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Angiogenesis is a physiological process for endometrial regeneration in the menstrual cycle and remodeling during pregnancy. Endogenous hydrogen sulfide (H2S), produced by cystathionine-β synthase (CBS) and cystathionine-γ lyase (CSE), is a potent proangiogenic factor; yet, whether the H2S system is expressed in the endometrium and whether H2S plays a role in endometrial angiogenesis are unknown. This study was to test whether estrogens stimulate endometrial H2S biosynthesis to promote endometrial microvascular endothelial cell (EMEC) angiogenesis. CBS messenger RNA/protein and H2S production significantly differed among endometria from postmenopausal (POM), premenopausal secretory (sPRM), and proliferative (pPRM) nonpregnant (NP) and pregnant (Preg) women (P < .05) in a rank order of POM approximately equal to sPRM is less than pPRM is less than Preg, positively correlating with angiogenesis indices and endogenous estrogens and with no difference in CSE expression. CBS and CSE proteins were localized to stroma, glands, and vessels in endometrium, and greater stromal CBS protein was observed in the pPRM and Preg states. Estradiol-17β (E2) (but not progesterone) stimulated CBS (but not CSE) expression and H2S production in pPRM endometrial stromal cells (ESCs) in vitro, which were attenuated by ICI 182 780. The H2S donor sodium hydrosulfide promoted in vitro EMEC angiogenesis. Co-culture with sPRM, pPRM, and Preg ESCs all stimulated EMEC migration with a rank order of sPRM less than pPRM approximately equal to Preg. CBS (but not CSE) inhibition attenuated ESC-stimulated EMEC migration. E2 did not affect EMEC migration but potentiated ESC-stimulated EMEC migration. Altogether, estrogens stimulate specific receptor-dependent stromal CBS-H2S production to promote endometrial EMEC angiogenesis in women.

Although many therapeutic interventions have shown promise in treating spinal cord injury, focusing on a single aspect of repair cannot achieve successful and functional regeneration in patients following spinal cord injury . In this study, we applied a combinatorial approach for treating spinal cord injury involving neuroprotection and rehabilitation, exploiting cell transplantation and functional sensorimotor training to promote nerve regeneration and functional recovery. Here, we used a mouse model of thoracic contusive spinal cord injury to investigate whether the combination of bone marrow mesenchymal stem cell transplantation and exercise training has a synergistic effect on functional restoration. Locomotor function was evaluated by the Basso Mouse Scale, horizontal ladder test, and footprint analysis. Magnetic resonance imaging, histological examination, transmission electron microscopy observation, immunofluorescence staining, and western blotting were performed 8 weeks after spinal cord injury to further explore the potential mechanism behind the synergistic repair effect. In vivo, the combination of bone marrow mesenchymal stem cell transplantation and exercise showed a better therapeutic effect on motor function than the single treatments. Further investigations revealed that the combination of bone marrow mesenchymal stem cell transplantation and exercise markedly reduced fibrotic scar tissue, protected neurons, and promoted axon and myelin protection. Additionally, the synergistic effects of bone marrow mesenchymal stem cell transplantation and exercise on spinal cord injury recovery occurred via the PI3K/AKT/mTOR pathway. In vitro, experimental evidence from the PC12 cell line and primary cortical neuron culture also demonstrated that blocking of the PI3K/AKT/mTOR pathway would aggravate neuronal damage. Thus, bone marrow mesenchymal stem cell transplantation combined with exercise training can effectively restore motor function after spinal cord injury by activating the PI3K/AKT/mTOR pathway.

Abstract Background In patients with cardiovascular diseases, it is reported that the triglyceride-glucose index (TGI) potentially indicates prognosis. However, the results are controversial. Moreover, whether age has an impact on the predictive value of TGI remains unclear. Methods Participants with cardiovascular diseases were enrolled using the China Health and Retirement Longitudinal Study (CHARLS) registry. TGI was calculated as ln (triglyceride×glucose/2). The survival status was recorded every 2 years in the follow-up waves. Multivariate regression analysis was carried out to determine the relationship between TGI levels and long-term all-cause mortality in patients grouped by different age. Patients younger than 65 years old were regarded as middle-aged group. Otherwise, they were classified as old group. Results In total, 2923 patients with cardiovascular diseases and baseline blood test results were included. After 7 years of follow-up, 242 (8.91%) patients died. Cox regression analysis revealed that higher TGI levels were associated with a higher risk of long-term all-cause mortality in middle-aged participants (hazard ratio [HR], 3.64; 95% confidence interval [CI] 1.44–9.22, P = 0.006) but not in old participants (HR 1.20, 95% CI 0.62–2.32, P = 0.594, P for interaction = 0.017), after adjusting physical activity and other factors. Kaplan–Meier estimate analysis and restricted cubic spline curves showed similar results. Conclusion TGI was a promising marker for predicting all-cause mortality in middle-aged patients after cardiovascular diseases. Patients younger than 65 years old who have a higher level of TGI may develop a higher risk of all-cause mortality, and they are encouraged to control vascular risk factors and take more physical activity to improve their prognosis. Additionally, whether intervention in regulating TGI levels is beneficial for the prognosis of these patients needs further investigation.

Abstract Background Since angiogenesis occurs as the pathological process following myocardial infarction to alleviate ischemia, therapeutic angiogenesis has been proposed to be a cardioprotective strategy. CD44 has been implicated in endothelial cell functions and its role has been well established in angiogenesis for years. Although recent studies indicate the close correlation between CD44 and exosome, as well as the two being implicated in myocardial ischemia pathological processes, the effect and the underlying mechanism of CD44 and its regulated plasma exosome in pathological angiogenesis post-myocardial infarction have not been fully elucidated. Methods In this study, we used CD44 knockout mice to study the in vivo impacts of CD44 on ischemic angiogenesis in myocardial infarction. Mouse cardiac function was measured by echocardiography, histological changes were observed by Evans Blue and TTC-double staining and Masson’s trichrome staining, and molecular changes were detected by immunofluorescence. In the in vitro study, CD44 knockout HUVECs were generated and CD44 inhibitor was used to study the mechanism of CD44 on angiogenesis. We performed the immunoprecipitation, proximity ligation assay, and super-resolution imaging to study the mechanistic regulation of FGFR2 signaling transduction by CD44. Importantly, we also isolated plasma exosomes from myocardial infarction model mice and studied the effect of plasma exosomes on the activation of the FGFR2 signaling pathway and the related phenotypic alterations, including exosomes uptake and angiogenic function in primary mouse microvascular endothelial cells, and further discovered the regulation mechanism of exosomal miRNAs. Results We observed that the expression of CD44 in the border zone of the infarcted heart was tightly related to pathological angiogenesis following myocardial ischemia. The depletion of CD44 impaired angiogenesis and impacts biogenesis and proangiogenic function of plasma exosomes. Subsequently, we found that CD44 mediated the activation of the FGFR2 signaling pathway as well as the caveolin 1-dependent uptake of exosomes in vascular endothelial cells. Most importantly, the proangiogenic therapeutic effect of plasma exosomal miRNAs depended upon the participation of CD44/FGFR2 signaling transduction in vascular endothelial cells. Conclusion CD44 and its regulated plasma exosomes have crucial potent angiogenic activity. Our studies elucidate that CD44 plays a key role in plasma exosomal miRNA-enhanced angiogenic FGFR2 singling transduction and ischemic angiogenesis in the early stage of myocardial infarction.

The popularity of Agrocybe cylindracea is increasing due to its unique flavor and nutritional value. The Agrocybe cylindracea cap is a key aspect of the growth process, and high-throughput observation of cap traits in greenhouses by machine vision is a future development trend of smart agriculture. Nevertheless, the segmentation of the Agrocybe cylindracea cap is extremely challenging due to its similarity in color to the rest of the mushroom and the occurrence of mutual occlusion, presenting a major obstacle for the effective application of automation technology. To address this issue, we propose an improved instance segmentation network called Agrocybe cylindracea R-CNN (AC R-CNN) based on the Mask R-CNN model. AC R-CNN incorporates hybrid dilated convolution (HDC) and attention modules into the feature extraction backbone network to enhance the segmentation of adhesive mushroom caps and focus on the segmentation objects. Furthermore, the Mask Branch module is replaced with PointRend to improve the network’s segmentation accuracy at the edges of the mushroom caps. These modifications effectively solve the problems of the original algorithm’s inability to segment adhesive Agrocybe cylindracea caps and low accuracy in edge segmentation. The experimental results demonstrate that AC R-CNN outperforms the original Mask R-CNN in terms of segmentation performance. The average precision (AP) is improved by 12.1%, and the F1 score is improved by 13.7%. Additionally, AC R-CNN outperforms other networks such as Mask Scoring R-CNN and BlendMask. Therefore, the research findings of this study can meet the high-precision segmentation requirements of Agrocybe cylindracea caps and lay a theoretical foundation for the development of subsequent intelligent phenotyping devices and harvesting robots.

BackgroundCardiac telerehabilitation offers a flexible and accessible model for patients with coronary artery disease (CAD), effectively transforming the traditional cardiac rehabilitation (CR) approach. ObjectiveThis systematic review and meta-analysis aimed to evaluate the long-term effectiveness of cardiac telerehabilitation. MethodsWe searched randomized controlled trials (RCTs) in 7 electronic databases: PubMed, Web of Science, EMBASE, the Cochrane Central Register of Controlled Trials, ClinicalTrials.gov, the China National Knowledge Infrastructure, and WANFANG. The primary outcome focused on cardiopulmonary fitness. For secondary outcomes, we examined cardiovascular risk factors (blood pressure, BMI, and serum lipids), psychological scales of depression and anxiety, quality of life (QoL), cardiac telerehabilitation adherence, and adverse events. ResultsIn total, 10 RCTs fulfilled the predefined criteria, which were reviewed in our meta-analysis. The results showed that after cardiac telerehabilitation, there was a significant difference in the improvement in long-term peak oxygen uptake compared to center-based CR (mean difference [MD] 1.61, 95% CI 0.38-2.85, P=.01), particularly after 6-month rehabilitation training (MD 1.87, 95% CI 0.34-3.39, P=.02). The pooled effect size of the meta-analysis indicated that there were no significant differences in the reduction in cardiovascular risk factor control. There was also no practical demonstration of anxiety scores or depression scores. However, cardiac telerehabilitation demonstrated an improvement in the long-term QoL of patients (MD 0.92, 95% CI 0.06-1.78, P=.04). In addition, the study reported a high completion rate (80%) for cardiac telerehabilitation interventions. The incidence of adverse events was also low during long-term follow-up. ConclusionsCardiac telerehabilitation proves to be more effective in improving cardiopulmonary fitness and QoL during the long-term follow-up for patients with CAD. Our study highlights monitoring-enabled and patient-centered telerehabilitation programs, which play a vital role in the recovery and development of CAD and in the long-term prognosis of patients.

An optically pumped magnetometer (OPM) for three-axis magnetic field measurement is demonstrated based on dual-pump polarization in a time-sharing regime. By detecting light absorption, each pump beam can achieve high-sensitive transverse measurement under modulation magnetic fields around a near-zero field. After the combination and orthogonalization of two pumps according to the scale factors along the reference axis, a three-axis orthogonal measurement system is obtained. Compared with existing methods, this configuration reduces misalignment errors introduced by the nonorthogonality of the sensitive directions and avoid coupling errors introduced by cross-axis DC magnetic fields. The coupling among the three axes is below 0.39%. On this basis, this OPM performs equivalent performances of each axis measurement with high accuracy and realizes a high sensitivity of 10 fT/Hz1/2. This SERF OPM can be employed in wide variety of applications including biological magnetic detection and sensitive tests of fundamental physics.

The treatment of cardiovascular and cerebrovascular diseases have undergone major advances in recent decades, allowing for a more effective prevention of cardiovascular and cerebrovascular events. However, cardiac and cerebral atherothrombotic complications still account for substantial morbidity and mortality worldwide. Novel therapeutic strategies are critical to improve patient outcomes following cardiovascular diseases. miRNAs are small non-coding RNAs, that regulate gene expression. Here, we discuss the role of miR-182 in regulating myocardial proliferation, migration, hypoxia, ischemia, apoptosis and hypertrophy in atherosclerosis, CAD, MI, I/R injury, organ transplant, cardiac hypertrophy, hypertension, heart failure, congenital heart disease and cardiotoxicity. Besides, we also summarize the current progress of miR-182 therapeutics in clinical development and discuss challenges that will need to be overcome to enter the clinic for patients with cardiac disease.