Culture

A novel system of chilled panels that can replace air conditioning can also help reduce the risk of indoor disease transmission, suggests new analysis from the University of British Columbia, University of Pennsylvania and Princeton University.

The researchers computed air conditioning requirements in 60 of the world's most populous cities--with the additional ventilation required due to COVID-19. Then, they compared the energy costs with their cooling method, using the chilled panels and natural ventilation.

The results, published in the COVID-19 edition of Applied Energy, showed that the alternative solution can save up to 45 per cent of the required energy, while ensuring building occupants are comfortable and rooms are adequately refreshed.

Dr. Adam Rysanek, a professor in the school of architecture and landscape architecture at UBC and co-author of the paper, notes that many public health guidelines, as well as building industry bodies, recommend increasing the flow of fresh, outdoor air into buildings in order to reduce the risk of spreading COVID-19 and other diseases.

"However, if we continue to rely on conventional HVAC systems to increase indoor fresh air rates, we may actually double energy consumption. That's the nature of conventional HVAC."

"Alternatively, we can encourage people to install new types of radiant cooling systems, which allow them to keep their windows open even when it's hot outside. These alternative systems can provide a sufficient level of thermal comfort, increase protection against disease while lessening the impact on the environment," noted Rysanek, director of the Building Decisions Research Group at UBC's faculty of applied science.

Rysanek and his colleagues earlier demonstrated their cooling system in the hot and humid climate of Singapore. They built a public pavilion featuring a system of chilled tubes enclosed within a condensation-preventing membrane. This allowed occupants to feel comfortable, and even cold, without changing the air temperature surrounding the human body.

"You can think of it as lean A/C--or, even better, as a green alternative to energy-guzzling air conditioning," said Rysanek.

Toronto is one of the cities included in the latest analysis, as are Beijing, Miami, Mumbai, New York and Paris. In all these regions, peak summer temperatures can soar past 35 degrees Celsius (95 degrees Fahrenheit).

"A key impact of climate change is the accelerating rise in average and peak temperatures, particularly in urban areas. We are expecting the appetite for indoor cooling will ramp up in the years ahead. Yet, if we want to mitigate urban heat and ensure people are healthy and comfortable while reducing our energy use, we need to seriously consider revolutionising our historical approach to air-conditioning," adds Rysanek.

Rysanek notes that, though chilled panel systems have been around for decades, adding the special membrane devised by the research team could be the key to making it a commercially viable alternative to traditional HVAC systems in all climates.

Interview languages: English

Musty, moldy, smoky or horse dung-like smelling cocoa is not suitable for chocolate production. As part of a larger research project, a team of scientists led by Martin Steinhaus from the Leibniz Institute for Food Systems Biology at the Technical University of Munich has identified the odorants responsible for such off-flavors. The food industry can now use these results to objectively assess the sensory quality of fermented cocoa based on odorant concentrations. The research team published the data in the Journal of Agricultural and Food Chemistry.

Who likes chocolate that smells like smoke or mold, or chocolate whose aroma is reminiscent of a horse stable or of mothballs? Off-flavors are a major problem, especially for small and medium-sized enterprises. However, also for larger companies, off-flavor-tainted cocoa batches can cause immense economic damage, posing the need for their reliable identification during the incoming goods inspection. Until now, this has only been possible with some limitations by using a trained sensory panel, since no approach to objectively evaluate off-flavors in cocoa on the basis of the concentrations of the causative odorants was available.

As part of a project of the Research Association of the German Food Industry, the team led by food chemist Martin Steinhaus has now made a significant contribution to solving this problem. Using the molecular sensory science concept established at the Leibniz Institute, the research group has identified the key odorants that chiefly contribute to typical off-flavors in fermented cocoa.

Off-flavors from hammy-smoky to moldy-musty

In cocoa samples with hammy-smoky off-flavors, the team identified six crucial odorants. The substances smelled smoky, hammy, phenolic or horse stable-like. In samples with a moldy-musty odor, the researchers found additional four off-flavor compounds. These smelled moldy, musty, beetroot-like, fecal- or mothball-like. The research team determined the odor threshold values of the identified substances in order to derive maximum concentration limits.

In its latest publication, for example, the team recommends a maximum tolerable concentration for the off-flavor substance geosmin of 1.6 micrograms per kilogram of fermented cocoa. Even in the lowest concentrations, this odorant has a musty, earthy smell reminiscent of beetroot. Geosmin is presumably of bacterial origin. For fecal, mothball-like smelling 3-methyl-1H-indole, the researchers recommend a limit of 1.1 micrograms per kilogram of fermented cocoa.

Odorant distribution is also important

The research team's findings also show that about 40 to 65 percent of total geosmin is found in the seed coat (testa) of fermented cocoa beans. In contrast, the off-flavor substance 3-methyl-1H-indole was predominantly found inside the beans. "The uneven distribution of the two odorants between the seed coat and the embryo is another important aspect that chocolate manufacturers should consider when testing fermented cocoa," says Martin Steinhaus. "At the moment, we do not know how much geosmin is transferred from the shells into the embryo during the roasting process. Therefore, it might be reasonable to remove the seed coats before roasting rather than after roasting."

The largest study of its type in the UK has identified differences in the immune response to COVID-19, between people with no symptoms, compared to those suffering a more serious reaction to the virus.

Researchers from the Wellcome Sanger Institute, Newcastle University, University College London, University of Cambridge, EMBL's European Bioinformatics Institute (EMBL-EBI) and their collaborators within the Human Cell Atlas initiative, found raised levels of specific immune cells in asymptomatic people. They also showed people with more serious symptoms had lost these protective cell types, but gained inflammatory cells. These differences in the immune response could help explain serious lung inflammation and blood clotting symptoms, and could be used to identify potential targets for developing therapies.

The research, published today (20th April 2021) in Nature Medicine, is one of the only studies to include people who were asymptomatic. This large-scale collaborative study is part of the Human Cell Atlas* initiative to map every cell type in the human body, to transform our understanding of health, infection and disease.

So far, the COVID-19 global pandemic has caused millions of deaths and many more infections worldwide. Symptoms vary widely in severity and can range from a mild cough to severe respiratory distress, blood clots and organ failure. Several previous studies have highlighted a complex immune response in the blood, but until now the full coordinated immune response and how this differs between symptomatic and asymptotic patients had not been investigated in detail.

In a new study to understand how different immune cells responded to the infection, a large team of researchers came together to analyse blood from 130 people with COVID-19. These patients came from three different UK centres (Newcastle, Cambridge and London) and ranged from asymptomatic to critically severe.

The team performed single-cell sequencing from ~800,000 individual immune cells, along with detailed analysis of cell surface proteins and antigen receptors found on immune cells in the blood. They revealed differences in multiple types of immune cells that are involved in the body's response to COVID-19.

In those with no symptoms, the team found increased levels of B cells that produce antibodies that are found in mucus passages, such as the nose. These antibodies may be one of our first line of defence in COVID-19. However, these protective B cells were missing in people with serious symptoms, indicating the importance of an effective antibody-associated immune response at the nose and other mucus passages.

The team discovered that whereas patients with mild to moderate symptoms, had high levels of B cells and helper T-cells, which help fight infection, those with serious symptoms had lost many of these immune cells, suggesting that this part of the immune system had failed in people with severe disease.

In contrast, people with more serious symptoms leading to hospitalisation had an uncontrolled increase in monocytes and killer T-cells, high levels of which can lead to lung inflammation. Those with severe disease also had raised levels of platelet-producing cells, which help blood to clot.

Professor Muzlifah Haniffa, senior author from Newcastle University and Senior Clinical Fellow at the Wellcome Sanger Institute, said: "This is one of the only studies of its kind that looks at samples collected from asymptomatic people, which helps us start to understand why some people react differently to COVID-19 infection. It could also explain symptoms such as lung inflammation and blood clots. The immune system is made up of lots of different groups of cells, similar to the way an orchestra is made up of different groups of instruments, and in order to understand the coordinated immune response, you have to look at these immune cells together."

While it is not yet understood how the infection stimulates these immune responses, the study gives a molecular explanation for how COVID-19 could cause an increased risk of blood clotting and inflammation in the lungs, which can lead to the patient needing a ventilator. This also uncovers potential new therapeutic targets to help protect patients against inflammation and severe disease. For example, it may be possible to develop treatments that decrease platelet production or reduce the number of killer T-cells produced, however more research is required.

Professor Menna Clatworthy, senior author and Professor of Translational Immunology at the University of Cambridge and Wellcome Sanger Institute Associate Faculty, said: "This is one of the most detailed studies of immune responses in COVID-19 to date, and begins to help us understand why some people get really sick while others fight off the virus without even knowing they have it. This new knowledge will help identify specific targets for therapy for patients that get sick with COVID-19."

In the future, research may identify those who are more likely to experience moderate to severe disease by looking at levels of these immune cells in their blood.

This study used samples from three centres in the UK, and found that some antibody responses were similar in individuals in one geographic area compared with those at a different centre, hinting that this part of the immune response may be tailored to different variants of the virus.

Dr John Marioni, senior author and Head of Research at EMBL's European Bioinformatics Institute (EMBL-EBI) and Senior Group Leader at the Cancer Research UK Cambridge Institute, said: "Using data from three different centres has allowed us to look at how people react to COVID-19 throughout the UK. The amount of data collected in this study has given us crucial insight into the immune reaction in various different severities of COVID-19 infection."

Professor Berthold Göttgens, senior author and Professor of Molecular Haematology at the University of Cambridge, said: "Along with the findings, the way this study was conducted is noteworthy, as it was a new way of doing biomedical science. By bringing different experts together, we were able to employ a divide and conquer approach, which allowed us to complete the work in extra quick time. This study required a large teamwork effort, in the middle of the pandemic when labs were being shut down. This was an incredibly rewarding study to work on, with everyone understanding the importance of the work and willing to go the extra mile."

Dr Sarah Teichmann, senior author from the Wellcome Sanger Institute and co-chair of the Human Cell Atlas Organising Committee, said: "This is a great example of using the Human Cell Atlas to understand COVID-19 and identify which of our cells are critical for infection and treatment. This information can be used to better understand why different people react to coronavirus in different ways. The data is openly accessible and can provide a basis for developing potential new therapies, to reduce the spread of the virus, or to protect those who start to develop severe disease."

Exposure to certain endocrine-disrupting chemicals could elevate the risk of breast cancer, according to a new comprehensive systematic review of epidemiological research. However, for many chemicals, evidence is inconsistent or still limited. The review was carried out by researchers at the universities of Hong Kong and Eastern Finland and published in Critical Reviews in Food Science and Nutrition.

Endocrine-disrupting chemicals (EDCs) can interfere with the body's hormonal system, also called the endocrine system, and are widely present in the environment. They originate from a variety of sources, including pesticides, plasticisers and other industrial and pharmaceutical chemicals, as well as natural sources. Humans are often exposed to EDCs through food, but other possible exposure routes include drinking water, skin contact and air.

Breast cancer accounts for the majority of women's cancers. There has been an increasing interest in the role of estrogene-mimicking EDCs, so called xenoestrogens, in the development of breast cancer. They comprise a broad range of pesticides, synthetic chemicals, phytoestrogens and certain mycotoxins. The researchers reviewed 131 epidemiological studies evaluating the link between xenoestrogen exposure and breast cancer. Most studies assessed exposures by measuring the EDCs and their metabolites in urine, serum, plasma or adipose tissues.

Some may be genetically more vulnerable to EDCs

According to the review, the nowadays widely banned pesticide DDT is one of the most studied EDCs in relation to breast cancer risk. Out of 43 epidemiological studies, eleven reported positive associations between DDT or its metabolites in lipid, serum or plasma and breast cancer incidence. Nine reported higher DDT levels among women with breast cancer than among controls. In a few studies, DDT was linked to estrogen-positive breast cancer or the association to breast cancer risk depended on genotype.

Polychlorinated biphenyls, PCBs, are a large group of compounds earlier much used in electrical devices, surface coatings and other purposes. The review of 50 studies found the association between total PCBs and breast cancer risk to be inconsistent. However, 19 studies linked certain PCBs to a higher breast cancer incidence. Similar to DTT, PCBs accumulate in the adipose tissue and in the food chain and can be excreted in breast milk.

Perfluorooctanoid acid (PFOA) found in some food packaging and cookware was linked to breast cancer risk in three out of five epidemiological studies. Some studies found an association between cancer risk and certain genotypes both for PCBs and PFOAs.

DDT, PCBs ja PFOA are POP substances, persistent organic pollutants, the use of which is strictly regulated. DDT ja PCBs are old POP substances and their levels in the environment are decreasing. PFOA is a newer POP substance.

Phytoestrogens were found beneficial in some, but not all studies

Phytoestrogens are natural plant estrogens that have been suggested to prevent breast cancer. Genistein is a phytoestrogen found in soy products. The review included 29 epidemiological studies focusing on genistein, 18 of which linked it to a lower breast cancer risk, although some only in certain age groups or populations.

For most EDCs included in the review, the link to breast cancer has been investigated in only a few epidemiological studies. Phtalates and bisphenol A (BPA), for example, are used in plastic packaging and can transfer to food. According to the review, four out of six studies linked phthalates to increased breast cancer risk. BPA was linked to more aggressive tumours in one study, but two other epidemiological studies found no link to breast cancer.

Parabens are common preservatives in foods and cosmetic products and considered possible endocrine disruptors. The only epidemiological study on the topic reported a link between paraben exposures, breast cancer risk and mortality following breast cancer.

Oral contraceptive use was linked to an increased breast cancer risk in seven out of eight epidemiological studies, but there were controversies on how duration or discontinuation of oral contraceptive use affected the risk.

The review also included the herbicide atrazine, the industrial by-product dioxine, mycotoxins produced by food and crop molds, and PBDEs found in household furniture coatings and appliances, but epidemiological studies on their links to breast cancer risk were still scarce and often inconsistent.

The writers point out that for EDCs to disrupt endocrine functions, dose, time, duration and age at exposure all matter. In addition, as multiple EDCs coexist in the environment, more research is needed to evaluate their interactive effects on breast cancer risk.

The review also suggests that genotypes could determine whether EDC exposure affects breast cancer risk, and more research is needed on this topic. "One example is the polymorphism of the CYP1A1 gene, which is responsible for estrogen metabolism."

According to the writers, next-generation technologies, such as genome sequencing, proteomics or epigenomics, can help identify new exposure biomarkers with better sensitivity and specificity. "These technologies will also pave way to better assessment of past exposure and prediction of future risks, by taking into account an individual's genetic profile."

As we accumulate more and more gene-sequencing information, cell-type databases are growing in both size and complexity. There is a need to understand where different types of cells are located in the body, and to map their gene expression patterns into specific locations in tissues and organs. For example, a gene can be actively expressed in one cell while suppressed in another.

One way of mapping genes into tissues is a technique called in situ hybridization. Simply put, a target gene is tagged ("hybridized") with a fluorescent marker within the sections of the tissue it is located in (the "in situ" part). The sections are then visualized under a specialized microscope to see where the gene "lights up". Consecutive photographs of each section are then put together to generate a "spatial" map of the gene's location inside the tissue.

The problem with methods that use in situ hybridization is that, as the number of target genes grows, they start to become complicated, require specialized equipment, and force scientists to select their targets beforehand, a process that can be laborious if the goal is to reconstruct a full map of gene distribution across tissues.

"Spatializing" sequencing data

Now, scientists at EPFL's School of Life Sciences have created a computational algorithm called Tomographer, which can transform gene-sequencing data into spatially resolved data such as images, and does so without needing a microscope. The work was carried out by the research group of Gioele La Manno, and is now published in Nature Biotechnology.

In the new Tomographer technique, the tissue is first cut along the axis of interest into consecutive sections, each of which is then sliced into tissue strips at different angles. Cells from the strips are then broken down to collect their total messenger RNA (mRNA). Each mRNA corresponds to a gene that was active in the cell. The measurements resulting from the strips can be then used as input to the Tomographer algorithm to reconstruct spatial gene-expression patterns across the tissue.

"The Tomographer algorithm opens a promising and robust path to "spatialize" different genomics measurement techniques," says Gioele La Manno. As an application, the scientists used Tomographer to spatially map the molecular anatomy of the brain of the Australian Bearded Dragon (Pogona vitticeps) - a non-model organism, demonstrating how versatile the algorithm can be.

"Ever since I started med school, I have been admiring the way computer tomography revolutionized the way we examine organs and body parts," says Christian Gabriel Schneider, one of the study's lead authors. "Today, I am very proud to be part of a team that has developed a molecular tomography technology. So far, we have focused on applications in neurodevelopmental biology, but in the future, we can certainly imagine molecular tomography becoming a constituent in personalized medicine."

"It was an exciting opportunity to develop an accessible and flexible computational method that has the potential to facilitate progress in the health sciences," adds Halima Hannah Schede, the study's other lead author. "I am very much looking forward to seeing what other spatially resolved biological data forms will be brought to light with Tomographer."

Lafora disease is an inherited neurodegenerative condition that initially develops with seizures in adolescence and evolves with progressive degeneration of the nervous system to death, about ten years after its onset. It is characterised by the accumulation of abnormal glycogen aggregates called Lafora bodies in the brain. There is currently no treatment for this condition, although some therapies are being tested in clinical trials.

Led by Dr. Joan Guinovart, emeritus professor of the University of Barcelona (UB) and also group leader of CIBERDEM, the Metabolic Engineering lab at IRB Barcelona has discovered that Lafora bodies that accumulate in glial cells, which are essential for the proper functioning of the nervous system, are responsible for the neurodegeneration associated with the disease.

For this study, Dr. Guinovart's group generated a mouse model of Lafora disease, in which they prevented glycogen from accumulating in glial cells. They found that these mice did not develop neurodegeneration.

"For years, it was believed that the disease was caused by the accumulation of Lafora bodies only in neurons, but now we have shown that neurodegeneration is caused by accumulations in glial cells," says Dr. Jordi Duran, co-director of the study.

"This discovery has important implications for the design of treatments for the disease and we now intend to investigate the mechanism by which glycogen deposits cause this damage. We will also study the possible role of this pathological mechanism in other neurodegenerative diseases," explains Dr. Duran.

The study also involved the laboratories led by Dr. José Antonio del Río, full professor of the UB (at the Institute for Bioengineering of Catalonia and the UB's Institute of Neurosciences) and Professor Matthew Gentry (at the University of Kentucky)..

A consortium supported by the association of affected families

This project has been developed within the framework of a global consortium for the study of Lafora disease, coordinated by the University of Kentucky in the US. In 2016, the consortium received $7.7 M from NIH (U.S. National Institutes of Health) for a period of five years. The consortium was promoted by Chelsea's Hope, an association of families in the US affected by Lafora disease, which in 2014 brought together leading specialists to foster research into the disease.

Scrobiculariaplana is a type of wedge clam widely found along the coasts and estuariesof northern Europe, the Mediterranean and West Africa. Like other mollusks, it is used as a bioindicator to study pollution in these types of ecosystems, for its ability to accumulate heavy metals and organic pollutants.

A new study has managed to identify the transcriptome and the associated proteome of this bivalve, a finding that could represent an important leap forward in the early detection of pollutants in coastal areas. While the genome is the DNA content comprising the genetic information essential for life, the transcriptome includes only the information on genes that are expressed, while the proteome is the totality of proteins expressed at a given time and under specific conditions. Therefore, its reconstruction is key to understanding the molecular effects of pollution.

Thanks to this finding, the study has managed to identify proteins associated with a total of 174 biological processes. Among these are various molecular functions related to stress response mechanisms suffered by these organisms when they are subjected to pollution and its effects.

The work began with collaboration with the Institute of Marine Sciences of Andalusia, the "Molecular Biology of Stress Response Mechanisms" at the University of Cordoba, and the Central Research Support Service (SCAI) of the university institution, which saw to the bio-informatics component, key to the reconstruction of the transcriptome.

After isolating RNA samples from this mollusk under controlled conditions, explained researcher Carmen Michán, small genetic sequences were extracted. The study managed to combine three mathematical algorithms to order all these small fragments, reconstruct entire genes, and bring together all the pieces of this great biological puzzle.

This software tool provides a solid database for biomolecular analysis ,and constitutes a beacon to guide future work. Furthermore, according to Professor José Alhama, another of the researchers who participated in the study, "having this tool increases the likelihood of success of new studies, not only in studies with this specific bivalve, but also in other similar mollusks." The researcher explained that no similar study had been carried out on organisms of this type. Now, this reference map could help better gauge the effects of pollution on marine ecosystems before the damage is irreparable.

KINGSTON, R.I., -- April 20, 2021 -- The Northwest Atlantic Shelf is one of the fastest-changing regions in the global ocean, and is currently experiencing marine heat waves, altered fisheries and a surge in sea level rise along the North American east coast. A new paper, "Changes in the Gulf Stream preceded rapid warming of the Northwest Atlantic Shelf," published in Communications Earth & Environment by recent URI Graduate School of Oceanography graduate Afonso Gonçalves Neto reveals the causes, potential predictability and historical context for these types of rapid changes.

"We used satellite data to show that when the Gulf Stream migrates closer to the underwater plateau known as the Grand Banks of Newfoundland, as it did after 2008, it blocks the southwestward transport of the Labrador Current that would otherwise provide cold, fresh, oxygen-rich water to the North American shelf," said lead author Gonçalves Neto. This mechanism explains why the most recent decade has been the hottest on record at the edge of the Northeast United States and Canada, as the delivery system of cold water to the region got choked off by the presence of the Gulf Stream.

The URI research team noted the importance of finding that the satellite-observed signature of the Gulf Stream's position relative to the Grand Banks precedes subsurface shelf warming by over a year. "By monitoring satellite observations for changes near the Grand Banks, we can predict changes coming to the Northeast U.S. shelf with potentially enough lead time to inform fishery management decision-making," said GSO graduate student and co-author Joe Langan.

The Grand Banks of Newfoundland is hardly a stranger to attention. It was near this feature that an iceberg sank the R.M.S. Titanic, one impetus for creation of the International Ice Patrol. The Ice Patrol has been collecting oceanographic data in this region for over a century, allowing the URI team to put recent satellite observations in a much longer-term context. Though the 2008 shift at the edge of the Grand Banks created warmer and saltier conditions than ever recorded since 1930, there was a similar shift in the 1970s relative to the decades preceding it. Thus, the circulation change directly observed by satellites might have had a precedent about 50 years ago.

Jaime Palter, GSO associate professor of oceanography and co-author of the study, marveled at the long record, and what remains unknown. "We still don't know what caused the abrupt shift of the circulation near the Grand Banks inferred in the 1970s and observed in 2008, or whether this is the new normal for the circulation and the temperatures of the northeast shelf," said Palter. "There are modeling studies that suggest that a slowdown of the Atlantic Meridional Overturning Circulation can cause the types of changes we observed, but the connection remains to be made in the observational record."

Almost 80% of South Africans speak one of the SEB family languages as their first language. Their origins can be traced to farmers of West-Central Africa whose descendants over the past two millennia spread south of the equator and finally into Southern Africa.

Since then, varying degrees of sedentism [the practice of living in one place for a long time], population movements and interaction with Khoe and San communities, as well as people speaking other SEB languages, ultimately generated what are today distinct Southern African languages such as isiZulu, isiXhosa and Sesotho.

Despite these linguistic differences, these groups are treated mostly as a single group in genetic studies.

Understanding genetic diversity in a population is critical to the success of disease genetic studies. If two genetically distinct populations are treated as one, the methods normally used to find disease genes could become error prone.

Consideration of these genetic differences is critical to providing a reliable understanding of the genetics of complex diseases, such as diabetes and hypertension, in South Africans.

Dr Dhriti Sengupta and Dr Ananyo Choudhury in the Sydney Brenner Institute for Molecular Bioscience (SBIMB) at the University of the Witwatersrand, Johannesburg, South Africa, were joint lead authors of the paper published in Nature Communications on 7 April 2021.

The study comprised a multidisciplinary team of geneticists, bioinformaticians, linguists, historians and archaeologists from Wits University (Michèle Ramsay, Scott Hazelhurst, Shaun Aron and Gavin Whitelaw), the University of Limpopo, and partners in Belgium, Sweden and Switzerland.

"South Eastern Bantu-speakers have a clear linguistic division - they speak more than nine distinct languages - and their geography is clear: some of the groups are found more frequently in the north, some in central, and some in southern Africa. Yet despite these characteristics, the SEB groups have so far been treated as a single genetic entity," says Choudhury.

The study found that SEB speaking groups are too different to be treated as a single genetic unit.

"So if you are treating say, Tsonga and Xhosa, as the same population - as was often done until now - you might get a completely wrong gene implicated for a disease," says Sengupta.

ABOUT THE STUDY

The study, titled: "Genetic substructure and complex demographic history of South African Bantu speakers" aimed to find out whether the SEB speakers are indeed a single genetic entity or if they have enough genetic differences to be grouped into smaller units.

Genetic data from more than 5000 participants speaking eight different southern African languages were generated and analysed.

These languages are isiZulu, isiXhosa, siSwati, Xitsonga, Tshivenda, Sepedi, Sesotho and Setswana.

Participants were recruited from research sites in Soweto in Gauteng, Agincourt in Mpumalanga, and Dikgale in Limpopo province.

Genetic differences reflect geography, language and history

The study detected major variations in genetic contribution from the Khoe and San into SEB speaking groups; some groups have received a lot of genetic influx from Khoe and San people, while others have had a very little genetic exchange with these groups.

This variation ranged on average from about 2% in Tsonga to more than 20% in Xhosa and Tswana.

This suggests that SEB speaking groups are too different to be treated as a single genetic unit.

"The study showed that there could be substantial errors in disease gene discovery and disease risk estimation if the differences between South-Eastern-Bantu speaking groups are not taken into consideration," says Sengupta.

The genetic data also show major differences in the history of these groups over the last 1000 years. Genetic exchanges were found to have occurred at different points in time, suggesting a unique journey of each group across the southern African landscape over the past millennium.

These genetic differences are strong enough to impact the outcomes of biomedical genetic research.

Sengupta emphasises, however, that ethnolinguistic identities are complex and cautioned against extrapolating broad conclusions from the findings regarding genetic differences.

"Although genetic data showed differences [separation] between groups, there was also a substantial amount of overlap [similarity]. So while findings regarding differences could have huge value from a research perspective, they should not be generalised," she says.

A GENETIC BLUEPRINT FOR FUTURE HEALTH

A common approach to identify if a genetic variant causes or predisposes us to a disease is to take a set of individuals with a disease (e.g., high blood pressure or diabetes) and another set of healthy individuals without the disease, and then compare the occurrence of many genetic variants in the two sets.

If a variant shows a notable frequency difference between the two sets it is assumed that the genetic variant could be associated with the disease.

"However, this approach depends entirely on the underlying assumption that the two groups consist of genetically similar individuals. One of the major highlights of our study is the observation that Bantu-speakers from two geographic regions - or two ethnolinguistic groups - cannot be treated as if they are the same when it comes to disease genetic studies," says Choudhury.

Future studies, especially those testing a small number of variants, need to be more nuanced and have balanced ethnolinguistic and geographic representation, he says.

This study is the second landmark study in African population genetics, published in the last six months, led by researchers in the Sydney Brenner Institute for Molecular Bioscience in the Faculty of Health Sciences at Wits University.

Professor Michèle Ramsay, director of the SBIMB and corresponding author of the study, says: "The in-depth analysis of several large African genetic datasets has just begun. We look forward to mining these datasets to provide new insights into key population histories and the genetics of complex diseases in Africa".

The Cyclostomata is an ancient group of aquatic colonial suspension-feeders from the phylum Bryozoa. The fact that they have unique placentae has been discovered by researchers at St Petersburg University and the University of Vienna. The coenocytes, i.e. large multinucleate cell structures, originate via nuclear multiplication and cytoplasmic growth among the cells surrounding the early embryo. Interestingly, the coenocytes are commonly found among fungi and plants, yet are quite rare in animals. It is the first time coenocytes have been discovered in placenta.

Biologists are well aware that the cells of the living organisms are incredibly different in the way that they behave. They may happen to form a multinucleate structure resulting from cell fusion, i.e. so-called syncytium with a single membrane. Such 'behaviour' ensures nutrient circulation with no resources and time spent on transporting between the cells. Yet similar structures can be formed through ways other than fusion, e.g. coenocytes originate via nuclear multiplication and cytoplasmic growth. Cell fusion is mainly typical of animals. For instance, in human placenta, syncytium covers embryonic placental villi, which invades the wall of the uterus to establish nutrient circulation between the embryo and the mother. In contrast, formation of coenocytes is typical of plants and fungi. Yet what these processes - cell fusion and cell growth, have in common is that they result in quite large irregular structures that resemble tissues.

'Initially, my postgraduate student Uliana Nekliudova, who is the first author of the article, and I expected to see syncytium in the Cyclostomata. Yet what we came across was coenocytes, i.e. multinucleate structures that were previously unknown in animal placentas,' said the head of the project and Professor at the Department of Invertebrate Zoology at St Petersburg University Andrew Ostrovsky. 'The embryos in this group of Bryozoa are not just abut the placenta, as happens normally, but embedded into it. The placenta consists of several large coenocytes, and the coenocytic "elements" are interconnected via cytoplasmic bridges and various cell contacts. Coenocytes have different ultra-structure. This tissue shows evidence of both nutrient synthesis and transport.'

Additionally, as the scientist said, forming such a structurally complex placenta may have contributed to evolving polyembryony in this group of animals. Polyembryony is a condition in which over a hundred embryos develop from a single fertilised egg, forming larvae. Yet, the unique combination of placentation, viviparity, and polyembryony is known to occur only in the nine-banded armadillo Dasypus.

The samples were collected near the Marine Biological Station of St Petersburg University at the White Sea. The scientists also discovered that placentation originated from the organ that was responsible for pushing off tentacles. All bryozoans release sperm into water column where zooids from other colonies catch it using tentacles. The membranous sac, i.e. an organ that contains circular muscles, pushes the tentacles off. After internal fertilisation, the membranous sac becomes part of the placenta transforming to coenocytes that provide embryonic nourishment. Evolution of the cyclostome placenta, involving transformation of the hydrostatic apparatus (membranous sac) and substitution of its function to embryonic nourishment, is an example of exaptation.

Most bryozoans eject a fertilised egg and then transport it into a special brood cavity for incubation. Yet the cyclostome bryozoans do it differently. The larvae develop inside the gonozooids, i.e. colony members that serve as a placental incubator. Larval production lasts almost all summer. Developed larvae gradually leave the gonozooids.

'Polyembryony is a so-called evolutional dead-end. You have offspring, yet they are clones. There is no genetic diversity', said Andrew Ostrovsky. 'The fact that the offspring are different is essential for the ability to survive. The question is why is polyembryony - that has been typical to Cyclostomata for about 200 million years according to the fossil evidence we have - resisted? What is the catch? Presumably, the bryozoans, producing clone-larvae during several months, "collide" them with a constantly changing environment. As a result, it is not genomes that change, but conditions where these genomes happen to find themselves.'

Although the problem of gender discrimination is already found in the music industry, music recommendation algorithms would be increasing the gender gap. Andrés Ferraro and Xavier Serra, researchers of the Music Technology research group (MTG) of the UPF Department of Information and Communication Technologies (DTIC), with Christine Bauer, of the University of Utrecht (Netherlands), have recently published a paper on gender balance in music recommendation systems in which they ask themselves how the system should work to avoid gender bias.

At the outset, the authors identified that gender justice was one of the artists' main concerns

Initially, the work by Ferraro, Serra and Bauer aimed to understand the fairness of music platforms available online from the artists' point of view. In interviews conducted with music artists, they identified that gender justice was one of their main concerns.

Women have less exposure

The authors tested a commonly used music recommendation algorithm based on collaborative filtering and analysed the results of two datasets. In both cases, they found that the algorithm reproduces the existing bias in the dataset, in which only 25% of artists are women. In addition, the algorithm generates a ranking with artists to recommend to the user. The authors saw that on average the first recommendation of a woman artist comes in 6th or 7th position, while that of a man artist is in first position. Ferraro, first author of the paper adds: "The bias in exposure comes from the way recommendations are generated". This means that women have less exposure based on the recommendations of the system.

The situation worsens when taking into account that as users listen to recommended songs, the algorithm learns. This creates a feedback loop.

With the help of the reordered algorithm, users begin to change their behaviour so that they listen to more female artists

A new approach to compensate for gender bias

The authors of the study propose a new approach that would allow greater exposure of female artists and would consist of reordering the recommendation, which would move a specified number of positions downwards in order to solve the existing gender bias.

In a simulation, the authors studied how classified recommendations would affect user behaviour in the long run. The results showed that, with the help of the reclassified algorithm, users would begin to change their behaviour and thus listen to more female artists than with other music recommendation algorithms and, moreover, the new algorithm, based on machine learning, would consolidate this change in behaviour.

MINNEAPOLIS/ST.PAUL (04/20/2021) -- University of Minnesota Medical School researchers have offered new ways to think about the immune system thanks to a recent study published in Nature. Their research, which indicates organ tissues become increasingly immune throughout life, may begin to alter fundamental ideas regarding the rules of vaccination and the immune system's function within the body.

Saythi Wijeyesinghe, PhD, the lead author on the study is a researcher in the Masopust Lab at the U of M Medical School, which focuses on T cell immunity. His research began with the goal to understand the lifespan of T cells in organ tissues, which are known to fight off viruses while also protecting from reinfection by the same virus.

"Historically, studies of the immune system have emphasized its renewable nature through bone marrow, lymphoid organs and blood. Our work shows how much this model fails to account for the many immune cells distributed throughout other organs of the body, where most infections and tumors arise," Wijeyesinghe said. "What we found ends up painting a much broader picture of how the immune system accomplishes surveillance of the entire body for pathogens, tissue damage and tumors."

The study's major findings, include:

- Antiviral T cells that reside in most organs of the body persist over time and in the face of extensive infectious exposures;

- Unlike other organ systems, the immune system becomes increasingly immune throughout life, which is a natural response to accumulated microbial exposures over time;

- Up to 25% of the cells in organs were immune cells, indicating that the immune system significantly contributes to the cellular makeup of the body;

- And, along with antiviral T cells, most other immune cells are durably tissue-resident in organs as well.

Wijeyesinghe hopes this study can further advance the ongoing change in how the broader scientific community conceptualizes the immune system and immune homeostasis.

During this study, Wijeyesinghe also unexpectedly discovered how tissue-resident T cells may serve as the origin for memory T cells in blood. As a next step in this research, the Masopust Lab is developing new techniques to trace the fate of these immune cells, hoping to further dissect the relationship between blood-borne and tissue-based immunity.

PHILADELPHIA - Renter protection policies that have curbed mass evictions during the COVID-19 pandemic have played a key role in preventing the spread of SARS-CoV-2 in U.S. cities, according to a new study published in Nature Communications.

Using an epidemiological model to predict how evictions and eviction moratoria would impact the epidemic, the researchers found, for instance, that in a city of 1 million in which 1 percent of households experience eviction monthly, this could lead to up to 49,000 excess COVID-19 infections. In Philadelphia alone, a fivefold increase in evictions, predicted by some economic analyses, could lead to 53,000 extra infections. The study was led by researchers in the Perelman School of Medicine at the University of Pennsylvania, Johns Hopkins University, and the University of Illinois at Urbana-Champaign.

"Our model shows clearly that policies to stem evictions are not only a warranted but a necessary component of COVID control. As long as the virus is circulating, ending these protections could have devastating implications in the United States," said co-senior author Michael Z. Levy, PhD/a>, an associate professor of Epidemiology in Penn's Perelman School of Medicine.

Record levels of unemployment have put millions of Americans at risk of losing their homes throughout 2020 and 2021. At the start of the pandemic, many cities and states enacted temporary legislation banning evictions, some of which have since expired. On September 4, 2020, the Centers for Disease Control and Prevention (CDC) imposed a national moratorium on evictions, which was extended in March 2021. This order is currently being challenged in various courts.

In addition to a number of well-documented adverse outcomes, evictions would also have outsized repercussions on the growth rate of the COVID-19 epidemic, Levy and his research team predicted in the summer of 2020. The effect emerges from increases in household sizes -- data suggest that, once evicted, households tend to "double-up," moving in with friends or family. Household transmission can also limit or delay the effects of measures like lockdowns, which aim to decrease the contact rate in the general population.

"Evictions were particularly concerning for us, because a growing number of contact tracing studies have shown that households are a major source of SARS-CoV-2 transmission. When households get bigger, that gives the virus a greater opportunity to get inside the home, and then, a greater chance to spread outside of it -- to coworkers, friends, and other family members," study co-author Alison Hill, PhD, an assistant professor at the Johns Hopkins University School of Medicine.

To quantify this effect, the research team modified an epidemiological model known as SEIR (susceptible, exposed, infectious, and recovered) to track the transmission of SARS-CoV-2 through a hypothetical metropolitan area of 1 million individuals. They then used a two-layer "network model" to show the contacts within a city population over which infection can spread: One layer described contacts within the household, estimated from the 2019 American Community Survey of the U.S. Census, and the second layer constituted contacts outside the household, such as work colleagues, classmates, and friends.

The researchers modeled evictions that resulted in the "doubling up" of households by merging each evicted household with one randomly selected household in the network. They then adjusted the number of contacts outside the household over the course of the simulations to capture the effects of lockdown measures and their subsequent relaxation.

The research team found that with a low monthly eviction rate of 0.25 percent, an estimated 0.5 percent more of the population could become infected with COVID-19 -- or about 5,000 excess cases per 1 million residents -- compared to if there were no evictions. A 1 percent monthly eviction rate could lead to 19,000 to 49,000 excess cases. With an eviction rate of 2 percent per month, that number jumps to 50,000 to 100,000 excess infections in a single city.

"Our results suggest that the CDC-mandated national order prohibiting evictions from Sept 4 - Dec 31, 2020 likely prevented thousands of excess COVID-19 infections for every million metropolitan residents," according to the study authors.

Their initial model assumed that mixing between households occurs randomly throughout a city and that evictions are uniformly distributed. However, data throughout the pandemic has consistently showed that both COVID-19 and evictions disproportionately affect poorer, minority communities. The research team therefore adjusted their model to evaluate the effect of evictions in a specific, diverse city - Philadelphia, Pennsylvania, which has one of the highest eviction rates among large U.S. cities.

In July 2020, Philadelphia's City Council passed the Emergency Housing Protection Act, in an effort to prevent evictions during the pandemic. The city was sued by a lobbyist group, which questioned whether the legislation was of broad societal interest, rather than protecting a narrow class of residents. This prompted Levy's team to assess the claim.

Their simulations showed that allowing evictions to resume in Philadelphia could substantially increase the number of COVID infections in the city, and that these increases would be felt among various socioeconomic populations, including those experiencing a low number of evictions. With evictions occurring at only their pre-pandemic rates, the epidemic would infect an extra 0.3 percent of the Philadelphia population, or 4,700 individuals. However, the researchers point out, many economic analyses predict the eviction crisis could be much higher if allowed to resume, due to the economic fallout associated with COVID-19. With a five-fold increase in evictions, excess infections would increase by 53,000 in the city.

"These simulations show that a change that seemingly only affects a small proportion of the population can have a great impact across interconnected communities," Levy said. "Evictions not only affect the evicted, but they can endanger an entire city."

An overgrowth of yeast in the gut within the first few months of life may cause changes to the immune system that increase the risk of asthma later on, shows a study published today in eLife.

Asthma is a common and sometimes difficult-to-manage, life-long lung condition that affects one in 10 children in developed countries. The findings explain a possible cause of asthma and may help scientists develop new strategies to prevent or treat the condition.

The period just after birth is a critical window for the development of a healthy immune system and gut microbiome. Disruptions to gut bacteria that produce anti-inflammatory compounds called short-chain fatty acids (SCFAs) early in life have previously been linked to asthma.

"We recently showed that overgrowth of a type of gut yeast called Pichia kudriavzevii in newborns in Ecuador is associated with an increased risk of asthma," says first author Rozlyn Boutin, an MD/PhD student in the Department of Microbiology and Immunology at the University of British Columbia, Vancouver, Canada. "In this study, we wanted to see if we could replicate these findings in children from an industrialised setting and identify how fungi of the gut microbiota affect the development of the immune system."

Boutin and colleagues began with a study of 123 newborns in Canada, who are part of the CHILD Cohort Study. They again found that an overgrowth of Pichia kudriavzevii in the stools of the newborns during the first three months of life was associated with a higher risk of asthma.

To understand how this yeast overgrowth might contribute to asthma later in life, the team applied Pichia kudriavzevii to newborn mice with immature gut microbiota communities. In this mouse model of asthma, the team found that the newborns exposed to the yeast experienced more lung inflammation than those who were unexposed. Applying Pichia kudriavzevii to an adolescent mouse model, however, did not cause this excess inflammation.

"Our findings show that there is a critical window in early life where disruptions in the gut microbiota caused by Pichia kudriavzevii affect the development of the immune system and increase the risk and severity of asthma later in life," Boutin says.

Previous studies have shown that bacterial SCFAs have beneficial effects on immune development that protect against asthma. In this study, the team also showed that anti-inflammatory SCFAs produced by gut bacteria inhibit the growth of Pichia kudriavzevii.

"Immune responses to gut microbe disruptions early in life have long-term consequences for diseases of the immune system later in life," concludes senior author Brett Finlay, Professor at the Michael Smith Laboratories and the Departments of Biochemistry and Molecular Biology, and Microbiology and Immunology, University of British Columbia. "Our study adds to our understanding of microbiota-associated asthma and suggests that inhibiting yeast overgrowth with SCFAs in early life could be an effective approach to preventing this condition."

FAYETTEVILLE, Ark. - The fearsome tyrannosaur dinosaurs that ruled the northern hemisphere during the Late Cretaceous period (66-100 million years ago) may not have been solitary predators as popularly envisioned, but social carnivores similar to wolves, according to a new study.

The finding, based on research at a unique fossil bone site inside Utah's Grand Staircase-Escalante National Monument containing the remains of several dinosaurs of the same species, was made by a team of scientists including Celina Suarez, University of Arkansas associate professor of geosciences.

"This supports our hypothesis that these tyrannosaurs died in this site and were all fossilized together; they all died together, and this information is key to our interpretation that the animals were likely gregarious in their behavior," Suarez said.

The research team also include scientists from the U.S. Bureau of Land Management, Denver Museum of Nature and Science, Colby College of Maine and James Cook University in Australia. The study examines a unique fossil bone site inside Grand Staircase-Escalante National Monument called the "Rainbows and Unicorns Quarry" that they say exceeded the expectations raised even from the site's lofty nickname.

"Localities [like Rainbows and Unicorns Quarry] that produce insights into the possible behavior of extinct animals are especially rare, and difficult to interpret," said tyrannosaur expert Philip Currie in a press release from the BLM. "Traditional excavation techniques, supplemented by the analysis of rare earth elements, stable isotopes and charcoal concentrations convincingly show a synchronous death event at the Rainbows site of four or five tyrannosaurids. Undoubtedly, this group died together, which adds to a growing body of evidence that tyrannosaurids were capable of interacting as gregarious packs."

In 2014, BLM paleontologist Alan Titus discovered the Rainbows and Unicorns Quarry site in Grand Staircase-Escalante National Monument and led the subsequent research on the site, which is the first tyrannosaur mass death site found in the southern United States. Researchers ran a battery of tests and analyses on the vestiges of the original site, now preserved as small rock fragments and fossils in their final resting place, and sandbar deposits from the ancient river.

"We realized right away this site could potentially be used to test the social tyrannosaur idea. Unfortunately, the site's ancient history is complicated," Titus said. "With bones appearing to have been exhumed and reburied by the action of a river, the original context within which they lay has been destroyed. However, all has not been lost." As the details of the site's history emerged, the research team concluded that the tyrannosaurs died together during a seasonal flooding event that washed their carcasses into a lake, where they sat, largely undisturbed until the river later churned its way through the bone bed.

"We used a truly multidisciplinary approach (physical and chemical evidence) to piece the history of the site together, with the end-result being that the tyrannosaurs died together during a seasonal flooding event," said Suarez.

Using analysis of stable carbon and oxygen isotopes and concentrations of rare earth elements within the bones and rock, Suarez and her then-doctoral student, Daigo Yamamura, were able to provide a chemical fingerprint of the site. Based on the geochemical work, they were able to conclusively determine that the remains from the site all fossilized in the same environment and were not the result of an attritional assemblage of fossils washed in from a variety of areas.

"None of the physical evidence conclusively suggested that these organisms came to be fossilized together, so we turned to geochemistry to see if that could help us. The similarity of rare earth element patterns is highly suggestive that these organisms died and were fossilized together," said Suarez.

Excavation of the quarry site has been ongoing since its discovery in 2014 and due to the size of the site and volume of bones found there the excavation will probably continue into the foreseeable future. In addition to tyrannosaurs, the site has also yielded seven species of turtles, multiple fish and ray species, two other kinds of dinosaurs, and a nearly complete skeleton of a juvenile (12-foot-long) Deinosuchus alligator, although they do not appear to have all died together like the tyrannosaurs.

"The new Utah site adds to the growing body of evidence showing that tyrannosaurs were complex, large predators capable of social behaviors common in many of their living relatives, the birds," said project contributor, Joe Sertich, curator of dinosaurs at the Denver Museum of Nature & Science. "This discovery should be the tipping point for reconsidering how these top carnivores behaved and hunted across the northern hemisphere during the Cretaceous."

Future research plans for the Rainbows and Unicorns Quarry fossils include additional trace element and isotopic analysis of the tyrannosaur bones, which paleontologists hope will determine with a greater degree of certainty the mystery of Teratophoneus' social behavior.

In stark contrast to the social interaction between humans and among many species of animals, paleontologists have long debated whether tyrannosaurs lived and hunted alone or in groups.

Based on findings at a site in Alberta, Canada, with over 12 individuals, the idea that tyrannosaurs were social with complex hunting strategies was first formulated by Philip Currie over 20 years ago. This idea has been widely debated, with many scientists doubting the giant killing machines had the brainpower to organize into anything more complex than what is observed in modern crocodiles. Because the Canadian site appeared to be an isolated case, skeptics claimed it represented unusual circumstances that did not reflect normal tyrannosaur behavior. Discovery of a second tyrannosaur mass death site in Montana again raised the possibility of social tyrannosaurs, but this site was still not widely accepted by the scientific community as evidence for social behavior. The researcher's findings at the Unicorns and Rainbows Quarry provides even more compelling evidence that tyrannosaurs may have habitually lived in groups.