Lifeboat Foundation

If you believe the headlines, seaweeds can do almost anything from storing tons of carbon and stopping cows from belching methane, to making biofuels and renewable plastics – all while sustaining vibrant coastal ecosystems and feeding communities.

Add to that list their potential wound-healing properties and possible anti-aging effects, and it’s no wonder the seaweed farming industry is booming.

A new study adds to that fanfare, with lab experiments based on human-like skin cells revealing extracts from two brown seaweeds can inhibit reactions linked to skin aging and boost collagen levels.

A typical vaccine teaches the human immune system to recognize a virus or bacteria as an enemy that should be attacked. The new “inverse vaccine” does just the opposite: it removes the immune system’s memory of one molecule. While such immune memory erasure would be unwanted for infectious diseases, it can stop autoimmune reactions like those seen in multiple sclerosis, type I diabetes, or rheumatoid arthritis, in which the immune system attacks a person’s healthy tissues.

The inverse vaccine, described in Nature Biomedical Engineering, takes advantage of how the liver naturally marks molecules from broken-down cells with “do not attack” flags to prevent autoimmune reactions to cells that die by natural processes. PME researchers coupled an antigen — a molecule being attacked by the immune system— with a molecule resembling a fragment of an aged cell that the liver would recognize as friend, rather than foe. The team showed how the vaccine could successfully stop the autoimmune reaction associated with a multiple-sclerosis-like disease.

“In the past, we showed that we could use this approach to prevent autoimmunity,” said Jeffrey Hubbell, the Eugene Bell Professor in Tissue Engineering and lead author of the new paper. “But what is so exciting about this work is that we have shown that we can treat diseases like multiple sclerosis after there is already ongoing inflammation, which is more useful in a real-world context.”

Purpose: Wolfiporia cocos is frequently used in traditional Chinese medicine to treat depression. However, antidepressant-like effects of the main active ingredients of Wolfiporia cocos, total triterpenes of Wolfiporia cocos (TTWC), are not well studied. This study aimed to investigate those effects and explore their specific mechanisms of action in depth. Methods: Chemical components of TTWC were analyzed using LC-MS. Depression-like behavior in rats were induced by chronic unpredictable mild stress (CUMS). The suppressive effects of TTWC (60120240 mg/kg) against CUMS-induced depression-like behavior were evaluated using the forced swimming test (FST), open field test (OFT) and sucrose preference test (SPT). Levels of 5-hydroxytryptamine (5-HT), glutamate (GLU), corticotropin-releasing hormone (CRH), interleukin-1 beta (IL-1beta), interleukin-18 (IL-18), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in different groups were determined by ELISA. Western blotting (WB) was used to detect the expression of NLRP3, ASC, pro-caspase-1, caspase-1, pro-IL-1beta, IL-1beta, pro-IL-18, and IL-18 in the prefrontal cortex. Additionally, the mRNA levels of NLRP3, ASC, caspase-1, IL-1beta and IL-18 were detected by RT-PCR. Results: A total of 69 lanostane-type triterpene acids of TTWC were identified. The results showed that TTWC exhibited an antidepressant-like effect in CUMS rats, reversed the decreased sugar preference in the SPT, reduction of immobility time in the FST, reduced the rest time, increased the total moving distance in the OFT. TTWC increased 5-HT levels and decreased GLU levels in the hippocampus. Moreover, TTWC decreased CRH levels in serum, indicating the regulation of over-activation of the hypothalamic-pituitary-adrenal (HPA) axis. In addition, reduced serum levels of IL-1beta, IL-18, IL-6, and TNF-alpha. The WB results implied that TTWC inhibited the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 in the prefrontal cortex and enhanced the expression of pro-caspase-1, pro-IL-1beta, and pro-IL-18. Although most of the results were not significant, PCR results showed that TTWC inhibited the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 in the prefrontal cortex. Conclusion: TTWC treatment exerted an antidepressant-like effect and regulates neurotransmitters, HPA axis and NLRP3 signaling pathway. These results indicated the potential of TTWC in preventing the development of depression.

Keywords: NLRP3 pathway; Wolfiporia cocos (schwein.) ryvarden & gilb; chronic unpredictable mild stress; depression; hypothalamic-pituitary-adrenal axis; neurotransmitter; triterpenes.

Copyright © 2022 Pan, Chen, Han, Luo, Zhang, Zhang, Zhang, Zhou, Li, Fang, Wang and Ye.

This is a ~50 minute talk by Michael Levin to a clinical audience about bioelectricity and why it represents a new approach to medicine.

Large-scale 3T MRI data enables fast whole-brain scanning at 0.055T via deep learning super-resolution and image reconstruction.

It could soon be possible to measure changes in depression levels like we can measure blood pressure or heart rate.

In a new study, 10 patients with depression that had resisted treatment were enrolled in a six-month course of deep brain stimulation (DBS) therapy. Previous results from DBS have been mixed, but help from artificial intelligence could soon change that.

Success with DBS relies on stimulating the right tissue, which means getting accurate feedback. Currently, this is based on patients reporting their mood, which can be affected by stressful life events as much as it can be the result of neurological wiring.

An artificial intelligence platform developed by an Israeli startup can reveal whether a patient is at risk of a heart attack by analyzing their routine chest CT scans.

Results from a new study testing Nanox. AI’s HealthCCSng algorithm on such scans found that 58 percent of patients unknowingly had moderate to severe levels of coronary artery calcium (CAC) or plaque.

CAC is the strongest predictor of future cardiac events, and measuring it typically subjects patients to an additional costly scan that is not normally covered by insurance companies.

“That’s what’s driving all this – the availability of this technology and better patient care,” he said.

As many as 20–30% of the Knoxville-based health system’s patients could receive virtual care through the program.

A new compound called d16 that reduces tumor growth and overcomes treatment resistance in mutant p53-bearing cancers has been developed by researchers at the Baylor College of Medicine. Their findings testing the compound, published in the journal Cancer Research Communications, suggests the new compound could be used in combination therapies to provide more effective treatment against these kinds of cancer.

“One of the most common alterations in many human cancers are mutations in p53, a gene that normally provides one of the most powerful shields against tumor growth,” says Helena Folly-Kossi, PhD, a postdoctoral associate in Weei-Chin Lin’s lab at Baylor and the study’s first author. “Mutations that alter the normal function of p53 can promote tumor growth, cancer progression and resistance to therapy, which are associated with poor prognosis. It is important to understand how p53 mutations help cancer grow to develop therapies to counteract their effects.”

According to Lin, finding ways to target p53 mutations directly as a form of therapy for cancer has been difficult. His lab has been working for many years to not interfere directly with p53, but rather to identify vulnerabilities in the cells carrying p53 mutations that they could target to prevent cancer growth. “One of the challenges has been to develop drugs that act on mutant p53 directly. Some of these drugs are under development, but they appear to be toxic,” he said.