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Introduction Current international guidelines recommend aerobic, resistance, and combined exercises for the management of type 2 diabetes mellitus (T2DM). In our study, we conducted a network meta-analysis to assess the comparative impact of different exercise training modalities on glycemic control, cardiovascular risk factors, and weight loss in patients with T2DM. Methods We searched five electronic databases to identify randomized controlled trials (RCTs) that compared the differences between different exercise training modalities for patients with T2DM. The risk of bias in the included RCTs was evaluated according to the Cochrane tool. Network meta-analysis was performed to calculate mean difference the ratio of the mean and absolute risk differences. Data were analyzed using R-3.4.0. Results A total of 37 studies with 2208 patients with T2DM were included in our study. Both supervised aerobic and supervised resistance exercises showed a significant reduction in HbA1c compared to no exercise (0.30% lower, 0.30% lower, respectively), however, there was a less reduction when compared to combined exercise (0.17% higher, 0.23% higher). Supervised aerobic also presented more significant improvement than no exercise in fasting plasma glucose (9.38 mg/dl lower), total cholesterol (20.24 mg/dl lower), triacylglycerol (19.34 mg/dl lower), and low-density lipoprotein cholesterol (11.88 mg/dl lower). Supervised resistance showed more benefit than no exercise in improving systolic blood pressure (3.90 mmHg lower]) and total cholesterol (22.08 mg/dl lower]. In addition, supervised aerobic exercise was more powerful in improving HbA1c and weight loss than unsupervised aerobic (HbA1c: 0.60% lower; weight loss: 5.02 kg lower) and unsupervised resistance (HbA1c: 0.53% lower) exercises. Conclusion Compared with either supervised aerobic or supervised resistance exercise alone, combined exercise showed more pronounced improvement in HbA1c levels; however, there was a less marked improvement in some cardiovascular risk factors. In terms of weight loss, there were no significant differences among the combined, supervised aerobic, and supervised resistance exercises. Trial registration Our study protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO); registration number: CRD42017067518 .

We recognize the stochastic collisions of dopamine contained phospholipid vesicle on carbon fiber nanoelectrode, extending the observation of discrete collision events on nanoelectrode to biologically relevant analytes. To decrease noise interference to the technique, the dimensions of nanoelectrode was systematically investigated and optimized. Scanning electron microscopy （SEM） further supported the comparable sizes of nanoelectrode and vesicles （-100 nm in diameter）. Vesicles collision and rupture on the surface of nanoelectrode led to the dopamine release from vesicles, which could be electrochemically oxidized to dopamine-o-quinone and detected via voltammetry. The comparable size of the nanoelectrode with vesicles and fast voltammetry allowed differentiation of single collision events from the current magnitudes and peak widths in the electrochemical collision experiments, which shows the efficacy of the method to characterize vesicle samples. This work provides a foundation upon which quantitative sensor technology might be built for the detection of dopamine contained vesicles with high spatial and temporal resolution.

Rejuvenation of telomeres with various lengths has been found in induced pluripotent stem cells （iPSCs）. Mechanisms of telomere length regulation during induction and proliferation of iPSCs remain elusive. We show that telomere dynamics are variable in mouse iPSCs during reprogramming and passage, and suggest that these differences likely result from multiple potential factors, including the telomerase machinery, telomerase-independent mechanisms and clonal influences including reexpression of exogenous reprogramming factors. Using a genetic model of telomerase-deficient （Terc^-/- and Terc^＋/-） cells for derivation and passages of iPSCs, we found that telomerase plays a critical role in reprogramming and self-renewal of iPSCs. Further, telomerase maintenance of telomeres is necessary for induction of true pluripotency while the alternative pathway of elongation and maintenance by recombination is also required, but not sufficient. Together, several aspects of telomere biology may account for the variable telomere dynamics in iPSCs. Notably, the mechanisms employed to maintain telomeres during iPSC reprogramming are very similar to those of embryonic stem cells. These findings may also relate to the cloning field where these mechanisms could be responsible for telomere heterogeneity after nuclear reprogramming by somatic cell nuclear transfer.

Tibial plateau fractures represent approximately 1% of all fractures which have been reported to commonly accompany by soft tissue injuriesY1 Neglect or missed diagnosis of such soft tissue injuries have negative effects on clinical outcome. In this article, we report a rare case of tibial plateau fracture combined with extensive soft tissue injuries, including bucket-handle tears （BHTs） of both the medial meniscus （MM） and the lateral meniscus （LM）. The patient also had an anterior cruciate ligament （ACL） tibial avulsion fracture, which led to the formation of a loose body in the joint. If left untreated, all of these concomitant injuries could cause unpleasant residual symptoms, such as joint locking and loss of extension.

Aim： SM934 is a novel water-soluble artemisinin derivative with immunoregulatory activities that has been used to treat murine lupus nephritis. In the current study, we investigated the effects of SM934 on rat experimental membranous nephropathy. Methods： Passive Heymann nephritis （PHN） was induced in SD rats by intraperitoneal injection of anti-FxlA serum. The rats were orally administered SM934 （12.5 and 25 mg.kg-1.d-1） or prednisolone （5 mg.kg-1.d-1） for 28 d. Blood and urine sample, and kidney tissue were collected for analyses. Human complement C3a-induced injury of HK-2 cells was used for in vitro experiments. Results： Treatment of PHN rats with SM934 or prednisolone attenuated the progression of glomerulonephritis and renal fibrosis, as evidenced by the reduced level of proteinuria and circulating antibodies, as well as by the reduced immune complex deposition, reversed podocyte injuries, and attenuated tubulointerstitial fibrosis in the kidneys. Furthermore, the two drugs suppressed TGF- β1 expression and Smad2/3 phosphorylation, and increased Smad7 expression in the kidneys. The two doses of SM934 produced almost identical therapeutic effects on PHN rats. Pretreatment with SM934 or a C3a receptor antagonist blocked the C3a-induced epithelial-mesenchymal transition in HK-2 cells in vitro. Conclusion： SM934 ameliorates kidney injury and attenuates the tubulointerstitial fibrosis in PHN rats by down-regulation of the TGF- β1/Smad signaling pathway.

The physical and chemical properties of spinnable pitch showed a huge impact on the performance of resultant pitch carbon fiber even if its physical and chemical properties were slightly changed. Various polycyclic aromatic compounds and abundant free radicals existed in spinnable pitch, and there are many interactions among molecules and free radicals. The molecular structure and composition of spinnable pitch were investigated during incubation, and the effect of molecular evaluation on rheological properties of spinnable pitch was illustrated using various characterization methods in this work. It indicated that n-hexane soluble fraction mainly occurred condensation or cleavage, and a small number of heavy components were generated after a long period. The fraction of n-hexane insoluble/toluene soluble underwent molecular condensation and cross-linking in the presence of oxygen-containing radicals and aromatic hydrocarbon radicals, while toluene insoluble/tetrahydrofuran soluble fraction tended to change in large molecules of polycyclic aromatic hydrocarbons. Lastly, tetrahydrofuran insoluble fraction was condensed due to its high aromaticity during the incubation process, and the content of aromatic carbon increased. These changes of composition and structure of spinnable pitch led to its softening point, increase in viscosity and flow activation energy, and deterioration of the rheological property.

Oligodendrocyte progenitor cells (OPCs) differentiate to myelin-producing mature oligodendrocytes and enwrap growing or demyelinated axons during development and post central nervous diseases. Failure of remyelination owing to cell death or undifferentiation of OPCs contributes to severe neurologic deficits and motor dysfunction. However, how to prevent the cell death of OPCs is still poorly understood, especially in hemorrhagic diseases. In the current study, we injected autologous blood into the mouse lateral ventricular to study the hemorrhage-induced OPC cell death in vivo. The integrity of the myelin sheath of the corpus callosum was disrupted post intraventricular hemorrhage (IVH) assessed by using magnetic resonance imaging, immunostaining, and transmission electron microscopy. Consistent with the severe demethylation, we observed massive cell death of oligodendrocyte lineages in the periventricular area. In addition, we found that ferroptosis is the major cell death form in Hemin-induced OPC death by using RNA-seq analysis, and the mechanism was glutathione peroxidase 4 activity reduction-resulted lipid peroxide accumulation. Furthermore, inhibition of ferroptosis rescued OPC cell death in vitro, and in vivo attenuated IVH-induced white matter injury and promoted recovery of neurological function. These data demonstrate that ferroptosis is an essential form of OPC cell death in hemorrhagic stroke, and rescuing ferroptotic OPCs could serve as a therapeutic target for stroke and related diseases.

As one of China’s most treasured traditional flowers, Rhododendron Subgen. Hymenanthes is renowned worldwide for its evergreen foliage, vibrant flowers, and significant ornamental, landscaping, and economic value. However, climate change poses a serious threat to its future, leading to population declines and endangerment of some species. Despite the ecological and economic importance of Rhododendron Subgen. Hymenanthes , the future distribution of suitable habitats and the most effective strategies for its conservation and utilization remain unclear. This study employs the MaxEnt model, which is well-known for its reliability in predicting species distribution under changing environmental conditions, to predict the potential global distribution of nine species of Rhododendron Subgen. Hymenanthes . The goal is to provide a solid foundation for their conservation, cultivation management, and breeding. The results indicate that, under future climate scenarios, suitable habitat areas for four species ( R. irroratum , R. agastum , R. decorum , and R. arboreum ) will significantly decrease, while suitable habitats for the remaining five species ( R. delavayi , R. fortunei , R. calophytum , R. simiarum , and R. wardii ) will experience slight expansion. Temperature and precipitation are identified as key environmental factors influencing the growth and distribution of these species, affecting their ability to colonize new regions. The migration direction of the expanding regions for all nine species is consistent, with their centroids shifting towards the northwest. These findings provide critical insights for developing targeted conservation strategies, including identifying potential refugia and prioritizing conservation areas under future climate conditions.

Esophageal squamous cell carcinoma (ESCC) is a highly lethal malignancy and remains a major public health burden worldwide, particularly in China, where both incidence and mortality rates are among the highest globally. Recent studies suggest that laminin subunit alpha 3 (LAMA3), a component of the basement membrane, may promote tumor progression; however, its specific role in ESCC remains unclear. In this study, we analyzed public RNA-sequencing data from TCGA and TIMER to evaluate LAMA3 expression and its clinical relevance in ESCC. We also validated LAMA3 protein and mRNA expression in clinical samples and cell lines using immunohistochemistry and RT-qPCR. Using siRNA, we established LAMA3-knockdown ESCC cell models and assessed cell proliferation, colony formation, migration, and invasion in vitro. LAMA3 expression was 2.4-fold higher in ESCC tumor tissues than in adjacent normal tissues ( p  < 0.001). High LAMA3 levels were associated with worse overall survival and disease-free survival ( p  < 0.05). Knockdown of LAMA3 suppressed cell proliferation by 57% ( p  < 0.001), migration by 49% ( p  < 0.001), and invasion by 47% ( p  < 0.001).Pathway enrichment analysis indicated involvement of LAMA3 and its co-expressed genes in cell adhesion, extracellular matrix organization, and the PI3K-AKT pathway. In summary, our results demonstrate that LAMA3 is a major promoter of ESCC progression and a potential biomarker and therapeutic target.

Apoptotic death of cardiac myocytes is associated with ischemic heart disease and chemotherapy‐induced cardiomyopathy. Chemoattractant receptor‐homologous molecule expressed on T helper type 2 cells (CRTH2) is highly expressed in the heart. However, its specific role in ischemic cardiomyopathy is not fully understood. Here, we demonstrated that CRTH2 disruption markedly improved cardiac recovery in mice postmyocardial infarction and doxorubicin challenge by suppressing cardiomyocyte apoptosis. Mechanistically, CRTH2 activation specifically facilitated endoplasmic reticulum (ER) stress‐induced cardiomyocyte apoptosis via caspase‐12‐dependent pathway. Blockage of m‐calpain prevented CRTH2‐mediated cardiomyocyte apoptosis under ER stress by suppressing caspase‐12 activity. CRTH2 was coupled with G αq to elicit intracellular Ca 2+ flux and activated m‐calpain/caspase‐12 cascade in cardiomyocytes. Knockdown of caspase‐4, an alternative to caspase‐12 in humans, markedly alleviated CRHT2 activation‐induced apoptosis in human cardiomyocyte response to anoxia. Our findings revealed an unexpected role of CRTH2 in promoting ER stress‐induced cardiomyocyte apoptosis, suggesting that CRTH2 inhibition has therapeutic potential for ischemic cardiomyopathy. Synopsis Chemoattractant receptor‐homologous molecule expressed on T‐helper type‐2 cells (CRTH2), which mediates the chemoattractant effect of prostaglandin (PG) D2 in leukocytes, is shown here to promote ER stress‐induced cardiomyocyte apoptosis through caspase‐12‐dependent pathway. PGD2/CRTH2 signaling in cardiomyocytes is activated upon ER stress such as anoxia and doxorubicin (DOX) challenge. CRTH2 promotes ER stress‐induced apoptosis in cardiomyocytes through Gαq/m‐calpain/caspase‐12 signaling pathway. CRTH2 inhibition confers cardioprotection against myocardial infaction or DOX treatment in mice by reducing cardiomyocyte apoptosis. Graphical Abstract Chemoattractant receptor‐homologous molecule expressed on T‐helper type‐2 cells (CRTH2), which mediates the chemoattractant effect of prostaglandin (PG) D2 in leukocytes, is shown here to promote ER stress‐induced cardiomyocyte apoptosis through caspase‐12‐dependent pathway.