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Category: biotech/medical – Page 34

Scientists now know why ovarian cancer spreads so rapidly in the abdomen

Ovarian cancer kills more women than any other gynecological cancer. Most patients receive their diagnosis only after the disease spreads throughout the abdomen. Until now, scientists have never fully understood why this cancer advances so fast.

A new study led by Nagoya University explains why. Published in Science Advances, the study shows that cancer cells recruit help from protective mesothelial cells that normally line the abdominal cavity. Mesothelial cells lead the invasion and cancer cells follow the pathways they create. These hybrid cell clusters resist chemotherapy better than cancer alone.

Researchers examined abdominal fluid from ovarian cancer patients and found something unexpected. Cancer cells do not float alone in the abdominal cavity. Instead, they often grab onto mesothelial cells and form hybrid spheres. About 60% of all cancer spheres contain these recruited mesothelial cells. The cancer cells release a protein called TGF-β1 that transforms the mesothelial cells and causes them to develop spike-like structures that cut through tissue.

ABCA1 protein releases molecular brakes on solid tumor immunotherapy, study finds

In recent years, cancer researchers have made major breakthroughs by using the body’s immune system to fight cancer. One of the most promising approaches, known as immune checkpoint blockade, works by releasing molecular “brakes” on T cells. This allows them to better recognize and attack cancer cells. While these therapies can be very effective for some patients, many solid tumors, including most forms of breast cancer, remain largely unaffected. Cancer Center at Illinois (CCIL) Program Co-leader Erik Nelson and his research group are working to understand why these treatments fail.

Elevated blood concentrations of cholesterol have long been linked to cancer outcomes. In a new study, they found that a protein called ABCA1 is involved in transporting cholesterol out of a type of immune cell called macrophages, and in so-doing shifts them to an “attack cancer” mode.

“Immune based therapies have revolutionized how we can treat cancer, basically taking the brakes off of a type of immune cell called T cells so they can attack cancer,” Nelson said. “While this approach works well for some patients, many so-called solid tumors fail to respond or develop resistance mechanisms.”

DNA marker in malaria mosquitoes may be pivotal in tackling insecticide resistance

A new study has detected a DNA marker in a gene encoding a key enzyme known as cytochrome P450 that helps mosquitoes to break down and survive exposure to pyrethroids, the main insecticides used for treating bed nets. This new finding, published on the bioRxiv preprint server and slated for publication in Science Translational Medicine, will help to better implement insecticide resistance management strategies and contribute to reducing the burden of malaria in sub-Saharan Africa, home to 90% of cases globally.

The work was jointly led by Liverpool School of Tropical Medicine and the Centre for Research in Infectious Diseases (CRID) in Cameroon.

Professor Charles Wondji, Professor of Genetics and Vector Biology at Liverpool School of Tropical Medicine and lead author on the study, said, “Our study designed field-applicable tools to easily track the spread of metabolic resistance in the major malaria mosquito species and assess its impact on control interventions. These important findings can help to maintain the effectiveness of insecticide-based tools such as bed nets, which remain a cornerstone of malaria prevention.”

Mutation in one Parkinson’s protein eases cellular traffic jams caused by another

A hallmark of Parkinson’s disease is the buildup of Lewy bodies—misfolded clumps of the protein known as alpha-synuclein. Long before Lewy bodies form, alpha-synuclein can interfere with neurons’ ability to transport proteins and other cargo along their axons to the synapses. When present at high levels, alpha-synuclein binds too tightly to structures inside the axon, creating the cellular equivalent of traffic jams. These disruptions may even help set the stage for the later accumulation of Lewy bodies in the brain.

Now, University at Buffalo researchers have identified a way to reduce these traffic jams and restore flow—by altering how alpha-synuclein interacts with another Parkinson’s-related protein known as leucine-rich repeat kinase 2 (LRRK2).

In a study published last month, the researchers increased levels of specific mutant forms of LRRK2 in fruit fly larvae. They found that one mutation had a downstream effect on alpha-synuclein, limiting its ability to bind to cargo and disrupt axonal transport. The research is published in the journal Frontiers in Molecular Neuroscience.

Self-regulating living implant could end daily insulin injections

A pioneering study marks a major step toward eliminating the need for daily insulin injections for people with diabetes. The study was led by Assistant Professor Shady Farah of the Faculty of Chemical Engineering at the Technion—Israel Institute of Technology, in co-correspondence with MIT, and in collaboration with Harvard University, Johns Hopkins University, and the University of Massachusetts. The findings are published in the journal Science Translational Medicine.

The research introduces a living, cell-based implant that can function as an autonomous artificial pancreas, essentially a living drug that is long-term, thanks to a novel crystalline shield-protecting technology. Once implanted, the system operates entirely on its own: it continuously senses blood-glucose levels, produces insulin within the implant itself, and releases the exact amount needed—precisely when it is needed. In effect, the implant becomes a self-regulating, drug-manufacturing organ inside the body, requiring no external pumps, injections, or patient intervention.

One of the study’s most significant breakthroughs addresses the longstanding challenge of immune rejection, which has limited the success of cell-based therapies for decades. The researchers developed engineered therapeutic crystals—called “crystalline shield”—that shield the implant from the immune system, preventing it from being recognized as a foreign object. This protective strategy enables the implant to function reliably and continuously for several years.

A new way to communicate with neurons using focused ultrasound stimulation

I still vividly remember the first time we observed neurons responding not to audible sound, but to concentrated, precisely calibrated ultrasonic pulses. On the screen in front of us, calcium signals from brain cells began to rise and fall in little waves. It was less about forcing the brain to adapt and more about listening to the brain and responding subtly.

Understanding how neurons interact and how neurological conditions like Parkinson’s disease affect this communication has been the focus of my study for many years. Calcium, a small ion that functions as a potent messenger inside cells, is at the center of this communication.

Neurons struggle to survive, connect, and operate correctly when calcium transmission is disrupted. Our team began to wonder if we might safely modify this fundamental signaling function without requiring invasive operations or drugs.

Engineered enzymes enable greener one-pot amide synthesis for drug manufacturing

A single type of chemical structure that shows up again and again in modern medicine is the amide bond that links a carbonyl group (C=O) to a nitrogen atom. They’re so ubiquitous that 117 of the top 200 small-molecule drugs by retail sales in 2023 feature at least one amide bond. And now, researchers have discovered a clever new way to reengineer natural enzymes to build amides from simple chemicals like aldehydes and amines.

The team chose a naturally abundant enzyme family called aldehyde dehydrogenases (ALDHs), specifically p-hydroxybenzaldehyde dehydrogenase (PHBDD), which can efficiently convert aldehydes into acids. The team turned it into a new catalyst, known as an oxidative amidase (OxiAm), by modifying its internal pocket of the enzyme in two major ways: making it hydrophobic to prevent the formation of unwanted acids and making it bigger to allow larger, diverse chemical parts to fit inside so they could be bonded together.

According to the results published in Science, the team was able to obtain amides directly from commercially available alcohols via a two-step enzymatic cascade reaction carried out in a single container. This approach could enable new, greener methods for producing five major drug molecules, including a key component of imatinib, an essential drug used to treat chronic myeloid leukemia and gastrointestinal stromal tumors.

New CRISPR tool spreads through bacteria to disable antibiotic resistance genes

Antibiotic resistance (AR) has steadily accelerated in recent years to become a global health crisis. As deadly bacteria evolve new ways to elude drug treatments for a variety of illnesses, a growing number of “superbugs” have emerged, ramping up estimates of more than 10 million worldwide deaths per year by 2050.

Scientists are looking to recently developed technologies to address the pressing threat of antibiotic-resistant bacteria, which are known to flourish in hospital settings, sewage treatment areas, animal husbandry locations, and fish farms. University of California San Diego scientists have now applied cutting-edge genetics tools to counteract antibiotic resistance.

The laboratories of UC San Diego School of Biological Sciences Professors Ethan Bier and Justin Meyer have collaborated on a novel method of removing antibiotic-resistant elements from populations of bacteria. The researchers developed a new CRISPR-based technology similar to gene drives, which are being applied in insect populations to disrupt the spread of harmful properties, such as parasites that cause malaria. The new Pro-Active Genetics (Pro-AG) tool called pPro-MobV is a second-generation technology that uses a similar approach to disable drug resistance in populations of bacteria.

Researchers demonstrate organic crystal emitting red light from UV and green from near-infrared

Invisible light beyond the range of human vision plays a vital role in communication technologies, medical diagnostics, and optical sensing. Ultraviolet and near-infrared wavelengths are routinely used in these fields, yet detecting them directly often requires complex instrumentation.

Developing materials that can convert invisible light into visible signals could serve as essential components for measurement technologies and sensors, and play a major role in understanding the fundamental photophysical processes. However, developing those materials remains a key challenge in photonics and materials science.

Measuring time at the quantum level depends on material symmetry

EPFL physicists have found a way to measure the time involved in quantum events and found it depends on the symmetry of the material. “The concept of time has troubled philosophers and physicists for thousands of years, and the advent of quantum mechanics has not simplified the problem,” says Professor Hugo Dil, a physicist at EPFL. “The central problem is the general role of time in quantum mechanics, and especially the timescale associated with a quantum transition.”

Quantum events, like tunneling, or an electron changing its state by absorbing a photon, happen at mind-bending speeds. Some take only a few tenths of attoseconds (10-18 seconds), which is so short that light would not even cross the width of a small virus. But measuring time intervals this small is notoriously difficult, also because any external timing tool can distort the very thing we want to observe.

“Although the 2023 Nobel prize in physics shows we can access such short times, the use of such an external time scale risks inducing artifacts,” says Dil. “This challenge can be resolved by using quantum interference methods, based on the link between accumulated phase and time.”

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