This study was conducted in the First Affiliated Hospital of Zhejiang Chinese Medical University for the project of Establishment and Assessment of Ethics Review Platform for TCM Clinical Research. The Ethics Review Platform for Clinical Research is a complete system, which is a Participant Protection System. It includes four as-pects, which are the medical and health institution, ethics committee, ethics committee office, research departments and researchers. In this system, the establishment of research departments and researchers platform is the most cru-cial part. All treatment, protection, risk control, adverse event supervision, which are closely related to the Partici-pant Protection System are completed by researchers. However, during the assessment process, a series of problems were found, such as the current weak ethical consciousness of researchers, less familiar with ethical review process and do not pay equal attention to the participant protection as clinical research. This kind of problem was also found in other hospital assessments in China, which has become a short board of the Participant Protection System.Therefore, from the aspect of the ethics committee, this article presented several ethics problems which should be paid more attention to by researchers such as participant protection, plan design and conduction during the clinical research and also gave some useful advices to change the situation, according to the Assessment Standard of Ethics Review Platform for TCM Clinical Research. In this way, researchers will develop their ethical consciousness and be more familiar with the ethics review process in order to complete key task of participant protection.

0.05). Chuansu Jiuxin Capsule could improve haemorheology (mainly act on blood viscosity, plasma viscosity and HCT), degrade platelet function (increase TXB2 level and decrease 6-keto-PGF1? level) and protect endothelia (increase ET and decrease NO level). Conclusions Chuansu Jiuxin Capsule was effective and safe for the treatment on AP patients with syndrome of blood stasis in collateral of heart.

Objective To analyze the influence of adenovirus latent infection on gamma-glutamylcysteine systhetase(γ-GCS) in rat alveolar epithelial cells. Methods The rat alveolar epithelial cells were stably transfected with the plasmid pE1Aneo and control plasmid. Glutathione(GSH) contents, the activity of γ-GCS were detected in oxidant stress. Then the leuel of protein expression, mRNA expression, and promoter transcriptional activity of glutamate-cysteine ligase catalytic subunit(GCLC) were further detected. Results GSH contents decreased because of adenovirus E1A expression in oxidant stress. E1A repressed the expression and activity of γ-GCS, messenger RNA expression, and promoter transcriptional activity of GCLC. Conclusion Adenovirus E1A decreased the activity of γ-GCS probably by repressed promoter transcriptional activity of GCLC. As a result, GSH contents were downregulated in oxidant stress. Thus Adenovirus latent infection amplified the oxidant/antioxidant imbalance in rat alveolar epithelial cells in oxidants stress, which may be an important mechanism of COPD.

Objective To observe the changes of respiratory musc]e strength by traditional Chinese medicine combined with cholinesterase inhibitors in myasthenia gravis (MG) patients.Methods Thirty-four cholinesterase inhibitor-resistant patients,of them 14 were MG patients with stage Ⅰ ,and 20 were stage Ⅱ ,were treated with bromide dimethylcarbamate ( 360-480 mg/d ).Traditional Chinese potion were administered in those without effectiveness,and the dosages of bromide dimethylcarbamate decreased with Traditional Chinese potion lasting for 4-6 months.Vital capacity ( VC ),maximal voluntary ventilation ( MVV ),maximal inspiratory pressure ( PIM ),maximal expiratory pressure ( PEM ),respiratory centre driving pressure ( P0.1 ),residual volume ( RV )were measured before and after treatment.Results The amelioration of VC,MVV,PIM,PEM,P0.1 ,RV,respiratory muscle strength and other indicators of 34 MG patients were not obviously after treatment with cholinesterase inhibitor alone ( P ＞ 0.05 ).After treatment with traditional Chinese medicine combined with cholinesterase inhibitors,VC,MVV,PIM,PEM ( before treatment:76.66% ± 18.59%,68.03 % ± 10.45 %,43.25 % ± 18.16%,21.75 % ±14.44% ) increased significantly in all 34 MG patients( after treatment:86.91% ± 14.87% ,75.11% ± 11.17%,52.66% ±20.32% ,28.56% ± 10.06% ) ( P ＜ 0.05).RV decreased from 164.94% ± 67.97% to 143.16% ±79.21% (P ＜0.01 ),and respiratory muscle strength,endurance and other indicators significantly improved (P ＜0.01).PIM(65.80% ±28.03% to 52.66% ±20.32%),and PEM (37.03% ±20.57% to 28.56% ±10.06%)improved more significantly in group stage than in group stage (P ＜0.01 ).Respiratory muscle endurance in stage Ⅰpatients ( 108.71% ± 17.56% ) improved significantly than stage Ⅱ patients (96.01% ± 14.12% ,P ＜ 0.01 ).Conclusions Traditional Chinese medicine combined with cholinesterase inhibitors could effectively improve the lung function and respiratory muscle strength in patients with resistance of the cholinesterase inhibitors.The improvement of lung function,respiratory muscle strength were more obviously in stage Ⅰ patients than in stage Ⅱ patients.Respiratory muscle strength and endurance were improved greater in stage Ⅱ than in stage Ⅰ patients.

ObjectiveTo explore the therapeutic effect of continuous veno-venous hemofiltration (CVVH) on the treatment of severe acute pancreatitis (SAP).MethodsAll data about forty-five patients with SAP admitted to the intensive care unit (ICU) from June 2005 through June 2010 were reviewed.These 45 patients were randomly (random number ) divided into routine treatment group (n =22 )and comprehensive treatment group ( n =23 ).In control group,patients were rapidly given with a suffficient liquid support,vasoactive drug to increase organ perfusion,trypsin secretion inhibitor,broad-spectrum antibiotics,enteral nutrition with intestine membrane protective agent in early stage.In the comprehensive treatment group,patients received CVVH integrated with routine treatment.On admission and 72 h posttreatment,the scores of acute physiology and chronic health evaluation Ⅱ ( APACHE Ⅱ ) and multiple organ dysfunction syndrome (MODS),and the results of standard bettery of biochemistry tests indcluding blood urea nitrogen (BUN),serum cratinine (Scr),total bilirubin (TBIL),alanine aminotransferase (ALT),amylase (AMS),C-reactive protein (CRP),TNF-α,IL-6,IL-8 were observed.Time of mechanical ventilation support,length of ICU stay,and survival rate were compared between two groups.ResultsOn admission between the two groups,no statistical significance was seen in the APACHE Ⅱ and MODS score,BUN,Scr,TBIL,ALT,AMS,CRP,TNF-α,IL-6,IL-8 (P ＞ 0.05).But APACHE Ⅱ and MODS score were decreased significantly in comprehensive treatment group than in the routine treatment group,as well as the the level of BUN,Scr,TBIL,ALT,AMS,TNF-α,IL-6,IL-8 and CRP after 72h post-treatment (P＜0.05 ).In routine treatment group and comprehensive treatment group,the time of respirator intervention and length of stay in ICU were (7.6±3.4) d vs.(11.5±4.7) d,(12.3±7.8) dvs.(17.6±9.2) d respectively,the statistical significance was shown ( P ＜ 0.05 ).Compared to the comprehensive treatment group ( 86.96％ ),the survival rate ( 59.09％ ) were lower in routine treatment group ( P ＜ 0.05 ).ConclusionsCVVH combined with routine treatment,which can remove inflammatory agents and toxins,maintain homoeostasis,and improve oxygenation,is effective in treatment of SAP and can improve patient survival rate.

Objective To explore the role of LiCl in microbial suppurative keratitis .Methods Western-blot assay was used to detect the efficacy of LiCl .Inflammatory cytokine levels were examined using Real-time PCR .Cell apoptosis was detected by using TUNEL and flow cytometry assays .Results LiCl promoted corneal resistance to PA infection .Real-time PCR data showed that LiCl enhanced IL-10 expression ,but suppressed TNF-expression .TUNEL and flow cytometry data showed that LiCl promoted the apoptosis of infiltrating cells .Conclusion LiCl promoted host resistance against microbial suppurative keratitis ,via regulating in-flammatory cytokine expression and cell apoptosis .

AIM:To observe the influence of adenovirus latent infection on the oxidant/antioxidant balance in rat alveolar epithelial cells.METHODS:The rat alveolar epithelial cells were stably transfected with the plasmid pE1Aneo and control plasmid pneo.GSH and MDA contents,the activities of major anti-oxidative enzymes including SOD,CAT,GPx,GST and ?-GCS were detected in oxidant stress.RESULTS:Adenovirus E1A expression repressed the activity of ?-GCS,and decreased GSH contents in oxidant stress.As a result,the activity of GPx and GST was decreased.The contents of MDA maintained high in oxidant stress.CONCLUSION:Adenovirus latent infection amplifies the oxidant/antioxidant imbalance in rat alveolar epithelial cells in oxidants stress,and adenovirus E1A protein decreases the activity of ?-GCS,which plays an important role in this process.

Objective To define the loci of the mutant gene in the loop-tail mouse.Methods To study the heredity pattern, loop-tail mice were mated with normal C57BL/6J and C3H mice.Their offsprings with loop-tail or normal phenotype were registered respectively.Microsatellite marker D1Mit113 and D1Mit149 were used to locate the mutant gene.Based on fine mapping, the candidate gene Vangl2 was found.Vangl2 gene from the loop-tail mice was amplified by PCR followed by sequencing.Incision enzyme FspBI ( BfaI ) identified the genotype of offspring from loop-tail mice intercrossing.Results Heredity test indicated that the loop-tail phenotype was controlled by a single dominant gene not with 100%penetrance but was affected by genetic background.A C-to-T transversion was at the 1345bp in Vangl2 gene of the loop-tail mice.Conclusions The C-to-T transversion introduces a pre-termination codon of amino acids and causes the phenotype of loop-tail phenotype.None homozygous mice were found in the offsprings, suggesting that the homozygous mice are lethal.

Streptococcus pneumoniae(S.pn) is an opportunity pathogenic bacteria,environmental factors play a key role in the pathogenicity of S.pn. It is important to study virulent gene in vivo. The S.pn suicide plasmid containing gfp reporter was constructed by fusing the genes pneumolysin and gfp,in which gfp is an excellent molecule probe in vivo. The plasmid was integrated to No.22 S.pn by homologous recombination. The recombinant S.pn was gained and evaluated in aspects of fluorescence excitation, biological character and physio-activity. The results showed it is efficient and available to report the expression of virulent genes in vivo and in vitro, which will provide a new easy method for evaluating and screening the virulent genes of S.pn in vivo.

Objective To investigate the association of the major histocompatibility complex class Ⅰ chain-related antigens A (MICA)-129 gene polymorphism and soluble MICA (sMICA) levels with ulcerative colitis (UC) in Hubei Han nationality. Methods The genetic polymorphism of MICA-129 was examined using a polymerase chain reaction-sequence based test (PCR-SBT) in 256 UC patients and 460 healthy controls. From the above subjects, 80 patients and 90 healthy individuals were randomly selected for determining serum sMICA concentrations by ELISA. Results The frequencies of variant allele (G) and genotype (GG) in MICA-129 gene were significantly higher in the UC patients than in the controls(76. 8%vs 72. 2%, P =0. 060; 55.9% vs 46. 3% ,P =0. 016). Serum sMICA levels were significantly elevated in the patients compared to the controls[(576. 47 ±279. 02) ng/L vs( 182. 17 ±73. 11 ) ng/L,P ＜0. 001]. In addition, the sMICA levels were higher in the patients carrying MICA-129 GG genotypes than in those carrying ( GA + AA) genotypes [( 638. 87 ± 347. 15 ) ng/L vs ( 507. 51 ± 152. 87 ) ng/L, P = 0. 035].Conclusions The genetic polymorphism of MICA-129 and sMICA levels are correlated with the UC patients in Hubei Han nationality. Our findings demonstrate that MICA-129 gene may contribute to the pathogenesis of UC.