Association between genetically proxied glucosamine and risk of cancer and non-neoplastic disease: A Mendelian randomization study.

Introduction: Observational investigations have examined the impact of glucosamine use on the risk of cancer and non-neoplastic diseases. However, the findings from these studies face limitations arising from confounding variables, reverse causation, and conflicting reports. Consequently, the establishment of a causal relationship between habitual glucosamine consumption and the risk of cancer and non-neoplastic diseases necessitates further investigation.

Axl promotes intracranial aneurysm rupture by regulating macrophage polarization toward M1 STAT1/HIF-1α.

Background: Macrophage infiltration and polarization are crucial for the pathogenesis of intracranial aneurysm (IA) rupture. Axl, a receptor tyrosine kinase, is involved in inflammation and efferocytosis in multiple organs. Upregulated soluble Axl in cerebrospinal fluid (CSF) and plasma is correlated with intracranial aneurysm rupture.

Inhibition of SIRT1 by miR-138-5p provides a mechanism for inhibiting osteoblast proliferation and promoting apoptosis under simulated microgravity.

Microgravity can inhibit osteoblast proliferation and promote apoptosis, which is related to a reduction in mechanical stress on the bones and results in disuse osteoporosis, but the detailed mechanism is still unclear. In this study, we first demonstrated that miR-138-5p was upregulated, inhibited osteoblast proliferation and induced osteoblast apoptosis under simulated microgravity. Moreover, miR-138-5p silencing partially mitigated the effects of proliferation and apoptosis of MC3T3-E1 cells.

Exosomes from Microvascular Endothelial Cells under Mechanical Unloading Inhibit Osteogenic Differentiation via miR-92b-3p/ELK4 Axis.

Mechanical unloading-related bone loss adversely harms astronauts' health. Nevertheless, the specific molecular basis underlying the phenomenon has not been completely elucidated. Although the bone microvasculature contributes significantly to bone homeostasis, the pathophysiological role of microvascular endothelial cells (MVECs) in bone loss induced by mechanical unloading is not apparent.

Bioinformatic analysis of the RNA expression patterns in microgravity-induced bone loss.

Researchers have linked microgravity in space to the significant imbalance between bone formation and bone resorption that induces persistent bone loss in load-bearing bones. However, the underlying molecular mechanisms are still unclear, which hinders the development of therapeutic measures. The aim of this study was to identify hub genes and explore novel molecular mechanisms underlying microgravity-induced bone loss using transcriptome datasets obtained from the GEO and SRA databases.

Methyltransferase Setdb1 Promotes Osteoblast Proliferation by Epigenetically Silencing Macrod2 with the Assistance of Atf7ip.

Bone loss caused by mechanical unloading is a threat to prolonged space flight and human health. Epigenetic modifications play a crucial role in varied biological processes, but the mechanism of histone modification on unloading-induced bone loss has rarely been studied. Here, we discovered for the first time that the methyltransferase Setdb1 was downregulated under the mechanical unloading both in vitro and in vivo so as to attenuate osteoblast proliferation.

Predictors of thromboembolic complications after stent-assisted coiling of acutely ruptured intracranial aneurysms: A retrospective multicenter study.

Background: Stent-assisted coiling (SAC) has been reported to safely and effectively treat wide-necked unruptured intracranial aneurysms. However, SAC of acutely ruptured aneurysms is controversial because of perioperative thromboembolic complications. We aimed to investigate the predictors of the thromboembolic complications after SAC of acutely ruptured aneurysms.

Stent-assisted coiling of acutely ruptured cerebral aneurysm: a multicenter prospective registry study (SAVE).

Background: Stent-assisted coiling (SAC) has been reported as a feasible and effective treatment of wide-neck cerebral aneurysms. However, the evidence of SAC of ruptured cerebral aneurysm is lacking. There are no prospective multicenter studies regarding SAC of acutely ruptured aneurysms within 72 hours after subarachnoid hemorrhage.

Circulating Exosomes from Mice with LPS-Induced Bone Loss Inhibit Osteoblast Differentiation.

Osteoimmunology focuses on the intermodulation between bone and the immune system. Lipopolysaccharide (LPS)-induced bone loss models are commonly used to investigate the interface between inflammation and osteoporosis. Circulating exosomes can regulate physiological and pathological processes through exosomal microRNAs and proteins.

HDAC6 Negatively Regulates miR-155-5p Expression to Elicit Proliferation by Targeting RHEB in Microvascular Endothelial Cells under Mechanical Unloading.

Mechanical unloading contributes to significant cardiovascular deconditioning. Endothelial dysfunction in the sites of microcirculation may be one of the causes of the cardiovascular degeneration induced by unloading, but the detailed mechanism is still unclear. Here, we first demonstrated that mechanical unloading inhibited brain microvascular endothelial cell proliferation and downregulated histone deacetylase 6 (HDAC6) expression.

The small protein MafG plays a critical role in MC3T3-E1 cell apoptosis induced by simulated microgravity and radiation.

Microgravity and radiation exposure-induced bone damage is one of the most significant alterations in astronauts after long-term spaceflight. However, the underlying mechanism is still largely unknown. Recent ground-based simulation studies have suggested that this impairment is likely mediated by increased production of reactive oxygen species (ROS) during spaceflight.

The combined effects of simulated microgravity and X-ray radiation on MC3T3-E1 cells and rat femurs.

Microgravity is well-known to induce Osteopenia. However, the combined effects of microgravity and radiation that commonly exist in space have not been broadly elucidated. This research investigates the combined effects on MC3T3-E1 cells and rat femurs.

Bone-targeted lncRNA OGRU alleviates unloading-induced bone loss via miR-320-3p/Hoxa10 axis.

Unloading-induced bone loss is a threat to human health and can eventually result in osteoporotic fractures. Although the underlying molecular mechanism of unloading-induced bone loss has been broadly elucidated, the pathophysiological role of long noncoding RNAs (lncRNAs) in this process is unknown. Here, we identified a novel lncRNA, OGRU, a 1816-nucleotide transcript with significantly decreased levels in bone specimens from hindlimb-unloaded mice and in MC3T3-E1 cells under clinorotation-unloading conditions.

Targeted overexpression of the long noncoding RNA ODSM can regulate osteoblast function in vitro and in vivo.

Ameliorating bone loss caused by mechanical unloading is a substantial clinical challenge, and the role of noncoding RNAs in this process has attracted increasing attention. In this study, we found that the long noncoding RNA osteoblast differentiation-related lncRNA under simulated microgravity (lncRNA ODSM) could inhibit osteoblast apoptosis and promote osteoblast mineralization in vitro. The increased expression level of the lncRNA ODSM partially reduced apoptosis and promoted differentiation in MC3T3-E1 cells under microgravity unloading conditions, and the effect was partially dependent on miR-139-3p.

Targeted silencing of miRNA-132-3p expression rescues disuse osteopenia by promoting mesenchymal stem cell osteogenic differentiation and osteogenesis in mice.

Background: Skeletal unloading can induce severe disuse osteopenia that often occurs in spaceflight astronauts or in patients subjected to prolonged bed-rest or immobility. Previously, we revealed a mechano-sensitive factor, miRNA-132-3p, that is closely related to the osteoblast function. The aim of this study was to investigate whether miRNA-132-3p could be an effective target for treating disuse osteopenia.

MiR-30 family members inhibit osteoblast differentiation by suppressing Runx2 under unloading conditions in MC3T3-E1 cells.

Disuse osteoporosis is common in prolonged therapeutic bed rest, space flight and immobilization due to limb fracture, which is related to reduction of mechanical stress on bone. Mechanical unloading can inhibit the differentiation of osteoblasts, but the detailed mechanism is still unclear. Runt-related transcription factor-2 (Runx2), is an important transcription factor, which plays a crucial role in disuse osteoporosis induced by unloading conditions.

MicroRNA-139-3p regulates osteoblast differentiation and apoptosis by targeting ELK1 and interacting with long noncoding RNA ODSM.

Recent studies have confirmed that microRNAs and lncRNAs can affect bone cell differentiation and bone formation. In this study, miR-139-3p was upregulated in the femurs of hindlimb unloading mice and MC3T3-E1 cells under simulated microgravity; this effect was related to osteoblast differentiation and apoptosis. Silencing miR-139-3p attenuated the suppression of differentiation and the promotion of MC3T3-E1 cell apoptosis induced by simulated microgravity.