改良肾大部切除大鼠诱发慢性肾衰模型的建立

对5/6切除大鼠肾脏诱发其慢性肾功能衰竭的动物模型进行改良,该方法省时省力,可以减少麻药用量不当造成的大鼠死亡,随差血肌酐(Scr)、尿素氮(BUN)的增加,肾衰逐渐加重,为药理研究及筛选治疗慢性肾衰的有效药物提供了一种实验对象。     

Unscheduled CDK1 activity in G1 phase of the cell cycle triggers apoptosis in X-irradiated lymphocytic leukemia cells

Cyclin-dependent kinase 1 (CDK1) is a major component of the cell cycle progression engine. Recently, several investigations provided evidence demonstrating that unscheduled CDK1 activation may also be involved in apoptosis in cancerous cells. In this article, we demonstrate that X-ray irradiation induced G1 arrest in MOLT-4 lymphocytic leukemia cells, the arrest being accompanied by reduction in the activity of CDK2, but increased CDK1 activity and cell apoptosis in the G1 phase. Interestingly, this increase in CDK1 and apoptosis by ionizing radiation was prevented by pretreatment with the CDK1 inhibitor, roscovitine, suggesting that CDK1 kinase activity is required for radiation-induced apoptotic cell death in this model system. Furthermore, cyclin B1 and CDK1 were detected co-localizing and associating in G1 phase MOLT-4 cells, with the cellular lysates from these cells revealing a genotoxic stress-induced increase in CDK1 phosphorylation (Thr-161) and dephosphorylation (Tyr-15), as analyzed by postsorting immunoprecipitation and immunoblotting. Finally, X-irradiation was found to increase Bcl-2 phosphorylation in G1 phase cells. Taken together, these novel findings suggest that CDK1 is activated by unscheduled accumulation of cyclin B1 in G1 phase cells exposed to X-ray, and that CDK1 activation, at the wrong time and in the wrong phase, may directly or indirectly trigger a Bcl-2-dependent signaling pathway leading to apoptotic cell death in MOLT-4 cells. Received 30 March 2006; received after revision 23 June 2006; accepted 24 August 2006 J. Wu and Y. Feng contributed equally to this work.     

Hedgehog signaling in pancreas development and disease

Since its discovery, numerous studies have shown that the Hedgehog (Hh) signaling pathway plays an instrumental role during diverse processes of cell differentiation and organ development. More recently, it has become evident that Hh signaling is not restricted to developmental events, but retains some of its activity during adult life. In mature tissues, Hh signaling has been implicated in the maintenance of stem cell niches in the brain, renewal of the gut epithelium and differentiation of hematopoietic cells. In addition to the basal function in adult tissue, deregulated signaling has been implicated in a variety of cancers, including basal cell carcinoma, glioma and small cell lung cancer. Here, we will focus on the role of Hh signaling in pancreas development and pancreatic diseases, including diabetes mellitus, chronic pancreatitis and pancreatic cancer. Received 5 August 2005; received after revision 4 November 2005; accepted 22 November 2005     

慢性能量缺乏症防护理论研究

慢性能量缺乏症是运动员常见症状。本研究目的在于深入了解慢性能量缺乏症影响及其防护理论的研究进展。通过相关文献的分析和归纳,本研究结论认为慢性能量缺乏是生殖系统功能失调的直接原因;“能量可用性”的引入来衡量能量平衡具有一定优势,“能量可用性”的阈值需要进一步确认。     

Chronic stress induced proliferation and activation of mast cells of gastric antrum in rats

To explore chronic eration and activation of mast heterotypic stressors induced prolifcells in gastric antrum mucosa by ultrastructure alterations of mast cells, chronic unpredictable heterotypic stressors were used as a study model. The mean immunofluorescence magnitude of mast cell protease 1 （MCP-1） taken from chronic stress rats were 37.4±7.7, significantly higher （p〈0.05） than the value of normal control group （24.8±5.6）. Chronic unpredictable haterotypic stressors appeared also to induce ultrastructure alterations of mast cells. It indicated that mast cells were proliferated and activated, while mast cell granules were hyperplasiaed. Most granules had obvious intragranular changes with loss of electron-dense material. The morphologic evidence showed that macrophages and leukocytes infiltrated in chronic stress rats. Some granules of leukocytes adhered to the surface of mast cell, and formed a bridge. Macrophages phagocytized the mast cell granules.     

Effects of mistletoe (Viscum album L.) extracts on cultured tumor cells

Summary Bacterially fermented mistletoe preparations (BFMP) were tested on rat hepatoma tissue culture (HTC) cells and human leukemia Molt 4 cells. A dose-dependent inhibition of the growth rate of the cells was observed. For both cell lines, cytostatic concentrations, expressed in weight of fresh plant, were 0.5 mg/ml culture medium for oak BFMP and 1 mg/ml for apple tree BFMP. However, the action of the two preparations was markedly different on each cell line. Non-viable HTC cells were not stained by trypan blue while non-viable Molt 4 cells were fully colored by this reagent. A lysis of cellular membranes of HTC cells was observed by electron microscopy. Furthermore, oak BFMP inhibited the growth of virus transformed 3T3-SV40 cells more than that of non-transformed 3T3 cells. In contrast to BFMP, non-fermented extracts and a purified mistletoe lectin showed a greater inhibition of the growth of Molt 4 cells than of HTC cells. Samples withdrawn at different times during fermentation gradually lost their inhibitory effect on the growth of Molt 4 cells while their action on HTC cells increased up to the 4th day of fermentation. These results are discussed in relation to the cytotoxic substances of mistletoe already characterized.The bacterially fermented mistletoe preparations, named BFMP in the text, were obtained from the Hiscia Institute, CH-4144 Arlesheim, Switzerland, under the name of Iscador. For oak BFMP, mistletoe was fromQuercus petraea Liebl. andQuercus robur L.; for apple tree BFMP fromMalus domestica Borkh.     

鼻内窥镜,柯—陆手术联合进路治疗慢性鼻窦？…

探讨鼻内窥镜,柯－陆手术联合进路治疗伴有上颌窦病变的慢性鼻窦炎,鼻息肉的疗效。方法：对１０４例伴有上颌窦病变的慢性鼻窦炎患者行鼻内窥镜、柯－陆手术联合进路鼻窦手术,彻底清除病变。结果：术后随访６－１２个月,治愈８５例,好转１５例,无效４例,总有效率为９６．１％。     

选择性COX-2抑制剂尼美舒利对白血病K562细胞增殖的影响

目的:观察选择性COX-2抑制剂尼美舒利对人类骨髓白血病K562细胞增殖和凋亡的影响。方法:分别以尼美舒利25、50、100μg.mL-1体外处理骨髓白血病K562细胞,采用MTT比色法、流式细胞仪分析技术及DNA片段凝胶电泳等方法,检测尼美舒利对K562细胞增殖和凋亡的影响。结果:尼美舒利剂量依赖性地抑制K562细胞增殖,其中等剂量组(50μg.mL-1)的抑制作用强于阿霉素组(25μg.mL-1);尼美舒利可诱导细胞凋亡,使细胞阻滞于G0/G1期,S期细胞明显减少,其诱导细胞凋亡的作用也呈剂量依赖性(剂量由低至高,凋亡率分别为(3.4±2.8)%,(16.8±1.8)%和(42.7±2.5)%;DNA条带分析也进一步证实了尼美舒利的促凋亡作用。结论:尼美舒利在体外可显著抑制K562细胞增殖,该作用可能与其干扰细胞周期、诱导细胞凋亡有关。     

异丙肾上腺素致大鼠心肌缺血型慢性心力衰竭的实验研究

目的:建立异丙肾上腺素(ISO)缺血型慢性心力衰竭(CHF)大鼠模型,为研究慢性心衰的发病机制和有效治疗措施提供理想的动物模型。方法:模型组大鼠首次按3.0 mg/(kg.d)腹腔注射ISO连续3 d,观察4周,第5周按2.0 mg/(kg.d)继续给药2 d,观察1周,第6周再按3.0 mg/(kg.d)给药2 d,1周后进行血流动力学指标、血清心肌肌钙蛋白-Ⅰ(cTn-Ⅰ)、血管紧张素Ⅱ(AngII)水平等测定和肺组织病理学观察。结果:模型组大鼠较正常对照组左室收缩最大速率降低25.2%,左室舒张最大速率绝对值降低了33.7%,肺组织病理改变明显,血清cTn-Ⅰ和AngII水平明显增加(P<0.01)。结论:采用大鼠间断性腹腔反复注射一定剂量ISO制备慢性心衰模型方法稳定、可靠、容易控制。     

慢性热应激对猪肠道CD3^＋T细胞表达的影响

以猪肠道CD3＋T细胞为研究对象,旨在观察慢性热应激对猪肠道黏膜免疫功能的影响。12头小型猪随机平均分成热应激组和常温对照组两组。人工气候室内,热应激组模拟夏季炎热气候,气温从26～39℃24h循环变温,在39℃时维持4h;常温对照组在24℃下饲养。试验持续10d,热应激10d后39℃高温持续期结束剖杀试验猪,取其十二指肠中段、空肠及回肠中段进行固定、石蜡切片、免疫组织化学染色,观察十二指肠、空肠及回肠中CD3＋T细胞数量的变化。结果显示：实验猪十二指肠黏膜上皮层、固有层及十二指肠肠腺均呈CD3强阳性,与对照组相比,CD3阳性面积系数显著上升（P〈0.05）;空肠和回肠黏膜上皮层的CD3阳性细胞数量也显著增加（P〈0.05）,而固有层中的CD3阳性细胞数量则无明显变化,增加的幅度小于十二指肠。慢性热应激中实验猪肠道结构严重受损,消化吸收功能严重下降,而肠道CD3＋T细胞的增多,可能是机体肠道黏膜免疫功能的一种代偿性增强反应。