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Objective. Inflammatory skin disorders are becoming major issues threatening public health with increasing prevalence. This study was to evaluate the anti-inflammatory, antioxidant, and antisenescent activities of traditional folk medicinal plant, Physalis alkekengi L. extracts to alleviate skin inflammation and its possible mechanisms. Methods. Lipopolysaccharides (LPS)-treated murine macrophages RAW264.7 and human skin keratinocytes HaCaT were incubated with the plant extracts, respectively. The production of nitric oxide (NO) was tested by using Griess reagents. The activity of nitric oxide synthase (NOS) was detected through a fluorescence microplate reader. Reactive oxygen species (ROS) production and cell apoptosis were quantified by flow cytometry. The proinflammatory cytokines were measured using ELISA and qRT-PCR. Human skin fibroblasts (HFF-1) were coincubated with D-galactose (D-gal) and the plant extracts. The senescence associated-galactosidase (SA-β-gal) was stained to evaluate cellular senescence. The senescence-associated secretory phenotype (SASP), IL-1β, was measured through ELISA. The mRNA of IL-1α in SLS-stimulated and PGE2 in UV-radiated 3D skin models were detected by qRT-PCR. In vivo ROS production and neutrophil recruitment in CuSO4-treated zebrafish models were observed by fluorescence microscopy. Inflammation-related factors were measured by qRT-PCR. Results. In vitro, Physalis alkekengi L. significantly reduced NO production, NOS activity, cell apoptosis, transcription of TNF-α, IL-6, IL-1β and ROS production. These plant extracts markedly attenuated SA-β-gal and IL-1β and downregulated the production of IL-1α and PGE2. In vivo, the plant extracts dramatically dampened ROS production, the number of neutrophils, and proinflammatory cytokines. Conclusions. Cumulatively, this work systematically demonstrated the anti-inflammatory, antioxidant, and antisenescent properties of Physalis alkekengi L. and proposed the possible roles of Physalis alkekengi L. in inflammatory signaling pathways, providing an effective natural product for the treatment of inflammatory skin disorders.

Background Emerging epidemiological evidence implicates pulmonary dysfunction in cardiovascular pathogenesis, yet its arrhythmogenic potential remains poorly defined. Objectives We aimed to assess the link between ventilatory parameters, pulmonary disease phenotypes and risk of incident arrhythmias across diverse populations. Methods We analyzed data from 17,684 adults in two prospective cohort studies-the Atherosclerosis Risk in Communities (ARIC; n = 12,929) and Cardiovascular Health Study (CHS; n = 4,755). Adjudicated arrhythmia diagnoses (atrial fibrillation/flutter [AF/AFL], ventricular arrhythmias [VAs], high-grade atrioventricular [AV] block, and premature atrial/ventricular complexes [PAC/PVC]) were identified via hospitalization records and mortality data. Multivariable-adjusted Cox proportional hazards models quantified associations between forced expiratory volume in 1 s (FEV1%) predicted and forced vital capacity (FVC%) predicted quartiles with arrhythmia risk, adjusting for traditional cardiovascular risk factors. Results Over a median follow-up of 12.6 years, impaired FEV1% and FVC% corresponded to a graded increase in arrhythmia risk. Compared to the highest quartile, the lowest FEV1% predicted quartile had elevated hazards for any arrhythmias (HR 1.32, 95% CI 1.23–1.42), AF/AFL (HR 1.68, 1.52–1.85), VAs (HR 1.55, 1.29–1.86), high-grade AV block (HR 1.37, 1.08–1.73), and PAC/PVC (HR 1.42, 1.20–1.69). Similar trends were observed for FVC% predicted quartiles. These associations remained consistent in never-smoking individuals and across cohorts. Obstructive spirometry pattern was associated with the strongest arrhythmia risk, while restrictive ventilatory patterns showed relatively lower risk elevations. No association was observed with sick sinus syndrome. Conclusions Reduced pulmonary function suggested independent associations with incident arrhythmias across supraventricular, ventricular, and conduction system pathologies in two historical cohorts. These findings suggest that spirometric indices could potentially represent novel independent indicators for arrhythmia development worthy of further validation in contemporary settings,, with associations distinct from conventional cardiometabolic risk factors.

The increased risk of cardiovascular events in patients prescribed macrolides has been subject to debate for decades. Medline, EMBASE databases and ClinicalTrials.gov were searched from inception until August 31, 2022 for studies investigating the link between macrolides and cardiovascular risk. A meta-analysis was performed using a random-effects model. A total of 80 studies involving 39,374,874 patients were included. No association was found between macrolides and all-cause death. However, compared with the non-macrolide group, macrolides were associated with a significantly increased risk of ventricular arrhythmia or sudden cardiac death (VA or SCD) (azithromycin, relative ratio [RR]: 1.53; 95% confidence interval [CI]: 1.19 to 1.97; clarithromycin, RR: 1.52; 95% CI: 1.07 to 2.16). Besides, administration of macrolides was associated with a higher risk of cardiovascular disease (CVD) death (azithromycin, RR: 1.63; 95% CI: 1.17 to 2.27) and a slightly increased risk of myocardial infarction (MI) (azithromycin, RR: 1.08; 95% CI: 1.02 to 1.15). Interestingly, no association was observed between roxithromycin and adverse cardiac outcomes. Increased risk of VA or SCD was observed for recent or current use of macrolides, MI for former use, and CVD death for current use. Administration of macrolide antibiotics and timing of macrolide use are associated with increased risk for SCD or VTA and cardiovascular death, but not all-cause death.

Inadequate trophoblast invasion and placentation are widely believed to contribute to preeclampsia, and multiple lines of evidence indicate the involvement of hypoxia in preeclampsia. However, the molecular mechanisms underlying the association of placental hypoxia with preeclampsia are not clear. The present study focused on the role in preeclampsia of heme oxygenase 1 (HO-1), which is an inducible isoform of HO in response to hypoxia, via examining the expression of HO-1 and the expression and phosphorylation (Tyr705) of Signal transducer and activator of transcription (STAT) 3 in preeclamptic placentas via the immunohistochemical method, western blotting assay and RT-qPCR method. Then we investigated the regulation by HO-1 of the expression and phosphorylation of STAT3 in human placental choriocarcinoma JEG-3 cells under hypoxia. There was upregulation of HO-1 at both mRNA (1.506 ±0.08347 ( = 37) vs. 1.000 ±0.08854 ( = 31), < 0.0001) and protein (0.630 ±0.155 ( = 35) vs. 0.310 ±0.052, 0.630 ±0.155 ( = 35), < 0.001) levels and a reduced level of STAT3 phosphorylation (Tyr 705) in the preeclamptic placental tissues, compared to normal placental tissues (0.143 ±0.027 ( = 35) vs. 0.194 ±0.028 ( = 35), < 0.01). Also, experiments demonstrated that HO-1 was markedly promoted by hypoxia in human placental choriocarcinoma JEG-3 cells, 6 or 12 h post treatment ( < 0.05 or < 0.01). However, the STAT3 phosphorylation (Tyr 705) was attenuated by sustained hypoxia ( < 0.01). Moreover, it was demonstrated that HO-1 overexpression significantly inhibited the hypoxia-promoted STAT3 phosphorylation (Tyr 705). HO-1 was overexpressed in PE placenta, in association with reduced STAT3 phosphorylation (Tyr 705). HO-1 inhibits the STAT3 phosphorylation in placental JEG-3 cells under hypoxia. Thus, we speculate that overexpressed HO-1 might contribute to the reduced STAT3 phosphorylation (Tyr 705) and the pathogenesis of preeclampsia.

ObjectiveThe purpose of this study was to perform a systematic review and meta-analysis to evaluate the effect of high-dose versus low-dose haemofiltration on the survival of critically ill patients with acute kidney injury (AKI). We hypothesised that high-dose treatments are not associated with a higher risk of mortality.DesignMeta-analysis.SettingRandomised controlled trials and two-arm prospective and retrospective studies were included.ParticipantsCritically ill patients with AKI.InterventionsContinuous renal replacement therapy.Primary and secondary outcome measuresPrimary outcomes: 90-day mortality, intensive care unit (ICU) mortality, hospital mortality; secondary outcomes: length of ICU and hospital stay.ResultEight studies including 2970 patients were included in the analysis. Pooled results showed no significant difference in the 90-mortality rate between patients treated with high-dose or low-dose haemofiltration (pooled OR=0.90, 95% CI 0.73 to 1.11, p=0.32). Findings were similar for ICU (pooled OR=1.12, 95% CI 0.94 to 1.34, p=0.21) and hospital mortality (pooled OR=1.03, 95% CI 0.81 to 1.30, p=0.84). Length of ICU and hospital stay were similar between high-dose and low-dose groups. Pooled results are not overly influenced by any one study, different cut-off points of prescribed dose or different cut-off points of delivered dose. Meta-regression analysis indicated that the results were not affected by the percentage of patients with sepsis or septic shock.ConclusionHigh-dose and low-dose haemofiltration produce similar outcomes with respect to mortality and length of ICU and hospital stay in critically ill patients with AKI.This study was not registered at the time the data were collected and analysed. It has since been registered on 17 February 2017 at http://www.researchregistry.com/, registration number: reviewregistry211.

Various diseases caused by disorders of glucose and lipid metabolism are increasing day by day. Although many drugs have certain therapeutic effects, they still produce some side effects. Therefore, this article chooses the natural medicinal plant mulberry leaves to reveal its mechanism of regulating glucose and lipid metabolism. By establishing an insulin resistance model and a 3T3‐L1 adipocyte model, it was found that mulberry leaf extract (MLE) and deoxynojirimycin (DNJ) significantly increased glucose consumption and glycogen consumption, while reducing total cholesterol (TC), triglycerides (TG) and low‐density lipoprotein cholesterol (LDL‐C) levels. Network pharmacology, molecular docking, and protein level showed that MLE and DNJ could improve glucose and lipid metabolism disorders through IRS1/PI3K/AKT signaling pathway. These results suggest that MLE and DNJ may have broad application prospects in regulating glycolipid metabolism in functional foods and healthcare products.

Background Mutations in human ether-à-go-go-related gene (hERG) potassium channels are closely associated with long QT syndrome (LQTS). Previous studies have demonstrated that macrolide antibiotics increase the risk of cardiovascular diseases. To date, the mechanisms underlying acquired LQTS remain elusive. Methods A novel hERG mutation I1025N was identified in an azithromycin-treated patient with acquired long QT syndrome via Sanger sequencing. The mutant I1025N plasmid was transfected into HEK-293 cells, which were subsequently incubated with azithromycin. The effect of azithromycin and mutant I1025N on the hERG channel was evaluated via western blot, immunofluorescence, and electrophysiology techniques. Results The protein expression of the mature hERG protein was down-regulated, whereas that of the immature hERG protein was up-regulated in mutant I1025N HEK-293 cells. Azithromycin administration resulted in a negative effect on the maturation of the hERG protein. Additionally, the I1025N mutation exerted an inhibitory effect on hERG channel current. Moreover, azithromycin inhibited hERG channel current in a concentration-dependent manner. The I1025N mutation and azithromycin synergistically decreased hERG channel expression and hERG current. However, the I1025N mutation and azithromycin did not alter channel gating dynamics. Conclusions These findings suggest that hERG gene mutations might be involved in the genetic susceptibility mechanism underlying acquired LQTS induced by azithromycin.

Inorganic-organic hybrid WOx-ethylenediamine （WO/-EDA） nanowires have been produced by a simple, low-cost and high-yield solvothermal method. These WO/-EDA hybrid nanowires have unique lamellar mesostructures with an alternate stacking of an interconnected [WO6] octahedral layer and a monolayer of ethylenediamine molecules. This hybrid structure integrated the functionality of ethylenediamine with the stability of the WOx frameworks. In situ synchrotron- radiation X-ray diffraction is used to elucidate a possible formation mechanism of the hybrid WOx-EDA. The nanowire morphology, lamellar structure and abundant functional amino groups endow them with versatile abilities. For example, in heavy metal ion adsorption the WOx-EDA nanowires display exceptional adsorption capabilities of 925 mg·g^-1 for Pb^2＋ and 610 mg·g^-1 for UO2^2＋. The nanowires also show outstanding stability and activity as a heterogeneous base catalyst in the Knoevenagel condensation reaction at room temperature. The catalyst can be recycled and reused for 20 cycles with nearly 100% yields. This study provides a new strategy to design inorganic-organic hybrid materials, and offers a multifunctional material that is a highly efficient adsorbent and sustainable catalyst.

Two new triterpenoids, 30-O-β-D-glucopyranosyloxy-2α,3α,24-trihydroxyurs-12, 18-diene-28-oic acid O-β-D-glucopyranosyl ester (1) and 2α,3β,3,30-tetrahydroxyurs-12, 18-diene-28-oic acid O-β-D-glucopyranosyl ester (2) were isolated from roots of Actinidia valvata Dunn. Their structures were elucidated by means of extensive spectroscopic studies. Both these two new compounds showed moderate cytotoxic activity in vitro against BEL-7402 and SMMC-7721 tumor cell line.

In order to solve the mobile robot trajectory tracking problem better, an iterative learning control (ILC) was applied. And the efficiency of mobile robot trajectory tracking was improved. From the simulation result, ILC with forgetting factor has very good performance for solving mobile robot trajectory tracking problem, and the smooth of trajectory tracking process also improved well.