Electric Stimulation Hyperthermia Relieves Inflammation via the Suppressor of Cytokine Signaling 3-Toll Like Receptor 4 Pathway in a Prostatitis Rat Model.

PURPOSE: Chronic prostatitis (CP), including chronic pelvic pain syndrome (CPPS), is the most commonly encountered manifestation of prostatitis. The aim of this study was to evaluate the effect of electric stimulation hyperthermia treatment (ESHT) on CP/CPPS and to explore the underlying mechanism. MATERIALS AND METHODS: RWPE-2 cells with lipopolysaccharide-induced inflammation and a prostatitis rat model induced by 17ß-estradiol and dihydrotestosterone underwent sham, electric stimulation, or ESHT treatment. Four weeks later, cells, supernatants, and rat prostates were collected for analysis using immunohistochemistry, Western blots, and enzyme-linked immunosorbent assays. RESULTS: We found that ESHT improved prostatitis in vivo and attenuated inflammation in vitro. ESHT significantly induced suppressor of cytokine signaling 3 (SOCS3) expression and subsequently promoted HSP70. It attenuated inflammation through decreased expression of toll-like receptor 4 (TLR4), nuclear factor kappa B, and subsequent inflammatory cytokines. ESHT also inhibited apoptosis and released growth factor in tissue affected by prostatitis. CONCLUSIONS: ESHT improved CP/CPPS and reversed pathologic changes of prostatitis by inhibiting the SOCS3-TLR4 pathway.

Profiling of remote skeletal muscle gene changes resulting from stimulation of atopic dermatitis disease in NC/Nga mouse model.

Although atopic dermatitis (AD) is known to be a representative skin disorder, it also affects the systemic immune response. In a recent study, myoblasts were shown to be involved in the immune regulation, but the roles of muscle cells in AD are poorly understood. We aimed to identify the relationship between mitochondria and atopy by genome-wide analysis of skeletal muscles in mice. We induced AD-like symptoms using house dust mite (HDM) extract in NC/Nga mice. The transcriptional profiles of the untreated group and HDM-induced AD-like group were analyzed and compared using microarray, differentially expressed gene and functional pathway analyses, and protein interaction network construction. Our microarray analysis demonstrated that immune response-, calcium handling-, and mitochondrial metabolism-related genes were differentially expressed. In the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology pathway analyses, immune response pathways involved in cytokine interaction, nuclear factor-kappa B, and T-cell receptor signaling, calcium handling pathways, and mitochondria metabolism pathways involved in the citrate cycle were significantly upregulated. In protein interaction network analysis, chemokine family-, muscle contraction process-, and immune response-related genes were identified as hub genes with many interactions. In addition, mitochondrial pathways involved in calcium signaling, cardiac muscle contraction, tricarboxylic acid cycle, oxidation-reduction process, and calcium-mediated signaling were significantly stimulated in KEGG and Gene Ontology analyses. Our results provide a comprehensive understanding of the genome-wide transcriptional changes of HDM-induced AD-like symptoms and the indicated genes that could be used as AD clinical biomarkers.

Anomalous origin of the left circumflex coronary artery from the first diagonal branch presented as acute myocardial infarction.

Coronary artery anomalies are diagnosed in 0.6 to 1.5% of patients who undergo coronary angiography (CAG). They may present with life threatening conditions but are generally asymptomatic. Recognition and adequate visualization of the anomaly is essential for correct management of the condition. However, in some cases the exact orifice and course of an anomalous coronary vessel cannot be selectively identified by CAG. In this report, a 54-year-old man was admitted to the hospital with acute inferior myocardial infarction and had an anomalous origin of the left circumflex coronary artery (LCX) from the first diagonal branch (D1). In CAG, the right CAG showed no significant stenosis and fortunately we found an anomalous origin of the LCX from the D1. The course of LCX was precisely established by 64-slice multi-detector computed tomography.

Palatal bone density in adult subjects: implications for mini-implant placement.

OBJECTIVES: To evaluate palatal bone density to allow for better selection of palatal implant anchorage sites. MATERIALS AND METHODS: Computed tomographic (CT) images were obtained from 15 males and 15 females (mean age, 27 years; range, 23-35 years). Bone density was measured in Hounsfield units (HU) at 80 coordinates at regular mediolateral and anteroposterior intervals along the midpalatal suture. RESULTS: Bone densities ranged from 805 to 1247 HU. A significant difference between male and female groups was noted, although no difference was found between left and right sides of individual palates. Palatal bone densities showed a tendency to decrease laterally and posteriorly. The midpalatal area within 3 mm of the midsagittal suture had the densest bone in the entire palate. CONCLUSION: Results suggest that mini-implants for orthodontic anchorage may be effectively placed in most areas with bone density equivalent to the palatal area if they are placed from 3 mm posterior to the incisive foramen and 1 to 5 mm to the paramedian side.