Using only DNA and glass, researchers made a material four times stronger and five times lighter than steel. It was inspired by Iron Man.
Category: biotech/medical – Page 338
Your immune system should ideally recognize and attack infectious invaders and cancerous cells. But the system requires safety mechanisms, or brakes, to keep it from damaging healthy cells. To do this, T cells—the immune system’s most powerful attackers—rely on immune “checkpoints” to turn immune activation down when they receive the right signal. While these interactions have been well studied, a research team supported in part by NIH has made an unexpected discovery into how a key immune checkpoint works, with potentially important implications for therapies designed to boost or dampen immune activity to treat cancer and autoimmune diseases.1
The checkpoint in question is a protein called programmed cell death-1 (PD-1). Here’s how it works: PD-1 is a receptor on the surface of T cells, where it latches onto certain proteins, known as PD-L1 and PD-L2, on the surface of other cells in the body. When this interaction occurs, a signal is sent to the T cells that stops them from attacking these other cells.
Cancer cells often take advantage of this braking system, producing copious amounts of PD-L1 on their surface, allowing them to hide from T cells. An effective class of immunotherapy drugs used to treat many cancers works by blocking the interaction between PD-1 and PD-L1, to effectively release the brakes on the immune system to allow the T cells to unleash an assault on cancer cells. Researchers have also developed potential treatments for autoimmune diseases that take the opposite tact: stimulating PD-1 interaction to keep T cells inactive. These PD-1 “agonists” have shown promise in clinical trials as treatments for certain autoimmune diseases.
Researchers from Nottingham Trent University (NTU) have developed realistic 3D printed heart and lung models that can bleed, beat and breathe like their real counterparts.
Designed for organ transplant training, the lifelike models reportedly reflect the tactile qualities of a human heart and can be produced with various tissue hardness levels. Using the models, medical professionals can plan surgeries and safely research and teach transplant procedures, without the risk of complications.
The project, which was led by research fellow Richard Arm, leveraged 3D scans of both healthy and diseased human hearts to 3D print the models to a high level of accuracy.
Scientists develop a human neuron model that efficiently simulates tau protein spread in Alzheimer’s, hinting at new therapeutic targets.
It reduces stress, boosts the immune system, and relieves pain. Touch is even crucial to our survival. Babies can die if they don’t get it. Additionally, the lack of it in a child’s‘life can stunt their growth in various ways.
Thus, scientists at Saarland University developed the smart textile with therapeutic and medicinal value in mind.
They claim that with this technology, seriously ill children in hospital isolation wards gain the chance to feel their parents’ closeness.
A groundbreaking study in the UK has revealed that reducing the duration of MRI scans for prostate cancer by a third would make them cheaper and more accessible without compromising on their accuracy. Lower costs would mean that more men could be offered scans and diagnosis for a disease which is highly treatable in its early stages.
As of today, doctors rely on a three-stage MRI scan to detect prostate cancer. The patient is injected with a contrast dye at the third stage, which helps to enhance the images from the scan. Now, the new research indicates the third step can be done away with if the first two scans are done with high precision and good quality.
Researchers from University College London (UCL) and University College London Hospitals conducted a study in which they assessed the impact of dropping the third stage. The study involved 555 patients from 22 hospitals in 12 countries.
New detection tools powered by AI have lifted the lid on what some are calling an epidemic of fraud in medical research and publishing. Last year, the number of papers retracted by research journals topped 10,000 for the first time.
One case involved the chief of a cancer surgery division at Columbia University’s medical center. An investigation found that dozens of his cancer treatment studies contained dubious data and recycled images. Other scandals have hit Harvard on the East Coast and on the West Coast it is Stanford University. A scandal there resulted in the resignation of the president last year.
Chapters:
0:00 What we think we know about medical research.
1:32 Arthur Caplan, NYU Langone Medical Center.
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Year 2008 I think that this reversing of the death processes in cancer could be genetically engineered in humans to essentially reverse death on the whole human body.
British Journal of Cancer volume 100, pages 118–122 (2009) Cite this article.
Study finds several species of cholesterol-metabolizing bacteria in people with lower cholesterol levels.
Year 2021 😗😁😘
Researchers Prof. Judith Haendeler from the Medical Faculty and the molecular biologist Prof. Joachim Altschmied from the Department of Biology, together with their teams, have shown for the first time in the cardiovascular system that telomerase reverse transcriptase (TERT) within the mitochondria, the powerhouses of the cells, has a protective function in myocardial infarction. This work, which was performed together with other groups from the University Hospital Düsseldorf and the University Hospital Essen within the frame of the Collaborative Research Center 1,116, was recently published in the journal Circulation.
Cardiac muscle cells benefit from the increased mitochondrial function and are protected from cell death. Other cell types also profit from increased mitochondrial function such as fibroblasts, which are essential for stable scarring after an infarction, and endothelial cells, which are needed for vascularization and thus blood supply in the infarct area.
In the cell nucleus, TERT is a component of the so-called “immortality enzyme” telomerase, for the discovery of which the Nobel Prize in Physiology or Medicine was awarded in 2009. Meanwhile, it has been shown by the two research groups at HHU, that TERT is also present in mitochondria in the cells of the cardiovascular system. However, until now it has not been possible to clearly distinguish between its functions in these two cell organelles.