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Pancreatic cancer is an aggressive disease in which malignant cells form in the tissues of the pancreas, a long and flat gland located behind the stomach that helps with digestion and blood sugar regulation. Because pancreatic cancer is difficult to detect early, it is associated with a low survival rate, accounting for just over 3% of all new cancer cases in the U.S., but leading to nearly 8% of all cancer deaths, according to the National Cancer Institute.
Through a pre-clinical study conducted in his former role at Moffitt Cancer Center and published in Clinical Cancer Research, Said Sebti, Ph.D., associate director for basic research at VCU Massey Cancer Center, identified a novel drug that effectively thwarts pancreatic tumors that are addicted to the cancer-causing mutant KRAS gene. Sebti recently met with clinical colleagues at Massey to discuss evaluating the drug in clinical trials in patients whose pancreatic tumors harbor mutant KRAS.
“We discovered a link between hyperactivation of the CDK protein and mutant KRAS addiction, and we exploited this link preclinically to counter mutant KRAS-driven pancreatic cancer, warranting clinical investigation in patients afflicted with this deadly disease,” said Sebti, who is also the Lacy Family Chair in Cancer Research at Massey and a professor of pharmacology and toxicology at the VCU School of Medicine. “Our findings are highly significant as they revealed a new avenue to combat an aggressive form of pancreatic cancer with very poor prognosis due mainly to its resistance to conventional therapies.”
KRAS is mutated in 90 percent of pancreatic cancers. Previous research from the Sebti lab and other labs has demonstrated that some tumors that harbor mutant KRAS are actually addicted to the mutant gene, meaning they cannot survive or grow without it. Sebti set out to discover if there is a drug that can specifically kill tumors that are addicted to mutant KRAS.
Sebti and collaborators used three scientific approaches to try and answer this question.
First, they mapped out the blueprint of pancreatic cancer cells through global phosphoproteomics, which gave them a snapshot of how the addicted and non-addicted tumors differ at the phosphoprotein level. They found two proteins — CDK1 and CDK2 — which were indicative of which cells were addicted to mutant KRAS.

An interdisciplinary group of researchers from across the globe has comprehensively examined the sources and health effects of air pollution — not just on a global scale, but also individually for more than 200 countries.
They found that worldwide, more than one million deaths were attributable to the burning of fossil fuels in 2017. More than half of those deaths were attributable to coal.
Findings and access to their data, which have been made public, were published today in the journal Nature Communications.
Pollution is at once a global crisis and a devastatingly personal problem. It is analyzed by satellites, but PM2.5 — tiny particles that can infiltrate a person’s lungs — can also sicken a person who cooks dinner nightly on a cookstove.
“PM2.5 is the world’s leading environmental risk factor for mortality. Our key objective is to understand its sources,” said Randall Martin, the Raymond R. Tucker Distinguished Professor in the Department of Energy, Environmental & Chemical Engineering at Washington University in St. Louis.
Martin jointly led the study with Michael Brauer, a professor of public health at the University of British Columbia. They worked with specific datasets and tools from the Institute for Health Metrics and Evaluation at the University of Washington, the Joint Global Change Research Institute at the University of Maryland and Pacific Northwest National Laboratory, as well as other researchers from universities and organizations across the world, amassing a wealth of data, analytical tools and brainpower.

Red seaweeds have been prevalent in the diets of Asian communities for thousands of years. In a new study, published in Marine Drugs, researchers have shown how these algae confer health benefits.
“In the past, people have wondered why the number of colon cancer patients in Japan is the lowest in the world,” said Yong-Su Jin (CABBI/BSD/MME), a professor of food microbiology. “Many assumed that it was due to some aspect of the Japanese diet or lifestyle. We wanted to ask whether their seaweed diet was connected to the lower frequency of colon cancer.”
Although several studies have shown that Asians who eat seaweed regularly have lower risk of colon, colorectal, and breast cancer, it was unclear which component was responsible for the anti-cancer effects.
In the study, the researchers broke down the structure of different types of red seaweed using enzymes and tested the sugars that were produced to see which one of them caused health benefits. Among the six different sugars produced, agarotriose and 3,6-anhydro-L-galactose, or AHG, showed the most promise.
“After we produced these sugars, we tested their prebiotic activity using the bacteria Bifidobacterium longum ssp. infantis,” said Eun Ju Yun, a former postdoctoral researcher at the Carl R. Woese Institute for Genomic Biology. B. infantis is a probiotic bacterium; it colonizes the gut of infants and provides health benefits. Among the seaweed-derived sugars, the bacteria could only consume agarotriose, indicating that it works as a prebiotic i.e., it improves the growth of probiotic bacteria.
“We also tested another strain, B. kashiwanohense, and found that it also consumed agarotriose,” Jin said. “These results show us that when we eat red seaweed, it gets broken down in the gut and releases these sugars which serve as food for the probiotic bacteria. It could help explain why Japanese populations are healthier compared to others.”
The researchers also tested the sugars to see if they had any anti-cancer activity. “We found that AHG specifically inhibits the growth of human colon cancer cells and does not affect the growth of normal cells,” Yun said. The anti-cancer activity of AHG is due to its ability to trigger apoptosis or cell death.
“There is a lot of information on how red seaweeds are degraded by microorganisms in the ocean and in the human body,” said Kyoung Heon Kim, a professor of biotechnology and the co-advisor on the paper. “Our work explains why red seaweeds are beneficial by providing the molecular mechanism. We will continue studying their function in animal models and hopefully we will be able to use them as a therapeutic agent in the future.”
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Materials provided by Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign. Original written by Ananya Sen. Note: Content may be edited for style and length.

In many parts of the world, mosquitoes are a common summertime nuisance.
But in places on the front lines of climate change, these disease-spreading insects may one day be a year-round problem, according to new research from the University of Florida.
“In tropical regions, mosquitoes are active all year, but that isn’t the case for the rest of the world. Outside of the tropics, winter temperatures cause mosquitoes to go into a kind of hibernation called diapause. We call these mosquitoes ‘cold bounded’ because their activity is limited by these lower temperatures,” said Brett Scheffers, senior author of the study and an assistant professor in the UF/IFAS wildlife ecology and conservation department.
“However, with climate change, we expect summers to get longer and winters to become shorter and warmer. What will that mean for those cold bounded mosquitoes? How will they respond?” Scheffers said.
To help answer those questions, the study’s authors conducted experiments with mosquitoes collected in and around Gainesville, a North Central Florida city on the dividing line between subtropical and temperate climates. Their study is published in the journal “Ecology.”
The researchers compared how mosquitoes collected during different parts of the year responded to changes in temperature.

In updated recommendations, the federal health agency said both domestic and international travel was low risk for fully vaccinated Americans. But travel remains far from simple.The Centers for Disease Control and Prevention updated its guidance for fully vaccinated Americans in April, saying that traveling both domestically and internationally was low risk.The long-awaited recommendations were issued by federal health officials after a series of studies found that vaccines administered in the United States were robustly effective in preventing infections in real-life conditions.One is considered fully vaccinated two weeks after receiving the single dose of the Johnson & Johnson vaccine, or two weeks after receiving the second dose of the Pfizer-BioNTech or Moderna shots.If you decide to travel, you might still have some questions. Here are the answers.Will I still need to wear a mask and socially distance while traveling?Yes. Under federal law, masks must be worn at airports in the United States, onboard domestic flights and in all transport hubs. The C.D.C. says that as long as coronavirus measures are taken in these scenarios, including mask wearing, fully vaccinated Americans can travel domestically without having to take a test or quarantine, although the agency warns that some states and territories may keep their local travel restrictions and recommendations in place.For those wishing to travel internationally, a coronavirus test will not be required before departure from the United States unless mandated by the government of their destination. Vaccinated travelers are still required to get tested three days before travel by air into the United States, and are advised to take a test three to five days after their return, but will not need to self-quarantine.Can I go abroad?Yes, but only to countries that will have you. More than half the world’s countries have reopened to tourists from the United States, including some countries in the European Union, which recently reopened their borders to vaccinated travelers in anticipation of the summer tourism season. Other places like Turkey, Croatia and Montenegro have already been welcoming Americans with negative test results. Greece also joined that growing list in May, ahead of most European countries, opening to fully vaccinated tourists and other foreigners with a negative test.Many Caribbean nations have reopened to American tourists, but each has its own coronavirus protocols and entry requirements.Here’s a full list of countries Americans can currently travel to.What about domestic travel? Is it free and clear to cross state borders?If you are fully vaccinated, the C.D.C. says you can travel freely within the United States and that you do not need to get tested, or self-quarantine, before or after traveling. But some states and local governments may choose to keep travel restrictions in place, including testing, quarantine and stay-at-home orders. Hawaii, for instance, still has travel restrictions in place. Before you travel across state lines, check the current rules at your destination. How are they going to check that I’m fully vaccinated?Right now, the best way to prove that you have been vaccinated is to show your vaccine card.Digital vaccine and health certificates showing that people have been vaccinated or tested are in various stages of development around the world and are expected, eventually, to be widely used to speed up travel.The subject of “vaccine passports” is currently one of the most hotly debated topics within the travel industry, with questions over the equity of their use and concerns over health and data privacy.In early April, Gov. Ron DeSantis of Florida issued an executive order that would ban local governments and state businesses from requiring proof of vaccination for services.And in March, the European Union endorsed its own vaccine certificate, but individual European countries are still expected to set their own rules for travel requirements this summer.But what about my kids? What’s the guidance on traveling with unvaccinated people?The C.D.C. advises people against travel unless they have been vaccinated. If you must travel, the agency recommends testing one to three days before a trip and following all coronavirus guidance at your destination.In May, the F.D.A. expanded its emergency use authorization of the Pfizer-BioNTech coronavirus vaccine to include adolescents between 12 and 15 years of age.All air passengers aged two and older coming into the United States, including fully vaccinated people, are required to have a negative Covid-19 test result taken no more than three days before they board their flight.What is my moral obligation to the places I visit where most people are not vaccinated?The United States inoculation rollout has been among the fastest in the world, but there is a stark gap between its rapid rollout and the vaccination programs in different countries. Some nations have yet to report a single dose being administered.Many countries are currently seeing a surge in new cases and are implementing strict coronavirus protocols, including mask mandates in public spaces, capacity limits at restaurants and tourist sites and other lockdown restrictions.It is important to check coronavirus case rates, measures and medical infrastructure before traveling to your destination and not to let your guard down when you get there. Even though you are fully vaccinated, you may still be able to transmit the disease to local communities who have not yet been inoculated.You can track coronavirus vaccination rollouts around the world here.Follow New York Times Travel on Instagram, Twitter and Facebook. And sign up for our weekly Travel Dispatch newsletter to receive expert tips on traveling smarter and inspiration for your next vacation.

Vermont has at least partially vaccinated 80 percent of residents 12 or older, allowing it to lift all remaining state pandemic restrictions, Gov. Phil Scott announced on Monday.Federal data confirmed that the state passed the 80 percent milestone first, while lagging vaccination rates elsewhere have imperiled President Biden’s national goal of getting shots into the arms of at least 70 percent of adults over 18 by July 4.“I’m very proud to announce that Vermont has now become the first state in the nation to vaccinate over 80 percent of its 12-and-over population,” Mr. Scott said at a news conference on Monday.Vermont has been very successful at handling the coronavirus. A New York Times database shows that the state has reported fewer cases and fewer deaths, relative to its population, than any state but Hawaii. Vermont has vaccinated 83 percent of its adult population, aged 18 or older; Hawaii and Massachusetts are the only other states so far that have exceeded 80 percent by that measure.“Not only do we lead the United States, but Vermont is now a global leader in vaccinations to defeat Covid-19,” Mr. Scott said. “Our state has shown the world what’s possible when you have a group of people with the right attitude following the data and trusting medical science.”The number of new positive tests reported daily across the country seems to be leveling off after having fallen steadily for months. Experts are worried that states with low rates of vaccination, particularly in the South, could incubate new outbreaks.Mr. Scott, a Republican, lifted his state’s mask mandate and capacity restrictions for vaccinated people on May 14. He said that Vermont’s state of emergency would end on Tuesday.“It’s really very simple: There are no longer any state Covid-19 restrictions,” he said.People in Vermont still have to abide by federal pandemic regulations, and businesses will be allowed to take safety measures like requiring masks if their owners choose to do so, he said.“This is something that businesses have to decide for themselves,” Mr. Scott said.Many states have relaxed or removed most of their pandemic restrictions, including some with far lower vaccination rates than Vermont’s.Mr. Scott praised public health officials for his state’s testing program and vaccine rollout. But he noted that Vermont’s work was far from done.“We’ll continue to vaccinate as many Vermonters as possible, because every shot given today, tomorrow and in the weeks to come is just as important as the ones we administered yesterday,” he said.Amy Schoenfeld Walker contributed reporting.

An international team of researchers led by the University of Bonn (Germany) has identified the cause of a rare, severe muscle disease. According to these findings, a single spontaneously occurring mutation results in the muscle cells no longer being able to correctly break down defective proteins. As a result, the cells perish. The condition causes severe heart failure in children, accompanied by skeletal and respiratory muscle damage. Those affected rarely live beyond the age of 20. The study also highlights experimental approaches for potential treatment. Whether this hope will be fulfilled, however, will only become clear in a few years. The results are published in the journal Nature Communications.
Anyone who has ever snapped a spoke on their bike or broken down with their car knows that mechanical stresses sooner or later result in damage that needs to be repaired. This also applies to the human musculature. “With each movement, structural proteins are damaged and have to be replaced,” explains adjunct professor Dr. Michael Hesse from the Institute of Physiology at the University of Bonn, who led the study together with his colleague Prof. Dr. Bernd Fleischmann.
The defective molecules are normally broken down in the cell and their components are then recycled. An important role in this complex process is played by a protein called BAG3. The results of the new study show how important this is: The researchers were able to demonstrate that a single change in the genetic blueprint of BAG3 results in a fatal disease.
“The mutation causes BAG3 to form insoluble complexes with partner proteins that grow larger and larger,” Hesse says. This brings the repair processes to a standstill — the muscles become less and less efficient. Moreover, toxic levels of proteins accumulate over time, eventually resulting in the death of the muscle cell. “The consequences are usually first seen in the heart,” Hesse says. “There, muscle is successively replaced by scar tissue. This causes the heart’s elasticity to decrease until it can barely pump blood.”
Affected individuals therefore usually require a heart transplant in childhood. Even this measure only provides temporary relief, as the disease also affects the skeletal and respiratory muscles. As a result, sufferers often die at a young age.
Very rare condition, therefore little research
The lethal mutation can arise spontaneously during embryo development. Fortunately, this is a very rare occurrence: There are probably only a few hundred affected children worldwide. However, due to its rarity, the disease has received little research attention to date. “Our study now takes us a great deal further,” stresses Bernd Fleischmann.
This is because the researchers have succeeded for the first time in replicating the disease in mice and using the new animal model to identify its causes. This allows it to be researched better than before — also with regard to possible therapies. Maybe the effect of the mutation can at least be reduced. Humans have two versions of each gene, one from the mother and the other from the father. This means that even if one version of BAG3 mutates during embryo development, there is still a second gene that is intact.
Unfortunately, however, the defective BAG3 also clumps with its intact siblings. The mutation in one of the genes is therefore sufficient to stop the breakdown of the defective muscle proteins. However, if the mutated version could be eliminated, the repair should work again. It would also prevent the massive accumulation of proteins in the cell that eventually results in its death.
There are indeed methods to specifically inhibit the activity of individual genes. “We used one of them to treat the sick mice,” explains Kathrin Graf-Riesen of the Institute of Physiology, who was responsible for most of the experiments along with Dr. Kenichi Kimura and her colleague Dr. Astrid Ooms. The animals treated in this way then showed significantly fewer symptoms. Whether this approach can be transferred to humans, however, remains the subject of further research.
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Materials provided by University of Bonn. Note: Content may be edited for style and length.

A funny thing happened on the way to discovering how zinc impacts kidney stones — two different theories emerged, each contradicting the other. One: Zinc stops the growth of the calcium oxalate crystals that make up the stones; and two: It alters the surfaces of crystals which encourages further growth. Now it can be told — both theories are correct as reported in the America Chemical Society journal Crystal Growth & Design by Jeffrey Rimer, Abraham E. Dukler Professor of Chemical and Biomolecular Engineering at the University of Houston, who conducted the first study to offer some resolution to the differing hypotheses.
“What we see with zinc is something we haven’t seen before. It does slow down calcium oxalate crystal growth and at the same time it changes the surface of the crystals, causing defects in the form of intergrowths. These abnormalities create centers for new crystals to nucleate and grow,” reports Rimer, who refers to the effect as a double-edged sword.
The formation of kidney stones is a pathological condition that has increased in frequency among patients, leading to an increased amount of suffering and steep rise in medical costs.
Though calcium oxalate crystals are found everywhere, the most naturally abundant form of these crystals are calcium oxalate monohydrates (COM), the kind found in human kidney stone disease. Along with COM, kidney stones are composed of various hard deposits of inorganic salts and organic compounds (e.g., proteins) crystallizing or sticking together in concentrated urine. They can be severely painful to pass through the urinary tract.
In this study, Rimer and his team used a combination of in vitro experiments and computational modeling to decode the effects of zinc on COM crystal growth.
“The techniques we’re using in our lab to investigate these systems enable us to get a better picture and to deconstruct these complex systems as a means of identifying new ways to prevent kidney stone formation,” said Rimer. “These are enabling tools that allow us to understand at an almost molecular level how various species in urine can regulate crystal growth.”
Rimer’s findings on the dual role of zinc on COM was confirmed by atomic force microscopy measurements showing a unique ability of zinc ions to alter the termination of crystal surfaces.
The team compared the impact of zinc on COM, with similar ions like magnesium.
“We wondered what would happen if we used alternative ions commonly found in urine, such as magnesium, and the answer was nothing. It had little to no effect, whereas zinc had a major effect. This is an excellent demonstration of how subtle differences in the nature of various species impacts their interaction with crystal surfaces,” said Rimer.
The paper’s first author is Bryan G. Alamani, a former doctoral student of Rimer’s and now a professor at University of the Philippines Diliman. Rimer also partnered with Julian Gale, Curtin University, Perth, Western Australia.
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Materials provided by University of Houston. Original written by Laurie Fickman. Note: Content may be edited for style and length.

The diet of microbes is vast: They are able to use different molecules as nutrients, including biomolecules such as proteins and lipids of dead and decaying organisms. This includes so called extracellular DNA molecules which are not or no longer present in intact cells. “From the bacteria’s perspective DNA is particularly nutritious,” says Kenneth Wasmund, a microbiologist at the Centre for Microbiology and Environmental Systems Science (CMESS) at the University of Vienna and lead author of the study. “It’s essentially a fertilizer. After all, it is a chain of millions of pieces of sugar and phosphorus- and nitrogen-containing bases.” Extracellular DNA is common in the environment because when any organism dies, its contents, including DNA, are released into the environment. The microbes that degrade such abundant biomolecules are critical for global biogeochemical cycles as they recycle organic material settling from ocean waters, thereby also influencing how much carbon ultimately remains in the ocean floor. Yet, not all microbes are capable of using DNA as a nutrient.
Marine sediments are a massive habitat for undescribed microbes
The muddy sediments of the sea floor are a massive global habitat for these ecologically important microorganisms; after all, our oceans cover more than 70 percent of the earth’s surface. Thousands of microbial species live here, most of which are still largely unknown. “Our study identifies some of these microbial players and reveals their lifestyles. At the same time, it tells us something about what happens to the vast amounts of DNA that are constantly released into the environment but do not accumulate anywhere and, accordingly, are obviously somehow being recycled,” Kenneth Wasmund explains. Previous research has shown that microorganisms grown in the laboratory might use DNA as an energy source. “Our research has now focused on microbes that actually live and actively function in the seafloor, while using DNA as a food source,” he adds.
Deciphering bacteria that use DNA for food by functional microbiome analyses
To this end, colleagues from the University of Calgary in Canada collected samples from the seafloor in the Baffin Bay, a marginal sea of the Atlantic Ocean between Greenland and Canada. To identify and characterise DNA-foraging microbes in these samples, the research team used an array of experimental, analytical, and bioinformatic methods. “In this collaboration of all four divisions at CMESS, we made full use of the excellent research infrastructure and unleashed the full expertise for functional microbiome analyses that is present at our Centre,” says Alexander Loy, head of the research group at the University of Vienna.
In laboratory incubations, the researchers fed purified DNA that was isotopically-labelled with heavy carbon atoms (13C) to the sediment bacteria. Using stable isotope probing, including a specific isotope imaging technique, they were then able to track the heavy carbon and as a result could see which bacteria degraded the labelled DNA. In addition, the scientists reconstructed the genetic information present in the cells, i.e. the genomes, of the DNA-eating microorganisms to learn about their functional potential and distribution in the world’s oceans.
Novel DNA-eating bacteria in the seafloor
The metagenomic analysis showed that the bacteria were equipped with DNA-degrading enzymes that enable them to chop-up DNA into small pieces to help them take it up and consume it. One bacterial species stood out as it had a particularly sophisticated set of tools for degrading DNA. Their appetite for DNA, also called nucleic acid, is now borne in their name: The research team named them Izemoplasma acidinucleici.
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Materials provided by University of Vienna. Note: Content may be edited for style and length.

The human gut microbiome is a complex community of trillions of microbes that are constantly interacting with each other and our bodies. It supports our wellbeing, immune system and mental health — but how is it sustained?
Researchers in the UK and Germany, alongside other international collaborators, have investigated the evolution of bacteria in the human gut microbiome — asking how these microbes persist throughout their lifetimes — taking into account internal and external influencing factors.
The results of the study will help inform tailored probiotics, live bacteria found in particular foods or supplements, as well as dietary or medical interventions, to treat gut disease and maintain a healthy gut microbiome.
Keeping a stable, healthy gut microbial population is mutually beneficial to us and the bacteria. In exchange for nutrition and a comfortable habitat, the microbe community returns the favour by providing us with health benefits, which we are now starting to understand.
Lead author and Group Leader Dr Falk Hildebrand from the Quadram Institute and Earlham Institute, explains: “We know that certain microbes colonise us at birth, and some can live with us for decades. Yet, although studies have looked at individual microbe species, the mechanisms and scale of persistence in the microbiome as a whole haven’t been explored.”
To examine this, a team of scientists at the Earlham Institute and Quadram Institute on the Norwich Research Park, along with the European Molecular Biology Laboratory (EMBL) in Germany, used metagenomics to analyse the evolutionary strategies and persistence of different bacteria in the human gut microbiome.