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When it comes to cancer, clarity is key. The ability to visualize cancerous tumors and metastatic tissue three dimensionally (3D) can help clinicians diagnose the precise type and stage of cancer, while also informing the best treatment methods. To obtain an even clearer tissue for imaging, a research team based in Japan has tested the effectiveness of specialized hydrogels. Acting as a 3D molecular network, these hydrogels can rapidly remove fats from tissues, which are a factor in tissue opacification, without losing their structure. The material is used in several biomedical devices, including contact lenses.
They published their results online on June 21 in Macromolecular Bioscience with the print edition issued on Sep. 16.
Since 1981, the leading cause of death in Japan has been cancer,” said first author Chie Kojima, associate professor in the Department of Applied Chemistry in the Graduate School of Engineering at Osaka Prefecture University. “We need new treatment methods and diagnostic techniques. 3D fluorescence imaging is one such approach that could prove indispensable for understanding multicellular systems on the scale of an organ, as it can give us more information than traditional 2D imaging. This could be useful for personalized medicine in diagnosis, as well as elucidating biological phenomena.
This type of imaging involves tagging certain molecular machines, such as proteins, so they fluoresce with different colors depending on what they are. The glowing signals can be viewed in a variety of samples, from whole organisms down to the cellular level. Most tissues are opaque, though, blocking the ability to see these signals. In 2D imaging, the samples are sliced thinly, which makes the signals easy to see but removes the ability to visualize the full system in 3D.
Previously, researchers have used an approach known as CLARITY, in which the tissues are embedded in polyacrylamide hydrogels. The fats are removed from the tissues and the refractive index of the media is adjusted. The tagged glowing signals can be visualized in 3D, but it takes a month for the cancerous tissue to clear — far too long for a patient waiting for a diagnosis, according to Kojima. In that time, the tumor would have likely spread.
The optical clearing process time in the CLARITY method needs to be shortened for practical applications,” Kojima said.

An unprecedented review of the aquatic foods sector has uncovered how fisheries and aquaculture can play a greater role in delivering healthy diets and more sustainable, equitable and resilient food systems around the world.
Five peer-reviewed papers in the journal Nature highlight the opportunities to leverage the vast diversity of aquatic, or “blue,” foods in the coming decades to address malnutrition, lower the environmental footprint of the food system, and provide livelihoods.
“People are trying to make more informed choices about the food they eat, in particular the environmental footprint of their food,” said Ben Halpern, a marine ecologist at UC Santa Barbara’s Bren School of Environmental Science & Management, who with colleagues examined the environmental sustainability of aquatic foods, the potential for the growth of small-scale producers and the climate risks that face aquatic food systems. “For the first time we pulled together data from hundreds of studies on a wide range of seafood species to help answer that question. Blue foods stack up really well overall and provide a great option for sustainable food.”
The research projects that global demand for blue foods will roughly double by 2050, and will be met primarily through increased aquaculture production rather than by capture fisheries.
Investing in innovation and improving fisheries management could increase consumption even more and have profound effects on malnutrition. For instance, a “high growth” modeling scenario showed that increasing supply by 15.5 million tons (8%), causing a drop in prices, would reduce cases of nutrient deficiencies by 166 million, especially among low-income populations.
“Small-scale fishers — the individuals and small boats that fish in places all around the world — are a huge part of the global seafood system and are incredibly diverse in who they are and how they fish,” said Halpern, who also directs the National Center for Ecological Analysis & Synthesis at UCSB. “That diversity creates both opportunities and challenges for sustainably managing the oceans. We unpacked this diversity to help guide better management.”
Blue foods were found to rank more highly than terrestrial animal-source foods in terms of their nutritional benefits and potential for sustainability gains.

New research shows that Multiple Sclerosis (MS) patients undergoing anti-CD20 (aCD20) treatment — which depletes the B cells that contribute to the MS attacks — are able to mount robust T-cell responses to the mRNA COVID-19 vaccines, despite having a muted antibody response to the vaccines.
Because B cells are responsible for antibody production, patients’ ability to produce antibodies that prevent the virus from entering and infecting a person’s cells is significantly muted when the B cells are depleted with aCD20 treatment. But the same patients are nonetheless able to mount very good responses of the second protective arm of their immune system, which uses T cells to eliminate cells once infected (thereby preventing viral spread to other cells), according to new research from the Perelman School of Medicine at the University of Pennsylvania in a new paper published in Nature Medicine.
“The message from this study is clear — it is worthwhile for patients with MS receiving aCD20 treatment to get a COVID-19 vaccine, which will prevent severe illness,” said one of the senior authors E. John Wherry, PhD, chair of Systems Pharmacology and Translational Therapeutics and director of the Penn Institute for Immunology. “Based on this body of evidence, we urge patients with MS receiving aCD20 treatment to get a COVID-19 vaccine if they haven’t already.”
The study measured both the antibody and T cell responses in 20 patients with MS who were undergoing aCD20 treatment, compared to those in a group of healthy controls. None of the participants in the study had prior clinical signs or symptoms of COVID-19. Researchers analyzed plasma and peripheral blood mononuclear cell samples five times over the study period: prior to the first vaccine dose, 10-12 days following the first vaccine dose, prior to the second vaccine dose, 10-12 days following the second vaccine dose, and 25-30 days following the second vaccine dose.
All healthy control subjects generated both anti-spike and anti-receptor-binding domain (RBD) antibodies following the first dose of mRNA vaccine, and the level of antibody increased further after the second dose. However, in patients with MS, the antibody response was far more varied. By 30 days after the second vaccine dose, 85% of participants developed anti-spike antibodies, and 50% mounted anti-RBD responses. For those subjects who did have detectable antibodies, the magnitude of response was generally lower, and the response was delayed compared to the control group.
The timing of a patient’s last aCD20 infusion — typically administered every six months — played a significant role in the immune response mounted. Patients with MS with higher percentages of circulating B cells prior to the vaccine had more robust antibody responses to the vaccine.
“This data not only reveal that patients undergoing anti-CD20 infusions are still able to mount important COVID-19 vaccine responses which are likely to protect from severe illness, but also informs our clinical practices in how we advise patients with MS and other autoimmune disorders on such therapies,” said another of the paper’s senior authors Amit Bar-Or, MD, FRCPC director of the Center for Neuroinflammation and Experimental Therapeutics and chief of the Division of MS and Related Disorders. “For example, knowing that responses are weakest immediately following an anti-CD20 infusion, we can now advise patients to wait a number of months after their therapy to get a COVID-19 vaccine.”
Researchers found that patients who had undergone aCD20 treatments had subpopulations of T cells that responded similarly to vaccination as healthy control subjects. Patients who underwent aCD20 therapy generated robust CD4 and CD8 T cell responses to the COVID-19 vaccination. Further, the CD8 T cell response was especially robust among the subgroup of patients with MS who didn’t generate RBD antibodies. This observation reveals that even without circulating B cells, the COVID-19 vaccine effectively primed patients’ immune response to the virus.
“Often when determining if a patient mounted a proper response to an mRNA vaccine, we test for the presence of antibodies, but this method neglects an entire arm of a person’s immune response,” said one of the lead authors Sokratis A. Apostolidis, MD, a fellow in the Department of Rheumatology. “Measuring both antibodies and T-cell response gives us a more complete picture of a patient’s immune response, and reveals that patients who can’t generate antibodies as well as a healthy person are actually still protected by the COVID-19 vaccine.”
The researchers do note that due to the limited antibody responses mounted by patients receiving aCD20 treatments, they might not be able to neutralize the virus as quickly before it infects other cells, which could result in them being contagious carriers of the virus for a longer period of time.
This work was supported by grants from the NIH (AI105343, AI082630, AI108545, AI155577, AI149680, AI152236, P30-AI0450080, R01 AI118694, UC4 DK112217, T32 AR076951-01, T32 CA009140, U19AI082630, UM1 AI144288, NMSS SI-2011-37160). This work was also supported by NIH contract (Nr. 75N9301900065).
Funding was also provided by the Allen Institute for Immunology, Chen Family Research Fund, the National Multiple Sclerosis Society-American Brain Foundation Clinician Scientist Award, the Parker Institute for Cancer Immunotherapy, the Penn Center for Research on Coronavirus and Other Emerging Pathogens, the University of Pennsylvania Perelman School of Medicine COVID Fund, the University of Pennsylvania Institute for Immunology Glick COVID-19 research award, the University of Pennsylvania Perelman School of Medicine 21st Century Scholar Fund, a philanthropic gift from Jeffrey Lurie, Joel Embiid, Josh Harris, and David Blitzer, the Penn Center for Neuroinflammation and Experimental Therapeutics and the Melissa and Paul Anderson Fund.

Results of a new study led by the University of Maryland School of Public Health show that people infected with the virus that causes COVID-19 exhale infectious virus in their breath — and those infected with the Alpha variant (the dominant strain circulating at the time this study was conducted) put 43 to 100 times more virus into the air than people infected with the original strains of the virus. The researchers also found that loose-fitting cloth and surgical masks reduced the amount of virus that gets into the air around infected people by about half. The study was published in Clinical Infectious Diseases.
“Our latest study provides further evidence of the importance of airborne transmission,” said Dr. Don Milton, professor of environmental health at the University of Maryland School of Public Health (UMD SPH). “We know that the Delta variant circulating now is even more contagious than the Alpha variant. Our research indicates that the variants just keep getting better at travelling through the air, so we must provide better ventilation and wear tight-fitting masks, in addition to vaccination, to help stop spread of the virus.”
The amount of virus in the air coming from Alpha variant infections was much more — 18-times more — than could be explained by the increased amounts of virus in nasal swabs and saliva. One of the lead authors, doctoral student Jianyu Lai explained that, “We already knew that virus in saliva and nasal swabs was increased in Alpha variant infections. Virus from the nose and mouth might be transmitted by sprays of large droplets up close to an infected person. But, our study shows that the virus in exhaled aerosols is increasing even more.” These major increases in airborne virus from Alpha infections occurred before the Delta variant arrived and indicate that the virus is evolving to be better at travelling through the air.
To test whether face masks work in blocking the virus from being transmitted among people, this study measured how much SARS-CoV-2 is breathed into the air and tested how much less virus people sick with COVID-19 exhaled into the air after putting on a cloth or surgical mask. Face coverings significantly reduced virus-laden particles in the air around the person with COVID-19, cutting the amount by about 50%. Unfortunately, the loose-fitting cloth and surgical masks didn’t stop infectious virus from getting into the air.
Dr. Jennifer German, a co-author said, “The take-home messages from this paper are that the coronavirus can be in your exhaled breath, is getting better at being in your exhaled breath, and using a mask reduces the chance of you breathing it on others.” This means that a layered approach to control measures (including improved ventilation, increased filtration, UV air sanitation, and tight-fitting masks, in addition to vaccination) is critical to protect people in public-facing jobs and indoor spaces.
The study, Infectious SARS-CoV-2 in Exhaled Aerosols and Efficacy of Masks During Early Mild Infection, was published in Clinical Infectious Diseases and conducted by researchers from the University of Maryland School of Public Health, University of Maryland School of Medicine, Walter Reed Army Institute of Research, Duke-NUS Medical School, and Rice University.
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Data sets that are biased by having too many genomes from people with European ancestry can still be applied to other ancestry groups to predict their risk of developing breast and prostate cancer. Lars Fritsche of the University of Michigan and colleagues report these findings in a new study published Sept. 16 in PLOS Genetics.
Genome-wide association studies (GWAS) use hundreds or thousands of genomes to find genetic variations linked to specific traits or diseases. Ultimately, geneticists hope to use GWAS results to assign individuals a polygenic risk score (PRS) that predicts their risk of developing a complex disease involving multiple genes, such as diabetes or heart disease, based on which variations they carry. However, most known genetic risk factors, especially for cancer, are based almost exclusively on studies of individuals with European ancestry. Currently, it is unclear if these results can be used to estimate a PRS for people from other groups.
In the new study, researchers used GWAS results from people with European ancestry and data from the UK Biobank to calculate a PRS for breast and prostate cancer for people with African, East Asian, European and South Asian ancestry. They discovered that when they scaled the risk scores within each group, they could identify individuals at higher risk of breast and prostate cancer. The findings suggest it is possible to apply existing European ancestry GWAS results to provide risk scores for people with diverse ancestry.
Of course, this is only a temporary solution. The researchers emphasize that scientists must recruit more diverse participants for GWAS analyses if they hope to realize the full potential of PRS in helping to detect and prevent cancer across ethnic groups.
“Surprisingly, the use of summary statistics from very large, European-based cancer GWAS for PRS construction and their ancestry specific scaling provided meaningful predictors of cancer risk,” the researchers add. “While the performance of the breast and prostate cancer PRS was decent across all analyzed ancestry groups, the applicability of such a compromise solution needs to be evaluated on a case-by-case basis.”
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A new discovery from researchers at The University of Texas MD Anderson Cancer Center has clarified the long-established connection between inflammation and pancreatic cancer development. According to the study published today in Science, pancreatic cells display an adaptive response to repeated inflammatory episodes that initially protects against tissue damage but can promote tumor formation in the presence of mutant KRAS.
The authors demonstrated that mutant KRAS — which is found in roughly 95% of all pancreatic cancers — supports this adaptive response, leading to selective pressure to maintain the cancer-causing mutation.
“We discovered that a single transient inflammatory event induced long-term transcriptomic and epigenetic reprogramming of epithelial cells that cooperated with oncogenic KRAS to promote pancreatic tumors long after the inflammation was resolved,” said corresponding author Andrea Viale, M.D., assistant professor of Genomic Medicine. “In the setting of repeated pancreatitis, KRAS mutations can be acquired early on to limit tissue damage, suggesting the existence of a strong evolutionary pressure to select mutated cells and providing a possible explanation for the nearly universal presence of mutant KRAS in pancreatic cancers.”
Clarifying the connection between inflammation and cancer
Inflammation has long been linked to tumor development in several cancer types, but the specific reasons behind this connection were previously unclear. The research team, led by co-first authors Edoardo Del Poggetto, Ph.D., postdoctoral fellow, and I-Lin Ho, graduate student in the Viale Laboratory, sought to study the effect of pancreatitis — a condition of inflammation in the pancreas linked with a higher risk of pancreatic cancer — on pancreatic epithelial cells.
The researchers stimulated transient inflammation in a model system of inducible KRAS-driven pancreatic cancer. Inflammation caused immediate pathological changes in pancreatic cells, but they resolved within one week. However, activation of KRAS even monthsfollowing the resolution of inflammation resulted in accelerated tumor formation compared with controls, suggesting that inflammation drives long-term changes in epithelial cells that cooperate with mutant KRAS to promote cancer development.

Hundreds of cancer-linked genes play a different role in causing disease than scientists had expected.
So-called tumor suppressor genes have long been known to block cell growth, preventing cancerous cells from spreading. Mutations in these genes, scientists believed, thus allow tumors to flourish unchecked.
Now, Howard Hughes Medical Institute Investigator Stephen Elledge’s team has uncovered a surprising new action for many of these defective genes. More than 100 mutated tumor suppressor genes can prevent the immune system from spotting and destroying malignant cells in mice , Elledge, a geneticist at Brigham and Women’s Hospital, reports September 16, 2021, in the journal Science. “The shock was that these genes are all about getting around the immune system, as opposed to simply saying ‘grow, grow, grow!'” he says.
Conventional wisdom had suggested that, for the vast major of tumor suppressor genes, mutations allow cells to run amok, growing and dividing uncontrollably. But that explanation had some gaps. For example, mutated versions of many of these genes don’t actually cause rampant growth when put into cells in a petri dish. And scientists couldn’t explain why the immune system, which is normally highly proficient at attacking abnormal cells, doesn’t do more to nip new tumors in the bud.
Elledge’s newpaper offers some answers. His team probed the effects of 7,500 genes, including genes known to be involved in human cancer. A third or more of those cancer-linked genes, when mutated, trigger mechanisms that prevent the immune system from rooting out tumors, often in a tissue-specific manner.
“These results reveal a fascinating and unexpected relationship between tumor suppressor genes and the immune system,” says HHMI Investigator Bert Vogelstein, a cancer geneticist at the Johns Hopkins University who was not involved in the research.

SharecloseShare pageCopy linkAbout sharingimage source, Getty ImagesItaly is to make it compulsory for all workers to have a Covid “green pass” – proof of vaccination, a negative test or recovery from the virus.The measures are a first for Europe and some of the strictest in the world. Anyone without a pass will reportedly face suspension from work and may have their pay stopped after five days.The measure, due to come into force on 15 October, aims to boost vaccinations in a country that has been badly hit by the virus. Green pass certificates for Covid-19, provided both digitally and on paper, are already required to access Italian train stations, cinemas, restaurants, gyms and swimming pools. School staff are also required to show a pass and some teachers have reportedly been turned away from work.On Thursday, the Italian government approved a new law to extend the requirements to all workplaces and employees across all sectors, including the self-employed. Businesses and staff could face fines of up to €1,500 (£1,280) if people are found to be working without a valid green pass.It is hoped the move will encourage more people to get fully vaccinated against the coronavirus.Despite a vocal anti-vaccination minority, Italians have broadly backed the government’s vaccination campaign.Nearly 65% of Italians have now been fully vaccinated, but infections have been rising, driven by the Delta variant. The EU vaccine ‘passport’ and what it means for travelCovid vaccines: How fast is progress around the world?Covid map: Where are cases the highest?Italy has recorded more than 4.6 million cases of Covid-19 and over 130,000 coronavirus-related deaths since the start of the pandemic, according to Johns Hopkins University data. The green pass was initially introduced to make travel within the EU more efficient, and several countries have since introduced requirements for people to show the certificate for different reasons. France requires a health pass for access to restaurants, bars, planes and trains, while Austria, Cyprus and Denmark are among other EU countries to have launched similar schemes.You may also be interested in…

The experience of a fruit fly dying from cancer may seem worlds away from that of a human with a life-threatening tumor, yet University of California, Berkeley, researchers are finding commonalities between the two that could lead to ways to prolong the lives of cancer patients.
Fruit fly research is already pointing to a new anti-cancer strategy distinct from the conventional goal of destroying the tumor or cancerous cells. Instead, the research suggests, launching an attack against the destructive chemicals the cancer is throwing off could increase survival rates and improve patients’ health.
“It’s a really complementary way of thinking about therapy,” said David Bilder, UC Berkeley professor of molecular and cell biology. “You’re trying to help the host deal with the effects of the tumor, rather than killing the tumor itself.”
Jung Kim, a postdoctoral fellow in Bilder’s lab, recently discovered that tumors in fruit flies release a chemical that compromises the barrier between the bloodstream and the brain, letting the two environments mix — a recipe for disaster in numerous diseases, including infection, trauma and even obesity. In collaboration with the labs of UC Berkeley professors David Raulet and Kaoru Saijo, Kim and Bilder subsequently demonstrated that tumors in mice that release the same chemical, a cytokine called interleukin-6 (IL-6), also make the blood-brain barrier leaky.
More importantly, they were able to extend the lifespan of both fruit flies and mice with malignant tumors by blocking the effect of the cytokine on the barrier.
“The IL-6 cytokine is known to cause inflammation. What’s new here is that this tumor-induced inflammation is actually causing the blood-brain barrier to open. If we interfere with that opening process but leave the tumor alone, then the host can live significantly longer and healthier with the same tumor burden,” Bilder said.

A Purdue University engineer’s patent-pending invention could improve the quality of life for millions of people suffering from diabetic foot ulcers.
Rahim Rahimi, an assistant professor in the School of Materials Engineering, has developed a flexible polymer composite microneedle array that can overcome the physicochemical bacterial biofilm present in chronic, nonhealing wounds and deliver both oxygen and bactericidal agents simultaneously. The results have been published in ACS Applied Bio Materials.
“The biofilm acts as a shield, hindering antibiotics from reaching infected cells and tissues,” Rahimi said. “When these microneedles pierce through the shield, they absorb the fluid underneath and dissolve, which delivers the antibiotic directly to the ulcerated cells and tissues.”
Rahimi said the traditional method to bypass biofilm is for physicians to peel it off, which is painful to patients and doesn’t discriminate unhealthy tissue from healthy tissue.
“The microneedles don’t cause pain because they are not long enough to touch nerve endings in the foot,” he said. “In this published study, the team assessed the microneedles on ex vivo porcine wound models. In fewer than five minutes, the microneedles dissolved, the antibiotic was delivered and the patch was removed.”
The lack of proper treatment of infected ulcers can lead to bacteremia and sepsis. As a result, chronic wounds are one of the key causes of limb amputations.
The next step to developing the microneedles beyond the proof-of-concept stage is to find partners to conduct human tests. Rahimi has disclosed the innovation to the Purdue Research Foundation Office of Technology Commercialization. OTC has filed a patent application on the intellectual property. The innovation is available for licensing.
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