胸腺注射供体脾细胞诱导移植心脏免疫耐受的实验研究

目的探讨诱导心脏移植免疫耐受的方法及其产生的可能机制. 方法采用大鼠腹部心脏移植模型,随机分成未处理(Ⅰ)组,胸腺注射供体脾细胞(Ⅱ)组,腹腔注射兔抗鼠淋巴细胞血清(Ⅲ)组,胸腺注射供体脾细胞联合应用兔抗鼠淋巴细胞血清(Ⅳ)组,每组6只大鼠.Ⅱ、Ⅳ组在移植前2 1 d将供体脾细胞2.5×107个注射到受体胸腺,Ⅲ、Ⅳ组受体腹腔注射兔抗鼠淋巴细胞血清(ALS)1 ml,然后行异位心脏移植.观察移植心脏存活时间,供心病理学改变及供、受体间的混合淋巴细胞反应(MLR). 结果Ⅳ组供心平均存活时间(MST)为(81.8±7.6)d,较Ⅰ组(7.3±1.0)d、Ⅱ组( 7.8±1.0)d、Ⅲ组(8.2±1.2)d显著延长,差异有显著性意义(P＜ 0.01 );供心仅见少量炎性细胞浸润;供、受体间MLR较正常对照组显著降低,差异有显著性意义(P＜0.01). 结论胸腺注射供体脾细胞联合应用ALS能成功诱导心脏移植的免疫耐受;胸腺内特异性T细胞克隆消除可能与免疫耐受的形成有关.     

股前外侧（肌）皮瓣交腿修复胫前大面积软组织缺损

目的寻求一种对胫前区大片软组织缺损修复的手术新方法,降低截肢率.方法对10例胫前严重的开放性损伤伴大面积软组织缺损病例,采用股前外侧(肌)皮瓣交腿血管吻合移植方法,移植皮瓣12×8～28×15cm2,随访6个月-5年.结果除2例,皮瓣边缘部分坏死外,其余8例皆一期愈合,外形、功能满意.结论交腿皮瓣移植术可降低某些小腿严重开放性创伤的伤残率.     

丙泊酚在家兔肾下主动脉阻断术中对肾功能的保护作用

目的　探讨丙泊酚在肾下主动脉阻断术中对肾功能的保护作用及其机制。方法　 2 4只家兔随机分为假手术组 (A组 )、阻断组 (B组 )及丙泊酚 (C组 ) ,每组 8只。B、C组肾下主动脉阻断4 0分钟后再灌注 1小时 ,C组于阻断前 10分钟静注丙泊酚 5mg/kg ,继以持续输注丙泊酚 2 0mg·kg-1·h-1至松开前 5分钟 ;余两组以等容量生理盐水作对照。测定给药前 (C-10 )、松开前 (C40 )、松开后 1小时 (R60 )血中内皮素 1(ET 1)水平及尿素氮 (BUN)、肌酐 (Cr)、K+ 、Ca2 + 含量 ,记录阻断前、阻断后、松开后尿量并测定尿 β2 微球蛋白 (β2 MG)含量。结果　 (1)B组再灌注后血浆ET 1水平明显高于阻断前及A组 (P <0 0 5 ) ,C组阻断后及松开后血ET 1较阻断前无明显变化。 (2 )B组R60 时的血浆BUN、血K+ 含量明显高于基础水平 (P <0 0 5 ) ,C组无明显变化。 (3)B组及C组阻断后尿量均明显升高 ,再灌注后B组尿量明显低于阻断前 (P <0 0 5 ) ,B组尿 β2 MG明显高于阻断前及C组 (P <0 0 5 )。结论　肾下主动脉阻断可导致肾小球及肾小管功能障碍。丙泊酚对肾功能有保护作用 ,其机制与其抑制ET 1水平升高有关     

�����Ե����׵����������̽��

目的 探讨术后急性胆囊炎的病因、诊断方法和治疗。方法 回顾性分析9例术后急性胆囊炎的临床资料并复习文献。结果 B超确诊为术后急性胆囊炎者7例。CT确诊1例,1例因胆囊穿孔而死亡,急性胆囊切除术病例无死亡。结论 胆汁淤积是引起卢术后急性胆囊炎的主要病因,早期确诊、及时治疗是降低病死率的关键。     

小鼠异体Sertoli细胞诱导胰岛移植免疫耐受的作用

Objective To study whether the sertoli cell allograft can achieve the immunotolerance and protect the co-transplant islet allograft on the heterotopic situation. Methods The diabetic C57 mice were used as recipients, and healthy BALB/C mice as islet donors,respectively. Healthy BALB/C and C57 mice were used as testis sertoli cell donors. The recipients were randomly divided into 4 groups,6 mice in each group : group A: only transplant with islet allograft;group B: co-transplant with islet allograft and serto-li isograft;group C:co-transplant with islet allograft and sertoli allograft;group D:sham-operated group. The blood and urine glucose levels in the models, and the survival time of the graft were observed. Results The mean survive time of graft in groups A, B, and C was (6.50±2.35 ), (55.67±4.84), and (51.33± 5.05 ) days respectively. In group D, blood glucose level was abnormal. The hyperglycemia of the diabetic C57 mice could be reversed by the transplant methods of groups B and C. The mean survival time in groups B and C was longer than in group A P < 0.05, but there was no significant differences between groups B and C,P > 0.05. Conclusion The sertoli cells can induce local immunotolerance and protect the co-transplant islet allograft. Sertoli cell isograft can obtain the same local immunotolerance as the sertoli cell allograft.     

Post-transplant Lymphoproliferative Syndrome in the Pediatric Liver Transplant Population

Post-transplant lymphoproliferative disease remains a complication with a high morbidity and mortality. The present study examined 291 pediatric liver transplants performed in 263 children from October 1984 to December 1999. Post-transplant lymphoproliferative disease has an overall incidence of 12%. Tacrolimus and cyclosporine had a similar incidence of post-transplant lymphoproliferative disease. Fifty-six per cent of patients who developed post-transplant lymphoproliferative disease were Epstein-Barr virus negative at the time of transplantation. Mean time of conversion to Epstein-Barr virus positivity was 1.1 years after liver transplantation. Ten per cent of those who developed post-transplant lymphoproliferative disease never had Epstein-Barr virus detected. Mean time from Epstein-Barr virus positivity to detection of post-transplant lymphoproliferative disease was 2.68 years, and 3.13 years from liver transplantation (OLTx) to post-transplant lymphoproliferative disease. There was a 35% incidence of mortality. Deaths occurred a mean of 0.76 years after diagnosis of post-transplant lymphoproliferative disease. Most cases of post-transplant lymphoproliferative disease had extranodal location. There was one recurrence in 10% of patients, and two in 3%. All recurrent cases were seen in recipients who became Epstein-Barr virus positive after transplantation. There has been a decrease in the incidence of post-transplant lymphoproliferative disease from 15% to 9% to 4%. Post-transplant lymphoproliferative disease should be diagnosed promptly and treated aggressively. The best treatment, however, seems to be prevention, starting in the immediate postoperative period. Survivors should be monitored for both recurrence of post-transplant lymphoproliferative disease and acute cellular rejection.     

Prostatic expression of hensin, a protein implicated in epithelial terminal differentiation

OBJECTIVES: Hensin induces terminal differentiation in rabbit kidney collecting tubule cells. Rabbit hensin and human DMBT1 result from alternative splicing of the same gene. The human DMBT1 gene is located on chromosome 10q25-26, a region often deleted in prostate cancer. In this study we examined the potential role of this gene in terminal differentiation of prostate, as well as its role in prostatic carcinogenesis. METHODS: We searched for deletions of this gene in prostatic cells cultured from cancer and benign tissues using PCR and cDNA cloning. The expression of hensin/DMBT1 in cultured cells and during prostate development was characterized by immunochemistry. RESULTS: No deletions of hensin/DMBT1 similar to those found in glioblastomas, lung and esophageal cancers were observed in prostate cancer or BPH cells. Hensin/DMBT1 protein was localized in intracellular vesicles of epithelial cells in neonatal and 6-week-old mouse prostates. By 6 weeks, hensin/DMBT1 began to localize in the basal lamina of the prostate and vas deferens. In matured 6-month-old prostates, there was extensive deposition of hensin/DMBT1 in the basal lamina. CONCLUSIONS: There is no evidence that hensin/DMBT1 is implicated in prostatic carcinogenesis. The localization of hensin/DMBT1 during maturation raises the possibility that hensin/DMBT1 is involved in terminal differentiation of the prostate and vas deferens.     

Morphologic and molecular evidence for gap junctions and connexin 43 and 45 expression in annulus fibrosus cells from the human intervertebral disc.

Data are presented which provide evidence for gap junction formation and connexin (Cx) 43 and 45 gene expression in human intervertebral disc cells in vivo and in vitro. These findings in cells from the annulus are important in conjunction with the well-recognized loss of disc cells during aging and disc degeneration. As a result of this loss of cells, cell-cell communication, which we propose is an important, but as yet poorly understood, mechanism which links and coordinates cellular function throughout the entire population of disc cells, is also disrupted. These studies provide additional information on the fundamental cell biology of the disc cell and provide an additional framework for understanding aging, degeneration and potential repair of the human disc.     

Can localization studies be used to direct focused parathyroid operations?

BACKGROUND: There is considerable controversy today concerning the most appropriate surgical approach for patients with primary hyperparathyroidism. The conventional surgical operation involves a bilateral neck exploration through a collar incision with identification of all parathyroid tissue and removal of abnormal parathyroid glands while the patient is under general anesthesia. The success rate of this operation is about 95% or greater in the hands of an experienced endocrine surgeon. Preoperative localization techniques are generally considered to be unnecessary before initial parathyroid operations. The purpose of this investigation was (1) to evaluate the individual and combined accuracy of ultrasonography and technetium 99m sestamibi scans in localizing abnormal parathyroid glands and (2) to determine whether such scans could be used to direct a focused operation. METHODS: We retrospectively studied 338 patients with sporadic primary hyperparathyroidism who had preoperative neck localization studies, ultrasonography and/or technetium 99m sestamibi scans, and parathyroid exploration (238 patients or, reexploration, 60 patients) from January 1996 to April 2000 at the University of California San Francisco/Mount Zion Medical Center. The preoperative localization studies were recorded as true-positive, false-positive, and false-negative and compared with the surgical and pathologic findings and with the outcome of the operation. RESULTS: All of the abnormal parathyroid glands were correctly identified by ultrasonography in 184 of 303 patients (60.7%) and by technetium 99m sestamibi scanning in 183 of 237 patients (77.2%). The sensitivities of ultrasonography and sestamibi were 65% and 80%, respectively. Among the 202 patients who received both ultrasonography and sestamibi scans, a parathyroid tumor was identified at the same site in 105 (52%) of them. When both techniques identified a parathyroid tumor at the same site, the tests were correct in 101 of 105 patients and the sensitivity increased to 96%. CONCLUSIONS: When both the ultrasonography and sestamibi scans identified the same, solitary parathyroid tumor in patients with sporadic primary hyperparathyroidism, this was the only abnormal parathyroid gland in 96% of the patients. A focused parathyroidectomy could therefore be performed in such patients with an acceptable ( approximately 95%) success rate.     

Human parathyroid hormone 1-34 reverses bone loss in ovariectomized mice.

The experimental work characterizing the anabolic effect of parathyroid hormone (PTH) in bone has been performed in nonmurine ovariectomized (OVX) animals, mainly rats. A major drawback of these animal models is their inaccessibility to genetic manipulations such as gene knockout and overexpression. Therefore, this study on PTH anabolic activity was carried out in OVX mice that can be manipulated genetically in future studies. Adult Swiss-Webster mice were OVX, and after the fifth postoperative week were treated intermittently with human PTH(1-34) [hPTH(1-34)] or vehicle for 4 weeks. Femoral bones were evaluated by microcomputed tomography (microCT) followed by histomorphometry. A tight correlation was observed between trabecular density (BV/TV) determinations made by both methods. The BV/TV showed >60% loss in the distal metaphysis in 5-week and 9-week post-OVX, non-PTH-treated animals. PTH induced a approximately 35% recovery of this loss and a approximately 40% reversal of the associated decreases in trabecular number (Tb.N) and connectivity. PTH also caused a shift from single to double calcein-labeled trabecular surfaces, a significant enhancement in the mineralizing perimeter and a respective 2- and 3-fold stimulation of the mineral appositional rate (MAR) and bone formation rate (BFR). Diaphyseal endosteal cortical MAR and thickness also were increased with a high correlation between these parameters. These data show that OVX osteoporotic mice respond to PTH by increased osteoblast activity and the consequent restoration of trabecular network. The Swiss-Webster mouse model will be useful in future studies investigating molecular mechanisms involved in the pathogenesis and treatment of osteoporosis, including the mechanisms of action of known and future bone antiresorptive and anabolic agents.