WR-2721对γ线照射小鼠胃排空的防护作用

小鼠经γ线1200rad照射后胃排空受到明显抑制,如照前15min腹腔注射WR-2721 5mg或10mg对照后3天胃排空的抑制有明显改善。虽然WR-2721药物本身对胃排空具有一定的抑制作用,但经过24～48h后则可表现出对胃排空有一定程度的改善效应,这可能与该药减轻急性放射损伤的过程有关。     

高脂血症患者血小板体积及有关参数的研究

本文报道242例高脂血症患者血小板(PLT)、平均血小板数(MPLT)及平均血小板体积(MPV)等参数的测定结果,其中高胆固醇并高甘油三酯患者,PLT、MPLT及巨大血小板比例(Macro-PLT)高于正常,MPV正常;而单纯高胆固醇或高甘油三酯患者,上述指标与正常人无显著性差异。提示高胆固醇并高甘油三酯患者,存在血小板生成动力学异常,其血小板的破坏增加,生成率加速、但处于一种高水平的动态平衡之中。这可能是高脂血症出现高凝状态的原因之一。同时表明此类患者使用抗血小板疗法具有一定的合理性和必要性。     

新疆出血热病毒与流行性出血热病毒的生物学特性比较

本文通过免疫荧光(IF)和电镜(EM)技术对新疆出血热(XHF)及流行性出血热(EHF)病毒的生物学特性在Vero E_6及LLC-MK_2两株传代细胞上进行了比较。两种病毒感染两株细胞后免疫荧光染色有两种不同的荧光形态特征,两种病毒对细胞的敏感性明显不同,XHF病毒在LLC-MK_2细胞上感染后6～8天可出现明显的细胞病变,而EHF病毒感染此细胞后则不引起病变。电镜观察到两种病毒在LLC-MK_2细胞中都能形成与布尼病毒相似的形态特征。     

Dedifferentiated liposarcoma of the liver

Among the rare occurrences of primary malignant mesenchymal tumors of the liver, the development of liposarcoma has been only theoretically listed--there is no proven example in the literature. This article documents a case of primary liposarcoma of the liver in a 30-year-old woman who presented with a huge intrahepatic tumor in the left lobe measuring 14 X 10 X 6 cm. It was composed of two distinct macroscopic and histologic features--the well-differentiated liposarcoma and the cellular, nonlipogenic pleomorphic sarcoma. The former was a mature, lipomatous tumor with various stages of lipoblasts. The latter was much more cellular, made up of pleomorphic cells admixed with a few areas of spindle cells with many mitotic figures, resembling a pleomorphic variant of malignant fibrous histiocytoma. Oil red O stain revealed multifocal, but a scanty amount, of fat-storing tumor cells in both compartments aside from large fat globules in the differentiated area. This is the first reported case of primary liposarcoma of the liver.     

γ线照后大鼠胃组织乙酰胆碱含量胆碱酯酶活性及平滑肌对乙酰胆碱反应性的变化

本文以大鼠为实验对象,观察了γ线8Gy照后胃组织内乙酰胆碱含量、胆碱酯酶活性及平滑肌对乙酰胆碱反应性的变化。结果表明,照后1/24～l天胃组织内乙酰胆碱含量明显下降,3天趋向正常,5天基本恢复至照前水平。胃组织的胆碱酯酶活性在照后l/24～5天基本无改变。在同一剂量照后1h,胃窦平滑肌对乙酰胆碱的反应与照前近似,l天后开始减弱,3天后明显下降,与正常相比有非常显著差异。     

Central Nervous System Lymphomatoid Granulomatosis Presenting with Parkinsonism

Lymphomatoid granulomatosis (LG) is a potentially malignant lymphoproliferative disorder. The lung is the most common involved site, followed by the skin and nervous system. However, LG of the central nervous system presenting with Parkinsonism is very rare. We report a patient with LG who presented with parkinsonian features such as bilateral rigidity, bradykinesia, and agitation. Brain magnetic resonance imaging showed multifocal punctuate enhanced lesions in both supra- and infratentorial areas. Steroid pulse therapy resulted in a dramatical improvement in the symptoms and MRI abnormalities.     

螺旋CT三维重建影像在胫骨平台骨折诊疗中的价值

目的探讨螺旋CT三维重建影像在胫骨平台骨折诊断和治疗中的临床使用价值。方法2001年8月～2005年4月收集38例胫骨平台骨折分别行X线片和螺旋CT三维重建影像检查,对照术中所见,分析比较螺旋CT三维重建影像在临床诊断和治疗中的作用。结果X线片检查2例无法明确诊断,骨折分型错误6例;螺旋CT三维重建诊断、分型均正确。X线片与螺旋CT三维重建影像在确立诊断方面未见明显差异,但在分型和指导治疗方面,螺旋CT三维重建影像明显优于前者。结论螺旋CT三维重建影像能直观、立体地显示胫骨平台骨折的形态,有助于骨折的分型及治疗。     

Differential gene expression in cultured osteoblasts and bone marrow stromal cells from patients with Paget's disease of bone.

Paget's disease is a focal condition of bone. To study changes in cells within pagetic lesions, we cultured osteoblasts and stromal cells from 22 patients and compared gene expression in these cells to cells from healthy bone. We identified several differentially regulated genes, and we suggest that these changes could lead to the formation of the lesions. INTRODUCTION: Paget's disease is a focal condition of bone of unknown cause. Although it is regarded as primarily an osteoclast disorder, the tight coupling of the activity of osteoclasts and osteoblasts suggests that the osteoblast could play a key role in its pathogenesis. The aim of the study was to identify possible changes in pagetic osteoblasts and stromal cells that might contribute to the development of pagetic lesions. MATERIALS AND METHODS: Candidate genes were identified based on known bone cell regulators, supplemented with microarray analysis. Gene expression was determined by real-time PCR in primary cultures of osteoblasts and bone marrow stromal cells from pagetic patients and control subjects. Concentrations of secreted proteins were determined by ELISA. RESULTS: Dickkopf1 mRNA and protein levels were increased in both pagetic osteoblast and stromal cell cultures, and interleukin (IL)-1 and IL-6 were overexpressed in pagetic osteoblasts. These changes parallel recent findings in myeloma bone disease, which shares some clinical similarities with Paget's disease. Alkaline phosphatase was overexpressed, and bone sialoprotein and osteocalcin were underexpressed in pagetic osteoblasts, consistent with their circulating levels in pagetic patients. It is hypothesized that overexpression of Dickkopf1, IL-1, and IL-6 would result in stimulation of osteoclast proliferation and inhibition of osteoblast growth, leading to the development of the characteristic lytic bone lesions. By stimulating osteoblast differentiation, Dickkopf1 and IL-6 may also promote mineralization, leading to the conversion of lytic lesions to sclerotic. CONCLUSIONS: These findings suggest that dysregulated gene expression in pagetic osteoblasts could cause the changes in bone cell number and function characteristic of Paget's disease.     

Enhanced chondrogenesis and Wnt signaling in PTH-treated fractures.

Studies have shown that systemic PTH treatment enhanced the rate of bone repair in rodent models. However, the mechanisms through which PTH affects bone repair have not been elucidated. In these studies we show that PTH primarily enhanced the earliest stages of endochondral bone repair by increasing chondrocyte recruitment and rate of differentiation. In coordination with these cellular events, we observed an increased level of canonical Wnt-signaling in PTH-treated bones at multiple time-points across the time-course of fracture repair, supporting the conclusion that PTH responses are at least in part mediated through Wnt signaling. INTRODUCTION: Since FDA approval of PTH [PTH(1-34); Forteo] as a treatment for osteoporosis, there has been interest in its use in other musculoskeletal conditions. Fracture repair is one area in which PTH may have a significant clinical impact. Multiple animal studies have shown that systemic PTH treatment of healing fractures increased both callus volume and return of mechanical competence in models of fracture healing. Whereas the potential for PTH has been established, the mechanism(s) by which PTH produces these effects remain elusive. MATERIALS AND METHODS: Closed femoral fractures were generated in 8-wk-old male C57Bl/6 mice followed by daily systemic injections of either saline (control) or 30 microg/kg PTH(1-34) for 14 days after fracture. Bones were harvested at days 2, 3, 5, 7, 10, 14, 21, and 28 after fracture and analyzed at the tissue level by radiography and histomorphometry and at the molecular and biochemical levels level by RNase protection assay (RPA), real-time PCR, and Western blot analysis. RESULTS: Quantitative muCT analysis showed that PTH treatment induced a larger callus cross-sectional area, length, and total volume compared with controls. Molecular analysis of the expression of extracellular matrix genes associated with chondrogenesis and osteogenesis showed that PTH treated fractures displayed a 3-fold greater increase in chondrogenesis relative to osteogenesis over the course of the repair process. In addition, chondrocyte hypertrophy occurred earlier in the PTH-treated callus tissues. Analysis of the expression of potential mediators of PTH actions showed that PTH treatment significantly induced the expression of Wnts 4, 5a, 5b, and 10b and increased levels of unphosphorylated, nuclear localized beta-catenin protein, a central feature of canonical Wnt signaling. CONCLUSIONS: These results showed that the PTH-mediated enhancement of fracture repair is primarily associated with an amplification of chondrocyte recruitment and maturation in the early fracture callus. Associated with these cellular effects, we observed an increase in canonical Wnt signaling supporting the conclusion that PTH effects on bone repair are mediated at least in part through the activation of Wnt-signaling pathways.