门诊老年冠心病患者用药知识需求的调查

冠心病是老年人的常见病、多发病,致残或死亡率已居常见病之首[1]。目前,药物治疗仍是冠心病二级预防的主要措施。近年来研究发现,83·3%的冠心病患者无法正确使用药物,用药依从性差[2]。分析原因,87%的门诊老年慢性病患者包括冠心病患者在内,主观不遵医用药是由于在用药过程中出现诸多用药问题时得不到相关知识信息支持所导致[3]。另外,通过调查证实冠心病患者对用药知识的需求亦居前列,尤其是出院后用药知识是首要需求[2,4-6]。由此表明,对门诊老年冠心病患者进行用药知识教育十分必要。依据健康教育学方法,分析患者的教育需求是制定教育…     

呼出气氢测定试验对飞行人员乳糖酶缺乏症的研究

对66名汉族飞行人员进行乳糖呼出气氢测定试验,乳糖吸收不良的发生率为83.3％,其中乳糖不耐受者占34.6％;与一般汉族人群无明显差别。对10名确定为中度以上乳糖吸收不良的飞行人员进行250ml鲜牛奶的试验结果,有50％呼出气氢含量在正常范围,并无一例出现胃肠道症状。提示较长期食用牛奶未能使乳糖酶缺乏状态发生改变,但每日食用适量牛奶属合理营养。     

Genetic imbalances in pleomorphic xanthoastrocytoma detected by comparative genomic hybridization and literature review.

Pleomorphic xanthoastrocytoma (PXA) is a rare, low-grade astrocytic tumor found in the central nervous system. Histologically, the tumor is characterized by markedly pleomorphic and lipidized cells. Although most of the patients have a favorable prognosis, a small number of cases undergoing recurrence or progression to anaplastic astrocytoma were reported. Very few genetic studies have been performed on PXA because of its rarity and the pathogenesis of this neoplasm is largely unknown. In order to provide an overview of genetic alterations in PXA, we performed comparative genomic hybridization to identify chromosomal imbalances (DNA gains and losses) in three cases of PXA. Genetic imbalance was detected on at least one chromosome for each case. One case, which revealed multiple genetic alterations, showed a poor prognosis. DNA gain on chromosome 7 and loss on 8p were demonstrated in two of three cases, suggesting that the candidate gene(s) located on these regions may play a role in the development of PXA. Further studies are needed to identify the residing candidate genes that are involved in the tumorigenesis of PXA. In addition, the histopathological features and previous genetic studies on PXA are reviewed.     

结核性淋巴结炎的“结节病”样变型

对１２例经病理学专家会诊、从病变上认定的淋巴结“结节病”石蜡包埋组织，应用结核杆菌ＤＮＡ特异性序列片段的聚合酶链反应（Ｍ．ＴＢ－ＰＣＲ）技术、ＢＣＧ免疫组化（ＢＣＧ－ＩＨＣ）技术和抗酸染色（ＡＦ）进行了分支杆菌／结核杆菌检测。在这１２例考虑为“结节病”的病例中：有１例呈ＢＣＧ－ＩＨＣ和Ｍ。ＴＢ－ＰＣＲ两项阳性；另１例呈ＡＦ、ＢＣＧ－ＩＨＣ和Ｍ．ＴＢ－ＰＣＲ三项阳性。研究结果提示：（１）某些结核性淋巴结炎可呈结节病样病变；（２）淋巴结结节病很可能与分支杆菌／结核杆菌感染有关。     

血清抗果蝇唾腺染色体抗体测定及临床意义探讨

以果蝇唾腺作为基质,用间接免疫荧光法检测血清抗果蝇唾腺染色体抗体[简称抗染色体抗体(Anti—chromosome antibody AchrA)]。正常人及其它风湿性疾病患者共151例,均为阴性,而系统性红斑狼疮(SLE)患者44例,AchrA阳性者占16例(36.4%)。揭示AchrA对SLE有高度特异性及一定的敏感性。对比SLE患者的AchrA及抗核抗体(ANA),双阳性占15例(34.1%),提示与两种抗体起反应的核成分不尽相同。     

Fgl2 prothrombinase expression in mouse trophoblast and decidua triggers abortion but may be countered by OX-2

Spontaneous abortion of normal karyotype embryos in mice and in humans is associated with an increase in uterine T helper (Th) 1 type proinflammatory cytokines, tumour necrosis factor (TNF)-alpha, interferon-gamma and interleukin (IL)-1, and a deficiency of Th2/3 type cytokines, IL-4, IL-10, and transforming growth factor (TGF)-beta2. In mice, Th1 cytokines up-regulate a novel prothrombinase, fgl2, which via thrombin, leads to activation of polymorphonuclear leukocytes that terminate the pregnancy. Here we show that Th1 cytokines up-regulate fgl2 mRNA in fetal trophoblast and secondary decidua of CBA/JxDBA/2 and CBA/JxBALB/c matings, and promote fibrin deposition. This pattern is accompanied by a high rate of abortion. However, the spontaneous abortion rates in abortion-prone CBAxDBA/2 matings and in low abortion rate CBAxBALB/c matings were significantly lower than that expected from the frequency of implantations with high levels of fibrin and fgl2 mRNA(hi). As the glycoprotein OX-2 occurs in the pregnant rat uterus and can deviate cytokine responses to Th2/3, we investigated OX-2 in pregnant CBA/J mice. We found OX-2 mRNA was present at the same sites as fgl2 mRNA, but was reduced in response to Th1 cytokines. Furthermore, anti-OX-2 raised the abortion rate to predicted levels, while recombinant OX-2 dramatically reduced the abortion rate. Fgl2 prothrombinase may provide a mechanism explaining pregnancy loss, and conversely, successful pregnancy may be due in part to OX-2-dependent activation of maternal tolerance mechanisms at the feto-maternal interface.     

高糖对体外培养Schwann细胞生长及细胞外信号调节激酶1／2磷酸化的影响

目的:探讨高糖对体外培养Schwann细胞生长及细胞外信号调节激酶(ERK)磷酸化的影响.方法:按照培养液中葡萄糖浓度的小同,分为对照组与高糖组.用MTT法检测Schwann细胞生长情况;用ELISA法检测对照组与高糖组ERK1/2磷酸化的程度,以及加入神经源性一氧化氮合成酶(nNOS)抑制剂后ERK1/2磷酸化的程度.结果:高糖浓度下,细胞虽有增殖但幅度及时程明显低于对照组,高糖抑制Schwann细胞生长;随着精浓度的升高.ERK1/2磷酸化的程度逐渐增加,并与加入nNOS抑制剂有相似的表现.结论:高糖抑制Schwann细胞生长,并且降低nNOS的量,减弱一氧化氮(NO)对ERK1/2的抑制作用,导致ERK1/2磷酸化水平升高.     

Bednar tumor (pigmented dermatofibrosarcoma protuberans). An analysis of six cases

Six cases of Bednar tumor were analyzed clinicopathologically along with a review of 39 published cases. The findings were then compared with data on 44 cases of ordinary dermatofibrosarcoma protuberans (DFSP) obtained from our files. The clinical manifestations of the patients and the anatomic locations of the tumors were similar between the two categories, but the rate of recurrence was lower in cases of Bednar tumor. The histologic pattern of Bednar tumor was indistinguishable from ordinary DFSP except for scattered melanosome-containing cells. Ultrastructural and immunohistochemical examinations showed no evidence of neuroectodermal differentiation of dominant spindle-shaped cells in Bednar tumor, supporting a fibroblastic line of differentiation. The origin and pathogenesis of the melanosome-containing cells were considered. These cells failed to react with HMB-45, a melanoma-specific antibody, and the large majority of melanosomes present were mature or at Stage IV, plus a few immature ones at Stage II. These pigmented cells do not appear to be neoplastic, and cannot be used as proof to indicate that Bednar tumor is a neuroectodermal neoplasm.