BACKGROUND: H-type vessels are mainly distributed in the metaphysis, which can promote the proliferation of osteocytes, further accelerating osteogenesis.OBJECTIVE: To investigate the expression of H-type vessels in the subchondral bone during the occurrence and development of osteoarthritis.METHODS: 8-week-old C57 mice were randomly divided into experimental and sham groups, followed by the right medial menisectomy to establish the osteoarthritis models or only articular capsulotomy. The knee samples were removed at 4 weeks postoperatively, and were stained with safranin-O-fast green to evaluate the degree of injury. The expression levels of CD31, Emcn and matrix metalloproteinase 13 were detected by immunofluorescent staining. The changes of the subchondral bone were observed by hematoxylin-eosin staining and the changes of bone mass in the subchondral bone were analyzed by micro-CT.RESULTS AND CONCLUSION: Compared with the sham group, the Osteoarthritis Research Society International scores, expression levels of CD31, Emcn, H-type vessels and matrix metalloproteinase 13, as well as the bone mass in the subchondral bone were significantly increased in the experimental group (P < 0.05). To conclude, the increased H-type vessels in the subchondral bone promote the hyperplasia and remodeling of subchondral bone in the progression of osteoarthritis.

Liver ischemia reperfusion injury (IRI) is one of the main causes of liver dysfunction or functional failure after liver transplantation or liver resection. As the main organ of lipid metabolism, liver is closely related to lipid metabolic balance. Lipoxygenase is a non-heme iron-containing oxidases that oxidizes polyunsaturated fatty acids to produce hydroxy-eicosanotetraenoic acid. Lipoxygenase is excessively expressed during liver ischemia, causing lipid metabolic disorders. High expression of several proinflammatory cytokines induced by lipoxygenase during liver reperfusion. Lipid peroxidation induced by lipoxygenase leads to the production of lipid oxygen free radicals, which induces iron death mainly characterized by lipid peroxidation, thus affecting apoptosis and tissue damage. This review mainly introduces the latest progress of lipoxygenase in liver IRI.

The review focuses upon the mechanism of exosome derived from mesenchymal stem cells in hepatic ischemia-reperfusion injury(IRI)to provide references for clinical application of exosomes in alleviating hepatic IRI.

Liver ischemia-reperfusion injury (IRI) is a significant factor contributing to liver dysfunction following surgical procedures such as liver transplantation and hepatectomy, and its pathogenesis is closely associated with oxidative stress and immune responses. However, effective prevention and therapeutic strategies are still lacking. Short-chain fatty acids (SCFAs), primarily produced by the fermentation of gut microbiota, are the major source of these acids in the human body. Research has indicated that SCFAs play a significant role in oxidative stress and immune response. This review primarily focuses on the advancements on the role of SCFAs, the main metabolic byproducts of gut microbiota, in liver IRI, with a view to provide insights for the development of prevention and treatment strategies for liver IRI.

Objective:To evaluate the feasibility of using cortical bone trajectory (CBT) screws in the osteoporotic thoracolumbar fixation by comparing the bone CT values at the bone-screw interface between traditional trajectory (TT) screws and CBT screws in patients with different bone densities.Methods:The high-resolution CT imaging data of thoracolumbar segments following thoracic or lumbar spine fractures from April 2020 to October 2022 were collected at The Second Hospital Affiliated to Wenzhou Medical University for retrospective analysis. They were divided into 3 groups: a normal bone mass group, an osteopenia group and an osteoporosis group. From each group 30 cases were chosen (90 cases in total, 36 males and 54 females). All the data were imported into Mimics 18.0 for three-dimensional bone reconstruction in which placement of TT and CBT screws was simulated on the vertebrae from T10 to L2 (non-fractured vertebrae). Regions of interest (ROI) where each simulated screw intersected the bone were segmented to measure their CT bone values. For each vertebra in each group, the relative difference percentage in average CT value of ROI between TT and CBT screws was calculated. The CT values of ROI were compared in the same group between TT and CBT screws from T10 to L2; the CT values of ROI were compared in the same screws among the 3 groups from T10 to L2; the CT values of ROI were compared between the CBT screws in the osteopenia and osteoporosis groups and the TT screws in the normal bone mass group; the relative difference percentages in average CT value of ROI between CBT and TT screws were compared between the 3 groups from T10 to L2.Results:The average CT value of ROI for CBT screws was significantly higher than that for TT screws from T10 to L2 in every group ( P< 0.001); as for the CT values of ROI for CBT and TT screws from T10 to L2, the osteoporosis group0.05). At T10, T12, and L1, the relative difference percentage in average CT value of ROI between CBT and TT screws was significantly higher in the osteopenia and osteoporosis groups than that in the normal bone mass group ( P<0.05), but there was no such a difference between the osteopenia and the osteoporosis groups ( P>0.05). At T11 and L2, there was no significant difference between the 3 groups in the relative difference percentage in average CT value of ROI between CBT and TT screws ( P>0.05). Conclusions:As bone mass decreases, both CBT and TT screws lead to a significant decrease in the bone density at the bone-screw interface. In patients with osteoporosis, CBT screws can still lead to a higher bone density at the bone-screw interface than TT screws, thus providing a higher strength at the bone-screw interface.

Although somatic cells can be reprogrammed to pluripotent stem cells (PSCs) with pure chemicals, authentic pluripotency of chemically induced pluripotent stem cells (CiPSCs) has never been achieved through tetraploid complementation assay. Spontaneous reprogramming of spermatogonial stem cells (SSCs) was another non-transgenic way to obtain PSCs, but this process lacks mechanistic explanation. Here, we reconstructed the trajectory of mouse SSC reprogramming and developed a five-chemical combination, boosting the reprogramming efficiency by nearly 80- to 100-folds. More importantly, chemical induced germline-derived PSCs (5C-gPSCs), but not gPSCs and chemical induced pluripotent stem cells, had authentic pluripotency, as determined by tetraploid complementation. Mechanistically, SSCs traversed through an inverted pathway of in vivo germ cell development, exhibiting the expression signatures and DNA methylation dynamics from spermatogonia to primordial germ cells and further to epiblasts. Besides, SSC-specific imprinting control regions switched from biallelic methylated states to monoallelic methylated states by imprinting demethylation and then re-methylation on one of the two alleles in 5C-gPSCs, which was apparently distinct with the imprinting reprogramming in vivo as DNA methylation simultaneously occurred on both alleles. Our work sheds light on the unique regulatory network underpinning SSC reprogramming, providing insights to understand generic mechanisms for cell-fate decision and epigenetic-related disorders in regenerative medicine.
Male ; Mice ; Animals ; Cellular Reprogramming/genetics* ; Tetraploidy ; Pluripotent Stem Cells/metabolism* ; Induced Pluripotent Stem Cells/metabolism* ; DNA Methylation ; Spermatogonia/metabolism* ; Germ Cells/metabolism*