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Objective: By meticulously tracking the evolving growth, development, and nutritional status of primary and secondary school students in Qiongzhong County from 2014 to 2021 post-implementation of the "Nutrition Improvement Program for Rural Compulsory Education Students"(NIPRCES, This project provides a supplementary food allowance of at least ￥4 per person per day for primary and secondary school students. The project area undergoes annual routine monitoring.), this study aims to offer a scientific basis for enhancing and promoting the project. Through thorough monitoring of students' nutritional status changes influenced by this program, we strive to establish a comprehensive and evidence-based framework for its future advancement. Methods: From 2014 to 2021, this study employed a multi-stage sampling method utilizing cluster sampling to select six primary and six secondary schools in Qiongzhong County, Hainan Province. Data on the growth and development of respondents were collected. This cohort was a dynamic cohort with a total of 18,762 final data recovered. The prevalence of malnutrition was evaluated using the Cochran Armitage Trend Test (CATT) to assess year-to-year changes. Furthermore, height/weight and the prevalence of malnutrition between groups were compared using the t-test, χ2 test, and Bonferroni's corrected analysis. Results: The average height of both boys and girls has increased. In 2021, boys and girls of all ages showed an average height increase of 2.31 cm and 1.98 cm, respectively, compared to 2014. Nevertheless, the growth and development levels, and rate of improvement of these students remain comparatively lower than their rural counterparts across China, who are of the same age. From 2014 to 2021, the prevalence of undernutrition (mainly wasting) showed a significant downward trend (P < 0.05) from 29.30% to 22.19%, and the prevalence of overnutrition showed an upward trend (both P < 0.05). The prevalence of undernutrition was higher among boys, students in grades 1–3 and those of Li nationality. Meanwhile, the prevalence of overnutrition was higher among boys, students in grades 1–3 and those of Han nationality. Conclusions: Over the 8-year period of NIPRCES, there has been progress in the growth and development of students, yet levels still lag behind the national average for rural students of the same age. While malnutrition prevalence have decreased, they remain high, with a concerning rise in overnutrition prevalence. Undernutrition and overweight/obesity are more prevalent among boys and younger students. Li students show higher prevalence of undernutrition, while overnutrition is a growing issue among Han students. Simultaneously, local education and health care departments must acknowledge the disparities in growth and nutritional status among primary and secondary school students residing in rural areas within the tropics and those in rural areas across the entire nation. Nutritional improvement measures should be tailored to local conditions. [ABSTRACT FROM AUTHOR]

Sjogren's syndrome (SS) is a complex systemic autoimmune disease. This study aims to elucidate a humanized NOD-PrkdcscidIl2rgem1/Smoc (NSG) murine model to better clarify the pathogenesis of SS. NSG female mice were adoptively transferred with 10 million peripheral blood mononuclear cells (PBMCs) through the tail vein from healthy controls (HCs), primary Sjogren's syndrome (pSS), and systemic lupus erythematosus (SLE) patients on D0. The mice were subcutaneously injected with C57/B6j submandibular gland (SG) protein or phosphate-buffered saline on D3, D17 and D31, respectively. NSG mice were successfully transplanted with human PBMCs. Compared with NSG-HC group, NSG-pSS and NSG-SLE mice exhibited a large number of lymphocytes infiltration in the SG, decreased salivary flow rate, lung involvement, decreased expression of genes related to salivary secretion, and the production of autoantibodies. Type I interferon-related genes were increased in the SG of NSG-pSS and NSG-SLE mice. The ratio of BAX/BCL2, BAX, cleaved caspase3, and TUNEL staining were increased in the SG of NSG-pSS and NSG-SLE mice. The expressions of p-MLKL and p-RIPK3 were increased in the SG of NSG-pSS and NSG-SLE mice. Increased expression of type I interferon-related genes, PANoptosis (apoptosis and necroptosis) were identified in the SG of this typical humanized NSG murine model of SS. [ABSTRACT FROM AUTHOR]

Aims: HNF1B syndrome is caused by defects in the hepatocyte nuclear factor 1B (HNF1B) gene, which leads to maturity‐onset diabetes of the young type 5 and congenital organ malformations. This study aimed to identify a gene defect in a patient presenting with diabetes and severe diarrhea, while also analyzing the prevalence of hypomagnesemia and its correlation with the HNF1B genotype. Materials and Methods: Whole exome sequencing was used to identify responsible point mutations and small indels in the proband and their family members. Multiplex ligation‐dependent probe amplification was carried out to identify HNF1B deletions. Furthermore, an analysis of published data on 539 cumulative HNF1B cases, from 29 literature sources, was carried out to determine the correlation between the HNF1B genotype and the phenotype of serum magnesium status. Results: Using multiplex ligation‐dependent probe amplification, we identified a de novo heterozygous HNF1B deletion in the patient, who showed dorsal pancreas agenesis and multiple kidney cysts, as detected by magnetic resonance imaging. Magnesium supplementation effectively alleviated the symptoms of diarrhea. Hypomagnesemia was highly prevalent in 192 out of 354 (54.2%) patients with HNF1B syndrome. Compared with patients with intragenic mutations, those with HNF1B deletions were more likely to suffer from hypomagnesemia, with an odds ratio of 3.1 (95% confidence interval 1.8–5.4). Conclusions: Hypomagnesemia is highly prevalent in individuals with HNF1B syndrome, and those with HNF1B deletion are more susceptible to developing hypomagnesemia compared with those with intragenic mutations. The genotype–phenotype associations in HNF1B syndrome have significant implications for endocrinologists in terms of genotype detection, treatment decisions and prognosis assessment. [ABSTRACT FROM AUTHOR]

Digital transformation and sustainability are both at the forefront of current supply chain developments. However, the specific mechanisms of how digital transformation and green supply chain development interact still need to be clarified, which can help supply chain business operators to enhance supply chain sustainability more effectively. This paper focuses on how the companies' organization structure and the socio-economic environment interact with digital technologies under the process of green supply chain development. Based on the "Technology–Organization–Environment" (TOE) framework, this paper analyze how digital transformation can drive green supply chain development. To test the TOE theoretical analysis framework, this paper calculates the digital transformation and green supply chain development index at the provincial level in China and conducts an empirical study. The main findings and implications of this paper can be summarized in the following aspects: First, according to the TOE theory, the external environment dimensions, such as the market and policy environments, affect the role of digital technology in promoting GSC development. Second, in the organizational dimensions, labor–capital relations, company size, and ownership factors can all affect the contribution of digital transformation to green supply chains. Third, there are differences in the impact of different types of digitization technologies on GSC development. [ABSTRACT FROM AUTHOR]

Moss-dominated biocrusts are widespread in degraded mining ecosystems and play an important role in soil development and ecosystem primary succession. In this work, the soil microbial community structure under moss-dominated biocrusts in ionic rare earth tailings was investigated to reveal the relationship between different types of moss and taxonomy/function of microbiomes. The results showed that microbial community structure was significantly influenced by four moss species (Claopodium rugulosifolium, Orthotrichum courtoisii, Polytrichum formosum, and Taxiphyllum giraldii). The microbial assembly was more prominent in Claopodium rugulosifolium soil than in the other moss soils, which covers 482 bacterial genera (including 130 specific genera) and 338 fungal genera (including 72 specific genera), and the specific genus is 40% to 1300% higher than that of the other three mosses. Although only 141 and 140 operational taxonomic units (OTUs) rooted in bacterial and fungal clusters, respectively, were shared by all four mosses grown in ionic rare earth tailings, this core microbiome could represent a large fraction (28.2% and 38.7%, respectively) of all sequence reads. The bacterial population and representation are the most abundant, which mainly includes Sphingomonas, Clostridium_sensu_stricto_1, and unclassified filamentous bacteria and chloroplasts, while the fungi population is relatively singular. The results also show that biocrust dominated by moss has a positive effect on soil microbe activity and soil nutrient conditions. Overall, these findings emphasize the importance of developing moss-dominated biocrusts as hotspots of ecosystem functioning and precious microbial genetic resources in degraded rare-earth mining areas and promoting a better understanding of biocrust ecology in humid climates under global change scenarios. [ABSTRACT FROM AUTHOR]

An efficient intermolecular C−H aminohalogenation of indoles with azoles and NXS (X = F, Cl, Br, I) has been developed. This mild protocol provides a straightforward entry to structurally valuable 2‐azolyl‐3‐halogenated indoles in one single operation. In addition, this attractive route for the synthesis of polyfunctionalized indoles is of great significance due to the product's versatile reactivity for further transformations. [ABSTRACT FROM AUTHOR]

Aiming at exploiting the discriminative deep features and encoding the high-level structures, this letter presents a deep-features-based high-order triple discriminative random field model, abbreviated as DF-HoTDF, for nonstationary polarimetric synthetic aperture radar (PolSAR) image classification. First, the DF-HoTDF model extracts the discriminative deep features by a graph-based complex-valued 3-D convolutional neural network (CV-3-D-CNN) and then constructs the unary potential by a negative log function. Second, it introduces an auxiliary field u to explicitly regulate the nonstationary label patterns of the PolSAR image and then constructs a pairwise potential guided by u to capture greater pairwise label interactions. Third, it defines a high-order potential on high-order cliques to encode high-level structures. Finally, under the discriminative model framework, the DF-HoTDF model has a weighted fusion of the unary potential, the pairwise potential, and the high-order potential. Then, with the DF-HoTDF model, we iteratively optimize the class label and the stationary maps until they converge. The experimental results demonstrate that the proposed DF-HoTDF model is of superior performances in nonstationary PolSAR image classification and that it can provide better label consistency in homogeneous region and better target structures and edge locations in heterogeneous region. [ABSTRACT FROM AUTHOR]

HighlightsThis study reports a novel frameshift mutation c.212dupG (p.Gly73fs) in the insulin (INS) gene causing maturity onset diabetes of the young (MODY) 10, one of the rare types of MODY, identified in seven family members.Screening for mutations in identified MODY genes is warranted in patients who require insulin, are negative for autoantibodies but have a family history of diabetes. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to investigate the prospective association of circulating adipocyte fatty acid-binding protein (A-FABP) levels with the development of subclinical atherosclerosis in patients with type 2 diabetes in an 8-year prospective study.Methods: A total of 170 patients with newly diagnosed type 2 diabetes were recruited in the study and 133 patients completed the follow-up of 8 years. Baseline plasma A-FABP levels were measured with enzyme-linked immunosorbent assays. The role of A-FABP in predicting the development of subclinical atherosclerosis over 8 years was analyzed using multiple logistic regression.Results: Of the 133 patients without subclinical atherosclerosis at baseline, a total of 100 had progressed to subclinical atherosclerosis over 8 years. Baseline A-FABP level was significantly higher in patients who had progressed to subclinical atherosclerosis at year 8 compared with ones who had not developed subclinical atherosclerosis after adjustment for sex (15.3 [12.1-23.2] versus 13.3 [10.0-18.9] ng/ml, P = 0.021). High baseline A-FABP level was an independent predictor for the development of subclinical atherosclerosis in patients with type 2 diabetes (odds ratio: 16.24, P = 0.022).Conclusions: Circulating A-FABP levels predict the development of subclinical atherosclerosis in type 2 diabetes patients. [ABSTRACT FROM AUTHOR]

The present study characterized the nutrients availability of three rare earth tailings deserted in different time stages in Southern Jiangxi of China, and revealed the influence of the soil nutrient properties on fungi composition and diversity by using an internal transcribed spacer (ITS) rRNA sequence approach. Three tailings (RS1, RS2 and RS3) and one reference soil (RS4) were sampled. Results showed that a higher levels of AN and TOC occurred in RS1 and RS4, whereas higher contents of SO2-4, TN, NO-3-N, NH+4-N and rare earth elements (REEs) existed in RS2 and RS3, suggesting a high environmental heterogeneity in the different tailings. Metagenomic analysis showed that RS1~RS4 harbored 355, 564, 366 and 507 operational taxonomic units (OTUs), respectively. Alpha diversity analysis showed that RS4, a control sample, had the highest Shannon diversity, whereas RS3, a newly formed tailings, exhibited the lowest Chao1 richness.Among the monitored environmental variables, AN and SO2-4 were the most important factors affecting the overall fungal community composition and the relative abundances of specific lineages. Additionally, genus Penicillium prevailed in RS1and RS4 while genus Aspergillus dominated in RS2 and RS3, indicating that the nitrification maybe conduct by different fungal genus in different tailings. Together, these results suggest that lower fungal community composition and diversity as well as the alteration in fungi-dominated heterotrophic nitrification may be due to the deteriorative nutrient in rare earth tailings, especially increasing level of sulfate and decreasing level of available nitrogen. [ABSTRACT FROM AUTHOR]

Highlights • The toxicity of OPs was slightly increased with the decrease of soil pH. • Mechanistic models were developed to interpret the phenomena. • Bioavailability and toxicodynamics are key factors for toxicity variation. • Bioavailability was related to hydrolysis and biodegradation characteristics. • Toxicodynamics were influenced by the interaction between AchE with OPs. Abstract Organophosphorus pesticides (OPs) have been widely used to control agricultural insects. Soil acidification is a major problem in soil of intensive agricultural systems, especially in red soil with a low pH buffer capacity. However, the effects of soil acidification on the toxicity of pesticides are still unclear. In the present study, the toxicity of three OPs on E. fetida was determined at individual (14-day lethal test) and biochemical levels (antioxidative defence enzymes) by using acidified soils (pH = 5.5, 4.3 and 3.1). The results showed that the toxicity of tested OPs was slightly increased with the decrease of soil pH. To interpret the phenomena, an optimum Quantitative Structure Activity Relationship (QSAR) model was developed based on the toxicity mechanism and the partial least squares regression (PLS) method. The model indicated bioavailability and toxicodynamics are key factors of soil acidification affecting the toxicity of the OPs. Further results revealed the bioavailability of the OPs was strongly related to their hydrolysis and biodegradation character, whereas the effects of soil acidification on toxicodynamics were mainly caused by the interaction between the acetylcholinesterase (AchE) and the OPs. Results will increase understanding of the effects of soil acidification on the toxicity of pesticides and its mechanism. [ABSTRACT FROM AUTHOR]

Objective: The aim of this work was to report an autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy with long-term follow-up in 7 patients. Methods: Antibodies were detected by indirect immunofluorescence assay and patient data were analyzed retrospectively. Results: Seven patients (4 female, 3 male) with ≥ 1 year follow-up were included. All patients had positive GFAP antibodies in their cerebral spinal fluid (CSF). Their median age at disease onset was 56 years (range 27–69) and the median disease duration was 1 year (range 1–4). In the initial attack, all patients received intravenous methylprednisolone (IVMP) followed by oral steroids, which were tapered. Six patients received intravenous immunoglobulin (IVIg). One patient had no response to IVIg and IVMP. Four patients received immunosuppressive agents. Five patients underwent the second lumbar puncture after treatment. CSF white blood cell counts, protein levels, and antibody titers were significantly decreased. CSF protein levels correlated positively with the Expanded Disability Status Scale score, which was elevated at each lumbar puncture. Four patients experienced relapse. To date, 6 patients had a bad prognosis, of which 2 died. Conclusions: Some patients with GFAP astrocytopathy experienced a poor response to treatment although they received steroids and immunosuppressive agents. [ABSTRACT FROM AUTHOR]

Intestinal ischemia-reperfusion (II/R) injury is a common clinical and pathological change; however, its underlying mechanisms remain unclear. Previous studies have shown that the inflammatory response induced by mast cell degranulation may be involved in the mechanism underlying II/R injury in rats. In this study, we established a human intestinal epithelial adenocarcinoma cell (Caco-2) hypoxia/reoxygenation (H/R) model and transwell system to investigate the effects of culture media (CM) from hypoxia conditioned human mast cell (HMC-1) and HMC-1 H/R on hypoxia/reoxygenation injury in Caco-2 under H/R conditions. Moreover, we assessed the barrier function of Caco-2 by measuring the 4-kDa fluorescein isothiocyanate (FITC)-dextran (FD4) flux and the tight junction protein expression. The results concluded that Caco-2 exposed to H/R insult showed an increase in lactate dehydrogenase (LDH) release, cell apoptosis index, cell permeability, Bax expression, phosphorylation of c-Jun N-terminal protein kinase (JNK) and p38, and a decrease in cell viability and expression of Bcl-2, ZO1, and occludin (all P < 0.05). Notably, preincubating Caco-2 with HMC-1CM resulted in an increase in cell injury (increased LDH levels and cell permeability, decreased cell viability), apoptosis index, p-JNK, and p-38 expression and a decrease in ZO1 and occludin expression by co-culture system (all P < 0.05). In conclusion, our results show that HMC-1 hypoxic and reoxygenated CM aggravates hypoxic and reoxygenated injury in Caco-2 by increasing the phosphorylation of JNK and p38 in vitro. • HMC-1 activates and releases hypoxia/reoxygenation-induced inflammatory factors. • HMC-1 hypoxic and reoxygenated CM aggravates hypoxic and reoxygenated injury in Caco-2. • CM from hypoxic and reoxygenated HMC-1 reduces the expression of tight junction proteins ZO1 and occludin. • H/R HMC-1 CM damages the intestinal epithelial barrier function in Caco-2. • HMC-1 hypoxic and reoxygenated CM increasing the phosphorylation of JNK and p38 in vitro. [ABSTRACT FROM AUTHOR]

Effects of miR-34a expression on cell metastasis-associated protein expression in hepatocellular cells. **P<0.01 vs. control cells. miR, microRNA; miRSCR, scramble miR-34a; SIRT, sirtuin; p53, tumor protein 53, Ac-p53, acetylated p53. [Extracted from the article]

Sevoflurane (SEV) preconditioning plays a protective effect against liver ischemia reperfusion (IR) injury, while the role of autophagy in SEV-mediated hepatoprotection and the precise mechanism is unclear. In the current study, mice were pretreated with SEV or autophagy inhibitor before liver IR injury. In vitro, primary rat hepatocytes were pretreated with SEV and then exposed to hypoxia/reoxygenation (H/R). Liver function was measured by biochemical and histopathological examinations, and markers associated with inflammation, oxidation, apoptosis and autophagy were subsequently measured. We found that SEV preconditioning dramatically reduced hepatic damage, alleviated cell inflammatory response, oxidative stress and apoptosis in mice suffering hepatic IR injury, whereas these protective effects were abolished by the autophagy inhibitor 3-MA. In addition, pretreatment with SEV markedly activated HGF/Met signaling pathway regulation. Besides, pretreatment with an hepatocyte growth factor (HGF) inhibitor or knocking down HGF expression significantly downregulated phosphorylated met (p-met) and autophagy levels, and abolished the protective effects of SEV against hepatic IR or hepatocyte H/R injury. Conversely, HGF overexpression efficiently increased the p-met and autophagy levels and strengthened the protective effects of SEV. These results indicated that sevoflurane preconditioning ameliorates hepatic IR injury by activating HGF/Met-mediated autophagy. • Sevoflurane preconditioning reduced mice hepatic ischemia reperfusion injuryby alleviating inflammation , oxidative stress and apoptosis. The protective effects of sevoflurane could be abolished by the autophagy inhibitor 3-MA. • Inhibiting hepatocyte growth factor (HGF) expression abolished the protective effects of sevoflurane against hepatic IR. • Sevoflurane preconditioning ameliorated hepatic IR injury by activating HGF/Met-mediated autophagy. [ABSTRACT FROM AUTHOR]

Antibiotic resistance genes (ARGs) have been widely detected around the world and are generally viewed as emerging pollutants with environmental persistence. The proliferation of ARGs can be easily promoted by antibiotics. However, the dynamics of ARGs in the environment are still unable to be quantified using a single parameter, which is vital to evaluating the ability of ARGs to spread by antibiotics and effectively controlling ARGs. A new parameter, termed the relative area ratio of sample to control (Δ A R), was developed based on the quantitative features determined by ARG-time curves in soils contaminated with sulfonamides (SAs) and verified by quantitative structure-activity relationships (QSARs) models. The results showed that Δ A R can not only be used to accurately quantify the characteristics of SAs resistance genes (Suls) over time but also be applied to reveal the relationships between the proliferation of Suls and important factors (i.e., concentrations and chemical structures). Moreover, the Δ A R-based QSARs model indicated that bioavailability and the frequency of conjugative transfer, rather than the ability of induced mutations in bacteria, tend to be key processes of the characteristics of the proliferation of Suls. Therefore, Δ A R is a useful parameter to perform environmental risk assessments of ARG proliferation in the environment. Unlabelled Image • Suls levels in SAs-spiked soil increased and then declined to the level of control. • A new parameter ΔAR was developed to interpret the dynamic of Suls. • ΔAR can reveal the relationships between Suls proliferation and important factors. • Bioavailability/frequency of conjugative transfer contributes to Suls proliferation. [ABSTRACT FROM AUTHOR]

The widespread occurrence and distribution of organotin compounds (OTCs) in both marine and freshwater ecosystems has aroused considerable concerns in most countries worldwide. In this work, individual kinetics of the elimination of three butyltins and three phenyltins from C. demersum L. were systematically studied for over 240 h in clean water after a 48h period of accumulation. All OTCs were rapidly metabolized to nontoxic inorganic tin by C. demersum L. through stepwise debutylation or dephenylation. In addition to inorganic tin, monobutyltin (MBT) and monophenyltin (MPT) were the primary degradation products of tributyltin (TBT) and triphenyltin (TPT), with small amounts of dibutyltin (DBT) and diphenyltin (DPT), respectively, also being present. The estimated half-life of TPT (240 h) in C. demersum L. was longer than that of TBT (100 h), although the TPT was less hydrophobic. The corresponding degradation mechanisms may be attributed to a cascade of enzymatic reactions of CYP450 enzymes in C. demersum L. The pH played an important role in both plant growth and TBT degradation. Although pH 8.9 was more suitable for C. demersum L. growth, it uptook and metabolized more TBT at pH 5.0, which may be because the cationic species TBT+ (at pH 5.0) was metabolized more easily than the neutral hydroxide species TBTOH (at pH 8.9). C. demersum L. may thus be the plant with the most potential for the remediation of OTC-contaminated freshwater environments. • OTCs can be rapidly metabolized to nontoxic inorganic tin by C. demersum L. (77 characters). • Degradation pathways are through the progressive removal of butyl or phenyl groups. (85 characters). • Mechanism is mainly attributed to a cascade of enzymatic reactions of CYP450. (79 characters). • OTC existence forms have a substantial impact on the degradation efficiency. (78 characters). [ABSTRACT FROM AUTHOR]

Comparatively limited knowledge is known about the accumulation processes of tributyltin (TBT) and triphenyltin (TPT) in fish and aquatic plant in the freshwater environment, which has hindered a full understanding of their bioaccumulation potential and ecological risks. In the present study, sorption of TBT and TPT on dead biota of both carp and C. demersum from water via the batch equilibrium technique as well as uptake of them on live biota of both carp and C. demersum from water at a static and a dynamic kinetics tests were investigated, respectively. Both TBT and TPT exhibit a high affinity in carps and C. demersum. And C. demersum has a faster metabolism either for TBT or TPT than carp. The apparent uptake values (C bio = 1904–8831 μg/kg) or bioconcentration factor (BCF = 3333–44000 L/kg) were one or two orders of magnitude higher than that of estimated by a simple sorption (405–472 μg/kg) or lipid model (74.5–149.6 μg/kg) for carp , indicating the uptake of TBT and TPT did not only depend on lipids but also oxygen ligands or macromolecules such as amino acids and proteins of the living organism. In contrast, the apparent C bio values (149.1–926.4 μg/kg) of both TBT and TPT were lower than that of estimated by sorption model (1341–1902 μg/kg) for C. demersum , which were due to the rapid metabolic rate of them, especially for TBT. But no relation was observed between TBT and TPT concentrations and lipid contents in C. demersum. • TBT and TPT exhibited a high affinity but a low speed of metabolism in carp. (79 characters). • C. demersum had a faster metabolism either for TBT or TPT than carp. (66 characters). • C. demersum can rapidly uptake and metabolize TBT and TPT. (61 characters). • Uptake limit of carp to OTC predicted by equilibrium sorption will be underestimated. (84 characters). [ABSTRACT FROM AUTHOR]

Photocatalysis is one of the most effective methods for treating antibiotic wastewater. Thus, it is of great significance to determine the relationship between degradation rates and structural characteristics of antibiotics in photocatalysis processes. In the present study, the photocatalytic degradation characteristics of 10 sulfonamides (SAs) were studied using two photocatalytic systems composed of nanophase titanium dioxide ( n TiO 2 ) plus ultraviolet (UV) and n TiO 2 /activated carbon fiber (ACF) plus UV. The results indicated that the largest apparent SA degradation rate constant ( K app ) is approximately 5 times as large as that of the smallest one. Based on the degradation mechanism and the partial least squares regression (PLS) method, optimum Quantitative Structure Activity Relationship (QSAR) models were developed for the two systems. Mechanistic models indicated that the degradation rule of SAs in the TiO 2 systems strongly relates to their highest occupied molecular orbital ( E homo ), the maximum values of nucleophilic attack ( f (+) x ), and the minimum values of the most negative partial charge on a main-chain atom ( q (C) min ), whereas the maximum values of OH radical attack ( f (0) x ) and the apparent adsorption rate constant values ( k ad ) are key factors affecting the degradation rule of SAs in the TiO 2 /ACF system. [ABSTRACT FROM AUTHOR]

2-Dimensional materials (2DMs) offer an attractive solution for the realization of high density and reliable memristors, compatible with printed and flexible electronics. In this work we fabricate a fully inkjet printed MoS 2 -based resistive switching memory, where graphene is used as top electrode and silver is used as bottom electrode. Memristic effects are observed only after annealing of each printed component. The printed memory on silicon shows low SET/RESET voltage, short switching times (less than 0.1 s) and resistance switching ratios of 10 3 -10 5 , comparable or superior to the performance obtained in devices with both printed silver electrodes on rigid substrates. The same device on Kapton shows resistance switching ratios of 10 2 -10 3 and remains stable at least up to 2% of strain. The memristor resistance switching is attributed to the formation of Ag conductive filaments, which can be suppressed by integrating graphene grown by chemical vapour deposition (CVD) onto the silver electrode. Temperature-dependent electrical measurements starting from 200 K show that memristic behavior appears at a temperature of ∼300 K, confirming that an energy threshold is needed to form the conductive filament. This work shows that inkjet printing is a very powerful technique for the fabrication of 2DMs-based resistive switches onto rigid and flexible substrates.

Purpose: Intravenous patient-controlled analgesia (IV-PCA) has been widely used; however, regimen criteria have not yet been established. In China, the most often used opioid is sufentanil, for which repeated doses are a concern, and empirical flurbiprofen axetil (FBP) as an adjuvant. We hypothesized that hydromorphone would be a better choice and also evaluated the effectiveness of FBP as an adjuvant. Methods: This historical cohort study was conducted in two tertiary hospitals in China and included 12,674 patients using hydromorphone or sufentanil for IV-PCA between April 1, 2017, and January 30, 2021. The primary outcome was analgesic insufficiency at static (AIS). The secondary outcomes included analgesic insufficiency with movement (AIM) and common opioid-related adverse effects such as postoperative nausea and vomiting (PONV) and dizziness. Results: Sufentanil, but not the sufentanil-FBP combination, was associated with higher risks of AIS and AIM compared to those for hydromorphone (OR 1.64 [1.23, 2.19], p < 0.001 and OR 1.42 [1.16, 1.73], p < 0.001). Hydromorphone combined with FBP also decreased the risk of both AIS and AIM compared to those for pure hydromorphone (OR 0.74 [0.61, 0.90], p = 0.003 and OR 0.80 [0.71, 0.91], p < 0.001). However, the risk of PONV was higher in patients aged ≤35 years using FBP (hydromorphone-FBP vs. hydromorphone and sufentanil-FBP vs. hydromorphone, OR 1.69 [1.22, 2.33], p = 0.001 and 1.79 [1.12, 2.86], p = 0.015). Conclusion: Hydromorphone was superior to sufentanil for IV-PCA in postoperative analgesia. Adding FBP may improve the analgesic effects of both hydromorphone and sufentanil but was associated with an increased risk of PONV in patients <35 years of age., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Song, He, Huang, Yang, Zhou, Xiao, Wang and Huang.)

Both innate and adaptive immune cells are critical players in autoimmune destruction of insulin-producing β cells in type 1 diabetes. However, the early pathogenic events triggering the recruitment and activation of innate immune cells in islets remain obscure. Here we show that circulating fatty acid binding protein 4 (FABP4) level was significantly elevated in patients with type 1 diabetes and their first-degree relatives and positively correlated with the titers of several islet autoantibodies. In nonobese diabetic (NOD) mice, increased FABP4 expression in islet macrophages started from the neonatal period, well before the occurrence of overt diabetes. Furthermore, the spontaneous development of autoimmune diabetes in NOD mice was markedly reduced by pharmacological inhibition or genetic ablation of FABP4 or adoptive transfer of FABP4-deficient bone marrow cells. Mechanistically, FABP4 activated innate immune responses in islets by enhancing the infiltration and polarization of macrophages to proinflammatory M1 subtype, thus creating an inflammatory milieu required for activation of diabetogenic CD8+ T cells and shift of CD4+ helper T cells toward Th1 subtypes. These findings demonstrate FABP4 as a possible early mediator for β cell autoimmunity by facilitating crosstalk between innate and adaptive immune cells, suggesting that pharmacological inhibition of FABP4 may represent a promising therapeutic strategy for autoimmune diabetes.

Objective: This study aims to clarify the changes and clinical significance of red cell distribution width (RDW) during HBV-related chronic diseases, including inactive hepatitis B virus (HBV) carriers, HBV immune tolerant individuals, chronic hepatitis B (CHB) patients and HBV-related hepatocirrhosis patients. Methods: RDW was measured 288 CHB patients, 100 patients with hepatitis B e antigen(HBeAg)-negative chronic HBV infection (inactive carriers), 92 patients with HBeAg-positive chronic HBV infection (immune tolerant), and 272 patients with HBV-related hepatocirrhosis. Their RDW changes were compared with 160 healthy controls. Correlations between RDW and clinical indicators were conducted. For HBeAg+ CHB patients, RDW was measured before and after antiviral therapy. The efficiency of RDW to distinguish hepatocirrhosis from CHB and/or inactive carriers was evaluated by receiver operating characteristic (ROC) curves. Results : RDW was higher in hepatocirrhosis patients than other groups of patients and healthy controls. Besides, HBeAg+ CHB patients possessed higher RDW than HBeAg- CHB patients. For HBeAg+ patients that underwent HBeAg seroconversion after antiviral therapy, RDW was decreased. RDW was positively correlated with total bilirubin and Child-Pugh scores and negatively correlated with albumin among hepatocirrhosis patients. The areas under the curve (AUC) of ROC curves to distinguish hepatocirrhosis from CHB patients was 0.7040 for RDW-standard deviation (RDW-SD) and 0.6650 for RDW-coefficient of variation (RDW-CV), and AUC to distinguish hepatocirrhosis from inactive carriers was 0.7805 for RDW-SD and 0.7991 for RDW-CV. Conclusions : RDW is significantly increased in HBeAg+ CHB patients and patients with HBV-related hepatocirrhosis and could reflect their severity. RDW could help to distinguish hepatocirrhosis from CHB patients and inactive HBV carriers., Competing Interests: Competing Interests: The authors have declared that no competing interest exists.

Objectives: Recent studies revealed that microRNAs (miRNAs) may play crucial roles in the responses and pathologic processes of spinal cord injury (SCI). This study aimed to investigate the effect and the molecular basis of miR-103 on LPS-induced injuries in PC12 cells in vitro and SCI rats in vivo ., Materials and Methods: PC12 cells were exposed to LPS to induce cell injuries to mimic the in vitro model of SCI. The expression of miR-103 and SOX2 in PC12 cells were altered by transient transfections. Cell viability and apoptotic cell rate were measured by CCK-8 assay and flow cytometry assay. Furthermore, Western blot analysis was performed to detect the expression levels of apoptosis- and autophagy- related proteins, MAPK/ERK pathway- and JAK/STAT pathway-related proteins. In addition, we also assessed the effect of miR-103 agomir on SCI rats., Results: LPS exposure induced cell injuries in PC12 cells. miR-103 overexpression significantly increased cell viability, reduced cell apoptosis and autophagy, and opposite results were observed in miR-103 inhibition. miR-103 attenuated LPS-induced injuries by indirect upregulation of SOX2. SOX2 overexpression protected PC12 cells against LPS-induced injuries, while SOX2 inhibition expedited LPS-induced cell injuries. Furthermore, miR-103 overexpression inhibited MAPK/ERK pathway and JAK/STAT pathway through upregulation of SOX2. We also found that miR-103 agomir inhibited cell apoptosis and autophagy in SCI rats., Conclusion: This study demonstrates that miR-103 may represent a protective effect against cell apoptosis and autophagy in LPS-injured PC12 cells and SCI rats by upregulation of SOX2 expression.

Hepatocellular carcinoma (HCC) remains one of the most common types of malignancy with high mortality and morbidity rates. Previous studies have suggested that microRNAs (miRs) serve pivotal functions in various types of tumor. The aim of the present study was to assess the association between miR-34a expression and HCC cell migration and invasion, and the potential underlying mechanisms. The miR-34a overexpression vector or scramble control was transfected into human Hep3B and Huh7 cell lines. Transwell assays, and Matrigel and wound healing assays were used to detect the effects of miR-34a expression on HCC cell invasion and migration, respectively. The expression of miR-34a and the mRNA expression of other associated proteins were detected using quantitative reverse transcription polymerase chain reaction, and protein levels were measured using western blot analysis. Compared with the control, miR-34a expression was significantly downregulated in Hep3B and Huh7 cells, but this was reversed by the transfection with exogenous miR-34a (P<0.01). The number of migrated or invaded cells was significantly reduced by the overexpression of miR-34a in Hep3B or Huh7 cells (P<0.01). The expression of sirtuin 1 was upregulated, while the level of acetylate-p53 was downregulated by overexpression of miR-34a. Taken together, the results of the present study suggested that the overexpression of miR-34a may have suppressed HCC metastasis via inhibited cell migration and invasion.

This study was designed to explore the effect of 3-methyladenine (3-MA) on sevoflurane anesthesia-induced cognitive dysfunction. A total of 60 C57BL/6 (5-8 months old) mice were randomly arranged into 3 groups: Control, sevoflurane (Sev) and Sev+3-MA group with 3-MA administration was performed during Sev administration. Morris water maze and Y-maze test were performed to examine the behavioral disorders. Moreover, hippocampal neuronal cell apoptosis and expression of autophagy related genes were detected. Sevoflurane induced cognitive dysfunction in mice showing significant longer escape latency, lower number of correct response, higher apoptotic neurons, and higher expression of autophagy related genes. However, additional 3-MA administration inhibited the effect of sevoflurane on cognitive dysfunction by shorting escape latency, reducing correct response number, inhibiting neurons apoptosis and autophagy genes expression. 3-MA additional administration inhibited sevoflurane anesthesia-induced cognitive dysfunction on mice. 3-MA might be usefull as an inhibitor for sevoflurane anesthesia-induced cognitive dysfunction in clinical trials.

It has been suggested that isoflurane may cause perioperative liver injury. However, the mechanism of its action remains unknown. The purpose of the present study was to determine this possible mechanism. Sprague-Dawley rats were randomly assigned into one of three groups (all n=12): Control group (exposed to mock anesthesia), isoflurane group (exposed to 2% isoflurane for 90 min), and isoflurane + insulin-like growth factor 1 (IGF-1) group (exposed to 2% isoflurane for 90 min and then treated with IGF-1). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were conducted to determine the levels of expression of IGF-1 and its receptor IGF-R. Liver necrosis was assessed by histological examination. TUNEL assay was performed to determine the apoptosis of hepatic cells. In addition, the levels of the proteins caspase-3 and B-cell lymphoma-extra large (Bcl-xL) were measured. Compared with the control group, levels of IGF-1 and IGF-1R mRNA and protein were significantly decreased following exposure to isoflurane (all P<0.05). The necrosis rate and liver apoptosis were significantly increased in the group treated with isoflurane alone compared with the control group (P<0.05), but were significantly decreased compared with the isoflurane group following application of IGF-1 (P<0.05). Additionally, isoflurane exposure significantly increased levels of caspase-3 compared with the control group (P<0.05), but decreased levels of Bcl-xL (P<0.05). By contrast, application of IGF-1 reversed these changes. The present study therefore suggests that isoflurane induces liver injury in part by regulating the expression of IGF-1 and that application of IGF-1 may protect against liver injury induced by isoflurane exposure.

The present study aimed to investigate bone microarchitecture of the proximal tibia in glucocorticoid-induced osteoporosis (GIOP) mice, and the underlying molecular mechanisms of curcumin in DXM-induced osteoporosis were performed. DXM-treated facilitated to induce hypercalciuria in mice, and curcumin-treated showed a decrease in urine calcium. Curcumin reversed DXM-induced bone resorption, including an increase in serum OCN and a decrease in bone resorption markers CTX and TRAP-5b. H&E staining showed the increased disconnections and separation in trabecular bone network as well as the reduction of trabecular thickness throughout the proximal metaphysis of tibia in GIOP group. Importantly, curcumin reversed DXM-induced trabecular deleterious effects and stimulated bone remodeling. The further evidence showed that curcumin supplement significantly decreased the TRAP-positive stained area and inhibited the activity of OPG/RANKL/RANK signaling in the GIOP mice. Moreover, bioinformatics analysis suggested that miR-365 was a regulator of MMP9. The levels of miR-365 were markedly suppressed; however, curcumin treatment could reverse the downregulation of miR-365 in the tibia of GIOP mice. Simultaneously, the results demonstrated that the mRNA and protein expression of MMP-9 were significantly increased in GIOP mice compared with that of the control group. Curcumin treatment could suppress the expression of MMP-9 in the tibia of GIOP mice. The present study demonstrated the protective effects of curcumin against bone deteriorations in the experimentally DIOP mice, and the underlying mechanism was mediated, at least partially, through the activation of microRNA-365 via suppressing MMP9.