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Background: The association between muscle defects and hypertension is well-established. However, the absence of pertinent and uncomplicated clinical indicators presents a challenge. Relative muscle strength (RMS) may offer a viable indicator. This study aimed to explore the association between RMS and hypertension. Methods: A total of 12,720 individuals aged ≥ 45 years from the 2011 wave of the China Health and Retirement Longitudinal Study (CHARLS) were included. Grip strength was recorded and appendicular skeletal muscle mass (ASM) was estimated using a validated mathematical formula. The RMS was calculated as the ratio of grip strength to ASM. Hypertension was determined based on previous diagnosis, history of hypertension medication use, and current blood pressure. Logistic regression models were employed to investigate the relationship between RMS and hypertension. Results: The prevalence of hypertension was 41.7% (5,307/12,720 patients). RMS was negatively correlated with hypertension with an OR (95% CI) of 0.68 (0.59–0.79) for males, 0.81 (0.73–0.90) for females, and 0.78 (0.72–0.85) for the entire population after adjusting for related covariates including age, education, marital history, smoking history, drinking history, diabetes, hyperlipidemia, and obesity. The trend test showed a linear association among males, females, or the entire population. Stratified analysis showed a consistent negative correlation between RMS and hypertension. Conclusions: Higher RMS is an independent protective factor against hypertension and efforts to promote RMS may be beneficial for the prevention and management of hypertension. [ABSTRACT FROM AUTHOR]

Morphogens act in developing tissues to control the spatial arrangement of cellular differentiation. The activity of a morphogen has generally been viewed as a concentration-dependent response to a diffusible signal, but the duration of morphogen signalling can also affect cellular responses. One such example is the morphogen sonic hedgehog (SHH). In the vertebrate central nervous system and limbs, the pattern of cellular differentiation is controlled by both the amount and the time of SHH exposure. How these two parameters are interpreted at a cellular level has been unclear. Here we provide evidence that changing the concentration or duration of SHH has an equivalent effect on intracellular signalling. Chick neural cells convert different concentrations of SHH into time-limited periods of signal transduction, such that signal duration is proportional to SHH concentration. This depends on the gradual desensitization of cells to ongoing SHH exposure, mediated by the SHH-dependent upregulation of patched 1 (PTC1), a ligand-binding inhibitor of SHH signalling. Thus, in addition to its role in shaping the SHH gradient, PTC1 participates cell autonomously in gradient sensing. Together, the data reveal a novel strategy for morphogen interpretation, in which the temporal adaptation of cells to a morphogen integrates the concentration and duration of a signal to control differential gene expression. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis (MS) is an immune-mediated demyelinated disease of the central nervous system. Activation of microglia is involved in the pathogenesis of myelin loss.Objective: This study is focused on the role of Hv1 in regulating demyelination and microglial activation through reactive oxygen species (ROS) production after lysophosphatidylcholine (LPC)-mediated demyelination. We also explored autophagy in this process.Methods: A model of demyelination using two-point LPC injection into the corpus callosum was established. LFB staining, immunofluorescence, Western blot, and electron microscopy were used to study the severity of demyelination. Microglial phenotype and autophagy were detected by immunofluorescence and Western blot. Morris water maze was used to test spatial learning and memory ability.Results: We have identified that LPC-mediated myelin damage was reduced by Hv1 deficiency. Furthermore, we found that ROS and autophagy of microglia increased in the demyelination region, which was also inhibited by Hv1 knockout.Conclusion: These results suggested that microglial Hv1 deficiency ameliorates demyelination through inhibition of ROS-mediated autophagy and microglial phenotypic transformation. [ABSTRACT FROM AUTHOR]

To broaden the stable operating range of hypersonic aircrafts, this work examined the mechanisms of the hysteresis phenomenon for hypersonic inlets under acceleration/deceleration process conditions. Guided by unsteady flowfield simulations on two typical 2D hypersonic inlets with different critical unstart modes of hard unstart and soft unstart, two dominant characteristics of the hysteresis phenomenon during the acceleration/deceleration processes were identified. The first characteristic is that, at the same free-stream Mach number in the hysteresis range, the main separation bubble at the cowl-lip station or the internal contraction section of the inlet during the acceleration process is considerably larger than that induced by the cowl shock wave/boundary layer interaction (SWBLI) during the deceleration process. The second characteristic is that the self-starting Mach number during the acceleration process exceeds the unstart Mach number during the deceleration process. Two mechanisms are proposed to explain such hysteresis. First, in the unstarting flowfield at relatively high incoming Mach numbers, the large-scale separation bubble under the unstarted state stems from the self-coupled SWBLI, instead of the throat blockage or the isolated SWBLI, the dimensionless pressure rise through the self-coupled SWBLI during acceleration is much larger than that of the isolated SWBLI during deceleration. Second, the transition between the unstarted state and the started state in the hysteresis range is, in essence, the conversion between the self-coupled SWBLI and the isolated one. [ABSTRACT FROM AUTHOR]

[Display omitted] • A novel host–guest nanoprobe is fabricated by adamantane-modified rhodamine B and cucurbit[7]uril. • The constructed nanoprobe exhibits highly selective and sensitive to detect salicylic acid. • The fluorescence signal amplification strategy is engineered to detect salicylic acid with 330-fold fluorescent enhancement. • The detection mechanism attributes to the synergetic effect of host–guest and hydrogen bond interactions. • The nanoprobe is useful for visually detecting SA in callus and plants. Salicylic acid (SA), the crucial phytohormone, is biosynthesized by plants in response to fight against multifarious phytopathogens and is a central mediator for regulating plant physiology and pathology processes including biotic and abiotic stress. However, current research still lacks of effective and simple tactics to track SA for understanding the underlying mechanisms in plants. Herein, we constructed a supramolecular host–guest nanoprobe (RAD&CB[7]) based on cucurbit[7]uril (CB[7]) and adamantane (AD)-modified rhodamine derivative, the nanoprobe selectivity and sensitivity for SA were very satisfactory. The nanoprobe RAD&CB[7] has been employed to (1) improve the fluorescent signal for detecting SA about 330-fold at lower concentration of SA (20 μM) in vitro, which is very difficult to realize by previous SA fluorescent probes. The density functional theory (DFT) calculations demonstrated the signal amplification is significantly higher than other fluorescent probes reported in literature due to the synergetic effects of host–guest and hydrogen-bond interaction. (2) realize the detection of SA in living Nicotiana glutinosa L. callus, Arabidopsis thaliana, and tomato seedlings even at ultra-low concentrations of RAD&CB[7] (minimum 1 μM) and SA (minimum 5 μM), compared with previous probes (minimum 10 μM) for detecting SA (minimum 25 μM) in vivo, thus realized quantitatively detected SA in callus and Arabidopsis thaliana roots. (3) verify SA-induced stomatal closure in the leaves of Arabidopsis thaliana by host–guest fluorescent probe technology for the first time. The remarkable in vitro and in vivo performance make this fluorescence signal amplification strategy a powerful tool for studying SA-related physiology and pathology in biological processes and discovering novel immune activators for crop protection. [ABSTRACT FROM AUTHOR]

Metformin (MET) is the first-line therapeutic option for patients with type 2 diabetes that has garnered substantial attention over recent years. However, an insufficient number of studies have been performed to assess its effects on insulin resistance and the expression profile of long noncoding RNAs (lncRNAs). The present study divided mice into three groups: Control group, high-fat diet (HFD) group and HFD + MET group. A high-throughput sequencing analysis was conducted to detect lncRNA and mRNA expression levels, and differentially expressed lncRNAs were selected. Subsequently, the differentially expressed lncRNAs were validated both in vivo and in vitro (mouse liver AML12 cells treated with Palmitic acid) models of insulin resistance. After validating randomly selected lncRNAs via reverse transcription-quantitative PCR a novel lncRNA, NONMMUT031874.2, was identified, which was upregulated in the HFD group and reversed with MET treatment. To investigate the downstream mechanism of NONMMUT031874.2, lncRNA-microRNA (miR/miRNA)-mRNA co-expression network was constructed and NONCODE, miRBase and TargetScan databases were used, which indicated that NONMMUT031874.2 may regulate suppressor of cytokine signaling 3 by miR-7054-5p. For the in vitro part of the present study, AML12 cells were transfected with small interfering RNA to knock down NONMMUT031874.2 expression before being treated with palmitic acid (PA) and MET. The results showed that the expression of NONMMUT031874.2 was significantly increased whereas miR-7054-5p expression was significantly decreased by PA treatment. By contrast, after knocking down NONMMUT031874.2 expression or treatment with MET, the aforementioned in vitro observations were reversed. In addition, it was also found that NONMMUT031874.2 knockdown and treatment with MET exerted similar effects in alleviating insulin resistance and whilst decreasing glucose concentration in AML12 cells. These results suggest that MET treatment can ameliorate insulin resistance by downregulating NONMMUT031874.2 expression. [ABSTRACT FROM AUTHOR]