Lifeboat Foundation

Inside of you, at all times, there are trillions of natural nano robots walking around, taking out the trash, and packaging strands of DNA. Below the calm, ordered exterior of a living organism lies a complex collection of molecular machines working together to create something greater than themselves. Physicist and author of “Life’s Ratchet” Peter Hoffmann shows us the tiny city beneath the surface.

Watch the full program here: https://youtu.be/FzFY5ms3AUc.
Original program date: May 30, 2013

Continue reading “The Nano Robots Inside You” »

How does the research conducted by Lige Leng at the Institute of Neuroscience of Xiamen University in China (I link it to you here)? It all starts with the study of the “inflamed brain”: many diseases of old age are associated with low-level chronic inflammation in the brain, organs, joints and circulatory system. A phenomenon sometimes called “inflammaging”.

You know it: over time all of our body’s repair systems deteriorate, our DNA and proteins accumulate damage, metabolism stumbles and cells stop doing their job. That’s life, beauty.

We’re all on our way to the exit, but research on worms, flies, mice and monkeys show that going at this speed isn’t inevitable. Diet and lifestyle changes (and, perhaps, upcoming anti-aging drugs) can curb decay and give us many more years of life, especially healthy life.

Continue reading “Discovered an aging ‘brake pedal’?” »

UChicago researchers’ design makes stable, suture-free medical monitoring in body possible.

Sometimes a knee replacement is considered too risky or too early to be recommended. These alternatives could help alleviate your knee pain.

Several factors contribute to the development of inflamm-aging, including genetic susceptibility, visceral obesity, microbiota and gut permeability, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by mitochondrial dysfunction, immune cells dysregulation, and chronic infection (Ferrucci & Fabbri, 2018). The immune system becomes gradually dysregulated during aging, leading to elevated blood levels of pro-inflammatory mediators, such as TNFα, IL6, and C-reactive protein (Harris et al., 1999 ; Mooradian et al., 1991). Energy homeostasis also becomes dysregulated with aging, which results in the redistribution of subcutaneous fat to visceral regions and contributes to inflammation (Bouchard et al., 1993 ; Chumlea et al., 1989 ; Curtis et al., 2005). Metabolism-induced inflammation, also known as metaflammation, shares similarities with inflamm-aging, including the elevation of certain circulating pro-inflammatory cytokines (Prattichizzo et al., 2018). Therefore, the molecules that play a key role in the regulation of metabolic homeostasis potentially mediate the development of chronic inflammation during aging.

Forkhead box O1 (FOXO1) transcription factor has been indicated to be involved in the regulation of nutrient metabolism and energy homeostasis (Cheng et al., 2009 ; InSug et al., 2015 ; Matsumoto et al., 2007 ; Yang et al., 2019 ; Zhang et al., 2012). Deletion of hepatic Foxo1 improves glucose homeostasis in insulin resistant mice (Dong et al., 2008). FOXO1 inhibition by AS1842856 attenuates hepatic steatosis in diet-induced obesity mice (Ding et al., 2020). In mature macrophages, FOXO1 promotes inflammation through the activation of TLR4-and STAT6-mediated signaling pathways (Fan et al., 2010 ; Lee et al., 2022). In invertebrates, DAF-16, the Foxo homolog gene, mediates the effect of insulin/IGF signaling on lifespan (Ogg et al., 1997). Overexpression of FOXO in Drosophila and C.elegans increases their lifespan (Giannakou et al., 2004 ; Henderson & Johnson, 2001). However, studies in mammalians show that FOXO1 does not have a significant correlation with longevity (Chiba et al., 2009 ; Kleindorp et al., 2011). Considering the role of FOXO1 in regulating glucose metabolism and inflammation, we hypothesize that FOXO1 plays an important role in the regulation of aging-induced inflammation and dysregulation of glucose homeostasis.

Liver is an important metabolic organ that plays a key role in maintaining whole-body nutrient homeostasis by regulating energy metabolism, clearing xenobiotic and endobiotic, and synthesizing necessary molecules (Rui, 2014). As a result, aging-induced changes in liver contribute to systemic susceptibility to aging-related diseases. Different types of liver cells, including hepatocytes, endothelial cells, hepatic stellate cells (HSC), and macrophages, are all affected by the aging process (Hunt et al., 2019). However, most studies on liver aging focused on whole-liver tissue, which is mainly composed of parenchymal cells, hepatocytes. Thus, the effects of aging on liver nonparenchymal cells (NPCs) are less understood. In this study, we used bulk RNA-Seq and single-cell RNA (scRNA)-Seq technologies to analyze aging-induced changes, and the role of FOXO1 in aging-related processes in both whole-liver and individual liver cells, particularly liver macrophages. We found that insulin resistance, liver fat accumulation, liver inflammation, and systemic inflammation were significantly aggravated in old mice. Additionally, aging significantly increased pro-inflammatory response in Kupffer cells (KCs) and induced a functional quiescence in monocyte-derived macrophages (MDMs). FOXO1 activity was significantly enhanced in the livers of old mice and FOXO1 inhibition improved insulin resistance, hepatic steatosis, and inflammation in old mice. Furthermore, we found that FOXO1 inhibition attenuated aging-induced pro-inflammation in KCs and had a limited effect on aging-induced functional quiescence in MDMs. Taken together, this study indicates that FOXO1 plays an important role in the liver aging processes and suggests that FOXO1 is a potential therapeutic target for the treatment of aging-induced chronic diseases.

Antipsychotic drugs treat incredibly vulnerable patients. Maintaining a treatment regimen is difficult for many patients, but not taking the medication is associated with a higher risk of poor health outcomes. These drugs are also very powerful with strong side effects, and blood tests are often used to calibrate a patient’s dosage and confirm that they are taking the recommended dose.

However, blood tests are invasive and potentially uncomfortable. Scientists have now discovered a way to test the levels of common antipsychotic drugs in the sweat from patients’ fingerprints, offering a quicker, more comfortable, and more convenient alternative to blood draws for patient monitoring.

“Our test offers patients a quick and dignified way of showing commitment to antipsychotic treatment,” said Katherine Longman of the University of Surrey, first author of the study in Frontiers in Chemistry. “This non-invasive approach can also be adapted to fit other therapeutic regimes.”

Researchers at Washington University School of Medicine in St. Louis have transformed stem cells into insulin-producing cells. They used the CRISPR gene-editing tool to correct a defect that caused a form of diabetes, and implanted the cells into mice to reverse diabetes in the animals. Shown is a microscopic image of insulin-secreting beta cells (insulin is green) that were made from stem cells produced from the skin of a patient with Wolfram syndrome.

CRISPR corrects genetic defect so cells can normalize blood sugar.

According to a Mass Common Brigham news release, the study, published in the Journal of Medical Web Analysis, revealed that ChatGPT was around 72% correct when it came to common decision-making from the first point of contact with a patient.

Stem cells can be classified based on their ability to specialize. Totipotent stem cells can become any tissue in the body, pluripotent stem cells can become any cell type except for a complete organ, and multipotent stem cells can only differentiate into specific tissue types.

Induced pluripotent stem cells (iPSCs) show promise in treating retinal degenerative diseases. They are created by reprogramming adult cells using Yamanaka factors, allowing them to revert to an embryonic state. These cells provide a virtually unlimited cell source for research and potential therapies.

Scientists are researching several diseases and drug development applications for these cells, highlighting the characteristics that make them an ideal therapy for macular degeneration.