Effects of Korean Red Ginseng (Panax ginseng), urushiol (Rhus vernicifera Stokes), and probiotics (Lactobacillus rhamnosus R0011 and Lactobacillus acidophilus R0052) on the gut–liver axis of alcoholic liver disease

AbstractBackgroundRoles of immune reaction and toll-like receptor-4 (TLR-4) have widely been established in the pathogenesis of alcoholic liver disease (ALD).MethodsWe evaluated the biologic efficacy of Korean Red Ginseng (KRG), urushiol, and probiotics (Lactobacillus rhamnosus R0011 and Lactobacillus acidophilus R0052) in mouse models of ALD. Sixty C57BL/6 mice were equally divided into six feeding groups for 10 weeks: normal diet, alcohol, control, alcohol + KRG, alcohol + urushiol, and alcohol + probiotics. Alcohol was administered via a Lieber–DeCarli liquid diet containing 10% alcohol. TLR-4 expression, proinflammatory cytokines, and histology, as well as the results of liver function tests were evaluated and compared.ResultsNo between-group differences were observed with regard to liver function. TLR-4 levels were significantly lower in the KRG, urushiol, and probiotics groups than in the alcohol group (0.37 ± 0.06 ng/mL, 0.39 ± 0.12 ng/mL, and 0.33 ± 0.07 ng/mL, respectively, vs. 0.88 ± 0.31 ng/mL; p < 0.05). Interleukin-1β levels in liver tissues were decreased among the probiotics and KRG groups. The tumor necrosis factor-α level of liver tissue was decreased in the KRG group.ConclusionThe pathological findings showed that alcohol-induced steatosis was significantly reduced by KRG and urushiol. As these agents improve immunologic capacity, they may be considered in potential anti-ALD treatments

Functional and Histologic Changes After Repeated Transcranial Direct Current Stimulation in Rat Stroke Model

Transcranial direct current stimulation (tDCS) is associated with enhancement or weakening of the NMDA receptor activity and change of the cortical blood flow. Therefore, repeated tDCS of the brain with cerebrovascular injury will induce the functional and histologic changes. Sixty-one Sprague-Dawley rats with cerebrovascular injury were used. Twenty rats died during the experimental course. The 41 rats that survived were allocated to the exercise group, the anodal stimulation group, the cathodal stimulation group, or the control group according to the initial motor function. Two-week treatment schedules started from 2 days postoperatively. Garcia, modified foot fault, and rota-rod performance scores were checked at 2, 9, and 16 days postoperatively. After the experiments, rats were sacrificed for the evaluation of histologic changes (changes of the white matter axon and infarct volume). The anodal stimulation and exercise groups showed improvement of Garcia's and modified foot fault scores at 16 days postoperatively. No significant change of the infarct volume happened after exercise and tDCS. Neuronal axons at the internal capsule of infarct hemispheres showed better preserved axons in the anodal stimulation group. From these results, repeated tDCS might have a neuroprotective effect on neuronal axons in rat stroke model

The determinants of stroke phenotypes were different from the predictors (CHADS2 and CHA2DS2-VASc) of stroke in patients with atrial fibrillation: a comprehensive approach

<p>Abstract</p> <p>Background</p> <p>Atrial fibrillation (AF) is a leading cause of fatal ischemic stroke. It was recently reported that international normalized ratio (INR) levels were associated with infarct volumes. However, factors other than INR levels that affect stroke phenotypes are largely unknown. Therefore, we evaluated the determinants of stroke phenotypes (pattern and volume) among patients with AF who were not adequately anticoagulated.</p> <p>Methods</p> <p>We analyzed data pertaining to consecutive AF patients admitted over a 6-year period with acute MCA territory infarcts. We divided the patients according to DWI (diffusion-weighted imaging) lesion volumes and patterns, and the relationship between stroke predictors (the CHADS₂and CHA₂DS₂-VASc score), systemic, and local factors and each stroke phenotype were then evaluated.</p> <p>Results</p> <p>The stroke phenotypes varied among 231 patients (admission INR median 1.06, interquartile range (IQR) 1.00-1.14). Specifically, (1) the DWI lesion volumes ranged from 0.04-338.62 ml (median 11.86 ml; IQR, 3.07-44.20 ml) and (2) 46 patients had a territorial infarct pattern, 118 had a lobar/deep pattern and 67 had a small scattered pattern. Multivariate testing revealed that the CHADS₂and CHA₂DS₂-VASc score were not related to either stroke phenotype. Additionally, the prior use of antiplatelet agents was not related to the stroke phenotypes. Congestive heart failure and diastolic dysfunction were not associated with stroke phenotypes.</p> <p>Conclusions</p> <p>The results of this study indicated that the determinants of stroke phenotypes were different from the predictors (i.e., CHADS2 and CHA₂DS₂-VASc score) of stroke in patients with AF.</p

Nanostring-based multigene assay to predict recurrence for gastric cancer patients after surgery

10.1371/journal.pone.0090133PLoS ONE93-POLN

Circulating Mesenchymal Stem Cells Microparticles in Patients with Cerebrovascular Disease

Preclinical and clinical studies have shown that the application of CD105+ mesenchymal stem cells (MSCs) is feasible and may lead to recovery after stroke. In addition, circulating microparticles are reportedly functional in various disease conditions. We tested the levels of circulating CD105+ microparticles in patients with acute ischemic stroke. The expression of CD105 (a surface marker of MSCs) and CXCR4 (a CXC chemokine receptor for MSC homing) on circulating microparticles was evaluated by flow cytometry of samples from 111 patients and 50 healthy subjects. The percentage of apoptotic CD105 microparticles was determined based on annexin V (AV) expression. The relationship between serum levels of CD105+/AV− microparticles, stromal cells derived factor-1α (SDF-1α), and the extensiveness of cerebral infarcts was also evaluated. CD105+/AV− microparticles were higher in stroke patients than control subjects. Correlation analysis showed that the levels of CD105+/AV− microparticles increased as the baseline stroke severity increased. Multivariate testing showed that the initial severity of stroke was independently associated with circulating CD105+/AV− microparticles (OR, 1.103 for 1 point increase in the NIHSS score on admission; 95% CI, 1.032–1.178) after adjusting for other variables. The levels of CD105+/CXCR4+/AV− microparticles were also increased in patients with severe disability (r = 0.192, p = 0.046 for NIHSS score on admission), but were decreased with time after stroke onset (r = −0.204, p = 0.036). Risk factor profiles were not associated with the levels of circulating microparticles or SDF-1α. In conclusion, our data showed that stroke triggers the mobilization of MSC-derived microparticles, especially in patients with extensive ischemic stroke

Effect of Repetitive Transcranial Magnetic Stimulation Over the Hand Motor Cortical Area on Central Pain After Spinal Cord Injury

Objective: To evaluate the analgesic effect of repetitive transcranial magnetic stimulation (rTMS) applied on the hand motor cortical area in patients with spinal cord injury (SCI) who have chronic neuropathic pain at multiple sites in the body, including the lower limbs, trunk, and pelvis. Design: Blinded, randomized crossover study. Setting: University hospital outpatient setting. Participants: Patients (N = 13) with motor complete or incomplete SCI and chronic central pain (11 completed the study). Interventions: rTMS was applied on the hand motor cortical area using a figure-of-eight coil. One thousand stimuli were applied daily on 5 consecutive days. Real and sham rTMS were separated by 12 weeks. Main Outcome Measures: Numeric rating scale (NRS) for average and worst pain and the Brief Pain Inventory (BPI). Results: At 1 week after the end of the rTMS period, the average NRS scores changed from 6.45 +/- 2.25 to 5.45 +/- 1.81 with real stimulation and from 6.18 +/- 1.83 to 5.91 +/- 2.07 with sham stimulation, and did not differ between treatments. The interference items of the BPI also did not differ between the real and sham rTMS. The effect of time on the NRS score for worst pain was significant with real stimulation but not with sham stimulation. Conclusions: The therapeutic efficacy of rTMS was not demonstrated when rTMS was applied to the hand motor cortical area in patients with chronic neuropathic pain at multiple sites in the body, including the lower limbs, trunk, and pelvis. However, the results for worst pain reduction suggest that further studies are required in which rTMS is applied with a more intensive stimulation protocol.Goto T, 2008, PAIN, V140, P509, DOI 10.1016/j.pain.2008.10.009Widerstrom-Noga E, 2008, SPINAL CORD, V46, P818, DOI 10.1038/sc.2008.64Turk DC, 2008, PAIN, V139, P485, DOI 10.1016/j.pain.2008.06.025Lefaucheur JP, 2008, CLIN NEUROPHYSIOL, V119, P2179, DOI 10.1016/j.clinph.2008.07.007Lam RW, 2008, CAN J PSYCHIAT, V53, P621Defrin R, 2007, ARCH PHYS MED REHAB, V88, P1574, DOI 10.1016/j.apmr.2007.07.025Passard A, 2007, BRAIN, V130, P2661, DOI 10.1093/brain/awm189Maarrawi J, 2007, NEUROLOGY, V69, P827Leo RJ, 2007, J PAIN, V8, P453, DOI 10.1016/j.pain.2007.01.009Fregni F, 2007, LANCET NEUROL, V6, P188Peyron R, 2007, NEUROIMAGE, V34, P310, DOI 10.1016/j.neuroimage.2006.08.037Bryce TN, 2007, J SPINAL CORD MED, V30, P421Lefaucheur JP, 2006, NEUROLOGY, V67, P1998Andre-Obadia N, 2006, CLIN NEUROPHYSIOL, V117, P1536, DOI 10.1016/j.clinph.2006.03.025Fitzgerald PB, 2006, AM J PSYCHIAT, V163, P88Jensen MP, 2005, SPINAL CORD, V43, P704, DOI 10.1038/sj.sc.3101777Nuti C, 2005, PAIN, V118, P43, DOI 10.1016/j.pain.2005.07.020Khedr EM, 2005, J NEUROL NEUROSUR PS, V76, P833, DOI 10.1136/jnnp.2004.055806Brown JA, 2005, NEUROSURGERY, V56, P290, DOI 10.1227/01.neu.0000148905.75845.98Dworkin RH, 2005, PAIN, V113, P9, DOI 10.1016/j.pain.2004.09.012Lefaucheur JP, 2004, J NEUROL NEUROSUR PS, V75, P612, DOI 10.1136/jnnp.2003.022236Yun YH, 2004, ONCOLOGY-BASEL, V66, P439, DOI 10.1159/000079497Siddall PJ, 2003, PAIN, V103, P249, DOI 10.1016/S0304-3959(02)00452-9Lefaucheur JP, 2001, NEUROPHYSIOL CLIN, V31, P247Bennett M, 2001, PAIN, V92, P147Garcia-Larrea L, 1999, PAIN, V83, P259Nguyen JP, 1999, PAIN, V82, P245NGUYEN JP, 1997, ADV STER F, V68, P54ACKERMANN H, 1992, J NEUROL, V239, P218WASSERMANN EM, 1992, ELECTROEN CLIN NEURO, V85, P1COHEN LG, 1990, ELECTROEN CLIN NEURO, V75, P350