Lifeboat Foundation

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.

Researchers have pioneered a 3D-SPI method that allows high-resolution imaging of microscopic objects, presenting a transformative approach for future biomedical research and optical sensing.

A research team led by Prof. Lei Gong from the University of Science and Technology (USTC) of the Chinese Academy of Sciences (CAS) and collaborators developed a three-dimensional single-pixel imaging (3D-SPI) approach based on 3D light-field illumination(3D-LFI), which enables volumetric imaging of microscopic objects with a near-diffraction-limit 3D optical resolution. They further demonstrated its capability of 3D visualization of label-free optical absorption contrast by imaging single algal cells in vivo.

The study titled “Optical Single-Pixel Volumetric Imaging by Three-dimensional Light-Field Illumination” was published recently in the journal Proceedings of the National Academy of Sciences (PNAS).

More than 20 years ago, the human genome was first sequenced. While the first version was full of “holes” representing missing DNA sequences, the genome has been gradually improved in successive rounds. Each has increased the quality of the genome and, in so doing, resolved most of the blank spaces that prevented us from having a complete reading of our genetic material.

The fundamental difficulty researchers faced in reading the genome from end to end is the enormous number of repeated sequences that populate it. The 20,000 or so genes we humans have occupy barely 2% of the entire genome. The remaining 98% is essentially made up of these families of repeated sequences, mobile elements known as transposons and retrotransposons, and—to a lesser but functionally important extent— gene expression regulatory sequences. These function as switches that determine when and where genes are turned on and off.

In March 2022, a major revision of the genome was published in the journal Science. An international consortium of researchers known as “T2T” (telomere to telomere, which are the ends of chromosomes) used a novel strategy based a type of cell (CHM13) that retains only one copy of each chromosome.

Scientists already have their ways of coaxing human cells into new forms, using a special concoction of chemicals to nudge humble skin cells into malleable tissues known as induced pluripotent stem cells.

In spite of this new lease on life, these particular cells still retain a few genetic reminders of their time as a fully developed tissue, affecting their use as a blank slate.

Now an international team of researchers has gone one better: finding a new way of wiping a cell’s memory clean so it can be better reprogrammed as a stem cell.