to consider tougher restrictions when the temperature drops just to maintain the same level of spread.

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Fewer kids may be carrying coronavirus without symptoms than believed, study says

(HealthDay)—Are infected-but-healthy children major “silent spreaders” of the new coronavirus? New research out of northern Italy, once a COVID-19 hotspot, suggests they might not be.

Rigorous COVID-19 testing of children and adults admitted to a hospital in Milan for reasons other than coronavirus found that just over 1% of kids tested positive for SARS-CoV-2, compared to more than 9% of adults.

That suggests a very low rate of asymptomatic infection among children, and does “not support the hypothesis that children are at higher risk of carrying SARS-CoV-2 asymptomatically than adults,” the researchers reported in the Sept. 14 online edition of JAMA Pediatrics.

One U.S. expert in infectious disease found the report encouraging.

“Since the start of the pandemic it has been very difficult to determine what the actual role of children in the spread of the virus is,” said Dr. Amesh Adalja, senior scholar at the Center for Health Security at Johns Hopkins University, in Baltimore.

“It is becoming clear that they do not amplify this virus the way they do influenza when it comes to community spread,” Adalja said.

In the new study, physicians led by Dr. Carlo Agostoni, of the Ca’Granda Foundation Maggiore Polyclinic Hospital in Milan, conducted two sets of nasal swab tests, up to two days apart, on 214 newly admitted patients.

Eighty-three of these new admissions were children and 131 were adults. All were admitted to the hospital in March and April, at the height of northern Italy’s COVID-19 outbreak. However, all of the patients were admitted for reasons unconnected to COVID-19, and none had shown any symptoms of the illness.

So how many were secretly carrying the virus nonetheless? Based on the swab tests, only 1.2% of the pediatric patients turned up positive for infection, compared to 9.2% of adults.

The low rate of carriage among kids in a city with a burgeoning number of COVID-19 cases suggests “that [children’s] role as facilitators of the spreading of SARS-CoV-2 infection could be reconsidered,” the study authors wrote.

Still, the researchers stressed that this is a small sample from just one hospital, so the findings shouldn’t be considered definitive.

And of course community outbreaks of COVID-19 tied to asymptomatic but infected children are happening in the United States. On Friday, researchers from the U.S. Centers for Disease Control and Prevention issued a report on a cluster of cases originating from two Salt Lake City day care facilities. The report found that 12 youngsters infected with coronavirus (only three showed any symptoms) enrolled at two day care centers easily passed SARS-CoV-2 to at least 12 family members, one of whom ended up hospitalized.

So as millions of children head back to school, uncertainty as to their role in the spread of COVID-19 continues, Adalja said.

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Genetic mutations may be linked to infertility, early menopause

A new study from Washington University School of Medicine in St. Louis identifies a specific gene’s previously unknown role in fertility. When the gene is missing in fruit flies, roundworms, zebrafish and mice, the animals are infertile or lose their fertility unusually early but appear otherwise healthy. Analyzing genetic data in people, the researchers found an association between mutations in this gene and early menopause.

The study appears Aug. 28 in the journal Science Advances.

The human gene—called nuclear envelope membrane protein 1 (NEMP1)—is not widely studied. In animals, mutations in the equivalent gene had been linked to impaired eye development in frogs.

The researchers who made the new discovery were not trying to study fertility at all. Rather, they were using genetic techniques to find genes involved with eye development in the early embryos of fruit flies.

“We blocked some gene expression in fruit flies but found that their eyes were fine,” said senior author Helen McNeill, Ph.D., the Larry J. Shapiro and Carol-Ann Uetake-Shapiro Professor and a BJC Investigator at the School of Medicine. “So, we started trying to figure out what other problems these animals might have. They appeared healthy, but to our surprise, it turned out they were completely sterile. We found they had substantially defective reproductive organs.”

Though it varied a bit by species, males and females both had fertility problems when missing this gene. And in females, the researchers found that the envelope that contains the egg’s nucleus—the vital compartment that holds half of an organism’s chromosomes—looked like a floppy balloon.

“This gene is expressed throughout the body, but we didn’t see this floppy balloon structure in the nuclei of any other cells,” said McNeill, also a professor of developmental biology. “That was a hint we’d stumbled across a gene that has a specific role in fertility. We saw the impact first in flies, but we knew the proteins are shared across species. With a group of wonderful collaborators, we also knocked this gene out in worms, zebrafish and mice. It’s so exciting to see that this protein that is present in many cells throughout the body has such a specific role in fertility. It’s not a huge leap to suspect it has a role in people as well.”

To study this floppy balloon-like nuclear envelope, the researchers used a technique called atomic force microscopy to poke a needle into the cells, first penetrating the outer membrane and then the nucleus’s membrane. The amount of force required to penetrate the membranes gives scientists a measure of their stiffness. While the outer membrane was of normal stiffness, the nucleus’s membrane was much softer.

“It’s interesting to ask whether stiffness of the nuclear envelope of the egg is also important for fertility in people,” McNeill said. “We know there are variants in this gene associated with early menopause. And when we studied this defect in mice, we see that their ovaries have lost the pool of egg cells that they’re born with, which determines fertility over the lifespan. So, this finding provides a potential explanation for why women with mutations in this gene might have early menopause. When you lose your stock of eggs, you go into menopause.”

McNeill and her colleagues suspect that the nuclear envelope has to find a balance between being pliant enough to allow the chromosomes to align as they should for reproductive purposes but stiff enough to protect them from the ovary’s stressful environment. With age, ovaries develop strands of collagen with potential to create mechanical stress not present in embryonic ovaries.

“If you have a softer nucleus, maybe it can’t handle that environment,” McNeill said. “This could be the cue that triggers the death of eggs. We don’t know yet, but we’re planning studies to address this question.”

Over the course of these studies, McNeill said they found only one other problem with the mice missing this specific gene: They were anemic, meaning they lacked red blood cells.

“Normal adult red blood cells lack a nucleus,” McNeill said. “There’s a stage when the nuclear envelope has to condense and get expelled from the young red blood cell as it develops in the bone marrow. The red blood cells in these mice aren’t doing this properly and die at this stage. With a floppy nuclear envelope, we think young red blood cells are not surviving in another mechanically stressful situation.”

The researchers would like to investigate whether women with fertility problems have mutations in NEMP1. To help establish whether such a link is causal, they have developed human embryonic stem cells that, using CRISPR gene-editing technology, were given specific mutations in NEMP1 listed in genetic databases as associated with infertility.

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