Cilia ; ultrastructure ; Humans ; Maxillary Sinus ; ultrastructure ; Microscopy, Electron, Scanning ; Mucous Membrane ; ultrastructure

Dendritic Cells ; Humans ; Rhinitis, Allergic, Perennial ; Rhinitis, Allergic, Seasonal

Clinically,heparin-induced thrombocytopenia (HIT) is an uncommon but serious disease,which is induced by the use of immune unfractionated heparin or low-molecular-weight heparin.The overall incidence of HIT is about 0.6％-5.0％.Nevertheless,in clinical practice it is profoundly dangerous,especially for patients who are receiving cardiovascular surgery or interventional therapy.At present,HIT is a hot clinical research subject.This paper aims to make a brief review about HIT pathogenesis,epidemiology,clinical evaluation and treatment,etc.

Objective To summarize the clinical experience of urethral realignment for treating early urethral injury under the guidance of ureteroscope,and evaluate its curative effect.Methods Twenty-nine male patients with urethral injury were selected,and 12 patients of posterior urethral injury,17 patients of former urethral injury.All the patients were treated with urethral realignment under the guidance of ureteroscope,postoperative indwelling catheter 3-8 weeks,every 7-16 days changed diameter increase 2 F the catheter 1 time.Results The 29 patients with urethral injury were a indwelling catheter success,all patients were no incontinence after operation 3 months.In the 29 patients,27 patients were urination unobstructed after catheter removal,2 patients were appeared urine line slim after 2 weeks,the 2 patients were normal urination after short urethral expansion.Conclusions The urethral realignment for treating early urethral injury under the guidance of ureteroscope has simple,lower complication,rapid recovery,better effect.The continuous flexible progressive urethral expansion and the strict nursing,which can effectively reduce the occurrence of urethral stricture.

Objective To investigated the role of the autophagy lysosomal pathway in PD cells and the possible molecular mechanisms. Methods A dopaminergic neuronal injury model was induced by 6-OHDA in PC12 cells . Autophagosomes in PC12 cells were examined by transmission electronmicro-scopy( TEM ). The expression of LC3- Ⅱ , Cathepsin B were assayed by western blot analysis. Results TEM revealed that the autophagosomes were increased in PC12 cells after 6-OHDA treatment and appeared apoptosis. The LC3-Ⅱ (2h:52.57 ±2.27,4h:56.83 ±3.51,6h:73.43 ±5.41,12h:103.90 ±2.57,24h: 100.40 ±3.91 )and Cathepsin B expression ( model group: 113.80 ± 4.46; normal group 35.89 ± 3.40) were increased after 6-OH DA treatments (P ＜ 0.05 or P ＜ 0.01 ). Conclusion The results indicate that autophagy lysosome pathway is involved in 6-OHDA-induced cell death in PC12 cells.

Based on domestic and international studies on Career-Life-Cycle theories,this paper analyzed the scientific research data of doctors to elucidate characters of varied steps in clinical and research practices,trying to construct Research Life-Cycle theory for doctors and provide theoretical references of talent cultivation in hospitals.

Objective: To explore the effects of ulinastatin on the level of MIF in rats with acute necrotic pancreatitis. Method: 52 healthy Wister rats were randomly divided into three groups: normal control group(group C, 12), ANP group(group A, 20)and UTI group(group U, 20). Severe acute pancreatitis rat model in group A were induced by injection of 315 % sodium taurocholate through retrogradely common biliopancreatic ducts via papilla duodeni. After inducing the rat model of ANP through the way above, rats in group U were treated by ulinastatin through portal vein injection. Pancreas and duodenum were only flipped after opening abdominal cavity in group C. Then rats were killed at 3rd, 6th ,12th ,24th hour after operation respectively. Cut the belly open at once, and draw blood in postcava. The levels of serum MIF were determined with ELISA. Blood amylase was detected through biochemistry instrument. Resected pancreas tissues was scored according to the standard of Kusske. Result: Compared to the normal control group, the level of serum MIF , blood amylase and histopathological scores were significantly increased in ANP group, P

AIM: To observe the effect of simvastatin on the proliferation of vascular smooth muscle cells(VSMCs) induced by serum and growth factor PDGF-BB and the effect of simvastatin on the expression of PTEN,a important regulator of G 1/S cell cycle transition. METHODS: The DNA synthesis was determined by -TdR incorporation, cell cycle was examined with flow cytometry, the protein level of PTEN was measured by Western blot method. RESULTS: (1)Simvastatin inhibited -TdR incorporation in a dose dependent manner. (2) Flow cytometric DNA analysis revealed that simvastatin induced significantly enhancement of G 0/G 1 phase and decrease in S phase VSMCs.(3)Simvastatin increased protein level of PTEN and mevalonate, a metabolite of HMG-COA, reversed the effect of simvastatin on PTEN protein expression. CONCLUSION: Simvastatin may inhibit proliferation of VSMCs and retarded cell cycle in G 0/G 1 phase by increasing PTEN expression through inhibiting synthesis of mevalonate.

AIM: Hydroxymethylglutaryl CoA (HMG-CoA) reductase inhibitors, such as simvastatin, have been shown to reduce atherosclerotic cardiovascular morbidity and mortality by mechanisms unrelated to its lipid-lowering effect. Several studies have shown that simvastatin induces apoptosis in a varieties of cell lines including vascular smooth muscle cells (VSMC). The aim of this study was to investigate the signal pathways involved in apoptosis induced by simvastatin. METHODS: Cultured VSMC were treated with simvastatin. Calpain activity was determined by measuring Ca 2+ ionophore-specific calpain substrate (suc-LLVY-AMC), caspase-3 activation was detected by Western blot, and apoptotic changes were distinguished by annexin Ⅴ binding and DNA laddering. RESULTS: After incubated with 30 ?mol/L simvastatin for 8 h, calpain activity had a marked increase ( P

Aim To construct a polysialic acid(PSA)and neural cell adhesion molecule(NCAM)differently expressing COS-7 cell line,and investigate the effects of PSA on the cell adhesion,migration and invasion,aiming to establish the base for further investigation of the signaling passway of the diverse celluar migration and invasion,and elucidate the molecular mechanism of PSA promoting cancer cell metastasis.Methods A polysialic acid and neural cell adhesion molecule differently expressing COS-7 cell line was constructed by transient cotransfection,and the cotransfection efficiency was determined by Western blot and flow cytometry.Adhesion assay was used to investigate the effect of PSA on cell adhesion ability;transwell assay was used to measure migration and invasion ability.Results The PSA and NCAM differently expressing COS-7 cell line was successfully constructed,which demonstrated PSA inhibited the cell adhesion to basement membrane,and promoted the migration and invasion ability.Conclusions The constructed polysialic acid and neural cell adhesion molecule differently expressing COS-7 cell line can be used to investigate molecular mechanism of promoting cancer cell metastasis induced by PSA in the future.