The adaptations in muscle architecture following whole body vibration training

Objective:This study aims to investigate the effect of 8-week whole-body vibration (WBV) added to conventional training on muscular architecture, dynamic muscle strength and physical performance compared to controls in young basketball players.Methods:Sixteen young basketball players between the ages of 14-16 years were randomly assigned to whole body vibration group (VG) or control group (CG). Both groups were trained with a conventional program. Pennation angle (PeA), fascicle length and muscle thickness of Rectus Femoris (RF) and Vastus lateralis were measured by ultrasonography. Isokinetic dynamic muscle testing at 180 °/s and 60°/s, squat jump (SJ) and flexibility were evaluated before and after 8 weeks of training programs. Primary outcome measure was the fascicle length.Results:Fascicle length of RF, SJ height and flexibility increased significantly within VG compared to pretraining (p<0.05). SJ height increased in VG compared to CG significantly following training (p<0.05). PeA, fascicle length, muscle thicknesses, strength and flexibility did not differ between groups.Conclusion:Eight weeks of WBV training improved fascicle length of RF, SJ height, and flexibility compared to pre-training. Addition of WBV to conventional training did not cause improvement in muscle architecture, strength and flexibility compared to conventional training alone.     

Acute adriamycin-induced cardiotoxicity is exacerbated by angiotension II

Adriamycin (ADR) increases the production of reactive oxygen species (ROS), which diminishes mitochondrial function. Angiotensin-II stimulates mitochondrial ROS generation. The aim of the study was to examine whether angiotensin converting enzyme (ACE) or renin inhibitors protect against ADR-induced mitochondrial function impairment. Rats were divided into five groups as control, ADR, co-treatment ADR with captopril, co-treatment ADR with aliskiren, co-treatment ADR with both captopril and aliskiren. Left ventricular function and blood pressures were assessed at the end of treatment period. Mitochondrial membrane potential (MMP) and ATP levels were determined. ADR treatment decreased the left ventricular pressure and increased the left ventricular end-diastolic pressure. ADR decreased MMP and ATP levels in myocyte mitochondria due to increasing oxidative stress. ADR decreased MMP and ATP levels due to increased oxidative stress in the heart. Inhibitors of ACE and renin caused the elevation of the decreased of MMP and ATP levels. The pathologic changes in electrocardiogram, blood pressure and left ventricular function were decreased by inhibition of Ang-II production. We concluded that inhibitors of angiotensin II are effective against ADR cardiotoxicity via the restoration of MMP and ATP production and prevention of mitochondrial damage in vivo.     

Specific haptoglobin expression in bronchoalveolar lavage during differentiation of circulating fibroblast progenitor cells in mild asthma

Haptoglobin is an acute-phase glycoprotein considered to be involved in tissue repair and is produced by fibroblasts and inflammatory cells. By using a gel-based proteomic approach, we show for the first time a possible role for haptoglobin in the differentiation of fibroblast progenitor cells, termed fibrocytes, in patients with mild asthma. Bronchoalveolar lavage fluid (BALF) was performed to sample circulating fibrocytes from patients with mild asthma and nonasthmatic control subjects. Fibrocytes from the airway lumen were characterized by triple staining of the markers CD34/CD45R0/alpha-smooth muscle actin, and subjected to confocal microscopy. The protein expression pattern was analyzed using two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF). Elevated levels of haptoglobin expression in BALF was reported in a sub-group of patients with mild asthma (p < 0.05) when compared to the other subjects. In addition, this increase in haptoglobin was accompanied by differentiation of fibrocytes into fibroblast-like cells. When further analyzing the expression pattern of haptoglobin isoforms, a heterozygous expression was detected in the patients where fibrocyte differentiation could be observed. These data raise the possibility that an acute and specific inflammatory state facilitates the differentiation of fibroblast progenitor cells into activated fibroblasts. Furthermore, this study proposes a novel role for haptoglobin in airway remodeling in patients with asthma.     

Latency of auditory P300 response is related with cognitive deficits in Obstructive Sleep Apnea Syndrome

Sleep and Biological Rhythms - Obstructive Sleep Apnea Syndrome (OSAS) is characterized by desaturation in blood oxygen level and sleep fragmentation because of repeated upper airway obstruction....     

Identification of potential microRNA markers related to Crimean-Congo hemorrhagic fever disease

Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne disease caused by the arbovirus Crimean-Congo hemorrhagic fever virus (CCHFV). The CCHFV has a single-stranded RNA genome of negative sense. MicroRNAs (miRNAs) are key players in virus-host interactions and viral pathogenesis. We investigated the miRNA gene expression profiles in patients with CCHF using microarray for the first time in the world. Microarray analysis was performed using mirBase Ver 21 (Agilent Technologies, Santa Clara, CA). All statistical analyses were performed across the case-control, fatal-control, and fatal-nonfatal case groups using Genespring (Ver 3.0). Fifteen miRNAs were statistical significant in patients with CCHF compared with the controls (5 were upregulated, 10 were downregulated). Seventy-five and sixty-six miRNAs are in fatal compared with control and nonfatal case, respectively (fold change ([FC] ≥50) were statistically significant. In this study, the target genes of important miRNAs were identified and Gene Ontology analyses were performed across all groups. As a result of this study, we propose that the detection of miRNAs in patients with CCHF will allow the determination of therapeutic targets in diseases. CCHF is an important public health problem that can often be fatal. In this study, we investigated miRNA expression in case-control, fatal-control, and fatal-nonfatal case groups. Significant miRNAs associated with fatality were detected in CCHF. This study will serve as a source of data for the development of an antagomir-based therapy against CCHF using miRNAs in the future.     

The protection of selenium on adriamycin-induced mitochondrial damage in rat

Although adriamycin (ADR) exhibits high anti-tumor efficacy in vitro, its clinical use in cancer chemotherapy is limited due to its high renal toxicity. This study investigated the mechanism of ADR nephropathy and the protective effect of selenium on ADR-induced kidney damage by analyzing of the relationship between selenium and mitochondria. Rats were divided into four groups. The first group was injected with saline i.p. for 21 days, the second group received the 4 mg/kg i.p. ADR every alternate day for 8 days, the third group received the 50 μg/kg i.p. Se for 21 days, and the fourth group received the Se. ADR co-administration i.p. blood pressures were assessed, the mitochondrial membrane potential (MMP) was assessed, and the adenosine triphosphate (ATP) levels were determined. The total antioxidant (TAS) and oxidant status (TOS) in cytosol, the mitochondria of kidney cells, and plasma were measured. Mitochondrial TAS decreased and TOS increased in the ADR group compared to the Se group. ADR-treated rats showed significantly lower MMP than did the control and Se groups. MMP was significantly restored in the Se + ADR group through selenium treatment compared to the ADR group (p < 0.01). In the ADR group, a reduction in ATP content was seen compared to the control and Se groups (p < 0.01). ATP level was significantly restored through treatment with selenium in the Se + ADR group compared to the ADR group (p < 0.01). We concluded that selenium is effective in vivo against ADR-induced kidney damage via the restoration of TAS and TOS, which prevented mitochondrial damage.     

A miR-206 regulated gene landscape enhances mammary epithelial differentiation

miR-206 is known to suppress breast cancer. However, while it is expressed in mammary stem cells, its function in such nontumor cells is not well understood. Here, we explore the role of miR-206 in undifferentiated, stem-like mammary cells using the murine mammary differentiation model HC11, genome-wide gene expression analysis, and functional assays. We describe the miR-206-regulated gene landscape and propose a network whereby miR-206 suppresses tumor development. We functionally demonstrate that miR-206 in nontumor stem-like cells induces a G1–S cell cycle arrest, and reduces colony formation and epithelial-to-mesenchymal transition markers. Finally, we show that addition of miR-206 accelerates the mammary differentiation process along with related accumulation of lipids. We conclude that miR-206 impacts a network of signaling pathways, and acts as a regulator of proliferation, stemness, and mammary cell differentiation in nontumor stem-like mammary cells. Our study provides a broad insight into the breast cancer suppressive functions of miR-206.