Interlayer and Phase Engineering Modifications of K-MoS2@C Nanoflowers for High-Performance Degradable Zn-Ion Batteries.

2D transition metal dichalcogenides (TMDs) have garnered significant interest as cathode materials for aqueous zinc-ion batteries (AZIBs) due to their open transport channels and abundant Zn2+ intercalation sites. However, unmodified TMDs exhibit low electrochemical activity and poor kinetics owing to the high binding energy and large hydration radius of divalent Zn2+. To overcome these limitations, an interlayer engineering strategy is proposed where K+ is preintercalated into K-MoS2 nanosheets, which then undergo in situ growth on carbon nanospheres (denoted as K-MoS2@C nanoflowers). This strategy stimulates in-plane redox-active sites, expands the interlayer spacing (from 6.16 to 9.42 Å), and induces the formation of abundant MoS2 1T-phase. The K-MoS2@C cathode demonstrates excellent redox activity and fast kinetics, attributed to the potassium ions acting as a structural "stabilizer" and an electrostatic interaction "shield," accelerating charge transfer, promoting Zn2+ diffusion, and ensuring structural stability. Meanwhile, the carbon nanospheres serve as a 3D conductive network for Zn2+ and enhance the cathode's hydrophilicity. More significantly, the outstanding electrochemical performance of K-MoS2@C, along with its superior biocompatibility and degradability of its related components, can enable an implantable energy supply, providing novel opportunities for the application of transient electronics.

Comparison of outcomes and characteristics of patients admitted to the ICU with COVID-19 and other community-acquired pneumonia based on propensity score matching.

OBJECTIVE: To compare the similarities and differences between patients with Coronavirus Disease 2019 (COVID-19) and those with other community-acquired pneumonia (CAP) admitted to the intensive care unit (ICU), utilizing propensity score matching (PSM), regarding hospitalization expenses, treatment options, and prognostic outcomes, aiming to inform the diagnosis and treatment of COVID-19. METHODS: Patients admitted to the ICU of the Third People's Hospital of Datong City, diagnosed with COVID-19 from December 2022 to February 2023, constituted the observation group, while those with other CAP admitted from January to November 2022 formed the control group. Basic information, clinical data at admission, and time from symptom onset to admission were matched using PSM. RESULTS: A total of 70 patients were included in the COVID-19 group and 119 in the CAP group. The patients were matched by the propensity matching method, and 37 patients were included in each of the last two groups. After matching, COVID-19 had a higher failure rate than CAP, but the difference was not statistically significant (73% vs. 51%, p = 0.055). The utilization rate of antiviral drugs (40% vs. 11%, p = 0.003), γ-globulin (19% vs. 0%, p = 0.011) and prone position ventilation (PPV) (27% vs. 0%, p < 0.001) in patients with COVID-19 were higher than those in the CAP, and the differences were statistically significant. The total hospitalization cost of COVID-19 patients was lower than that of CAP patients, and the difference was statistically significant (27889.5 vs. 50175.9, p = 0.007). The hospital stay for COVID-19 patients was shorter than for CAP patients, but the difference was not statistically significant (10.9 vs. 16.6, p = 0.071). CONCLUSION: Our findings suggest that limited medical resources influenced patient outcomes during the COVID-19 pandemic. Addressing substantial demands for ICU capacity and medications during this period could have potentially reduced the mortality rate among COVID-19 patients.

OSMR deficiency aggravates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling.

BACKGROUND: Oncostatin M (OSM) is a secreted cytokine of the interleukin (IL)-6 family that induces biological effects by activating functional receptor complexes of the common signal transducing component glycoprotein 130 (gp130) and OSM receptor ß (OSMR) or leukaemia inhibitory factor receptor (LIFR), which are mainly involved in chronic inflammatory and cardiovascular diseases. The effect and underlying mechanism of OSM/OSMR/LIFR on the development of cardiac hypertrophy remains unclear. METHODS AND RESULTS: OSMR-knockout (OSMR-KO) mice were subjected to aortic banding (AB) surgery to establish a model of pressure overload-induced cardiac hypertrophy. Echocardiographic, histological, biochemical and immunological analyses of the myocardium and the adoptive transfer of bone marrow-derived macrophages (BMDMs) were conducted for in vivo studies. BMDMs were isolated and stimulated with lipopolysaccharide (LPS) for the in vitro study. OSMR deficiency aggravated cardiac hypertrophy, fibrotic remodelling and cardiac dysfunction after AB surgery in mice. Mechanistically, the loss of OSMR activated OSM/LIFR/STAT3 signalling and promoted a proresolving macrophage phenotype that exacerbated inflammation and impaired cardiac repair during remodelling. In addition, adoptive transfer of OSMR-KO BMDMs to WT mice after AB surgery resulted in a consistent hypertrophic phenotype. Moreover, knockdown of LIFR in myocardial tissue with Ad-shLIFR ameliorated the effects of OSMR deletion on the phenotype and STAT3 activation. CONCLUSIONS: OSMR deficiency aggravated pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling, which provided evidence that OSMR might be an attractive target for treating pathological cardiac hypertrophy and heart failure.

Kinetics of ester-105 degradation by La/TiO2 photocatalysis.

Lanthanum-doped titanium (La/TiO2) nano-photocatalysts were prepared using the sol-gel method and characterized by X-ray diffraction (XRD), zeta potential, and low-temperature nitrogen adsorption analyses. Ester-105, a flotation collector from beneficiation wastewater, was chosen as the target pollutant. The influence of the initial ester-105 concentration, pH, and photocatalyst dosage on the photocatalytic degradation of ester-105 was investigated. To examine the kinetics of the adsorption and photocatalytic degradation of ester-105, a Langmuir adsorption model and Langmuir-Hinshelwood kinetic models were established and discussed. The synthesized photocatalyst comprised anatase-phase TiO2, with an isoelectric point of pH = 6.5, specific surface area of 56.1626 m2·g-1, and average pore size of 7.78 nm. The maximum adsorption and the adsorption equilibrium constant of La/TiO2 for ester-105 were determined as 0.338 mg·g-1 and 1.008 L·mg-1, respectively. The first-order kinetic reaction rate constant (k) exhibited a linear relationship with the initial ester-105 concentration. The optimal pH for ester degradation was theoretically determined to be 6.95, and the optimum photocatalyst dosage was found to be 0.2739 g·L-1. Experiments confirmed that the photocatalytic degradation of ester-105 using La/TiO2 followed the Langmuir-Hinshelwood kinetics model, thereby providing a theoretical foundation for the photocatalytic degradation of ester-105 for industrial application.

By restoring autophagic flux and improving mitochondrial function, corosolic acid protects against Dox-induced cardiotoxicity.

Despite effective anticancer effects, the use of doxorubicin (Dox) is limited due to its side effects as cardiotoxicity. Corosolic acid (CRA) is a pentacyclic triterpene acid isolated from Lagerstroemia speciosa L. (Banaba) leaves, and it has also been shown to improve myocardial hypertrophy and myocardial infarction which expected to be used in clinical pharmaceuticals. The purpose of this study was to explore whether CRA can improve myocardial injury caused by Dox and to clarify potential mechanisms. C57 BL/6J mice and AMPKα2 knockout mice were given a single intraperitoneal (i.p.) injection of Dox (5 mg/kg) every week for 4 weeks, while normal saline (NS) was used as control. Mice were given CRA (10 mg/kg or 20 mg/kg) or equal volumes of normal saline daily after the first time i.p. injection of Dox. After 4 weeks, echocardiography, gravimetric, hemodynamic, histological, and biochemical analyses were conducted. After Dox injury, compared with the control group, CRA increased the survival rate of mice, improved the cardiac function, decreased the oxidative stress, and reduced the apoptosis. CRA may function by promoting transcription factor EB (TFEB) nuclear translocation and thus restoring autophagic flux. We also observed that CRA protected mitochondrial structure and function, which may benefit from oxidative stress reduction or TFEB activation. In vitro, the protective effect of CRA is reversed by TFEB deletion. Then, we evaluated the expression of AMPKα2/mTOR C1 signaling pathway, the main pathway of TFEB activation. In vivo and in vitro, CRA promoted TFEB nuclear translocation by activating AMPKα2/mTOR C1 signaling, while ablating AMPKα2 reversed these results and accompanied with a decrease in the ability of CRA to resist Dox-induced cardiotoxicity. Thus, we suggested that CRA activated TFEB in an AMPKα2-dependent manner to protect against Dox cardiotoxicity. This study confirms the role and mechanism of CRA in the treatment of Dox-induced cardiac injury. Dox-induced damage to autophagy includes autophagosomes maturation disorders and autophagolysosomes acidification defects, CRA restored autophagic flux, and promoted lysosomal degradation by activating TFEB in an AMPKα2-depended manner, stabilized mitochondrial function, ultimately protected against Dox-induced cardiotoxicity.

Clinical observation and analysis of skin reactions caused by COVID-19 vaccination.

The novel coronavirus disease 2019 (COVID-19) vaccination is now an essential strategy for controlling the COVID-19 epidemic. This study included 132 cases of adverse skin reactions after the injection of COVID-19 vaccination from January 2021 to January 2022. The rate of adverse skin reactions after the 1st, 2nd, and 3rd doses of the COVID-19 vaccine were 52%, 40%, and 8% of total adverse skin reactions, respectively. The Urticaria-like rash was the most common manifestation of all adverse skin reactions, accounting for 40.15% of all adverse reactions. The Eczema-like rash was 27.27%. The rates of adverse skin reactions after vaccination with the COVID-19 vaccine in patients with a previous skin disease was 12.12%. Other rare skin adverse reactions after COVID-19 vaccination included herpes zoster, pityriasis rosea, erythema multiforme, chickenpox, herpes simplex, psoriasis, erythrodermatitis, arthus reaction, lichen planus recurrence, measles-like rash, frostbite rash, seborrhea, and vitiligo. There were 23 cases of adverse skin reactions in the same individual after two doses of COVID-19 vaccine. There were three cases of adverse skin reactions in the same person after three doses of the vaccine. Treatment measures are mostly mild regimens, such as oral antihistamines, compounded glycopyrrolate and topical weak to moderately potent corticosteroid creams. The total duration of these skin adverse reactions ranged from 2 weeks to 1 month.

TMEM173 protects against pressure overload-induced cardiac hypertrophy by modulating autophagy.

TMEM173 has been reported to participate in endoplasmic reticulum stress, inflammation and immunology, all of which closely involved with cardiac hypertrophy. But its role in autophagy is not fully figured out. In our research, Tmem173 global knockout (KO) mice manifested more deteriorated hypertrophy, fibrosis, inflammatory infiltration and cardiac malfunction compared with wild type C57BL/6 mice after 6 weeks of transverse aortic constriction. And KO mice showed inhibited autophagosome degradation in myocardium observed under transmission electron microscope and in protein level. In in vitro experiments conducted in neonatal rat cardiomyocytes under phenylephrine treatment, the abundance of Tmem173 gene was negatively related to the abundance of LC3-Ⅱ and the number of red and yellow fluorescent dots, of which reflected the capacity of autophagosome degradation. These results indicated that TMEM173 might be a promoter of autophagic flux and protected against pressure overload-induced cardiac hypertrophy. It may serve as a potential therapeutic target for cardiac hypertrophy in the future.

RelB regulates the homeostatic proliferation but not the function of Tregs.

BACKGROUND: RelB, a member of the NF-κB family, plays a critical role in the development of T cells. However, the role of RelB in Foxp3+ regulatory T cells (Tregs) remains controversial. RESULTS: Using a bone marrow chimeric mouse model, we demonstrated that the expansion of Foxp3+ Tregs in vivo could be mediated by extrinsic mechanisms. RelB plays an important role in inhibiting the homeostatic proliferation of Tregs, but not their survival. Even with the heightened expansion, RelB-/- Treg cells displayed normal suppressive function in vitro. Among the expanded populations of Treg cells, most were nTreg cells; however, the population of iTregs did not increase. Mechanistically, RelB seems to regulate Treg proliferation independently of the signal transducer and activator of transcription 5 (STAT5) pathway. CONCLUSIONS: These data suggest that RelB regulates Treg proliferation independently of the STAT5 pathway, but does not alter the function of Tregs. Further studies are warranted to uncover such mechanisms.

ERCC6L promotes the progression of hepatocellular carcinoma through activating PI3K/AKT and NF-κB signaling pathway.

BACKGROUND: Excision Repair Cross-Complementation group 6-like (ERCC6L) has been shown to exhibit carcinogenic effect in several malignant tumors. However, the function and molecular mechanism of the ERCC6L in hepatocellular carcinoma (HCC) have not been investigated extensively. METHODS: Immunohistochemistry analyses were used to detect ERCC6L expression in a HCC tissue microarray, and the Chi-square test was used to assess the correlation between ERCC6L expression and patients' clinicopathological features. shRNA was used to down-regulation ERCC6L expression in HCC cell lines. MTT assay, plate clone formation assay, flow cytometry, caspase 3/7 activity and migration assays were performed to evaluate the impact of ERCC6L on HCC cells in vitro. Nude mice xenograft models were used to assess the role of ERCC6L in vivo. The regulatory of mechanism of PI3K/AKT pathway was evaluated by western blotting. RESULTS: ERCC6L was highly expressed in HCC tissue compared with tumor adjacent tissues in 90 paired samples. ERCC6L expression positively correlated with gender, tumor encapsulation, and pathological stage. Patients with low ERCC6L expression had significantly longer OS than those with high ERCC6L expression. Knockdown of ERCC6L expression significantly inhibited proliferation, invasion and metastasis in vitro and tumor growth in vivo, and it promoted cell cycle arrest and apoptosis. Mechanistic analyses revealed that PI3K/AKT and NF-κB signaling pathway were inhibited by silencing ERCC6L. CONCLUSION: These results demonstrate that ERCC6L plays a critical role in HCC progression, and thereby might be a potential therapeutic target for HCC patients.

Protective role of berberine in isoprenaline-induced cardiac fibrosis in rats.

BACKGROUND: Cardiac fibrosis is a crucial aspect of cardiac remodeling that can severely affect cardiac function. Cardiac fibroblasts surely influence this process. Besides, macrophage plays an essential role in cardiac remodeling after heart injury. However, whether macrophage influence fibroblasts remain a question worth exploring. This study aimed to define the role of berberine (BBR) on isoprenaline (ISO)-induced cardiac fibrosis in an in vivo rat model and try to figure out the mechanism in vitro study. METHODS: The Sprague-Dawley rats were divided into five groups: control group, ISO-treated group, and ISO + BBR (10 mg/kg/d, 30 mg/kg/d, and 60 mg/kg/d orally)-pretreatment groups. Fibrosis was induced by ISO administration (5 mg/kg/d subcutaneously) for 10 days. One day after the last injection, all of the rats were sacrificed. Using picrosirius red (PSR) straining, immunohistochemistry, immunofluorescence, flow cytometry, western blot, RT-qPCR and cell co-culture, we explored the influence of pretreatment by BBR on ISO-induced cardiac fibrosis. RESULTS: Our results showed that BBR pretreatment greatly limited ISO-induced cardiac fibrosis and dysfunction. Moreover, BBR administration reduced macrophage infiltration into the myocardium of ISO-treated rats and inhibited transforming growth factor (TGF)-ß1/smads signaling pathways in comparison to that seen in the ISO group. Besides, in vitro study showed that BBR-pretreatment reduced ISO-induced TGF-ß1 mRNA expression in macrophages and ISO stimulation of macrophages significantly increased the expression of fibrotic markers in fibroblasts, but BBR-pretreatment blocked this increase. CONCLUSION: Our results showed that BBR may have a protective role to cardiac injury via reducing of macrophage infiltration and forbidding fibroblasts transdifferent into an 'activated' secretory phenotype, myofibroblasts.

[Mechanism of Polypeptide Extract from Scorpion Venom Combined Rapamycin in Enhancing Autophagy of H22 Hepatoma Cells: an Experimental Study].

OBJECTIVE: To observe enhanced effects of polypeptide extract from scorpion venom (PESV) combined Rapamycin on autophagy of H22 hepatoma cells in mice and to explore its possible mechanism. METHODS: The H22 hepatocarcinoma cell suspension was subcutaneously inoculated into 40 Kunming mice. Then tumor-bearing mice were randomly divided into four groups, i.e., the control group,the high dose PESV group, the low dose PESV group, and the combination group (high dose PESV + Rapamycin), 10 in each group. Mice in high and dose PESV groups were administered with 20 mg/kg and 10 mg/kg PESV respectively by gastrogavage. Mice in the combination group were administered with 2 mg/kg rapamycin and 20 mg/kg PESV by gastrogavage. The intervention lasted for 14 successive days. The tumor volume was measured once every other day, the tumor growth curve was drawn, and then the tumor inhibitory rate calculated. Pathological changes of the tumor tissue were observed by HE staining. Protein expression levels of mammal target of rapamycin (mTOR), UNC-51-like kinase-1 (ULK1), microtubule-associated protein1 light chain3 (MAPILC3A), and Beclin1 were detected by immunohistochemical assay. RESULTS: The growth of H22 hepatoma transplantation tumor was inhibited in high and low dose PESV groups and the combination group (P < 0.05). And there was statistical difference in tumor weight and tumor volume between the combination group and high and low dose PESV groups (P < 0.05). There was no statistical difference in tumor weight or tumor volume between the high dose PESV group and the low dose PESV group (P > 0.05). lmmunohistochemical assay showed that the protein expression of mTOR was higher, but protein expressions of ULK1, MAP1LC3A, Beclin1 were lower in the control group than in the rest 3 groups (P < 0.05, P < 0.01). Compared with the high dose PESV group, protein expressions of ULK1, MAP1LC3A, and Beclin1 were obviously lower (P < 0.05). CONCLUSION: PESV combined Rapamycin might inhibit the development of H22 hepatoma transplantation tumor in mice possibly through inhibiting the activity of mTOR, enhancing expressions of ULK1, MAP1LC3A, and Beclin1.

[Study on the mechanism of polypeptide extract from scorpion venom on inhibition of angiogenesis of H 22 hepatoma].

OBJECTIVE: To explore the mechanism of polypeptide extract from scorpion venom (PESV) on inhibiting angiogenesis. METHODS: The H22 hepatoma tumor model was established by subcutaneously implanting H22 hepatoma cells into mice. The tumor-bearing mice were randomly divided into 4 groups, i.e., the control group, the high dose PESV group, the low dose PESV group, and the 5-fluorouracil (5-Fu) group, 10 mice in each group. The intervention was lasted for 14 days. The growth curve of the tumor volume was drawn and the inhibition rate calculated. Pathological changes of the tumors were observed by HE staining. The microvessel density (MVD) was detected using SP method. The protein expression levels of phosphatidylinositol 3-kinase (P13K), phosphoprotein kinase B (P-Akt), hypoxia-inducible factor-1 alpha (HIF-1 )alpha, and vascular endothelial growth factor-A (VEGF-A) were detected by immunohistochemical assay and Western blot. RESULTS: The tumor inhibitory rate was 64.8%, 43.7%, and 32.4% in the 5-Fu group, the high dose PESV group, and the low dose PESV group. Compared with the control group, the protein expression of PI3K, P-Akt, HIF-1alpha, and VEGF-A were obviously inhibited by PESV and 5-Fu (P <0. 05,P <0. 01). The MVD also decreased in the high and low dose PESV groups (P < 0.05). CONCLUSIONS: PESV could inhibit the angiogenesis of H22 hepatoma. The mechanisms might be associated with suppressing the expression of PI3K, P-Akt, HIF-1 alpha, and VEGF-A.

Association between preoperative hemoglobin with length of hospital stay among non-cardiac and non-obstetric surgery patients: a secondary analysis of a retrospective cohort study.

BACKGROUND: Previous studies concerning the association between preoperative Hemoglobin (HB) level and the Length Of hospital Stay (LOS) in patients with non-cardiac surgery and non-obstetric surgery remain inconclusive. Herein, the objective of this study was to analyze whether and to what extent the preoperative HB level was connected with the LOS in non-cardiac and non-obstetric surgery patients. METHODS: This retrospective cohort study was performed at a single institution, involving patients who underwent elective non-cardiac, non-obstetric surgery from April 2007 to September 2013. Clinical characteristics of patients such as demographics, comorbidities, preoperative HB level, LOS, mortality, procedure length, and pulmonary hypertension (PHTN) Severity Class data were collected. A univariate analysis was used to determine the association between clinical characteristics and LOS. Multivariate regression analysis was conducted to investigate the relationship between preoperative HB level and LOS. RESULTS AND DISCUSSION: In this study, 311 patients were included. We observed that compared with the LOS > 7 days group, the average HB level of patients in the LOS ≤ 7 days group was higher (12.04 ± 2.20 g/dl vs. 10.92 ± 2.22 g/dl, p < 0.001). In addition, there were fewer patients with moderate-to-severe anemia in LOS ≤ 7 days group than the LOS > 7 days group (32.74% vs 58.82%, p < 0.001). In addition, we found that patients with LOS ≤ 7 days were accompanied with lower mortality (0.44% vs. 7.06%, p < 0.001) and lower mean combined pulmonary artery systolic pressure (PASP) and right ventricular systolic pressure (RVSP) than that in patients with LOS > 7 days (42.56 ± 11.97 vs. 46.00 ± 12.37, p < 0.05). After controlling for relevant confounders, we discovered a nonlinear association between preoperative HB level and LOS as well as a threshold effect based on LOS. Specifically, when preoperative HB level was less than 11.9 g/dL, LOS decreased by 2 days for each 1 g/dL increase in HB level. However, LOS did not alter substantially with the rise of preoperative HB level when it was higher than 11.9 g/dL. CONCLUSION: Our study showed a close non-linear association between preoperative HB level and LOS in patients with non-cardiac surgery and non-obstetric surgery. In particular, for patients with preoperative HB less than 11.9 g/dL, increasing the preoperative HB level can help shorten the LOS after operation.

No Evidence of Causal Association Between Atopic Dermatitis and Primary Open-Angle Glaucoma: A Bidirectional Two-Sample Mendelian Randomization Study.

Background: Atopic dermatitis (AD) can present with open-angle glaucoma, but powerful evidence to support their causal relationship is absent. Objective: To investigate the causal association of AD with primary open-angle glaucoma (POAG). Methods: A bidirectional 2-sample Mendelian randomization (MR) study was performed with the software R. Results: Eighteen single nucleotide polymorphisms (SNPs) were used in the forward MR analysis with AD as exposure. The inverse-variance weighted (IVW) method produced a result that genetically predicted AD was not associated with POAG (odds ratio [OR] = 1.10, 95% confidence interval [CI]: 0.95-1.27, P = 0.215). Fifty-one SNPs were used in the reverse MR analysis with POAG as exposure. The IVW method yielded a result that genetically predicted POAG was not correlated with AD (OR = 0.98, 95% CI: 0.95-1.01, P = 0.191). The bidirectional causal effect estimates were consistent with supplementary MR methods (MR-Egger, weighted median, simple mode, and weighted mode). The sensitivity analysis showed stable results. Conclusions: This bidirectional 2-sample MR study did not give evidence of causal association between AD and POAG.

[Distribution Prediction of Soil Heavy Metals Based on Remote Sensing Temporal-Spatial-Spectral Features and Random Forest Model].

Obtaining soil heavy metal content characteristics and spatial distribution is crucial for preventing soil pollution and formulating environmental protection policies. We collected 304 surface soil samples (0-20 cm) in the Changqing district. At the same time, the spectral, temporal, and spatial features of soil heavy metals were derived from multi-remote sensing data; the temporal-spatial-spectral features closely related to soil heavy metals were selected via correlation analysis and used as input independent variables. The measured soil arsenic (As) content was used as the dependent variable to establish a spatial prediction model based on the random forest (RF) algorithm. The results showed the following:the As content in the soils exceeded the background value by 43.17% but did not exceed the risk screening values and intervention values, indicating slight heavy metal pollution in the soil. The accuracy ranking of the spatial prediction models with one feature type from high to low was spatial features (ratio of performance to inter-quartile range (RPIQ)=3.87)>temporal features (RPIQ=2.57)>spectral features (RPIQ=2.50). The spatial features were the most informative for predicting soil heavy metals. The models using temporal-spatial, temporal-spectral, and spatial-spectral features were superior to those using only one feature type, and the RPIQ values were 4.81, 4.21, and 4.70, respectively. The RF model with temporal-spatial-spectral features achieved the highest spatial prediction accuracy (R2=0.90; root mean square error (RMSE)=0.77; RPIQ=5.68). The As content decreased from the northwest to the southeast due to Yellow River erosion and industrial activities. The spatial prediction of soil heavy metals incorporating remote sensing temporal-spatial-spectral features and the random forest model provides effective support for soil pollution prevention and environmental risk control.

Exploring the influencing factors on acne, melasma, and rosacea: A case-control study in China.

BACKGROUND: The severity and treatment response of acne, melasma, and rosacea may be influenced by various currently unclear internal and external factors. This study aimed to provide evidence to the influencing factors for the mentioned conditions through a real-world case-control study. METHODS: An online survey consisting of 60 questions was implemented, collecting information on demographics, socioeconomics, genetic factors, lifestyle habits, environmental exposures, and skin care behaviors. Then we constructed univariate and multivariate logistic regressions. Furthermore, we analyzed the dose-response relationship between exposure and outcome. RESULTS: A total of 399 individuals, including 94 acne patients, 107 melasma patients, and 91 rosacea patients were included. Acne and melasma were positively correlated with screen time (acne: odds ratio [OR]: 2.24, 95% confidence interval [CI]: 1.25-4.02; melasma: OR: 1.59, 95% CI: 1.09-2.31), while exercise exerted a protective effect on both acne (OR: 0.31, 95% CI: 0.13-0.77) and melasma (OR: 0.42, 95% CI: 0.22-0.80) in a dose-response relationship. In addition, males were associated with an elevated risk of acne (OR: 6.62, 95% CI: 1.01-43.26). Aging (OR: 1.15, 95% CI: 1.07-1.24) and irregular bowel movements (OR: 2.99, 95% CI: 1.11-8.08) were independent risk factors for melasma. Rosacea was positively associated with BMI (OR: 1.17, 95% CI: 1.01-1.35). CONCLUSION: In our study, we highlighted exercise as an independent protective factor for both acne and melasma in a dose-response trend. Inversely, extended use of electronic equipment was independently associated with higher risks of acne and melasma. Rosacea, however, was more likely to be related with BMI.

Wireless and Opto-Stimulated Flexible Implants: Artificial Retina Constructed by Ferroelectric BiFeO3-BaTiO3/P(VDF-TrFE) Composites.

The degeneration of retinal photoreceptors is one of the primary causes of blindness, and the implantation of retinal prostheses offers hope for vision restoration in individuals who are completely blind. Flexible bioelectronic devices present a promising avenue for the next generation of retinal prostheses owing to their soft mechanical properties and tissue friendliness. In this study, we developed flexible composite films of ferroelectric BiFeO3-BaTiO3 (BFO-BTO) particles synthesized by the hydrothermal method and ferroelectric poly(vinyldene difluoride-trifluoroethylene) (P(VDF-TrFE)) polymer and investigated their applications in artificial retinas. Owing to the coupling of the photothermal effect of BFO-BTO particles and the pyroelectric effect of the P(VDF-TrFE) polymer, the composite films demonstrate a strong photoelectric response (a maximum peak-to-peak photovoltage > 80 V under blue light of 100 mW/cm2) in a wide wavelength range of light (from visible to infrared) with the inherent flexibility and ease of preparation, making it an attractive candidate for artificial retinal applications. Experimental results showed that blind rats implanted with artificial retinas of the composites display light-responsive behavior, showcasing the effectiveness of vision restoration. This study demonstrates a novel approach for employing ferroelectric materials in vision restoration and offers insights into future artificial retina design.

Correction: Fang et al. Study on Dispersion, Adsorption, and Hydration Effects of Polycarboxylate Superplasticizers with Different Side Chain Structures in Reference Cement and Belite Cement. Materials 2023, 16, 4168.

In the original publication [...].

Membrane-Active All-Hydrocarbon-Stapled α-Helical Amphiphilic Tat Peptides: Broad-Spectrum Antibacterial Activity and Low Incidence of Drug Resistance.

Multidrug resistance against conventional antibiotics has dramatically increased the difficulty of treatment and accelerated the need for novel antibacterial agents. The peptide Tat (47-57) is derived from the transactivating transcriptional activator of human immunodeficiency virus 1, which is well-known as a cell-penetrating peptide in mammalian cells. However, it is also reported that the Tat peptide (47-57) has antifungal activity. In this study, a series of membrane-active hydrocarbon-stapled α-helical amphiphilic peptides were synthesized and evaluated as antibacterial agents against Gram-positive and Gram-negative bacteria, including multidrug-resistant strains. The impact of hydrocarbon staple, the position of aromatic amino acid residue in the hydrophobic face, the various types of aromatic amino acids, and the hydrophobicity on bioactivity were also investigated and discussed in this study. Among those synthesized peptides, analogues P3 and P10 bearing a l-2-naphthylalanine (Φ) residue at the first position and a Tyr residue at the eighth position demonstrated the highest antimicrobial activity and negligible hemolytic toxicity. Notably, P3 and P10 showed obviously enhanced antimicrobial activity against multidrug-resistant bacteria, low drug resistance, high cell selectivity, extended half-life in plasma, and excellent performance against biofilm. The antibacterial mechanisms of P3 and P10 were also preliminarily investigated in this effort. In conclusion, P3 and P10 are promising antimicrobial alternatives for the treatment of the antimicrobial-resistance crisis.

Cardiac tumour necrosis factor receptor-associated factor 7 mediates the ubiquitination of apoptosis signal-regulating kinase 1 and aggravates cardiac hypertrophy.

AIMS: Cardiac remodelling is a common pathophysiological process in the development of various cardiovascular diseases, but there is still a lack of effective interventions. Tumour necrosis receptor-associated factor 7 (TRAF7) belongs to the tumour necrosis factor receptor-associated factor family and plays an important role in biological processes. Previous studies have shown that TRAF7 mutations lead to congenital defects and malformations of the heart. However, the molecular mechanisms of TRAF7 in the underlying pathogenesis of pathological cardiac hypertrophy remain unknown. We aim to study the molecular mechanisms and effects of TRAF7 in cardiac remodelling and whether it has the potential to become a therapeutic target for cardiac remodelling. METHODS AND RESULTS: The pressure overload-induced cardiac hypertrophy model in mice was established via transverse aortic constriction (TAC) surgery, and cardiomyocytes were treated with phenylephrine (PE) to induce hypertrophic phenotype. Levels of cardiac dysfunction and remodelling were measured with echocardiography and tissue or cell staining. RNA sequencing, western blot, qRT-PCR, co-immunoprecipitation, and in vivo ubiquitination assays were used to explore the molecular mechanisms. The results showed that the expression of TRAF7 increased gradually during the development of hypertrophy. Accordingly, TRAF7 significantly exacerbated the PE-induced enlargement of primary neonatal Sprague-Dawley rat cardiomyocytes, whereas TRAF7 knockdown alleviated the hypertrophic phenotype in primary cardiomyocytes. Cardiac-specific overexpression of TRAF7 accelerated hypertrophic phenotype in mice and cardiac-specific Traf7 conditional knockout mice improved hypertrophic phenotype induced by TAC. Mechanistically, TRAF7 directly interacted with apoptosis signal-regulating kinase-1 (ASK1) and promoted ASK1 phosphorylation by mediating the K63-linked ubiquitination of ASK1 in response to PE stimulation, which then promoted ASK1 activation and downstream signalling during cardiac hypertrophy. Notably, the pro-hypertrophic effect of TRAF7 was largely blocked by GS4997 in vitro and cardiac-specific Ask1 conditional knockout in vivo. CONCLUSION: In summary, we identified TRAF7 as an essential regulator during cardiac hypertrophy, and modulation of the regulatory axis between TRAF7 and ASK1 could be a novel therapeutic strategy to prevent this pathological process.