Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: final results of a prospective, multicenter clinical trial. The Atakr Multicenter Investigators Group

BACKGROUND: The purpose of this study was to evaluate the safety and efficacy of a temperature-controlled radiofrequency catheter ablation system. METHODS AND RESULTS: The patient population included 1050 patients who had undergone ablation of atrioventricular nodal reentrant tachycardia (AVNRT), an accessory pathway (AP), or the atrioventricular junction (AVJ). Ablation was successful in 996 patients. The probability of success was highest among patients who had undergone ablation of the AVJ, lowest in patients who had undergone ablation of an AP, and in between for patients who had undergone ablation of AVNRT. A major complication occurred in 32 patients. Four variables predicted ablation success (AVJ, AVNRT, or left free wall AP ablation and an experienced center). Four factors predicted arrhythmia recurrence (right free wall, posteroseptal, septal, and multiple APs). Two variables predicted development of a complication (structural heart disease and the presence of multiple targets), and 3 variables predicted an increased risk of death (heart disease, lower ejection fraction, and AVJ ablation). CONCLUSIONS: These findings may serve as a guide to clinicians considering therapeutic options in patients who are candidates for ablation.     

卡马西平对癫痫患者染色体畸变率和姐妹染色单体交换频率的影响及与叶酸的

目的 研究卡马西平（ＣＢＺ）的诱变性及其与叶酸的关系,探讨ＣＢＺ致畸及叶酸防止致畸的机制。方法 应用细胞遗传学方法,检测１５例单服ＣＢＺ及１５例ＣＢＺ加叶酸的癫痫患者外周血淋巴细胞染色体畸变率（ＣＡＲ）、姐妹染色单体交换（ＳＣＥ）频率,同时用放免法测定血清叶酸含量,并与未服药癫痫对照组及正常对照组进行比较。结果 单服ＣＢＺ组患者的ＣＡＲ和ＳＣＥ频率较对照组增高,其血清叶酸含量较正常对照组下降;单服ＣＢＺ组患者的ＣＡＲ和ＳＣＥ频率较服ＣＢＺ加叶酸组增高;ＣＢＺ血药浓度与叶酸水平ＣＡＲ及ＳＣＥ之间未发现明显相关性。结论 ＣＢＺ具有ＤＮＡ损伤效应,其损伤效应可能与ＣＢＺ干扰叶酸代谢有关,补充叶酸可以有效防止ＣＢＺ引起的ＤＮＡ损伤。     

Interaction of Inflammatory Cells and Oral Microorganisms VII. In Vitro Polymorphonuclear Responses to Viable Bacteria and to Subcellular Components of Avirulent and Virulent Strains of Actinomyces viscosus

Both virulent (V) and avirulent (AV) strains of Actinomyces viscosus T14 are capable of colonizing the oral cavity of gnotobiotic rats, but only T14-V causes destructive periodontal disease. The basis for this difference in in vivo pathogenicity has not been adequately defined. In the present study we compared the capacities of T14-AV and T14-V to provoke in vitro extracellular release of lysosomal constituents from human polymorphonuclear leukocytes (PMNs). In serum-free cultures, viable T14-V but not T14-AV stimulated discharge of PMN lysosomes. The release response was correlated with PMN phagocytic activity; thus, PMNs readily ingested T14-V but not T14-AV. To explain these differences in PMN-bacteria interactions, subcellular fractions of T14-AV or T14-V were incubated with PMNs. A crude, insoluble sonic extract derived from T14-V caused PMN lysosome release, but a similar fraction from T14-AV was inactive. However, following extensive washing and treatment with deoxyribonuclease or sodium dodecyl sulfate, cell wall fractions of T14-AV stimulated lysosome release. These procedures apparently removed an extracellular polysaccharide slime which is synthesized by T14-AV but not by T14-V. There was a significant reduction in the capacities of viable T14-V or cell wall fractions of T14-V or T14-AV to provoke PMN lysosome release when these agents were preincubated with a slime material isolated from T14-AV. This inhibitory influence of slime was overcome by the addition of fresh or heated (56°C, 30 min) serum to the PMN-bacteria cultures. The data suggest a relationship between the abilities of the avirulent and virulent strains of A. viscosus T14 to act as periodontal pathogens in vivo and to serve as stimuli for PMN lysosome release in vitro.     

柴胡皂甙q及其甙元的结构鉴定

从小叶黑柴胡(Bupleurum smithii Wolffvar;parvifolium ShanetY.Li)的根中得到3个化合物,柴胡皂甙元A和Q及柴胡皂甙q。柴胡皂甙元Q和柴胡皂甙q为新化合物,根据理化性质和波谱分析,确定其结构分别为齐墩果烷-11,13(18)-二烯-3β,16β,23,28,30-五醇和3β,16β,23,28,3O-五羟基齐墩果烷-11,13(18)-二烯-3-O-β-D-吡喃葡萄糖基(1→6)-[α-L-吡喃鼠李糖基(1→4)]-β-D-吡喃葡萄糖甙。     

Prostate carcinoma skeletal metastases: cross-talk between tumor and bone

The majority of men with progressive prostate cancer develop metastases with the skeleton being the most prevalent metastatic site. Unlike many other tumors that metastasize to bone and form osteolytic lesions, prostate carcinomas form osteoblastic lesions. However, histological evaluation of these lesions reveals the presence of underlying osteoclastic activity. These lesions are painful, resulting in diminished quality of life of the patient. There is emerging evidence that prostate carcinomas establish and thrive in the skeleton due to cross-talk between the bone microenvironment and tumor cells. Bone provides chemotactic factors, adhesion factors, and growth factors that allow the prostate carcinoma cells to target and proliferate in the skeleton. The prostate carcinoma cells reciprocate through production of osteoblastic and osteolytic factors that modulate bone remodeling. The prostate carcinoma-induced osteolysis promotes release of the many growth factors within the bone extracellular matrix thus further enhancing the progression of the metastases. This review focuses on the interaction between the bone and the prostate carcinoma cells that allow for development and progression of prostate carcinoma skeletal metastases.     

胸腺瘤临床病理的预后因素研究

目的 探讨胸腺瘤临床病理特点与预后的关系。方法 对130例胸腺瘤的重症肌无力、肿瘤大小、坏死、核分裂及包膜情况、组织学分型（按照L－B分类及M－H分类）、Massaoka临床分期等诸多因素进行分析,观察其5,10年生存率的差别,所得数据进行统计学U检验及χ^2检验。结果 重症肌无力的有无、肿瘤大小、坏死、核分裂及L－B分类均与预后无关（P＞0．05）;而肿瘤有无包膜、M－H分类及临床分期与生存率有明显相关性。有包膜者5,10年生存率分别为100％和93．1％,无包膜者分别为54．4%和40．0％（P＜0．05）。按M－H分类,髓质型5,10年生存生存率分别为100％和79．8％,混合型分别为97．5％和88．4％,皮质为主型分别为83．3％和50．1％,皮质型分别为60．2％和29．9％,分化好的胸腺癌（WDTC）分别为43．4％和0％（P＜0．05）。临床分期中Ⅰ期5,10年生存率分别为100％和93．2％,Ⅱ期分别为84．6％和78．4％,Ⅲ期分别为45．3％和19．8％,Ⅳ期分别为38．0％和0（P＜0．01）。其中以细胞的异型性及有无侵犯胸腺周围器官对预后尤为重要。结论 L－B分类与预后无关;M－H分类、临床分期与预后有关,尤其是瘤细胞呈多角形和大圆形、临床侵犯胸腺外器官者对预后影响较明显。     

Endothelial cell seeding of polytetrafluoroethylene vascular prostheses coated with a fibroblastic matrix

One of the most serious problems with endothelial cell (EC) seeding of prosthetic materials is the poor adhesion and stability of the cells. Although several substrates that improve the initial adhesion have been assayed, the EC are lost within a limited period of time. In this study we attempted to modify the hydrophobic conditions of expanded polytetrafluoroethylene (ePTFE) by treating it with ethanol prior to seeding. In addition, we created a fibroblastic matrix that was also fixed by ethanol to the prosthetic material. In vitro studies were carried out at intervals of 24 hours and 15 days after seeding. EC from umbilical cord vein and fibroblasts from skin were seeded onto disks of PTFE with a porosity of 30 µm. The results obtained show that treatment of ePTFE with ethanol prior to EC seeding modifies its permeability, preventing cellular adhesion. The seeding of fibroblasts onto ePTFE allows a coating to form at 24 hours. The EC seeded onto this matrix adhere to it, forming a monolayer that persisted throughout the entire study period. The fibroblastic matrix allows the long-term survival of the EC on ePTFE.Supported by a grant from the CICYT SAF 92-0875.     

Abscisic acid regulates dormancy of prostate cancer disseminated tumor cells in the bone marrow

Prostate cancer (PCa) commonly metastasizes to the bone where the cells frequently undergo dormancy. The escape of disseminated tumor cells from cellular dormancy is a major cause of recurrence in marrow. Abscisic acid (ABA), a phytohormone, is known to regulate dormancy of plant seeds and to regulate other stress responses in plants. Recently, ABA was found to be synthesized by mammals cells and has been linked to human disease. Yet the role of ABA in regulating tumor dormancy or reactivation is unknown. We found that ABA is produced by human marrow cells, and exogenous ABA inhibits PCa cell proliferation while increasing the expression of p27, p21, and p16 and decreasing the expression of the proliferation marker, Ki67. Further, ABA significantly increased the percentage of PCa cells in the G₀ phase of the cell cycle as well as the duration the cells were arrested in G₀. We found that ABA regulates an increase of PPARγ receptor expression and suppressed phosphorylation of mTOR/p70S6K signaling and resulting in the induction of the cellular dormancy. We then confirmed that ABA regulates G₀ cell cycle arrest through PPARγ receptor signaling in vitro and under co-culture conditions with osteoblasts. Finally, we demonstrate that ABA regulates PCa dormancy in vivo following intratibial injection in an animal model. Together these data suggest that the ABA and PPARγ signaling pathways contribute to the establishment of PCa cellular dormancy in the bone marrow microenvironment. These findings may suggest critical pathways for targeting metastatic disease.