01). Compared with blank control group, the model group had obviously increased content of TNF-α and IL-6 (P less then 0.01), decreased content of IL-10 (P less then 0.01), more apoptotic neurons (P less then 0.01), higher expression of caspase-3 (P less then 0.01), and obviously lower Bcl-2/Bax (P less then 0.01). Moreover, expression of phosphorylated (p)-PTEN, PI3K and p-Akt in brain tissues was remarkably lower in the model group than those in the blank control group (P less then 0.01). selleck chemicals llc The expression level of miR-130a in brain tissues of CI rats is significantly increased. miR-130a promotes the release of inflammatory factors and facilitates neuronal apoptosis through suppressing the PTEN/PI3K/Akt signaling pathway. Copyright © Wang et al.Changes in the expression of serum chemokine CXC ligand 13 (CXCL13) and interleukin-6 (IL-6), and the relationship with lower limb vein thrombus were explored. A total of 128 patients undergoing hip replacement in The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine from May 2017 to June 2019 were selected, and the patients suffering from lower limb vein thrombus were enrolled as group A and other patients not suffering from it were enrolled as group B. Enzyme-linked immuno-sorbent assay was employed to determine the levels of serum chemokine CXCL13 and IL-6, and receiver operating characteristic curves of serum chemokine CXCL13 and IL-6 levels in diagnosing restenosis after surgery were drawn. Pearson’s correlation coefficient was adopted to analyze the correlation between serum chemokine CXCL13 and IL-6, and the logistic regression analysis to analyze the risk factors affecting hip replacement in patients. The levels of serum CXCL13 and IL-6 in group A were significantly higher than those in group B (both P less then 0.001). The specificity and sensitivity of serum CXCL13 level in diagnosis of lower limb vein thrombus after hip replacement were 61.76 and 80.00%, respectively, and those of serum IL-6 level in diagnosis were 70.59 and 66.67%, respectively. Serum CXCL13 level was positively correlated with serum IL-6 level (P less then 0.001), and age, body mass index (BMI), CXCL13 level and IL-6 level of the patients were independent risk factors affecting the efficacy of hip replacement. Serum CXCL13 level and serum IL-6 level can be used as biological indexes for prediction of early lower limb vein thrombus after hip replacement, and logistic regression analysis revealed that the age of the patients, BMI, diabetes history, hyperlipidemia history, hypertension history, CXCL13 level and IL-6 level are independent risk factors affecting the efficacy of hip replacement. Copyright © 2020, Spandidos Publications.Numerous cases of spinal cord injury following seizure have been previously reported. However, whether spinal cord injury is a common occurrence after seizures and its underlying mechanisms remain unclear. The present study generated a Sprague-Dawley rat model of temporal lobe epilepsy (TLE), and Nissl staining and transmission electron microscopy were used to detect tissue damage. In addition, Evans blue staining was used to detect damage to the blood-brain barrier (BBB) and albumin extravasation. In addition, double-staining was used to detect the association between neurons and extravasated albumin. Furthermore, neuronal degeneration was assessed using Fluoro-Jade C staining, while fluorescence staining and western blotting were used to detect apoptosis and inflammation. In the present study, spinal cord injury was only observed in rats with grade IV-V seizures, whereas Nissl staining showed structural damage and decreased neuronal cell numbers in the brain and the spinal cord. The present study identified BBB damage and albumin extravasation in rats of the TLE groups. Double-staining for albumin and neurons showed a significant match of neurons positive for albumin. Fluoro-Jade C staining indicated neuronal degeneration in the brain, but not the spinal cord in the TLE rats. High levels of caspase-3 were also detected in the injured spinal cord. A small number of albumin+ neurons in the spinal cord presented caspase-3+ signals in rats of the TLE groups. The expression levels of intercellular adhesion molecule 1, CD11b and inflammatory factors such as tumor necrosis factor-α and interleukin-6 were significantly elevated in the injured spinal cord. The present results suggested that spinal cord injury occurred in rats as a result of severe seizure attacks, and that BBB damage, albumin extravasation, inflammation and apoptosis contributed to the pathological changes observed during spinal cord injury. Copyright © Liu et al.Protective effect of fluvastatin (Flu) on myocardial cells in mice with acute myocardial infarction (AMI) and the mechanism were explored. Forty C57B/L6 mice in similar physiological status were selected and randomly divided into sham operation (Sham) group (n=10), AMI group (n=10), Flu group (n=10) and Flu + Angiotensin II (Ang II) (Ang II) group (n=10). The pathological changes in heart tissues were detected via hematoxylin and eosin (H&E) staining, and apoptosis of myocardial cells was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the expression levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined using relevant kits, and the expression levels of Ras homolog gene family (Rho)-associated coiled-coil protein kinase 1 (ROCK1), ROCK2, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax) and nuclear factor-κB (NF-κB) in the infarction region were determined using Western blotting. The infarction area in mice in Flu group was significantly smaller than that in AMI group. In AMI group, the level of MDA in the serum and infarction tissues was remarkably higher than that in Sham group (P less then 0.05), while that of SOD significantly declined (P less then 0.05). The level of MDA in Flu group was obviously lower than that in AMI group (P less then 0.05). The expression levels of Bax, NF-κB, ROCK1 and ROCK2 were obviously higher in AMI group than those in Sham group, while they were obviously lower in Flu group than those in AMI group (P less then 0.05). After the Rho member A (RhoA)/ROCK pathway agonist Ang II was added, the mitigation effect of Flu on myocardial apoptosis in the infarction region in AMI mice was evidently weakened. Flu mitigates AMI-induced myocardial apoptosis in mice, and the possible mechanism is that the inflammatory and oxidative stress responses activated and mediated by RhoA/ROCK are effectively inhibited. Copyright © Yi et al.