甘露聚糖肽联合吗啡对癌痛治疗的临床研究

目的：观察甘露聚糖肽联合阿片类药物治疗癌痛的临床效果。方法：采取随机、对照试验方法,64例晚期恶性肿瘤伴疼痛的患者,年龄37~69岁,VAS评分≥6,随机分为两组：吗啡组32例,甘露聚糖肽＋吗啡组32例。达到疼痛缓解时（VAS评分≤3分）维持给药直至观察终点,然后比较治疗前后的疼痛缓解程度、吗啡日均消耗量、生活质量的改变。结果：与治疗前相比,两组癌痛均有不同程度的缓解,联合用药组总缓解率高于单药组（P〈0.05）;联合用药组的吗啡日均消耗量比单药组少（P〈0.05）;联合用药组患者生活质量较单药组明显提高。结论：甘露聚糖肽联合吗啡能有效地控制癌痛,减少吗啡的用量,并能提高患者生活质量。     

585名学龄儿童血铅水平测定分析

目的:探讨呼和浩特市学龄儿童血铅水平及铅中毒现状.方法:采用原子吸收光谱法对受测试儿童进行血铅测定.结果:受测试的585名7～12岁儿童血铅平均值为52.14 μg/L,其中47名儿童血铅≥100 μg/L,铅中毒率为8.03%;不同年龄组间血铅水平及铅中毒率差异无统计学意义;不同性别儿童血铅水平及铅中毒率比较差异有显著性意义.结论:呼和浩特市学龄儿童血铅水平不容忽视.     

MSCs成骨分化中BMP2对成骨转录因子SATB2表达的调控作用

目的探索间充质干细胞（MSCs）成骨分化中骨形态发生蛋白2（BMP2）对成骨转录因子SATB2表达的调控作用。方法体外培养小鼠间充质细胞系C2C12,腺病毒介导的BMP2（Adv-BMP2）诱导其向成骨细胞分化,建立并验证C2C12细胞成骨分化细胞模型。Real-Time PCR和Western blotting分别检测C2C12细胞成骨分化过程中经不同浓度Adv-BMP2处理不同时间时SATB2 mRNA和SATB2蛋白表达;以经相应浓度Adv-β-Gal处理细胞作对照。结果经150 pfu/cell Adv-BMP2处理C2C12细胞5 d后,成骨细胞标志基因Ⅰ型胶原、骨唾液酸蛋白和骨钙素表达以及碱性磷酸酶活性均显著增加,MSCs成骨分化模型构建成功。150 pfu/cell Adv-BMP2诱导C2C12细胞成骨分化过程中,SATB2 mRNA和SATB蛋白表达随分化进程而增加;Adv-BMP2浓度为0～225 pfu/cell时,SATB2表达随Adv-BMP2浓度升高而增加。结论 BMP2可调控SATB2的表达,从而影响MSCs成骨分化。     

抗肿瘤药羟喜树碱对Wnt通路抑制剂FrpHE的表达作用

目的研究加入羟喜树碱后Wnt通路抑制因子FrpHE(frizzled relatd protein)在人肿瘤细胞株中的表达调控作用。方法选择人肝癌HepG2(HepG2,含野生型p53;Hep3B,p53缺失)和人大肠癌(Lovo,含野生型p53),人神经胶质瘤细胞(U251,p53突变)细胞株为模型,观察抑制剂FrpHE以及反映Wnt通路功能变化的-βcatenin的表达。以RT-PCR技术检测Wnt通路抑制因子FrpHE表达的调节作用,以流式细胞术检测肿瘤细胞中Wnt通路的关键调节因子-βcatenin的表达。结果加入羟喜树碱24h后FrpHE mRNA表达水平在人肝癌细胞(HepG2,含野生型p53;Hep3B,p53缺失)中与对照组相比表达水平显著增加。在人大肠癌细胞(Lovo,含野生型p53)和人神经胶质瘤细胞(U251,p53突变型)中,未见FrpHE mRNA表达。-βcatenin的阳性细胞百分比强度和平均荧光量强度与对照组相比,表达水平降低。结论羟喜树碱在人肝癌细胞中能明显诱导抑制剂FrpHE mRNA的表达。     

颗粒细胞抑制素B的表达及其在女性生殖中的意义

目的探讨抑制素B(INH-B)在颗粒细胞的表达与卵巢反应、卵子成熟及胚胎发育之间的关系。方法收集39名实施体外受精-胚胎移植(IVF-ET)者的颗粒细胞,通过免疫组化技术测定颗粒细胞INH-B表达强度。按照获卵数将患者分为三组,A组:获卵≤5枚;B组:获卵61~5枚;C组:获卵≥16枚。分析比较各组INH-B表达强度、胚胎实验室数据及临床结局。结果①A组的INH-B表达强度显著低于其他二组(P<0.001),B组与C组间INH-B表达强度无显著差异(P>0.05)。②颗粒细胞INH-B表达强度与获卵数、受精卵数、卵裂数及可用胚胎数呈正相关(均P<0.001)。③颗粒细胞INH-B表达强度与IVF-ET临床妊娠率无显著相关(P>0.05)。结论颗粒细胞INH-B表达可反映细胞自身的功能状态,颗粒细胞功能减退是卵巢反应减低、发育卵泡数目减少的主要原因之一。     

The Tall R Wave in Lead V1 in Posterior Myocardial Infarction: A Reciprocal Sign or a His-Purkinje Conduction Disturbance?

The significance of the tall R wave in lead V1 with an R/S ratio greater than or equal to 1 in posterior myocardial infarction (PMI) was investigated in 28 patients during programmed electrical stimulation. The patients had been admitted with acute PMI documented by electrocardiogram and proven by enzymatic increase. Electrophysiological study was performed 3 weeks after acute PMI. In 17 of the 28 patients (group 1), the tall R wave in V1 disappeared during stimulation: In 13 of them a premature atrial extrastimulus was responsible for an abrupt normalization of QRS complex in V1 related to an increase in AH or HV interval. In the 4 remaining patients the disappearance of the tall R wave in V1 was related to a sinus pause. In 14 patients of group 1, a different prematurity in atrial stimulation induced a right or left bundle branch block (BBB). In 11 of the 28 patients (group 2) the tall R wave in V1 was unchanged but a premature atrial extrastimulus induced a right BBB in 5 patients and a left BBB in 6. In conclusion, the normalization of QRS complex in lead V1 during atrial stimulation or alterations in cycle length suggests that the tall R wave in V1 in PMI is not a simple reciprocal sign of leads V8 V9. Its association with different varieties of BBB and changes in AH or HV intervals could suggest a relationship with a His-Purkinje conduction disturbance in some patients.     

Metabolic, membrane, and functional responses of human polymorphonuclear leukocytes to platelet-activating factor

The phospholipid mediator of anaphylaxis, platelet-activating factor (PAF) is chemotactic for polymorphonuclear leukocytes (PMN). We have examined this agent's effects on several other PMN functions. Human PMN were prepared from heparinized venous blood by Ficoll gradient. Metabolic burst was examined by measurement of O2 use and O2.- production in the presence or absence of PAF (10(-6)--10(-9) M). Unless cells were treated with cytochalasin-B (5 micrograms/ml), no significant respiratory burst was demonstrated. However, pretreatment with PAF (10(-7) M) enhanced approximately threefold the O2 utilization found when cells were subsequently stimulated with 10(-7) M FMLP. PAF also stimulated arachidonic acid metabolism in 14C-arachidonic acid- labeled PMN. Thin-layer chromatography analysis of chloroform-methanol extracts showed substances that comigrated with authentic 5- hydroxyeicosatetraenoic acid had a marked increase in radioactivity following PAF stimulation at 10(-7) M. PAF failed to stimulate release of granule enzymes, B-glucuronidase, lysozyme, or myeloperoxidase unless cytochalasin-B were added. PAF from 10(-6) M to 10(-10) M affected PMN surface responses. PMN labeled with the fluorescent dye, chlorotetracycline, showed decreased fluorescence upon addition of PAF, suggesting translocation of membrane-bound cations. Further, the rate of migration of PMN in an electric field was decreased following PAF exposure, a change consistent with reduced cell surface charge. PMN self-aggregation and adherence to endothelial cells were both influenced by PAF (10(-6) M--10(-9) M). Aggregation was markedly stimulated by the compound, and the percent PMN adhering to endothelial cell monolayers increased almost twofold in the presence of 10(-8) M PAF. Thus, PAF promotes a variety of PMN responses: enhances respiratory burst, stimulates arachidonic acid turnover, alters cell membrane cation content and surface charge, and promotes PMN self- aggregation as well as adherence to endothelial cells.     

Interleukin-6 synergizes with M-CSF in the formation of macrophage colonies from purified human marrow progenitor cells

We examined the in vitro stimulative effects of recombinant human interleukin-6 (IL-6, or interferon-beta 2) on purified human bone marrow progenitor cells. IL-6 alone or in combination with erythropoietin (Epo), IL-3, GM-CSF, or G-CSF did not induce colony formation. However, IL-6 strongly synergized with M-CSF in stimulating macrophage colony formation (colony numbers and size). The magnitude of IL-6 synergism with M-CSF was dose dependent; maximal potentiation of M- colony formation was evident at approximately 100 to 1,000 U/mL IL-6. When the addition of IL-6 to M-CSF-supplemented cultures was delayed for more than one day after the beginning of culture, enhancement of macrophage colony formation was lost. IL-6 stimulation of M-CSF- responsive colony formation was not apparent when nonpurified marrow cells were plated, most likely due to endogenous IL-6 release. These observations suggest that IL-6, in addition to playing a role in B- lymphocyte proliferation can potentiate the human immune defence mechanism by stimulating monocyte-macrophage development as well.     

Granulocyte colony-stimulating factor (G-CSF) production and G-CSF receptor structure in patients with congenital neutropenia

Congenital neutropenia (Kostmann's syndrome [KS]) is an autosomal recessive syndrome that is characterized by profound neutropenia, resulting in major clinical infections and death. Since the neutropenia and symptoms in KS improve in response to exogenous administration of granulocyte colony-stimulating factor (G-CSF), we studied bone marrow cytokine (G-CSF, granulocyte-macrophage CSF [GM-CSF], and interleukin- 6) production under both basal and stimulated conditions. No differences in G-CSF, GM-CSF, or IL-6 gene expression were found in bone marrow stromal cells between normal controls and KS patients, and all three cytokines were detected by enzyme-linked immunosorbent assay (ELISA) in medium conditioned by bone marrow stromal cells from normal donors and patients with KS. Each KS patient tested had detectable, functional G-CSF in their own serum before exogenous G-CSF administration. Since G-CSF production appeared normal in KS patients, we then asked whether we could detect structural defects in the signaling portion of G-CSF receptor genes. Polymerase chain reaction (PCR) amplification of the G-CSF receptor transmembrane region alone, and of the transmembrane plus cytosolic portions of the receptor, yielded the size products predicted from the sequences of the normal G- CSF receptor. Single-strand conformational polymorphism (SSCP) analysis of G-CSF receptor PCR products demonstrated no variance in structural conformation between KS patients and normal subjects. These results demonstrate that bone marrow stromal cells in patients with KS secrete normal concentrations of functional G-CSF and suggest that the neutropenia in KS patients is caused by an inability of neutrophilic progenitor and precursor cells to respond to normal, physiologic levels of G-CSF. Such a defect, clinically responsive to pharmacologic doses of G-CSF, might be caused by defects in the post-G-CSF receptor signal transduction pathway.     

Detection of Bm86 antigen in different strains of Boophilus microplus and effectiveness of immunization with recombinant Bm86

The control of tick populations by using conventional strategies poses several problems, including the appearance of organophosphate resistant strains, among others. The possibility of using alternative strategies such as vaccination with tick antigens has been suggested by several authors. One particular antigen (Bm86) has been described and shown to be able to induce a protective immunity against the cattle tick Boophilus microplus. In this paper we demonstrate by means of immunohistochemical staining that this antigen is conserved among several strains of this species. These results correlate with those showing that animals vaccinated with a preparation of recombinant Bm86 were protected against challenge with the four different strains tested, including one resistant to organophosphates. These results favour the immunization with recombinant Bm86 for the control of the cattle tick B. microplus.