The Tohoku journal of experimental medicine
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Tohoku J. Exp. Med. · Dec 2020
Randomized Controlled TrialVirtual-reality balance training with a video-game system improves dynamic balance in chronic stroke patients.
Stroke is one of the most serious healthcare problems and a major cause of impairment of cognition and physical functions. Virtual rehabilitation approaches to postural control have been used for enhancing functional recovery that may lead to a decrease in the risk of falling. In the present study, we investigated the effects of virtual reality balance training (VRBT) with a balance board game system on balance of chronic stroke patients. ⋯ There was greater improvement on BBS (4.00 vs. 2.81 scores) and TUG (-1.33 vs. -0.52 sec) in the VRBT group compared with the control group (P < 0.05), but not on static balance in both groups. In conclusion, we demonstrate a significant improvement in dynamic balance in chronic stroke patients with VRBT. VRBT is feasible and suitable for chronic stroke patients with balance deficit in clinical settings.
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Tohoku J. Exp. Med. · Dec 2020
Melanoma differentiation-associated gene 5 regulates the expression of a chemokine CXCL10 in human mesangial cells: implications for chronic inflammatory renal diseases.
Mesangial cells play an important role in inflammatory reactions in kidney. Although viral infections often trigger the worsening of chronic inflammatory renal diseases, the mechanisms are largely unknown. Melanoma differentiation-associated gene 5 (MDA5) is a member of RNA helicase family with a conserved Asp-Glu-x-His (DExH) box. In the present study, we examined the effect of polyinosinic-polycytidylic acid (poly IC), an authentic double-stranded RNA (dsRNA) that mimics viral dsRNAs, on MDA5 expression using primary culture of human mesangial cells. The cells were simply treated or transfected with poly IC; the former procedure is a model of cells exposed to viral dsRNA released from dying cells, and the latter is a model of entry of RNA virus into the cytoplasm. Expression levels of MDA5 mRNA in mesangial cells were increased about 70-100 fold in response to either treatment or transfection with poly IC. MDA5 protein expression was significantly induced as well. RNA interference experiments revealed that poly IC treatment induced MDA5 expression via Toll-like receptor 3 (TLR3) and interferon (IFN)-β, and that poly IC trasnfection induced MDA5 expression via another DExH box RNA helicase, retinoic acid-inducible gene-I (RIG-I), and IFN-β. Moreover, MDA5 induced by poly IC, in turn, increased the expression of a chemokine CXCL10. In addition, immunohistochemical staining demonstrated a high level of MDA5 expression in glomeruli, mainly in mesangial cells, of patients with severe lupus nephritis or proteinuric IgA nephropathy. MDA5 may be involved not only in physiological antiviral reactions but also in chronic inflammation in glomerular mesangial cells.
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Tohoku J. Exp. Med. · Dec 2020
Clinical TrialVisceral adipose tissue volume estimated at imaging sites 5-6 cm above L4-L5 is optimal for predicting cardiovascular risk factors in obese Japanese men.
The association between visceral adipose tissue (VAT) with cardiovascular disease (CVD) has been clearly demonstrated. Although typical VAT area at 4th and 5th lumbar vertebrae (L4-L5) is used to approximate VAT volume, growing evidence has suggested that this measurement site may not be ideal. However, these findings for Asian people remain unclear. Thus, we searched for the better VAT measurement sites associated with CVD risk factors in obese, Japanese men. Eighty-two obese men were included in a cross-sectional study. Among these participants, 37 men completed the 12-week intervention (90 min and 3 d/week) were used for addressing longitudinal association between the VAT measurement sites and CVD risk factors. Consecutive MRI images (from 3 cm below L4-L5 to 20 cm above L4-L5) were used to explore the relationship between each VAT area and CVD risk factors (total cholesterol, HDL cholesterol, triglycerides, glucose, insulin and blood pressure). The images located only 5-9 cm above L4-L5 had significant correlations with HDL cholesterol and triglycerides, but L4-L5 site did not in the cross-sectional analysis. In response to exercise, the image located 5 cm above L4-L5 showed the highest correlations with changes in total cholesterol (r = 0.46) and glucose (r = 0.36). Also, the image located 6 cm above L4-L5 showed highest correlations with changes in triglycerides (r = 0.37) and insulin (r = 0.37). Thus, the range of VAT images located 5-6 cm above L4-L5 may be optimal for identifying CVD risk factors compared to a typical site of L4-L5.
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Tohoku J. Exp. Med. · Dec 2020
The C-681G polymorphism of the PPAR-γ gene is associated with susceptibility to non-alcoholic fatty liver disease.
Non-alcoholic fatty liver disease (NAFLD) is defined as excessive accumulation of fatty acid in the liver, a common disease in the world. The research of single nucleotide polymorphisms (SNPs) provides a new approach for managing NAFLD. SNPs may increase or decrease the functions of the target genes and their encoding proteins. Peroxisome proliferator-activated receptor (PPAR) plays a key role in modulating metabolism of hepatic triglycerides and consequently magnitude of NAFLD. In this study, we investigated the effect of three SNPs in the PPAR-γ gene i.e. rs10865710 (C-681G), rs7649970 (C-689T) and rs1801282 (C34G, also termed Pro12Ala) on susceptibility to NAFLD. The participants were selected from our epidemiological survey. Totally 169 participants were enrolled in NAFLD group, and 699 healthy subjects were included as controls. PCR-RFLP was applied to detect the SNPs. The G allele frequency of rs10865710 in NAFLD group (41.1%) was significantly higher than that (34.8%) in controls (p = 0.03). Differences in other two loci (rs7649970 and rs1801282) were not statistically significant between the two groups (p > 0.05). This result was confirmed by haplotype analysis. The GCC haplotype (a set of 3 adjacent SNPs in linkage disequilibrium, corresponding to the three alleles of above polymorphisms in order) was a risk factor for the susceptibility to NAFLD (p = 0.03). This study has revealed that the G allele of rs10865710 in the PPAR-γ gene is associated with the increased susceptibility to NAFLD. Our findings may provide novel diagnostic biomarkers and therapeutic targets for NAFLD.
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Tohoku J. Exp. Med. · Dec 2020
Artemisinin attenuates post-infarct myocardial remodeling by down-regulating the NF-κB pathway.
Myocardial infarction (MI) leads to progressive left ventricular (LV) dilatation and is associated with interstitial fibrosis in the non-infarcted myocardium. The NF-κB signaling pathway plays an important role in ventricular remodeling after MI. Recent studies have indicated that the anti-malarial agent artemisinin can inhibit NF-κB activation, which may attenuate post-infarct myocardial remodeling. In this study, we investigated the effect of artemisinin on post-infarct myocardial remodeling using a rat model of MI. Adult male Sprague Dawley rats were divided into a sham group (n = 10) and MI groups that were treated either with oral gavage of artemisinin (75 mg/kg/day, n = 20) or vehicle (0.5% carboxymethyl cellulose, n = 20) three times a day for 4 weeks. Each treatment was started at 24 hours after ligation of the left anterior descending coronary artery. Four weeks after MI, the artemisinin-treated group showed a significantly improved survival rate compared with that of the vehicle-treated group (65% vs. 40%, P < 0.05). Although infarct size was similar in both groups, echocardiography showed significant improvements in cardiac function and left ventricular dimensions in the artemisinin-treated group. Moreover, the degree of myocardial fibrosis and elevated levels of fibrosis-related factors [transforming growth factor-β1, collagen type I, matrix metalloproteinase (MMP)-2 and MMP-9] in the non-infarcted myocardium were remarkably ameliorated by artemisinin (all P < 0.05). Importantly, artemisinin inhibited the NF-κB pathway by blocking IKBα phosphorylation. In conclusion, artemisinin may attenuate post-infarct myocardial remodeling by down-regulating the NF-κB pathway.