The treatment of cerebral palsy is still a big medical problem.The pathogenesis of spasticity,as result of a variety of lesions of the cerebral cortex,brain stem,spinal cord,is caused by involvement of the inhibitory pyramidal and parapyramidal descending tracts terminating on the spinal facilitatory myotatic reflex.A lesion of the descending tracts disturbs this equilibrium leading to spasticity,which is cha-racterized by muscle resistance at rest that is velocity dependent and associated with an increase in tonic stretch reflexes resulting from hype-rexcitability of the stretch reflex.Spasticity caused abnomal posture,caused special movement,and higher multilation,which affect children's life severely.There are so many ways to lower hypermyotonia,such as:drugs,rehabilitation care,acupuncture and so on.Bioelectric stimulation therapy is a new ways in the zone.Its curative effect and the mechanism are still in explore,this article just to give an overview about bioelectric stimulation therapy in curing spastic cerebral palsy.

Aim To observe the changes of diaphragm contractility and cytoskeletal proteins titin,nebulin and sarcoplasmic reticulum Ca~(2+)-ATPase gene expressions in adriamycin-induced cytotoxicity in rats.Methods The animal models of diaphragm damage were duplicated by injecting adriamycin into abdominal cavity one time.Forty male sprague-dawley rats were randomly divided into four groups(n=10):Three groups received adriamycin in low,middle and high dosage(10,20 and 40 mg·kg~(-1))respectively.Meanwhile,the normal saline was given to rats in control groups.Three days later,these rats were killed,and the diaphragm was removed by thoracotomy.The diaphragm contractility was assessed in isolated diaphragm strips perfusion by these paramemters including peak twitch tension(Pt),maximum tetanic tension(Po),time to peak contraction(CT),half relaxaion time(1/2RT),maximal rates of contraction(+dt/dt_(max))and maximal rates of relaxation(-dt/dt_(max)).The expressions of titin,nebulin and sarcoplasmic reticulum Ca~(2+)-ATPase(SERCA)at mRNA level were detected by RT-PCR analysis.Results In contrast to those in control group,Po,Pt,±dt/dt_(max) in the adriamycin group were lower(P<0.01);CT,1/2RT in the adriamycin group increased significantly(P<0.01).The levels of titin,nebulin and SERCA gene expressions in middle-dose group were lower than those in control group(P<0.01).Conclusions The mRNA levels of titin,nebulin and SERCA of diaphragm are down-regulated in adriamycin-induced cytotoxicity in rats.It may be associated with the decline of diaphragm contractility.

Botulinum Toxins, Type A ; administration & dosage ; adverse effects ; therapeutic use ; Cerebral Palsy ; drug therapy ; Child ; Child, Preschool ; Dose-Response Relationship, Drug ; Female ; Humans ; Male

Aim To observe the effects of liver cirrho-sis on the expression of transforming growth factor-β1 ( TGF-β1 ) and ColⅠin rat myocardium and interven-tion of erythropoietin ( EPO ) . Methods Thirty-six male Sprague-Dasley rats were randomly divided into three groups:control group, liver cirrhosis group and EPO group, then the cardic hemodynamic parameters in vivo and levels of serum lactate dehydrogenase ( LDH ) as well as creatine kinase isoenzyme ( CK-MB) were measured. With Masson′s trichrome stain, changes of collagen formation of myocardial tissue in different groups were observed. Also the mRNA ex-pressions of TGF-β1 and ColⅠin myocardium were de-tected by RT-PCR. Results In contrast to control group, rats in liver cirrhosis group showed a decline in systolic and diastolic function of left ventricule, rising myocardial enzyme, a distinct increase of cardiac colla-gen deposition, as well as an elevation of TGF-β1 and ColⅠmRNA expressions. In contrast to liver cirrhosis group, rats in EPO group demonstrated an improve-ment in systolic and diastolic function of left ventricule as well as in cardiac collagen deposition, and a de-crease in both myocardial enzyme and TGF-β1 and ColⅠmRNA expressions. Conclusion Liver cirrhosis can lead to the changes of myocardial structure and function in rats,and it can accelerate myocardial inter-stitial fibrosis; EPO can protect the myocardial injury in liver cirrhosis rats.

AIM: To investigate the dynamic variety of frequency and function of FoxP3~+ regulatory T cells in patients with acute hepatitis B (AHB). METHODS: Peripheral blood mononuclear cells (PBMCs) from 15 AHB patients at acute phase (week 1 of illness), convalescent phase (primary occurrence of both ALT level normalization and HBsAg negative conversion), resolved phase (at least 8 weeks after both ALT normalization and HBsAg seroconversion, and 15 health subjects were analyzed for FoxP3 (Forkhead/winged helix transcription factor) mRNA expression in MACS magnetic beads-purified CD4~+ T cells by real-time RT-PCR assay. The effects of Treg cells on the proliferation of CD4~+CD25~- T cells were examined by a ~3[H]-thymidine incorporation assay. RESULTS: AHB patients presented a significantly higher FoxP3 mRNA expression at convalescent phase than acute phase (t=-6.04, P<0.01) and resolved phase (t=4.45, P<0.01), and healthy controls (t=3.44, P<0.01). We also observed that the suppression efficiency of Treg cells on proliferation of CD4~+CD25~- T cells was lower at acute phase than convalescent phase (t=-5.30, P<0.01) and resolved phase (t=-3.20, P<0.05), but there was no significant difference between healthy controls and any phase of AHB. CONCLUSION: AHB patients presented lower circulating Treg frequency and suppression function at acute phase, and both of them are increased at convalescent phase, and then return to normal level along with disease resolved. This follow-up study furthers our understanding of Treg' s role in immunopathogenesis of hepatitis B.

In order to study the analgesic effect of Shaoyao Gancao Decoction, this paper discussed material basis and mechanism from the perspective of macromolecules in traditional Chinese medicine. Inspired by the phenomenon of turbidity after boiling Chinese medicine, this experiment took Shaoyao Gancao Decoction as the research object to study the formation process of precipitation during boiling. The results showed that aggregates with a certain shape were formed in the solvent during the boiling process, and the precipitate was obtained by standing and centrifuging. Analysis found that the precipitation was mainly composed of small molecules such as paeoniflorin, albiflorin, liquiritin, glycyrrhizic acid, isoliquiritin and gallic acid, and macromolecules such as protein and polysaccharide. The composition of precipitate was consistent with that of Shaoyao Gancao Decoction, but the analgesic effect of Shaoyao Gancao Decoction after removing the precipitate was significantly reduced. Based on these results, we isolated small molecular compounds, polysaccharides and protein from Shaoyao Gancao Decoction and their contents are 60.4, 700.7 and 207.2 mg·g^-1 respectively. We get the ratio, polysaccharide: small molecule = 11.6∶1, protein: small molecule = 3.4∶1, the precipitate is prepared in the state of boiling. The characterization results showed that the particle size of the precipitate will change significantly after co-heating, and the content determination results showed that the content of the six small molecular compounds which was free in solvent was significantly reduced after the formation of the precipitate. The acetic acid writhing experiment proved that the precipitate has a good analgesic effect, and effectively reduced the levels of inflammatory factors prostaglandin E2 and nitric oxide, and increased the level of anti-inflammatory factor interleukin-10. These results proved that the precipitate in Shaoyao Gancao Decoction is an important material basis for analgesic effect, and macromolecules such as protein and polysaccharide are the main components of the precipitate. The study of macromolecules in the precipitate of Shaoyao Gancao Decoction not only provides new ideas and methods for elucidating the pharmacodynamic material basis of Shaoyao Gancao Decoction, but also provides a reference for analyzing the scientificity of traditional decoction.

BACKGROUND: Research has been reported that serum soluble CD146 (sCD146) expression was improved on the surface of endothelial cells and activated T cells by the stimulation of inflammatory factor. Therefore, it predicts that CD146 may participate in inflammatory reaction of tissue.OBJECTIVE: To investigate the expression and clinical significance of serum sCD146 in peripheral blood from patients with ankylosing spondylitis.METHODS: A total of 62 patients with ankylosing spondylitis were selected from the Sixth People's Hospital AffiUated to Shanghai Jiao Tong University. All patients were divided into two groups: active group (n=46) and inactive group (n=16); while, 20 healthy subjects were selected as the control group. Indicators including Bath Ankylosing SpondyUtis Disease ActivityIndex (BASDAI),Bath Ankylosing Spondylitis Functional Index (BASFI), patient's global assessment (PGA), night pain, visual analogue scale (VAS),morning stiffness time, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were measured in all patients. The serum concentration of sCD146 from 62 patients with ankylosing spondlitis and 20 healthy controls was measured by enzyme-linked immunosorbent assay. Westergren method was used to measure ESR and immunoturbidimetry for CRP. Clinical data of the patients were collected as well.RESULTS AND CONCLUSION: sCD146 levels of patients with ankylosing spondlitis were significantly higher than normal control group (P ＜ 0.05). The sCD146 expression in the active group was significantly higher than inactive and normal control groups (P ＜0.05). Positive correlations were observed between sCD146 and BASDAI index of patients with ankylosing spondlitis (P ＜ 0.05).The sCD146 levels of ankylosing spondUtis patients with peripheral joint involvement were significantly higher than the patients with axial involvement alone or the normal controls (P ＜ 0.05).The expression level of sCD146 in peripheral blood was positively correlated with disease activities of patients with ankylosing spondlitis. It may play important roles in the pathogenesis in ankylosing spondlitis.

Objective To evaluate the inhibitory effect of photocatalytic titanium dioxide (TiO2)on the growth of a human epidermal squamous cell carcinoma cell line A431 and its mechanism.Methods Cultured A431 cells were classified into various groups to remain untreated (blank control group),be treated with different concentrations (100,200,300,400,500,600 mg/L) of TiO2 nanoparticles alone or in combination with ultraviolet (UV,main wavelength 253.7 nm,power 30 W,distance 30 cm,exposure duration 15 min) irradiation.After additional culture for different durations,methyl thiazolyl tetrazolium (MTT) assay was performed to evaluate cell growth,annexin V-fluorescein isothiocyanate/propidium iodide (PI) double staining to observe cell apoptosis,and Rho123 staining to determine mitochondrial transmembrane potential.Statistical analysis was carried out using SPSS 13.0 software.Analysis of variance (AOV),t test and Student-Newman-Keuls (SNK) test were performed to assess the differences in these parameters between these groups.Results The growth of A431 cells was inhibited by pretreatment with TiO2 nanoparticles followed by UV irradiation,and the inhibitory effect was enhanced as the dose of TiO2 nanoparticles increased.As AOV and SNK test showed,there were significant differences in the growth inhibition rate among A431 cells treated with different concentrations of TiO2 nanoparticles at the three time points (24,48 and 72 hours) after UV irradiation (n =6,F =21.54,77.56,20.27,respectively,all P ＜ 0.05).No statistical inhibition was observed in the growth of A431 cells treated with TiO2 nanoparticles alone compared with untreated A431 cells (all P ＞ 0.05).Photocatalytic TiO2 nanoparticles also induced the apoptosis but decreased the mitochondrial transmembrane potential in A431 cells.In detail,the apoptosis rate was 8.86％ ± 0.22％,11.72％ ± 0.29％ and 31.24％ ± 0.78％ in A431 cells treated with TiO2nanoparticles of 100,200,400 mg/L followed by UV irradiation,respectively,compared to 2.69％ ± 0.28％ in the blank control group (n =3,F =256.61,P ＜ 0.05).Decreased mitochondrial transmembrane potential (expressed as total fluorescence intensity) was observed in A431 cells treated with TiO2 nanoparticles of 100,200,400 mg/L followed by UV irradiation compared with blank control group (758.48 ± 15.42,676.60 ± 14.35,557.71 ± 13.12vs.2943.65 ± 70.26,F =208.57,P ＜ 0.05,n =3),and SNK test also revealed statistical differences between these groups.Conclusions TiO2 nanoparticles combined with UV can inhibit the growth of but induce the apoptosis in A431 cells,which may be associated with the reduction in mitochondrial transmembrane potential in A431 cells,while TiO2 nanoparticles alone show no inhibitory effect on the growth of A431 cells.

Aim To observe whether the activation of aldehyde dehydrogenase 2 ( ALDH2 ) can protect a-gainst diabetes induced liver injury in rat model, and analyze the role of JNK pathway in the liver protection induced by activation of ALDH2 . Methods All male SD rats were randomly divided into three groups: nor-mal control group ( Con ) , diabetes group ( DM ) and ethanol + diabetes group ( EtOH + DM ) . After 8 weeks, the fasting blood glucose ( FBG) level, glyco-sylated hemoglobin ( HbA1c) level, serum AST and ALT levels were measured. The changes of hepatic pa-thology were observed by hematoxylin and eosin ( HE) staining method. The protein expressions of ALDH2, JNK and p-JNK in liver tissue were measured. Result Compared with control group, in DM group, the lev-els of FBG and HbA1c, serum AST and ALT levels were increased significantly. The structure of liver mor-phology was destroyed, disarranged and unclear, the hepatocyte was swollen, and a large number of inflam-matory cells were infiltrated. ALDH2 protein expres-sion was decreased, while the expressions of JNK, p-JNK and the ratio of p-JNK/JNK were increased. Com-pared with DM group, in EtOH+DM group, the levels of FBG and HbA1c, serum AST and ALT levels were decreased. The expression of ALDH2 protein was in-creased, accompanying with the decrease of JNK, p-JNK protein expressions and the ratio of p-JNK/JNK. Conclusion Activation of ALDH2 can protect the liv-er against diabetes induced liver damage in rat model, which may be relevant with inhibiting the JNK path-way.

Aim To investigate the role of mitochondrial aldehyde dehydrogenase 2 ( ALDH2) in the cardio-protection of ischemic postconditioning in isolated rat hearts. Methods Hearts isolated from male Sprague-Dawley rats were perfused on a langendorff apparatus and subjected to 30 min of regional ischemia( occlusion of left anterior descending artery) followed by 120 min reperfusion. Ischemic postconditioning was achieved by 6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of reperfusion. The ventricular hemodynamic parameters and lactate dehydrogenase ( LDH) release during reperfusion were measured. The infarct size was measured by TTC staining method. The expressions of ALDH2,Bcl-2 and Bax at mRNA level of left anterior myocardium were detected by RT-PCR analysis. Results In contrast to ischemia and reperfusion,ischemic postconditioning improved the recovery of left ventricular developed pressure,rate pressure product during reperfusion,and reduced LDH release and infarct size. The expressions of ALDH2 mRNA level and the ratio of Bcl-2 /Bax were increased. Adminis-tration of ALDH2 antagonist cyanamide at the beginning of reperfusion attentuated the role of ischemic postconditioning. Conclusion Ischemic postconditioning plays a role in the cardioprotection partially through increasing mitochondrial ALDH2 mRNA expression.