Driven by the overuse of antimicrobials, pathogens are quickly building up resistances to once-successful treatments. It’s estimated that antimicrobial-resistant infections killed more than 1 million people worldwide in 2019, according to the World Health Organization.
“There are worries that at the rate things are going, in perhaps 20 or 30 years, few of our drugs will be effective at all,” said Xuefei Huang, a Michigan State University Research Foundation Professor in the departments of Chemistry and Biomedical Engineering.
“This would bring us back to the pre-antibiotic age.”
Now, in a new Nature Communications study, Huang and his collaborators have reported a breakthrough that will help tackle this global threat head-on. Specifically, the team has created a promising vaccine candidate for antibiotic-resistant bacteria.
Bacterial vaccines, along with antibiotics, are a crucial tool in the fight against deadly microbes.
In the latest paper, Huang announced several discoveries that will help the development of a carbohydrate-based vaccine for infections caused by Staphylococcus aureus and its “superbug” relative methicillin-resistant Staphylococcus aureus, or MRSA.
Staph aureus, or staph, and MRSA are among the most prevalent causes of bacterial infections.

Using an innovative delivery platform created by the Huang group at MSU, the team’s preclinical vaccine formulation offered high levels of immunity from lethal levels of staph and MRSA in animal trials.
With this work, Huang and his team have expanded the frontiers of vaccine science, equipping fellow researchers with new knowledge to improve and refine future bacterial vaccines.
Carbohydrate hurdles
To develop a vaccine, researchers must identify an effective antigen. This is a substance or molecule that the body flags as foreign, helping to trigger an immune response and the creation of antibodies that will fight future infection.
While most vaccines rely on protein antigens, Huang is an expert in the chemistry and biology of carbohydrates. These are chemical compounds comprised of saccharides, or sugars.
Developing carbohydrates to use as antigens in vaccines comes with its own unique challenges and advantages.

“Sugar structures are very specific to certain bacteria,” Huang explained. “A vaccine that works against one bacterium might not work at all against another, even if they’re very similar.”
This is why a single dose of a bacterial vaccine can contain many different antigens. For instance, the “20” in Pfizer’s PREVNAR 20 pediatric pneumonia vaccine refers to the 20 unique strains of bacteria it protects against.
If researchers can develop an antigen that’s shared among many — if not all — bacteria, vaccination coverage would be greatly improved.
Gerald Pier, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital and a collaborator on the latest MSU-led paper, has studied one such antigen candidate for years.
Polysaccharide poly-β-(1−6)-N-acetylglucosamine, or PNAG, is a carbohydrate found on the cell wall of staph, many other bacteria and even fungi. This prevalence makes it extremely useful, offering potential protection against numerous pathogens at once.
By examining PNAG as an antigen candidate for staph, Pier, Huang and their colleagues are unlocking the secrets needed to make a more effective vaccine.
A molecular mosaic
Imagine creating a mosaic made from multicolored tiles.
Arrange these tiles in a precise pattern and you’ll end up with a striking work of art. Move just a few tiles around, however, and you’ll find yourself looking at a very different image.
PNAG — and carbohydrates in general — are kind of like mosaics. There are myriad ways to arrange their individual pieces, but only a select few have the effects that researchers desire.
Just as changing a few tiles in a mosaic can give you a completely different image, swapping out these pieces or even changing their location within a PNAG molecule changes its performance as a potential antigen.
“We were very interested in this molecule and these different patterns,” Huang said.
“We wanted to know: Was there a best combination to improve Staph aureus vaccine efficiency, and does the arrangement matter?”
The pieces that Huang and his colleagues were most interested in were biologically active molecular components known as amines and acetyl groups that adorn PNAG’s sugary backbone.
PNAG molecules can contain many amines. These amines can be acetylated, meaning they’re modified with an acetyl group, or they can be free and not bound to anything else.
Currently, most researchers investigating PNAG as an antigen focus on forms of the sugar that are either fully free or fully acetylated.
Huang and his colleagues believed there were promising opportunities in the understudied in-between space where there’s a mixture of free and acetylated amines.
For its research, the team created a library of 32 different PNAG structures. The structures were all pentasaccharides — made from five saccharides — but they differed in how they were decorated with amines and acetyl groups.
By screening these 32 structures with antibody studies, they made their discovery.
“The fine pattern matters quite a bit,” Huang said. “And the impact is drastic.”
An MSU mutant
The team identified two PNAG combinations that were especially promising. Going a step further, the researchers attached them to a groundbreaking vaccine delivery platform.
The platform is based on a bacteriophage, which is a virus that infects bacteria, called Qbeta, also written as Qβ (pronounced “cue beta”). Huang’s team modified the bacteriophage, giving it the power to deliver antigens for carbohydrate-based pathogens.
PNAG and other carbohydrates typically don’t provoke strong immune responses in our bodies, but the mutant Qbeta, or mQβ, helps create an enhanced reaction.
This breakthrough delivery platform — which also has vaccine applications for cancer and even opioid addiction — earned Huang MSU’s 2024 Technology Transfer Achievement Award.
When coupled with mQβ, Huang and his collaborators found that the two most promising PNAG pentasaccharides offered high levels of protection in mice against staph and MRSA.
In animal studies, the team’s new vaccine construct outperformed another PNAG-vaccine delivery system that is currently in human trials.
The team also found their formulation had minimal impact on the biochemistry of the gut microbiome in tests.
As the team prepares for future tests of their new vaccine candidate, Huang is looking forward to the role bacterial vaccines will play in the larger fight against antibiotic resistance.
“Vaccines reduce the overall infection rate, which means there’s less of a need for antibiotics,” Huang said. “This reduces the chance for bacteria to develop resistance, breaking the cycle.
“The two go hand in hand.”

New research has found a significant association between participating in low to moderate intensity exercise and reduced rates of depression.
Researchers from Anglia Ruskin University (ARU) carried out an umbrella review of studies carried out across the world to examine the potential of physical activity as a mental health intervention.
The analysis, published in the journal Neuroscience and Biobehavioural Reviews, found that physical activity reduced the risk of depression by 23% and anxiety by 26%. A particularly strong association was found between low and moderate physical activity, which included activities such as gardening, golf and walking, and reduced risk of depression. However, this was not strongly observed for high intensity exercise.
Physical activity was also significantly associated with reduced risk of severe mental health conditions, including a reduction in psychosis/schizophrenia by 27%.
The results were consistent in both men and women, and across different age groups and across the world.
Lead author Lee Smith, Professor of Public Health at Anglia Ruskin University (ARU), said: “Preventing mental health complications effectively has emerged as a major challenge, and an area of paramount importance in the realm of public health. These conditions can be complex and necessitate a multi-pronged approach to treatment, which may encompass pharmacological interventions, psychotherapy, and lifestyle changes.
“These effects of physical activity intensity on depression highlight the need for precise exercise guidelines. Moderate exercise can improve mental health through biochemical reactions, whereas high-intensity exercise may worsen stress-related responses in some individuals.
“Acknowledging differences in people’s response to exercise is vital for effective mental health strategies, suggesting any activity recommendations should be tailored for the individual.
“The fact that even low to moderate levels of physical activity can be beneficial for mental health is particularly important, given that these levels of activity may be more achievable for people who can make smaller lifestyle changes without feeling they need to commit to a high-intensity exercise programme.”

If a patient is successfully resuscitated after a cardiac arrest and circulation resumes, they are not out of the woods yet. A number of factors can influence whether and how they survive the trauma in the subsequent phase. The administration of the anaesthetic midazolam has a positive effect, as shown by a multicenter study of 571 patients conducted by the Research Association for Emergency Medicine Ostwestfalen-Lippe led by the University Clinic for Anaesthesiology, Intensive Care and Emergency Medicine at the Johannes Wesling clinic in Minden, hospital of Ruhr University Bochum, Germany, at the Chair of Emergency Medicine headed by Professor Jochen Hinkelbein.
In cases where the patient required anesthesia after successful resuscitation, midazolam improved the chances of optimal oxygen saturation and CO2 levels in the blood. The risk of a renewed drop in blood pressure or a renewed circulatory arrest didn’t increase. “This specific group of patients who have been successfully resuscitated should definitely be included in the guidelines for pre-hospital anesthesia. Midazolam has proven to have a particularly positive effect in this group,” concludes Dr. Gerrit Jansen, lead author of the study, which was published in the journal Deutsches Ärzteblatt International on April 8, 2024.
In the event of a cardiac arrest, rapid intervention is essential: If first aiders carry out resuscitation measures in good time, the patient’s circulation can be restarted in the best-case scenario. “However, it’s often the case that the patient hasn’t yet regained consciousness,” explains Gerrit Jansen. In this phase, there are various factors that can affect the chances of survival and subsequent permanent limitations due to the circulatory arrest.
“Some patients display protective reflexes after resuscitation, such as coughing or defensive movements, which make the emergency responders’ work more difficult. They often have to perform extended airway management, for example by intubating the patient in the same way as during surgery. This frequently requires sedation or anesthesia,” explains Jansen. Until now, there has been concern that anaesthetic drugs could have a negative impact on the circulatory system, which has only just been restored. According to the study, however, this is not the case.
Of the 571 people included in the study who survived a cardiac arrest and were admitted to hospital, 395 were sedated, 249 of them with midazolam. The chance that their blood oxygen saturation levels were in the optimal range following a cardiac arrest increased twofold when midazolam was administered. The chance that carbon dioxide was effectively exhaled increased by a factor of 1.6 with the drug. “Our statistical methods confirmed a correlation between these results and the administration of midazolam, without any indication of negative circulatory effects,” says Gerrit Jansen.
“The European guidelines of the European Resuscitation Council don’t yet set out any specific recommendations for possible anesthetic drugs,” explains Jansen. “The German guideline for pre-hospital anesthesia for patients with cardiovascular risk doesn’t mention patients in cardiac arrest. We’ve therefore carried out pioneering research in this field, the results of which should be incorporated into the recommendations for the benefit of the patients.”

A group of researchers have expanded conventional knowledge on a critical enzyme that controls cell migration. In a recent publication in the journal Nature Communications, they reported that phosphoinositide 3-kinase (PI3K) not only acts as an accelerator to prompt cell motility, but it also has a built-in brake mechanism that impedes migration.
“PI3K is a major signaling enzyme that has been extensively studied for over 30 years due to its roles in fundamental cellular functions like growth, survival, movement and metabolism,” points out Hideaki Matsubayashi, lead author of the study and assistant professor at Tohoku University’s Frontier Research Institute for Interdisciplinary Sciences (FRIS). “It plays a critical part in cell migration and invasion, something that, when dysregulated, can cause many pathologies. Our work revealed that PI3K can also actively restrain these same migratory processes through a separate non-catalytic endocytic mechanism originating from its p85β subunit.”
Using a combination of bioinformatics, molecular modeling, biochemical binding assays and live-cell imaging, Matsubayashi and his colleagues demonstrated that a disordered region within p85β’s inter-SH2 domain directly binds to the endocytic protein AP2. This part of PI3K can activate a cellular process that pulls certain molecules into the cell, and it does so without needing the enzyme’s typical lipid-modification function.
When the researchers disrupted the binding, the mutated p85β did not function as it should. Instead of regulating cell movement through its brake mechanism, it built up in specific sites within the cell. This leads to cells moving faster and more persistently, indicating a loss of the brake mechanism’s control over cell migration.
“Remarkably, this single PI3K enzyme has opposing accelerator and brake pedals built into its molecular framework,” added Matsubayashi. “The endocytic mechanism helps regulate PI3K’s activity to ensure that cell movement is controlled at the right times and in the right places for important biological processes.”
This braking role was found to be specific to just the p85β subunit. And since the p85β subunit of PI3K is linked to cancer-promoting properties, deeper understanding of PI3K regulation and its isoform specificity could lead to novel therapeutic strategies, such that selectively inhibit the cancerous aspect of PI3K, while preserving the normal functions of PI3K in healthy cells.

LMU researchers have developed a method to determine how reliably target proteins can be labeled using super-resolution fluorescence microscopy.
Modern microscopy techniques make it possible to examine the inner workings of cells in astonishing detail. “We can now observe the arrangement and interaction of individual proteins under the microscope,” says Professor Ralf Jungmann, Chair of Molecular Physics of Life at LMU and Max Planck Fellow at the MPI of Biochemistry. The biophysicist’s team recently developed the revolutionary RESI (Resolution Enhancement by Sequential Imaging) method. This technique can be used to improve the resolution of fluorescence microscopy down to the Ångström scale — far below the classical diffraction limit of light. DNA-conjugated marker molecules, which the researchers attach precisely to the molecules they want to understand better, are crucial for this.
Jungmann’s team has now presented a technique in the journal Nature Methods that can be used to quantify how well biomarker molecules bind to the target proteins. “This is absolutely crucial if you want to make quantitatively reliable statements,” explains the physicist. If you know the labeling efficiency, you can carry out spatially resolved proteomics in this way. This allows you to find out not only what individual proteins do in a cell, but also to what extent they are present and how their quantity and behavior change under certain circumstances. “But this is only possible if we can assess how well the labeling has worked.” This is because only labeled proteins emit flashes of light under the microscope and thus become visible.
Reliable and versatile
The method developed by Jungmann’s team makes this assessment possible by adding a reference biomarker to the target proteins. This marker “glows” in a different color during microscopy, so that successfully marked proteins appear in two colors. Jungmann’s team demonstrated this using the membrane protein CD86, among others: The reference produces a pink fluorescence, the actual marker a bluish one. This creates a pattern of innumerable pink and blue points of light. Where the marking did not work, only the reference lights up individually. The marking efficiency is calculated from the ratio of double and single illuminated molecules.
The method offers several advantages compared to previous methods for determining binding efficiency: “It works not only in vitro, but also in vivo, i.e. in the context of intact cells,” explains Jungmann. “The technique can also be applied to a variety of different target molecules, biomarkers, and samples and is compatible with a whole range of super-resolution methods.” A reliable and widely applicable means of assessing marker efficiency is crucial to ensure accurate data evaluation and enable reliable comparisons between different binders, labeling conditions, and research laboratories.
The authors of the study are certain that the new quantification method has paved the way for significantly expanding the potential of their super-resolution microscope method: “Now we can also consider specific biomedical applications in which the quantitative detection of proteins and processes is of great importance,” says Jungmann. This includes cancer research, for example, where information about interactions between proteins on the cell surface and drugs with molecular resolution is essential for the development of new types of medication.

A research team including scientists from the CNRS1 has discovered that cancer, one of the leading causes of death worldwide, can be caused entirely by epigenetic changes2, in other words, changes that contribute to how gene expression is regulated, and partly explain why, despite an identical genome, an individual develops very different cells (neurons, skin cells, etc.).
While studies have already described the influence of these processes in the development of cancer, this is the first time that scientists have demonstrated that genetic mutations are not essential for the onset of the disease. This discovery forces us to reconsider the theory that, for more than 30 years, has assumed that cancers are predominantly genetic diseases caused necessarily by DNA mutations that accumulate at the genome level3.
To show this, the research team focused on epigenetic factors that can alter gene activity. By causing epigenetic dysregulation4 in Drosophila, and then restoring the cells to their normal state, scientists have found that part of the genome remains dysfunctional. This phenomenon induces a tumour state that is maintained autonomously and continues to progress, keeping in memory the cancerous status of these cells even though the signal that caused it has been restored.
These conclusions, to be published on April 24, 2024, in the journal Nature, open up new therapeutic avenues in oncology.
Notes
1 — Working at the Institut de Génétique Humaine (CNRS/Université de Montpellier).
2 — Epigenetics is the study of the mechanisms that allow the inheritance of different gene expression profiles in the presence of the same DNA sequence.
3 — The genome is defined as the set of genetic material — and therefore the entire DNA sequence — contained in a cell or organism.
4 — Scientists focused on epigenetic factors called Polycomb proteins, which regulate the expression of key genes, and are dysregulated in many human cancers. When these proteins are experimentally removed, the activity of the targeted genes is disrupted: some can activate their own transcription and self-maintain. When Polycomb proteins are integrated back into the cell, a subset of the genes are resistant to the proteins and remain dysregulated through cell division, allowing the cancer to continue its progression.

Nursing homes in disadvantaged communities are more likely to overmedicate residents with antipsychotics, especially homes that are understaffed, according to a new study published in JAMA Network Open.
“The neighborhood in which a nursing home is located seems to influence how widely antipsychotics are used, even when they may not be indicated,” said Jasmine Travers, assistant professor at NYU Rory Meyers College of Nursing and the study’s senior author.
Antipsychotic medications are used to treat serious psychiatric disorders such as schizophrenia. These medications have long been given to nursing home residents with and without dementia who are agitated or have behavioral issues. — Sometimes staff rely on their sedating side effects for “chemical restraint” rather than redirecting residents in distress.
“We know that nursing homes with lower staffing levels use more antipsychotics. These medications may be compensating for understaffing by sedating residents instead of having adequate staff to support their needs,” said Travers.
Antipsychotic use in older adults can be dangerous, increasing their risk for falls, strokes, and even death. As a result, in recent years, there has been a significant push by the Centers for Medicare and Medicaid Services (CMS) to reduce the use of antipsychotics to manage behaviors such as aggression or wandering in nursing homes.
However, this may be more challenging in disadvantaged neighborhoods, where residents may be exposed to greater stressors, including higher crime rates, noise pollution, and less green space, all of which can harm their mental and physical health. For older adults, these stressors might translate to poor sleep or agitation, increasing the risk that an antipsychotic medication is used, even without an appropriate diagnosis.
To better understand the connection between nursing home staffing, neighborhood factors, and antipsychotic use, Travers and her colleagues looked at data from 10,666 nursing homes across the U.S., 1,867 of which were in severely disadvantaged neighborhoods. Neighborhood socioeconomics were measured using data on income, education, employment, and housing for small geographic units called census blocks.

The researchers also looked at what percentage of residents received an antipsychotic drug in the last week but didn’t have a qualifying diagnosis of schizophrenia, Tourette syndrome, or Huntington’s disease. (The study did not take into account residents who are falsely diagnosed with schizophrenia to get around the CMS reporting requirement, a troubling practice documented in a 2022 report by the U.S. Department of Health and Human Services.)
The researchers found that nursing homes that were understaffed — measured as having less than three hours of nurse staffing per resident each day — had greater antipsychotic medication use in severely disadvantaged neighborhoods (19.2%) compared to less disadvantaged neighborhoods (17.1%).
“This means that in a 100-bed nursing home that is understaffed, two additional residents would inappropriately receive an antipsychotic medication if the nursing home was in a disadvantaged neighborhood versus a more well-off area,” said Travers.
Notably, when nursing homes met or exceeded the federal government’s proposed staffing levels of at least three hours of nursing per resident per day, there was not a significant difference in antipsychotic use based on neighborhood, providing support for having minimum staffing levels. The researchers call for a more focused effort on improving staffing in nursing homes in lower income areas, which could include additional funding — similar to funds provided to federally qualified health centers — or other tailored interventions to address gaps in staffing.
“Addressing staffing deficiencies, particularly in nursing homes in disadvantaged neighborhoods, will be critical for reducing the overuse of antipsychotics,” said Travers. “Understanding this vulnerability can help inform policy solutions to support, not penalize, nursing homes in disinvested communities.”
In addition to Travers, study authors include Erinn Hade and Steven Friedman of NYU Grossman School of Medicine, Aasha Raval and Kimberly Hadson of NYU Meyers, and Jason Falvey of the University of Maryland School of Medicine. The research was supported by the National Institute on Aging (K76AG074922, K76AG074926, P30AG028747) and the Patrick and Catherine Weldon Donaghue Medical Research Foundation.

Mount Sinai researchers have published the first study to use single-cell analysis in identifying several pathophysiological mechanisms of abnormal passageways in the digestive system known as perianal fistulae, a common complication of Crohn’s disease. These findings were published in the journal Med on April 24.
Crohn’s disease is an inflammatory bowel disease that causes chronic inflammation at any part of the gastrointestinal (GI) tract and impacts more than half a million people in the United States. Perianal fistulae, abnormal connections between the anal canal and perianal skin, are a common complication of Crohn’s disease that often result in painful abscesses and impact patients’ quality of life.
This Mount Sinai study is the first to apply single-cell transcriptomics of perianal fistulous tracts, and to recruit Black patients with the chronic condition for a diverse and comprehensive study cohort. Patients with African ancestry have been substantially underrepresented in genome-wide association studies of Crohn’s disease, and inflammatory bowel disease overall, reflecting in part the lower prevalence of Crohn’s disease in African American populations compared to patients with European ancestry. However, patients of African ancestry are about twice as likely to have perianal fistulae, according to studies in adult and pediatric populations.
The researchers profiled more than 140,000 single cells from diverse Crohn’s disease patients with perianal fistulae. The team identified several key pathways underlying fistulizing Crohn’s disease, including cellular aging and loss of proliferation, reaction to microenvironmental stimuli, and a destructive gene signature in connective tissues that is unique to perianal fistulae. The researchers also determined that subpopulations of fibroblasts — cells forming the connective tissues — with this destructive gene signature may originate from mononuclear cells in the immune system, a phenomenon observed in greater magnitude from patients with African ancestry. The experts found evidence for key transcription factor binding events in relevant gene promoter regions that suggests a potential epigenetic phenomenon underlying this apparent difference in cell behavior between patients of African and European ancestry.
“Circulating blood monocytes can traffic to disease tissues and form a critical first step in fighting microbes throughout the body,” said corresponding author Judy H. Cho, MD, Dean and Ward-Coleman Chair in Translational Genetics at the Icahn School of Medicine at Mount Sinai. “In this study, we have defined population-specific differences in how blood monocytes respond, which contribute to the higher rates of perianal fistulous complications in African American patients with Crohn’s disease.”
A range of anti-inflammatory medications can treat Crohn’s disease, but they show limited efficacy for closure of perianal fistula tracts. In severe cases, patients may require surgical removal of all or part of the rectum. But researchers said their findings provide avenues to identify new therapeutic options. The team said future studies should examine similar epigenetic patterns in white blood cells of the immune system from diverse, healthy patients and from patients with other immune-mediated inflammatory diseases to further explore the role of the transcription factor underlying race or ancestry-based disparities.
“We have leveraged transcriptomic, epigenetic, genetic, cellular, and tissue-based data from patients with a history of this devastating complication to better understand reasons for the discrepancy in prevalence between Black and white patients,” said first author Rachel M. Levantovsky, PhD, who is working on her MD in the Mount Sinai Medical Scientist Training Program. “Our discovery of unique fistula fibroblasts, distinct monocyte differentiation in African-ancestry individuals, and key transcription factor binding events helps us illuminate mechanistic underpinnings of perianal fistula — critical for the optimization of future treatment.”
The study was supported by funding from the National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health (U01DK062422, U24DK062429, R01DK123758, and F30DK127736), Leona M. and Harry B. Helmsley Charitable Trust, Sanford J. Grossman Charitable Trust, and David and Margot Lowy Foundation Trust.

The Agriculture Department finalized a new rule to bring the meals more in line with federal dietary standards.School meals will soon contain less salt and sugar, but can still include chocolate milk, under new nutrition guidelines released by the Biden administration.The Agriculture Department on Wednesday finalized the regulation it had first proposed in February 2023, having weakened several provisions after feedback from food companies, school nutrition professionals and over 136,000 public comments.“All of this is designed to ensure that students have quality meals and that we meet parents’ expectation that their children are receiving healthy and nutritious meals at school,” Tom Vilsack, the agriculture secretary, said in a call with reporters on Tuesday.The new guidelines, which seek to better align school meals with federal dietary standards, build on a 2010 law that aimed to make cafeteria breakfasts and lunches healthier. That law, championed by Michelle Obama when she was the first lady, became embroiled in political debate almost immediately. The Trump administration tried repeatedly to roll back nutrition standards, and the Biden administration relaxed certain provisions to provide more flexibility during the coronavirus pandemic.When the Agriculture Department proposed updates to the standards last year, school nutrition professionals called the guidelines unrealistic to enforce and dairy groups expressed concerns over what they called a push to limit milk.The final rule reflects some of those concerns.Under the rule, schools will need to limit the amount of added sugars in cereals and yogurts beginning in the 2025-26 academic year and gradually step up reductions in other foods.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.

A single spillover, from a bird to a cow, led to the infections, a review of genetic data has found.The bird flu outbreak in American dairy cattle may have begun in January, or even as early as December, a new analysis of genetic data suggests.The Department of Agriculture announced in late March that dairy cattle in Texas and Kansas had tested positive for the virus, called H5N1. It has since reported cases in dozens of herds in eight states.On Tuesday, federal health officials said they had discovered fragments of H5N1 in milk samples obtained at various sites across the nation. The fragments pose no threat to consumers, the officials said.It is unclear exactly how the cows became infected, but the most likely source is feces or other secretions from a wild bird infected with the virus.Scientists in the United States and elsewhere have criticized federal agencies for withholding key information about the outbreaks, including genetic sequences of the virus from infected cows, The New York Times reported on Friday. The data may hold valuable clues to the evolution of the virus and the extent of the outbreak.On Sunday, the department published 239 genetic sequences, but it omitted some details regarding the locations from which they were obtained and the dates.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.