The Relationship Between the Neutrophil to Lymphocyte Ratio, The Platelet to Lymphocyte Ratio, and Cardiac Syndrome X.

Objective: This study aims to investigate the relationship between the neutrophil to lymphocyte ratio (NLR), the platelet to lymphocyte ratio (PLR), and cardiac syndrome X (CSX). Methods: A total of 102 patients with CSX who were hospitalized in the Cardiology Department of our hospital from December 2018 to December 2020 were enrolled in the CSX group, and 102 subjects who underwent physical examinations during the same period were included in the control group. An automatic blood cell analyzer was adopted to detect the neutrophil count (NC), lymphocyte count (LC), and number of platelets (PLT) in the whole blood of the subjects in both groups, and the NLR and PLR were calculated. Electrocardiography was conducted on the subjects in both groups to detect whether any abnormality existed in the ST segment. The receiver operating curve (ROC) was used to evaluate the diagnostic value of each indicator of CSX, and multivariate logistic regression analysis was adopted for the analysis of the influencing factors. Results: No significant differences existed in age, gender, smoking history, or family history of diabetes mellitus, hypertension, and tumors between the two groups (p > 0.05). When compared with the control group, the NC, PLT, NLR, PLR, and rate of abnormality of the ST segment on the electrocardiogram were significantly higher, and the LC was significantly lower in the CSX group (p < 0.05). Multivariate logistic regression analysis showed that the ST-segment abnormality (3.95 [2.10~7.41]; NLR > 2.21, 3.46 [1.87~6.39]; and PLR > 119.77, 3.66 [1.99~6.73]) was a correlated risk factor for the occurrence of CSX (p < 0.05). Conclusion: Both the NLR and PLR in patients with CSX were significantly elevated, and both have a certain predictive value for the occurrence of CSX and are expected to be effective biomarkers for CSX.

Focal adhesion kinase-related non-kinase ameliorates liver fibrosis by inhibiting aerobic glycolysis via the FAK/Ras/c-myc/ENO1 pathway.

BACKGROUND: Hepatic stellate cell (HSC) hyperactivation is a central link in liver fibrosis development. HSCs perform aerobic glycolysis to provide energy for their activation. Focal adhesion kinase (FAK) promotes aerobic glycolysis in cancer cells or fibroblasts, while FAK-related non-kinase (FRNK) inhibits FAK phosphorylation and biological functions. AIM: To elucidate the effect of FRNK on liver fibrosis at the level of aerobic glycolytic metabolism in HSCs. METHODS: Mouse liver fibrosis models were established by administering CCl4, and the effect of FRNK on the degree of liver fibrosis in the model was evaluated. Transforming growth factor-ß1 was used to activate LX-2 cells. Tyrosine phosphorylation at position 397 (pY397-FAK) was detected to identify activated FAK, and the expression of the glycolysis-related proteins monocarboxylate transporter 1 (MCT-1) and enolase1 (ENO1) was assessed. Bioinformatics analysis was performed to predict putative binding sites for c-myc in the ENO1 promoter region, which were validated with chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. RESULTS: The pY397-FAK level was increased in human fibrotic liver tissue. FRNK knockout promoted liver fibrosis in mouse models. It also increased the activation, migration, proliferation and aerobic glycolysis of primary hepatic stellate cells (pHSCs) but inhibited pHSC apoptosis. Nevertheless, opposite trends for these phenomena were observed after exogenous FRNK treatment in LX-2 cells. Mechanistically, the FAK/Ras/c-myc/ENO1 pathway promoted aerobic glycolysis, which was inhibited by exogenous FRNK. CONCLUSION: FRNK inhibits aerobic glycolysis in HSCs by inhibiting the FAK/Ras/c-myc/ENO1 pathway, thereby improving liver fibrosis. FRNK might be a potential target for liver fibrosis treatment.

Effect of Long-Term Systolic Blood Pressure Trajectory on Kidney Damage in the Diabetic Population: A Prospective Study in a Community-Based Chinese Cohort.

BACKGROUND: Previous studies have shown that hypertension is an important factor contributing to the occurrence and progression of diabetic kidney damage. However, the relationship between the patterns of blood pressure (BP) trajectory and kidney damage in the diabetic population remains unclear. This prospective study investigated the effect of long-term systolic BP (SBP) trajectory on kidney damage in the diabetic population based on an 8-year follow-up community-based cohort. METHODS: This study included 4556 diabetic participants among 101,510 participants. BP, estimated glomerular filtration rate (eGFR), and urinary protein were measured every 2 years from 2006 to 2014. SBP trajectory was identified by the censored normal modeling. Five discrete SBP trajectories were identified according to SBP range and the changing pattern over time. Kidney damage was evaluated through eGFR and urinary protein value. A multivariate logistic regression model was used to analyze the influence of different SBP trajectory groups on kidney damage. RESULTS: We identified five discrete SBP trajectories: low-stable group (n = 864), moderate-stable group (n = 1980), moderate increasing group (n = 609), elevated decreasing group, (n = 679), and elevated stable group (n = 424). The detection rate of kidney damage in the low-stable group (SBP: 118-124 mmHg) was the lowest among the five groups. The detection rate of each kidney damage index was higher in the elevated stable group (SBP: 159-172 mmHg) compared with the low-stable group. For details, the gap was 4.14 (11.6% vs. 2.8%) in eGFR <60 ml·min-1·1.73 m-2 and 3.66 (17.2% vs. 4.7%), 3.38 (25.0% vs. 7.4%), and 1.8 (10.6% vs. 5.9%) times in positive urinary protein, eGFR <60 ml·min-1·1.73 m-2 and/or positive urinary protein, and eGFR decline ≥30%, respectively (P < 0.01). CONCLUSION: An elevated stable SBP trajectory is an independent risk factor for kidney damage in the diabetic population.

Low expression of the FoxO4 gene may contribute to the phenomenon of EMT in non-small cell lung cancer.

Because of its importance in tumor invasion and metastasis, the epithelial-mesenchymal transition (EMT) has become a research focus in the field of cancer. Recently, evidence has been presented that FoxO4 might be involved in EMT. Our study aimed to detect the expression of FoxO4, E-cadherin and vimentin in non-small cell lung cancers (NSCLCs). We also investigated clinical features and their correlations with the markers. In our study, FoxO4, E-cadherin and vimentin were assessed by immunohistochemistry in a tissue microarray (TMA) containing 150 cases of NSCLC. In addition, the expression level of FoxO4 protein was determined by Western blotting. The percentages of FoxO4, E-cadherin and vimentin positive expression in NSCLCs were 42.7%, 38.7% and 55.3%, respectively. Immunoreactivity of FoxO4 was low in NSCLC when compared with paired normal lung tissues. There were significant correlations between FoxO4 and TNM stage (P<0.001), histological differentiation (P=0.004) and lymph node metastasis (P<0.001), but no significant links with age (P=0.323), gender (P=0.410), tumor size (P=0.084), smoking status (P=0.721) and histological type (P=0.281). Our study showed that low expression of FoxO4 correlated with decreased expression of E-cadherin and elevated expression of vimentin. Cox regression analysis indicated FoxO4 to be an independent prognostic factor in NSCLC (P=0.046). These data suggested that FoxO4 might inhibit the process of EMT in NSCLC, and might therefore be a target for therapy.

The monitoring results of electromagnetic radiation of 110-kV high-voltage lines in one urban location in Chongqing P.R. China.

To understand electromagnetic radiation field strength and its influencing factors of certain 110-kV high-voltage lines in one urban area of Chongqing by measuring 110-kV high-voltage line's electromagnetic radiation level. According to the methodology as determined by the National Hygienic Standards, we selected certain adjacent residential buildings, high-voltage lines along a specific street and selected different distances around its vertical projection point as monitoring points. The levels of electromagnetic radiations were measured respectively. In this investigation within the frequency of 5-1,000 Hz both the electric field strength and magnetic field strength of each monitoring sites were lower than the public exposure standards as determined by the International Commission on Non-Ionizing Radiation Protection. However, the electrical field strength on the roof adjacent to the high-voltage lines was significantly higher than that as measured on the other floors in the same buildings (p < 0.05). The electromagnetic radiation measurements of different monitoring points, under the same high-voltage lines, showed the location which is nearer the high-voltage line maintain a consistently higher level of radiation than the more distant locations (p < 0.05). Electromagnetic radiation generated by high-voltage lines decreases proportionally to the distance from the lines. The buildings can to some extent shield (or absorb) the electric fields generated by high-voltage lines nearby. The electromagnetic radiation intensity near high-voltage lines may be mitigated or intensified by the manner in which the high-voltage lines are set up, and it merits attention for the potential impact on human health.