Publisher Health

A new Danish study may be the first step towards much faster and more accurate diagnosis of a wide range of conditions that require regulation of the body’s stress hormone: cortisol.
The researchers have discovered a groundbreaking method of measuring levels of free cortisol directly from a blood sample very simply and quickly with just a few drops of blood.
This is in sharp contrast to the current practice, which is both demanding and imprecise.
“The current methods of measuring free cortisol from blood or saliva are very onerous and require processing of the sample. The most common method is therefore to collect urine over a few days instead. Unfortunately, collecting every drop of urine over several days requires great perseverance from patients. It can be almost impossible, even if the patients are hospitalised, and this is probably why we see up to 60 per cent variation in the urine free cortisol measurements in the individual patient,” explains Andreas Lodberg, MD and postdoc at the Department of Biomedicine, Aarhus University.
Accurate and reliable method
The new method addresses many of these challenges, as it uses a so-called cell-based assay. This not only improves the accuracy and reliability of cortisol measurements, but also evens out the high variation normally observed in patient samples.
An assay is the analytical procedure used to measure the level of a substance — in this case cortisol.

Currently, immunoassays using antibodies is the most common method, but the possibility of using the cell-based assay HEK293F-GRE opens completely new doors.
This makes it possible to measure the total level of cortisol, including both natural free cortisol and synthetic cortisol from medicinal products.
Measures total hormone level
The new approach has the potential to remove the limitations associated with current methods. Traditional tests, for example, cannot distinguish synthetic cortisol from natural cortisol, which is problematic in patients who have received treatment with synthetic cortisol.
This can lead to misdiagnoses or incorrect dosage of medication. The cell-based test eliminates this problem by measuring the total hormone level.
“Being able to measure the total cortisol level accurately means we can potentially adapt treatment more precisely and reduce the risk of side effects,” explains Andreas Lodberg.

A possible game changer
In this way, the test can be a game changer for diagnosing and treating patients who need cortisol regulation. This may be stress-related illnesses such as anxiety and depression, chronic illnesses such as diabetes and cancer, and inflammatory diseases such as allergies and asthma.
Andreas Lodberg emphasises that there is still a need to explore how the method can best be integrated into clinical practice.
The goal is to make the test available using a standard blood sample for doctors to improve patient care.
“Our validation shows that this method meets the stringent criteria set by the U.S. Food and Drug Administration, making it a promising candidate for future use in clinical laboratories,” says Andreas Lodberg.

A synthetic chemical called Bisphenol A, or BPA, is widely used in the production of durable plastic products including eyewear, water bottles and epoxy resins. But it’s also an endocrine disruptor, which means that it can interfere with normal hormone functions in the body. Studies suggest that high levels of exposure may be detrimental to human health in a variety of ways; it may also alter the gut microbiome.
But the connections aren’t clear. Researchers in Spain recently studied a group of over 100 children to identify microbes that play a role in BPA exposure and degradation, with the larger goal of understanding the complicated relationship between that process and childhood obesity. In their study, published this week in mSystems, the researchers found more unique bacteria taxa in children of normal weight than in overweight or obese children.
The findings suggest that BPA exposure could promote different microbial communities in normal weight children than those in children with obesity or who are overweight.
“We found that the gut microbial community responds differently to BPA exposure depending on the BMI (body-mass index) of the individual,” said microbiologist Margarita Aguilera, Ph.D., at the University of Granada in Spain. Aguilera is a senior author on the study. Those connections, she said, “underscore the intricate interplay between gut microbiota and potential human pathophysiology resulting from cumulative BPA exposure.”
Previous studies have investigated symptoms and effects associated with BPA exposure. Others have used mouse models and 16S rRNA gene sequencing, which can reveal microbes in complex mixtures of materials, like those from the gut or water. For the new study, the researchers, including Ana López-Moreno, Ph.D., who led the experimental work as part of her doctoral thesis, instead combined analyses of cultured samples with amplicon sequencing — an approach that, to their knowledge, hasn’t been used before.
The results came from a study of 106 children in Spain, roughly half boys and half girls, all between the ages of 5 and 10. They had participated in the OBEMIRISK project, an effort to understand the interplay between BPA and the gut microbiome sponsored by the European Food Safety Authority. Sixty of the children were normal weight; the rest were either overweight or obese. Fecal samples from the children were exposed to several levels of BPA and allowed to incubate for 3 days. Then, the researchers used 16s rRNA sequencing and amplicon sequencing, ultimately identifying 333 BPA-resistant bacterial species.
Notably, species of Clostridium and Romboutsia found in the BPA-cultured samples promoted the richness of microbiota communities. Generally, Aguilera’s team noted, normal-weight children hosted a more diverse, enriched and structured network of bacteria than those found in the groups of overweight and obese children. Those results, she said, suggest that the gut microbiota in normal-weight children may be more resilient when exposed to xenobiotic substances like BPA.
Knowing which microbes participate in the complex network connecting BPA, obesity and the gut microbiome, Aguilera said, could point to future interventions and policy changes that may reduce the risk of childhood obesity worldwide. In future work, she said the researchers plan to similarly investigate how exposure to other synthetic chemicals, including parabens and phthalates, may influence the composition of the gut microbiome. Her group’s overarching goal, however, is to elucidate the mechanisms behind an invisible but widespread threat.
“We want to raise awareness about the health risks associated with microplastics that enter our bodies, and those that circulate in the environment,” Aguilera said. “It’s crucial for individuals to be mindful of these concerns.”

The most recent COVID-19 booster shot reduces adults’ risk of moderate or severe COVID by more than half, according to a new nationwide data study from September 2023 through January 2024, a period of JN.1 variant dominance.
The new study is one of the first to evaluate protection provided by the updated shot against COVID-19-associated emergency department and urgent care visits (markers for moderate disease) and against hospitalizations (a marker for severe disease), in individuals 18 and older, due to JN.1, the most recently predominant strain of COVID.
“Halving your risk of needing to visit an E.D. or urgent care center or to be treated in the hospital for COVID is significant,” said study co-author Shaun Grannis, M.D., M.S., Regenstrief Institute vice president for data and analytics and a professor at Indiana University School of Medicine. “As an informatician I want to highlight that the data we analyzed came from different populations and geographic locations, adults of all ages and the most recent COVID strain. This analysis strongly supports the benefit of getting a booster shot and as a clinician, I encourage my patients to do so.”
“These are encouraging findings,” said study co-author Brian Dixon, PhD, MPA, interim director of Regenstrief Institute’s Clem McDonald Center for Biomedical Informatics and professor at Indiana University Richard M. Fairbanks School of Public Health. “These estimates of vaccine effectiveness are what we would expect for an annual booster designed for an endemic virus that continues to evolve. We looked at a longer time period than similar studies in Europe, and we found good performance. Yet we do need to be alert to the presumed waning of the updated booster’s effectiveness, which we have seen in earlier COVID-19 vaccines. Americans should expect the CDC to recommend future boosters, likely on an annual schedule.”
These findings of protection against moderate and severe disease provided by the booster in this large study are consistent with those of an earlier, small scale study of individuals seen for testing at a pharmacy. That study did not include hospitalized patients.
The authors of the new study, co-authored by Drs. Grannis and Dixon, concluded, “In this analysis of updated COVID-19 VE [vaccine effectiveness], receipt of an updated COVID-19 vaccine dose provided protection against COVID-19-associated ED/UC [emergency department/critical care] visits and hospitalizations among immunocompetent adults. CDC will continue monitoring VE of updated COVID-19 vaccines. All adults should stay up to date with recommended COVID-19 vaccines, including receiving a dose of updated vaccine.”
“Interim Effectiveness of Updated 2023-2024 (Monovalent XBB.1.5) COVID-19 Vaccines Against COVID-19-Associated Emergency Department and Urgent Care Encounters and Hospitalization Among Immunocompetent Adults Aged ≥18 Years — VISION and IVY Networks, September 2023-January 2024” is published in Morbidity and Mortality Report (MMWR). The study was funded by the CDC.

Researchers have discovered how “leaky” mitochondria — the powerhouses of our cells — can drive harmful inflammation responsible for diseases such as lupus and rheumatoid arthritis. Scientists may be able to leverage the findings to develop better treatments for those diseases, improve our ability to fight off viruses and even slow aging.
The new discovery reveals how genetic material can escape from our cellular batteries, known as mitochondria, and prompt the body to launch a damaging immune response. By developing therapies to target this process, doctors may one day be able to stop the harmful inflammation and prevent the toll it takes on our bodies.
“When mitochondria don’t correctly replicate their genetic material, they try to eliminate it. However, if this is happening too often and the cell can’t dispose of all of it, it can cause inflammation, and too much inflammation can lead to disease, including autoimmune and chronic diseases,” said researcher Laura E. Newman, PhD, of the University of Virginia School of Medicine. “Now that we are beginning to understand how this inflammation starts, we might be able to prevent this process, with the ultimate goal of limiting inflammation and treating disease.”
Powering Inflammation
Mitochondria have their own set of genetic material, separate from the DNA that serves as the operating instructions for our cells. Scientists have known that this mitochondrial DNA, known as mtDNA, can escape into our cells and cause inflammation. But exactly what caused this has been a mystery until now.
“We knew that mtDNA was escaping mitochondria, but how was still unclear,” said Gerald Shadel, PhD, director of the San Diego-Nathan Shock Center of Excellence in the Basic Biology of Aging at the Salk Institute. “Using imaging and cell biology approaches, we’re able to trace the steps of the pathway for moving mtDNA out of the mitochondria, which we can now try to target with therapeutic interventions to hopefully prevent the resulting inflammation.”
Shadel and Newman, then a postdoctoral researcher in Shadel’s lab, and their collaborators used sophisticated imaging techniques to determine what was happening inside the leaky mitochondria. They found that the leak was triggered by a malfunction in mtDNA replication. This caused the accumulation of protein masses caused nucleoids.

To try to fix this problem, the cell containing the faulty mitochondrion begins to export the excess nucleoids to its cellular trash bins. But the trash bins, called endosomes, can become overwhelmed by the volume of debris, the scientists found. These overburdened endosomes respond by releasing mtDNA into the cell — in short, the trash can overflows.
“We had a huge breakthrough when we saw that mtDNA was inside of a mysterious membrane structure once it left mitochondria. After assembling all of the puzzle pieces, we realized that structure was an endosome,” Newman said. “That discovery eventually led us to the realization that the mtDNA was being disposed of and, in the process, some of it was leaking out.”
The cell responds to this hazardous waste spill by flagging the nucleoids as foreign DNA, like a virus, and launches an immune response that results in harmful inflammation, the scientists determined.
“Using our cutting-edge imaging tools for probing mitochondria dynamics and mtDNA release, we have discovered an entirely novel release mechanism for mtDNA,” said researcher Uri Manor, PhD, former director of the Waitt Advanced Biophotonics Core at Salk and current assistant professor at UC San Diego. “There are so many follow-up questions we cannot wait to ask, like how other interactions between organelles control innate immune pathways, how different cell types release mtDNA, and how we can target this new pathway to reduce inflammation during disease and aging.”
Newman will continue to seek these answers in her new role at the UVA School of Medicine’s Department of Cell Biology. “We want to understand the physiological and disease contexts where this process can become activated,” she said. “For example, many viruses attack mitochondria during infection, so we will be testing whether mitochondria purposely use this pathway to sound the alarm against invading viruses, and whether over-reliance on this pathway to fight off infection can later trigger chronic diseases.”
Findings Published
The researchers have published their findings in the scientific journal Nature Cell Biology. The research team consisted of Newman, Sammy Weiser Novak, Gladys R. Rojas, Nimesha Tadepalle, Cara R. Schiavon, Danielle A. Grotjahn, Christina G. Towers, Marie-Ève Tremblay, Matthew P. Donnelly, Sagnika Ghosh, Michaela Medina, Sienna Rocha, Ricardo Rodriguez-Enriquez, Joshua A. Chevez, Ian Lemersal, Manor and Shadel.
The work was supported by the National Institutes of Health, grants R01 AR069876, P30AG068635, 1K99GM141482, 1F32GM137580, T32GM007198, 5R00CA245187 and 5R00CA245187-04S1; an Allen-AHA Initiative in Brain Health and Cognitive Impairment award, 19PABH134610000H; a National Science Foundation NeuroNex Award, 2014862; a Chan-Zuckerberg Initiative Imaging Scientist Award; the LIFE Foundation; a George E. Hewitt Foundation for Medical Research Postdoctoral Fellowship; the Paul F. Glenn Foundation for Medical Research Postdoctoral Fellowship; the Salk Pioneer Fund Postdoctoral Scholar Award; the Waitt Foundation; Yale School of Medicine’s Center for Cellular and Molecular Imaging; a Canada Research Chair (Tier 2) in Neurobiology of Aging and Cognition; and the Canada Foundation for Innovation John R. Evans Leaders Fund, grant 39965.

Microbial life will flourish in mountain streams because of ongoing glacier shrinkage. This is what a team of scientists from EPFL and Charles University, Prague, report in a paper published in Nature Geoscience. Their observations are based on samples collected from 154 glacier-fed streams worldwide as part of the EPFL-led Vanishing Glaciers project, which is funded by the NOMIS Foundation.
Glacier-fed streams are murky, raging torrents in the summer. Large quantities of glacial meltwater churn up rocks and sediment, allowing very little light to reach the streambed, while freezing temperatures and snow in other seasons provide little opportunity for a rich microbiome to develop. But, as glaciers shrink under the effects of global warming, the volume of water originating from glaciers is declining. That means the streams are becoming warmer, calmer, and clearer, giving algae and other microorganisms an opportunity to become abundant and to contribute more to local carbon and nutrient cycles. “We’re witnessing a process of profound change at the level of the microbiome in these ecosystems — nothing short of a ‘green transition’ because of the increased primary production,” says Tom Battin, a full professor at EPFL’s River Ecosystems Laboratory (RIVER).
Changing composition In their paper, the scientists looked at the nutrients, such as nitrogen and phosphorus, in the stream water as well as the enzymes that microorganisms living in the streambed sediment produce in order to use these nutrients. Then, they looked at changes in both of these over a very large gradient of streams fed by glaciers that differ in size. “Glacier-fed-stream ecosystems generally have limited quantities of carbon and nutrients, particularly phosphorus,” explains Tyler Kohler, a former postdoc at RIVER and the paper’s lead author. “As glaciers shrink and the demand for phosphorus by algae and other microorganisms grows, phosphorus may become more limiting in high-mountain streams.” Hence phosphorus, a critical building block for life, will become even more rare in downstream ecosystems, including larger rivers and lakes, with yet unknown impacts for their food webs.
Advanced stage in Uganda
These findings are supported by a paper published in Royal Society Open Science in August 2023 by scientists from the Vanishing Glaciers project. In this study, the authors analyzed the microbiome of a small glacier-fed stream in the Rwenzori Mountains, in Uganda, where the “green transition” was already at an advanced stage. Here, the nutrient and enzyme composition was also much different, and algae were abundant. “What’s happening with the Rwenzori glacier gives us a glimpse of what Swiss glacier-fed streams will look like 30 or 50 years from now,” says Battin. One outcome of this change is that as glacier-fed streams host more microbial life, they will play a bigger role in biogeochemical cycles such as CO2 fluxes.
The RIVER team plans to build on this research. They are conducting a census of the microbial biodiversity in glacier-fed streams and, using various lines of genomic information, are exploring how diverse microorganisms are able to dwell in one of Earth’s most extreme freshwater ecosystems.

Suppose two speakers of the same language are playing a guessing game where each has the same color swatches, and Player 1 tries to get Player 2 to guess a hue by naming the color. If the second player consistently guesses correctly as often as possible, that indicates their language has an efficient color naming system.
Past research has shown that efficient color vocabularies are constrained both by how people perceive colors and by how much they want or need to communicate about a given color. For example, Penn researchers found in a 2021 study that the need to communicate about reds and yellows is high across languages, while greens are more important in some languages.
Now, Penn scientists have identified another constraint: history. Colin R. Twomey, interim executive director of the Data Driven Discovery Initiative in the School of Arts & Sciences, worked with psychology professor David H. Brainard and biology professor Joshua B. Plotkin in a new paper showing how a language’s past color vocabulary shapes its ability to evolve, shedding light on how the number and meaning of color words have changed over time. Their work is published in Proceedings of the National Academy of Sciences.
“The main takeaway is that, once you as a linguistic community have an efficient vocabulary, that starting point restricts the next possible efficient vocabulary that you could have when you introduce a new term,” says Twomey, the first author. “As the vocabulary grows, the number of different vocabularies that you could move to is increasingly constrained.”
This takeaway shares a principle with evolutionary biology. The existence of an evolutionary pathway limits available future pathways, compared to the number of options available if a species were to arise anew. Plotkin and Twomey come from a background in evolutionary theory for biology, and here they are trying to better understand how some of the same theory applies to cultural evolution.
The authors used the publicly available World Color Survey (WCS), in which about 25 speakers from each of 110 languages were asked to name the same set of 330 color stimuli. This dataset provides the likelihood that a speaker from each of the languages would use a certain term to describe a color.
The WCS was the work of anthropologist Brent Berlin and linguist Paul Kay, who identified 11 color categories in English: red, orange, yellow, green, blue, purple, pink, black, white, brown, and gray. While English uses 11 color categories, the most common color vocabulary size among WCS languages is six words.

Using the WCS, the Penn researchers explored the introduction of new terms and the probability that a given word will change meaning as the size of the color vocabulary increases. For example, a term identified as green-blue could shift in meaning to “green” if a new term is established as “blue.” Green-blue and blue are quite susceptible to changes in meaning as new terms are added, whereas red, black, and yellow remain relatively stable in meaning.
One example the authors show is a color vocabulary that evolved into a six-word set with red, pink, yellow, black, white, and a green-blue shade. But if one were to make a six-word vocabulary from scratch — de novo — based on the same communicative needs for that language, the vocabulary could instead have separate colors for green and blue and still include red but have no word for pink, and it would still be efficient. Moreover, and despite facing the exact same constraints, from there the historical vocabulary would most likely split green-blue into separate terms whereas the de novo vocabulary is more likely to introduce light green or orange than pink.
“Since we know that history matters, it means we can infer history from the present language state. In principle, we can infer what ancestral color vocabularies were and then compare that to the historical record,” Plotkin says. An example he provides is that at certain points in history, certain commercial dyes were introduced that became economically important to a culture.
The paper also notes that history should also constrain how people talk about and categorize aspects of culture aside from color; Plotkin and Brainard respectively point to the ways we categorize consumer products and weather conditions, for example.
Their color study “represents a general theory that categories are refined based on communicative needs, historical constraints, and this principle of efficiency,” Brainard says. “The ideas, we would hope, would apply to how we name and categorize and communicate about all kinds of things.”
This study was supported by a postdoctoral fellowship through the University of Pennsylvania’s Data Driven Discovery Initiative and the John Templeton Foundation (Grant 62281).
Colin R. Twomey is the interim executive director of the Data Driven Discovery Initiative and at the time of this study was a postdoctoral fellow in the Department of Biology in the University of Pennsylvania School of Arts & Sciences.
Joshua B. Plotkin is the Walter H. and Leonore C. Annenberg Professor of the Natural Sciences in the Department of Biology in Penn Arts & Sciences.
David H. Brainard is the RRL Professor of Psychology in in Penn Arts & Sciences.

Cleveland Clinic researchers have discovered a key mechanism used by Kaposi’s sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), to induce cancer. The research points to effective new treatment options for KSHV-associated cancers, including Kaposi’s sarcoma, primary effusion lymphoma, and HHV8-associated multicentric Castleman disease.
“Our findings have significant implications: viruses cause between 10% to 20% of cancers worldwide, a number that is constantly increasing as new discoveries are made. Treating virus-induced cancers with standard cancer therapies can help shrink tumors that are already there, but it doesn’t fix the underlying problem of the virus,” said Jun Zhao, Ph.D., of Cleveland Clinic Florida Research & Innovation Center. “Understanding how pathogens transform a healthy cell into a cancer cell uncovers exploitable vulnerabilities and allows us to make and repurpose existing drugs that can effectively treat virus-associated malignancies.”
The Nature Communicationsstudy, led by Dr. Zhao, reveals that KSHV manipulates two human enzymes called CDK6 and CAD to reshape the way human cells produce new nucleotides — the building blocks of DNA and RNA — and process glucose. The changes to how infected cells grow and how KSHV persists put cells at a much higher risk of forming tumors and play a crucial role in causing cancer.
The team showed the virus activates a specific pathway driving cell metabolism and proliferation. Inhibiting this process with existing FDA-approved breast cancer drugs reduced KSHV replication, blocked lymphoma progression and shrunk existing tumors in preclinical models.
Like other herpesviruses, KSHV often has no symptoms initially and remains in the body after primary infection. The virus stays dormant, suppressed by the immune system. However, KSHV can reactivate when immunity is weakened — as in older people, those with HIV/AIDS, and transplant recipients. In these high-risk groups, the now active virus can trigger aggressive cancers.
KSHV-induced cancers are fast-acting, aggressive and difficult to treat. An estimated 10% of people in North America and Northern Europe have KSHV, but this ranges throughout the globe. More than 50% of individuals in parts of Northen Africa are estimated to have the virus. Experts estimate these rates are higher, as KSHV often goes undiagnosed because of lack of symptoms. These findings have implications that reach past KSHV; researchers can apply knowledge about KSHV to other cancer-associated viruses that might use the same process to cause cancer.
To understand the cells’ metabolic processes to uncover the virus’s vulnerabilities, Dr. Zhao collaborated with Michaela Gack, Ph.D., Scientific Director of the Florida Research & Innovation Center.

Rapidly replicating cancer cells reprogram metabolism to fuel growth. Meanwhile, most viruses cannot produce energy or necessary molecules on their own, so they rely on human cells to do the work for them. The team found that the virus takes over the host protein CDK6 and CAD, causing the infected cells to produce extra metabolites, which allows faster replication of the virus and an uncontrolled proliferation of the cells.
The research team treated pre-clinical models with a CDK6-blocking drug, Palbociclib, an FDA-approved breast cancer medication, as well as a compound targeting CAD. They saw significant decreases in tumor size and increases in cancer survival rates: most tumors virtually disappeared after about a month of treatment, and remaining tumors shrank around 80%. Survival increased to 100% for selected lymphoma cell lines.
Dr. Zhao and his team are working to better understand the connections among KSHV, CDK6/CAD pathway, and cancer formation. With the knowledge they obtain, they plan to implement and refine their experimental drug combinations for clinical trials.
“Cellular metabolism could be hijacked by both viruses and cancers for pathogenesis,” said Dr. Zhao. “By investigating these metabolic rewiring mechanisms, we aim to find the Achilles’ heel of cancer-causing viruses and non-viral cancers. I’m excited to see what the future of this work holds.”

Published8 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, EPABy Aurelia FosterHealth reporterMore than 91,000 NHS appointments had to be rescheduled due to this week’s junior doctor strike in England.Members of British Medical Association (BMA) took industrial action for five days in their tenth strike since last March in a dispute over pay.More than 23,000 staff were absent due the strike, NHS England says.There have now been 1,000 hours of disruption to routine care due to industrial action by junior doctors and consultants, it says.More than 1.4 million operations and appointments in total have been cancelled due to strike action by health workers including doctors, nurses and other healthcare professionals since December 2022.The junior doctor walkout this week affected critical care, neonatal care, maternity, and trauma units in hospitals across England. It meant senior doctors had to be drafted across from other services to staff emergency care.The NHS’ national medical director Professor Sir Stephen Powis said: “NHS staff worked incredibly hard to keep patients safe and cover striking colleagues and we are extremely grateful for their huge efforts and for the time and skill that went into the planning.”The strike was among members of the BMA, which wants a 35% pay increase – a proposal previously rejected by ministers.Junior doctors have so far taken 39 days of strike action during this dispute. Nearly half of NHS doctors are junior doctors – a group spanning recent graduates to some who have 10 years or more experience – and two-thirds are members of the BMA.NHS Confederation, which represents healthcare employers, said it was patients who “bear the brunt” of the dispute.”It is important to remember that behind every number is a patient who may be living in pain or discomfort waiting for treatment that could turn their lives around,” chief executive Matthew Taylor said.Pay dealThe union said more strikes are likely unless a deal is made with the government on pay.Junior doctors received a pay rise averaging nearly 9% this financial year – and during talks at the end of last year, the option of an extra 3% on top of that was discussed.But those talks ended in early December without a deal being reached.The BMA says it wants an offer that makes up for what it says has been 15 years of below-inflation pay rises.The union is balloting members on further strike action, with a result expected at the end of this month.Health Secretary Victoria Atkins said: “Now that this latest round of industrial action is over, I once again urge the BMA Junior Doctors’ Committee to demonstrate they have reasonable expectations so we can come back to the negotiating table to find a fair deal that works for the NHS, doctors and patients.”Junior doctors in Wales also recently held a strike, while in Northern Ireland they are planning to strike in early March.Earlier, the BMA rejected a pay offer for specialist, associate specialist and specialty (SAS) doctors in England – very experienced doctors who are more senior that junior doctors, but who are not consultants.More on this storyJunior doctors strike for 10th time over payPublished6 days agoJunior doctors to strike over five days, BMA saysPublished9 FebruaryThousands of appointments hit by doctor walkoutPublished27 December 2023Thousands of junior doctors begin 72-hour strikePublished21 FebruaryRelated Internet LinksBritish Medical AssociationNHS EnglandThe BBC is not responsible for the content of external sites.

Americans with Covid or other respiratory infections may return to daily activities if they don’t have a fever and their symptoms are improving.Americans with Covid or other respiratory infections need not isolate for five days before returning to work or school, the Centers for Disease Control and Prevention said on Friday, a striking sign of changing attitudes toward the coronavirus.People with respiratory illnesses may resume daily activities if they have been fever-free for at least 24 hours without the aid of medications and if their symptoms are improving, agency officials said. Acknowledging that people can be contagious even without symptoms, the C.D.C. urged those who end isolation to limit close contact with others, wear well-fitted masks, improve indoor air quality and practice good hygiene, like washing hands and covering coughs and sneezes.The guidelines apply to Covid, influenza and respiratory syncytial virus, among other respiratory ailments, which should make it easier for people to comply, Dr. Mandy Cohen, the C.D.C.’s director, told reporters on Friday.“Our goal here is to continue to protect those at risk for severe illness, while also reassuring folks that these recommendations are simple, clear, easy to understand and can be followed,” she said.Dr. Cohen noted the sharp decreases in the numbers of Covid-related hospitalizations and deaths this winter compared with those in previous years, and said a vast majority of hospitalizations had occurred among Americans who did not receive the latest shots.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

The pill mifepristone will be available with a prescription at pharmacy counters in a few states to start.The two largest pharmacy chains in the United States will start dispensing the abortion pill mifepristone this month, a step that could make access easier for some patients.Officials at CVS and Walgreens said in interviews on Friday that they had received certification to dispense mifepristone under guidelines that the Food and Drug Administration issued last year. The chains plan to make the medication available in stores in a handful of states at first. They will not be providing the medication by mail. Both chains said they would gradually expand to all other states where abortion was legal and where pharmacies were legally able to dispense abortion pills — about half of the states.Walgreens will start providing the pill within the next week in a small number of its pharmacies in New York, Pennsylvania, Massachusetts, California and Illinois, said Fraser Engerman, a spokesman for the chain. “We are beginning a phased rollout in select locations to allow us to ensure quality, safety and privacy for our patients, providers and team members,” he said.CVS will begin dispensing in all of its pharmacies in Massachusetts and Rhode Island “in the weeks ahead,” Amy Thibault, a spokeswoman for the company, said.The chains will be monitoring the prospects in a few states, including Kansas, Montana and Wyoming, where abortion bans or strict limitations have been enacted but are enjoined because of legal challenges.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.