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A study from researchers at The University of Texas MD Anderson Cancer Center, published today in Nature Cell Biology, details a previously unexplained type of cell death called disulfidptosis that could open the door for novel cancer therapeutic strategies.

As described in the study, disulfidptosis is triggered when cells with high levels of the SLC7A11 protein are subjected to glucose starvation. In preclinical models, treatment with glucose inhibitors induced disulfidptosis in cancer cells with high SLC7A11 expression, effectively suppressing tumor growth without significant toxicity in normal tissues.

The study was led by Boyi Gan, Ph.D., and Junjie Chen, Ph.D., both professors of Experimental Radiation Oncology.

The viruses Kaposi sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) have been linked to several cancers. For the first time, UNC School of Medicine scientists have discovered that these viruses use a human protein called barrier-to-autointegration factor 1, or BAF, to evade our innate immune response, allowing the viruses to spread and cause disease.

These findings, published in Nature Communications, suggest that BAF and related proteins could be therapeutic targets to prevent these viruses from spreading and leading to cancers, such as Kaposi sarcoma, non-Hodgkin lymphoma, Hodgkin lymphoma, multicentric Castleman disease, nasopharyngeal carcinoma, and gastric cancer.

“Viruses are in a constant battle with the cellular immune system, which includes the protein cyclic GMP-AMP synthase, or cGAS, which binds to viral DNA and sounds the alarm to trigger immune responses and fight the viral invaders,” said senior author Blossom Damania, Ph.D., the Boshamer Distinguished Professor of Microbiology and Immunology and member of the Lineberger Comprehensive Cancer Center. “We’ve discovered that KSHV and EBV use a different host cell protein, BAF, to prevent cGAS from sounding the alarm.”

The Microsoft cofounder talked to Forbes about his work with AI unicorn OpenAI and back on Microsoft’s campus, AI’s potential impact on jobs and in medicine, and much more.

In 2020, Bill Gates left the board of directors of Microsoft, the tech giant he cofounded in 1975. But he still spends about 10% of his time at its Redmond, Washington headquarters, meeting with product teams, he says. A big topic of discussion for those sessions: artificial intelligence, and the ways AI can change how we work — and how we use Microsoft software products to do it.

Knees in this X-ray have severe osteoarthritis which affects 1 in 7 adult Americans. Is there progress on alternatives to knee replacement surgery?

Stem cell therapies were supposed to end the need for knee replacement surgery. Progress in this field has been very slow.

Magicmine/iStock.

After a few weeks, these transplants developed key features of the human immune system, introducing a model that could be used to effectively simulate the human intestinal system.

Osaka University researchers discover that taking tricaprin regularly in your diet leads to a reduction in coronary artery plaque and an improvement of symptoms for patients with triglyceride deposit cardiomyovasculopathy.

As children, our parents encouraged us to take vitamins for growth and strength. Now, Japanese researchers have found that a specific supplement may even repair a broken heart.

In a study that was recently published in the European Heart Journal, researchers from Osaka University discovered that a dietary supplement can significantly improve heart disease symptoms in a subset of patients.

Rejuvenating an older person’s blood may now be within reach, based on recent findings from Passegué’s lab published in Nature Cell Biology(link is external and opens in a new window).

Passegué, with her graduate student Carl Mitchell, found that an anti-inflammatory drug, already approved for use in rheumatoid arthritis, can turn back time in mice and reverse some of the effects of age on the hematopoietic system.

Nature article:

Continue reading “Will Revitalizing Old Blood Slow Aging?” »

A 1967 publication titled “Mortality of Bereavement” discovered that bereaved relatives had a 7-fold increased risk of dying within the following year. Despite that the cause of death was undetermined, this is the first scientific evidence indicating that extreme sadness kills.

Coined in 1991, Takotsubo cardiomyopathy — or broken heart syndrome — mimic aspects of a heart attack such as shortness of breath, fainting, and chest pain. But, oddly, they have no blocked arteries. Instead, some parts of the heart stopped moving and other heart muscles try to compensate for this. This turns the heart into an irregular shape, like that of an octopus pot — hence, the name “Takotsubo” (‘Tako’ means octopus and ‘tsubo’ means pot in Japanese). This condition is reversible but can be fatal at times. Takotsubo cardiomyopathy is triggered by intense emotions or stressful life events such as the death of a loved one and losing (or even winning) a lot of money. This is why “heartbroken” from sadness is a legitimate phenomenon.

Research advances further confirm that sadness, or more accurately emotional stress, destroy the heart in many ways. The mind-heart connection extends to far more than just the broken heart syndrome. Convincing epidemiological evidence ascertains that emotional pains can lead to heart diseases, the major killer worldwide, and this linkage is underpinned by biology.

Though it’s been around for nearly 3,500 years, scientists are still missing many basic facts about the disease.