Potential contribution of nuclear factor-kappaB to cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.

Nuclear factor-kappaB (NF-kappaB) plays a key role in inflammation, which is involved in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). In the present study, we assessed the potential role of NF-kappaB in regulation of cerebral vasospasm. Nuclear factor-kappaB DNA-binding activity was measured in cultured vascular smooth muscle cells (VSMCs) treated with hemolysate and pyrrolidine dithiocarbamate (PDTC, 80 micromol/L), an inhibitor of NF-kappaB. Forty-two rabbits were divided into three groups: control, SAH, and PDTC groups (n=14 for each group). The caliber of the basilar artery was evaluated. Nuclear factor-kappaB DNA-binding activity and the gene expression levels of cytokines and adhesion molecules in the basilar artery were measured. Immunohistochemical study was performed to assess the expression and localization of tumor necrosis factor (TNF)-alpha, intercellular adhesion molecule (ICAM)-1, and myeloperoxidase (MPO). It was observed that NF-kappaB DNA-binding activity was significantly increased by treatment with hemolysate in cultured VSCMs, but this increase was suppressed by pretreatment with PDTC. Severe vasospasm was observed in the SAH group, which was attenuated in the PDTC group. Subarachnoid hemorrhage could induce increases of NF-kappaB DNA-binding activity and the gene expression levels of TNF-alpha, interleukin (IL)-1 beta, ICAM-1, and vascular cell adhesion molecule (VCAM)-1, which were reduced in the PDTC group. Immunohistochemical study demonstrated that the expression levels of TNF-alpha, ICAM-1, and MPO were all increased in the SAH group, but these increases were attenuated in the PDTC group. Our results suggest that NF-kappaB is activated in the arterial wall after SAH, which potentially leads to vasospasm development through induction of inflammatory response.     

臀上血管深上支的应用解剖

本文观察了52侧(男46,女6)成人尸体臀上动、静脉深上支进入髂嵴情况.臀上动、静脉深上支分为前、中、后支;本文测量了臀上动、静脉深上支的外径及各分支进入髂嵴的距离.臀上动、静脉深上支的分支在髂嵴前部及中部分布较多,前支的分支为3～8支,其中以4～6支者为多见,占78.8±5.5％;中支的分支1～4支,其中以2～3者为多见,占73.1±6.1％.因此,臀上动脉深上支作为游离髂骨移植术取髂嵴的前部和中部较宜.     

Adeno-associated virus vector-mediated systemic delivery of IFN-beta combined with low-dose cyclophosphamide affects tumor regression in murine neuroblastoma models.

PURPOSE: Type I IFNs (IFN-alpha/beta) have shown significant antitumor activity in preclinical models but limited efficacy and significant toxicity in clinical trials. We hypothesized that the antitumor activity of type I IFNs could be enhanced by chronic, low-dose systemic delivery and sought to test this in murine neuroblastoma models. EXPERIMENTAL DESIGN: Continuous liver-generated expression of human IFN-beta (hINF-beta) was achieved through a gene therapy-mediated approach using adeno-associated virus vectors encoding hIFN-beta (AAV hINF-beta). Orthotopic localized retroperitoneal and disseminated models of neuroblastoma were established using three different xenografts. Immunohistochemical analysis and ELISA were used to evaluate the antiangiogenic effect of therapy. RESULTS: The development of both localized orthotopic (retroperitoneal) and disseminated neuroblastoma was prevented in all mice expressing hINF-beta. Continued growth of established retroperitoneal tumors, treated with AAV hINF-beta as monotherapy, was significantly restricted, and survival for mice with established, disseminated disease was significantly prolonged following administration of AAV hINF-beta. Analysis of treated tumors revealed a significant antiangiogenic effect. Mean intratumoral vessel density was diminished and expression of the angiogenic factors vascular endothelial growth factor and basic fibroblast growth factor were both decreased. Finally, combination therapy in which AAV hIFN-beta was used together with low-dose cyclophosphamide resulted in regression of both established retroperitoneal and disseminated disease. CONCLUSIONS: AAV-mediated delivery of hIFN-beta when used as monotherapy was able to restrict neuroblastoma growth due in part to inhibition of angiogenesis. When used in combination with conventional chemotherapy, AAV hIFN-beta was able to effect complete tumor regression.     

持续压力超负荷对兔左心室细胞凋亡的影响

OBJECTIVE: To study the effect of chronic pressure overload on the apoptosis of the left ventricle myocytes in rabbits. METHODS: Rabbit models of chronic pressure overload-induced heart failure were prepared in which dynamic changes of apoptotic myocytes in the left ventricle were observed by way of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. RESULTS: Only a few apoptotic cells was observed in the sham-operated group, while in the experimental group, the apoptotic left ventricle myocytes significantly increased after operation, presenting a peak level between day 3 and day 7. Seven days after the operation, the apoptotic myocytes began to decrease and till day 14, the apoptotic cell number had been smaller than that measured on day 1. When signs of heart failure set in, the apoptotic myocytes were again increased (P<0.001). CONCLUSION: During chronic pressure overload, myocyte apoptosis in the left ventricle is elevated at the early stages and undulates subsequently, with the peak occurring before hypertrophy is obvious.     

Breast Volume Measurement in Young Chinese Women and Clinical Applications

The authors carried out research on breast volume and body surface anatomy of 125 women. As a result, an average breast volume for Chinese women was obtained (325.36 ± 12.66 ml), and a table with several linear equations for calculating breast volume was derived. The authors applied these results to their clinical work and succeeded in making mammaplasty more precise in 178 patients.