Publisher Health

A UAB research team has managed to track the behaviour of microplastics during their “journey” through the intestinal tract of a living organism and illustrate what happens along the way. The study, carried out on Drosophila melanogaster using electron microscopy equipment developed by the researchers themselves, represents a significant step towards a more precise analysis of the health risks of being exposed to these pollutants.
The behaviour of micro and nanoplastics (MNPLs) inside the organism is a question impossible to answer at present in humans, and in vitro models are not useful. Hence, there is a need to look for models that allow us to answer this question. Furthermore, there are limitations in the current methodologies for detecting and quantifying their presence in different human biological samples, which prevents an accurate assessment of the health risk of exposure.
In this context, researchers from the Mutagenesis Research Group of the Universitat Autònoma de Barcelona (UAB) have managed to monitor the tracking of MNPLs in their “journey” from the environment to the interior of a living organism. They have done it by developing tools based on electron microscopy and in larvae of the Drosophila melanogaster fly, a model organism widely used to study biological phenomena and processes.
The research team has studied the behaviour of MNPLs along their pathway with commercial polystyrene of nanometric sizes. The “photographic report” obtained has allowed them to see the interaction of MNPLs with the microbiota and cells of the membrane that recovers the inside of the intestines, their ability to cross the intestinal barrier and their presence in haemolymph, which is equivalent to blood in humans, and in blood cells, which correspond to our lymphocytes.
“In addition to establishing a new methodological approach, our study confirms the great advantages of Drosophila melanogaster as a model to determine the potential harmful effects associated with the ingestion of these pollutants,” explains Ricard Marcos, researcher at the Department of Genetics and Microbiology of the UAB and coordinator of the study.
Effects at the nanometric level
The evaluation of the biological effects at different stages of the larvae’s life showed that, although no significant toxicity was observed, the exposure produced a broad molecular response, altering the expression of genes involved in the general response to stress, oxidative damage and genotoxicity, as well as in genes related to the response to physical damage on the intestinal barrier.
“Our work adds information on what happens, in terms of effects, when the exposure is to nanoplastics, which, due to their small size, are of particular relevance to us, because of their greater capacity to break down biological barriers and produce toxicological effects that can affect the health of organisms, including humans,” says Alba Hernández Bonilla, a researcher at the UAB and co-author of the study.
So far, most of the effects of MNPLs have been carried out in micro- and even millimetric ranges, and in aquatic models, mainly marine. In vivo studies using nanoplastics are almost non-existent. It is in this context that the relevance of the study, which has used methodologies that have never before been used for these purposes, is clear, researchers point out.
The study has been published recently in the journal Environmental Sciences: Nano and is part of the European project PLASTICHEAL, coordinated by the UAB, which aims to provide regulators with new methodologies and solid scientific evidence to establish the knowledge base for an adequate risk assessment of MNPLs.

Men all over the world are suffering from deteriorating semen quality — often referred to as an outright fertility crisis.
Now, however, there may be good news for some of the men who are experiencing problems.
In a new clinical study, researchers from the University of Copenhagen and Hvidovre Hospital show that men with obesity improve their semen quality if they lose weight — and maintain the weight loss.
“It was surprising to us that such a big improvement can be shown in the semen quality in connection with a weight loss. And as 18 percent of Danes have obesity, this new knowledge may actually make a difference,” says Professor Signe Torekov who headed the study together with Professor Romain Barres at the Novo Nordisk Foundation Center for Basic Metabolic Research.
The new findings may be good news for the fertility, as a link between higher sperm count and faster achievement of pregnancy has previously been shown.
The study has been published in the recognised journal Human Reproduction which enjoys one of the highest rankings in the field of fertility. A total of 56 men with obesity participated, aged 18-65 years and with a body mass index between 32 and 43.

LMU scientists have shown that small aggregates function as temporary RNA repositories, which are regulated by neural activity.
Cells constantly have to adapt the level of activity of certain genes to specific requirements. This applies particularly to neurons, where synapses have to be repeatedly re-formed, re-wired, and restructured. For these processes — without which learning and remembering, for example, would not be possible — messenger molecules (mRNAs) deliver protein blueprints to the right place at the right time.
In regulating these complex processes, so-called RNA granules — small aggregates of various RNA binding proteins and mRNA — play an important role. In a paper just published in the journal Nature Communications, a team led by LMU cell biologist Prof. Michael Kiebler details how certain RNA granules change depending on neural activity.
The researchers investigated granules containing the RNA binding protein DDX6. It was already known that this protein is an essential component of the granules and that it can regulate translation — that is to say, the conversion of genetic information into proteins. “We used DDX as a marker to investigate the regulation of these granules under physiological conditions in neurons,” says Karl Bauer, lead author of the study.
The researchers were able to demonstrate both in cell cultures and in an animal model that the size of these granules diminishes while the neuron matures, but that their number increases. “This suggests that the granules dissolve and that their components are redistributed in the cell,” says Bauer. “In an independent study (back to back in the same issue), our cooperation partner in Nice, led by Prof. Florence Besse, managed to demonstrate that these RNA granules take on important roles in the further life of an organism, all the way through to physiological aging.”
DDX6-RNA granules function as temporary “RNA repositories”
As neurons mature, their synaptic activity increases exponentially. This being so, the researchers suspected that there was a correlation between neural activity and the size of the RNA granules. Further experiments confirmed this hypothesis: When the cells were stimulated, the granules shrank; and when synaptic activity was curbed, they got bigger again.
In addition, the scientists discovered that a further RNA binding protein — Staufen2 — also plays a role in the formation of the granules: Without Staufen2, which is involved in mRNA transport in the cell among other functions, the granules did not grow again even when synaptic activity was suppressed. Furthermore, the supply of RNA to the granules was also necessary for growth to take place even when activity was curbed.
Taking all this evidence together, the scientists conclude from their results that DDX6-RNA granules function as temporary “RNA repositories” and are involved in the regulation of neural activity: Specific mRNAs might be brought to the granules by Staufen2 and kept there in an inactive state until they are released when needed.
The authors expect that mRNAs are also regulated in other cell types by the formation of granules. As such, the results obtained here will make a long-term contribution to a first mechanistic understanding of how cells respond to external and internal influences by temporally and spatially regulating mRNAs and their translations.
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Sometimes, even the alteration of a single nucleotide in a gene can cause serious disease. In a young boy with epilepsy, this kind of mutation has not just affected the functioning of the protein in question — it could also curb the functioning of several closely related proteins. This has been shown in a study, published in the journal PNAS, by researchers in Sweden and the USA. The study sheds light on the molecular biology behind some forms of genetic epilepsy.
In this study, the researchers have found a previously unknown mutation in a child with epilepsy. He has a very subtle change — a single nucleotide that is different — in the gene KCNA2,which produces an ion channel protein. Ion channels are proteins which form pores in the cell surface membrane. When the channels open, they allow the flow of specific electrically charged ions into or out of the cell. This triggers or terminates electrical impulses in cells, such as nerve or muscle cells. Thus, ion channels are important for, among other things, brain function.
Ordinarily, there is a balance in the brain between signals that increase cell activity and ones which suppress it. In epilepsy, the balance is disturbed, and the nerve cells send signals in an uncontrolled manner. The ion channel which has mutated in the patient normally has a dampening effect on nerve signalling.
“What is interesting with this ion channel is that both mutations that increase function and those that decrease function have been connected to epilepsy. It seems that you need just the right amount of activity, otherwise the risk to develop seizures increases,” says Antonios Pantazis, associate professor at the Department of Biomedical and Clinical Sciences, and the Wallenberg Center for Molecular Medicine at Linköping University.
Using diverse experimental methods, the research team found that cells could produce the mutant channel proteins, but they could not transport them to their surface membrane. As mutant channels stayed trapped inside the cell, there was no measurable ion channel activity.
There are two copies of most of our genes. The patient had one mutated copy and one normal one, so one would expect that he had 50% of functional ion channels. But when the scientists reproduced this condition in the lab, it turned out that the channel activity was as low as 20 percent, compared to normal. The mutation apparently decreased the function of the normal proteins, too: a “dominant negative” mutation. To understand how this happened, we need to consider that this ion channel comprises four interconnected proteins. The researchers showed that proteins from the mutant gene can connect with proteins made by the normal copy, and also keep them trapped inside the cell.
And here comes the crux of the story: there are, in fact, several ion-channel genes related to KCNA2. Proteins made from these different genes often mix together to form ion channels. When the scientists mixed proteins from mutant KCNA2 with those of related gene KCNA4, they found that KCNA4 proteins were also prevented from transporting to the cell surface.
Pantazis explains that when different channel proteins combine with each other to create mixed ion channels, this contributes to the great diversity and complexity of nerve cell signalling. This diversity is important for the processes that we associate with the functioning of the brain, such as thoughts, consciousness and the ability to imagine. Yet this ability of channel proteins to combine also confers a disadvantage, as the brain becomes vulnerable to single, dominant-negative mutations, which can perturb the function of several ion channels, and cause neurological disease, as in this story.
“Studying the effects of mutations on ion channels can give us vital clues about the mechanisms of disease and potential therapeutic strategies,” says Michelle Nilsson, a PhD student in Pantazis’ research group, and principal author on the study.
“Since these mutations can have unexpected effects on ion-channel function, studying them can also lead to new discoveries about how our bodies work at the molecular level,” Antonios Pantazis says.
The study has been funded by the Knut and Alice Wallenberg Foundation through the Wallenberg Center for Molecular Medicine (WCMM) at Linköping University, and the Swedish Research Council.
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Materials provided by Linköping University. Original written by Karin Söderlund Leifler. Note: Content may be edited for style and length.

The drug gabapentin, currently prescribed to control seizures and reduce nerve pain, may enhance recovery of movement after a stroke by helping neurons on the undamaged side of the brain take up the signaling work of lost cells, new research in mice suggests.
The experiments mimicked ischemic stroke in humans, which occurs when a clot blocks blood flow and neurons die in the affected brain region.
Results showed that daily gabapentin treatment for six weeks after a stroke restored fine motor functions in the animals’ upper extremities. Functional recovery also continued after treatment was stopped, the researchers found.
The Ohio State University team previously found that gabapentin blocks the activity of a protein that, when expressed at elevated levels after an injury to the brain or spinal cord, hinders re-growth of axons, the long, slender extensions of nerve cell bodies that transmit messages.
“When this protein is high, it interferes with neurological recovery,” said lead author Andrea Tedeschi, assistant professor of neuroscience in Ohio State’s College of Medicine.
“Imagine this protein is the brake pedal and recovery is the gas pedal. You can push on the gas pedal but can’t accelerate as long as you’re also pushing on the brake pedal,” Tedeschi said. “If you start lifting the brake pedal and continuously press on the gas, you can really speed up recovery. We think that is gabapentin’s effect on neurons, and there is a contribution of non-neuronal cells that tap into this process and make it even more effective.”
The study is published today (May 23, 2022) in the journal Brain.

A lifestyle intervention program of increased physical activity, healthy eating and aiming for weight loss of 7% or more, or taking the medication metformin were effective long-term to delay or prevent Type 2 diabetes in adults with prediabetes. Neither approach, however, reduced the risk of cardiovascular disease for study participants over 21 years of the study, according to the findings of the multicenter Diabetes Prevention Program Outcomes Study (DPPOS), published today in the American Heart Association’s flagship, peer-reviewed journal Circulation.
Type 2 diabetes (T2D) is the most common form of diabetes, affecting more than 34 million people in the U.S., representing nearly 11% of the U.S. population, according to the U.S. Centers for Disease Control and Prevention’s 2020 National Diabetes Statistics Report, and cardiovascular disease (CVD) is the leading cause of death and disability among people with T2D. Type 2 diabetes occurs when the body is unable to efficiently use the insulin it makes and the pancreas is unable to produce sufficient amounts of insulin. Adults with T2D are twice as likely to die from CVD — including heart attack, stroke or heart failure — compared to adults who do not have T2D. People with T2D often have other cardiovascular disease risk factors, including being overweight or having obesity, high blood pressure or high cholesterol.
The DPPOS evaluated 21-years of follow-up (through 2019) for the 3,234 adults who participated in the original, 3-year Diabetes Prevention Program (DPP) trial. This analysis of the DPPOS was focused on determining whether the medication metformin or lifestyle intervention might reduce the risk of cardiovascular disease or the rate of major cardiac events such as heart attack, stroke or death due to cardiovascular disease.
“The risk of cardiovascular disease in people with prediabetes is increased, and CVD risk further increases over time after Type 2 diabetes develops and progresses,” said Ronald B. Goldberg, M.D., chair of the writing group for the DPPOS and a professor of medicine, biochemistry and molecular biology in the division of diabetes, endocrinology and metabolism, and senior faculty member and co-director of the Diabetes Research Institute Clinical Laboratory at the University of Miami’s Miller School of Medicine in Miami, Florida. “We were focused on assessing the impact of lifestyle or metformin interventions for prevention of Type 2 diabetes in people with prediabetes to reduce cardiovascular disease.”
The DPP was a landmark, 27-center randomized trial across the U.S. from 1996-2001 to assess how to prevent or delay the onset of T2D in people with prediabetes. Study participants were screened and accepted in the DPP based upon these criteria: initially, a 2-hour glucose reading of 140-199 mg/dL on an oral glucose tolerance test; fasting glucose levels of 95-125 mg/dL; and body mass index of 24 kg/m2 or higher.
A racially diverse group of 3,234 adults were studied in the original DPP for almost three years. The participants were an average age of 51 years, and nearly 70% of the participants were women. People in the intensive lifestyle intervention group (nutritional improvement and physical activity aimed at achieving a weight loss of 7%) reduced the incidence of developing T2D by 58%, and participants who took twice daily doses of metformin had a reduced incidence of 31% for T2D, when compared to people in the placebo group who received standard care, which included information about effective treatment and management of T2D at the time of diagnosis.

American Heart Association. “Statement updates ambulatory blood pressure classification in children and adolescents.” ScienceDaily. ScienceDaily, 23 May 2022. .
American Heart Association. (2022, May 23). Statement updates ambulatory blood pressure classification in children and adolescents. ScienceDaily. Retrieved May 23, 2022 from www.sciencedaily.com/releases/2022/05/220523093350.htm
American Heart Association. “Statement updates ambulatory blood pressure classification in children and adolescents.” ScienceDaily. www.sciencedaily.com/releases/2022/05/220523093350.htm (accessed May 23, 2022).

Researchers at the Centre for Genomic Regulation (CRG) in Barcelona have identified a potential new diagnostic marker that predicts the successful and efficient development of mammalian egg cells. The findings could pave the way for generating artificial oocytes in the laboratory, helping researchers study the causes and treatments of infertility disorders and test the impact of drugs and chemicals on women’s reproduction. The research is published in The EMBO Journal.
Humans have 23 pairs of chromosomes. Between males and females, 22 pairs are shared, with the 23rd pair being the sex chromosomes. Males usually have an X and a Y chromosome, while females have two X’s. This presents a potential problem for the female cellular machinery, as two active X chromosomes generates an overdose of gene products, which is fatal for developing embryos or leads to cancer in adult life. To avoid this scenario, female cells inactivate one X chromosome by turning off its genes and compacting it.
Little is known about how X-chromosome inactivation affects the development of reproductive cells. In mammals, oocytes develop from germ cells, precursor cells that migrate from early embryonic tissue to the developing gonads. Germ cells then undergo meiosis, an important chromosomal rearrangement process, which is responsible for the genetic uniqueness of each individual germ cell. Germ cells mature and eventually turn into functional sperm or oocytes.
To address this question, researchers at the Centre for Genomic Regulation (CRG) built an X-chromosome reporter system (XRep), a tool which allowed them to study how the chromosome shapeshifts over time during germ cell development in vitro.
Using female mouse cells, the method revealed a carefully orchestrated act of X-chromosome ‘yoyo’. If one X chromosome briefly inactivated and then reactivated, it resulted in germ cells being four times more efficient for entering meiosis and transforming into egg cells compared to germ cells that have never turned their X chromosome ‘off and on’ again. In comparison, germ cells that failed to inactivate the X chromosome in the first place or reactivated it too rapidly showed abnormal gene expression and cell differentiation patterns.
The study also found that cells with two active X chromosomes divided faster and easily reverted into a state of pluripotency. According to the authors, these characteristics are similar to human germ cell tumors, which come form germ cells that got lost during their migration to the gonads or failed to differentiate properly once inside the testicles and ovaries. The researchers deduced that a correct X-chromosome inactivation and reactivation sequence is an indicator of normal germ cell differentiation. The research team notes that further studies will be needed to confirm whether an abnormal X-chromosome state is a diagnostic indicator, or whether it could be a causal factor responsible for the cell abnormality.
“Our findings have important implications for reproductive research because XRep allows us to assess cellular X-chromosome status in real time, helping identify and isolate germ cells with a high success rate of turning into oocytes,” says Dr. Bernhard Payer, Group Leader at the CRG and senior author of the study.
“Human oocytes have never been generated completely in vitro. Monitoring the X-chromosome state during in vitro germ cell differentiation might therefore be a way to optimize the protocol to produce high quality human eggs in the lab. Human eggs for research are scarce and difficult to obtain because they are currently only available from egg donors and mostly used for reproductive purposes. In vitro-generated human eggs could therefore provide an unlimited resource to study the causes and treatments of infertility disorders and as well to test the safety of drugs and chemicals for women’s reproduction,” concludes Dr. Payer.
Dr. Moritz Bauer, co-first author of the study, adds: “Our results also highlight how we need specific tools to study female cells. The vast majority of studies are performed using male cells, leading to a gender-gap in scientific knowledge. We therefore need to stop looking at female development through the lens of male cells, which will contribute to our understanding of sex-specific disease progressions.”
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A shipment that arrived on Sunday was the first of two intended to address shortages in the United States. Another shipment is set to arrive this week, the White House said.A shipment of infant formula intended to fill a nationwide shortage arrived in the United States from Europe on Sunday, and a second flight was expected to bring additional supplies in the coming days, the Biden administration said.The shipment, equivalent to about 500,000 eight-ounce bottles, contained a hypoallergenic formula for children with cow’s milk protein allergy, the White House said in a statement. It provides enough formula to take care of 9,000 babies and 18,000 toddlers for a week, Tom Vilsack, the agriculture secretary, said in televised remarks at the airport in Indianapolis, where the shipment arrived on a military plane from Ramstein Air Base in Germany.“This shipment of formula serves a critical medical purpose and will help infants with specific dietary needs requiring specialized formula,” Mr. Vilsack said on Twitter.A second shipment, which is expected to arrive this week, would bring the supply of formula up to the equivalent of 1.5 million eight-ounce bottles of three formulas, which would later be distributed from a Nestlé facility in Pennsylvania.U.S. troops moved pallets of baby formula at Ramstein Air Base in Germany on Saturday.Thomas Lohnes/Getty ImagesThe transports are part of a series of measures taken by the Biden administration to address the shortage of infant and toddler formula that had threatened to become a political and public health disaster, as frustrated families searched depleted supermarket shelves.President Biden invoked the Defense Production Act last week to increase production and authorized the use of Defense Department planes for “Operation Fly Formula” to respond to the crisis.In February, Abbott Nutrition, which controls 48 percent of the formula market in the United States, voluntarily recalled some of its most popular brands — Similac, Alimentum and EleCare — after four babies were hospitalized with bacterial infections. At least two babies died, although the company said this month that there was no evidence its formula caused any known infant illnesses.Abbott also shut down its plant in Sturgis, Mich., and the Food and Drug Administration warned consumers not to use the recalled brands that were produced there.Shelves normally meant for baby formula sat nearly empty on Sunday at a store in downtown Washington, D.C.Samuel Corum/Agence France-Presse — Getty ImagesThe effects of the closure of the Sturgis plant have been widespread, with stores limiting purchases of formula and parents desperately seeking supplies or trying to make formula at home, which pediatricians discourage. The shortage has also been exacerbated by supply-chain woes and labor shortages associated with the pandemic.The statement from the White House said the pallets of formula that arrived on Sunday were “prioritized because they serve a critical medical purpose” and were in short supply because of the plant closure in Sturgis.In another step to address the acute shortages, the F.D.A. announced last week that it would relax some of its regulations to encourage new suppliers to provide formula. The United States normally produces about 98 percent of the formula it consumes, with imports coming primarily from Mexico, Ireland and the Netherlands.

Pfizer and BioNTech said on Monday that preliminary findings of a clinical trial of children younger than five showed three doses of their coronavirus vaccine produced a strong enough immune response to meet the criteria for regulatory authorization.In a news release, the companies announced results from a subset of a trial of 1,678 children ages 6 months through 4 years, saying the three-dose regimen had been 80 percent effective in preventing symptomatic infection. No supporting data was disclosed, and the companies did not say how many children were in the subset. A spokeswoman for Pfizer said comprehensive results from the trial will be disclosed next month.Both Pfizer and Moderna are hoping to soon win authorization to vaccinate the nation’s youngest children. About 18 million children under the age of 5 are the only Americans not yet eligible for vaccination against the coronavirus, and parents’ expectations for when shots will be offered have been repeatedly dashed.Pfizer and its partner BioNTech said the number of children in the trial who fell ill with Covid was too small to make a definitive statement on efficacy. Only 10 children participating in the trial became ill with Covid after those in the vaccination group were given the third dose. The clinical trial’s protocol specified that analysis of vaccine efficacy required at least 21 Covid cases. The companies said that final data on efficacy, a secondary endpoint for the clinical trial, would be shared “once available.”The Biden administration had hoped to offer vaccine doses to those under 5 as early as February. The Food and Drug Administration initially pressed Pfizer to submit data on how well two doses worked for young children, but pulled back after Pfizer said two doses were not sufficiently effective in preventing symptomatic infection from the highly contagious Omicron variant.But Pfizer said that the new results showed that three doses, with the third given at least two months after the second, stimulated the immune system to strongly protect against the virus, with no safety concerns. Researchers said the immune response of the subset of trial participants, measured one month after the third dose, compared favorably to that of people 16 to 25 who received two doses.“We are pleased that our formulation for the youngest children, which we carefully selected to be one-tenth of the dose strength for adults, was well tolerated and produced a strong immune response,” Dr. Albert Bourla, Pfizer’s chief executive, said in a statement. Dr. Ugur Sahin, chief executive of BioNTech, said the companies would complete their F.D.A. application for emergency authorization of the pediatric vaccine this week.The new findings heat up a competition between Moderna and Pfizer over which company will produce the best vaccine for the youngest Americans. Moderna is proposing a two-dose regimen for children younger than 6, using a quarter the strength of its adult dose. The company has said it anticipates that a third dose will be necessary as a booster shot, but it has not yet submitted any data on that to the government.The question of which vaccine works better will be put to a committee of outside advisers to the F.D.A., likely in mid-June. With both Pfizer and Moderna proposing different dosing regimens for the youngest children and presenting different clinical trial results, the committee could sway regulators on which vaccine should be authorized, or whether both deserve clearance.In late April, Moderna sought emergency authorization of its pediatric vaccine after interim results showed that clinical trial participants had a similar immune response to young adults when given a dose one-fourth as strong.Like Pfizer, the firm said its results met the clinical trial criteria for success. Moderna has said its vaccine appeared to be 51 percent effective against symptomatic infection among children younger than 2, and 37 percent effective among those 2 to 5.If Pfizer’s results are borne out by subsequent data, its efficacy would be better than Moderna’s. Both companies say their vaccines produce similar side effects to other pediatric vaccines that have been used for decades.