Objective To compare the effects of neutral posture training (NPT) and gas resistance training on balance and motor func-tion in stroke patients. Methods From June, 2014 to February, 2016, 44 hemiplegic patients were randomly divided into control group (n=22) and experimental group (n=22). The control group received conventional decubitus trunk muscle training and sitting gas resistance train-ing. The experimental group received NPT. They were assessed with Fugl-Meyer Assessment-Upper Extremities (FMA-UE), Fugl-Meyer Assessment-Lower Extremities (FMA-LE), and Berg Balance Scale (BBS) before and after training. Results There was no significant differ-ence in the scores of FMA-UE, FMA-LE and BBS between two groups (t<0.962, P>0.05). The scores significantly increased after training in both groups (t>12.248, P<0.001), and were higher in the experimental group than in the control group (t>1.972, P<0.05). Conclusion The NPT could improve the motor and balance function of stroke patients, rather than gas resistance training.

Forms and Records Control ; methods ; Humans ; Pathology, Clinical ; methods

To explore the role of mechanosensitive potassium channel TREK-1, Western blot analysis was used to investigate the expression changes of TREK-1 in left ventricle in acute mechanically stretched heart. Forty Wistar rats were randomly divided into 8 groups (n=5 in each group), subject to single Langendorff perfusion for 0, 30, 60, 120 min and acute mechanical stretch for 0, 30, 60, 120 min respectively. With Langendorff apparatus, an acute mechanically stretched heart model was established. There was no significant difference in the expression of TREK-1 among single Langendorff perfusion groups (P>0.05). As compared to non-stretched Langendorff-perfused heart, only the expression of TREK-1 in acute mechanically stretched heart (120 min) was greatly increased (P<0.05). This result suggested that some course of mechanical stretch could up-regulate the expression of TREK-1 in left ventricle. TREK-1 might play an important role in mechanoelectric feedback, so it could reduce the occurrence of arrhythmia that was induced by extra mechanical stretch.
Feedback ; Heart Ventricles/*metabolism ; Mechanotransduction, Cellular ; Potassium Channels, Tandem Pore Domain/*metabolism ; Random Allocation ; Rats, Wistar ; Stress, Mechanical

BACKGROUND: Multiple sclerosis(MS) is a chronic autoimmune disease induced by the interaction between genetic and environmental factors. Its pathogen and the mechanism of the relapse and remission m the course of the disease are still unknown. Most of the MS research centers are looking for the pathogenic polypeptide epitope in proteolipid protein(PLP), myelin sheath basic protein (MBP) and oligodendrocyte glycoprotein (MOG) OBJECTIVE: To compare the proliferation of T cell lines(TCL) in MS induced by myelin sheath and delipidated myelin sheath towards 11 components of myelin sheath to mainly search the possible pathogenic polypeptide epitope in PLP, and investigate the possible effects of abnormal dcgrease in myelin sheath.DESIGN: A case-controlled trial.SETTING: Department of neurology in a hospital of a university.PARTICIPANTS: Mononuclear cells(MNC) of 16 MS cases(clinical relapsing-remitting type, patients did not receive any immunosuppresant for at least 3 months when their peripheral blood samples were taken) and 12 HLA-DR15 healthy volunteers were furnished by Dr. Trotter JL of MS Research Center of Washington University from the cell database.INTERVENTIONS: MS-TCL and normal TCL were induced twice by stimulation with myelin sheath and delipidated myelin sheath in vitro by cell culture in vitro. TCL proliferation was tested by 11 antigens including PLP,MBP, M87-106, P30-49, P40-60, P89-106, P95-117, P117-137,P139-151, P178-191, and P185-206.MAIN OUTCOME MEASURES: Difference of scintillation counting in every minute of every well, and the stimulative index of each well were calculated, and the mean wells with positive proliferation of TCL towards each antigen were confirmed as well.RESULTS: The general specific proliferation towards myelin sheath antigens was bigger in MS group than control group 5.49 ±5.31 to 3.10 ± 3. 17, and delipidated myelin sheath-induced TCL was bigger than myelin sheath-induced one 5. 49 ± 5.31 to 3.41 ± 4. 83 . Delipidated myelin sheath significantly changed the immune responses of MS group,especially the changes of responses towards P30-49, P40-60, P89-106,P117-137, P139-161, and P185-206 were significant compared with that the control group only responded to two polypeptides, which indicated that the antigen epitope of MBP, PLP, M87-106, P95-117, P40-60, and P185-206 might have significance in the triggering of MS autoimmune responses.CONCLUSION: TCL induced by MS myelin sheath has different proliferation towards antigen components of myelin sheath from control group. Delipidated myelin sheath significantly increases TCL proliferation in MS group, which suggests that if MS patients developed abnormal degrease in myelin sheath, TCL would produce autoimmune response towards self-myelin sheath, MBP, PLP and its polypeptide segments all can trigger MS or aggravate the state of the illness. Our finding supports the hypothesis of MS autoimmune pathogenic mechanism.

[ ABSTRACT] AIM:To observe the treatment effect and its immune regulation of human amnion epithelial cells ( hAECs) on Alzheimer’ s disease ( AD)-like pathology rat model.METHODS: The hAECs were isolated from amnion with trypsin digestion, and the phenotype of hAECs was analyzed by flow cytometry.SD rats ( n=48) were randomly divid-ed into sham control group, model group, medium group and hAECs group.AD-like pathology rat model was induced by bilateral intraventricular injection of lipopolysaccharide (LPS).hAECs (5 ×105) were injected into the hippocampus of the AD-like pathology rats.At 2 weeks after transplantation, the animals were tested by Morris water maze to observe the function of learning and memory.The pathological change of the brain was observed by HE staining.The expression of am-yloid β-protein 42 (Aβ42) and Tau protein and the level of acetylcholine (ACh) in the injury brain were determined by immunohistochemistry.The survival and differentiation of hAECs in the hippocampus were measured by immunofluorescent technique.The percentages of lymphocyte subsets in the peripheral blood mononuclear cells were analyzed by flow cytome-try.The contents of serum cytokines were detected by cytometric bead array.RESULTS:Compared with model group and medium group, hAECs group showed shortened escape latency ( P<0.01) , increased frequency of going through the plat-form (P<0.05), reduced loss of hippocampal neurons, decreased expression of Tau protein and Aβ42 in the hippocampus (P<0.05), increased ACh level in the hippocampus (P<0.05), decreased percentages of Th1 and Th17 subsets, in-creased percentages of Th2 and Treg cells ( P<0.05) , decreased concentrations of IFN-γand IL-2 in the serum, and in-creased concentration of IL-4 ( P<0.05 ) .CONCLUSION: hAECs improve the cognitive learning and memory function and alleviate pathologic damage of hippocampus through immune regulation in AD-like pathology rats.

Humans ; Interferons ; administration & dosage ; therapeutic use ; Lymphoma, Mantle-Cell ; drug therapy ; Male ; Middle Aged ; Thalidomide ; administration & dosage ; therapeutic use

Objective To analyze the changes of PAIgG, CD62P, CD4+CD25+ Foxp3+Tr,and IL-18 before and after treatment in peripheral blood of children with acute idiopathic thrombocytopenic purpura(ITP) and investigate the function of these factors in the pathogenesis of ITP.Methods Forty-one cases of acute ITP children were divided into the effective group(35cases) and the ineffective group (6cases) according to the clinical treatment. To detect PAIgG,CD62P,and the number of Tr cells by using flow cytometry ,IL-18 plasma levels by ELISA assay,and analyze the variations of these indicators before and after treatment in children with acute ITP. Results In the effective treatment group, PAIgG, CD62P before treatment were 53.05%,(14.18±5.04 )%, which were significantly higher than that after treatment [18.62%, ( 8.36±1.95 )%] and control group[5.26%,(2.65±0.59) %,all P<0.01],and PAIgG,CD62P after treatment were also higher than that in control group [all P<0.05].IL-18,CD4 + T lymphocytes, Tr/CD4+T-lymphocyte ratios before treatment [415.47 ±38.92 ) ng/L,( 25.64 ± 5.81 )%,( 2.67 ± 0.14 )%]were significantly lower than that after treatment [(512.85±42. 17)ng/L,(35.08±6.07)% ,(4.76±0.58)%] and control group[(506. 39±32.28) ng/L,(35.32±2.27)% ,(5.37 ±0.69)% ,all P<0.01]. IL-18, CD4 +T lymphocytes, Tr/CD4 +T-lymphocyte ratios after treatmenthad no statistically significant difference compared with control group( all P<0.05 ). In ineffective group, the test results of PAIgG, CD62P, IL-18, CD4 +T lymphocytes, Tr/CD4+ T-lymphocyte ratios showed no significant change before and after treatment( all P<0.05 ).IL-18 had negative correlations with PAIgG,CD62P respectively before and after treatment(all P<0.05 ). Tr cells / CD4 + T had negative correlations with PAIgG,CD62P respectively (all P<0.05). Conclusions The amount of Tr, IL-18 were reduced, while CD62P and PAIgG increased in peripheral blood of children with acute ITP. IL-18, Tr , CD62P and PAIgG play important roles in the pathogenesis of acute ITP.

The endothelial-to-mesenchymal transition (EndMT) in endothelial cells contributes to the development of cardiac fibrosis,ultimately leading to cardiac remodeling.In this study,the effects and molecular mechanisms of celastrol (CEL) on transforming growth factor-β1 (TGF-β1)-induced EndMT in human umbilical vein endothelial (HUVEC-12) cells were investigated.The presented data demonstrated.that CEL significantly blocked the morphology change of HUVEC-12 cells induced by TGF-β1 without cell cytotoxicity.In accordance with these findings,CEL blocked TGF-β1-induced EndMT as evidenced by the inhibition of the mesenchymal markers,including collagen Ⅰ,Ⅲ,α-SMA,fibronectin mRNA expression,and the increase in the mRNA expression of endothelial cell marker CD31.These changes were also confirmed by double immunofluorescence staining of CD31 and vimentin.The in vitro scratch assay showed that CEL inhibited the migration capacity of the transitioned endothelial cells induced by TGF-β1.Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-β1/Smads signalling pathway,which was also confirmed by the inhibition of its downstream transcription factor snail1,twistl,twist2,ZEB1 and ZEB2.These results indicate that CEL blocks TGF-β1-induced EndMT through TGF-β1/Smads signalling pathway and suggest that it may be a feasible therapy for cardiac fibrosis diseases.

Objective To investigate the feature of diabetic foot ulcer and the relative mechanism, and to analyze its predilection site. Methods The precipitating factors and the areas of ulcer were analyzed in 121 diabetic patients with foot ulcer. The peripheral neuropathy was diagnosed by measuring the skin sensation, tendon reflex, electromyogram or vibration perception threshold (VPT). The diabetic peripheral neuropathy (DPN) was evaluated by positive symptoms, ultrasound or magnetic resonance angiography. According to morbid changes, the patients were divided into neuropathic ulcer group (n = 33), ischemic ulcer group (n = 27), and mixed type ulcer group (n = 61). Results The ulcers of 97 cases (80. 2%) were distributed in digital pedis and plantar pedis. In neurogenic ulcer group, there were 48.5% lesion at planta pedis, 30.3% at dorsum pedis, and 21.2% at digiti pedi. In ischemie ulcer group, there were 59.3% at digiti pedis, 29.6% at dorsum pedis, and 11.1% at planta pedis. In mixed type ulcer group, there were 49. 2% at digiti pedis, 41% at planta pedis, and 9.8% at dorsum pedis. The difference of ulcer distribution was apparent in these groups. Among these three groups, patients in mixed type ulcer group was the oldest, and had the longest duration of diabetes (P<0.05) and the largest area of ulcer at diagnosis. However, the BMI and blood pressure in isehemic ulcer group were higher than those of the other groups (P>0.05). Conclusions The difference of lesion basis affects the position of diabetic foot ulcer, and the thumbs and plantar pedis are the predilection area of diabetic foot.

380 mmHg) while the PaCO2 increased slightly at T5 and decreased gradually. The PCWP decreased slightly at T2, T3 , T4 and increased quickly at T5 , T6, levelling with T0 at T9. PVRI was on gradual increase beginning ahepatic stage and falling to the level of T0 at T7. The changes of PAP were similar with PCWP, the value at T6 being higher than that at T3, T4 significantly. Conclusion DO2 -directed hemodynamic management protects pulmonary function from damage during LTx.