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.

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.

HPLC is widely applied in the analysis of chemical drugs. In order to regulate the use and maintenance of HPLC col-umn and guarantee the analysis quality of HPLC, the classified management of HPLC column was explored in the paper from the follow-ing five aspects:file establishment, recipient and return management, column performance evaluation, information accumulation of ap-plication range, and maintenance and abandonment of HPLC column.

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.

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