Analysis of the clinical features and risk factors of kidney injury in patients with chronic heart failure-a retrospective cohort study.

Background: Heart failure (HF) often leads to kidney injury and increased morbidity and mortality. Factors contributing to kidney injury in HF patients had not been elucidated completely. This study sought to comprehensively evaluate the risk factors and clinical features of kidney injury in patients with chronic heart failure (CHF) and to provide more evidence for the management of these patients. Methods: Adult patients with CHF admitted to Beijing Anzhen Hospital, Capital Medical University from January 2022 to May 2022 were included in this study. The primary endpoints were the independent risk factors for the development of kidney injury. A multivariate logistic regression model was used for the exploration of the risk factors. Results: A total of 193 patients were included in this study, of whom 86 (44.5%) developed kidney injury. The independent risk factors for kidney injury in patients with CHF included sex (male) [odds ratio (OR): 4.30, 95% confidence interval (CI): 1.72-10.7, P=0.001], hypertension (OR: 3.68, 95% CI: 1.64-8.29, P=0.001), and stroke (OR: 3.82, 95% CI: 1.25-11.6, P=0.01). Kidney injury was significantly positively correlated with age (OR: 1.03, 95% CI: 1.008-1.06, P=0.01) and potassium (OR: 3.70, 95% CI: 1.58-8.67, P=0.002), and significantly negatively correlated with angiotensin receptor blocker (ARB) application (OR: 0.26, 95% CI: 0.11-0.61, P=0.001), serum albumin concentration (OR: 0.88, 95% CI: 0.81-0.96, P=0.005), hemoglobin concentration (OR: 0.97, 95% CI: 0.95-0.99, P=0.006), and left ventricular ejection fraction (LVEF; OR: 0.95, 95% CI: 0.92-0.98, P=0.01). Conclusions: Kidney injury occurred in more than half of the patients with CHF during hospitalization. The independent risk factors for kidney injury in the CHF patients included sex (male), hypertension, and stroke. Kidney injury was positively correlated with age and serum potassium, and negatively correlated with serum albumin, hemoglobin concentration, LVEF, and ARB application.

Responses of Rice and Related Cadmium Transporter Genes to the Passivating Microbial Agent MBLHAP.

Alkali-producing microorganisms and hydroxyapatite (HAP), a chemical passivation agent, have a certain remediation effect on cadmium (Cd) -contaminated soil. They can decrease the available Cd content in the soil to a certain extent and reduce the overall Cd content of rice planted in the soil. The Cd-contaminated soil was treated with the passivating bacterial agent that had been developed. Changes in the Cd concentration of rice leaves and soil were observed. Real-time PCR was used to analyse the expression levels of Cd transport protein genes in rice. Then, we determined the activities of super-oxide dismutase (SOD), catalase (CAT) and peroxidase (POD) at different stages of rice growth. The results showed that after HAP, alkali-producing microorganisms and passivating microbial agents were applied to the Cd treated soil. The total Cd content in rice leaves was reduced by 66.80%, 80.32% and 81.35%. The expression differences of genes related to Cd transporter proteins were measured, and the results showed that the changes in gene regulation were consistent with the changes in Cd content of rice leaves. The changes in SOD activity, CAT activity and POD activity further indicated that the three enzymes could alleviate the adverse effects of Cd stress by regulating the related enzyme activities in rice. In conclusion, alkali-producing microorganisms, HAP and passivating bacterial agents can effectively reduce the toxicity of Cd to rice, and reduce the absorption and accumulation of Cd in rice leaves.

Engineering of Defect-Rich Cu2WS4 Nano-homojunctions Anchored on Covalent Organic Frameworks for Enhanced Gaseous Elemental Mercury Removal.

Fabricating two-dimensional transition-metal dichalcogenide (TMD)-based unique composites is an effective way to boost the overall physical and chemical properties, which will be helpful for the efficient and fast capture of elemental mercury (Hg0) over a wide temperature range. Herein, we constructed a defect-rich Cu2WS4 nano-homojunction decorated on covalent organic frameworks (COFs) with abundant S vacancies. Highly well-dispersed and uniform Cu2WS4 nanoparticles were immobilized on COFs strongly via an ion pre-anchored strategy, consequently exhibiting enhanced Hg0 removal performance. The saturation adsorption capacity of Cu2WS4@COF composites (21.60 mg·g-1) was 9 times larger than that of Cu2WS4 crystals, which may be ascribed to more active S sites exposed in hybrid interfaces formed in the Cu2WS4 nano-homojunction and between Cu2WS4 nanoparticles and COFs. More importantly, such hybrid materials reduced adsorption deactivation at high temperatures, having a wide operating temperature range (from 40 to 200 °C) owing to the thermostability of active S species immobilized by both physical confined and chemical interactions in COFs. Accordingly, this work not only provides an effective method to construct uniform TMD-based sorbents for mercury capture but also opens a new realm of advanced COF hybrid materials with designed functionalities.

A Retrospective Study of the Clinical Characteristics of Japanese Encephalitis in Adults.

OBJECTIVE: This study aimed to explore the diagnostic points and treatment modes of the clinical characteristics of Japanese encephalitis (JE) in the middle-aged and elderly population. METHODS: Six patients aged 47-72 who were diagnosed with JE at the Beijing Chaoyang Hospital Affiliated with the Capital Medical University between August 2018 and September 2019 were enrolled in the study. Their clinical manifestations, biochemical indicators, imaging data, diagnostic methods, and the evolution and outcomes of the treatments they underwent were retrospectively analyzed. RESULTS: (1) All six patients had severe clinical symptoms and poor prognoses that were more likely to be associated with other systemic diseases. (2) Lesions were most commonly distributed in the thalamus, basal ganglia, and midbrain. The appearance of hyperintensity in the corpus callosum, hippocampus, and subcortical white matter was more specific. The hyperperfusion metabolism in the lesion area in head computed tomography perfusion imaging indicated the state of inflammatory activity in the lesion. In cranial magnetic resonance imaging (MRI), T2 and fluid-attenuated inversion recovery (FLAIR) were more sensitive. (3) After a patient has been systematically treated in the intensive care unit (ICU), the patient gradually recovered and the level of consciousness improved (p < 0.05). CONCLUSIONS: In brain MRI-especially T2 and FLAIR-intracranial infection is often accompanied by abnormal signals in the thalamus, midbrain, hippocampus, and white matter hyperintensity (WMH), which is highly suggestive of JE. The positive detection of anti-JE virus immunoglobulin M antibodies in a patient's serum and/or cerebrospinal fluid can confirm the diagnosis of JE, and comprehensive ICU treatment (hormones combined with anti-inflammatory, antiviral, and mild hypothermic cerebral protection therapies) can improve the survival rate.

HDAC3 of dorsal hippocampus induces postoperative cognitive dysfunction in aged mice.

Postoperative cognitive dysfunction (POCD) affects a substantial number of aged individuals. Although advanced age has been regarded as the only independent risk factor for cognitive decline following anesthesia and surgery, the exact cellular and molecular mechanisms remain poorly understood. Histone deacetylase 3 (HDAC3), an epigenetic regulator of memory plays an important role in age-dependent disease. In this study, we investigated the role of HDAC3 in POCD using a laparotomy mouse model. The results showed that the level of HDAC3 in the dorsal hippocampus (DH) was elevated in aged mice compared with young mice. The surgery impaired the spatial-temporal memory in aged mice, as indicated in the object location memory (OLM) and temporal order memory (TOM) tests. Model mice also exhibited increased expression of HDAC3 protein and decreased levels of dendritic spine density and synaptic plasticity-related proteins in the DH. Selectively blocking HDAC3 in the DH of aged mice reversed spatial-temporal memory impairment induced by surgery and restored dendritic spine density and synaptic plasticity-related proteins in the DH. Overexpression of HDAC3 by adeno-associated virus in the DH of young mice mimicked the behavioral deficits induced by anesthesia and surgery. Our results indicated that HDAC3 negatively regulates spatial-temporal memory in aged mice after anesthesia and surgery. Targeting HDAC3 might represent a potential therapy to avoid POCD.

The role of autophagy-related proteins in the pathogenesis of neuromyelitis optica spectrum disorders.

This study aimed to investigate the expression of autophagy-related proteins in a mouse model of neuromyelitis optica (NMO). Mice were assigned to one of four groups: an animal experimental model group (NMO-EAE group, given with exogenous IL-17A), Interleukin-17 monoclonal antibody intervention group (NMO-EAE_0IL17inb), No exogenous interleukin-17 enhanced immune intervention group (NMO-EAE_0IL17), and a control group. Behavioral scores were assessed in each group, and the protein expressions of sequestosome 1 (P62), Beclin-1, the mammalian target of rapamycin (mTOR), phosphoinositide 3-kinase (PI3K-I), and LC3II/LC3I were detected using Western blotting. In the NMO-EAE_0IL17 group, the expression of Beclin-1 decreased, the LC3II/LC3I ratio was lower, and the expressions of P62, mTOR, and PI3K-I increased; after administration of IL-17A inhibitor into the brain tissue, however, the expression of Beclin-1 increased significantly, along with the LC3II/LC3I ratio, while the expressions of P62, mTOR and PI3K-I protein decreased significantly. In terms of behavioral scores, the scores of optic neuritis and myelitis were more serious, onset occurred earlier and the progress was faster, after the administration of IL-17A. In the mechanism of NMO animal model, IL-17A may regulate autophagy and affect the disease process through the activation of the PI3K-mTOR signaling pathway.

Tire pyrolysis wastewater treatment by a combined process of coagulation detoxification and biodegradation.

Recycling waste tires through pyrolysis technology generates refractory wastewater, which is harmful to the environment if not disposed properly. In this study, a combined process of coagulation detoxification and biodegradation was used to treat tire pyrolysis wastewater. Organics removal characteristics at the molecular level were investigated using electrospray ionization (ESI) coupled with Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR MS). The results showed that nearly 90% of the organic matter from the wastewater was removed through the process. Preference of the two coagulants for different classes of organics in tire pyrolysis wastewater was observed. The covalently bound inorganic-organic hybrid coagulant (CBHyC) used in this work had a complementary relationship with biodegradation for the organics removal: this coagulant reduced toxicity and enhanced the biodegradation by preferentially removing refractory substances such as lignin with a high degree of oxidation (O/C > 0.3). This study provides molecular insight into the organics of tire pyrolysis wastewater removed by a combined treatment process, supporting the advancement and application of waste rubber recycling technology. It also contributes to the possible development of an effective treatment process for refractory wastewater.

Vicenin-2 inhibits the Helicobacterium pylori infection associated gastric carcinogenic events through modulation of PI3K/AKT and Nrf2 signaling in GES-1 cells.

Helicobacter pylori (H. pylori), a microbial carcinogen of Gram-negative bacteria, has been recognized to be the highest risk factor for the growth of human gastric cancer (GC). Therefore, the inhibition of the growth rate of H. pylori has been considered an effective vital strategy to prevent GC development. This study highlights the inhibitory effect of vicenin-2 against H. pylori-induced gastric carcinogen signaling in human gastric epithelial cells (GES-1). In vitro cytotoxicity studies reported that 40 µM of vicenin-2  remarkably protects the gastric cells and this concentration shows 85% cell viability also does not produce toxicity. In addition, vicenin-2 prevents H. pylori-infected increased depletion of antioxidants mediated by reactive oxygen species generation, DNA damage, malondialdehyde, and nuclear fragmentation. Here, we noticed that vicenin-2 remarkably suppressed the expression range of the phosphorylated form of phosphatidylinositol 3-kinase/protein kinase B, phosphorylated p38 kinases, phosphorylated extracellular signal-regulated kinase-1, phosphorylated c-Jun N-terminal kinase, tumor necrosis factor-α, interleukin-6, cyclooxygenase-2 in GES-1 infected with H. pylori. Moreover, we observed that vicenin-2 enhanced the antioxidants protein nuclear factor erythroid factor-2 and phosphatase and tensin homolog expression in H. pylori-infected cells. Thus, vicenin-2 prevents the H. pylori-associated infection, and its resistance might be a potential strategy in preventing GC induced by H. pylori.

LncRNA H19 induced by helicobacter pylori infection promotes gastric cancer cell growth via enhancing NF-κB-induced inflammation.

BACKGROUND: The aim of this study was to investigate the role of long non-coding RNA (lncRNA) H19 in gastric cancer (GC) with Helicobacter pylori (H. pylori). METHODS: H19 expression in peripheral blood from H. pylori+/- GC patients and healthy donors (control) as well as in GC tissues and cells were detected by qRT-PCR. Cell proliferation was evaluated by CCK-8 assay. Cell migration and invasion were evaluated by Transwell assay. The levels of pro-inflammatory cytokines were determined by ELISA. The protein levels of IκBα, p-IκBα and p65 were determined by western blotting. RESULTS: H19 expression was upregulated in H. pylori-infected GC tissues and cells. Furthermore, H. pylori promoted GC cell viability, migration, invasion and inflammatory response. Moreover, H19 overexpression promoted the proliferation, migration and invasion of H. pylori-infected GC cells via enhancing NF-κB-induced inflammation. CONCLUSIONS: LncRNA H19 promotes H. pylori-induced GC cell growth via enhancing NF-κB-induced inflammation.

The Association between Infertility and Helicobacter pylori Infection: a Meta-Analysis of Case-control Studies.

BACKGROUND: Helicobacter pylori (H. pylori) is increasingly associated with extra-digestive diseases. Infertility is a common condition, with an incidence of 10 to 15% of couples. Studies examining the association of H. pylori infection and infertility have reported conflicting results. This meta-analysis aimed to investigate the association between H. pylori infection and infertility. METHODS: Studies of H. pylori infection and infertility were identified in PubMed, EMBASE, the Cochrane Library, and China National Knowledge Infrastructure. We performed a meta-analysis of all case-control studies. RESULTS: Seven studies that analyzed the relationship between H. pylori infection and infertility, with a combined study population of 1,902 patients, were included in the meta-analysis (n = 626 for patients; n = 1,276 for controls). In the infertility group, 344 (54.9%) patients were H. pylori-positive, and 495 (38.8%) were H. pylori-positive in the control group. Our result suggested that H. pylori infection was associated significantly with infertility (OR = 1.45, 95% CI: 1.197 - 2.160; I2 = 36.5%, Z = 3.15, p = 0.002). Begg's and Egger's funnel plot showed no publication bias (p = 0.807). CONCLUSIONS: Our meta-analysis identified a possible association between H. pylori infection and infertility.

Potential Role of MicroRNA-375 as Biomarker in Human Cancers Detection: A Meta-Analysis.

The association between circulating microRNA-375 (miR-375) expression and cancers has been studied; however, the results are inconsistent. We searched PubMed, Embase, and Web of Science for studies concerning the diagnostic value of miR-375 for cancer. The bivariate meta-analysis model was employed to summarize sensitivity, specificity, and diagnostic odds ratio (DOR) for miR-375 in the diagnosis of cancer. Summary receiver operating characteristic (SROC) curve analysis and the area under the curve (AUC) were also used to check the overall test performance. A total of 645 cancer patients and 421 cancer-free individuals from 12 studies were contained in this meta-analysis. The summary estimates revealed that the pooled sensitivity was 78% (95% confidence interval (CI): 64%-87%), the specificity was 74% (95% CI: 62%-84%), the DOR was 10.04 (95% CI: 6.01-16.77), and the AUC was 0.82 (95% CI: 0.79-0.85). In addition, we found that the diagnostic effect of miR-375 varies according to the race and cancer type. Our data suggest that miR-375 profiling has a potential to be used as a screening test for cancers but the specific race and cancer should be considered. More studies on the diagnostic value of miR-375 for cancer are needed in the future.

Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway.

BACKGROUND: Long noncoding RNA (lncRNA) H19 is emerging as a vital regulatory molecule in the progression of different types of cancer and miR-675 is reported to be embedded in H19's first exon. However, their function and specific mechanisms of action have not been fully elucidated. The aim of this study was to identify a novel lncRNA-microRNA-mRNA functional network in gastric cancer. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the relative expression of H19 and miR-675 in normal (GES-1) and gastric cancer cell lines (SGC-7901, SGC-7901/DDP) as well as in tumor tissues. Gain and loss of function approaches were carried out to investigate the potential roles of H19/miR-675 in cell proliferation and apoptosis. Moreover, Fas associated via death domain (FADD) was validated to be the target of miR-675 via luciferase reporter assay. Western blotting was used to evaluate the protein expression of related signaling pathway. RESULTS: In our study H19 and miR-675 were increased in gastric cancer cell lines and tissues. Overexpression of H19 and miR-675 promoted cell proliferation and inhibited cell apoptosis, whereas knockdown of H19 and miR-675 inhibited these effects. By further examining the underlying mechanism, we showed that H19/miR-675 axis inhibited expression of FADD. FADD downregulation subsequently inhibited the caspase cleavage cascades including caspase 8 and caspase 3. CONCLUSION: Taken together, our results point to a novel regulatory pathway H19/miR-675/ FADD/caspase 8/caspase 3 in gastric cancer which may be potential target for cancer therapy.

MicroRNA-150 as a Potential Biomarker in Diagnosis of Cancer: a Meta-Analysis.

BACKGROUND: Altered expression of microRNAs contributes to human carcinogenesis. Previous studies assessed the association of aberrant circulating microRNA (miR)-150 level with the risk in developing various human cancers, but the data were inconsistent. METHODS: This meta-analysis further assessed the potential diagnostic value of miR-150 in cancer. PubMed, Embase, and Web of Science for publications were searched using the keywords of miR-150 and human cancer. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were obtained to assess the diagnostic value. RESULTS: The summary estimates revealed that the pooled sensitivity was 80% (95% CI: 74% - 85%), the specificity was 81% (95% CI: 71% - 87%), the DOR was 16.47 (95% CI: 10.41 - 26.06), and the AUC was 0.86 (95% CI: 0.82 - 0.89) for miR-150 as a tumor marker. CONCLUSIONS: miR-150 may be a potential noninvasive tumor marker for various human cancers and further studies with a large sample size are needed to confirm.

The effect of activin A on signal transduction pathways in PC12 cells subjected to oxygen and glucose deprivation.

The processes and mechanisms underlying brain injuries due to ischemia and anoxia have yet to be determined. Additionally, few clinical treatements are currently available. Activins have a protective role in the restoration, differentiation, and survival of injured cells, including Activin A (ActA), which acts as a neuroprotectant. However, its exact mechanism of action remains to be determined. ActA has been shown to protect neurons following ischemic brain injury. In this study, PC12 cells were differentiated into neuron-like cells after stimulation with nerve growth factor to prepare an oxygen/glucose deprivation (OGD) model in neurons. The differentiated PC12 cells, subjected to the OGD model, were exposed to ActA. Results showed that the PC12 survival rate decreased after OGD, leading to an increase in caspase-3 expression in these cells. Pretreatment with ActA was able to partially prevent OGD-induced apoptosis, likely through the downregulation of caspase-3. Futhermore, ActA pretreatment increased the expression of key proteins in the ActA/Smads signal transduction pathway, which may promote neuroprotection after OGD. Therefore, exogenous ActA may function as a neuroprotectant and provide a novel therapeutic treatment for ischemic brain injury.

Emodin prevents hypoxic-ischemic neuronal injury: Involvement of the activin A pathway.

Emodin, an extract of dried rhizomes and the root of the Rhizoma Polygoni Cuspidati, can protect neurons from hypoxic-ischemic brain damage. This study aimed to verify the underlying mechanism. After PC12 cells had differentiated into neuron-like cells under the induction of mouse nerve growth factor, cells were subjected to oxygen-glucose deprivation and treated with emodin. Results showed that the viability of neuron-like cells cultured under an ischemia-hypoxia environment decreased, while the expression of activin A and caspase-3 in cells increased. Emodin raised the survival rate of oxygen-glucose deprived neuron-like cells, increased activin A expression, and decreased caspase-3 expression. Experimental findings indicate that emodin can inhibit neuronal apoptosis and alleviate the injury of nerve cells after oxygen-glucose deprivation through the activin A pathway.