中西医结合治疗男性免疫性不育症1806例

0 引言近年来的免疫学研究发现,不明原因的不育患者体内存在着抗精子抗体(Anti-sperm antibody, ASAb)并对不育产生影响[1,2]. 我院近年来对抗体阳性者进行了中西医结合治疗,有效消除了抗体,取得了较好的临床效果,现报道如下.     

卡西霉素对血小板在脑微血管内皮细胞粘附的影响及药物的阻断作用

体外实验表明calcimycin0.01μmol·L^-1刺激牛脑微血管内皮细胞25min,使兔血小板与脑微血管内皮细胞的粘附率增高17.1%。PAF受体拮抗剂WEB20860.1,1.0和10.0μumol·L^-1对血小板在脑微血管内皮细胞上粘附的抑制率分别为9.0,22.9和23.1%。DMPP0.1,1.0,10.0μmol·L^-1及Tet0.1,1.0,10。Oμmol·L^-1的抑制率分别为9.7,15.6,22.1%和7.8,15.6及24.6%,提示DMPP和Tet对脑血管有保护作用。     

血小板激活因子对大鼠脑血管通透性的影响及药物的保护作用

颈内动脉注射血小板激活因子(PAF),再给伊文思蓝,可见脑实质染色程度加深,而颈内动脉只注射伊文思蓝,脑实质未见染色。而我们合成的新药SZ-1可剂量依赖性地抑制PAF诱导的脑实质伊文思蓝染色程度的加深。在体外培养的脑微血管平滑肌细胞上,PAF能显著刺激¹⁴C-花生四烯酸的释放,而SZ-1能剂量依赖性地抑制这种释放,提示PAF在脑内产生的损害除与其他因素相关外,还与其刺激花生四烯酸释放有密切关系,SZ-1对PAF引起的脑部损害有保护作用。     

四氢巴马汀等单胺排空作用的比较

利血平(1.5mg/kg,ip)单独给药后24h能显著降低大鼠脑内NA(—60%)和DA(—75%)。预先给予dl-THP(60mg/kg)能使脑内NA和DA进一步下降,分别为正常对照组的15和5%,与单给利血平组有显著性差别。dl-THP同样亦能协同利血平排空5HT的作用。相反,预先给予丁苯那嗪(50mg/kg)则部分拮抗利血平的排空作用。此外,dl-THP与利血平不同,对Na⁺K⁺-ATP酶和Mg²⁺-ATP酶活性无显著影响。l-或d-THP在10^-4mol/L的较高浓度下能诱发豚鼠输精管节律性收缩,并不被多种受体阻断剂拮抗。在体研究表明,dl-THP在较大剂量下与利血平相似,降低犬鼠体温。     

蝙蝠葛碱和粉防己碱对[3H]WEB 2086与体外牛脑前动脉平滑肌细胞结合的影响(英文)

用标记的血小板活化因子拮抗剂[³H]WEB 2086,在培养的牛脑前动脉平滑肌细胞上鉴定了血小板活化因子受体。结果表明在25℃时该细胞上存在两种与配基具有不同亲和力的受体结合位点,其中K_d-1=22.8±5.0 nmol·L^-1,K_d-2=186+20.5 nmol·L^-1;B_max-1=2.1±0.3 pmol/10⁴细胞,B_max-2=12.1±1-5 pmol/10⁶细胞。蝙蝠葛碱和粉防己碱均能抑制[³H]WEB2086与上述细胞的结合。     

香荚兰素对抗大鼠杏仁核点燃效应

用大鼠杏仁核点燃模型研究了香荚兰素的抗癫痫作用。每日一次低电流刺激杏仁基底外侧核可在第15天使大鼠产生典型的五期反应,刺激后放电显著延长。香荚兰素在不产生中枢抑制作用的剂量即可抑制点燃效应的五期反应,ED₅₀为286 mg/kg(ip),同时使刺激后放电时程比对照组下降28.6%。苯妥英钠抑制五期反应的ED₅₀为56mg/kg,也能明显缩短刺激后放电时程。本文提供了一种新型慢性实验性癲痫模型。     

木脂素类化合物的精细立体结构与生物活性关系

对胡椒属(Piper Ruizet Pavon)植物中的木脂素类化合物精细立体结构与生物活性进行研究。选择该类化合物三种骨架的3个化合物进行了X衍射单晶结构分析,获得其立体结构参数;应用分子图形学,分子力学等诸方法,获得3种骨架中的9个分子的自由态下立体结构数据;并以已有的药理(血小板活化因子拮抗活性)实验数据为基础进行结构与活性分析。     

三氧化二β-锗丙酸对硝基苯酯的合成和结构性质

The title compound was synthesized with the view of finding anticancer agents since organogermanium have been reported to have such actions. Tts structure and properties were determined and examined by elemental analysis, IR spectrum, FAB-MS and TG-DTA. The IR spectrum showed the characteristic absorption band of Ge-O bonds at 800～900 cm^-1,indicating the formation of organogermanium sesquioxide. Under fast acom bombardment, the Ge-O-Ge-O network was split, the fragments with R-Ge could combine with 3-mercapto-1,2-propanediol or glycerin easily, forming the new compounds of R-Ge-O-CH and R-Ge-O-CH type. When heated in air, the compound decomposed in three steps, the possible mechanism of thermal decomposition was discussed. The biological activity of the compound is to be determined.     

Histopathological changes of Macaca mulatta infected with Plasmodium knowlesi

目的　探讨诺氏疟原虫 (Plasmodiumknowlesi)感染恒河猴 (Macacamulatta)引起有关脏器的病理组织学变化。方法　病解 3例感染疟原虫未经治疗病死的猴 ;2例感染疟原虫经青蒿琥酯 (artesunate)栓剂治疗后又复发的猴 ;1例感染疟原虫经磷酸哌喹 (piperaquinephosphate)治愈后死于上肢坏死感染的猴。对有关脏器均进行切片检查。结果　 3例 (1号、7号和 12号 )未经治疗而病死的猴和 1例 (72号 )虽经青蒿琥酯栓剂治疗但很快被排出体外的猴的心、肝、脾、肺、肾、大小脑、胰腺、甲状旁腺、脑垂体和淋巴结等均有严重病变 ,含原虫的红细胞和疟色素聚集于这些脏器的毛细血管内。 1例 (131号 )经用哌喹治愈而死于上肢坏死的猴 ,除见多个脏器内有色素沉积或被巨噬细胞吞噬外 ,可见胰岛细胞、甲状旁腺和垂体细胞萎缩和消失等病变。 1例 (33号 )用青蒿琥酯栓剂治疗后短期原虫转阴 ,但又复燃的猴被灌药致死 ,多个脏器所见与感染后未经治疗者明显不同 ,仅见肝脏Kupffer细胞和大脑基质细胞内含原虫和疟色素 ,多个脏器均呈修复。结论　本文报导了诺氏疟原虫感染恒河猴后各有关脏器的病理组织学变化 ,特别是观察到胰岛细胞、甲状旁腺和垂体细胞的萎缩和消失与心肌细胞的溶解是国内外文献所未记载过的。     

In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins

It has been shown recently in China that arsenic trioxide (As2O3) is a very effective treatment for acute promyelocytic leukemia (APL). APL patients resistant to all-trans retinoic acid (ATRA) and conventional chemotherapy can still respond to AS2O3. In this study, we addressed the possible cellular and molecular mechanisms of this treatment by using NB4 cells as a model. The results show that: (1) As2O3 triggers relatively specific NB4 cell apoptosis at micromolar concentration, as proved by morphology, histogramic related nuclear DNA contents, and DNA gel eletrophoresis. (2) As2O3 does not influence bax, bcl-x, c-myc, and p53 gene expression, but downregulates bcl-2 gene expression at both mRNA and protein levels. (3) As2O3 induces a significant modulation of the PML staining pattern in NB4 cells and HL-60 cells. The micropunctates characteristic of PML-RAR alpha in NB4 cells dissappear after treatment with As2O3, whereas a diffuse PML staining occurs in the perinuclear cytoplasmic region. In addition, a low percentage of untreated NB4 cells exhibits an accumulation of PML positive particles in a compartment of cytoplasm. The percentage of these cells can be significantly increased after As2O3 treatment. A similar PML staining pattern is observed in apoptotic cells. (4) ATRA pretreatment does not influence As2O3-induced apoptosis. These results suggest that induction of cell apoptosis can be one of the mechanisms of the therapeutic effect of As2O3. Moreover, this apoptosis induction occurs independently of the retinoid pathway and may be mediated, at least partly, through the modulation of bcl-2, as well as PML-RAR alpha and/ or PML proteins.