Comparison and correlation study of synovial ultrasound indices and serum VEGF in rheumatoid wrist arthritis before and after treatment.

OBJECTIVE: Rheumatoid wrist arthritis is a chronic autoimmune disease, resulting in joint deformity and functional impairment. We aimed to compare the wrist synovial ultrasound indices and serum vascular endothelial growth factor (VEGF) level in patients with RA before and after treatment, and to explore the correlation between the two. METHODS: Forty patients with RA in wrist underwent ultrasound examination to determine wrist synovial thickness, synovial blood flow grade, and synovial artery resistive index (RI) before and after treatment. The serum level of VEGF was detected by enzyme-linked immunosorbent assay. Correlation between synovial ultrasound indices and serum VEGF level was assessed. RESULTS: Pre-treatment synovial thickness, synovial artery RI, and serum VEGF level were 8.60 ± 2.82 mm, 0.62 ± 0.07, and 419.49 ± 19.27 pg/mL, respectively. The corresponding post-treatment levels were 4.05 ± 1.89 mm, 0.83 ± 0.10, and 199.30 ± 16.18 pg/mL. Pre-treatment distribution of synovial blood flow grades was as follows: grade 0, nil; grade I, 1 case; grade II, 17 cases; grade III, 22 cases. The post-treatment distribution was as follows: grade 0, 6 cases; grade I, 23 cases; grade II, 11 cases; and grade III, nil. There were significant differences between pre- and post-treatment wrist synovial thickness, artery RI, and blood flow grading. Wrist synovial thickness and synovial blood flow grade showed a strong positive correlation with serum VEGF level (P < 0.01). There was strong negative correlation between wrist synovial artery RI and serum VEGF level (P < 0.01). CONCLUSION: The strong correlation between wrist synovial ultrasound indicators and serum VEGF may be clinically useful for diagnosis and therapy.

The therapeutic effect of CORM-3 on acute liver failure induced by lipopolysaccharide/D-galactosamine in mice.

BACKGROUND: Acute liver failure (ALF) is a severe and life-threatening clinical syndrome resulting in a high mortality and extremely poor prognosis. Recently, a water-soluble CO-releasing molecule (CORM-3) has been shown to have anti-inflammatory effect. The present study was to investigate the effect of CORM-3 on ALF and elucidate its underlying mechanism. METHODS: ALF was induced by a combination of LPS/D-GalN in mice which were treated with CORM-3 or inactive CORM-3 (iCORM-3). The efficacy of CORM-3 was evaluated based on survival, liver histopathology, serum aminotransferase activities (ALT and AST) and total bilirubin (TBiL). Serum levels of inflammatory cytokines (TNF-alpha, IL-6, IL-1beta and IL-10) and liver immunohistochemistry of NF-kappaB-p65 were determined; the expression of inflammatory mediators such as iNOS, COX-2 and TLR4 was measured using Western blotting. RESULTS: The pretreatment with CORM-3 significantly improved the liver histology and the survival rate of mice compared with the controls; CORM-3 also decreased the levels of ALT, AST and TBiL. Furthermore, CORM-3 significantly inhibited the increased concentration of pro-inflammatory cytokines (TNF-alpha, IL-6 and IL-1beta) and increased the anti-inflammatory cytokine (IL-10) productions in ALF mice. Moreover, CORM-3 significantly reduced the increased expression of iNOS and TLR4 in liver tissues and inhibited the nuclear expression of NF-kappaB-p65. CORM-3 had no effect on the increased expression of COX-2 in the ALF mice. An iCORM-3 failed to prevent acute liver damage induced by LPS/D-GalN. CONCLUSION: These findings provided evidence that CORM-3 may offer a novel alternative approach for the management of ALF through anti-inflammatory functions.

Analysis on the interaction domain of VirG and apyrase by pull-down assay.

VirG is outer membrane protein of Shigella and affects the spread of Shigella. Recently it has been reported that apyrase influences the location of VirG, although the underlying mechanism remains poorly understood. The site of interaction between apyrase and VirG is the focus of our research. First we constructed recombinant plasmid pHIS-phoN2 and pS-(v1-1102, v53-758, v759-1102, v53-319, v320-507, v507-758) by denaturation-renaturation, the phoN2:kan mutant of Shigella flexneri 5a M90T by a modified version of the lambda red recombination protocol originally described by Datsenko and Wanner and the complemented strain M90TΔphoN2/pET24a(PhisphoN2). Second, the recombinant plasmid pHIS-phoN2 and the pS-(v1-1102, v53-758, v759-1102, v53-319, v320-507, v507-758) were transformed into E. coli BL21 (DE3) and induced to express the fusion proteins. Third, the fusion proteins were purified and the interaction of VirG and apyrase was identified by pull-down. Fourth, VirG was divided and the interaction site of apyrase and VirG was determined. Finally, how apyrase affects the function of VirG was analyzed by immunofluorescence. Accordingly, the results provided the data supporting the fact that apyrase combines with the α-domain of VirG to influence the function of VirG.

[Protective effect of Tongxinluo Ultramicro-pulverization on experimental myocardial infarction of rats].

OBJECTIVE: To study the effects of Tongxinluo ultramicro-pulverization (TXLU) on experimental myocardial infarction and platelet aggregation of rats, investigate its mechanisms on ischemia heart disease and offer a reference to clinical usage. METHOD: Rats were separated randomly into 7 groups: sham, model, diltiazem (0.15 mg x kg(-1)), TXL(1.2 g x kg(-1)), TXLU (1.2, 0.6, 0.3 g x kg(-1)). The experimental myocardial infarction was induced with ligating the left anterior descending branch of the coronary of rats. The infarction size was determined after myocardium tissue was stained with 2,3,5-triphenyltetrazolium chloride (TTC). And the serum of rats was separated to analyze CK, LDH, SOD, MDA. Another 60 rats were separated randomly into 6 groups: control, aspirin (0.15 mg x kg(-1)), TXL (1.2 g x kg(-1)), TXLU (1.2 ,0.6,0.3 g x kg(-1)). The rat platelet aggregation was induced with adenosine diphosphate (ADP) and collagen to observe the inhibitory effects of TXLU. RESULT: TXLU could relieve the myocardial infarction size and weight stained with TTC significantly, the myocardial infarction size of the three groups of TXLU were (2.7 +/- 2.1)%, (3.4 +/- 1.2)%, (2.8 +/- 1.8)%, compared with model group (8.9 +/- 5.9)%, P < 0.05 or P < 0.01. The myocardial infarction weight of the three groups of TXLU were (8.4 +/- 3.5)%, (8.7 +/- 4.1)%, (9.7 +/- 4.1)%, compared with model group (l2.2 +/- 3.6)% P < 0.05 or P < 0. 01. And the content of MDA and the activities of CK and LDH in rats subjected with ligation of coronary artery were inhibited obviously too, compared with model group P < 0.05 or P < 0.01, then the activity of SOD increased. TXLU could inhibit the maximum percentage of rats platelet aggregation induced with ADP and collagen, the maximum percentage of platelet aggregation induced with ADP were (26.9 +/- 9.2)%, (24.4 +/- 13.4)%, (30.6 +/- 12.2)%, compared with control group (44.3 +/- 15. 7)% P < 0.05 or P < 0.01; The maximum percentage of platelet aggregation induced with collagen were (33.8 +/- 6.9)%, (32.1 +/- 8.3)%, (41.5 +/- 7.8)%, compared with control group (49.2 +/- 15.9)%, P < 0.05 or P < 0.01. CONCLUSION: The experiment results indicated that TXLU could protect myocardial tissue of rats from ischemic injury and the mechanism may be related with antioxidation and inhibiting platelet aggregation, and the results also suggested TXLU could lower clinical dosage.