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A new study shows how an anticancer drug triggers an “outside in” signal that gets it sucked into a cancer cell. The work, published Jan. 29 in Nature Communications, reveals a new signaling mechanism that could be exploited for delivering other drugs.

Many malignant cancers overexpress a protein called P-cadherin, which is embedded in the cell membrane. Because cancer cells have a lot of P-cadherin sticking out of their surface, the protein has been targeted for drug development.

Monoclonal antibodies against P-cadherin can carry a drug payload to the cancer cells. It has not been clear, though, exactly how the antibodies attach to P-cadherin or how they get inside the cancer cell once attached.

Researchers have found that Artemisia herba-alba, a medicinal herb, contains compounds capable of fighting colorectal cancer. The plant extract halted cancer cell growth, disrupted key pathways, and showed potential as a less harmful alternative to chemotherapy.

Scientists from the University of Sharjah have discovered that Artemisia herba-alba, a naturally occurring aromatic herb, contains compounds with potential therapeutic effects against colorectal cancer.

This herb, commonly known as common wormwood, white wormwood, or herba alba, grows naturally in North Africa and the Middle East, where it has long been used in traditional medicine. Local populations have historically relied on it to treat conditions such as bronchitis, diarrhea, hypertension, and diabetes.

Some people will do anything to live forever: injecting young blood, freezing their heads, even zapping themselves with electricity in places you’d rather not imagine. On today’s episode of The Infographics Show, we’re diving into the strangest and most extreme attempts to cheat death, and why they might make you rethink wanting to live forever!

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Summary: New research reveals that brain cells use a muscle-like signaling mechanism to relay information over long distances. Scientists discovered that dendrites, the branch-like extensions of neurons, contain a structured network of contact sites that amplify calcium signals—similar to how muscles contract. These contact sites regulate calcium release, activating key proteins involved in learning and memory.

This mechanism explains how neurons process information received at specific points and relay it to the cell body. Understanding this process sheds light on synaptic plasticity, which underlies learning and memory formation. The findings could provide new insights into neurodegenerative diseases like Alzheimer’s.

Nerve cells have amazing strategies to save energy and still perform the most important of their tasks. Researchers from the University Hospital Bonn (UKB) and the University of Bonn as well as the University Medical Center Göttingen found that the neuronal energy conservation program determines the location and number of messenger RNA (mRNA) and proteins and differs depending on the length, longevity and other properties of the respective molecule. The work has now been published in Nature Communications.

We have all experienced the need to save energy in recent years. To do this, we all had to come up with strategies to save energy while still meeting our most important needs.

Our are facing a similar dilemma: They have to supply their synapses, i.e., their contact points with other neurons, but also organize their in such a way that they don’t produce too much or too little proteins.

Many describe this as the experience of seeing their life ‘flash before their eyes.’

The recording was made when an 87-year-old patient underwent cardiac arrest while being treated for epilepsy.

Doctors had strapped a device on his head to monitor brain activity, but the man died during the process.

A complex molecular machine, the spliceosome, ensures that the genetic information from the genome, after being transcribed into mRNA precursors, is correctly assembled into mature mRNA. Splicing is a basic requirement for producing proteins that fulfill an organism’s vital functions. Faulty functioning of a spliceosome can lead to a variety of serious diseases.

Researchers at the Heidelberg University Biochemistry Center (BZH) have succeeded for the first time in depicting a faulty “blocked” at high resolution and reconstructing how it is recognized and eliminated in the cell. The research was published in Nature Structural & Molecular Biology.

The of all living organisms is contained in DNA, with the majority of genes in higher organisms being structured in a mosaic-like manner. So the cells are able to “read” the instructions for building proteins stored in these genetic mosaic particles, they are first copied into precursors of mRNA, or messenger RNA. The spliceosome then converts them into mature, functional mRNA.

Xenon gas inhalation reduced neurodegeneration and boosted protection in preclinical models of Alzheimer’s disease. Most treatments being pursued today to protect against Alzheimer’s disease focus on amyloid plaques and tau tangles that accumulate in the brain, but new research from Mass General Brigham and Washington University School of Medicine in St. Louis points to a novel — and noble — approach: using Xenon gas. The study found that Xenon gas inhalation suppressed neuroinflammation, reduced brain atrophy, and increased protective neuronal states in mouse models of Alzheimer’s disease. Results are published in Science Translational Medicine, and a phase 1 clinical trial of the treatment in healthy volunteers will begin in early 2025.

“It is a very novel discovery showing that simply inhaling an inert gas can have such a profound neuroprotective effect,” said senior and co-corresponding author Oleg Butovsky, PhD, of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital (BWH), a founding member of the Mass General Brigham healthcare system. “One of the main limitations in the field of Alzheimer’s disease research and treatment is that it is extremely difficult to design medications that can pass the blood-brain barrier — but Xenon gas does. We look forward to seeing this novel approach tested in humans.”

“It is exciting that in both animal models that model different aspects of Alzheimer’s disease, amyloid pathology in one model and tau pathology in another model, that Xenon had protective effects in both situations,” said senior and co-corresponding author David M. Holtzman, MD, from Washington University School of Medicine in St. Louis.

Dense crowds form some of the most dangerous environments in modern society. Dangers arise from uncontrolled collective motions, leading to compression against walls, suffocation and fatalities. Our current understanding of crowd dynamics primarily relies on heuristic collision models, which effectively capture the behaviour observed in small groups of people. However, the emergent dynamics of dense crowds, composed of thousands of individuals, remains a formidable many-body problem lacking quantitative experimental characterization and explanations rooted in first principles. Here we analyse the dynamics of thousands of densely packed individuals at the San Fermín festival (Spain) and infer a physical theory of dense crowds in confinement. Our measurements reveal that dense crowds can self-organize into macroscopic chiral oscillators, coordinating the orbital motion of hundreds of individuals without external guidance. Guided by these measurements and symmetry principles, we construct a mechanical model of dense-crowd motion. Our model demonstrates that emergent odd frictional forces drive a non-reciprocal phase transition7 towards collective chiral oscillations, capturing all our experimental observations. To test the robustness of our findings, we show that similar chiral dynamics emerged at the onset of the 2010 Love Parade disaster and propose a protocol that could help anticipate these previously unpredictable dynamics.