General physiology and biophysics最新文献

The low-frequency pulsed electromagnetic field (PEMF) may have possible cytoprotective effects against the destructive effects of oxidative stress. The goal was to investigate if shortterm low-frequency PEMF has cytoprotective effects in glioblastoma cell line following high-dose hydrogen peroxide (H2O2) treatment. U87-MG cells were divided into four groups: Sham-control group; PEMF group (cells exposed to PEMF); H2O2 group (cells treated with H2O2 at time intervals 30 min and 48 h, respectively); H2O2+PEMF group (cells exposed to PEMF after H2O2 treatment at time intervals 30 min and 48 h, respectively). The cell viability, levels of reactive oxygen species, glutathione peroxidase activity, and the amount of glutathione were measured. The cytoprotective effect of PEMF against deleterious effects of oxidative stress triggered by different time interval of H2O2 treatment might be mediated by the increase in the cell viability, the elevation in the antioxidant enzyme activity/amount, and the decrease in the reactive oxygen species level. In addition, the cytoprotective effect of PEMF varies depending on different time intervals of H2O2 treatment. In the light of these findings, further in vivo and/or in vitro studies on neurophysiological effects of PEMFs and their underlying molecular mechanisms are needed to elucidate neurotoxic or neuroprotective role against antioxidant defense mechanisms.

Our study aimed to detect the effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) on exacerbating cardiomyocyte hypoxia/reoxygenation (H/R) injury and the possible mechanism. A cell model of H/R was constructed. PCSK9 mRNA and protein levels were significantly upregulated during AC16 cardiomyocyte H/R. Flowmetry detection of apoptosis, as well as JC-1, confirmed that PCSK9 upregulation of autophagy levels was accompanied by apoptosis. Furthermore, in the H/R+si-PCSK9 group, the expression of autophagy-related protein LC3 decreased and P62 increased. At the same time, the presentation of the autophagic pathway Pink1/Parkin was also downregulated. In conclusion, in AC16 cardiomyocytes treated with H/R, PCSK9 expression and autophagy levels were increased; a possible molecular mechanism was the activation of the Pink1/Parkin pathway.

A high-fructose intake is metabolically analogous to a high-fat diet. The impact of highfructose intake was investigated in spontaneously hypertensive (SHR) and hypertriacylglycerolemic (HTG) rats to find out the impact of which risk factor of metabolic syndrome - hypertension or hypertriacylglycerolemia - will cause more complications. Rats were fed a standard or a fructose diet (F60) with 60% of added fructose for 5 weeks. The F60 diet increased the total serum cholesterol content of both HTG-F60 and SHR-F60 rats. Further, in SHR-F60 it increased serum triacylglycerols, TBARS in the liver, a specific activity of NAGA in the kidney, aggravated glucose tolerance, deteriorated synaptic plasticity, and reduced somatic and dendritic responses in the hippocampus. SHR rats were more sensitive to the F60 diet, suggesting that hypertension along with a high-fructose intake result in a more pronounced disorder compared to hypertriacylglycerolemia. This work wants to draw attention to fructose-induced health risks associated with hypertension.

This study aimed to identify immune-based prognostic biomarkers associated with metastasis of osteosarcoma. Based on the GEO and TCGA databases, 437 differentially expressed genes were screened between primary and metastatic osteosarcoma. Weighted gene co-expression network analysis (WGCNA) revealed 496 genes in turquoise module which had the highest correlation with osteosarcoma metastasis. Within these two group genes, 122 common genes involved in osteosarcoma metastasis were identified. These genes were enriched in chemokine activity, chemokine receptor binding, TNF signaling pathway, etc. Survival analysis revealed 8 prognostic genes (ANK3, EGR1, FBP1, FOS, KIFC3, MAOB, ISLR and MFAP4) from the 122 genes. RT-qPCR showed that all of these eight genes were differentially expressed between 143B and MNNG/HOS Cl cells. Various infiltrating immune cells showed significant differences between primary and metastatic osteosarcoma. Expression of all the 8 prognostic genes was correlated with infiltration abundance of multiple immune cells, such as follicular helper T cells, activated dendritic cells. In addition, 10 microRNAs and 7 transcription factors that targeted these prognostic genes were predicted. In conclusion, 8 immune-based prognostic genes associated with osteosarcoma metastasis were identified.

Parkinson's disease (PD) is an oxidative stress-linked neurodegenerative disorder, with the highest prevalence among seniors. The objective of this study were: (1) to analyse levels of following oxidative stress parameters: total antioxidant capacity (TAC), uric acid (UA), total glutathione (tGSH), bilirubin (Bil) and albumin (Alb), in blood of PD patients and healthy controls; (2) to find possible associations of examined oxidative stress parameters with PD subtypes and levodopa treatment status; and (3) to evaluate power and relevance of the aforementioned oxidative stress parameter for the prediction of onset and progression of PD by utilizing Random Forest machine learning (RFML). Oxidative stress parameters were determined in 125 PD patients and 55 healthy controls. Evaluated with frequentist statistics, our data revealed that UA is the only oxidative stress parameter associated with PD. However, when the PD cohort was divided in gender-dependent manner, tGSH and Bil were also significantly associated with PD in subgroup of female patients. RFML rendered no predictive power of any of the tested oxidative stress parameters in respect to PD, its subtypes, and/or status of levodopa treatment. In conclusion, despite the positive association of UA with PD (in complete cohort of PD patients) and of tGSH and Bil with PD but only in female patients, these oxidative stress parameters are of no use in clinical practice due to the lack of the predictive/diagnostic power.

Amyloid-β peptide interactions with model lipid membranes have been studied by means of small angle neutron scattering and molecular dynamics simulations. These interactions had been indicated recently as an origin of the membrane structure reorganizations between spherical small unilamellar vesicles and planar bicelle-like structures. In present work, we investigate the influence of charge on the peptide-triggered morphological changes by introducing the anionic lipid DMPS to the underlying DMPC membrane. Changes to the membrane thickness and the overall membrane structure with and without Aβ25-35 incorporated have been investigated over a wide range of temperatures. Our results document the previously reported morphological reformations between bicelle-like structures present in gel phase and small unilamellar vesicles present in fluid phase to be independent from the charge existence in the system.