Toggle light / dark theme

Scientists identify an important protein that increases “bacterial virulence,” when mutated, changing harmless bacteria to harmful ones.

As far as humans are concerned, bacteria can be classified as either harmful, pathogenic bacteria and harmless or beneficial non-pathogenic bacteria. To develop better treatments for diseases caused by pathogenic bacteria, we need to have a good grasp on the mechanisms that cause some bacteria to be virulent. Scientists have identified genes that cause virulence, or capability to cause disease, but they do not fully know how bacteria evolve to become pathogenic.

To find out, Professor Chikara Kaito and his team of scientists from Okayama University, Japan, used a process called experimental evolution to identify molecular mechanisms that cells develop to gain useful traits, and published their findings in PLoS Pathogens. “We’re excited by this research because no one has ever looked at virulence evolution of bacteria in an animal; studies before us looked at the evolution in cells,” said Prof Kaito.

While there are ways to alleviate some symptoms, there is currently no way to prevent or cure Parkinson’s disease, so the prospect of a one-off treatment that completely eliminates it is certainly an exciting one. While such a therapy remains a while off, scientists have demonstrated an exciting proof of concept in mice, whereby inhibiting a single gene as a one-time treatment eradicated the disease entirely, and kept it at bay for the remainder of their lives.

The research was carried out at the University of California, San Diego (UCSD), and centers on a protein called PTB, which plays a role in which genes are switch on and off in a cell. The team was experimenting with techniques whereby the gene that encodes for PTB is switched off so researchers can determine the flow-on effects of a reduction in the that protein on other cell types, and found peculiar results when working with connective tissue cells called fibroblasts.

In one experiment, the team created a cell line that was permanently lacking PTB, and after a couple of weeks found that there was only a small amount of fibroblasts remaining in the dish, which was brimming with neurons instead. Building on this, the team was able to use a single treatment to inhibit the activity of PTB in mice, which reprogrammed support cells in the brain called astrocytes into neurons that produce the neurotransmitter dopamine.

Leading futurist Tracey Follows has written an article at Forbes on #transhumanism documentary IMMORTALITY OR BUST. Check it out!


Zoltan has a more radical idea of change than almost anything else you are seeing on your TV screens today but the mainstream media continue to miss him. That’s why it’s good to see he has made his own documentary film explaining to a broader audience what he’s doing, how it all works, and why they should be interested in transhumanism at all.

‘Immortality or Bust’, winner of the Breakout Award at the Raw Science Film Festival in Los Angeles, follows Zoltan on his 2 year campaign running for President of the US. The film starts by explaining his passion for this transhumanist cause and shows him building a custom-made Bluebird motorhome like his father drove when he was a kid, turning it into a mobile coffin to take him on his journey to Washington DC. There he is to deliver his Transhumanist Bill of Rights.

Tweaking an immune protein called interleukin-18 can overcome tumors that lure it into binding with a decoy receptor protein and render it harmless to cancer cells, new research in mice shows. In conjunction with the paper, published Wednesday in Nature, a company founded by senior author Aaron Ring announced $25 million in initial financing to create and commercialize a drug based on the discovery.

The approach adds another weapon to an immunotherapy arsenal that activates immune responses hijacked by cancer. Checkpoint inhibitors, for example, take the brakes off immune cells that should battle invaders. IL-18 is a cytokine that normally activates T cells and natural killer cells, two immune forces that fight infection, but it’s disarmed by the decoy wielded by tumors.

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.