Regression Analysis of Factors Based on Cluster Analysis of Acute Radiation Pneumonia due to Radiation Therapy for Lung Cancer.

We conducted in this paper a regression analysis of factors associated with acute radiation pneumonia due to radiation therapy for lung cancer utilizing cluster analysis to explore the predictive effects of clinical and dosimetry factors on grade ≥2 radiation pneumonia due to radiation therapy for lung cancer and to further refine the effect of the ratio of the volume of the primary foci to the volume of the lung lobes in which they are located on radiation pneumonia, to refine the factors that are clinically effective in predicting the occurrence of grade ≥2 radiation pneumonia. This will provide a basis for better guiding lung cancer radiation therapy, reducing the occurrence of grade ≥2 radiation pneumonia, and improving the safety of radiotherapy. Based on the characteristics of the selected surveillance data, the experimental simulation of the factors of acute radiation pneumonia due to lung cancer radiation therapy was performed based on three signal detection methods using fuzzy mean clustering algorithm with drug names as the target and adverse drug reactions as the characteristics, and the drugs were classified into three categories. The method was then designed and used to determine the classification correctness evaluation function as the best signal detection method. The factor classification and risk feature identification of acute radiation pneumonia due to radiation therapy for lung cancer based on ADR were achieved by using cluster analysis and feature extraction techniques, which provided a referenceable method for establishing the factor classification mechanism of acute radiation pneumonia due to radiation therapy for lung cancer and a new idea for reuse of ADR surveillance report data resources.

Corilagin decreases insulin resistance in polycystic ovary syndrome rat model through regulating AMPK/GSK3ß pathway.

BACKGROUND: This study aims to explore the effects of Corilagin on insulin resistance (IR) of polycystic ovary syndrome (PCOS) and the underlying mechanisms. METHODS: The PCOS rat model was established by subcutaneously injected with dehydroepiandrosterone (DHEA) of 6 mg/kg/day. Body weight and ovary weight were recorded. Serum glucose and insulin concentration were analyzed with commercial kits. The expression of adenosine monophosphate-activated protein kinase (AMPK) and glycogen synthase kinase 3ß (GSK3ß) was detected by Western blot. RESULTS: The results showed that DHEA could induce ovarian dysfunction of rats and Corilagin alleviated DHEA-induced ovarian dysfunction. Corilagin reduced DHEA-induced increase of serum glucose and insulin concentration. Corilagin increased the expression level of p-AMPK/AMPK and p-GSK3ß/GSK3ß of rat ovarian induced by DHEA. CONCLUSIONS: The present research reported the protective effects of Corilagin on PCOS, and demonstrated the protection effect was related to decreasing IR through regulating AMPK/GSK3ß pathway.

Adiponectin Relieves Human Adult Cardiac Myocytes Injury Induced by Intermittent Hypoxia.

BACKGROUND Obstructive sleep apnea (OSA) is associated with many cardiovascular disorders. Intermittent hypoxia (IH) is a key pathological hallmark of OSA. This study was conducted to evaluate the potential therapeutic effects and the associated mechanisms of adiponectin (APN) on IH induced human adult cardiac myocytes (HACMs) injury. MATERIAL AND METHODS HACMs were exposed to normoxia or IH (1% to 21% O2) using a novel cell culture bio-reactor with gas-permeable membranes. Cell viability was detected by Cell Counting Kit-8 assay. Cell membrane integrity was assessed by the detection of lactate dehydrogenase (LDH) release. Cell apoptosis was analyzed by flow cytometry. Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were determined using specific assay kits. P-AMPK (AMP-activated protein kinase), p-LKB1, and p-p65 protein levels were measured by western blotting. Pro-inflammatory factors including interleukin (IL)-1ß, IL-6, IL-8 expressions were detected by enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction. RESULTS The results showed that APN had no cytotoxic to HACMs. Compared with the control group, HACMs cell viability significantly decreased, LDH release increased and cell apoptosis increased in the IH group. The levels of IL-1ß, IL-6, IL-8, MDA, and p-p65 were higher, while the levels of SOD, GSH-Px, p-AMPK, and p-LKB1 were lower in HACMs cells in the IH group than that in the control group. However, APN treatment significantly rescued these effects compared with the IH group in a dose-dependent manner. CONCLUSIONS In conclusion, these results indicated that APN protected against IH induced HACMs injury possibly mediated by AMPK and NF-κB pathway.