Osmanhull1371

41 eV to 3.12 eV). The peak intensity of PL spectra of In2O3 NPs also reduces with the increment of Ag ions suggesting the hindrance of the recombination rate of e-/h+. The photocatalytic activity was measured by the degradation of Rh B dye under UV irradiation. The degradation efficiency of Ag-doped (6%) In2O3 NPs was 92%. Biochemical data indicated that Ag-doping enhances the anticancer performance of In2O3 NPs against human lung cancer cells (A549). Moreover, Ag-doped In2O3 NPs displayed excellent biocompatibility in normal human lung fibroblasts (IMR90). Overall, this study demonstrated that Ag-doping enhances the photocatalytic activity and anticancer efficacy of In2O3 NPs. This study warrants further investigation on the environmental and biomedical applications of Ag-In2O3 NPs.Ambient cold is associated with substantial population attributable fraction of mortality in China, and respiratory health is vulnerable to cold exposure. This study aimed to examine the effect of cold spells on risk of deaths from chronic obstructive pulmonary disease (COPD). We collected daily data on deaths from COPD and climatic factors from 1 January 2016 to 31 December 2019 in 13 cities of Jiangsu Province, China. We used a quasi-Poisson generalized linear model coupled with a distributed lag non-linear model to quantify the association between risk of COPD deaths and exposure to cold spells (defined as 2 or more consecutive days with mean temperature ≤ 5th percentile of daily mean temperature distribution in cold months). Stratification analyses by age, sex, education, and occupation were undertaken to identify vulnerable subgroups. Cell Cycle inhibitor The results suggested that exposure to cold spells was associated with a higher risk of COPD deaths in Lianyungang (relative risk (RR) 1.70; 95% confidence interval (CI) 1.31, 2.21), Nanjing (RR 1.54; 95% CI 1.16, 2.04), Nantong (RR 1.97; 95% CI 1.68, 2.31), Suzhou (RR 1.97; 95% CI 1.55, 2.50), Suqian (RR 1.68; 95% CI 1.23, 2.29), Taizhou (RR 1.70; 95% CI 1.32, 2.19), Wuxi (RR 1.99; 95% CI 1.53, 2.60), Xuzhou (RR 1.71; 95% CI 1.01, 2.90), Yancheng (RR 1.78; 95% CI 1.53, 2.06), Yangzhou (RR 2.78; 95% CI 2.06, 3.76), and Zhenjiang (RR 1.79; 95% CI 1.26, 2.55). All subgroups seemed to be vulnerable to the effect of cold spells. The recommendation of this study is that individuals with pre-existing COPD, regardless of age, sex, education, or occupation, should be made aware of the health risk posed by cold spells and should be encouraged to take cold adaptation actions before cold season arrives. The main limitation of this study is that it is subject to ecological fallacy.Mechanical deformation and chemico-osmotic consolidation of clay liners can change its intrinsic transport properties in all direction and can alter fluid and solute transport processes in the entire model domain. These phenomena are described inadequately by lower-dimensional models. Based on the Biot's consolidation theory, fluid and solute mass conservation equations, a three-dimensional (3D) fully-coupled hydro-mechanical-chemical (HMC) model has been proposed in this study. The impacts of mechanical consolidation and chemico-osmotic consolidation on permeability, hydrodynamic dispersion, solute sorption, membrane efficiency, and chemical osmosis are considered in the model. The model is applied to evaluate performances of a single compacted clay liner (CCL) and a damaged geomembrane-compacted clay composite liner (GMB/CCL) to contain a generic landfill contaminant. Effect of model dimensionality on solute spread for CCL is found to be marginal, but for GMB/CCL the effect is significantly large. After 50-d negative excess pore water pressure at deeper portion of a clay liner.

Hepatoblastoma is a rare but devastating pediatric liver malignancy. Overexpressed methyltransferase-like 1 (METTL1) is a methyltransferase that catalyzes essential N7-methylguanosine (m7G) modification of eukaryotic mRNA. Accumulating evidence has revealed the oncogenic potential of METTL1. However, whether METTL1 gene polymorphisms confer susceptibility to hepatoblastoma has not been reported. This study aimed to identify causal relationships between genetic variants of this gene and susceptibility to hepatoblastoma.

Using the TaqMan assay, we genotyped three METTL1 polymorphisms (rs2291617 G > T, rs10877013 T > C, rs10877012 T > G) in germline DNA samples from 1759 Chinese children of Han ethnicity (313 cases vs. 1446 controls).

None of these polymorphisms were associated with hepatoblastoma risk. However, combination analysis showed that children with 1 to 3 risk genotypes were associated with increased hepatoblastoma risk (adjusted odds ratio = 1.47, 95% confidence interval  1.07-2.02; P = 0.018). Stratified analyses revealed significant effects of combined polymorphisms mainly among young children (< 17 months of age), boys, and those with advanced hepatoblastoma.

We identified some potential functional METTL1 gene polymorphisms that work together to increase the risk of hepatoblastoma among Chinese Han children; single polymorphism showed only weak effects. These METTL1 polymorphisms may be promising biomarkers for screening high-risk individuals for hepatoblastoma. These findings are inspiring and deserve to be validated among individuals of different ethnicities.

We identified some potential functional METTL1 gene polymorphisms that work together to increase the risk of hepatoblastoma among Chinese Han children; single polymorphism showed only weak effects. These METTL1 polymorphisms may be promising biomarkers for screening high-risk individuals for hepatoblastoma. These findings are inspiring and deserve to be validated among individuals of different ethnicities.

The combination of atezolizumab and bevacizumab (Atezo-Bev) has become the standard first-line therapy for patients with advanced hepatocellular carcinoma (HCC), but the prognosis and treatment pattern after its treatment failure are unclear.

We reviewed the medical records of patients who failed first-line Atezo-Bev treatment for advanced HCC from January 2018 to May 2021 in four Taiwan medical centers. Post-first-line survival (PFLS) was defined as the date from the failure of Atezo-Bev treatment to the date of death or last follow-up.

A total of 41 patients were included in the study. All patients had Child-Pugh A liver reserve before the initiation of Atezo-Bev treatment, but the liver reserve of 6 (15%) and 7 (17%) patients deteriorated to Child-Pugh B and C, respectively, after treatment failure. The median PFLS was 5.9months. PFLS significantly differed among patients with various liver reserves after the failure of Atezo-Bev treatment (median 9.6 vs 3.8 vs 1.2months, for Child-Pugh A, B, and C; p < 0.001). In total, 30 (73%) patients received second-line systemic therapy, and they exhibited significantly longer PFLS (median 8.0 vs 1.8months, p = 0.033) than patients who did not. Deteriorated liver function and not receiving second-line therapy remained associated with inferior PFLS in multivariate analysis. The most common second-line therapies were sorafenib (n = 19, 63%) and lenvatinib (n = 9, 30%), with no significant differences in efficacies.

Receiving second-line therapy and good liver reserve were associated with favorable PFLS after the failure of first-line Atezo-Bev treatment.

Receiving second-line therapy and good liver reserve were associated with favorable PFLS after the failure of first-line Atezo-Bev treatment.The aim of the present study was to investigate the browning effects mechanism of Smilax china L. polyphenols (SCLP) and its monomer. In this study, polyphenols (SCLP, engeletin, quercetin and caffeic acid) markedly suppressed lipid accumulation. Polyphenols significantly up-graded the expression of protein kinase A (PKA), adipose triglyceride lipase (ATGL), peroxisome proliferators-activated receptors alpha (PPARα), carnitine palmitoyl transferase (CPT) and acyl-CoA oxidase (ACO) to promote lipolysis and β-oxidation. Moreover, polyphenols greatly enhanced mitochondrial biogenesis in adipocytes, as demonstrated by the expression of Nrf1 and Tfam were up-regulated. Furthermore, polyphenols treatment greatly up-regulated the browning program in adipocytes by increased brown-specific genes and proteins uncoupling protein 1 (UCP-1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) and PR domain containing 16 (PRDM16), as well as beige-specific genes (Tmem26, Tbx1, CD137, Cited1), especially engeletin. Further research found that the brown-specific markers were decreased by antagonist treatment of AMPK or β3-AR, but polyphenols treatment reversed the effect of antagonists and improved the expression of UCP-1, PRDM16 and PGC-1α. In conclusion, these results indicated that polyphenols stimulate browning in adipocytes via activation of the β3-AR/AMPK signaling pathway, and SCLP and its monomer may be worth investigating to prevent obesity.The purpose of this study is to explore the effect and mechanism of neuritin overexpression in the bone marrow on peripheral neuropathy in type 2 diabetic (db/db) mice. We analyzed the impact of bone marrow neuritin overexpression on diabetic peripheral neuropathy and migration of bone marrow mesenchymal stem cells in db/db mice. Antagonists were used to inhibit the stromal cell-derived factor (SDF)-1α/C-X-C chemokine receptor type 4 (CXCR4)-phosphoinositide 3-kinase (PI3K)/Akt signaling pathway in primary cultured bone marrow mesenchymal stem cells. Immunofluorescence, transmission electron microscopy, Oil Red O staining, and transwell migration assays were used. Bone marrow-specific overexpression of neuritin in db/db mice was successfully established. Overexpression of neuritin in the bone marrow ameliorated hyperglycemia, prevented diabetic peripheral neuropathy, protected the ultrastructure of the sciatic nerve and intra-epidermal nerve fiber density, and promoted Schwann cell proliferation and remyelination in the sciatic nerve. Moreover, it ameliorated fat accumulation, adipocyte number, and vascular and nerve densities; decreased glutamate content in serum and bone marrow; restored gradient SDF-1α contents between bone marrow, blood, and sciatic nerve; and promoted impaired diabetic bone marrow mesenchymal stem cell migration. Neuritin improves bone marrow mesenchymal stem cell migration via the SDF-1α/CXCR4-PI3K/Akt signaling pathway in vitro. Overexpression of neuritin in the bone marrow can locally ameliorate neuropathy in the bone marrow. This improves the migration capability of bone marrow mesenchymal stem cells and repairs diabetic peripheral neuropathy, at least partly by activating the PI3K/Akt pathway through the SDF-1α/CXCR4 axis.Trimethylamine lyases are expressed in a wide range of intestinal microbiota which metabolize dietary nutrients like choline, betaine, and L-carnitine to form trimethylamine (TMA). Trimethylamine N-oxide (TMAO) is an oxidative product of trimethylamine (TMA) catalyzed by the action of flavin monooxygenases (FMO) in the liver. Higher levels of TMAO in the plasma and cerebrospinal fluid (CSF) have been shown to contribute to the development of risk factors and actively promote the pathogenesis of metabolic, cardiovascular, and cerebrovascular diseases. The investigations on the harmful effects of TMAO in the development and progression of neurodegenerative and sleep disorders are summarized in this manuscript. Clinical investigations on the role of TMAO in predicting risk factors and prognostic factors in patients with neurological disorders are also summarized. It is observed that the mechanisms underlying TMAO-mediated pathogenesis include activation of inflammatory signaling pathways such as nuclear factor kappa B (NF-κβ), NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome, and MAPK/JNK in the periphery and brain.