Association between low handgrip strength and incontinence among Chinese middle-aged and older people: A cross-sectional study.

Objective: Incontinence seriously affects the lives of middle-aged and older people. Pelvic floor muscle assessment is very important for incontinence, and handgrip strength can be used as an auxiliary diagnostic tool. Our study aims to find new cutoff points of handgrip strength as early indicators of incontinence and analyze the association between low handgrip strength and incontinence among Chinese middle-aged and older people. Methods: Participants were recruited from the 2015 China Health and Retirement Longevity Study. Receiver operating characteristic (ROC) curves were used to find the handgrip strength cutoff point. Logistic regression analysis was performed to explore other incontinence-related risk factors. Results: The study included 10,229 middle-aged and older people. Compared with normal handgrip strength participants, medium strength participants had 1.510 [men, 95% confidence interval (CI) = 1.017-2.243] and 1.792 (women, 95% CI = 1.294-2.480) times greater risk of incontinence, and low strength participants had 2.420 (men, 95% CI = 1.787-3.277) and 1.516 (women, 95% CI = 1.130-2.032) times greater risk of incontinence. Trend test results showed that the risk of incontinence increased with decreasing handgrip strength in middle-aged and older people. Conclusions: Our study suggests that handgrip strength < 31 kg in men and < 20.5 kg in women is significantly associated with higher risk of incontinence in Chinese middle-aged and older people. The risk of incontinence increases with decreasing handgrip strength. Handgrip strength should be measured in routine physical examinations in middle-aged and older people for timely assessment and intervention in incontinence.

Mauritone A, a new polyketide from a fungal-bacterial symbiont Aspergillus spelaeus GXIMD 04541/Sphingomonas echinoides GXIMD 04532.

A new polyketide, mauritone A (1) with six known polyketides curvulone B (2), curvularin (3), 12-oxocurvularin (4), (10E,15S)-10,11-dehydrocurvularin (5), (11R,15S)-11-hydroxycurvularin (6), and (11S,15S)-11-hydroxycurvularin (7) were isolated from the fungal-bacterial symbiont Aspergillus spelaeus GXIMD 04541/Sphingomonas echinoides GXIMD 04532 derived from Mauritia arabica. Their structures were elucidated by extensive spectral analysis. All compounds (1-7) were evaluated for their anti-inflammatory effects. The inhibitory effects of 4, 5, and 7 on nitric oxide (NO) production were found to be significant, with IC50 values of 5.5 ± 0.26, 2.0 ± 0.31, and 8.3 ± 0.62 µM, respectively, surpassing that of the positive control quercetin (10.6 ± 0.64 µM). Compounds 3 and 6 exhibited moderate inhibition of NO, with IC50 values of 18.6 ± 0.53 and 12.7 ± 0.45 µM, respectively.

Hainanenin-1, an oncolytic peptide, triggers immunogenic cell death via STING activation in triple-negative breast cancer.

BACKGROUND: In triple-negative breast cancer (TNBC) therapy, insufficient tumor infiltration by lymphocytes significantly hinders the efficacy of immune checkpoint inhibitors. We have previously demonstrated that Hainanenin-1 (HN-1), a host defense peptide (HDP) identified from Hainan frog skin, induces breast cancer apoptosis and boots anti-tumor immunity via unknown mechanism. METHODS: We used in vitro experiments to observe immunogenic cell death (ICD) indicators in HN-1-treated TNBC cell lines, a mouse tumor model to verify HN-1 promotion of mice anti-tumor immune response, and an in vitro drug sensitivity test of patient-derived breast cancer cells to verify the inhibitory effect of HN-1. RESULTS: HN-1 induced ICD in TNBC in a process during which damage-associated molecular patterns (DAMPs) were released that could further increase the anti-tumor immune response. The secretion level of interleukin 2 (IL-2), IL-12, and interferon γ in the co-culture supernatant was increased, and dendritic cells (DCs) were activated via a co-culture with HN-1-pretreated TNBC cells. As a result, HN-1 increased the infiltration of anti-tumor immune cells (DCs and T lymphocytes) in the mouse model bearing both 4T1 and EMT6 tumors. Meanwhile, regulatory T cells and myeloid-derived suppressor cells were suppressed. In addition, HN-1 induced DNA damage, and double-strand DNA release in the cytosol was significantly enhanced, indicating that HN-1 might stimulate ICD via activation of STING pathway. The knockdown of STING inhibited HN-1-induced ICD. Of note, HN-1 exhibited inhibitory effects on patient-derived breast cancer cells under three-dimensional culture conditions. CONCLUSIONS: Collectively, our study demonstrated that HN-1 could be utilized as a potential compound that might augment immunotherapy effects in patients with TNBC.

F wave analysis based on the compound muscle action potential scan.

INTRODUCTION/AIMS: Conventional F wave analysis involves a relatively uniform physiological environment induced by supramaximal stimulations. The F wave characteristics in a dynamic physiological condition, however, are rarely investigated. This study aimed to improve understanding of F wave properties in the more dynamic process by introducing a novel method to analyze F waves based on the compound muscle action potential (CMAP) scan technique. METHODS: Twenty four healthy subjects participated in the study. The CMAP scan was applied to record muscle responses in the abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles, respectively. F wave characteristics including mean F wave amplitude and latency (F-M latency), persistence and activating threshold were quantified. RESULTS: An average of 200 F waves per muscle were obtained from the CMAP scan recording. Weak to moderate correlations between F wave amplitude and stimulating intensity were observed in most of the APB (19 muscles; r = 0.33 ± 0.14, all p < .05) and ADM (23 muscles, r = 0.46 ± 0.16, all p < .05) muscles. Significantly longer mean F latency and lower activating F-threshold were found in the ADM muscles (F-M latency: APB: 25.43 ± 2.39 ms, ADM: 26.15 ± 2.32 ms, p < .05; F-threshold: APB: 7.68 ± 8.96% CMAP, ADM: 2.35 ± 2.42% CMAP, p < .05). DISCUSSION: This study introduces new features of F waves using the CMAP scan technique and identifies differences of F wave characteristics between the hand muscles. The CMAP scan based F waves analysis can be combined with the motor unit number estimation to assess functional alterations in motor neurons in neurological disorders.

Cell-free hemoglobin and hemin catalyzing triclosan oxidative coupling in plasma: A novel exogenous phenolic pollutants coupling pathway.

Previous studies reported that hemoprotein CYP450 catalyzed triclosan coupling is an "uncommon" metabolic pathway that may enhance toxicity, raising concerns about its environmental and health impacts. Hemoglobin, a notable hemoprotein, can catalyze endogenous phenolic amino acid tyrosine coupling reactions. Our study explored the feasibility of these coupling reactions for exogenous phenolic pollutants in plasma. Both hemoglobin and hemin were found to catalyze triclosan coupling in the presence of H2O2. This resulted in the formation of five diTCS-2 H, two diTCS-Cl-3 H, and twelve triTCS-4 H in phosphate buffer, with a total of nineteen triclosan coupling products monitored using LC-QTOF. In plasma, five diTCS-2 H, two diTCS-Cl-3 H, and two triTCS-4 H were detected in hemoglobin-catalyzed reactions. Hemin showed a weaker catalytic effect on triclosan transformation compared to hemoglobin, likely due to hemin dimerization and oxidative degradation by H2O2, which limits its catalytic efficiency. Triclosan transformation in the human plasma-like medium still occurs with high H2O2, despite the presence of antioxidant proteins that typically inhibit such transformations. In plasma, free H2O2 was depleted within 40 minutes when 800 µM H2O2 was added, suggesting a rapid consumption of H2O2 in these reactions. Antioxidative species, or hemoglobin/hemin scavengers such as bovine serum albumin, may inhibit but not completely terminate the triclosan coupling reactions. Previous studies reported that diTCS-2 H showed higher hydrophobicity and greater endocrine-disrupting effects compared to triclosan, which further underscores the potential health risks. This study indicates that hemoglobin and heme in human plasma might significantly contribute to phenolic coupling reactions, potentially increasing health risks.

Insight into the Metal-Involving Chalcogen Bond in the PdII/PtII-Based Complexes: Comparison with the Conventional Chalcogen Bond.

The metal-involving Ch···M chalcogen bond and the conventional Ch···O chalcogen bond between ChX2 (Ch = Se, Te; X = CCH, CN) acting as a Lewis acid and M(acac)2 (M = Pd, Pt; Hacac = acetylacetone) acting as a Lewis base were studied by density functional theory calculations. It has been observed that the nucleophilicity of the PtII complexes is higher than that of the corresponding PdII complexes. As a result, the PtII complexes tend to exhibit a more negative interaction energy and larger orbital interaction. The strength of the chalcogen bond increases with the increase of the chalcogen atom and the electronegativity of the substituent on the Lewis acid and vice versa. The metal-involving chalcogen bond shows a typical weak closed-shell noncovalent interaction in the (HCC)2Ch···M(acac)2 complexes, while it exhibits a partially covalent nature in the (NC)2Ch···M(acac)2 complexes. The conventional Ch···O chalcogen bond displays the character of a weak noncovalent interaction, and its strength is generally weaker than that of metal-involving Ch···M interactions. It could be argued that the metal-involving chalcogen bond is primarily determined by the correlation term, whereas the conventional chalcogen bond is mainly governed by the electrostatic interaction.

HIF-1α activation impairs dendrites formation and elongation in osteocytogenesis.

Osteocytes are terminally differentiated cells derived from osteoblasts and are deeply embedded within the bone matrix. They play a critical role in bone remodeling by generating a lacuno-canalicular network (LCN) and controlling the transport of nutrients. Due to the absence of blood vessels within the bone matrix, it is widely believed that osteocytes develop in a hypoxic environment. However, the mechanisms of osteocytogenesis and the role of oxygen sensing in this process remain unclear. Hypoxia-inducible factors (HIFs) are major transcriptional factors involved in oxygen sensing. Previous studies have shown that accumulation of HIFs in osteoblasts leads to abnormal bone remodeling, potentially linked with the alterations of the LCN network. Specifically, HIF-1α is hypothesized to play a more significant role in regulating bone remodeling compared to HIF-2α. Therefore, we investigated the functions of HIF-1α in dendrite formation and the establishment of the LCN network during osteocytogenesis. Immunostaining and scanning electron microscopy revealed that the E11 protein aggregates to form a ring structure that defines the site for dendrite initiation. This process is followed by activation of the ERM/RhoA pathway and recruitment of matrix metalloproteinase 14 (MMP14) to facilitate extracellular matrix degradation, enabling dendrite elongation. However, both hypoxic treatment and overexpression of HIF-1α impair ring formation, resulting in reduced ERM/RhoA activity and decreased matrix degradation capability. These findings suggest that abnormal HIF-1α activity in local areas could contribute to impaired LCN network formation and abnormal bone remodeling observed in bone diseases such as osteopenia and aging.

Cyclosporine A protects podocytes by regulating transgelin in adriamycin-induced podocyte injury.

INTRODUCTION: The calcineurin inhibitor cyclosporine A (CsA) has been shown to effectively reduce proteinuria. However, its precise mechanism is still not fully understood. Our previous study showed that CsA reduced proteinuria by directly stabilizing the foot process (FP) cytoskeletal structure via cofilin-1, suggesting that synaptopodin, a podocyte-specific actin protein, is not the sole target of CsA in podocytes. METHODS: In this study, we established an adriamycin (ADR)-induced nephropathy rat model and a cultured podocyte injury model. We employed Western blotting and immunofluorescence techniques to assess the expression and distribution of transgelin, KLF-4, nephrin, and synaptopodin. RESULTS: We observed a significant increase in proteinuria levels accompanied by loss of normal FP structure in the ADR-induced nephropathy rat model. The levels of the actin cross-linking protein transgelin were increased significantly, while those of the podocyte-specific molecules nephrin and synaptopodin were decreased in vivo. Treatment with CsA effectively reduced proteinuria while restoring FP effacement stability in ADR-induced nephropathy models, and restoring the expression of transgelin, nephrin, and synaptopodin both in vivo and in vitro. Furthermore, CsA treatment dose-dependently decreased transgelin levels while significantly increasing KLF-4 expression in injured podocytes. In addition, CsA failed to downregulate transgelin when KLF-4 was specifically knocked down. CONCLUSION: Our findings suggest that CsA protects against podocyte injury by downregulating abnormally high levels of transgelin via upregulation of KLF-4 expression.

Analyzing Spatio-Temporal Dynamics of Grassland Resilience and Influencing Factors in the West Songnen Plain, China, for Eco-Restoration.

Grassland plays an indispensable role in the stability and development of terrestrial ecosystems. Quantitatively assessing grassland resilience is of great significance for conducting research on grassland ecosystems. However, the quantitative measurement of resilience is difficult, and research on the spatio-temporal variation of grassland resilience remains incomplete. Utilizing the Global Land Surface Satellite (GLASS) leaf area index (LAI) product derived from MODIS remote sensing data, along with land cover and meteorological data, this paper constructed the grassland resilience index (GRI) in the west Songnen Plain, China, a typical region with salt and alkali soils. This paper analyzed the spatio-temporal changes of the GRI and explored the contribution of climate factors, human activities, and geographical factors to the GRI. The results revealed that from 2000 to 2021, the GRI in the study area ranged from 0.1 to 0.22, with a multi-year average of 0.14. The average GRI exhibited a pattern of high-value aggregations in the north and low-value distributions in the south. Trend analysis indicated that areas with an improved GRI accounted for 59.09% of the total grassland area, but there were still some areas with serious degradation. From 2000 to 2015, the latitude and mean annual temperature (MAT) were principal factors to control the distribution of the GRI. In 2020, the mean annual precipitation (MAP) and MAT played important roles in the distribution of the GRI. From 2000 to 2021, the influence of human activities was consistently less significant compared to geographical location and climate variables.

Mmp14-dependent remodeling of the pericellular-dermal collagen interface governs fibroblast survival.

Dermal fibroblasts deposit type I collagen, the dominant extracellular matrix molecule found in skin, during early postnatal development. Coincident with this biosynthetic program, fibroblasts proteolytically remodel pericellular collagen fibrils by mobilizing the membrane-anchored matrix metalloproteinase, Mmp14. Unexpectedly, dermal fibroblasts in Mmp14-/- mice commit to a large-scale apoptotic program that leaves skin tissues replete with dying cells. A requirement for Mmp14 in dermal fibroblast survival is recapitulated in vitro when cells are embedded within, but not cultured atop, three-dimensional hydrogels of crosslinked type I collagen. In the absence of Mmp14-dependent pericellular proteolysis, dermal fibroblasts fail to trigger ß1 integrin activation and instead actuate a TGF-ß1/phospho-JNK stress response that leads to apoptotic cell death in vitro as well as in vivo. Taken together, these studies identify Mmp14 as a requisite cell survival factor that maintains dermal fibroblast viability in postnatal dermal tissues.

High Density 3D Carbon Tube Nanoarray Electrode Boosting the Capacitance of Filter Capacitor.

Electric double-layer capacitors (EDLCs) with fast frequency response are regarded as small-scale alternatives to the commercial bulky aluminum electrolytic capacitors. Creating carbon-based nanoarray electrodes with precise alignment and smooth ion channels is crucial for enhancing EDLCs' performance. However, controlling the density of macropore-dominated nanoarray electrodes poses challenges in boosting the capacitance of line-filtering EDLCs. Herein, a simple technique to finely adjust the vertical-pore diameter and inter-spacing in three-dimensional nanoporous anodic aluminum oxide (3D-AAO) template is achieved, and 3D compactly arranged carbon tube (3D-CACT) nanoarrays are created as electrodes for symmetrical EDLCs using nanoporous 3D-AAO template-assisted chemical vapor deposition of carbon. The 3D-CACT electrodes demonstrate a high surface area of 253.0 m2 g-1, a D/G band intensity ratio of 0.94, and a C/O atomic ratio of 8. As a result, the high-density 3D-CT nanoarray-based sandwich-type EDLCs demonstrate a record high specific areal capacitance of 3.23 mF cm-2 at 120 Hz and exceptional fast frequency response due to the vertically aligned and highly ordered nanoarray of closely packed CT units. The 3D-CT nanoarray electrode-based EDLCs could serve as line filters in integrated circuits, aiding power system miniaturization.

A carboxymethyl-resistant starch/polyacrylic acid semi-IPN hydrogel with excellent adhesive and antibacterial properties for peri-implantitis prevention.

Hydrogels possess inherent characteristics that render them promising for the prevention of peri-implantitis. Nonetheless, hydrogels with singular network structures are incapable of concurrently achieving the desired adhesion and mechanical properties. In this work, a carboxymethyl resistant starch/polyacrylic acid semi-interpenetrating (CMRS/PAA semi-IPN) hydrogel was successfully prepared in one step. Its morphology, structure, mechanical properties, and adhesion properties were systematically assessed, which revealed a homogeneously porous structure with a commendable mechanical strength of 67.317 kPa and an adhesion strength of 63 kPa. Ciprofloxacin (Cip) was loaded in the CMRS/PAA hydrogel via in situ compounding. The in vitro kinetic study of drug release shows that the slow drug release efficiency exceeds 90 % in the weakly acidic microenvironment at the infection site after 72 h, indicating enhanced antimicrobial properties. The Cip-loaded hydrogel also exhibits a remarkable bacterial inhibition rate exceeding 99 % against the pathogenic bacterium P. gingivalis and good cytocompatibility and hemocompatibility in vitro. In summary, the current work explored a novel solution and direction for the development of anti-infective medical materials applicable to dental implants.

Detection of minimal hepatic encephalopathy in patients with cirrhosis based on the Stroop-CN model (NCRCID-CHESS 2106): a prospective multicenter study.

Minimal hepatic encephalopathy (MHE) has a substantial impact on the clinical outcomes and quality of life (QOL) of patients with cirrhosis. However, timely diagnosis and intervention are challenging due to sophisticated diagnostic methods. In this study, 673 healthy controls and 905 patients with cirrhosis were screened, and 660 healthy controls and 757 patients with cirrhosis, divided into the test (292 patients) and validation (465 patients) cohort, were analyzed after screening. A diagnostic model of the Stroop test (Stroop-CN) was constructed by multivariate linear regression based on the results of healthy controls. The prevalence of MHE and the comparison results with psychometric hepatic encephalopathy score through the Stroop-CN model were stable in the test and validation cohorts. Moreover, the prevalence of MHE remained significantly higher in patients with worse disease conditions marked as high Child-Pugh grades and the Model for End-stage Liver Disease and Sodium (MELD-Na) scores in the test and validation cohort. The EuroQol 5-D questionnaire revealed that patients with MHE had a worse QOL than those without MHE both in the test and validation cohort. In conclusion, an easy and practical Stroop-CN model for MHE diagnosis based on the EncephalApp is established. It is found that a considerable number of Chinese patients with cirrhosis experience MHE, which significantly impacts their QOL.

Integrating serum pharmacochemistry and network pharmacology to explore potential compounds and mechanisms of Alpiniae oxyphyllae fructus in the treatment of cellular senescence in diabetic kidney disease.

Background: Diabetic kidney disease (DKD), one of the microvascular complications in patients with diabetes mellitus, is a common cause of end-stage renal disease. Cellular senescence is believed to be an essential participant in the pathogenesis of DKD. Although there is evidence that Alpiniae oxyphyllae fructus (AOF) can ameliorate DKD progression and organismal senescence, its ability to ameliorate renal cellular senescence in DKD as well as active components and molecular mechanisms remain to be explored. Purpose: This study aimed to investigate the role of AOF in the treatment of cellular senescence in DKD and to explore its active components and potential molecular mechanisms. Methods: The pharmacological efficacy of AOF in ameliorating cellular senescence in DKD was assessed by establishing DKD mouse models and HK-2 cells under high glucose stress. UHPLC-QTOF-MS was used to screen the active compounds in AOF, which were used in conjunction with network pharmacology to predict the molecular mechanism of AOF in the treatment of cellular senescence in DKD. Results: In vivo experiments showed that AOF reduced GLU, mAlb, Scr, BUN, MDA, SOD levels, and ameliorated renal pathological damage and renal cell senescence in DKD mice. In vitro experiments showed that AOF-containing serum improved the decline in HK-2 cell viability and alleviated cellular senescence under high glucose intervention. The results of the UHPLC-QTOF-MS screened 26 active compounds of AOF. The network pharmacological analyses revealed that Cubebin, 2',6'-dihydroxy-4'-methoxydihydrochalcone, Chalcone base + 3O,1Prenyl, Batatasin IV, and Lucidenolactone were the five core compounds and TP53, SRC, STAT3, PIK3CA, and AKT1 are the five core targets of AOF in the treatment of DKD. Molecular docking simulation results showed that the five core compounds had good binding ability to the five core targets. Western blot validated the network pharmacological prediction results and showed that AOF and AOF-containing serum down-regulate the expression of TP53, and phosphorylation of SRC, STAT3, PIK3CA, and AKT. Conclusion: Our study shows that AOF may delay the development of cellular senescence in DKD by down-regulating the levels of TP53, and phosphorylation of SRC, STAT3, PIK3CA, and AKT.

National and subnational mortality trends of multiple myeloma in China, 2013-2020: Empirical evidence from national mortality.

The incidence of multiple myeloma (MM) has increased over time in China. Despite this increase, comprehensive and up-to-date statistics on its mortality at national and provincial scales are lacking. To bridge this gap, we used mortality data from the disease surveillance points system operated by the Chinese Center for Disease Control and Prevention. Mortality rates were standardized against the 2010 census population of China (ASMRC) and Segi's world population (ASMRW). Joinpoint regression models were used to analyze temporal trends. Our findings indicated an estimated 14,568 MM-related deaths in China. The observed crude mortality rates ASMRC, and ASMRW were 1.04, 0.80, and 0.62 per 100,000 individuals, respectively. A notable sex-related difference in mortality rates was evident, with male mortalities (8,319) surpassing female mortalities (6,249) by a factor of 1.33. Age-wise, mortality rates tended to increase after 55 years, reaching a maximum in those over 85 years (7.09 per 100,000 individuals). Provincial data revealed that the highest ASMRCs were in Zhejiang, Beijing, and Jiangxi, whereas the lowest were in Tibet, Qinghai, and Hainan. The period from 2013 to 2020 exhibited a significant increase of 58.09 % in MM mortality, with urban and rural areas exhibiting a 44.97 % and 70.94 % increase, respectively. This analysis highlights the growing mortality burden of MM across various demographics and regions, emphasizing the need for tailored disease management and preventive measures.

Deciphering the mitochondria-inflammation axis: Insights and therapeutic strategies for heart failure.

Heart failure (HF) is a clinical syndrome resulting from left ventricular systolic and diastolic dysfunction, leading to significant morbidity and mortality worldwide. Despite improvements in medical treatment, the prognosis of HF patients remains unsatisfactory, with high rehospitalization rates and substantial economic burdens. The heart, a high-energy-consuming organ, relies heavily on ATP production through oxidative phosphorylation in mitochondria. Mitochondrial dysfunction, characterized by impaired energy production, oxidative stress, and disrupted calcium homeostasis, plays a crucial role in HF pathogenesis. Additionally, inflammation contributes significantly to HF progression, with elevated levels of circulating inflammatory cytokines observed in patients. The interplay between mitochondrial dysfunction and inflammation involves shared risk factors, signaling pathways, and potential therapeutic targets. This review comprehensively explores the mechanisms linking mitochondrial dysfunction and inflammation in HF, including the roles of mitochondrial reactive oxygen species (ROS), calcium dysregulation, and mitochondrial DNA (mtDNA) release in triggering inflammatory responses. Understanding these complex interactions offers insights into novel therapeutic approaches for improving mitochondrial function and relieving oxidative stress and inflammation. Targeted interventions that address the mitochondria-inflammation axis hold promise for enhancing cardiac function and outcomes in HF patients.

High expression of RUNX1 in colorectal cancer subtype accelerates malignancy by inhibiting HMGCR.

Colorectal cancer (CRC) presents a complex landscape, characterized by both inter-tumor and intra-tumor heterogeneity. RUNX1, a gene implicated in modulating tumor cell growth, survival, and differentiation, remains incompletely understood regarding its impact on CRC prognosis. In our investigation, we discerned a positive correlation between elevated RUNX1 expression and aggressive phenotypes across various CRC subtypes. Notably, knockdown of RUNX1 demonstrated efficacy in restraining CRC proliferation both in vitro and in vivo, primarily through inducing apoptosis and impeding cell proliferation. Mechanistically, we unveiled a direct regulatory link between RUNX1 and cholesterol synthesis, mediated by its control over HMGCR expression. Knockdown of RUNX1 in CRC cells triggered HMGCR transcriptional activation, culminating in elevated cholesterol levels that subsequently hindered cancer progression. Clinically, heightened RUNX1 expression emerged as a prognostic marker for adverse outcomes in CRC patients. Our findings underscore the pivotal involvement of RUNX1 in CRC advancement and its potential as a therapeutic target. The unique influence of RUNX1 on cholesterol synthesis and HMGCR transcriptional regulation uncovers a novel pathway contributing to CRC progression.

Design, Synthesis, Bioactivity, and Tentative Exploration of Action Mode for Benzyl Ester-Containing Derivatives.

The active splicing strategy has witnessed improvement in bioactivity and antifungal spectra in pesticide discovery. Herein, a series of simple-structured molecules (Y1-Y53) containing chloro-substituted benzyl esters were designed using the above strategy. The structure-activity relationship (SAR) analysis demonstrated that the fatty acid fragment-structured esters were more effective than those containing an aromatic acid moiety or naphthenic acid part. Compounds Y36 and Y41, which featured a thiazole-4-acid moiety and trifluoromethyl aliphatic acid part, respectively, exhibited excellent in vivo curative activity (89.4%, 100 mg/L Y36) and in vitro fungicidal activity (EC50 = 0.708 mg/L, Y41) against Botrytis cinerea. Determination of antifungal spectra and analysis of scanning electron microscopy (SEM), membrane permeability, cell peroxidation, ergosterol content, oxalic acid pathways, and enzymatic assays were performed separately here. Compound Y41 is cost effective due to its simple structure and shows promise as a disease control candidate. In addition, Y41 might act on a novel target through a new pathway that disrupts the cell membrane integrity by inducing cell peroxidation.

Unveiling the Roles of Alloyed Boron in Hexavalent Chromium Removal Using Borohydride-Synthesized Nanoscale Zerovalent Iron: Electron Donor and Antipassivator.

Nanoscale zerovalent iron synthesized using borohydride (B-NZVI) has been widely applied in environmental remediation in recent decades. However, the contribution of boron in enhancing the inherent reactivity of B-NZVI and its effectiveness in removing hexavalent chromium [Cr(VI)] have not been well recognized and quantified. To the best of our knowledge, herein, a core-shell structure of B-NZVI featuring an Fe-B alloy shell beneath the iron oxide shell is demonstrated for the first time. Alloyed boron can reduce H+, contributing to more than 35.6% of H2 generation during acid digestion of B-NZVIs. In addition, alloyed B provides electrons for Fe3+ reduction during Cr(VI) removal, preventing in situ passivation of the reactive particle surface. Meanwhile, the amorphous oxide shell of B-NZVI exhibits an increased defect density, promoting the release of Fe2+ outside the shell to reduce Cr(VI), forming layer-structured precipitates and intense Fe-O bonds. Consequently, the surface-area-normalized capacity and surface reaction rate of B-NZVI are 6.5 and 6.9 times higher than those of crystalline NZVI, respectively. This study reveals the importance of alloyed B in Cr(VI) removal using B-NZVI and presents a comprehensive approach for investigating electron pathways and mechanisms involved in B-NZVIs for contaminant removal.

A High-Performance Passive Radiative Cooling Metafabric with Janus Wettability and Thermal Conduction.

With the development of industry and global warming, passive radiative cooling textiles have recently drawn great interest owing to saving energy consumption and preventing heat-related illnesses. Nevertheless, existing cooling textiles often lack efficient sweat management capacity and wearable comfort under many practical conditions. Herein, a hierarchical cooling metafabric that integrates passive radiation, thermal conduction, sweat evaporation, and excellent wearable comfort is reported through an electrospinning strategy. The metafabric presents excellent solar reflectivity (99.7%, 0.3-2.5 µm) and selective infrared radiation (92.4%, 8-13 µm), given that the unique optical nature of materials and wettability gradient/micro-nano hierarchical structure design. The strong moisture-wicking effect (water vapor transmission (WVT) of 2985 g m-2 d-1 and directional water transport index (R) of 1029.8%) and high heat-conduction capacity can synergistically enhance the radiative cooling efficiency of the metafabric. The outdoor experiment reveals that the metafabric can obtain cooling temperatures of 13.8 °C and 19.3 °C in the dry and sweating state, respectively. Meanwhile, the metafabric saves ≈19.3% of annual energy consumption compared with the buildings with HAVC systems in Shanghai. The metafabric also demonstrates desirable breathability, mechanical strength, and washability. The cost-effective and high-performance metafabric may offer a novel avenue for developing next-generation personal cooling textiles.