Publisher Health

Reproduction permanently alters females’ bones in ways not previously known, a team of anthropologists has found. Its discovery, based on an analysis of primates, sheds new light on how giving birth can permanently change the body.
“Our findings provide additional evidence of the profound impact that reproduction has on the female organism, further demonstrating that the skeleton is not a static organ, but a dynamic one that changes with life events,” explains Paola Cerrito, who led the research as a doctoral student in NYU’s Department of Anthropology and College of Dentistry.
Specifically, the researchers found that calcium, magnesium, and phosphorus concentrations are lower in females who have experienced reproduction. These changes are linked to giving birth itself and to lactation.
However, they caution that while other clinical studies show calcium and phosphorus are necessary for optimal bone strength, the new findings do not address overall health implications for either primates or humans. Rather, they say, the work illuminates the dynamic nature of our bones.
“A bone is not a static and dead portion of the skeleton,” notes NYU anthropologist Shara Bailey, one of the study’s authors. “It continuously adjusts and responds to physiological processes.”
The other authors of the study, which appears in the journal PLOS ONE, are Timothy Bromage, a professor in NYU College of Dentistry, Bin Hu, an adjunct professor at NYU College of Dentistry, Justin Goldstein, a doctoral candidate at Texas State University, and Rachel Kalisher, a doctoral candidate at Brown University.
It’s been long-established that menopause can have an effect on females’ bones. Less clear is how preceding life-cycle events, such as reproduction, can influence skeletal composition. To address this, the researchers studied the primary lamellar bone — the main type of bone in a mature skeleton. This aspect of the skeleton is an ideal part of the body to examine because it changes over time and leaves biological markers of these changes, allowing scientists to monitor alterations during the life span.
In the PLOS ONE study, the researchers examined the growth rate of lamellar bone in the femora, or thigh bones, of both female and male primates who had lived at the Sabana Seca Field Station in Puerto Rico and died of natural causes. Veterinarians at the field station had monitored and recorded information on these primates’ health and reproductive history, allowing the researchers to match bone-composition changes to life events with notable precision.
Cerrito and her colleagues used electron microscopy and energy-dispersive X-ray analysis — commonly deployed methods to gauge the chemical composition of tissue samples — to calculate changes in concentrations of calcium, phosphorus, oxygen, magnesium, and sodium in the primates’ bones.
Their results showed different concentrations of some of these elements in females who gave birth compared males as well as females who did not give birth. Specifically, in females who gave birth, calcium and phosphorus were lower in bone formed during reproductive events. Moreover, there was a significant decline in magnesium concentration during these primates’ breastfeeding of infants.
“Our research shows that even before the cessation of fertility the skeleton responds dynamically to changes in reproductive status,” says Cerrito, now a research fellow at ETH Zurich. “Moreover, these findings reaffirm the significant impact giving birth has on a female organism — quite simply, evidence of reproduction is ‘written in the bones’ for life.”
The research was supported by grants from the National Science Foundation (2018357) and the National Institutes of Health (1S10OD026989-01).

Inside tiny cellular machines called ribosomes, chains of genetic material called messenger RNAs (mRNAs) are matched with the corresponding transfer RNAs (tRNAs) to create sequences of amino acids that exit the ribosome as proteins. Unfinished proteins are called nascent chainsm and they are left attached to the ribosome.
Scientists know that some of these nascent chains can regulate the activity of the ribosome and that the nascent chains can sometimes interfere with antibiotics — many of which work by targeting bacterial ribosome activity. Scientists do not know why this happens, mainly because it is hard to visualize what the ribosome-peptide-drug interactions look like while the unfinished proteins are still tethered to the ribosome.
Now, scientists at the University of Illinois Chicago are the first to report a method for stable attachment of peptides to tRNAs, which has allowed them to gain new fundamental insights into ribosome function by determining the atomic-level structures of ribosomes and the shapes that these peptides take inside the ribosome.
Their method is newly reported in the journal Nature Chemistry.
“The challenge has been to see up close the structure of the ribosome and the exit tunnel in the presence of the nascent peptides because, in nature, the ribosome is very quick for us to capture images or conduct experiments,” said Yury Polikanov, associate professor in the biological sciences department at the College of Liberal Arts and Sciences. “Until the advent of this new method, we’ve essentially been blinded from seeing what is happening in the active site of the ribosome at this critical moment in time.”
Polikanov and his colleague Egor Syroegin, a PhD candidate in biological sciences at UIC, used a method called native chemical ligation to fuse custom peptides with the tRNA to yield what is called a peptidyl-tRNA.

The protein kinase CK2 is involved in a wide range of biological processes and cellular functions, including inflammatory responses and pathologies associated with inflammation. Also, its aberrant expression and activity are characteristic of many cancers. Yet the basic function of CK2 in CD8+ immune T cells has remained completely unknown.
CD8+ T cells, also known as killer T cells, are critical to maintain health by controlling infections by intracellular pathogens, including viruses and intracellular bacteria. CD8+ T cells also can control cancer progression by directly killing cancer cells, and through recruiting and activating other immune cells.
Now in a study published in The Journal of Immunology, University of Alabama at Birmingham researchers report that protein kinase CK2 controls CD8+ T cell effector and memory functions during infection. These experiments were done in mouse CD8+ T cells and a mouse model of infection by the intracellular pathogenic bacteria Listeria monocytogenes.
The CK2 kinase is known to act in cellular signaling pathways by phosphorylating target proteins at specific serine or threonine amino acids. The CK2 kinase has two catalytic subunits and two regulatory subunits. The UAB researchers, led by Hongwei Qin, Ph.D., and Etty “Tika” Benveniste, Ph.D., deleted the CK2α catalytic subunit from mouse CD8+ T cells and compared them to CD8+ T cells with an intact CK2 kinase.
The researchers first showed that the CK2 subunits were induced, and that CK2 kinase activity was increased, when intact CD8+ T cells were activated by stimulating the T cell receptor to trigger an immune response. That showed a potential role of CK2 in CD8+ T cell responses.
In contrast, the CK2α-/- deletion mutants showed significantly less CD8+ T cell activation and proliferation, indicating that the CK2α activity was required for those steps.
Furthermore, the researchers say their findings suggest that CK2α is involved in CD8+ T cell metabolic reprogramming during activation, specifically through increases in glycolytic metabolism and mitochondrial respiration. Mitochondria are the powerhouses of cells, supplying most of the cellular energy. Upon activation, intact T cells are known to undergo substantial metabolic reprogramming; but the UAB researchers found that CK2α-/- deletion mutants had significantly less glucose uptake and metabolism, and decreased mitochondrial respiration, compared to T cells with normal CK2.
Mechanistically, the UAB team showed that CK2α controlled the reprogramming of CD8+ T cell metabolism by regulating the well-known AKT/mTOR signaling pathway.
Using a mouse Listeria monocytogenes infection model, Qin, Benveniste and colleagues found that CK2α was required for CD8+ T cell expansion, maintenance and effector function in both primary and memory stages during infection by the intracellular bacterial pathogen.
“Taken together, our study demonstrates that CK2α regulates CD8+ T cell activation and differentiation both in vitro and in vivo,” Benveniste said. “However, the biological function of CK2α in CD8+ T cells, particularly CD8+ T cell cytotoxic function, remains to be explored.”
Co-authors with Benveniste and Qin in the study, “Protein kinase CK2 controls CD8+ T cell effector and memory function during infection,” are Wei Yang, Hairong Wei, William J. Turbitt, Jessica A. Buckley, Lianna Zhou and Laurie E. Harrington, UAB Department of Cell, Developmental and Integrative Biology; and Gloria A. Benavides, Xiaosen Ouyang, Jianhua Zhang and Victor M. Darley-Usmar, UAB Department of Pathology.
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Humans have just as many microbes in their microbiota as there are cells in the body, and most of these are in the large intestine (colon). They are an important part of our ‘digestion’ because they can harvest energy from many foods that evade our digestive enzymes. Unfortunately, whilst it is easy to collect fecal samples, it has been largely impossible to study the lower small intestine because this can only be reached during a surgical operation or after purging the intestinal contents to allow safe passage of an endoscope.
The small intestinal microbiome has remained almost “terra incognita” within the human gastrointestinal tract, despite the fact that the small intestine is essential for life and it absorbs 90% of all our calories. Researchers led by Andrew Macpherson and Bahtiyar Yilmaz from the Department for Biomedical Research at the University of Bern and the University Clinic for Visceral Surgery and Medicine at the Inselspital have now been able to examine the intestinal bacteria of the human small intestine in a simple and innovative way to show how they support the digestive process by reacting dynamically to the human nutritional status. While the gut bacteria (microbiota) of the large intestine remain relatively stable throughout life, those in the small intestine have been shown to be very unstable: they largely disappear when we fast overnight and reappear when we eat in the morning. These findings are important for a better understanding of the development of intestinal diseases such as celiac disease or Crohn’s disease. The study is published in the journal Cell Host and Microbe.
Direct access to intestinal bacteria
The researchers were able to examine patients whose lower small intestine (ileum) had needed surgery for cancer. Once these patients have healed, in some cases the ileum ends as an artificial opening on the abdominal wall. In this way, the researchers had direct access to the small intestinal bacteria and were able to examine what was happening in “real time.” The bacterial samples were analyzed using the latest sequencing methods. It was shown that the number of bacteria in the ileum depends to a large extent on the nutritional status of the patient: periods without food largely eliminate the bacteria in the small intestine. After a meal, the bacteria “bloom” again. Despite these diet-related fluctuations in “biomass,” the various types of bacteria do not become extinct, even if their numbers are very small. “Rather, each species is made up of a large number of subspecies that coexist — much like the different variants of COVID-19 that appear and disappear in the human population — and the proportions of each subspecies change very quickly, even within hours of eating a meal,” said Dr. Bahtiyar Yilmaz, first author and corresponding author of the study.
Effective and simple method
The close collaboration between clinic and basic research, that exists between the University Hospital Bern and the University of Bern, proved to be particularly valuable here: “The availability of different types of samples, combined with an unprecedented documentation of the clinical details by the medical staff of the University Hospital Bern and the in-depth microbial sequencing with the University of Bern’s next-generation sequencing platform make our study unique,” says Yilmaz. The results show that the use of ‘ostomy samples is very effective and simple to characterize the intestinal flora of the small intestine. The researchers were also able to demonstrate that the samples from patients with a stoma of the small intestine are representative of the intestinal flora of the small intestine without surgery.
“Ecosystem” in the small intestine
“We think of these changes in the intestinal bacteria in the small intestine as an ecosystem,” explained Andrew Macpherson, head of the study and senior author. “Because the system is so flexible, each bacterial species can adapt to a changing environment in the small intestine by changing the proportions of subspecies and thus prevent the species as a whole from dying out.” In this way, the intestinal bacteria avoid species extinctions — unless there are “bottlenecks” due to illness, malnutrition or environmental pollution. The findings can help to understand the interactions between the host and intestinal bacteria in intestinal diseases such as Crohn’s disease, celiac disease or chronic inflammation of the large intestine (ulcerative colitis) and form the basis for new therapeutic approaches.
This study was funded by the Swiss National Science Foundation (SNSF) and the European Research Council (ERC).
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Peering inside common atmospheric particles is providing important clues to their climate and health effects, according to a new study by University of British Columbia chemists.
Secondary organic aerosol (SOA) particles are ubiquitous in the atmosphere and play an important role in air quality and climate. They can add to air pollution and damage the lungs, as well as help deflect solar radiation or aid cloud formation.
Different types of SOA can mix together in a single particle and their environmental impacts are governed by the new particles’ physical and chemical properties, particularly the number of phases — or states — it can exist in.
In a new research letter published in the European Geosciences Union’s open access journal Atmospheric Chemistry and Physics, an international team of researchers found that particles with two phases can form when different types of SOA mix. The finding could help improve current models that predict SOA climate and health effects.
“Up until now, models have often assumed that when SOA types mix into the same particle, they have just one phase. But we found that’s not always the case, meaning current models might not correctly capture some of these effects,” says lead author Fabian Mahrt, a postdoctoral fellow at the Paul Scherrer Institute and UBC Department of Chemistry. The work was funded by the European Union’s Horizon 2020 research and innovation program.
The team found that six out of 15 mixtures of two SOA types commonly found in the atmosphere resulted in two-phase particles. Importantly, they also discovered that the number of phases depends on the difference in the average oxygen-to-carbon ratio between the given SOA types. It’s a fairly simple but potentially powerful way to represent such effects in models. When this difference is 0.47 or higher, the researchers found particles would have two phases.
“Now we can work with very complex organic molecules, calculate a single parameter which gives us information about the properties of a particular SOA mixture, and then potentially map quite large-scale impacts,” says aerosol scientist and senior author Allan Bertram, professor in the UBC Department of Chemistry.
This kind of SOA mixing might occur include when plumes of SOA particles, which have been in the atmosphere for some time, blow from rural environments over cities where newly produced SOA particles are being emitted, explains Mahrt.
“If we assume this mixing of the plumes forms particles with a single phase, we might over-predict the total organic particulate mass in these areas, and so, the effects on those people’s health.” The team of scientists hopes the finding can help improve models and ultimately ensure that policies and regulations are based on a rigorous scientific understanding.
Building on previous work, the researchers used fluorescence microscopy to look inside the mixed SOA particles in their current experiments, injecting them with a dye that causes the particle phases to emit different coloured light depending on their polarity. The researchers then used these colours to directly infer the number of phases of the mixtures, providing a direct visual proof of multiple phases.
“The study is evidence that we need to look at this phenomenon more carefully to get the full picture. We have one more piece of the puzzle but we have not necessarily finished the jigsaw yet,” says Mahrt. The research team hopes other scientists will now extend the number of SOA mixtures experimentally, as well as include the findings in atmospheric models going forward.
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A C.D.C. study estimates that, over five years, one in eight deaths of people ages 20 to 64 occurred because of alcohol-related injuries or illness.An estimated one in eight deaths of Americans ages 20 to 64 in the years 2015-19 was the result of injuries or illness caused by excessive alcohol use, according to a new study from the Centers for Disease Control and Prevention.The study, published on Tuesday in the journal JAMA Network Open, assessed the effects of alcohol on people of working age, who accounted for nearly two-thirds of the country’s annual average of 140,000 alcohol-related deaths.The rates of excessive alcohol use and related deaths have most likely climbed since the period the C.D.C. researchers analyzed. After the onset of the pandemic, a variety of data showed Americans drank more frequently, and deaths due to a narrower set of causes attributable to alcohol rose 25 percent in 2020 over the previous year.Although alcohol takes a progressively heavier toll on older age groups, its effects are more noticeable in younger people who are less likely to die of other causes. Among those ages 20 to 49, one in five deaths was attributable to drinking, and for those ages 20 to 34, it was one in four, the study found.“This is really affecting adults in the prime of their life,” said Marissa Esser, who leads the C.D.C.’s alcohol program and was a co-author of the study. She said the large share of people dying in their working years meant excess drinking had an outsize effect on economic productivity.The researchers analyzed data from the nation’s vital records and identified deaths due to excessive alcohol use over the five-year period. Some causes of death, such as alcoholic liver disease, could be wholly attributable to excess drinking. For other causes of death, like cancers related to drinking or injuries where intoxication was a known risk factor, the researchers estimated the share of fatalities due to excessive alcohol use based on surveyed drinking behavior and sales in various populations. The data are only updated every few years because the calculations rely on multiple sources of data.If anything, the study underestimated the true number of deaths, Dr. Esser said, because the researchers did not include every cause of death in which alcohol played at least some role.Dr. Gordon Smith, a professor of epidemiology at the West Virginia University School of Public Health who was not involved with the study, said that even after decades of studying alcohol, he was taken aback by the sheer magnitude of its toll. “I knew it was a big problem, but I think it was important to see just how much of a problem it is,” he said.He credited the study’s authors for their methods of measuring the influence of excess drinking on various causes of death. “They’ve come up with probably the best estimates to date of the amount that alcohol contributes to these other conditions,” he said.Alcohol is a leading cause of preventable death in the United States, but it is often overshadowed by tobacco or opiates. And its effects on Americans’ health has been growing. Nearly a decade ago, a similar study found one in 10 deaths of working-age people was due to drinking, although researchers have changed the methodology, so a perfect apples-to-apples comparison is not possible.Katherine Keyes, a professor of epidemiology at Columbia University who was not involved in the latest study, said it painted a stark picture of the problem. “Where the science needs to go,” she said, “is what do we do about it?”She took a hopeful view of variations in alcohol’s effects that the study found across the states. In Mississippi, alcohol accounted for 9.3 percent of working-age deaths, whereas in New Mexico, it accounted for 21.7 percent, including one in three deaths of people ages 20 to 34, which Dr. Keyes called “horrifying.”But she said those differences were also indicative of the profound role that the surrounding environment has in any individual’s drinking habits. That suggests the most affected communities may be able to learn from others where drinking is less perilous, she said.There is ample opportunity to improve access to treatment services, experts say. Millions of Americans struggle with alcohol use disorders, but their medical providers do not typically counsel them to reduce excessive use or offer them medications that can blunt cravings.Dr. Esser said policymakers should take steps to make their communities safer. “Evidence-based strategies are out there and underused,” she said. The C.D.C.’s Community Preventive Services Task Force recommends a number of measures, including raising alcohol taxes and regulating the number and concentration of businesses that sell alcohol.Last year, Congress permanently reduced federal alcohol tax rates, and state alcohol taxes have generally not kept up with inflation. But in some hard-hit states, advocates have begun pushing back. In Oregon, there was a campaign to raise alcohol taxes, and lawmakers in New Mexico recently held hearings about doing so.

In a small study, most adults seeking to lose weight overestimated the healthiness of their diet, according to preliminary research to be presented at the American Heart Association’s Scientific Sessions 2022. The meeting, held in person in Chicago and virtually, Nov. 5-7, 2022, is a premier global exchange of the latest scientific advancements, research and evidence-based clinical practice updates in cardiovascular science.
“We found that while people generally know that fruits and vegetables are healthy, there may be a disconnect between what researchers and health care professionals consider to be a healthy and balanced diet compared to what the public thinks is a healthy and balanced diet,” said study author Jessica Cheng, Ph.D., a postdoctoral research fellow in epidemiology at the Harvard T. H. Chan School of Public Health and in general internal medicine at Massachusetts General Hospital, both in Boston. This research was conducted while Dr. Cheng was a predoctoral fellow/Ph.D. candidate in the department of epidemiology at the University of Pittsburgh School of Public Health.
Nearly half of adults in the U.S. try to lose weight each year, according to the Centers for Disease Control and Prevention, with a majority attempting to eat more fruits, vegetables and salads. Healthy eating is essential for heart and general health, and longevity. Dietary guidance from the American Heart Association issued in 2021 advises adults to eat a variety of fruits and vegetables; opt for whole grains rather than refined grains; choose healthy protein sources; substitute nonfat and low-fat dairy products for full-fat versions; choose lean cuts of meat (for those who eat meat); use liquid plant oils instead of tropical oils and animal fats; choose minimally processed over ultra-processed foods; minimize foods and beverages with added sugar; choose foods with little or no added salt; and limit or avoid alcohol.
Researchers evaluated the diets of 116 adults aged 35-58 years old in the greater Pittsburgh, PA, area who were trying to lose weight. Study participants met one-on-one with a dietitian to discuss their nutrition and then tracked everything they ate and drank every day for one year on the Fitbit app. They also weighed themselves daily and wore a Fitbit device to track their physical activity.
Researchers calculated a Healthy Eating Index (HEI) score at the beginning and end of the study based on the types of foods that participants reported eating. Participants were asked to complete a 24-hour food recall for two days at each time point. The HEI is a measure for assessing how closely a dietary pattern aligns with the U.S. government’s Dietary Guidelines for Americans. A score of 0 to 100 is possible, with a higher score indicating a healthier diet. The score is based on the frequency of eating various dietary components such fruits, vegetables, whole and refined grains, meat and seafood, sodium, fats and sugars.
Participants self-scored their beginning and ending diet quality to determine their perceived scores. Their scores were also on a 0-100 scale based on the components of the HEI. The self-assessment of their beginning diet was a “look back” as they scored both their starting and ending diets at the end of the study. The difference in their starting and ending score was their perceived diet change. A difference of 6 points or less between the researchers’ HEI score and the participant’s perceived score was considered “good agreement.”
At the end of the study, about 1 in 4 participants’ scores had good agreement between their perceived diet score and the researcher-assessed score. The remaining 3 out of 4 participants’ scores had poor agreement, and most reported a perceived score that was higher than the HEI score assigned by researchers. The average perceived score was 67.6, and the average HEI score was 56.4.

Common gut bacteria can enhance the effects of cocaine in mice, researchers report November 1 in the journal Cell Host & Microbe. Their study demonstrates how cocaine use supports the growth of the bacteria, which in turn eat up a chemical, glycine, that contributes to normal brain function. As levels of glycine become depleted, mice exhibit a higher response to the drug with behavior abnormalities, such as significantly increasing drug-induced locomotion and seeking behaviors.
Additionally, by supplementing glycine back systemically or using a genetically modified bacteria that cannot use glycine, the response of the mice to cocaine falls back to normal levels, demonstrating that this amino acid can act as an addiction-like behavior mediator in animal models.
“I was interested in the gut-brain axis, and I found it very new and exciting,” says first author Santiago Cuesta, a neuroscientist at the University of Wisconsin School of Medicine and Public Health.
Cuesta and colleagues found that when cocaine enters the gut of the mice, it triggers the activation of the QseC protein that aids in the growth of γ-proteobacteria, such as E. coli. These bacteria, fueled by glycine, outcompete the normal gut bacteria that already exist in our digestive tracks, taking up most of the space and resources.
“The gut bacteria are consuming all of the glycine and the levels are decreasing systemically and in the brain,” says senior author Vanessa Sperandio, a microbiologist from the University of Wisconsin School of Medicine and Public Health. “It seems changing glycine overall is impacting the glutamatergic synapses that make the animals more prone to develop addiction.”
“Usually, for neuroscience behaviors, people are not thinking about controlling the microbiota, and microbiota studies usually don’t measure behaviors, but here we show they’re connected” says Cuesta. “Our microbiome can actually modulate psychiatric or brain-related behaviors.”
“I think the bridging of these communities is what’s going to move the field forward, advancing beyond correlations towards causations for the different types of psychiatric disorders,” says Sperandio.
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The urge to vomit after eating contaminated food is the body’s natural defensive response to get rid of bacterial toxins. However, the process of how our brain initiates this biological reaction upon detecting the germs remains elusive. For the first time, researchers mapped out the detailed neural pathway of the defensive responses from the gut to the brain in mice. The study, presented November 1 in the journal Cell, could help scientists develop better anti-nausea medications for cancer patients who undergo chemotherapy.
Many foodborne bacteria produce toxins in the host after being ingested. The brain, after sensing their presence, will initiate a series of biological responses, including vomit and nausea, to get rid of the substances and develop an aversion toward foods that taste or look the same.
“But details on how the signals are transmitted from the gut to the brain were unclear, because scientists couldn’t study the process on mice,” says Peng Cao, the paper’s corresponding author at the National Institute of Biological Sciences in Beijing. Rodents cannot vomit, likely because of their long esophagus and weaker muscle strength compared to their body size. As a result, scientists have been studying vomit in other animals like dogs and cats, but these animals are not comprehensively studied and thus failed to reveal the mechanism of nausea and vomiting.
Cao and his team noticed that while mice don’t vomit, they retch — meaning they also experience the urge to vomit without throwing up. The team found that after receiving Staphylococcal enterotoxin A (SEA), which is a common bacterial toxin produced by Staphylococcus aureus that also leads to foodborne illnesses in humans, mice developed episodes of unusual mouth opening. Mice that received SEA opened their mouths at angles wider than those observed in the control group, where mice received saline water. Moreover, during these episodes, the diaphragm and abdominal muscles of the SEA-treated mice contract simultaneously, a pattern seen in dogs when they are vomiting. During normal breathing, animals’ diaphragm and abdominal muscles contract alternatively.
“The neural mechanism of retching is similar to that of vomiting. In this experiment, we successfully build a paradigm for studying toxin-induced retching in mice, with which we can look into the defensive responses from the brain to toxins at the molecular and cellular levels,” Cao says.
In mice treated with SEA, the team found the toxin in the intestine activates the release of serotonin, a type of neurotransmitter, by the enterochromaffin cells on the lining of the intestinal lumen. The released serotonin binds to the receptors on the vagal sensory neurons located in the intestine, which transmits the signals along the vagus nerves from the gut to a specific type of neurons in the dorsal vagal complex — Tac1+DVC neurons — in the brainstem. When Cao and his team inactivated the Tac1+DVC neurons, SEA-treated mice retched less compared with mice with normal Tac1+DVC neuron activities.
In addition, the team investigated whether chemotherapy drugs, which also induce defensive responses like nausea and vomiting in recipients, activate the same neural pathway. They injected mice with doxorubicin, a common chemotherapy drug. The drug made mice retch, but when the team inactivated their Tac1+ DVC neurons or serotonin synthesis of their enterochromaffin cells, the animals’ retching behaviors were significantly reduced.
Cao says some of the current anti-nausea medications for chemotherapy recipients, such as Granisetron, work by blocking the serotonin receptors. The study helps explain why the drug works.
“With this study, we can now better understand the molecular and cellular mechanisms of nausea and vomiting, which will help us develop better medications,” Cao says.
Next, Cao and his colleagues want to explore how toxins act on enterochromaffin cells. Preliminary research shows that enterochromaffin cells don’t sense the presence of toxins directly. The process likely involves complex immune responses of damaged cells in the intestine.
“In addition to foodborne germs, humans encounter a lot of pathogens, and our body is equipped with similar mechanisms to expel these toxic substances. For example, coughing is our body’s attempt to remove the coronavirus. It’s a new and exciting field of research about how the brain senses the existence of pathogens and initiates responses to get rid of them.” Cao says, adding that future research may reveal new and better targets for drugs, including anti-nausea medicines.
This work was supported by the National Key R&D Program of China and the National Natural Science Foundation of China.
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Many medical devices for treating heart failure generate nonphysiological shear flow. This can trigger the destruction of red blood cells after implantation of ventricular assist devices (VADs), artificial heart valves, vascular stents, or interventional thrombectomy devices.
The destruction of red blood cells, or mechanical hemolysis, is an inevitable complication of interventional devices, so scientists want to gain a better understanding of the phenomenon.
In Physics of Fluids, from AIP Publishing, researchers from Tsinghua University developed a red blood cell destruction model based on simulations of dissipative particle dynamics within a high shear flow. They used the results to make recommendations for improvements of VADs.
“After interventional medical devices are implanted inside the human body, the nearby flow field generates a shear flow with a very high shear rate,” said co-author Xiwen Zhang. “The velocity change rate of the fluid will deform the red blood cell membrane. Eventually, deformation of the membrane exceeds the ultimate strain, and the membrane is disrupted by shear flow.”
The team discovered that acceleration during shearing is a major factor in red blood cell destruction, beyond exposure time and shear stress. They recommend adding a flow buffer structure to the structural design of VADs to reduce part of the hemolysis caused by shear acceleration.
For hemolysis-related research, many researchers focus on macroscale experiments to obtain a series of empirical fitting formulas.
“But our team is exploring the shear destruction process of red blood cells in more detail at the red blood cell scale by using dissipative particle dynamics,” said Zhang.
“We hope our study can serve as a bridge between macroscopic hemolysis experiments and microscopic red blood cell simulations (molecular dynamics simulations),” said Zhang. “In future work, we will continue constructing shear failure models of multiple red blood cells and perform shear failure simulations based on whole blood to be able to compare them with macroscopic hemolysis experiments.”
The researchers are currently developing a new index to predict the hemolysis of VADs more accurately and help optimize the shape of VADs, which should improve hydraulic performance and reduce hemolysis.
They plan to better represent the diffusion process of hemoglobin after shear damage by adding a transport dissipation particle dynamics model based on this work.
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