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

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

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.

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 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.

Objective To investigate the location of receptor interacting protein 3( RIP3) in Necroptosis and its function in this signal passage, and explore the relationship between receptor interacting protein 1 ( RIP1 ) and RIP3 in nuclear translocation. Methods Primary cerebrocortical neurons were cultured for 12 days,then pre-treated with zVAD-fmk(20μ,mol/L) for half an hour to block apoptosis. ①Extracting nuclear and cytoplasmic protein after neurons were exposed to TNF for different time ,then protein levels of RIP3 were analyzed by western blot and immunofluorescence for qualitative observation;②In the following research,the neurons were treated with Nec-1 and shRlPl ,then the protein level of RIP1 and RIP3 with western blot were analyzed, cell viability were determined by measuring LDH levels. Results ①In signaling pathways of necroptosis, the protein level of RIP3 in cytoplasmic decreased gradually with prolonged TNF exposure, to the corresponding it rolled up in nucleus and a-chieved the peak in 12 hours of TNF treatment ( Cytoplasmic 0. 45 ± 0. 03 ,0. 41 ± 0. 02,0. 73 ± 0. 03 ,0. 90 ± 0.01,1.15 ±0.04,1.30 ±0.02,0.99 ±0.03,0.63 ±0. 03;Nucleus 0. 07 ±0.02,0. 26 ±0.02,0. 57 ±0. 02,0. 68 ± 0.02,0. 80 ± 0.01,0.92 ± 0.02,1.28 ± 0.03,0. 87 ± 0.02) (P < 0.01). ②Blocking the relationship between RIP1 and RIP3 with necrostatin-1 and shRIPl , nuclear translocation of RIP3 decreased and caused a great increase in cell viability( 1.00 ±0.05,0.39 ±0.03,0.50 ±0. 03) (P<0. 01). Conclusion RIP3 mainly locates in cy-tolymph of normal cells,it translocates into nucelus as necroptosis takes place. RIP1 function with RIP3 in nuclear translocation. Block nuclear translocation of RIP3 is a potential way to protect cells.

Objectiye To study the mechanism by which transcranial magnetic stimulation (rTMS) affects cognitive dysfunction in vascular dementia (VD). Methods Thirty-six male Wistar rats were randomly divided into a control group, a VD group, a low frequency rTMS group and a high frequency rTMS group. Two-vessel occlusion was employed to induce VD models. Low frequency rTMS group rats were given 0.5 Hz rTMS for six weeks. High frequency rTMS group rats were given 5 Hz rTMS for six weeks. Morris' water maze test was used to measure their spatial learning ability and memory. The ultrastructures of the synapses in the four groups were detected with transmission electron microscopy. The expression of synaptophysin (SYN), brain derived neurotrophic factor (BDNF) and Nmethyl-D-aspartate receptor 1 ( NMDAR1 ) mRNA and protein in the hippocampus were determined by real-time PCR and Western blotting. Results The behavior and morphology of the rats treated with rTMS improved. The average expression of SYN, BDNF and NMDAR1 mRNA and protein in the low frequency rTMS group and the high frequency rTMS group were significantly higher than in the VD group. Conclusion rTMS can provide a rehabilitative effect for VD. The mechanism might be associated with enhancing the expression of SYN, BDNF and NMDAR1 in the hippocampus.

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

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