BAFF is an essential ligand essential for survival and differentiation of peripheral B cells. By interacting with three receptors, BAFF can promote B cell maturation and class switching, enhance humoral immunity and T cell co-stimulation. Over-expression of BAFF leads to autoimmune diseases such as systemic lupus erythematosus (SLE) in mouse model. Treating the mice model with BAFF antagonists can slow-down disease progression and enhance survival rate. Moreover, in some SLE patients serum level of BAFF is elevated and correlated with serum anti-dsDNA titer. The preliminary clinical trial of anti-BAFF monoclonal antibody has shown to be safe and effective. BAFF antagonists are promising therapeutic drugs for SLE.

Objective To detect of clostridium perfringens by qPCR in mouse models and a clinical case in order to offer early diagnosis.Methods 40 Kunming mice were randomly grouped and intramuscular injected clostridium perfringens type A in leg 0.1 ml(3.5 × 109cfu/ml or 3.5 × 108cfu/ml or 3.5× 107cfu/ml,diluted with saline),while control group was injected with 9% sodium chloride 0.1ml.The mouse models and a clinical case were detected by qPCR.Results The death rate of 3.5 × 109,3.5 × 108,3.5 × 107cfu/ml and the blank group were 90%,70%,10% and 0% after intramuscular injection for 72 h spectively.The mean Ct values among these groups were 21.21 ±2.69,28.45 ±2.74,32.49 ±2.87 and 0.00 ± 0.00(P ＜ 0.05).The Ct values of the patient were 30.67 and 30.44.Conclusions Cclostridium perfringens could be successful identified with qPCR in mouse models when the mice still did not show any symptoms.

Objective To compare the phenotypes of abnormal CD4+CD25-Foxp3+ T cells with traditional regulatory T cells (CD4+CD25+Foxp3+) in patients with untreated new-onset lupus (UNoL) and investigate their clinical relevance. Methods The expressions of surface markers (CD25, CD127, CCR4, GITR, CTLA-4) and intracellular marker(Foxp3) on the peripheral blood mononuclear cells from twenty-two UNoL patients were analyzed by flow cytometry analysis, and their clinical relevance were assessed. Results There were no significant differences between CD4+CD25-Foxp3+ and CD4+CD25+Foxp3- T cells in the expressions of GITR, CTLA--4 and CCR4 (P>0.05), but they were significantly lower than those of CD4+CD25+ Foxp3+ T cells in UNoL patients (P<0.01). The percentages of CD127low- in CD4+Foxp3+CD25high,CD4+Foxp3+ CD25low and CD4+Foxp3+CD25+ T cells were (93.8±3.5 )%, (93.7±2.3)% and (92.0±2.1)% respectively (P> 0.05), whereas the expressions of Foxp3 on CD4+CD127low- T subpopulations showed significant differences in CD4+CDI27low-CD25high (91.4±2.6)%, CD4+CD127low-CD25low (71.9±3.3)% and CD4+CD127low-CD25- (9.0± 2.2)% T cells(P<0.01 ). The frequency of CD+CCR4+CD25high T cells correlated negatively with SLEDAI (r=-0.695,P<0.001).and it was significantly lower in lupus nephritis patients(1.10±0.17)%compared with SLE patients without nephritis [(1.61±0.23)%,P<0.01]and healthy controls [(1.75±0.10)%,P<0.01], furthermore,the frequency of CD4+CCR4+CD25low-T cells in lupus nephritis was significantly higher than that in healthy controls[(11.5±2.3)%vs (8.0±1.0)%,P<0.01].Conclusion The increased CD4+CD25-Foxp3+ T cells in the Untreated Newonset Lupus(UNoL)patients mimic activated T effector cells.CD4+CD25high-CD127low-T cells can be used to isolate live CD4+CD25highFoxp3+regulatory T cells.CCR4+regulatory T cells may be involved in the pathogenesis of lupus nephritis.

Objective To identify the association between fatigue and depression in Parkinson's disease(PD).Methods 56 PD patients were enrolled in this study.The degree of fatigue was measured by Fatigue Severity Scale (FSS).Hamilton Depression Scale (24 items) was used to evaluate the degree of depression.PD Quality of Life Questionnaire (PDQL) were tested to evaluate the quality of life in PD patients.While other clinical information such as Unified Parkinson's Disease Rating Scale (UPDRS) Ⅲ,Hoehn-Yahr Scale and modified Webster Scale were investigated.Results The incidence of fatigue in this group is 71.4％ (40/56).Score of HAMD and PDQL exhibited a significant correlation to patients' fatigue,coefficient of partial correlation was 0.451 (P ＜ 0.01),-0.346 (P ＜ 0.05).The incidence of fatigue in non-depressive patients was low,27.3 ％.While in depressive patients,the incidence of fatigue is relatively high,for mild depression 75％,moderate depression 100％,severe depression 100％ respectively.Conclusions Fatigue is a prominent symptom of depression in PD patients,sometimes independent of depression also influencing the patients' quality of life.

Objective To investigate the effects of Thalidomide(THD)on transdifferentiation of human fetal lung fibroblast(HFL-F) to myofibroblast(MF) induced by Transforming Growth Factor-?1(TGF-?1) and the effects on trans differentiated MF.Methods HFL-F to MF trans-differentiation was induced with 5 ?g/L TGF-?1.The effect of 50 ?g/L THD on HFL-F to MF transdifferentiation was evaluated by measuring hydroxyproline(HYP) content with alkaline hydrolysis colorimetry,?-smooth muscle actin(?-SMA) protein with Western Blot,?-SMA and collagen Ⅲ(COL Ⅲ) mRNA with semiquantitative RT-PCR.Results THD inhibited TGF-?1 induced up-regulation of HYP and COLⅢ mRNA expressions(all P0.05).For HFL-F treated with 5 ?g/L TGF-?1 for 96 h,THD inhibited COLⅢ mRNA expression(P

Objective To investigate that p53 expression in fibroblast-like synoviocytes (FLS) and its effects on CD4+ T lymphocytes from active rheumatoid arthritis (RA) patients. Methods Human FLS was transfected with p53siRNA and cocultured with CD4+ T lymphocytes from active RA patients. The expression of osteoprotegerin and IL-6 secretion was detected in the transfected FLS. In addition, the expressions of IFN-γ, IL-17, IL-4 and CD25 as well as mRNA levels of IFN-γ RORγt, IL-17 and Foxp3 in cocuhured CD4+ T lymphocytes were also measured. Results IL-6 secretion decreased in p53-inhibited FLS while osteopro-tegerin expression was not altered, p53-inhibited FLS could significantly increase IL-17 and IFN-γ expres-sions. It also upregulated Foxp3 expression though had no effect on CD4+CD25high T lymphocytes. Conclusion p53 expression in FLS regulates Th1 and Th17 cells of RA patients, and therefore participate in the pathogenesis of RA.

Objective To evaluate the effect of angiotensin Ⅱ ( Ang Ⅱ ),angiotensin- (1-7) [ Ang- ( 1-7 ) ],and co-action of Ang Ⅱ and Ang-( 1-7 ) on β cell insulin signaling pathway.Methods Mouse pancreatic β cell line NIT-1 was incubated with( 1 )0,10-7,10-6,10-s,10-4 mol/L concentrations of Ang Ⅱ for 24 h ; ( 2 )0,10-7,10-6,10 -5,10-4 mol/L concentrations of Ang- ( 1-7 ) for 24 h; ( 3 ) co-administration of Ang Ⅱ and Ang- ( 1-7 ) was divided into control,10-5mol/L Ang Ⅱ,10-6mol/L Ang-( 1-7 ),10-5mol/L Ang Ⅱ + 10-6mol/L Ang-( 1-7 ) group.Tyrosine phosphorylation of insulin receptor β subunit(IR-β-Tyr) and serine phophorylation of protein kinase B(Akt-Ser) were detected by Western blot.ResultsInsulin-stimulated IR-β-Tyr and Akt-Ser phosphorylation was significantly decreased in Ang Ⅱ 10-5 and 10-4 mol/L group; no significant changes in insulin-stimulated IR-β-Tyr and Akt-Ser phosphorylation were detected between Ang-( 1-7 ) treatment groups and control; Ang-( 1-7 ) blocked the inhibitory effect of Ang Ⅱ on Akt-Ser phosphorylation,yet exerted no effect on Ang Ⅱ-induced IR-β-Tyr phosphorylation inhibition.Conclusion Ang Ⅱ significantly inhibits insulin signaling pathway in β cell; Ang-( 1-7 ) reverts the inhibitory effect of Ang Ⅱ on insulin-stimulated Akt-Ser phosphorylation in β cell.

Objective To identify a novel pathogenicity mutation of acid alpha‐glucosidase(GAA) gene in a Chinese family with two siblings affected with juvenile onset form glycogen storage disease Ⅱ(GSD Ⅱ) .Methods The clinical and family data of two siblings presenting recurrent respiratory tract infections ,respiratory failure associated with systemic muscle weakness ,were an‐alyzed and diagnosed with GSD Ⅱ by detecting alpha‐1 ,4‐glucosidase activity .DNA was extracted from peripheral blood of the proband ,younger brother and his parents .All 20 exons and the intron‐exon splice sites of GAA gene were amplified by polymerase chain reaction (PCR) .Mutations were detected by direct sequencing the PCR products .Results The younger brother was found to be compound heterozygous for two mutations in the GAA gene :c .1216G>A (p .Asp406Asn) missense mutation in the exon 8 from his father and c .1935C>A (p .Asp645Glu) missense mutation in the exon 14 from his mother .Conclusion The compound hetero‐zygous c .1216G>A and c .1935C>A mutations caused the juvenile onset form GSD Ⅱ characterized by dyspnea and cardiac hyper‐trophy .The novel c .1216G>A mutation may be related to the juvenile onset form GSD Ⅱ .

Objective To perform the sample survey on the recognition degree of abdominal compartment syndrome (ACS) among domestic pediatric healthcare providers (PHCP) Methods Three hundred self‐designed questionnaires were distributed to the participants at the twelfth Chinese Medical Association Congress of Pediatric Critical Care Medicine in November 2011 .Results A total of 194 effective questionnaires were reclaimed with the recovery rate of 64 .7% .28 .9% (56/194)of respondents did not heard of ACS .49 .5% (96/194)of them heard of ACS ,but did not contact ACS .Only 21 .6% (42/194)of respondents were well fa‐miliar with ACS .Among the medical staffs who were aware of ACS (familiar or just heard of ) ,only 7 .2% (10/138)knew the real definition of ACS .83 .3% (35/42) of respondents who were familiar with ACS used the intravesical route to measure the intra -ab‐dominal pressure(IAP) .However ,only 57 .1% (20/35)of respondents knew the correct saline volume for measuring IAP .Conclusion The recognition degree of ACS is low among domestic PHCP .It is necessary to strengthen the ACS related education among do‐mestic PHCP for increasing the awareness of ACS and promoting its treatment .

Objective · To explore the biological characteristics of platelet-rich fibrin (PRF) and its effects on proliferation and differentiation of adipose derived stem cells (ADSCs). Methods · The whole blood was collected from the forelimb vein of healthy beagles to prepare the PRF membrane, which were observed with optical microscope and scanning electron microscope. ADSCs were collected from the inguinaladipose tissue and were isolated and cultured. Identification of multi-directionaldifferentiation potential was performed. ADSCs were assigned to the PRF group and the control group, the former was treated with PRF in vitro. Cell proliferation wasmeasured with CCK-8. Osteogenesis induction was performed for two groups and the expression of genes associated with osteogenesis, including osteocalcin (OCN), osteopontin (OPN) and collagen I (Col- Ⅰ ), was measured with RT-PCR before induction and 4 and 7 days after induction. The alkaline phosphatase (ALP) activitywas measured 7 days after induction. Results · PRF is a milk white fibrin glue with elasticity and toughness. PRF can form loose and porous three dimensional network structure, which harbors lots of platelets and leucocytes. The cell proliferation activity was significantly higher in the PRF group than in the control group. After osteogenesis induction, the ALP activity and the mRNA levels of OCN, OPN, and Col- Ⅰ were significantly increased. Conclusion · PRF is a fibrin glue with three dimension network structure and contains lots of platelets, which can slowly release growth factors. PRF can promote the proliferation and osteogenic differentiation of ADSCs.