Protein ubiquitination in postsynaptic densities after transient cerebral ischemia.

The mechanisms underlying neurologic deficits and delayed neuronal death after ischemia are not fully understood. In the present study, we report that transient cerebral ischemia induces accumulation of ubiquitinated proteins (ubi-proteins) in postsynaptic densities (PSDs). By immunoelectron microscopy, we demonstrated that ubi-proteins were highly accumulated in PSD structures after ischemia. On Western blots, ubi-proteins were markedly increased in purified PSDs at 30 minutes of reperfusion, and the increase persisted until cell death in the CA1 region after ischemia. In the resistant DG area, however, the changes were transient and significantly less pronounced. Deposition of ubi-proteins in PSDs after ischemia correlates well with PSD structural damage in the CA1 region as viewed by electron microscopy. These results suggest that the ubiquitin-proteasome system fails to repair and remove damaged proteins in PSDs. The changes may demolish synaptic neurotransmission, contribute to neurologic deficits, and eventually lead to delayed neuronal death after transient cerebral ischemia.     

超声心动图对62例房间隔缺损封堵术后心功能变化的评价

目的：应用超声心动图评价房间隔缺损(ASD)封堵术前后左、右心室功能的变化。方法：对62例成功施行经皮穿刺ASD封堵术的患者进行研究。所有患者在术前、术后1周及1个月分别进行超声心动图检查．观察心脏大小及功能的改变。结果：ASD封堵术后，左室舒张末期前后径、左室舒张末期容积、左室每搏量及左室射血分数增大，而左室收缩末期容积未见明显改变；右室舒张末期前后径、右室舒张末期容积、右室收缩末期容积、右室每搏量、右室射血分数及右室心肌工作指数均减小。结论：经皮穿刺ASD封堵治疗既可减轻右室容量负荷，改善右室功能，也可改善左室的收缩功能：超声心动图对ASD封堵前后心脏血流动力学评价及疗效的观察起了重要的作用。     

Reduced expression of CD69 and adhesion molecules of T lymphocytes in asthmatic children receiving immunotherapy

T lymphocytes play a fundamental role in the initiation and regulation of chronic inflammatory responses in patients with asthma. CD69 is an early marker of T‐cell activation. The levels of intercellular adhesion molecule‐1 (ICAM‐1, CD54) and L ‐selectin have been reported to increase in patients with allergic diseases and asthma. The present study was therefore undertaken to investigate the expression of CD69, CD54, and L ‐selectin by T lymphocytes of children with asthma, before and after immunotherapy. Eighteen children newly diagnosed with asthma, 11 good and nine poor responders to immunotherapy, and 16 normal subjects, were enrolled in this study. The percentages of CD69⁺, CD54⁺, and CD62L⁺ cells in T lymphocytes were measured by using flow cytometry. The levels of CD69, CD54, and CD62L in serum and culture supernatants were determined by using enzyme‐linked immunosorbent assay (ELISA). The expression of CD69 and CD54 on CD3⁺ T lymphocytes was significantly higher in children with asthma than in control patients. All the patient groups expressed (spontaneously and following stimulation with phorbol myristate acetate and ionomycin together with mite‐extract proteins) greater amounts of CD69 and CD54 than did control subjects. With long‐term immunotherapy, the percentages of CD69⁺ and CD54⁺ T lymphocytes were significantly lower in patients with a good response to immunotherapy. Our results also showed significantly lower serum L ‐selectin levels following immunotherapy. In conclusion, successful immunotherapy resulted in decreased expression and production of CD69 and CD54. These results may explain, in part, the clinical efficacy of immunotherapy.     

斑点免疫金渗滤法的改进

目的 :改进斑点免疫金渗滤法的渗滤装置 ,降低成本 ,使之更适用于现场操作。方法 :用自制的圆形渗滤片替代塑料渗滤盒 ,并比较二者的效果。结果 :自制的渗滤片体积更小 ,成本更低 ,为一次性使用材料 ;检测抗体的效果与塑料渗滤盒法一致。结论 :自制的渗滤片优于常用的塑料渗滤盒     

Cell transplantation to improve ventricular function in the failing heart

Current therapies for congestive heart failure are limited in efficacy or in applicability. Cardiac cell transplantation offers a novel therapeutic approach to improve heart function. Although significant progress has been made over the past decade in the development of cell transplantation, only recently have investigators studied the changes in ventricular function following cell transplantation. This review article describes the latest research developments, evaluates recent studies of ventricular function after cell transplantation, and discusses the future directions of cell transplantation as a new therapy to ‘repair broken hearts’.     

瘢痕内切除术在治疗瘢痕疙瘩中的临床应用

目的：探讨一种较为经济有效地综合治疗瘢痕疙瘩的临床途径，方法：在瘢痕内切除大部分瘢痕组织，将保留的创缘两侧瘢痕皮肤修薄，无张力缝合，拆线后给予曲安缩松注射，一般3-5次，共治疗220例。结果：213例痊愈，随访6个月未复发，7例因月经紊乱等原因而放弃治疗，导致部分复发。结论：该方法简单、经济，不产生新的供皮区，给予曲安缩松注射次数少，较传统方法留瘢痕小。     

RANK signaling is not required for TNFalpha-mediated increase in CD11(hi) osteoclast precursors but is essential for mature osteoclast formation in TNFalpha-mediated inflammatory arthritis.

To address the controversy of whether TNFalpha can compensate for RANKL in osteoclastogenesis in vivo, we used a TNFalpha-induced animal model of inflammatory arthritis and blocked RANKL/RANK signaling. TNFalpha increased osteoclast precursors available for RANK-dependent osteoclastogenesis. RANK signaling is not required for the TNFalpha-stimulated increase in CD11b(hi) osteoclast precursors but is essential for mature osteoclast formation. INTRODUCTION: Although critical roles of TNFalpha in inflammatory arthritis and RANKL in bone resorption have been firmly established, a central controversy remains about the extent to which TNFalpha can compensate for RANKL during osteoclastogenesis and the stage at which RANK signaling is required for osteoclastogenesis. Here, we used the human TNFalpha transgenic mouse model (TNF-Tg) of erosive arthritis to determine if there are both RANK-dependent and -independent stages of osteoclastogenesis in TNFalpha-induced erosive arthritis. MATERIALS AND METHODS: Osteoclastogenesis and osteoclast precursor (OCP) frequency were analyzed using histology, fluorescence-activated cell sorting (FACS), and cell culture from (1) TNF-Tg mice treated with the RANKL antagonist, RANK:Fc, or (2) TNF-Tg X RANK -/- mice generated by crossing TNF-Tg mice with RANK-/- mice. RESULTS: Treatment of TNF-Tg mice, which have increased OCPs in their spleens, with RANK:Fc dramatically reduced osteoclast numbers on the surface of their arthritic joints and within their bones, but did not decrease CD11b(hi) OCP numbers in their spleens. Long-term RANK:Fc administration alleviated joint erosion. Furthermore, TNF-Tg x RANK -/- mice had severe osteopetrosis, no osteoclasts, and no joint erosion, but increased CD11b(hi) precursor numbers that failed to form mature osteoclasts in vitro. CONCLUSION: RANK signaling is essential for mature osteoclast formation in TNFalpha-mediated inflammatory arthritis but not for the TNFalpha-induced increase in CD11b(hi) OCP that subsequently can differentiate into osteoclasts in inflamed joints.     

宫腔镜辅助下分段诊刮术与单纯分段诊刮术诊断子宫内膜癌的比较

为比较宫腔镜辅助下分段诊刮术与单纯分段诊刮术在诊断子宫内膜癌中的临床意义 ,将经手术后病理证实的子宫内膜癌患者分为 2组 :宫腔镜辅助下分段诊刮组 (A组 ) 3 1例 ;单纯分段诊刮组 (B组 ) 3 9例。比较 2组术前诊断子宫内膜癌的准确性及开腹手术时腹水细胞学的检查结果。 2组患者的年龄、临床病理分期、病理分级及组织学类型差异无显著性。A组诊断宫颈受累的准确率为 96.77% (3 0 / 3 1 ) ,假阳性率为 3 .2 3 % (1 / 3 1 ) ;B组分别为 79.49%(3 1 / 3 9) ,1 5 .3 8% (6/ 3 9)。 2组准确率比较 ,差异有显著性 (P <0 .0 5 )。取腹水或腹腔冲洗液行细胞学检查。A组细胞学阳性率为 6.45 % (2 / 3 1 ) ,B组为 1 4.2 9% (3 / 2 1 ) ,2组间差异无显著性 (P >0 .0 5 )。提示 :宫腔镜辅助下分段诊刮术可提高术前诊断子宫内膜癌的准确性 ,从而避免不必要地扩大手术范围 ,而且不增加腹腔内播散的危险。     

大鼠慢性应激性水浸溃疡模型的复制

本文复制了慢性、应激性水浸溃疡模型,23℃每天拘束水浸4小时,4天后所得溃疡病变明显,溃疡指数是13.8士4.5mm~2,且再现性良好,是一个较好的慢性、应激性溃疡模型。哌哌西平对此溃疡具有较强的防治作用。     

The characteristics of Hep-2 cell with multiple drug resistance induced by Taxol.

OBJECTIVE: To investigate the characteristics of Hep-2 cell with multidrug resistance (MDR) induced by Taxol. STUDY DESIGN: Hep-2 cells were exposed in stepwise escalating concentration of Taxol to develop the resistant cell line-Hep-2T. Cell cycle distribution, apoptosis, and rhodamine accumulation were studied through flow cytometry. The MDR1 and MRP1 genes were detected through real-time quantitative RT-PCR, and the corresponding proteins were detected through Western blotting. RESULTS: The drug resistance of Hep-2T cells to Taxol, doxorubicin, gemcitabine, 5-FU, and cisplatin all increased. The percentage of G0/G1 phase and the antiapoptosis ability increased significantly compared with Hep-2 cells. Both MDR1 and MRP1 also increased at gene and protein level, though MDR1 was more prominent. CONCLUSION: More emphasis should be laid on MDR1/Pgp, the non-Pgp substrate chemotherapeutic agents, and the changes of cell cycle distribution to prevent MDR induced by Taxol. SIGNIFICANCE: These findings may provide theoretical support for the reverse of MDR.