Mesenchymal stem cells (MSCs), a non-hematopoietic stem cell population first discovered in bone marrow, are multipotent cells capable of differentiating into mature cells of several mesenchymal tissues, such as fat and bone. As common progenitor cells of adipocytes and osteoblasts, MSCs are delicately balanced for their differentiation commitment. Numerous in vitro investigations have demonstrated that fat-induction factors inhibit osteogenesis, and, conversely, bone-induction factors hinder adipogenesis. In fact, a variety of external cues contribute to the delicate balance of adipo-osteogenic differentiation of MSCs, including chemical, physical, and biological factors. These factors trigger different signaling pathways and activate various transcription factors that guide MSCs to commit to either lineage. The dysregulation of the adipo-osteogenic balance has been linked to several pathophysiologic processes, such as aging, obesity, osteopenia, osteopetrosis, and osteoporosis. Thus, the regulation of MSC differentiation has increasingly attracted great attention in recent years. Here, we review external factors and their signaling processes dictating the reciprocal regulation between adipocytes and osteoblasts during MSC differentiation and the ultimate control of the adipo-osteogenic balance.

/pdf/fate-decision-of-mesenchymal-stem-cells-adipocytes-or-2wh3vislf0.pdf

Fate decision of mesenchymal stem cells: adipocytes or osteoblasts?

The importance of the vascular supply for bone is well-known to orthopaedists but is still rather overlooked within the wider field of skeletal research. Blood supplies oxygen, nutrients and regulatory factors to tissues, as well as removing metabolic waste products such as carbon dioxide and acid. Bone receives up to about 10% of cardiac output, and this blood supply permits a much higher degree of cellularity, remodelling and repair than is possible in cartilage, which is avascular. The blood supply to bone is delivered to the endosteal cavity by nutrient arteries, then flows through marrow sinusoids before exiting via numerous small vessels that ramify through the cortex. The marrow cavity affords a range of vascular niches that are thought to regulate the growth and differentiation of hematopoietic and stromal cells, in part via gradients of oxygen tension. The quality of vascular supply to bone tends to decline with age and may be compromised in common pathological settings, including diabetes, anaemias, chronic airway diseases and immobility, as well as by tumours. Reductions in vascular supply are associated with bone loss. This may be due in part to the direct effects of hypoxia, which blocks osteoblast function and bone formation but causes reciprocal increases in osteoclastogenesis and bone resorption. Common regulatory factors such as parathyroid hormone or nitrates, both of which are potent vasodilators, might exert their osteogenic effects on bone via the vasculature. These observations suggest that the bone vasculature will be a fruitful area for future research.

/pdf/the-key-role-of-the-blood-supply-to-bone-5ihsvbjeek.pdf

The Key Role of the Blood Supply to Bone.

A biphasic artificial vascularized bone construct with regional bioactive factors is presented using dual 3D bioprinting platform technique, thereby forming a large functional bone grafts with organized vascular networks. Biocompatible mussel-inspired chemistry and "thiol-ene" click reaction are used to regionally immobilize bioactive factors during construct fabrication for modulating or improving cellular events.

/pdf/hierarchical-fabrication-of-engineered-vascularized-bone-12bdjeyi79.pdf

Hierarchical Fabrication of Engineered Vascularized Bone Biphasic Constructs via Dual 3D Bioprinting: Integrating Regional Bioactive Factors into Architectural Design.

3D biofabrication of vascular networks for tissue regeneration: A report on recent advances

3D printing of concentrated alginate/gelatin scaffolds with homogeneous nano apatite coating for bone tissue engineering

Background Studies have shown that high-intensity interval training (HIIT) is superior to moderate-intensity continuous training (MICT) for increasing peak oxygen uptake (VO2peak) and reducing cardiovascular disease (CVD) and mortality. To our knowledge, previously published systematic reviews have neither compared different HIIT models with MICT nor investigated intervention frequencies of HIIT vs. MICT for purposes of improving cardiorespiratory fitness in patients with CVD. Objective The purpose of this meta-analysis was to compare the effects of different training models, intervention frequencies and weeks of HIIT vs. MICT on changes in cardiorespiratory fitness during cardiac rehabilitation (CR). Methods A systematic search was carried out for research articles on randomized controlled trials (RCTs) indexed in the PubMed, Cochrane Library, Web of Science, Embase and Scopus databases for the period up to December 2021. We searched for RCTs that compared the effect of HIIT vs. MICT on cardiorespiratory fitness in patients with CVD. Results Twenty-two studies with 949 participants (HIIT: 476, MICT: 473) met the inclusion criteria. Sensitivity analysis revealed that HIIT increased VO2peak more than MICT (MD = 1.35). In the training models and durations, there was a greater increase in VO2peak with medium-interval HIIT (MD = 4.02) and more than 12 weeks duration (MD = 2.35) than with MICT. There were significant improvements in VO2peak with a HIIT frequency of 3 times/week (MD = 1.28). Overall, one minor cardiovascular and four non-cardiovascular adverse events were reported in the HIIT group, while six non-cardiovascular adverse events were reported in the MICT group. Conclusion HIIT is safe and appears to be more effective than MICT for improving cardiorespiratory fitness in patients with CVD. Medium-interval HIIT 3 times/week for more than 12 weeks resulted in the largest improvement in cardiorespiratory fitness during CR. Systematic Review Registration https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021245810, identifier: CRD42021245810.

/pdf/effects-of-high-intensity-interval-vs-moderate-intensity-1svjonbb.pdf

Effects of High-Intensity Interval vs. Moderate-Intensity Continuous Training on Cardiac Rehabilitation in Patients With Cardiovascular Disease: A Systematic Review and Meta-Analysis

Background & Aims: Peroxisome proliferator-activated receptor α (PPARα) is a ligand-activated transcription factor abundantly expressed in liver. PPARα activator has been previously reported to protect against acetaminophen-induced hepatotoxicity, but fenofibrate, a lipid-lowering drug that activates PPARα, has a common side-effect causing liver injury. Thus, the exact effect of liver PPARα on drug-induced liver injury remains obscure. Methods: Hepatocyte-specific Ppara knockout mice and littermate wild-type control mice were intraperitoneally injected with acetaminophen (400 mg/kg body weight). Blood and liver samples were collected at different time points. We measured phase I and II cytochrome P450 enzymes, glutathione, reactive oxygen species, cytokines including Il6, and pSTAT3 by reverse transcriptase quantitative PCR, colorimetric, immunohistochemistry analyses and Western blotting. Results: Hepatic expression of PPARα was significantly decreased in DILI patients. Disruption of the Ppara gene in hepatocytes significantly reduced acetaminophen-induced liver injury in mice. ROS production rather than the expression levels of phase I and II cytochrome P450 enzymes was reduced in hepatocyte-specific Ppara knockout mice compared to control mice after acetaminophen administration. Mechanistically, hepatocyte-specific Ppara knockout mice had upregulated activation of the hepatoprotective pathway IL-6/STAT3 compared to wild-type mice, as evidenced by hepatic Il6 mRNA levels, hepatic protein levels of STAT3 and phosphorylated STAT3 were much higher in hepatocyte-specific Ppara knockout mice than in wild-type mice post acetaminophen injection. Conclusions: Hepatocyte-specific disruption of the Ppara gene protects against acetaminophen-induced liver injury by reducing oxidative stress and upregulating the hepatoprotective IL-6/STAT3 signaling pathway.

/pdf/disruption-of-peroxisome-proliferator-activated-receptor-a-bkg6d3p1.pdf

Disruption of peroxisome proliferator-activated receptor α in hepatocytes protects against acetaminophen-induced liver injury by activating the IL-6/STAT3 pathway

Transcriptome, Lipidome, and Phytohormone Analyses Elucidate the Mechanism of Chilling Injury During Postharvest Cold Storage in Different Cold-Sensitive Peach Fruit

Printing Assembly of Flexible Devices with Oxidation Stable Mxene for High Performance Humidity Sensing Applications

Hypoxia inhibits the differentiation of mesenchymal stem cells into osteoblasts by activation of Notch signaling.

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