Objective To understand the clinical profiles of arthritis after human parvovirus B19(B19) infection.Methods Four cases were described and the clinical and laboratory characteristics were analyzed. Results The median onset age of the 4 patients(2 females and 2 males)was 34 years old.Typical clinical manifestations included joint symptoms,flu-like malaise and erythematous rash.Anti-Bl9 IgM antibodies were all positive in 4 patients.B19 DNA was detected in blood samples of 3.Other types of arthritis were excluded. No relapses were noticed after followed-up of 1～3 years.Conclusion The Anti-B19 lgM and B19 DNA should be detected in patients suffer from arthritis with unknown origin.

The insecurity factors of third-class steel implants in the clinical application are introduced.A method for organizing the stocking way and improving the management in hospital are used to monitor and manage all the processes of the steel implants.All problems in management are solved,and this can insure the operation security and depress the costs of patients.

Background:Damage of intestinal mucosal barrier is a key factor in the development and progress of acute pancreatitis(AP),and is closely related with the prognosis of the disease. Aims:To investigate the protective effect and possible mechanism of mucoprotective agent teprenone on intestinal mucosal barrier in rats with experimental AP. Methods:Forty-five adult male Sprague-Dawley rats were randomly divided into normal control group(n = 5),AP model group(n = 20)and teprenone treated group(n = 20). AP model was established by subcutaneous injection of cerulein at abdominal wall. Rats in treated group were intervened with teprenone intragastrically before and after model establishment. ELISA was used for measurement of serum interleukin-1(IL-1),IL-6,tumor necrosis factor-α(TNF-α)and amylase;histopathological and ultrastructural changes of small intestinal mucosa were observed by light microscope and transmission electron microscope;Western blotting was used to detect the expressions of tight junction protein occludin and ZO-1. Results:Serum levels of IL-1,IL-6,TNF-α and amylase in AP model group were significantly higher than those in normal control group(P < 0. 05),accompanied by necrosis and exfoliation of small intestinal villus,widening of intercellular tight junctions and downregulation of occludin and ZO-1 expression. While in teprenone treated group,serum levels of proinflammatory cytokines and amylase were significantly decreased as compared with AP model group(P < 0. 05),the villus of small intestine remained intact,and dense tight junctions were observed. Expressions of occludin and ZO-1 in teprenone treated group were upregulated. Conclusions:Teprenone may protect against intestinal mucosal barrier injury in AP model rats by upregulating tight junction protein expression.

Objective To observe the changes of zymophagy during experimental acute pancreatitis (AP) induced by caerulein.Methods Pancreatic acinar cell line AR42J cells were cultured in 6-well plates till 90％ confluent and then divided into AP group and control group.Caerulein (1 × 10-8 mol/L) was added into AP group to establish AP cell model,and 1640 cell culture medium was added into control group.After caerulein treated for one,four,six,eight,12 and 24 hours,cells and cell culture supernatant were collected.The levels of cytokine interleukin (IL)-1,tumor necrosis factor (TNF)α,trypsinogen activation (TAP) and amylase were measured with enzyme-linked immunosorbent assay (ELISA) method.The expression of LC3 and Beclin1 at mRNA of each group were detected by reverse transcription-polymerase chain reaction (RT-PCR).The LC3B protein level of each group were detected by Western blotting.The changes of autophagosome and zymophagosome were observed by transmission electron microscopy.The difference between AP group and control group was analyzed by analysis of variance.Results The level of IL-1,TNFα,amylase and TAP in cell culture supernatant of control group was (18.83±7.10) pg/mL,(14.20±3.79) pg/mL,(10.03±2.85) U/L and (39.48±8.62) pg/mL,respectively.Those of AP group significantly increased at first hour ((62.13±11.25) pg/mL,F=3.32,P＜0.01 ; (30.98±7.11) pg/mL,F=3.05,P＜0.05; (25.06±6.82) U/L,F=2.90,P＜0.05 and (128.51± 18.30) pg/mL),F=2.62,P＜0.01,at fourth or sixth hour reached peak (IL-1 at fourth hour:(71.96± 15.82) pg/mL,F=7.25,P＜0.01;TNFα at sixth hour:(39.92±8.94) pg/mL,F=4.93,P＜0.05; amylase at fourth hour:(28.83 ± 8.31) U/L,F=2.06,P＜0.05; TAP at fourth hour:(146.29± 29.36) pg/mL,F=0.14,P＜0.01) and then gradually decreased.At fourth and sixth hour,the expression of LC3 at mRNA level in AP group was 3.18±0.82,1.71±0.14,respectively,while the expression of Beclin-1 rnRNA at first,fourth hour was 2.44±0.34 and 4.13±0.30,all of them were significantly increased compared with those of control group (0.21±0.04 and 0.30±0.08,LC3 mRNA F=0.79、0.06; Beclin mRNA F=2.31、0.36,all P＜ 0.05).There were no significant differences at other time points.The numbers of autophagosome and zymophagosome of AP group were significantly higher than those of control group under transmission electron microscopy.Conclusion Zymophagy occurred during AP cell model induced by caerulein,which suggested that zymophagy might involve in the mechanism of AP.

Objective To explore the role of PADI4 mRNA in the initiation and development of rheumatoid arthritis(RA)and its correlation with clinical features.Methods Fifty-three RA patients,27 OA patients and 30 healthy volunteers were included in the study.The real-time-fluorescence quantitative PCR method was used to measure the expression level of PADI4 mRNA.The level of Anti-CCP antibody and DAS 28 of the RA patients were measured at the same time.Results It was shown that the level of PADI4 mRNA from RA was significantly higher than that of the OA and control group(P

Objective To investigate the relationship between high-sensitivity C-reactive protein(hsCRP), pulse pressure(PP) and microalbuminuria(MAU) in patients with essential hypertension.Methods Consecutive 60 patients with essential hypertension were classified based on the MAU level:patients with MAU(n=30) and the group of patients with normoalbuminuria(NMAU,n=30) with 30 healthy subjects as control.MAU,hsCRP,PP were determined.Results The level of hsCRP and pulse pressure in MAU group were higher than those in NMAU patients and healthy subjects (P

Objective To explore the effects of H2S on cerebral injury after cardiopulmonary resuscitation (CPR) and its mechanism.Methods Forty-five healthy Sprague-Dawley (SD) rats were randomly (random number) divided into shame-operated group ( group A,n =5 ),resuscitation group ( group B,further divided into four subgroups as per rats sacrificed 6 h,12 h,24 h,and 72 h after resuscitation,n =5),and NaHS pretreatment group ( group C,further divided into 4 subgroups as done in group B).The ratio of water content in brain tissue was calculated.The content of H2S in cerebral cortex of rats in all groups was determined by using universal microplate reader. Immunohistochemistry method was used to count the Nestin-positive cells. Results The content of H2S in hippocampus area of brain showed dramatic changes from rising up at first and then to lowering down to the minimum and finally returning to the original level in 72 h in B group.Compare to group B,brain water content was lesser ( P ＜0.05 or P ＜ 0.01 ) and the levels of Nestin in hippocampus increased in group C(P＜0.05 or P ＜0.01).The neurological deficit score (NDS) was improved (P ＜0.05 or P ＜0.01) and pathological changes in hippocampus of rat brain detected by using hemotoxylin - eosin staining were slighter in group C in comparison with group B.Conclusions Endogenous H2S may involve in the course of formation and progress of cerebral injury after CPR and small dose of NaHS (exogenous H2S) can improve NDS by decreasing cerebral edema and up-regulating Nestin level in hippocampus of brain,playing a protection role in cerebral injury after CPR.

Objective To investigate the protective effects of atorvastatin on hyperphosphate-induced rat vascular smooth muscle ceils (RVSMCs) calcification and to discuss the mechanism. Methods RVSMCs were placed in various culture media, including normal phosphate medium, high phosphate medium, ZVAD-FMK medium and atorvastatin medium.Calcium content and cell protein content were quantified by the o-cresolphthalein complexone method and BCA protein assay respectively. Calcification was visualized by yon Kossa staining. And cell apoptosis was quantified by ELISA. Results (1)At day 3, 6, 9, RVSMCs calcification occurred more frequently in high phosphate medium than that in normal phosphate medium (P<0.05). (2)At day 6, RVSMCs calcification was significantly inhibited in 1.0 μmol/L and 2.0 μmol/LZVAD-FMK medium (P<0.05). And in 10 nmol/L and I00 nmol/L statin medium, RVSMCscalcium deposition significantly decreased (P<0.05). (3)RVSMCs apoptosis and calcification occurredfrequently in high phosphate medium. And atorvastatin significantly inhibited RVSMCs apoptosisboth in long-term and short-term (P<0.05). Conclusions Hyperphosphate can induce the calcium deposition of RVSMCs in vitro. Atorvastatin protects RVSMCs from phosphate-induced calcification by inhibiting apoptosis.

Objective To evaluate the effect of parathyroid hormone (PTH) on the expression of connective tissue growth factor (CTGF) in human renal tubular epithelial cells, and to explore the role of MAPK signaling pathway. Methods Real time RT-PCR, Western blot, and reporter gene assay were employed to detect PTH-induced CTGF expression in HK-2 cells. Inhibitors (PD98059 and U0126) of MAPK signaling pathway were used to confirm involved signal pathway. Results HK-2 cells had basic expression level of CTGF mRNA and protein, which were increased significantly after treatment with PTH. The luciferase activity was up-regulated to a higher level as compared with control group after treatment with 10-10 mol/L PTH for 12 h [(1.8884±0.0780) vs (0.9891±0.0300) A, P<0.01]. Moreover, a small amount of p-ERK1/2 was detected in normal HK-2 cells, but it was increased significantly in response to PTH activation, most remarkably when treated with 10-10 mol/L PTH for 30 min. Inhibitors of MAPK signaling pathway, PD98059 and U0126, noticeably inhibited the expression of CTGF mRNA and protein as well as gene promoters in HK-2 cells. Conclusion PTH can induce higher expression of CTGF in HK-2 cells probably via MAPK signaling pathway.

Objective To investigate the effect of parathyroid hormone (PTH) on the transition and connective tissue growth factor (CTGF) expression of human renal proximal tubular epithelial cell line HK-2 . Methods The expression of CTGF mRNA and protein of HK-2 cells were measured by real time RT-PCR and Western blot respectively . The effect of PTH on the phenotypic transformation of HK-2 cells was examined by light microscopy . The expression of α-smooth muscle actin (α-SMA) in HK-2 cells was detected by immunofluorescence . Results Basal level of CTGF mRNA and the protein expression were detected in HK-2 ceils . PTH upregulated the expression of CTGF mRNA and protein with the maximal response at the concentration of 10-10 mol/L and the best stimulating time was at 72 h . After exposure to PTH (10-10tool/L) for 12 hours, the highest level of luciferase activity was 1 .96 fold as compared to control (1 .888±0 .078 vs 0 .989±0 .030, P＜0 .01 ) . Untreated cells showed negligible expression of ±-SMA,whereas ±-SMA expression was significantly increased in cells treated with PTH . Conclusion PTH up-regulates CTGF expression and induces transition of HK-2 cells .