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Stryhn Upton posted an update 6 months, 4 weeks ago
X-ray and MRI differences of calcaneal epiphysis between Sever’s disease patients and normal children were compared and analyzed to raise awareness of Sever’s disease. A total of 98 children with Sever’s disease were enrolled in the study, including 72 males and 26 females. Among them, 6 patients underwent MRI. There were 120 patients in the control group, including 73 males and 47 females, aged 8 to 15 years. The calcaneus epiphysis density (compact and cancellous bone type), the difference of the radiolucent line and the signal changes of Sever’s disease on MRI of the two groups were observed and analyzed. Among the patients with Sever’s disease, the male incidence rate was 79.59%, the female incidence rate was 20.41%, the average age of onset was 11.35, the average age of onset for male was 11.49, and the average age of onset for female was 10.80. There were significant statistical differences between the two groups in terms of epiphysis density (compact and cancellous type) and translucent line (χ2=38.85, 137.51, P less then 0.05). Six cases of MRI showed partial or complete different degrees of bone marrow, ligament, soft tissue edema, and joint effusion. Sever’s disease is mainly characterized by increased density of the calcaneus epiphysis and a radiolucent line of the epiphysis. It manifests as heel edema on MRI image.The ability to inhibit host macrophage apoptosis is one of the survival strategies of intracellular bacteria, including Brucella. In the present study the role of Mg2+/Mn2+ dependent protein phosphatase 1A (PPM1A) in the apoptosis of Brucella suis (B. click here suis) strain 2 vaccine-infected BV2 cells was investigated. Compared with control cells, the protein expression levels of cleaved caspase-3 were markedly increased in PPM1A short hairpin (sh)RNA-transfected BV2 cells. Flow cytometry analysis showed that treatment with JNK activator anisomycin significantly increased the rate of apoptosis in BV2 cells in comparison with the control cells. Furthermore, PPM1A shRNA significantly increased the levels of JNK phosphorylation and the levels of cleaved caspase-3 in BV2 cells infected with B. suis strain 2 in comparison with the control cells. DAPI staining showed nuclear condensation in B. suis infected BV2 cells transfected with PPM1A shRNA in comparison with the control shRNA cells. Flow cytometry analysis showed that PPM1A shRNA significantly increased the percentage of apoptotic BV2 cells infected with B. suis strain 2 compared with those transfected with control shRNA. Taken together, these data suggested that knockdown of PPM1A promotes apoptosis in B. suis strain 2-infected BV2 cells and that PPM1A may be a potential target in the development of treatments to inhibit intracellular growth of B. suis.Patients with heart disease often suffer from ischemia, which can be treated by reperfusion. However, this treatment can lead to the development of ischemia/reperfusion (I/R) injury, an inflammatory condition that can cause further heart damage. Dexmedetomidine (Dex), an α2-adrenoceptor agonist, and the microRNA (miR)-17-3p, have both been suggested to alleviate I/R injury and cardiac tissue inflammation. The aim of the present study was to investigate whether Dex and miR-17-3p could act together to prevent I/R injury. H9C2 cells, a myoblast cell line used as a model of rat cardiomyocytes, were cultured in a hypoxic environment for 3 h, and then reoxygenated for 3 h. This hypoxia/reoxygenation (H/R) was used to model I/R. Cell Counting kit-8 was used to determine cell viability and an annexin V-FITC/propidium iodide apoptosis kit used to analyze cell apoptosis. A dual luciferase reporter assay was used to determine the interaction between miR-17-3p and toll-like receptor 4 (TLR4). Western blotting and reverseon of inflammatory signaling pathways, and these inflammatory factors could be regulated by miR-17-3p.Expression levels of serum cyclooxygenase (COX)-2 and forkhead box O3a (FOXO3a) in patients with rheumatoid arthritis (RA) and the correlation with disease activity were investigated. Sixty patients with RA admitted to the People’s Hospital of Guangxi Zhuang Autonomous Region (study group; 28 active patients and 32 remissive patients), and further 30 healthy subjects undergoing physical examinations during the same period (control group) were enrolled in this study. RT-qPCR and enzyme-linked immunosorbent assay (ELISA) were used to detect the expression levels of COX-2 and FOXO3a in serum. According to DAS28 score, the patients were divided into active and remissive patients, between whom the expression levels were compared. Receiver operating characteristic (ROC) curves were plotted to analyze the diagnostic values of COX-2 and FOXO3a for disease activity. Pearson’s correlation coefficient was used to analyze the correlation of the two markers with erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and DAS28 score. The expression levels of COX-2 and FOXO3a in active and remissive patients were significantly higher than those in the control group (both P less then 0.05), and those in active patients were significantly higher than those in remissive patients (both P less then 0.05). The areas under the ROC curves (AUCs) of COX-2 and FOXO3a were 0.748 and 0.802, respectively, suggesting that the two markers have high diagnostic value. The expression levels of COX-2 and FOXO3a were positively correlated with ESR, CRP, and DAS28 score of active and remissive patients (both P less then 0.05). In conclusion, the expression levels of COX-2 and FOXO3a in patients with RA are upregulated, thus, the two markers may be involved in the development and progression of the disease. The expression levels of COX-2 and FOXO3a are related to the disease activity of RA, and therefore can be used as diagnostic indicators for the disease activity.Neonatal vascular ophthalmopathy is a refractory ophthalmologic disease, and is a major cause of blindness. Occurrence of neonatal vascular ophthalmopathy may be associated with Paxillin, a cellular adhesion molecule which promotes the migration of endothelial cells and angiogenesis. To explore the role of PXN in corneal angiogenesis, human umbilical vein endothelial cells were divided into five groups i) Control group; ii) Empty vector-transfected control group; iii) PXN knockdown group (shPXN group); iv) PXN-negative control (NC) group; and v) PXN over-expressed group (overExp group). PXN protein levels, migration and tube formation were assessed in the different experimental groups. Mice were divided into four groups i) Control; ii) Model; iii) shPXN; and iv) overExp groups. Tube formation was significantly increased in the overExp group compared with the empty vector-transfected control group (P less then 0.01). Tube formation was significantly decreased in the shPXN group compared with the PXN-NC group (P less then 0.