Chinese Medicinal Herbs for Childhood Pneumonia: A Systematic Review of Effectiveness and Safety

Objective. To assess the efficacy and safety of Chinese medicinal herbs for Childhood Pneumonia. Methods. We included randomized controlled trials (RCTs). The searched electronic databases included PubMed, the Cochrane Central Register of Controlled Trials, EMBASE, CBM, CNKI, and VIP. All studies included were assessed for quality and risk bias. Review Manager 5.1.6 software was used for data analyses, and the GRADEprofiler software was applied to classify the systematic review results. Results. Fourteen studies were identified (n=1.824). Chinese herbs may increase total effective rate (risk ratio (RR) 1.18; 95% confidence interval (CI), 1.11–1.26) and improve cough (total mean difference (MD), −2.18; 95% CI, (−2.66)–(−1.71)), fever (total MD, −1.85; 95% CI, (−2.29)–(−1.40)), rales (total MD, −1.53; 95% CI, (−1.84)–(−1.23)), and chest films (total MD, −3.10; 95% CI, (−4.11)–(−2.08)) in Childhood Pneumonia. Chinese herbs may shorten the length of hospital stay (total MD, −3.00; 95% CI, (−3.52)–(−2.48)), but no significant difference for adverse effects (RR, 0.39; 95% CI, 0.09–1.72) was identified. Conclusion. Chinese herbs may increase total effective rate and improve symptoms and signs. However, large, properly randomized, placebo-controlled, double-blind studies are required

Chronic Kidney Disease Increases Atrial Fibrillation Inducibility: Involvement of Inflammation, Atrial Fibrosis, and Connexins

Chronic kidney disease (CKD) causes atrial structural remodeling and subsequently increases the incidence of atrial fibrillation (AF). Atrial connexins and inflammatory responses may be involved in this remodeling process. In this study, nephrectomy was used to produce the CKD rat model. Three months post-nephrectomy, cardiac structure, function and AF vulnerability were quantified using echocardiography and electrophysiology methods. The left atrial tissue was tested for quantification of fibrosis and inflammation, and for the distribution and expression of connexin (Cx) 40 and Cx43. An echocardiography showed that CKD resulted in the left atrial enlargement and left ventricular hypertrophy, but had no functional changes. CKD caused a significant increase in the AF inducible rate (91.11% in CKD group vs. 6.67% in sham group, P < 0.001) and the AF duration [107 (0–770) s in CKD vs. 0 (0–70) s in sham, P < 0.001] with prolonged P-wave duration. CKD induced severe interstitial fibrosis, activated the transforming growth factor-β1/Smad2/3 pathway with a massive extracellular matrix deposition of collagen type I and α-smooth muscle actin, and matured the NLR (nucleotide-binding domain leucine-rich repeat-containing receptor) pyrin domain-containing protein 3 (NLRP3) inflammasome with an inflammatory cascade response. CKD resulted in an increase in non-phosphorylated-Cx43, a decrease in Cx40 and phosphorylated-Cx43, and lateralized the distribution of Cx40 and Cx43 proteins with upregulations of Rac-1, connective tissue growth factor and N-cadherin. These findings implicate the transforming growth factor-β1/Smad2/3, the NLRP3 inflammasome and the connexins as potential mediators of increased AF vulnerability in CKD

EMT and Stem Cell-Like Properties Associated with HIF-2α Are Involved in Arsenite-Induced Transformation of Human Bronchial Epithelial Cells

Arsenic is well-established as a human carcinogen, but the molecular mechanisms leading to arsenic-induced carcinogenesis are complex and elusive. It is not been determined if the epithelial-mesenchymal transition (EMT) and stem cell-like properties contribute in causing to carcinogen-induced malignant transformation and subsequent tumor formation.To investigate the molecular mechanisms underlying EMT and the emergence of cancer stem cell-like properties during neoplastic transformation of human bronchial epithelial (HBE) cells induced by chronic exposure to arsenite. HBE cells were continuously exposed to arsenite. Spheroid formation assays and analyses of side populations (SPs) were performed to confirm that arsenite induces the acquired EMT and cancer stem cell-like phenotype. Treated HBE cells were molecularly characterized by RT-PCR, Western blots, immunofluorescence, Southwestern assays, reporter assays, and chromatin immunoprecipitation.With chronic exposure to arsenite, HBE cells undergo an EMT and then acquire a malignant cancer stem cell-like phenotype. Twist1 and Bmi1 are involved in arsenite-induced EMT. The process is directly regulated by HIF-2α. The self-renewal genes, Oct4, Bmi1, and ALDH1, are necessary for arsenite-mediated maintenance of stem cells.EMT, regulated by HIF-2α, and the development of a cancer stem cell-like phenotype are associated with arsenite-induced transformation of HBE cells

Identification of Potential Hub Genes Related to Aflatoxin B1, Liver Fibrosis and Hepatocellular Carcinoma via Integrated Bioinformatics Analysis

The molecular mechanism of the hepatotoxicant aflatoxin B1 to induce liver fibrosis and hepatocellular carcinoma (HCC) remains unclear, to offer fresh perspectives on the molecular mechanisms underlying the onset and progression of AFB1-Fibrosis-HCC, which may offer novel targets for the detection and therapy of HCC caused by AFB1. In this study, expression profiles of AFB1, liver fibrosis and liver cancer-related datasets were downloaded from the Gene Expression Omnibus (GEO), and differentially expressed genes (DEGs) were identified by the GEO2R tool. The STRING database, CytoHubba, and Cytoscape software were used to create the protein-protein interaction and hub genes of the combined genes, and the ssGSEA score for inflammatory cells related gene sets, the signaling pathway, and immunotherapy were identified using R software and the GSEA database. The findings revealed that AFB1-associated liver fibrosis and HCC combined genes were linked to cell process disruptions, the BUB1B and RRM2 genes were identified as hub genes, and the BUB1B gene was significantly increased in JAK-STAT signaling gene sets pathways as well as having an immunotherapy-related impact. In conclusion, BUB1B and RRM2 were identified as potential biomarkers for AFB1-induced fibrosis and HCC progression

Multi-walled carbon nanotubes-induced alterations in microRNA let-7 and its targets activate a protection mechanism by conferring a developmental timing control

Abstract Background Multi-walled carbon nanotubes (MWCNTs) have been produced and applied for diverse purposes. MWCNTs can potentially cause the adverse effects on organisms. MicroRNA let-7 and its targets of HBL-1 and LIN-41 play a central role in regulating developmental timing by acting as a developmental switch. The sequence of let-7 and the underlying mechanisms for let-7 in the control of developmental timing are conserved among different species. In this study, we investigated the potential effect of MWCNTs exposure on the molecular basis for developmental timing mediated by let-7 and its targets of HBL-1 and LIN-41. Results MWCNTs exposure decreased let-7 expression, and increased expressions of hbl-1 and lin-41. let-7 mutant was resistant to MWCNTs toxicity, whereas hbl-1 or lin-41 mutant was susceptible to MWCNTs toxicity. hbl-1 or lin-41 mutant suppressed the resistance of let-7 mutant to MWCNTs toxicity. HBL-1 acted upstream of TIR-1, an adaptor protein, and SYM-1, a protein containing leucine-rich repeats, and ALG-1 and ALG-2, two RDE-1 proteins related to RNA interference (RNAi) pathway, acted upstream of LIN-41 to regulate MWCNTs toxicity. Moreover, we identified a feedback loop between let-7 and its targets of HBL-1 and LIN-41 in the regulation of MWCNTs toxicity. The observed increase in let-7::GFP expression in MWCNTs exposed nematodes with mutation of hbl-1 or lin-41 implied that a feedback mechanism may exist to strengthen the function of let-7 suppression in protecting the animals from MWCNTs toxicity. Conclusions Our results demonstrate the protection function of let-7 suppression for animals from MWCNTs toxicity by conferring a robust developmental timing control. Our results highlight the importance of molecular basis for developmental timing in influencing MWCNTs toxicity

Identification of Potential Hub Genes Related to Aflatoxin B1, Liver Fibrosis and Hepatocellular Carcinoma via Integrated Bioinformatics Analysis

The molecular mechanism of the hepatotoxicant aflatoxin B1 to induce liver fibrosis and hepatocellular carcinoma (HCC) remains unclear, to offer fresh perspectives on the molecular mechanisms underlying the onset and progression of AFB1-Fibrosis-HCC, which may offer novel targets for the detection and therapy of HCC caused by AFB1. In this study, expression profiles of AFB1, liver fibrosis and liver cancer-related datasets were downloaded from the Gene Expression Omnibus (GEO), and differentially expressed genes (DEGs) were identified by the GEO2R tool. The STRING database, CytoHubba, and Cytoscape software were used to create the protein-protein interaction and hub genes of the combined genes, and the ssGSEA score for inflammatory cells related gene sets, the signaling pathway, and immunotherapy were identified using R software and the GSEA database. The findings revealed that AFB1-associated liver fibrosis and HCC combined genes were linked to cell process disruptions, the BUB1B and RRM2 genes were identified as hub genes, and the BUB1B gene was significantly increased in JAK-STAT signaling gene sets pathways as well as having an immunotherapy-related impact. In conclusion, BUB1B and RRM2 were identified as potential biomarkers for AFB1-induced fibrosis and HCC progression

Indoxyl Sulfate Serum Level in Chronic Renal Failure Patients detected using Fluorescence-HPLC

Indoxyl sulfate (IS) is a protein-bound typical uremic toxin that accumulates in patients with impaired kidney function. The laboratory methods used to quantify serum concentrations of IS require improvement. We report an optimal, cost-effective alternative to the methods currently used.The methods is as follows: serum samples were extracted and deproteinized using acetonitrile and then further purified using dichloromethane. The samples were then analyzed using high-performance liquid chromatography (HPLC) with a fluorescence detector at a flow rate of 1.0mL/min. The isocratic mobile phase consisted of acetonitrile−0.2% (V/V) trifluoroacetic acid in phosphate buffered saline, pH 2.5 (8:92, V/V). Detector settings were λex 280nm/λem 390nm. Under the indicated conditions, IS was well separated. The retention time was approximately 6.59±0.11min. The results of the precision and reproducibility tests were <3%, and the recovery rate was greater than 95%,(98.44±3.21%).In conclusion, HPLC with a fluorescence detector is a simple, sensitive, and reliable method for quantifying IS concentration in the serum of patients with chronic renal failure

Identification of interneurons required for the aversive response of Caenorhabditis elegans to graphene oxide

Abstract Background So far, how the animals evade the environmental nanomaterials is still largely unclear. In this study, we employed in vivo assay system of Caenorhabditis elegans to investigate the aversive behavior of nematodes to graphene oxide (GO) and the underlying neuronal basis. Results In this assay model, we detected the significant aversive behavior of nematodes to GO at concentrations more than 50 mg/L. Loss-of-function mutation of nlg-1 encoding a neuroligin with the function in connecting pre- and post-synaptic neurons suppressed the aversive behavior of nematodes to GO. Moreover, based on the neuron-specific activity assay, we found that the NLG-1 activity in AIY or AIB interneurons was required for the regulation of aversive behavior to GO. The neuron-specific activities of NLG-1 in AIY or AIB interneurons were also required for the regulation of GO toxicity. Conclusions Using nlg-1 mutant as a genetic tool, we identified the AIY and AIB interneurons required for the regulation of aversive behavior to GO. Our results provide an important neuronal basis for the aversive response of animals to environmental nanomaterials