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While some cholesterol is a healthy thing for properly functioning cells, too much of it can cause blockages in the arteries and heart trouble, along with a host of other negative health outcomes. Scientists have discovered a new mechanism by which a “bad” type of cholesterol gains entry to the cells, identifying a pair of proteins that work like an entry tunnel. These proteins show promise as new targets for drugs that could lower cholesterol levels in the blood to help prevent disease.

The discovery made by an international team of researchers was only possible thanks to advances in imaging technology that enabled them to inspect proteins at a near-atomic level. In this case, the team were investigating the role two proteins, NPC1 and NPC2, play in transporting low-density lipoprotein (LDL) cholesterol, often referred to as “bad” cholesterol, into our cells.

“Before 2013 we often had to theorise about how membrane proteins worked and how they functioned, but now we can actually see them, and seeing is believing,” says study author Prof Rob Yang from the UNSW in Australia. “We were able to look at the NPC1 and NPC2 proteins and see exactly the role they play in transporting this LDL cholesterol into the cell.”

NDSU researchers recently developed a new method of creating quantum dots made of silicon. Quantum dots, or nanocrystals, are tiny nanometer-scale pieces of semiconductor that emit light when their electrons are exposed to UV light. The most common application of quantum dots is in QLED displays. Through their use, digital displays have become brighter and much thinner, resulting in improvements to television and, potentially, cell-phone technology.

Because silicon is abundant and nontoxic, silicon have unique technological appeal. Silicon quantum dots are currently being used for applications such as windows that remain transparent while serving as active photovoltaic collectors of energy, and they hold promise in medicine where quantum dots are coated with organic molecules to create nontoxic fluorescent biomarkers.

While traditional methods for creating silicon quantum dots require such as silicon tetrahydride (silane) gas or , the NDSU team’s research uses a liquid form of silicon to make the tiny particles at room temperature using relatively benign components.

As part of their studies, the scientists also examined the mechanisms by which some of the modified drugs were altered by the cultured microbiomes. To understand exactly how the transformations occurred, they traced the source of the chemical transformations to particular bacterial species and to genes within those bacteria. They also showed that microbiome-derived metabolic reactions discoverable using their approach could be recapitulated in a mouse model, which is the first step in adapting the approach for human drug development.

The framework could feasibly be used to aid drug discovery by identifying potential drug-microbiome interactions early in development, and so inform on formulation changes. It could also be used during clinical trials to better analyze drug toxicity and efficacy, and be harnessed to help personalize treatment to the microbiome of each patient. This could help to predict how a certain drug will behave, and suggest changes to the therapeutic strategy if undesired effects are predicted. “Our framework identifies novel drug-microbiome interactions that vary between individuals and demonstrates how the gut microbiome might be used in drug development and personalized medicine,” the team concluded.

“This is a case where medicine and ecology collide,” said Jaime Lopez, a graduate student in the Lewis-Sigler Institute for Integrative Genomics and a co-first author on the study, who contributed the computational and quantitative analysis of the data. “The bacteria in these microbial communities help each other survive, and they influence each other’s enzymatic profiles. This is something you would never capture if you didn’t study it in a community.”


Researchers at Princeton University have developed a way of systematically evaluating how the microbial communities in our intestines can chemically transform, or metabolize, drugs that are taken orally, in ways that impact on their efficacy and potentially safety. The new methodology—which the team used to evaluate the gut microbiome’s effect on hundreds of common medications already on the market—provides a more complete picture of how gut bacteria metabolize drugs. The framework could also feasibly help in the development of drugs that are more effective, have fewer side effects, and are personalized to an individual’s microbiome.

Previous studies have examined how single species of gut bacteria can metabolize oral medications, but the new framework enables evaluation of a person’s entire intestinal microbial community. “Basically, we do not run and hide from the complexity of the microbiome, but instead, we embrace it,” said Mohamed S. Donia, PhD, assistant professor of molecular biology. “This approach allows us to gain a holistic and more realistic view of the microbiome’s contribution to drug metabolism.”

Donia and colleagues reported on their findings in Cell, in a paper titled, “Personalized Mapping of Drug Metabolism by the Human Gut Microbiome.”

The loose alliance, whose backers include Infosys Ltd. co-founders Nandan Nilekani and Kris Gopalakrishnan as well as prominent startups from Practo to Policybazaar, will be formally unveiled as soon as this week in an attempt to salvage a decrepit system by digitizing everything from patient data and records to creating online platforms for hospital care and doctor consultations. Called Swasth — meaning health in Hindi — its 100-plus members have pledged to build new services and coordinate efforts to improve emergency responses.


Some of India’s richest people form an alliance with tech entrepreneurs to fix the country’s broken healthcare system.

A team of researchers at Memorial Sloan Kettering Cancer Center (MSK) reported on the epidemiology of COVID-19 illness experienced at an NCI-designated during the height of pandemic in New York City.

The characterization of COVID-19 in patients with cancer remains limited in published studies and nationwide surveillance analyses. Reports from China and Italy have raised the possibility that patients with cancer on active therapy have a higher risk of COVID-19 related severe events, although there is a knowledge gap as to which aspects of cancer and its treatment increase the risk of severe COVID-19 .

According to a new study from Memorial Sloan Kettering published June 24 in Nature Medicine, patients in active who develop COVID-19 infection don’t fare any worse than other hospitalized patients. Notably, , recent chemotherapy, or within the previous 30 days did not show a significant association with either hospitalization or severe respiratory illness due to COVID-19. Researchers say their findings suggest that no one should delay cancer treatment because of concerns about the virus.

Xiang-Dong Fu, PhD, has never been more excited about something in his entire career. He has long studied the basic biology of RNA, a genetic cousin of DNA, and the proteins that bind it. But a single discovery has launched Fu into a completely new field: neuroscience.

For decades, Fu and his team at University of California San Diego School of Medicine studied a protein called PTB, which is well known for binding RNA and influencing which genes are turned “on” or “off” in a cell. To study the role of a protein like PTB, scientists often manipulate cells to reduce the amount of that protein, and then watch to see what happens.


But then he noticed something odd after a couple of weeks — there were very few fibroblasts left. Almost the whole dish was instead filled with neurons.

In this serendipitous way, the team discovered that inhibiting or deleting just a single gene, the gene that encodes PTB, transforms several types of mouse cells directly into neurons.

More recently, Fu and Hao Qian, PhD, another postdoctoral researcher in his lab, took the finding a big step forward, applying it in what could one day be a new therapeutic approach for Parkinson’s disease and other neurodegenerative diseases. Just a single treatment to inhibit PTB in mice converted native astrocytes, star-shaped support cells of the brain, into neurons that produce the neurotransmitter dopamine. As a result, the mice’s Parkinson’s disease symptoms disappeared.

A trove of DNA sequences from 141,456 people — and counting — offers researchers an unparalleled look at genetic variation across the general population1,2. The resource has been helping researchers to identify variants that contribute to autism since it was released online about four years ago3,4.

The genomes of autistic people harbor hundreds of potentially harmful mutations. But to firmly connect a specific variant to the condition, researchers need to see if it is common among typical people — a sign that that variant may actually be benign.

In 2014, researchers debuted one of the first tools to probe the prevalence of a mutation in the general population. Known as the Exome Aggregation Consortium (ExAC), it contained 60,000 sequences of exomes — the protein-coding regions of the genome5.

How does the neural activity evoked by visual stimuli support visual awareness? In this paper we report on an individual with a rare type of neural degeneration as a window into the neural responses underlying visual awareness. When presented with stimuli containing faces and target words—regardless of whether the patient was aware of their presence—the neurophysiological responses were indistinguishable. These data support the possibility that extensive visual processing, up to and including activation of identity, can occur without resulting in visual awareness of the stimuli.

Visual awareness is thought to result from integration of low- and high-level processing; instances of integration failure provide a crucial window into the cognitive and neural bases of awareness. We present neurophysiological evidence of complex cognitive processing in the absence of awareness, raising questions about the conditions necessary for visual awareness. We describe an individual with a neurodegenerative disease who exhibits impaired visual awareness for the digits 2 to 9, and stimuli presented in close proximity to these digits, due to perceptual distortion. We identified robust event-related potential responses indicating 1) face detection with the component and 2) task-dependent target-word detection with the P3b component, despite no awareness of the presence of faces or target words.

The number of deaths linked to a Listeria outbreak from meat products in 2019 has doubled.

It had been thought 21 people were infected with Listeria monocytogenes in the Netherlands and Belgium. One person fell sick in October 2017, eight in 2018, and 12 in 2019. Three people died. All patients were hospitalized and one woman had a miscarriage. Two Dutch patients were pregnant women in their 30s. The others were from 64 to 94 years old and 10 were men.

Now it is known that Listeria in processed meats from Offerman, a Ter Beke subsidiary, made 35 people sick. Two women miscarried and six patients died. The information was revealed in the Dutch Food and Consumer Product Safety Authority’s (NVWA) annual report.