Objective To evaluate the efficacy and safety of urethroplasty via transpubie ap-proach in treatment of complex posterior urethral strictures after pelyic fracture. Methods Urethroplas-ty via transpubic approach was done on 26 patients (21 males and 5 females, at mean age of 26 years) with complex posterior urethral strictures. Posterior urethral stricture was 2.5-4.0 cm long in 23 patiens and > 4.0 em in three. There were five patients with urethratresia. The perioporative complications and operative effect were evaluated after the broken ends of the urethra was thoroughly resected and treated with end-to-end anastomosis. Results A follow-up for 1-7 years ( mean 4 years) showed successful op-eration in 22 patients (85%), with normal urination and without complications like osteitis pubis, pelvic disassociation, pelvic instability or urinary incontinence. But obstructed urination was found in one (4%) and failed operation in three (11%). Conclusions Urethroplasty via transpubic approach takes advantages of precise and thorough scar excision, less complications and long term curative effect and is clinically feasible and safe for patients with complex posterior urethral stricture.

The change of PKC activity and cytosolic free Ca 2+ induced by oxLDL and simvastatin in ASMC were measured by its ability to transfer phosphate from 32P-ATP to lysine-rich histone and flow cytometric analysis loading with the Ca 2+ dye fluo-3/Am, respectively. As a result, oxLDL increased total PKC activity in a dose-dependent manner with phase peaking at 14 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic [Ca 2+]i responses including rapid initial transient phase and sustained phase. Removal of extracellular Ca 2+did not inhibit the rapid phase of oxLDL-induced rise in [Ca 2+]i, but abolished the sustained phase of [Ca 2+]i in response to oxLDL. Activity of PKC was markedly decreased and simvastatin did not impair the initial peak in response to oxLDL but significantly reduced the subsequent plateau phase when simvastatin was added. The results suggested that oxLDL can induce dynamic changes of signal transduction of PKC and cytosolic free Ca 2+in ASMC. The rapid initial transient phase was due to the mobilization of [Ca 2+]i from intracellular Ca 2+ pool and the sustained phase resulted from the influx of extracellular Ca 2+. The inhibition of PKC activity induced by simvastatin may contribute to the changes of intracellular Ca 2+.

To investigate the clinical significance of the expression of CD40L on peripheral blood monocytes and the changes in serum soluble CD40L in patients with acute coronary syndrome, 16 normal controls and fifty-six patients including 24 with SA (8 patients after PTCA), 20 with UA and 12 with AMI entered in this study. The expression of CD40L on monocytes was analyzed by indirect immonofluorescence flow cytometry and serum sCD40L levels were measured by ELISA. The results showed: (1) The expression of CD40L on monocytes in UA and AMI were higher compared with SA and controls ( P 0.05). (2) Patients with UA and AMI had significantly raised serum levels of sCD40L when compared with patients with SA and controls( P

AIM: To investigate whether human umbilical vein endothelial cells and human atherosclerotic plaque lesions can coexpress CD40 and CD40 ligand . METHODS: The expression of CD40 and its ligand CD40L on human endothelia cells were measured by fluorescence microscope , flow cytometry(FCM), reverse transcription PCR(RT-PCR) and Western blotting, respectively. Both CD40 and CD40L expression in atheroma plaques were determined by immunohistochemistry. RESULTS: Cultured human endothelial cells constitutively coexpressed CD40 and CD40L in mRNA and protein levels. Stimulation with interleukin-1?, interleukin-6, tumor necrosis factor-? and interferon-? increased expression of CD40 and CD40L on endothelial cells . Human atherosclerotic lesions( n =6) showed coexpression of immunoreactive CD40 and CD40L. However, no expression of CD40 and CD40L in nonatherosclerotic human arteries. CD40L mainly expressed on the shoulder and base of the plaque. But CD40 was widespreadly expressed in plaque. CONCLUSION: Our results demonstrated that CD40 and CD40L coexpressed on human umbilical vein endothelial cells and in human atherosclerotic plaque lesions. These findings suggest a previously unsuspected role for CD40-CD40L interactions in atherosclerosis.

Objective： To investigate the effect of oxLDL and VitE on the expression of CD40 and CD40 ligand(CD40L) in cultured human monoc ytes. Methods： The expression of CD40 and CD40L on monocytes su rface were measured by indirect immunorescence technique in combination with flo w cytometry. Results： Low concentration of oxLDL（≤200 μg/L） significantly increased the expression of CD40 and CD40L in a dose and time dep endent manner. High concentration (>200 μg/L）of oxLDL markedly reduced the exp ression of CD40 and CD40L. When VitE was added, it significantly reduced the ex pression of CD40 and CD40L on monocytes surface induced by oxLDL in a dose-depe ndent manner. Conclusion：It is an important mechanism that the high expression of CD40 and CD40L induced by oxLDL may be contributed to the for mation of atherosclerosis. Antioxidan VitE can partially inhibit the high expres sion of CD40 and CD40L on monocytes surface induced by oxLDL.

200 ?g/L)of oxLDL markedly reduced the expression of CD40 and CD40L. When VitE was added, it significantly reduced the expression of CD40 and CD40L on monocytes surface induced by oxLDL in a dose dependent manner. Conclusion:It is an important mechanism that the high expression of CD40 and CD40L induced by oxLDL may be contributed to the formation of atherosclerosis. Antioxidan VitE can partially inhibit the high expression of CD40 and CD40L on monocytes surface induced by oxLDL. [

Objective To investigate the ability of single photon emission computed tomography (SPECT) and MRI in detecting skull-base invasion in nasopharyngeal carcinoma. Methods Sixty-one patients with nasopharyngeal carcinoma received whole body and skull-base tomography SPECT, and nasopharynx and skull-base MRI before radiotherapy. The results were double-blind compared and evaluated. Results The overall positive rates of skull-base invasion detected by SPECT and MRI were 51% and 46% (P=0.508). In paitents with headache, cranial nerve palsy or both, the rates were 83% and 86% (P=1.000) ,80% and 80% (P=1.000), 88% and 94% (P=1.000), respectively. In patients with T1+T2 and T3+T4lesions,the rates were 22% and 0(P=0.031) ,74% and 82% (P=0.250) ,repectively. In patients with N0+N1and N2+N3lesions,they were 50% and 48% (P=1.000) ,53% and 40% (P=0.500) ,respectively. The conformation rate between SPECT and MRI was 85%. Binary Logistic regression analysis showed that T stage was a risk factor for positive SPECT(χ2=4.23,P=0.040, OR=3.04). Headache tended to be a risk factor for both positive SPECT and positive MRI (χ2=3.13, P=0.077, OR=4.54;χ2=3.64,P=0.056,OR=12.00). Conclusions The detection sensitivity of SPECT in skull-base invasion in nasopharyngeal carcinoma is equivalent to that of MRI. The consistency between SPECT and MRI is good. Moreover, there is a good correlation between SPECT and symptoms, signs and stage. SPECT of skullbase tomography is necessary for patients with severe headache, negative CT and those who can not receive MRI. When SPECT result is positive,skull-base should be considered to be invaded and should be defined as gross tumor volume in radiotherapy planning.

AIM: To investigate effects of OX-LDL and VitE on the levels of IL-6,IL-8 and TNF-? in human umbilical vein endothelial cells(HUVEC). METHODS: Human umbilical vein endothelial cells were obtained by in vitro culture. HUVEC treated with or without Vit E was incubated with OX-LDL, and the levels of IL-6, IL-8 and TNF-? were determined by enzyme-linked immunosorbent assy technique. RESULTS:50 ?g/L,100 ?g/L, 200 ?g/L OX-LDL induced the release of IL-6,IL-8 and TNF-? by HUVEC in a dose-dependent manner. Compared with the control group , the levels of IL-6 and IL-8 were significantly increased at 6-12 h of stimulation with OX-LDL . Maximal levels of IL-6 and IL-8 occurred after 24-36 h, reaching a plateau maintained for at least 48 h. TNF-? rose after 2-6 h in HUVEC, and reached a maximum after 12 h. In contrast to IL-6 and IL-8, TNF-? declined after 48 h. However, when VitE (50 mg/L,100 mg/L,200 mg/L)was added, it can significant inhibited the release of IL-6, IL-8 and TNF-? in a dose-dependent manner, and after 48 h these cytokines have no diference between OX-LDL+VitE groups and OX-LDL groups. CONCLUSION: OX-LDL can obviously stimulate the production of IL-6,IL-8 and TNF-? in vascular endothelial cells, which can significantly be inhibited by VitE in a short time.

AMI: To clarify whether OX-LDL and simvastatin can induce the changes of PKC activity and cytosolic free Ca 2+ in rat aortic smooth muscle cells (ASMC). METHODS: PKC activity and cytosolic free Ca 2+ were measured by its ability to transfer phosphate from ATP to lysine-rich histone and flow cytometric analysis after loading with the Ca 2+ dye fluo 3/Am, respectively. RESULTS: OX-LDL increased PKC total activity in a dose-dependent manner and induced translocation of PKC from the cytosolic to membrane, while OX-LDL induced biphasic [Ca 2+ ]i responses including the rapid initial transient phase and the sustained phase. When simvastatin was added, the translocation of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but significantly reduced the subsequent plateau phase. CONCLUSSION: OX-LDL can induce dynamic changes of signal transduction of PKC and cytosolic free Ca 2+ in ASMC and these two events are closely linked.