New research amongst the world’s biggest consumers of dairy foods has shown that those with higher intakes of dairy fat — measured by levels of fatty acids in the blood — had a lower risk of cardiovascular disease compared to those with low intakes. Higher intakes of dairy fat were not associated with an increased risk of death.
Researchers then combined the results of this study in just over 4,000 Swedish adults with those from 17 similar studies in other countries, creating the most comprehensive evidence to date on the relationship between this more objective measure of dairy fat consumption, risk of cardiovascular disease (CVD) and death.
Dr Matti Marklund from The George Institute for Global Health, Johns Hopkins Bloomberg School of Public Health, and Uppsala University said that with dairy consumption on the rise worldwide, a better understanding of the health impact was needed.
“Many studies have relied on people being able to remember and record the amounts and types of dairy foods they’ve eaten, which is especially difficult given that dairy is commonly used in a variety of foods.
“Instead, we measured blood levels of certain fatty acids, or fat ‘building blocks’ that are found in dairy foods, which gives a more objective measure of dairy fat intake that doesn’t rely on memory or the quality of food databases,” he added.
“We found those with the highest levels actually had the lowest risk of CVD. These relationships are highly interesting, but we need further studies to better understand the full health impact of dairy fats and dairy foods.”
Dairy and dairy product consumption in Sweden is among the highest worldwide. An international collaboration between researchers in Sweden, the US and Australia assessed dairy fat consumption in 4150 Swedish 60-year-olds by measuring blood levels of a particular fatty acid that is mainly found in dairy foods and therefore can be used to reflect intake of dairy fat.

A group of researchers including a Concordia PhD student have developed a new method of bioprinting adult neuron cells. They’re using a new laser-assisted technology that maintains high levels of cell viability and functionality.
PhD candidate and 2020-21 Public Scholar Hamid Orimi and his co-authors present the feasibility of a new bioprinting technology they developed in a recent paper published in the journal Micromachines. They demonstrate how the methodology they created, called Laser-Induced Side Transfer (LIST), improves on existing bioprinting techniques by using bioinks of differing viscosities, allowing for better 3D printing. Orimi, his Concordia co-supervisor Sivakumar Narayanswamy in the Gina Cody School of Engineering and Computer Science, CRHMR co-supervisor Christos Boutopoulos and co-authors at the Université de Montréal first presented the method in the Nature journal Scientific Reports in 2020.
Orimi co-wrote the newer paper with lead author Katiane Roversi, Sebastien Talbot and Boutopoulos at UdeM and Marcelo Falchetti and Edroaldo da Rocha at Federal University of Santa Catarina in Brazil. In it, the researchers demonstrate that the technology can be used to successfully print sensory neurons, a vital component of the peripheral nervous system. This, they say, is promising for the long-term development of bioprinting’s potential, including disease modelling, drug testing and implant fabrication.
Viable and functional
The researchers used dorsal root ganglion (DRG) neurons from the peripheral nervous system of mice to test their technology. The neurons were suspended in a bioink solution and loaded into a square capillary above a biocompatible substrate. Low-energy nanosecond laser pulses were focused on the middle of the capillary, generating microbubbles that expanded and ejected a cell-laden microjet onto the substrate below it. The samples were briefly incubated, then washed and re-incubated for 48 hours.
The team then ran several tests to measure the printed cells’ capacities. A viability assay found that 86 per cent of the cells remained alive two days after printing. The researchers note that viability rates improved when the laser used lower energy. The thermomechanics associated with higher laser energy use was more likely to damage the cells.
Other tests measured neurite outgrowth (in which developing neurons produce new projections as they grow in response to guidance cues), neuropeptide release, calcium imaging and RNA sequencing. Overall, the results were generally encouraging, suggesting that the technique could be an important contribution to the field of bioprinting.
Good for people and animals
“In general, people often leap to conclusions when we talk about bioprinting,” Orimi says. “They think that we can now print things like human organs for transplants. While this is a long-term objective, we are very far from that point. But there are still many ways to use this technology.”
Nearest at hand is drug discovery. The team hopes to get approval to continue their research into cell grafting, which can assist greatly in drug discovery, such as for nerve recovery medicines.
Another advantage to using this technology, Orimi says, is a decrease in animal testing. This not only has a humanitarian aspect — fewer animals will be euthanized to carry out experiments meant to benefit humans — but it will also produce more accurate results, since testing will be carried out on human, not animal, tissue.
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Materials provided by Concordia University. Original written by Patrick Lejtenyi. Note: Content may be edited for style and length.

If I’m the only person wearing a mask in a store or other indoor location, am I really protected from infection?It’s true that masks work best when everyone in the room is wearing one. That’s because when an infected person wears a mask, a large percentage of their exhaled infectious particles are trapped, stopping viral spread at the source. And when fewer viral particles are floating around the room, the masks others are wearing would likely block those that have escaped.But there is also plenty of evidence showing that masks protect the wearer even when others around them are mask-free. The amount of protection depends on the quality of the mask and how well it fits. During a hotel outbreak in Switzerland, for instance, several employees and a guest who tested positive for the coronavirus were wearing only face shields (with no masks); those who wore masks were not infected. And a Tennessee study found that communities with mask mandates had lower hospitalization rates than areas where masks weren’t required.“Health care workers, scientists who work with nasty pathogens, and workers who may be exposed to hazardous airborne particles on the job rely on specialized masks like N95s for protection, so we know that properly-fitted, high-efficiency masks work,” said Linsey Marr, a Virginia Tech engineering professor and one of the world’s leading experts on viral transmission.A number of laboratory studies have also documented that a mask protects the person who is wearing it, though the level of that protection can vary depending on the type of mask, the material its made from, the experimental setup and how particle exposure was measured. But the bottom line of all the studies is that a mask reduces the potential exposure of the person wearing it. Here are some of the findings.One study from the Centers for Disease Control and Prevention found that a standard surgical mask only protected the wearer from about 7.5 percent of the particles generated by a simulated cough. But knotting the loops and tucking in the sides of the medical mask reduced exposure by nearly 65 percent. (Watch this video to see the “knot and tuck” method.) Covering the surgical mask with a cloth mask, a technique known as double masking, reduced exposure to the simulated cough particles by 83 percent.A Virginia Tech study looked at how well homemade masks, surgical masks and face shields protected the wearer, based on particle size. The research showed that most masks could block very large particles, like those from a sneeze. But when the researchers looked at smaller aerosol particles that are hardest to block, protection ranged from near zero with a face shield to about 30 percent protection with a surgical mask. (The percentages in the study can’t be directly compared to the C.D.C. knot-and-tuck study because the testing methods were different.) Based on the findings, Dr. Marr and her colleagues concluded that a two-layer cloth mask made of flexible, tightly-woven fabric, combined with a filter material (like a coffee filter or surgical mask), could offer good protection, reducing 70 percent of the most penetrating particles and trapping 90 percent or more of the larger particles. They also found that head straps or ties created a better fit than ear loops.A study from Tokyo tested how well different types of masks protected the wearer from actual coronavirus particles. The study showed that even a simple cotton mask offered some protection (17 to 27 percent) to the wearer. Medical masks performed better, including a surgical mask (47 to 50 percent protection), a loose fitting N95 (57 to 86 percent protection) and a tightly sealed N95 (79 to 90 percent protection).While many lab studies test masks using mannequin heads, a 2008 study used real people to measure how well masks could protect the wearer against a respiratory virus. The study subjects wore different kinds of masks fitted with special receptors that could measure particle concentration on both sides of the masks. In this study, cloth masks reduced exposure by 60 percent, surgical masks by 76 percent and N95 masks by 99 percent.Getty ImagesWhile the lab studies all show a mask can protect the wearer, how well the masks perform in the real world depends on a number of variables, including how consistently people use them, whether a person is in high-risk situations and the rate of infection in the community. A Danish study of 6,000 participants, half of whom were told to wear masks, didn’t show a benefit to mask wearing, but the study has been widely criticized for its poor design. The laboratory studies showed that a high-quality medical mask, like an N95, KN95 or KF94, works best. While vaccination is the best protection against Covid-19, even vaccinated people are advised to avoid crowds or large groups indoors when the vaccination status of others isn’t known. Given that the Delta variant is far more contagious than other variants, Dr. Marr also recommended wearing the highest-quality mask possible when you can’t keep your distance or be outdoors — or when nobody around you is masking up.“If I’m in a situation where I have to rely solely on my mask for protection — unvaccinated people may be present, it’s crowded, I don’t know anything about the ventilation — I would wear the best mask in my wardrobe, which is an N95,” said Dr. Marr. “Because Delta has proved to be so much more easily transmitted and because vaccinated people can transmit, we need to wear the best masks possible in high-risk situations.”

A new guideline has been developed to help scientists publish their research accurately and transparently. Published in JAMA, the AGReMA Statement (A Guideline for Reporting Mediation Analyses) provides recommendations for researchers who want to describe mediation analysis in their paper. Mediation analysis is primarily used to understand how an intervention works or why it does not.
The checklists can be found on the AGReMA website, and the explanation and elaboration paper in JAMA explains the importance of each item and how the checklist can be used by authors, peer reviewers and journal editors.
Hopin Lee, NHMRC Postdoctoral Research Fellow at NDORMS and lead author explained: “The use of mediation analysis has grown rapidly over the past ten years across a wide range of disciplines. Our research has shown that their reporting has been poor and inconsistent, which makes it difficult to understand how the research was conducted and how reliable the findings are. We hope that the AGReMA statement will fix some of these issues.”
Gary Collins, director of the UK EQUATOR centre noted: “AGReMA was developed through a rigorous evidence- and consensus-based process using the EQUATOR methodological framework. We think it will be a useful tool for many researchers conducting mediation analyses of trials and observational studies.”
Developed by an international team of methodologists, statisticians, clinical trialists, epidemiologists, psychologists, applied clinical researchers, clinicians, implementation scientists, evidence synthesis experts, representatives from the EQUATOR Network, and journal editors, the consensus-based checklist provides detailed steps to help researchers present clear and transparent reports that will raise the standard of reporting of mediation analyses.
“AGReMA is not tied to a particular disease condition or subspecialty of medicine,” said Hopin. “Our working group will liaise with journal editors and funding agencies to increase awareness and encourage its use. Our hope is that it will be endorsed by journal editors, peer reviewers, and authors and improve the accuracy, completeness and consistency in reporting mediation analyses.”
The development of AGReMA was supported by the Berkeley Initiative for Transparency in the Social Sciences, the Center for Effective Global Action, and the Laura and John Arnold Foundation.
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Materials provided by University of Oxford. Note: Content may be edited for style and length.

Charles Darwin was obsessed with domestic pigeons. He thought they held the secrets of selection in their beaks. Free from the bonds of natural selection, the 350-plus breeds of domestic pigeons have beaks of all shapes and sizes within a single species (Columba livia). The most striking are beaks so short that they sometimes prevent parents from feeding their own young. Centuries of interbreeding taught early pigeon fanciers that beak length was likely regulated by just a few heritable factors. Yet modern geneticists have failed to solve Darwin’s mystery by pinpointing the molecular machinery controlling short beaks — until now.
In a new study, biologists from the University of Utah discovered that a mutation in the ROR2 gene is linked to beak size reduction in numerous breeds of domestic pigeons. Surprisingly, mutations in ROR2 also underlie a human disorder called Robinow syndrome.
“Some of the most striking characteristics of Robinow syndrome are the facial features, which include a broad, prominent forehead and a short, wide nose and mouth, and are reminiscent of the short-beak phenotype in pigeons,” said Elena Boer, lead author of the paper who completed the research as a postdoctoral fellow at the U and is now a clinical variant scientist at ARUP Laboratories. “It makes sense from a developmental standpoint, because we know that the ROR2 signaling pathway plays an important role in vertebrate craniofacial development.”
The paper published in the journal Current Biology on Sept. 21, 2021.
Mapping genes and skulls
The researchers bred two pigeons with short and medium beaks — the medium-beaked male was a Racing Homer, a bird bred for speed with a beak length similar to the ancestral rock pigeon. The small-beaked female was an Old German Owl, a fancy pigeon breed that has a little, squat beak.

Cancer-fighting immune cells in patients with lung cancer whose tumors do not respond to immunotherapies appear to be running on a different “program” that makes them less effective than immune cells in patients whose cancers respond to these immune treatments, suggests a new study led by researchers at the Johns Hopkins Kimmel Cancer Center Bloomberg~Kimmel Institute for Cancer Immunotherapy.
The findings, published in the August 5 issue of Nature, could lead to new ways to overcome tumor resistance to these treatments.
“Cancer immunotherapies have tremendous promise, but this promise only comes to fruition for a fraction of patients who receive them,” says study leader Kellie N. Smith, Ph.D., assistant professor of oncology and Johns Hopkins Bloomberg~Kimmel Institute of Immunotherapy investigator. “Understanding why patients do or don’t respond could help us raise these numbers.”
Cancer immunotherapies have gained traction in recent years as a way to harness the immune system’s inherent drive to rid the body of malignant cells, Smith explains. One prominent type of immunotherapy, known as checkpoint inhibitors, breaks down molecular defenses that allow cancer cells to masquerade as healthy cells, enabling immune cells known as CD8 T cells to attack the cancer cells. Different populations of these immune cells recognize specific aberrant proteins, which prompt them to kill malignant cells as well as cells infected by various viruses.
Although checkpoint inhibitors have shown tremendous success in some cancer types — even sometimes eradicating all evidence of disease — the portion of patients with these dramatic responses is relatively low. For example, only about a quarter of patients with non-small cell lung cancer (NSCLC) have significant responses to these treatments.
Searching for differences between responders and nonresponders, Smith and her colleagues turned to results of a previous immunotherapy study. They gathered blood, tumor and healthy tissue samples taken from 20 early-stage NSCLC patients who took part in the previous study, which tested the effects of administering immune checkpoint inhibitors before surgery to remove tumors. Nine of the patients had a dramatic response to checkpoint inhibitors, with 10% or less of their original tumors remaining at the time of surgery. The other 11 patients were nonresponders and had either significantly lower responses or no response at all.
After isolating CD8 T cells from each of these samples, the researchers used a technology developed at Johns Hopkins called MANAFEST (Mutation Associated NeoAntigen Functional Expansion of Specific T cells) to search specifically for those cells that recognize proteins produced by cancerous mutations (known as mutation-associated neoantigens, or MANA), influenza or Epstein-Barr, the virus that causes infectious mononucleosis. They then analyzed these cells using a commercially available technique called single cell transcriptomics to see which genes were actively producing proteins in individual cells — the “program” that these cells run on.
The researchers found that responders and nonresponders alike had similarly sized armies of CD8 T cells in their tumors, with similar numbers of cells in both populations that respond to MANA, influenza and Epstein-Barr. However, when they compared the transcriptional programs between responders and nonresponders, they found marked differences. MANA-oriented CD8 T cells from responders showed fewer markers of exhaustion than those in nonresponders, Smith explains. Responders’ CD8 cells were ready to fight when exposed to tumor proteins and produced fewer proteins that inhibit their activity, she says. In one patient who showed a complete response to checkpoint inhibitors — no evidence of active cancer by the time of surgery — the MANA-oriented CD8 T cells had been completely reprogrammed to serve as effective cancer killers. In contrast, nonresponders’ MANA-oriented CD8 T cells were sluggish, with significantly more inhibitory proteins produced.
Both responders and nonresponders’ MANA-, influenza- or Epstein-Barr-oriented CD8 T cells had significant differences in their programming as well. The MANA-oriented cells tended to be incompletely activated compared with the other CD8 T cell types. The MANA-oriented cells were also significantly less responsive to interleukin-7, a molecule that readies immune cells to fight, compared with influenza-oriented cells.
Together, Smith says, these findings suggest numerous differences in MANA-oriented cells between checkpoint inhibitor responders and nonresponders that could eventually serve as drug targets to make nonresponders’ CD8 T cells act more like responders’ — both for NSCLC and a broad array of other cancer types.
“By learning how to reprogram these immune cells, we could someday facilitate disease-free survival for more people with cancer,” says Smith. She adds that “an important and interesting finding was that nonresponders had cells that recognized the tumor. So there is ‘hope’ for developing treatments for patients who don’t respond to single agent immunotherapy. We just need to figure out the right target to activate these cells to help them do what they were made to do.”

The EVONANO platform allows scientists to grow virtual tumours and use artificial intelligence to automatically optimise the design of nanoparticles to treat them.
The ability to grow and treat virtual tumours is an important step towards developing new therapies for cancer. Importantly, scientists can use virtual tumours to optimise design of nanoparticle-based drugs before they are tested in the laboratory or patients.
The paper, ‘Evolutionary computational platform for the automatic discovery of nanocarriers for cancer treatment,’ is published today in the Nature journal Computational Materials. The paper is the result of the European project EVONANO which involves Dr Sabine Hauert and Dr. Namid Stillman from the University of Bristol, and is led by Dr Igor Balaz at the University of Novi Sad.
“Simulations enable us to test many treatments, very quickly, and for a large variety of tumours. We are still at the early stages of making virtual tumours, given the complex nature of the disease, but the hope is that even these simple digital tumours can help us more efficiently design nanomedicines for cancer,” said Dr Hauert.
Dr Hauert said having the software to grow and treat virtual tumours could prove useful in the development of targeted cancer treatments.
“In the future, creating a digital twin of a patient tumour could enable the design of new nanoparticle treatments specialised for their needs, without the need for extensive trial and error or laboratory work, which is often costly and limited in its ability to quickly iterate on solutions suited for individual patients,” said Dr Hauert.

A team of engineers and biotechnologists at the University of Freiburg has for the first time shown in mammals that the concentration of antibiotics in the body can be determined using breath samples. The breath measurements also corresponded to the antibiotic concentrations in the blood. The team’s biosensor — a multiplex chip that allows simultaneous measurement of several specimens and test substances — will in future enable personalized dosing of medicines against infectious diseases on-site and help to minimize the development of resistant strains of bacteria.
The sensor developed by the research group headed by Dr. Can Dincer and H. Ceren Ates, FIT Freiburg Center for Interactive Materials and Bioinspired Technologies, and Prof. Dr. Wilfried Weber, Professor of Synthetic Biology and a member of the team of speakers at the Cluster of Excellence CIBSS — Centre for Integrative Biological Signalling Studies, is based on synthetic proteins that react to antibiotics and thus generate a current change. The researchers’ results are now being published in the journal Advanced Materials.
Previously researchers could only detect traces of antibiotics in the breath
The researchers tested the biosensor on the blood, plasma, urine, saliva and breath samples of pigs who had received antibiotics. They were able to show that the result achieved with biosensors in the pigs’ plasma were as accurate as the standard medical laboratory process. Previously, measurement of antibiotic levels in exhaled breath samples was not possible: “Until now researchers could only detect traces of antibiotics in the breath. With our synthetic proteins on a microfluidic chip, we can determine the smallest concentrations in the breath condensate and they correlate with the blood values,” explains Dincer.
Sensor will help to keep antibiotic level stable in severely ill
Physicians need to keep the antibiotics level within a personalized therapeutic range for patients suffering severe infections, at the risk of threats such as sepsis and organ failure or even the death of the patient. Inadequate administration of antibiotics could allow bacteria to mutate so that the medicines no longer work: they become resistant. “Rapid monitoring of antibiotic levels would be a huge advantage in hospital,” says Ates, “it might be possible to fit the method into a conventional face mask.” In another project at the University of Freiburg, Dincer is developing wearable paper sensors for the continuous measurement of biomarkers from exhaled breath. Clinical trials to validate the antibiotic biosensor by testing the system with human samples are planned.
Bacterial proteins as sensor
The microfluidic biosensor bears proteins that can recognize beta-lactam antibiotics such as penicillin, affixed to a polymer film. Antibiotic of interest in the sample and an enzyme-coupled beta-lactam are in competition to bind these bacterial proteins. This competition generates a current change — like in a battery: the more antibiotic there is present in the sample, the less enzyme product develops, which leads to a lower measurable current. The process is based on a natural receptor protein that resistant bacteria uses to detect the antibiotics that threatens them. “You could say we are beating the bacteria at their own game,” Weber says of the process developed by his group.
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Materials provided by University of Freiburg. Note: Content may be edited for style and length.

Patients in most countries of the world do not have access to basic cancer medicines, according to new research from King’s College London Global Oncology Group Professor Richard Sullivan and collaborators at Kingston University and the World Health Organization. Their paper, published in The Lancet Oncology, asked oncologists worldwide to list the most important cancer medicines and to describe whether patients could access these medicines in their home country.
The World Health Organization (WHO) has updated and released an Essential Medicines List (EML) every two years since 1977. This list helps policy-makers worldwide prioritize which medicines to provide for patients.
Professor Sullivan and the international team surveyed 948 frontline cancer doctors from 82 countries to learn which cancer medicines they considered the most important for patient care
The research team found that the most important medicines identified by oncologists are primarily older inexpensive chemotherapy and hormone medicines. With one exception, all of the top 20 high-priority cancer medicines are already included on the EML. Oncologists consider these medicines to be the most important because they have large benefits for patients across many common cancers.
15 of 20 medications are common to all three top 20 lists, however although the list for low-income and lower-middle-income countries does not include any immunotherapy agents and the only hormone therapy listed is tamoxifen, the lists for upper-middle-income countries and high-income countries include and newer hormonal treatments.
The paper also reports that in most health systems, patients are unable to afford even these basic cancer medicines. In lower and middle-income countries, most patients face major financial barriers to accessing anticancer medications — even older, generic, and inexpensive chemotherapy drugs. Financial barriers also exist in many high-income countries.
Professor Richard Sullivan, from King’s College London, said: “Our study demonstrates that the most important cancer medicines are not sufficiently prioritized by many government health systems. This leads to limited access to even the most fundamental regimens for cancer care. The primary reason why medicines are not available to patients is because they are not affordable. This is tragic as most of these medicines are older generic drugs and provide major benefits to patients. These problems are most pressing in low-middle and upper-middle income countries where the rates of cancer are most rapidly escalating” the researchers found.
He added: “There is an urgent need for global and country-level policy action to ensure patients with cancer globally have access to affordable high priority effective medicines.”
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In a new paper published in Nature, scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, describe the structure of a key protein on the surface of the hepatitis C virus (HCV) and how it interacts with its receptor found on some human cells. The findings provide new leads for developing an HCV vaccine. Hepatitis C is one of the most common bloodborne infections in the United States. Although it may not cause any symptoms in its early stages, untreated chronic infections can lead to severe liver damage, cancer, and death. Concerningly, infections are on the rise among young adults, largely due to exposure resulting from shared drug-injectables. No vaccine is available to prevent HCV infection.
HCV is usually transmitted via blood, such as during birth or when drug-injection equipment is shared. Because HCV may not cause any symptoms for years after initial infection, infections often go undetected. According to the U.S. Centers for Disease Control and Prevention, an estimated 2.4 million people are living with hepatitis C infection in the United States. More than half of all people infected with HCV are thought to develop chronic infection. HCV is a leading cause of cirrhosis, liver failure requiring transplant, and the leading cause of death from liver disease. Although effective antiviral drugs are available to treat HCV infection, they are expensive and do not prevent reinfection.
In their new paper in Nature, researchers from NIAID and other organizations describe the interaction between a protein expressed on the surface of the HCV, known as HCV E2, and a receptor called CD81 found on the surface of some human cells. Prior research had shown that antibodies interfered with interactions between these two proteins. This suggested that the interaction between HCV E2 and CD81 allowed HCV to enter and infect human cells. However, exactly how this occurred was unknown.
The researchers determined the exact structure of HCV E2 and CD81 and studied how the two proteins interacted when exposed to each other under different conditions. They found that under acidic conditions, HCV E2 easily binds to the CD81 receptor. Once the interaction between virus and receptor begins, HCV E2 changes shape, facilitating its entrance into the cell by putting the virus in closer contact with the cell membrane.
Identifying these structures and the ways they interact with each other may provide the foundation for a vaccine against HCV, the researchers say. A vaccine potentially could cause a person to make specific antibodies that prevent HCV E2 from binding with CD81, stopping the virus from entering the cell, and preventing HCV infection.
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Materials provided by NIH/National Institute of Allergy and Infectious Diseases. Note: Content may be edited for style and length.