Lifeboat Foundation

Your pancreas is a little sweet potato-shaped organ that sits snug behind your stomach. The pancreas is studded with islets, the cell clusters that house insulin-producing beta cells. In people with type 1 diabetes, the body’s own immune cells head for the islets and start attacking the beta cells. No one knows exactly what triggers this attack.

One clue may lie in the pattern of beta cell death. Many beta cells are killed off in big patches while other beta cells are mysteriously untouched. Something seems to be drawing immune cells to attack specific groups of beta cells while ignoring others.

In a new Science Advances study, researchers at La Jolla Institute for Immunology (LJI) report that the nervous system may be driving this patchy cell die-off. Their new findings in a mouse model suggest that blocking nerve signals to the pancreas could stop patients from ever developing type 1 diabetes.

Obesity is the main cause of type 2 diabetes and related chronic illnesses that together will kill more people around the globe this year than the COVID-19 coronavirus. Scientists at Joslin Diabetes Center have delivered a proof of concept for a novel cell-based therapy against this dangerous condition.

The potential therapy for obesity would transplant HUMBLE (human brown-like) fat cells, human white fat cells that have been genetically modified to become similar to heat-generating brown fat cells, says Yu-Hua Tseng, Ph.D., a Senior Investigator in Joslin’s Section on Integrative Physiology and Metabolism.

Brown fat cells burn energy instead of storing energy as white fat cells do, says Tseng, senior author on a paper about the work in Science Translational Medicine. In the process, brown fat can lower excessive levels of glucose and lipids in the blood that are linked to metabolic diseases such as diabetes.

Research looking at a possible new therapeutic approach for Alzheimer’s disease was recently published in the Journal of Neuroinflammation. The paper out of the University of Kentucky’s Sanders-Brown Center on Aging (SBCoA) is titled “Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition”. The work looked at targeting inflammation by using an antibody. Alzheimer’s disease and related dementias have no disease-modifying treatments at this time and represent a looming public health crisis given the continually growing aging population.

The paper explains that current therapeutic approaches to the treatment of Alzheimer’s disease focus on the major pathological hallmarks of the disease which are amyloid plaques and neurofibrillary tangles. They are the requirements for a diagnosis of Alzheimer’s disease. However, the authors say there has been an explosion of genetic data suggesting the risk for sporadic Alzheimer’s disease is driven by several other factors including neuroinflammation, membrane turnover and storage, and lipid metabolism.

In this study the researchers focused on triggering receptor expressed on myeloid cell-2 (TREM2). “TREM2 was identified several years ago as a gene that, when there’s a mutation, significantly increases risk of Alzheimer’s disease. The field thinks that this mutation reduces the function of the receptor, so we hypothesized that targeting TREM2 to increase its function might be a valid treatment for Alzheimer’s,” explained Donna Wilcock, SBCoA associate director.

Elon Musk’s Neuralink will likely show off its design for a brain-computer interface Friday evening. The concept it unveiled last summer involves surgically implanting it into the brain to detect the activity of neurons. The US military also wants to develop a brain-computer interface, as we explain in this story from October. But here’s the kicker: no surgery required—and the device could be put on and taken off like a helmet or headband.

In August, three graduate students at Carnegie Mellon University were crammed together in a small, windowless basement lab, using a jury-rigged 3D printer frame to zap a slice of mouse brain with electricity.

The brain fragment, cut from the hippocampus, looked like a piece of thinly sliced garlic. It rested on a platform near the center of the contraption. A narrow tube bathed the slice in a solution of salt, glucose, and amino acids. This kept it alive, after a fashion: neurons in the slice continued to fire, allowing the experimenters to gather data. An array of electrodes beneath the slice delivered the electric zaps, while a syringe-like metal probe measured how the neurons reacted. Bright LED lamps illuminated the dish. The setup, to use the lab members’ lingo, was kind of hacky.

Continue reading “The US military is trying to read minds” »

Our kidneys are crucial for keeping us alive and healthy. A sort of chemical computer that keeps our blood chemistry stable—whether we’re eating a sugary birthday cake or a vitamin-filled salad—they prevent waste buildup, stabilize our electrolyte levels, and produce hormones to regulate our blood pressure and make red blood cells.

Kidneys clean our blood using nephrons, which are essentially filters that let fluid and waste products through while blocking blood cells, proteins, and minerals. The latter get reintegrated into the blood, and the former leave the body in urine.

Scientists have struggled to come up with viable treatments for kidney disease and renal failure, and their complexity means kidneys are incredibly hard to synthetically recreate; each kidney contains around one million intricately-structured nephrons.

British scientists have discovered that an active ingredient found in insect repellent can kill COVID-19, according to a report.

Researchers at the UK’s Defense Science and Technology Laboratory determined that Citriodiol can help fight coronavirus in a preliminary study, Sky News reported.

Insect repellents containing Citriodiol are not believed to be enough alone to protect people from the virus but can be used as an additional layer of defense along with face masks, hand washing and other health recommendations, according to the report.

Dr. Shigeaki Hinohara had an extraordinary life for many reasons. For starters, the Japanese physician and longevity expert lived until the age of 105.

When he died, in 2017, Hinohara was chairman emeritus of St. Luke’s International University and honorary president of St. Luke’s International Hospital, both in Tokyo.

Perhaps best known for his book, “Living Long, Living Good,” Hinohara offered advice that helped make Japan the world leader in longevity. Some were fairly intuitive points, while others were less obvious:

White fat cells can be turned into energy-burning brown fat using CRISPR gene-editing technology. These engineered cells have helped mice avoid weight gain and diabetes when on a high-fat diet, and could eventually be used to treat obesity-related disorders, say the researchers behind the work.

Human adults have plenty of white fat, the cells filled with lipid that make up fatty deposits. But we have much smaller reserves of brown fat cells, which burn energy as well as storing it. People typically lose brown fat as they age or put on weight. While brown fat seems to be stimulated when we are exposed to cold temperatures, there are no established methods of building up brown fat in the body.

Researchers at the Fred Hutchinson Cancer Research Center in Seattle, USA, have used gene editing to remove latent herpes simplex virus 1 (HSV-1), also known as oral herpes.

In mice, the technique showed a 92% decrease in the latent virus – enough to keep the infection from coming back, according to the scientists. The study used two sets of “genetic scissors” to damage the virus’s DNA, fine-tune a delivery vehicle to the infected cells, and target the nerve pathways connecting the neck with the face, reaching the tissue where the virus lies dormant. The findings are published in Nature Communications.

“This is the first time that scientists have been able to go in and actually eliminate most of the herpes in a body,” said senior author Dr. Keith Jerome, Professor in the Vaccine and Infectious Disease Division at Fred Hutch. “We are targeting the root cause of the infection: the infected cells where the virus lies dormant and are the seeds that give rise to repeat infections.”