ObjectiveTo determine the serum level of anti-aminoacyl-tRNA synthetase (ARS)antibody in patients with polymyositis (PM) and dermatomyositis (DM) and to investigate the value of anti-ARS antibody for diagnosing interstitial lung diseases(ILD) in patients with PM/DM compared with anti-Jo-1 antibody.MethodsSerum anti-ARS antibody concentrations were measured by ELISA in 109 adult PM/DM patients,20 patients with SLE,20 patients with RA and 50 healthy controls.T test,Mann-Whitney U test,chi-square test or Fisher exact test were used to compare the sensitivity and specificity for diagnosing ILD in PM/DM patients between anti-ARS antibody and anti-Jo-1 antibody.Moreover,McNemar test was employed to analyze the correlation between the clinical features and anti-MDA5 antibody in PM/DM patients.Results The serum positive rate of anti-ARS antibody was 37.9％,7.8％,10％,0 and 0 in PM/DM patients with ILD and without ILD,patients with SLE and RA and healthy controls,respectively.Serum anti-ARS antibody levels and positive rate in the PM/DM patients with ILD were significantly higher when compared with PM/DM patients without ILD,patients with SLE and RA and healthy controls (X2=-13.5,5.45,10.57,15.17; P＜0.01 ).Anti-ARS antibody presented a significantly higher sensitivity for diagnosing ILD in patients with PM/DM compared to anti-Jo-1 antibody (P＜0.01).The rate of fever and ILD were significantly higher in anti-ARS positive group than anti-ARS negative group(X2=12.55,13.53; P＜0.05),while heliotrope rash and shawl sign occurred more often in anti-ARS negative group(X2=5.7,5.8; P＜0.05).Additionally,follow-up study showed that the serum anti-ARS antibody were all negative in nine patients who died of PM/DM with ILD (P＜0.05).ConclusionSerum anti-ARS antibody is a stronger predictor for early diagnosis of PM/DM with ILD compared to anti-Jo-1 antibody.The detection of anti-ARS antibody can be widely applied to clinical practice.

Objective:To investigate the expression of activin A in paraventricular nucleus (PVN)of the WKY rats and its influence in arterial blood pressure,and to clarify the mechanism of activin A in the regulation of arterial blood pressure by PVN.Methods:The WKY rats were selected.The expressions of activin A,ActRⅡA,ActRⅡB,and Smads mRNA in PVN of the WKY rats were measured by RT-PCR.The expression of ActRⅡA protein in PVN was detected by immunohistochemical staining.The microinjection of exogenous activin A into PVN was used to observe the changes of arterial blood pressure.The primary cultured PVN neurons from the WKY rats were divided into control group and activin A group.The mRNA expression levels of ActRⅡA,ActRⅡB,and Smads in the PVN neurons were analyzed by RT-PCR.Results:Activin A,ActRⅡA,ActRⅡB,Smad2 and Smad3 mRNA were expressed in PVN of the WKY rats.The ActRⅡ A protein expression in PVN was further confirmed by immunohistochemical staining.After microinjection of activin A or angiotensin Ⅱ (AgⅡ)into PVN,the mean arterial blood pressure was increased obviously compared with before treatment (P <0.05).Moreover,compared with control group,the expression levels of ActRⅡA and Smad3 mRNA in primary cultured PVN neurons of the rats in vitro were significantly increased (P <0.05).Conclusion:Activin A can regulate the arterial blood pressure in PVN in an autocrine or paracrine manner,which is related to ActRⅡA-Smad3 signal pathway.

Objective To identify the accurate measurement of glomerular filtration rate (GFR) in chronic glomerulonephritis (CGN)patients. Methods Forty-two patients were enrolled in the study, including 15 females with age from 18 to 73 years old (mean 46 years old) and 27 males with age from 20 to 77 years old (mean 48 years old). The methods used for measuring GFR were classical dual plasma sample clearance method (tGFR), considered to be the gold standard,renal dynamic imaging method (dGFR), 24-hour creatinine clearance method (24hCcr). The difference and correlation amony them were analyzed. When the difference was significant, Pearson correlation and linear regression analysis were further performed. The difference of GFR detected by dGFR between left and right kidney of patients was compared simultaneously. A two-sided P value＜0.05 was considered as statistically significant. Results Either dGFR or 24hCcr was statistically different from tGFR, but had excellent correlation with tGFR, and the coefficient was 0.916 (P=0.000) and 0.957 (P=0.000) respectively. The linear regressions correlation existed and the regression equations were tGFR=0.936 dGFR-4.648 (F=208.941, P=0.000), tGFR =0.887 24hCcr+2.919 (F=376.513, P=0.000) respectively. Difference had not statistically significance between left and right kidney of patients (P=0.591). Conclusions Neither dGFR nor 24hCcr can substitute tGFR, but both can reflect the GFR of the CGN patients safely and effectively. The decrease of GFR is homochronous for left and right kidney of CGN patients. Therefore, the 24hCcr can be chosen to evaluate the GFR in the hospitals without SPECT.

Objective To establish model of the chicken embryo transplantation of human colon cancer cells ,and investigate the effect of Solanine、VEGF antibody and Solanine combined with VEGF antibody on human colon cancer cells induce tumor angio‐genesis and tumor proliferation .Methods The model of the chicken embryo transplantation of human colon cancer HT‐29 cells were divided into three experimental group and control group .We added to the chick embryo chorioallantoic membrane with Sola‐nine、VEGF antibody and Solanine+ VEGF antibody mixture ,PBS was added to the control group .Then we analysed picture through the stereomicroscope and IPP 6 .0 image analysis software ,using immunohistochemistry envision method to detect of CD34 antigen and ki‐67 antigen ,and observing effect of Solanine group ,VEGF antibody group ,Solanine+ VEGF antibody group and the effect on the tumor angiogenesis and tumor proliferation .Results The tumor angiogenesis ,CD34 antigen and ki‐67 antigen of Sola‐nine+VEGF antibody group were significantly better than those of VEGF antibody group and Solanine group(P<0 .01);VEGF antibody group had statistical significant difference with Solanine group(P<0 .01);the effect of other three groups were better than that of the control group(P<0 .01) .Conclusion Solanine、VEGF antibody and Solanine combined with VEGF antibody could in‐hibit tumor angiogenesis and tumor proliferation of human colon cancer cell line HT‐29 to induce .It provides a new way for anti‐an‐giogenes .

Objective:To investigate the content and mode of pharmaceutical care for the patients with severe burn and promote the rational use of drugs. Methods:Taking the treatment for one patient with severe burn as example,pharmacists provided pharmaceu-tical care in respects of anti-infection therapy,organ preservation,nutritional support, drug interactions, drug precautions, drug incom-patibility, adverse drug reactions and the effect evaluation . Results:The program of rational drug use was provided for clinics through the implementation of pharmaceutical care. The vital signs of the patient were stable, and then the patient left on pass and continued to be treated with rehabilitation therapy. Conclusion:It is necessary for clinical pharmacists to perform pharmaceutical care for the pa-tients with severe burn,reduce the abuse of drugs and improve the medication safety and effectiveness. Meanwhile, the collaborative service of doctors,pharmacists,nurses and inspectors to patients reflects the value of clinical pharmacists.

Objective To observe the effects of salidroside regulating glucose metabolism in type 2 diabetic mice,then to explore the molecular mechanism. Methods Type 2 diabetes model was induced by feeding high-fat diet and intraperitoneal injecting STZ to male C56BL/6J mice,then the glucose related indexes,micro RNA-370 levels in the serum and liver tissue and the expression of gluconeogenesis key protein(G6Pase and PEPCK) in the liver tissue to observe the treatment effects of salidro-side on type 2 diabetic-caused gluose metabolic disorder.In cell test,we isolated primary hepatocytes,then silenced or over-ex-pressed micro RNA-370 in mouse primary hepatocytes to observe the molecular mechanism of glucose metabolic regulation of the micro RNA-370 and salidroside. Results Treated with salidroside 40,80 and 160 mg·kg-1,the results showed that compared with the model control group,the glucose related indexes were all improved significantly.The relative expression levels of micro RNA-370 in serum and liver,and that of PEPCK and G6Pase all reduced in different degrees,dose-dependently.The changes of middle and high dose group decreased significantly(P<0.05),that of low dose group had a decreasing trend but no statistically significant.In the cell test,compared with the normal control group,salidroside alone group and micro RNA-370 inhibitor group were able to reduce the protein expression level of PEPCK and G6Pase(P<0.05),micro RNA-370mimic alone group can signifi-cantly increase the protein expression level of PEPCK and G6Pase(P<0.05),compared with the micro RNA-370mimic alone group,combining micro RNA-370 mimic and salidroside can significantly reverse the increasing caused by micro RNA-370 mimic alone(P<0.05). Conclusion Our research found that salidroside can improve glucose metabolism disorder in type 2 diabetic mice,and at least in part,through the suppression of micro RNA-370 expression for the first time.

Although the functions of metabolic enzymes and nuclear receptors in controlling physiological homeostasis have been established, their crosstalk in modulating metabolic disease has not been explored. Genetic ablation of the xenobiotic-metabolizing cytochrome P450 enzyme CYP2E1 in mice markedly induced adipose browning and increased energy expenditure to improve obesity. CYP2E1 deficiency activated the expression of hepatic peroxisome proliferator-activated receptor alpha (PPARα) target genes, including fibroblast growth factor (FGF) 21, that upon release from the liver, enhanced adipose browning and energy expenditure to decrease obesity. Nineteen metabolites were increased in Cyp2e1-null mice as revealed by global untargeted metabolomics, among which four compounds, lysophosphatidylcholine and three polyunsaturated fatty acids were found to be directly metabolized by CYP2E1 and to serve as PPARα agonists, thus explaining how CYP2E1 deficiency causes hepatic PPARα activation through increasing cellular levels of endogenous PPARα agonists. Translationally, a CYP2E1 inhibitor was found to activate the PPARα-FGF21-beige adipose axis and decrease obesity in wild-type mice, but not in liver-specific Ppara-null mice. The present results establish a metabolic crosstalk between PPARα and CYP2E1 that supports the potential for a novel anti-obesity strategy of activating adipose tissue browning by targeting the CYP2E1 to modulate endogenous metabolites beyond its canonical role in xenobiotic-metabolism.