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Links have been reported between schizophrenia and proteins produced by the immune system that can act against one’s own body, known as autoantibodies. In a study published last month in Brain Behavior and Immunity, Japanese researchers identified autoantibodies that target a ‘synaptic adhesion protein’, neurexin 1α, in a subset of patients with schizophrenia. When injected into mice, the autoantibodies caused many schizophrenia-related changes.
What is a synaptic protein, and why might it be linked to schizophrenia? Synaptic adhesion proteins are specialized proteins that bind to create physical connections between brain cells. These connections, called synapses, allow the cells to communicate by passing molecules back and forth. Both synapses and autoimmunity are known to be associated with schizophrenia, so the research team from Tokyo Medical and Dental University (TMDU) decided to investigate autoantibodies that target synaptic proteins in patients with schizophrenia.
“In around 2% of our patient population, we identified autoantibodies against the synaptic protein neurexin 1α, which is expressed by one cell in the synapse and binds to proteins known as neuroligins on the other cell in the synapse,” says lead author of the study Hiroki Shiwaku. “Once we had identified these autoantibodies, we wanted to see if they were able to cause schizophrenia-related changes.”
To do this, the researchers isolated autoantibodies from some of the patients with schizophrenia and injected them into the cerebrospinal fluid of mice, so that the autoantibodies would travel into the brain. In these mice, the autoantibodies blocked neurexin 1α and neuroligin binding and altered some related synaptic properties. The administration of these autoantibodies also resulted in fewer synapses in the brains of mice and schizophrenia-related behaviors, such as reduced social behavior toward unfamiliar mice and reduced cognitive function.
“Together, our results strongly suggest that autoantibodies against neurexin 1α can cause schizophrenia-related changes, at least in mice,” explains Hiroki Shiwaku. “These autoantibodies may therefore represent a therapeutic target for a subset of patients with schizophrenia.”
Schizophrenia has a wide variety of both symptoms and treatment responses, and many patients have symptoms that are resistant to currently available treatment options. Therefore, the identification of possible disease-causing autoantibodies is important for improving symptom control in patients with schizophrenia. It is hoped that the results of this investigation will allow patients with autoantibodies that target neurexin 1α — all of whom were resistant to antipsychotic treatment in the present study — to better control their symptoms in the future.

About two-thirds of the risk for Alzheimer’s disease (AD) is thought to arise from genetic influences, but about a third could be influenced by environment and lifestyle, opening the door for behavioral interventions that could delay or prevent pathophysiological changes that occur with AD. Now a new study in a mouse model of AD examines the effects of environmental enrichment on AD symptom progression and pathology. The study appears in Biological Psychiatry, published by Elsevier.
Gerd Kempermann, PhD, from the German Center for Neurodegenerative Diseases in Dresden, Germany, and senior author of the study, emphasized the importance of studying the early stages of disease, when interventions might be most effective.
Dr. Kempermann commented, “AD does not start when the symptoms become obvious. There is a decades-long silent period, during which the pathology progresses undetected. Clinicians and researchers have become increasingly interested in what happens during this phase.”
To study this early pathology, Dr. Kempermann and colleagues used a mouse model of AD that replicates this silent period. The model contains several mutations associated with human AD in the gene encoding amyloid precursor protein (App). These AppNL-F mice develop toxic amyloid-beta plaques by age 6 months and cognitive impairment by 18 months.
Dr. Kempermann said, “However, we discovered that there are already subtle but important behavioral changes long before the first plaques appear, and the cognitive deficits become detectable.”
The mice were housed in an enriched environment, which consisted of 60 interconnected cages, from age 6 weeks to 23 weeks and were then moved to standard cages after 4 months. Living in the enriched environment improved several measures of metabolism, which are known risk factors for AD.
Dr. Kempermann explained, “The [AD model] mice in our study showed a reduction in individual behaviors. They became more similar and more rigid. As this individualization is to a large degree driven by individual behavior and depends on brain plasticity, we can conclude that the affected mice had behavioral deficits very early in the course of the disease. They did not respond normally to the offerings of their environment. This finding is important, because it will help us to understand how we can best tailor preventive measures during the pre-clinical phase. It also underscores that prevention has to start early.”
The researchers also examined markers of neurogenesis in the mice. Paradoxically, the AppNL-F mice had higher rates of neurogenesis than control mice, which is interpreted as a failing attempt at compensation and as paradoxically counterproductive. This overshooting compensation was normalized by exposure to enrichment.
John Krystal, MD, Editor of Biological Psychiatry, said of the work, “This novel study suggests that environmental enrichment may reduce the early accumulation of amyloid plaques in a mouse model of AD. This insight may suggest a strategy for delaying the development of symptoms associated with this disorder.”

A new “molecular editing” technique from Scripps Research enables chemists to add new elements to organic molecules at locations that were previously out of reach.
The researchers described their new method in a paper that appeared on May 31, 2023, in Nature. The method uses a designer molecule called a ligand that helps a palladium-atom catalyst reach from one side of a carbon-atom ring to break a carbon-hydrogen bond on the other side, allowing a new set of molecules to join at that site. This molecule-building feat was previously impossible for so-called “saturated” rings of carbon atoms, which are common features in drug molecules.
“Previously, to achieve the same result, one would have to undertake a de novo approach — what we call a cyclization reaction — involving the formation of a new ring structure from an acyclic chain, using this new method, we can directly modify an existing ring to avoid a cyclization process that can often prove challenging,” says study senior author Jin-Quan Yu, PhD, the Bristol Myers Squibb Endowed Chair in Chemistry and the Frank and Bertha Hupp Professor in the Department of Chemistry at Scripps Research. “In addition to saving steps, this unprecedented synthetic strategy can introduce new chemical space for drug discovery as structurally distinct substrates are incorporated into the ring.”
Yu and his laboratory are already known for their innovations in C-H functionalization, which is a powerful way of building complex organic molecules to make new pharmaceuticals and other valuable commercial compounds. In this approach, chemists use ligands and catalysts to disconnect a hydrogen (H) atom from a carbon (C) atom at a desired position on an organic molecule. This disconnection allows a new cluster of molecules, known as a functional group, to bond where the hydrogen atom had been.
Most molecules that are used to build new drugs include rings of carbon atoms, also called carbocycles. Thanks in part to Yu’s group, the C-H functionalizations of carbon atoms on these rings have become relatively easy in many cases. This approach is often not applicable, though, in cases where the existing functional group needed to anchor the ligand and catalyst is directly across the ring from the desired C-H functionalization site.
“We call this scenario ‘crossing the river,’ and it has been extremely challenging because the palladium catalyst must form a strained ‘bridge’ connecting the existing functional group and the desired carbon site on the other side of the ring,” Yu says.
The most challenging cases are those in which the carbon-ring structures are “saturated,” which means their carbons are connected only with single carbon-carbon bonds. Saturated carbon rings are common in pharmaceutical chemistry, but are harder targets for C-H functionalization, in part because the C-H bonds have less affinity for metal catalysts, compared to the double C-C bonds of unsaturated carbon rings. The Yu lab has achieved C-H functionalization across unsaturated rings, but there has been no way to do this across a saturated ring — until now.
In the study, Yu and his team, including co-first authors Guowei Kang, PhD, Daniel Strassfeld, PhD, and Tao Sheng, PhD, all postdoctoral research associates in the Yu lab, were able — after months of trial and error — to develop quinuclidine-pyridone and sulfonamide-pyridone ligands enabling cross-ring functionalization with saturated carbon rings. They showed that the approach can work for rings containing from four to eight carbon atoms, within a wide variety of molecules.
The researchers demonstrated the new technique by easily functionalizing molecules that are being used to develop future drugs, including compounds called histone deacetylase inhibitors, which are under investigation as potential cancer treatments.
“We anticipate that this new tool will greatly simplify the synthesis of a large class of carbocyclic molecules used in pharmaceutical chemistry, expanding chemical space for the discovery of new and better drugs,” Yu says.
The research was supported by grants from the National Institute of General Medical Sciences (2R01GM084019 and F32GM143921).

An international team, led by UBC Okanagan researchers, suggests a simple tweak to the first meal of the day might help people living with Type 2 diabetes (T2D) better control their blood sugar levels.
Dr. Barbara Oliveira conducts research with Dr. Jonathan Little’s Exercise, Metabolism and Inflammation Lab in UBCO’s Faculty of Health and Social Development. Their latest study, published this week in the American Journal of Clinical Nutrition, confirms that switching from a traditional western-style low-fat breakfast, like oatmeal, toast and fruit, to a low-carb meal higher in protein and fat, like eggs with bacon or cheese, can help people with T2D better manage their blood sugar for most of the day.
In fact, changing just one meal helped keep the blood sugar in check.
“We’re not talking about a complete diet overhaul,” says Dr. Oliveira. “One of many complications for people living with T2D is rapid or large increases in blood glucose levels after a meal. Our research indicates a low-carbohydrate meal, first thing in the morning, seems to help control blood sugar throughout the day.”
Controlling glucose levels is critical for reducing the complications of T2D including inflammation and cardiovascular disease — the major cause of morbidity in patients with T2D.
“Treatment strategies that can help lower post-meal glucose swings and rapid changes in glucose are crucial to managing this condition,” she adds. “We’ve determined that if the first meal of the day is low-carb and higher in protein and fat we can limit hyperglycemic swings.”
Low-carb diets have become trendy in recent years and have been recognized as a dietary strategy to improve glucose control, Dr. Oliveira explains. However, similar to all diets, it’s tough to follow, especially long term. Instead of asking patients to commit to every meal being low-carb, she and Dr. Little examined the idea of making just the first meal of the day low-carb to see how that impacts diet adherence, and more importantly, blood glucose levels.

Their 12-week study had 121 participants split into two groups. One was advised to eat from a selection of low-carb breakfasts containing approximate amounts of 8g of carbohydrate, 25g of protein and 37g of fat while the other was advised to eat from a selection of low-fat higher-carb options containing about 56g of carbohydrates, 20g of protein and 15g of fat. All the breakfast options in both groups provided 450 calories.
Participants had a variety of breakfast choices and were required to upload a photo of their meal, which was reviewed by a study dietitian to confirm compliance.
All participants were provided with a continuous glucose monitoring device they wore throughout the study and also undertook A1C blood tests, before and after the 12 weeks, to measure their average blood sugar levels. They also measured their weight and waist circumference at the beginning and end of the trial. As the study continued they reported feelings of satiety, energy and activity levels.
Dr. Oliveira notes while there were no significant differences between the low-carb and other group for weight, body mass index or waist circumference, the low-carb group did see a reduction in blood sugar levels and some were able to reduce their glucose-lowering medication. The upward and downward swings in blood glucose levels, known as glycemic variability, with the low-carb group was also significantly lower, suggesting the benefits of a low-carbohydrate breakfast for stabilizing blood sugars throughout the day.
One additional interesting finding was that people who had the low-carb breakfast self-reported lower calorie and carbohydrate intake at lunch and during the remainder of the day. This could suggest that a breakfast rich in fat and protein, while lower in carbs, can impact daily eating habits.
“Having fewer carbs for breakfast not only aligns better with how people with T2D handle glucose throughout the day, but it also has incredible potential for people with T2D who struggle with their glucose levels in the morning,” she adds. “By making a small adjustment to the carb content of a single meal rather than the entire diet, we have the potential to increase adherence significantly while still obtaining significant benefits.”
The research was conducted in collaboration with the University of Wollongong in Australia and was funded, in part, by peer-reviewed grants from the Egg Farmers of Canada and the American Egg Board.

Influenza epidemics, caused by influenza A or B viruses, result in acute respiratory infection. They kill half a million people worldwide every year. These viruses can also wreak havoc on animals, as in the case of avian flu. A team from the University of Geneva (UNIGE) has identified how the influenza A virus manages to penetrate cells to infect them. By attaching itself to a receptor on the cell surface, it hijacks the iron transport mechanism to start its infection cycle. By blocking the receptor involved, the researchers were also able to significantly reduce its ability to invade cells. These results, published in the journal PNAS, highlight a vulnerability that could be exploited to combat the virus.
Influenza viruses represent a major risk to human and animal health. Their potential for mutation makes them particularly elusive. ”We already knew that the influenza A virus binds to sugar structures on the cell surface, then rolls along the cell surface until it finds a suitable entry point into the host cell. However, we did not know which proteins on the host cell surface marked this entry point, and how they favoured the entry of the virus,” explains Mirco Schmolke, Associate Professor in the Department of Microbiology and Molecular Medicine and in the Geneva Centre for Inflammation Research (GCIR) at the UNIGE Faculty of Medicine, who led this work.
A receptor as a key to infection
The scientists first identified cell surface proteins present in the vicinity of the viral haemagglutinin, the protein used by the influenza A virus to enter the cell. One of these proteins stood out: transferrin receptor 1. This acts as a revolving door transporting iron molecules into the cell, which are essential for many physiological functions.
”The influenza virus takes advantage of the continuous recycling of the transferrin receptor 1 to enter the cell and infect it,” explains Béryl Mazel-Sanchez, a former post-doctoral researcher in Mirco Schmolke’s laboratory and first author of this work. ”To confirm our discovery, we genetically engineered human lung cells to remove the transferrin receptor 1, or on the contrary to overexpress it. By deleting it in cells normally susceptible to infection, we prevented influenza A from entering. Conversely, by overexpressing it in cells normally resistant to infection, we made them easier to infect”.
Inhibiting this mechanism
The research team then succeeded in reproducing this mechanism by inhibiting the transferrinreceptor 1 using a chemical molecule. ”We tested it successfully on human lung cells, on human lung tissue samples and on mice with several viral strains,” says Béryl Mazel-Sanchez. ”In the presence of this inhibitor, the virus replicated much less. However, in view of its potentially oncogenic characteristics, this product cannot be used to treat humans.” On the other hand, anti-cancer therapies based on the inhibition of the transferrin receptor are under development and could also be interesting in this context.
”Our discovery was made possible thanks to the excellent collaboration within the Faculty of Medicine as well as with the University Hospitals of Geneva (HUG) and the Swiss Institute of Bioinformatics (SIB),” the authors add. In addition to the transferrin receptor 1, scientists have identified some 30 other proteins whose role in the influenza A entry process remains to be deciphered. It is indeed likely that the virus uses a combination involving other receptors. ”Although we are still far from a clinical application, blocking the transferrin receptor 1 could become a promising strategy for treating influenza virus infections in humans and potentially in animals.”

Some foods and medicines, such as many COVID-19 vaccines, must be kept cold. As a step toward a robust, stable technique that could indicate when these products exceed safe limits, researchers in ACS Nano report a class of brilliantly colored microcrystals in materials that become colorless over a wide range of temperatures and response times. As a proof of concept, the team packaged the color-changing materials into a vial lid and QR code.
Walk-in freezers and refrigerated trucks generally maintain their set temperatures, but accidents can happen. Wireless sensors can monitor the temperature of individual products, but these devices produce a lot of electronic waste. Recently, researchers have suggested using materials that act as visual indicators to provide this information with less waste. Yet some current options using colorful reactions or dyes produce hues that can fade. Or they only track above-freezing temperatures, which isn’t useful for some COVID-19 vaccines that can actually start breaking down below freezing — above -4 or -94 degrees Fahrenheit. So, Yadong Yin, Xuemin Du and colleagues wanted to develop a better color-changing material with tunable melting to track a wide range of temperatures.
The researchers used structural colors, instead of dyes, for their indicator system. The team made glycerol-coated silicon dioxide nanoparticles, which appeared bright green or red when they clustered together into microcrystals in water. Next, they created liquids with variable melting points by mixing different proportions of polyethylene glycol or ethylene glycol and water. When these two parts were put together, they could produce an irreversible color loss when the temperature-triggered solution melted and the microcrystals broke apart. The materials could be customized to track temperature exposures from -94 to +99 degrees Fahrenheit that lasted from a few minutes to multiple days. In other experiments, the two-part indicator systems were packaged into flexible round vial labels and a QR code. These systems were very sensitive and successfully indicated when the materials got too warm. The researchers say that structural color-changing materials hold promise for the diverse scenarios encountered in medical cold supply chains.
The authors acknowledge funding from the National Natural Science Foundation of China, the National Key R&D Program of China, the Youth Innovation Promotion Association of Chinese Academy of Sciences, the Guangdong Regional Joint Fund-Key Project, the Chinese Academy of Sciences Key Laboratory of Health Informatics, the Shenzhen Institutes of Advanced Technology and the Fundamental Research Program of Shenzhen.

Consuming nutritious food can improve metabolic health and delay aging. But what are the appropriate quantities of dietary macronutrients that can help achieve this? To answer this, researchers from Japan fed isocaloric diets with varying amounts of protein to young and middle-aged male mice. They found that the mice were metabolically healthier when fed moderate-protein diets. These findings could provide valuable insights into developing nutritional interventions and improving metabolic health in people.
As the proverb “You are what you eat” goes, the type of food we consume influences our health and longevity all through our lives. In fact, there is a direct association between age-related nutritional requirements and metabolic health. Optimal nutrition according to age can help maintain metabolic health, thereby improving the health span (period of life without diseases) and lifespan of an individual. Different nutritional interventions involving varied calorie and protein intake have been known to improve the health and lifespan of rodents and primates. Furthermore, recent studies have also reported the association of dietary macronutrients (proteins, carbohydrates, fats) with cardio-metabolic health and aging in mice. However, the amount of protein that must be consumed to maintain metabolic health is not known.
In a new study published in GeroScience on April 28, 2023, a team of researchers led by Assistant Professor Yoshitaka Kondo from Waseda University, Japan, investigated the amount of dietary protein needed to improve metabolic health in mice approaching old age. The team, which also included Dr. Takuya Chiba, Faculty of Human Sciences, Waseda University, Dr. Akihito Ishigami, Molecular Regulation of Aging, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Dr. Hitoshi Aoki, Research and Development Division, Nichirei Foods Inc, and Dr. Shin-Ichiro Takahashi, Department of Animal Sciences and Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, University of Tokyo. They recruited young (6 months old) and middle-aged (16 months old) male C57BL/6NCr mice who were fed isocaloric diets with varying protein content (5 to 45 %) for two months. After two months, the effect of varying protein diets was assessed based on measurements of skeletal muscle weight, liver and plasma lipid profiles, and self-organizing map (SOM) cluster analysis of plasma amino acid profiles.
When asked about the motivation behind their study, Kondo explains, “The optimal balance of macronutrients for ideal health outcomes may vary across different life stages. Previous studies show the possibility of minimizing age-specific mortality throughout life by changing the ratio of dietary protein to carbohydrates during approach to old age in mice. However, the amount of protein that should be consumed to maintain metabolic health while approaching old age is still unclear.”
The team observed that the consumption of a low-protein diet led to the development of mild fatty liver, with increased levels of hepatic lipids in middle-aged mice as compared to young mice. In contrast, a moderate-protein diet led to reduced blood glucose concentrations and lipid levels in both liver and plasma. These findings indicate that a moderate-protein diet (25% and 35%) kept both young and middle-aged mice metabolically healthier.
On examining the effect of varying protein diets on plasma amino acid concentrations in mice of both age groups, the researchers observed that the plasma concentration of individual amino acids varied with age and varying dietary protein content. This was further validated using SOM analysis of the plasma amino acids. Furthermore, the plasma amino acid profiles revealed using SOM analysis showed the correlation between different protein intake and the varying amounts of hepatic triglycerides and cholesterol levels.
Discussing the impact of their study on public health, Kondo remarks, “Protein requirements change through the course of life, being higher in younger reproductive mice, reducing through middle age, and rising again in older mice as protein efficiency declines. The same pattern is likely to be observed in humans. Therefore, it could be assumed that increasing daily protein intake in meals could promote metabolic health of people. Moreover, ideal dietary macronutrient balance at each life stage could also extend health span.”
In conclusion, a balanced diet with moderate amounts of protein could be the key to a long and healthy life.

Estudios recientes muestran que la mayoría de las muertes relacionadas con el embarazo ocurren en el año posterior al parto. El hallazgo está cambiando la manera en que los médicos atienden a las nuevas madres.El bebé de Sherri Willis-Prater tenía dos meses de nacido y ella estaba a punto de regresar a trabajar en la cafetería de una escuela de Chicago. Pero cuando una noche subió el pequeño tramo de escaleras para ir a la cocina, casi se desploma, jadeando para respirar.En el hospital, a Willis-Prater, quien en ese momento tenía 42 años, la conectaron a un respirador que le bombeaba aire hacia los pulmones. Los médicos dijeron que su corazón estaba trabajando a menos del 20 por ciento de su capacidad. Había desarrollado un tipo poco común de insuficiencia cardiaca que se presenta después del embarazo.Ese diagnóstico era lo último que esperaba escuchar. Tras dar a luz, Willis-Prater pensó que “había logrado cruzar la meta”, recordó en una entrevista. “Ya no tengo que preocuparme por nada”.La mayoría de la gente cree que el trabajo de parto y dar a luz son las partes más difíciles del embarazo, pero las investigaciones científicas recientes están cuestionando esta idea y han descubierto que durante el año posterior al nacimiento todavía sigue habiendo un riesgo considerable. De hecho, el periodo más letal para la madre es posterior al nacimiento del bebé.Por cada mujer que fallece, alrededor de 50 a 100 mujeres sufren complicaciones graves que pueden dejarlas con problemas de salud por el resto de su vida. Las cifras van en aumento, ya que cada vez más mujeres estadounidenses tienen sobrepeso, además de que la hipertensión y la diabetes se han vuelto más comunes.Asimismo, cada vez más mujeres posponen la maternidad para una época posterior de su vida, por lo que es más probable que inicien el embarazo con padecimientos crónicos de salud que pueden dar lugar a complicaciones.Estas nuevas cifras aparecen en medio de un inquietante incremento de muertes de mujeres embarazadas y madres recientes en Estados Unidos, país que tiene la tasa más elevada de mortalidad materna de los países industrializados. Estas cifras se dispararon durante la pandemia: de 20,1 muertes por cada 100.000 nacimientos vivos en 2019 a 32,9 muertes por cada 100.000 en 2021. Hay de dos a tres veces más fallecimientos de mujeres negras y nativas estadounidenses que de las mujeres blancas.Pero esas cifras corresponden a una definición tradicional de mortalidad materna: muertes que ocurren durante la gestación o hasta seis semanas después del parto.Un panorama más completo del problema salió a la luz en septiembre, cuando los Centros para el Control y la Prevención de Enfermedades (CDC, por su sigla en inglés) observaron con mayor amplitud las muertes maternas, las analizaron durante un año entero luego del nacimiento e incluyeron los fallecimientos resultantes de trastornos de salud mental.Con base en los datos de 36 estados sobre 1018 muertes relacionadas con el embarazo de 2017 a 2019, los CDC llegaron a la conclusión de que cerca de una tercera parte de estas ocurrían durante el embarazo o el día del parto y que más o menos otra tercera parte antes de que el bebé cumpliera seis meses. Un 30 por ciento tenía lugar a partir de ese momento hasta el primer año de vida del bebé, periodo en el que no se habían enfocado las investigaciones sobre la mortalidad materna.Estos datos han ocasionado que se pida que se dé una atención posterior más exhaustiva y que se otorgue más apoyo a las madres recientes durante lo que se ha denominado el “cuarto trimestre”, así como atención especial a las mujeres vulnerables.“Nuestro planteamiento de la natalidad ha sido que el bebé es el caramelo y la mamá la envoltura, y una vez que el bebé está fuera de la envoltura, la hacemos a un lado”, señaló Alison Stuebe, profesora de ginecología y obstetricia de la Facultad de Medicina de la Universidad de Carolina del Norte. “Tenemos que reconocer que la envoltura es una persona y que las mamás se pueden poner muy mal y morir”.Después de dar a luz, Sherri Willis-Prater recordó haber pensado: “Ya no tengo que preocuparme por nada”. Pero poco después le diagnosticaron insuficiencia cardíaca. Anjali Pinto para The New York TimesLas causas principales de muerte materna entre las mujeres blancas y latinas son los trastornos de salud mental que dan pie a suicidios y sobredosis fatales. Entre las mujeres asiáticas, la principal causa de muerte son las hemorragias.Entre las mujeres negras, como Willis-Prater, los padecimientos cardíacos fueron la principal causa de muerte. La hipertensión, un factor predisponente, es más común entre las mujeres negras, las cuales con frecuencia tienen poco acceso a atención médica debido tanto a la pobreza como al racismo.El riesgo de muerte materna posterior —de seis meses a un año después del parto— es 3,5 veces más alto para las mujeres negras, en comparación con el de las mujeres blancas..La práctica de la medicina suele cambiar con lentitud, pero estas cifras están acelerando modificaciones a Medicaid, el plan de atención médica que cubre a los estadounidenses de bajos ingresos, que incluyen a más del 40 por ciento de las mujeres embarazadas en Estados Unidos.La cobertura de Medicaid para las madres recientes se ha ampliado hasta todo un año después del parto para que las mujeres estén aseguradas mientras se recuperan del embarazo en 33 estados y en Washington D. C., y otros ocho estados tienen planes de hacer lo mismo, de acuerdo con Kaiser Family Foundation (KFF, por sus sigla en inglés).Según KFF, tres estados, entre ellos Texas, están ampliando solo la cobertura limitada, y seis —incluyendo Arkansas, el cual ha tenido una de las tasas de mortalidad materna más elevadas del país— no tienen planes de ampliar la cobertura de Medicaid.Otras iniciativas incluyen una nueva ley en Nueva Jersey que exige que los médicos de la sala de emergencias pregunten a las mujeres en edad fértil sobre su historial de embarazo. Algunas enfermedades que llevan a las mujeres al hospital pueden diagnosticarse con mayor rapidez si los médicos saben que dieron a luz recientemente.En Carolina del Norte, los proveedores de salud ganan un bono de 150 dólares si una paciente acude a una consulta posparto. Históricamente, casi la mitad de las nuevas madres no acuden a sus controles posparto.Ahora se les está recomendando a los médicos revisar a las madres dentro de las tres semanas posteriores al parto, en vez de esperar a la revisión a las seis semanas de dar a luz que solía acostumbrarse.“Ahora es así: ‘Nos vemos en dos semanas, ¿de acuerdo? Y, sí, en definitiva, tiene que venir’”, comentó Tamika Auguste, autora, junto con Stuebe, de los nuevos lineamientos para los cuidados posteriores al parto del Colegio Americano de Obstetras y Ginecólogos.Según Auguste, las madres recientes que tienen padecimientos de salud como la hipertensión deben acudir a revisión incluso antes.Sin embargo, es todavía más importante que los médicos y otros profesionales de la salud escuchen a las mujeres cuando éstas expresan alguna preocupación y que pongan atención especial cuando las mujeres negras y nativas estadounidenses digan que algo no está bien.“Ya nada de ‘Estás bien querida, no hay problema’”, señaló Auguste. “Nada de eso. Más bien: ‘Vamos a ver si podemos revisarte hoy o mañana’”.El embarazo ha sido llamado “la prueba de esfuerzo cardíaco de la naturaleza” debido a las tensiones que ejerce sobre el corazón y el sistema circulatorio de la mujer.Lea Suzuki/The San Francisco Chronicle, vía Getty ImagesMúltiples riesgosMuchos médicos se refieren al embarazo como “la prueba de esfuerzo cardíaco de la naturaleza”. Esta condición sobrecarga el corazón y el sistema circulatorio de una mujer: el volumen de sangre aumenta hasta en un 50 por ciento, el corazón trabaja más y la frecuencia cardíaca aumenta.Las elevaciones en la presión arterial pueden afectar otros órganos vitales y dejar a una mujer en mayor riesgo de enfermedad cardiovascular durante el embarazo o incluso décadas después, dijo Rachel Bond, cardióloga y directora del sistema del programa de salud cardíaca de la mujer en el centro médico Dignity Health en Chandler, Arizona“Les decimos a las mujeres: ‘Has atravesado tu primera prueba de estrés, o pasas o fallas’”, dijo Bond. “El fracaso no significa necesariamente que tendrá una enfermedad cardíaca, pero significa que nosotros, como médicos, debemos tratarlo de manera más agresiva”.Una vez que nace el bebé, el útero se encoge y la presión arterial puede aumentar, lo que puede provocar un derrame cerebral.Las nuevas madres también son más propensas a experimentar coágulos de sangre e infecciones potencialmente mortales. Al mismo tiempo, los cambios hormonales pueden provocar fluctuaciones en el estado de ánimo. Algunos de estos son transitorios, pero también se puede desarrollar una depresión posparto más grave y duradera.Pese a que la mayor parte de las mujeres sobreviven a las complicaciones relacionadas con el embarazo después de dar a luz, es importantísimo que reciban atención médica inmediata.Deidre Winzy, una asistente médica de 28 años de Nueva Orleans, ya era hipertensa cuando se embarazó de su tercer hijo. Los médicos le proporcionaron un tensiómetro para que lo usara en su casa junto con la aplicación Babyscripts, un sistema de monitoreo a distancia que enviaba las lecturas a su obstetra.Tras diagnosticarla con preeclampsia, un padecimiento de hipertensión muy peligroso, le indujeron el parto dos semanas y media antes. Pero tres semanas después de dar a luz, Winzy despertó a mitad de la noche sintiéndose desorientada y mareada y, balbuceando, llamó a una amiga para que la ayudara.Los paramédicos creyeron que lo que tenía era un ataque de pánico y al principio no querían llevarla al hospital, pero en realidad estaba teniendo un derrame cerebral. “Llegué justo a tiempo”, recuerda Winzy. “Si no lo hubiera logrado, tal vez habría quedado paralítica el resto de mi vida”.Ahora Winzy tiene problemas de pérdida de memoria a corto plazo y debilidad, pero puede trabajar. De todas maneras, por ser madre soltera de tres niños, no deja de preocuparse.“Mi peor temor es faltarles a mis hijos”, recalcó Winzy. “¿Qué tal si vuelvo a tener otro derrame y este me deja paralítica de manera permanente o me mata? Es aterrador”.Aryana Jacobs, sosteniendo a su hijo Caleb, mientras su esposo, Brendan Hurley, observa. Su primer embarazo transcurrió sin incidentes, pero tenía antecedentes familiares de hipertensión y tenía un tensiómetro en casa.Shuran Huang para The New York TimesEntre las mujeres blancas, las condiciones de salud mental son responsables del 35 por ciento de las muertes relacionadas con el embarazo, según datos de los CDC. Entre las mujeres hispanas, la cifra es del 24 por ciento. La ansiedad o la depresión preexistentes pueden dejar a las mujeres vulnerables a la depresión posparto, al igual que un embarazo difícil o tener un bebé enfermo.El estrés de ser padre puede desencadenar una recaída en alguien que se está recuperando de un trastorno por uso de sustancias, dijo Katayune Kaeni, psicóloga y presidenta de la junta del Postpartum Support International.Karen Bullock, de 39 años, que vive en las afueras de Peoria, Illinois, tuvo un embarazo difícil y un parto prematuro traumático, y tuvo problemas para amamantar.“Nada salió de forma natural”, dijo. “No estaba feliz cuando nació el bebé, estaba asustada. Cada vez que lo miraba, pensaba, ‘no sé qué hacer contigo’”. Bullock finalmente fue diagnosticada con depresión posparto y comenzó a tomar medicamentos.Las complicaciones pueden sorprender incluso a las mujeres cuyos embarazos han transcurrido sin problemas. A Aryana Jacobs, una analista de tecnología de la salud de 34 años que vive en Washington D. C., le dijeron después de una cesárea que su presión arterial estaba fluctuando. Jacobs la verificaba en casa con un tensiómetro que tenía debido a sus antecedentes familiares de hipertensión. En unos cuantos días, la lectura llegó a ser de 170/110.La llevaron al hospital y le dieron tratamiento para la preeclampsia, la cual casi siempre se desarrolla durante el embarazo, no después.“Me gustaría que a todas las madres las enviaran a casa con una caja de chocolates y un tensiómetro para recalcar que al ser madres no dejan de ser pacientes. Su cuerpo se está recuperando de algo muy fuerte”, señaló Jacobs.

Gratitude ceremonies give students and faculty members a chance to recognize the sacrifice of those who gave their bodies for medical research and education, and the loved ones they left behind.A solemn gathering at Columbia University last month had the trappings of a traditional memorial service. Students and faculty members performed music and gave speeches. The university’s chaplain closed the ceremony with a reflection.But there was one key difference: No one in the room had ever met the people whose lives were being honored. The attendees were all students and faculty members at Columbia’s medical school, and they were gathered to show gratitude for the people who had donated their bodies for the students to study in the anatomy lab.“Who were they before?” said Bree Zhang, a first-year dental student. “A parent, a child, a co-worker, a friend? What books did they read? How is their family doing now, and do they know how much their loved one has given me and the rest of us?”Similar scenes played out across the country this spring as medical, dental and physical therapy students assembled to offer tributes to whole-body donors and their families. At the ceremonies, students perform music, light candles, read letters and share art. (A heart diagram from Ms. Zhang’s anatomy studies, overlaid with her whimsical drawings of books, tree roots and human figures, was projected behind her as she spoke at Columbia.) A nondenominational spiritual leader often plays a role. Sometimes a tree designation or an offering of flowers to a donor’s family, is included.Bree Zhang, a first-year dental student at Columbia, spoke at the ceremony and shared artwork inspired by her experience in the anatomy lab.Diana Cervantes for The New York TimesIt is not clear how many people in the United States donate their bodies for medical research and education, though estimates suggest that about 20,000 people or their families do so each year. Criteria vary by program and by state; generally anyone over 18 can become a donor, though people with certain transmissible diseases, such as hepatitis B or C, tuberculosis, H.I.V. or AIDS, are typically excluded. Many programs also exclude bodies that have been autopsied or have had organs removed for donation.Even with the introduction of elaborate 3-D visualization software, dissection remains a cornerstone of a medical education for most first-year students, as it has for centuries. Students spend months methodically studying the structures of the body, including organs, tendons, veins and tissue. The experience teaches more than the foundations of medicine. Treating the donor, who is viewed as a doctor’s first patient, with respect and care gives students a grounding in ethics and professionalism, said Joy Balta, the chair of the American Association for Anatomy’s human body donation committee.Recognizing a sacrificeBody donation is a selfless act by the donors, as well as by their families, who can wait as long as a couple of years to receive the ashes. The memorials, often called ceremonies of appreciation or gratitude, recognize the sacrifice.“You’re able to think about the donor that you’ve been working with,” said Dr. Balta, who is also the director of the Anatomy Learning Institute at Point Loma Nazarene University in San Diego. “These are people,” he added, “that donated their bodies, that wanted you to work with them to improve science and health care.”The Vagelos College of Physicians and Surgeons at Columbia began hosting a donor gratitude ceremony in the late 1970s as a way of marking an experience that “is very difficult for some students and really transformative,” said Paulette Bernd, who runs the school’s clinical gross anatomy course.Georgetown University medical students, from left, Justine Mann, Lauren Bierman and Jacqueline Antonishek, with a donor body in an anatomy lab in 2011.Bill O’Leary/The Washington Post via Getty ImagesRelatives of the donors are invited to the events at some schools. At others, the ceremonies are only for students and faculty members, an extension of the anonymity that is provided to the donors in the lab. At Brown University, for instance, only a donor’s age, cause of death, marital status and occupation are shared with students, and the donor’s hands and faces are covered for much of the process.“The bodies go through this whole process of being de-identified,” said Nidhi Bhaskar, a first-year medical student who helped coordinate a gratitude ceremony at Brown this month. “And this is a really great way to re-humanize them. We take into account the very real gift they left, and the family members who are still processing their loss.”The anatomy lab can be a fraught experience for medical students, for whom “it may be their first experience where they’re dealing with death and dying,” said Dr. Daniel Topping, a clinical associate professor in the department of anatomy and cell biology at the University of Florida College of Medicine.Abby Carey-Ewend, a second-year student at the Washington University School of Medicine in St. Louis, remembers being incredibly nervous about it.“But when I started it,” she said, “I realized that it was really a phenomenal opportunity to be able to work with three other students and one donor, and to really learn the intricacies of the human body from something beyond a textbook or videos.”Ms. Carey-Ewend helped plan the appreciation ceremony for her medical program, which was held in April. A priority, she said, was acquainting family members of the donors with the campus community and the students their loved ones had helped educate.‘I knew she was helping somebody.’Among the guests at the ceremony at Washington University was Regina Dunn. When her mother, Louise Dunn, died in July at 90, she was too distraught to plan a funeral. The donor remembrance was Louise Dunn’s first memorial service, she said.“They just made you feel so comfortable,” Regina Dunn said of the students. “And a lot of people wanted that closure.”Louise Dunn, who opened a modeling school for women of color in St. Louis in 1960, was driven throughout her life by a desire to help people, her daughter said. So it was not surprising that she wanted to continue to help others after her death, Ms. Dunn said, even if some of her survivors had to overcome a degree of apprehension over her decision to donate her body to science.Medical students paying their respects to body donors at Zhejiang University in Hangzhou, China, in 2018.Agence France-Presse — Getty ImagesRegina Dunn said that a Black student told a friend who accompanied her to the ceremony that having a Black donor in the lab, when most donors are white, had a profound impact.“I felt honored, I really did,” Ms. Dunn said, “because I knew she was helping somebody.”For the family of Michael Haas, who donated his body to the Indiana University School of Medicine, a gratitude ceremony last month was a full-circle moment in several ways.It was held on April 16, four days before the anniversary of Mr. Haas’s death, his wife, Molly Haas, said. The ceremony was held on the university’s campus in Bloomington, Ind., where the couple were engaged in 1970. The families received white and red carnations; Ms. Haas recalled that her husband always bought her red carnations.Both decided to donate their bodies in 2012, around the time that the symptoms of Mr. Haas’s Alzheimer’s disease began to show. For Mr. Haas, a former social worker and Episcopal priest, becoming a whole-body donor was a way of extending a lifelong mission of service, his wife said.“His values, his ethics were always very generous,” Ms. Haas said.‘A great sense of gratitude’The appreciation ceremonies are typically planned by students, but they also give the faculty members who run the anatomy labs a way of processing their relationships with the people who donate their bodies for medical education.“I feel a great sense of gratitude and responsibility and honor every time I’m around a donor,” said Dr. Topping, of the University of Florida. “It’s a very sacred thing for me.”When the Zucker School of Medicine at Hofstra University, on Long Island, made its gratitude ceremony a virtual event during the coronavirus pandemic, it allowed donor relatives from across the country and around the world to participate, said Robert Hill, an associate professor. In 2020, relatives of one donor logged on from India, he said.The Vagelos College of Physicians and Surgeons at Columbia has been hosting donor gratitude ceremonies since the 1970s, said Paulette Bernd, who runs the school’s clinical gross anatomy course.Diana Cervantes for The New York Times“It’s a way of bringing closure to their shared journey,” he said. “Our students are on an educational journey, and our donor families are navigating the world without their loved one.”Nirusha Lachman, the chair of the department of clinical anatomy at the Mayo Clinic College of Medicine and Science, attended her first gratitude ceremony about 40 years ago when she was a student in South Africa, and she has since spoken at several.The gatherings, she said, serve to drive home the point that donors live on through the education that their bodies have provided.“You want this to resonate, even with the families,” Dr. Lachman said, “that death was not the end for their loved ones.”

St. Jude Children’s Research Hospital scientists discovered how the current epizootic H5N1 avian influenza virus (bird flu) gained new genes and greater virulence as it spread west. Researchers showed that the avian virus could severely infect the brains of mammalian research models, a notable departure from previous related strains of the virus. The researchers genetically traced the virus’ expansion across the continent and its establishment in wild waterfowl populations to understand what makes it so different. The study was recently published in Nature Communications.
“We haven’t seen a virus quite like this one,” said corresponding author Richard Webby, Ph.D., St. Jude Department of Infectious Diseases. “In 24 years of tracing this particular H5N1 flu lineage, we haven’t seen this ability to cause disease but also be maintained in these wild bird populations.”
When the scientists tested the newer avian flu strains for their ability to cause disease in mammals by infecting a ferret model, they found an unexpectedly high amount of pathogenicity.
“Some of these are really nasty viruses,” Webby said. “There’s a huge amount of the virus in the brain of infected animals. That’s the hallmark of what we saw with these flu strains — increased pathogenicity associated with high virus load in the brain. That’s not the first time we’ve seen H5 viruses in the brain, but these are probably some of the most virulent we’ve looked at over 24 years of following these viruses.”
Previous influenza viruses that caused severe disease in North America “burned out” in their main host bird population, and the outbreaks ended quickly. This current strain was detected at high levels in sick chickens but has expanded into other species.
“This is not just a chicken virus now,” Webby said. “It’s also infecting other avian and mammal species in the U.S. It’s a higher exposure risk for humans and other mammals than we’ve ever had in North America. We’ve never really been exposed to this level of circulation of these highly pathogenic flu viruses.”
A low risk to humans (for now)

While the newer strains of this H5N1 influenza show a greater ability to cause disease in mammals than earlier viruses, the scientists found it to be low-risk to humans. This is because the virus appears well-adapted to transmit between birds rather than between mammals.
“Overall, their risk to humans is still low,” Webby said. “But that risk does seem to be changing, and these viruses are doing things that we haven’t seen H5s do before. They’ve come into the continent’s wild bird population, they’ve reassorted, and they’ve been maintained over time. There are now many different types out there, and they’re very nasty.”
Even though the risk of spreading infection is low, the research suggests humans should be cautious interacting with wildlife.
“Someone would have to work pretty hard to infect themselves with this virus. But if they do happen to be infected, there’s a real chance of getting a severe disease from it,” Webby said. “People just need to be careful and remember that some of the wild animals out there potentially harbor these highly pathogenic viruses.”
Genetic change supercharges spread and severity
In the past, similar strains of influenza viruses have not caused similarly severe diseases, nor have they become far-flung in wild bird populations. Since the new strains have done so much more damage, the scientists looked for what was different. The group identified the direct ancestor to the current strains, which spread from Europe to the Americas after gaining a different version of the viral protein, neuraminidase. This new protein increased the virus’s ability to transmit between birds. Then it arrived on the East Coast of Canada and traveled to the United States.

As the researchers studied the virus further, they pinpointed which viruses — distinct from previous ones — caused the current outbreaks. They found that after reaching North America, the virus rapidly changed again to become more virulent. It mixed with flu viruses in North American wild birds, swapping several genes. This reassortment of genes had two effects. One, the virus seemed to become even more adapted to the bird population, infecting many different types of birds. This included atypical hosts, such as buzzards and eagles, which typically do not get the flu. Second, the virus gained its severe disease-causing properties.
“The surprising thing was that just a few reassortment events did change these viruses’ ability to cause disease in our models,” Webby said. “And those events generated many different genotypes from that mixing. Then those viruses spread and have now become established in the North American wild bird population.”
Webby’s group and others continue to monitor the ongoing avian flu pandemic globally to assess its continually evolving risk to both humans and birds.