重组人肿瘤坏死因子诱导HL－60白血病细胞分化及调控原癌基因表达的作用

采用２０～２００Ｕ／ｍｌ的重组人肿瘤坏死因子（ｒｈＴＮＦ－α）处理体外液相培养的人早幼粒白血病细胞珠ＨＬ－６０，观察到５０～２００Ｕ／ｍｌ的小剂量ＴＮＦ具有诱导其向单核－巨噬细胞途径分化及抑制其增殖的效应。采用细胞总ＲＮＡ打点杂交技术检测１～１００Ｕ／ｍｌＴＮＦ诱导ＨＬ－６０细胞早期（１２小时内）对其ｃ－ｍｙｃ，ｃ－ｆｏｓ原癌基因表达的影响，发现ＴＮＦ可抑制ｃ－ｍｙｃｍＲＮＡ水平及ｃ－ｆｏｓ短暂性表达增高。结果表明此小剂量ｒｈＴＮＦ－α具有诱导白血病细胞分化的效应及调控多癌基因表达的作用。     

大鼠肺微血管和肺泡铸型的扫描电镜观察

用扫描电镜观察以甲基丙烯酸甲酯灌注鼠的肺微血管和肺泡。胸膜下毛细血管较稀疏,网孔粗大。毛细血管部分成锐角折返,亦可见毛细血管盲端。肺泡隔毛细血管均成扁平状膨大,且相互吻合成单层密集网。肺泡铸型为大小不等、不规则的多面体,表面可见肺泡Ⅱ型细胞核之压迹。两肺泡之间可见呈桥式连接的肺泡孔,亦可见部分呈三通管样相连。     

Formoterol and salbutamol inhibit bradykinin- and histamine-induced airway microvascular leakage in guinea-pig.

1. The effects of the beta 2-adrenoceptor agonists, salbutamol and formoterol, on the increase of microvascular permeability induced by histamine or bradykinin in guinea-pig airways have been studied in vivo. Extravasation of intravenously injected Evans blue dye was used as an index of permeability. The effects of salbutamol and formoterol on the increase in pulmonary airway resistance induced by histamine or bradykinin have also been studied. 2. The increase in pulmonary airway resistance induced by histamine or bradykinin was totally inhibited by salbutamol and formoterol. The ED50 of the two mediators were 0.59 +/- 0.21 (n = 5) and 0.20 +/- 0.14 (n = 5) micrograms kg-1 respectively for salbutamol, and 0.13 +/- 0.12 (n = 6) and 0.02 +/- 0.01 (n = 6) micrograms kg-1 respectively for formoterol. 3. Salbutamol (10 and 30 micrograms kg-1) and formoterol (1 and 10 micrograms kg-1) inhibited the increase of microvascular permeability induced by histamine (30 micrograms kg-1) in the guinea-pig airways. The inhibitory effect was predominant in the trachea and the main bronchi, with a maximum inhibition of 20 to 50%. The two drugs had little or no inhibitory effect on the other structures studied, viz. nasal mucosa, larynx, proximal and distal intrapulmonary airways. 4. Salbutamol and formoterol (1 and 10 micrograms kg-1) abolished the increase in microvascular permeability induced by bradykinin (0.3 micrograms kg-1). This inhibitory effect of two beta-adrenoceptor stimulants was predominant in the trachea and the nasal mucosa where it was observed with 1 microgram kg-1 of the beta-adrenoceptor agonists.(ABSTRACT TRUNCATED AT 250 WORDS)     

脆性X综合征中不稳定的DNA序列和异常甲基化研究

采用ＰＣＲ结合序列胶分析的方法，对８２条正常中国人Ｘ染色体ＦＲＡＸＡ位点（ＣＧＧ）ｎ重复序列拷贝数的多态性进行了测定，其范围为２１～３１，高峰为２７。并通过Ｓｏｕｔｈｅｒｎ杂交分析了来自６个Ｆｒａ（Ｘ）家系的１５名成员（ＣＧＧ）ｎ的拷贝数与该重复序列上游ＣｐＧ岛的甲基化状态。Ｆｒａ（Ｘ）患者（ＣＧＧ）ｎ大量扩增并伴随ＣｐＧ岛异常甲基化。Ｆｒａ（Ｘ）携带者女性（ＣＧＧ）ｎ扩增较少，有嵌合现象。其子代或产生更大扩增，或保持原来状态，呈动态突变遗传特征。     

Surgical Management of PICA Aneurysm and Incidental Facial Nerve Schwannoma: Case Report.

We report a patient with a posterior inferior cerebellar artery (PICA) aneurysm and an incidental facial nerve schwannoma at the cerebellopontine angle (CPA). A 46-year-old woman presented with the sudden onset of a severe headache, nausea, and vomiting. She had no other abnormal neurological symptoms and signs. Computed tomography (CT) showed hemorrhage in the fourth ventricle. Cerebral angiography demonstrated an aneurysm arising from the tonsillomedullary segment of the left PICA. A facial nerve schwannoma was incidentally found as the aneurysm was being clipped. The aneurysm was clipped via a left transcondylar approach. Subsequently, the schwannoma (2 x 3 x 2 mm) was resected from the facial nerve fascicles, and the facial nerve was preserved. Postoperatively, the patient developed mild to moderate dysfunction of the facial nerve (House-Brackmann grade III [H-B III]) but her hearing was intact. Both a facial nerve schwannoma involving the CPA and an aneurysm involving the PICA can be managed through the transcondylar approach. An asymptomatic facial nerve schwannoma can be resected safely with minimal facial nerve dysfunction.     

In vivo 13C saturation transfer effect of the lactate dehydrogenase reaction.

Lactate dehydrogenase (LDH, EC 1.1.1.27) catalyzes an exchange reaction between pyruvate and lactate. It is demonstrated here that this reaction is sufficiently fast to cause a significant magnetization (saturation) transfer effect when the 13C resonance of pyruvate is saturated by a continuous-wave (CW) RF pulse. Infusion of [2-(13)C]glucose was used to allow labeling of pyruvate C2 at 207.9 ppm to determine the pseudo first-order rate constant of the unidirectional lactate-->pyruvate flux in vivo. During systemic administration of GABAA receptor antagonist bicuculline, this pseudo first-order rate constant was determined to be 0.08+/-0.01 s-1 (mean+/-SD, N=4) in halothane-anesthetized adult rat brains. In 9L and C6 rat glioma models, the 13C saturation transfer effect of the LDH reaction was also detected in vivo. Our results demonstrate that the 13C magnetization transfer effect of the LDH reaction may be useful as a novel marker for utilizing noninvasive in vivo MRS to study many physiological and pathological conditions, such as cancer.     

西藏地区农牧民生活习俗与包囊虫病的关系调查

目的　探讨西藏地区农、牧民生活习俗与包囊虫病的关系。方法　自制问卷对 7个县 2 40个家庭 163 1名成员与包囊虫感染有关的生活习俗进行调查分析。结果　饭前便后洗手的人仅有 16 1%,餐具一般都用天然水洗 ,大部家庭用天然绵羊绒擦洗茶具。大多数人都喝过河溪水 ,池塘水 ,人人都吃半生不熟的肉 ,半数以上的吃生肉和生血肠 ,绝大多数人喝未经消毒的鲜牛、羊奶。 10 0 %家庭养狗 ,所有人员与狗、羊、牛、马接触密切。包囊虫病人占调查人数 0 43 %( 7/ 163 1) ,有典型症状者占 0 67%( 11/ 163 1)。结论　当地居民感染包囊虫与不良生活习俗有关     

我国原料药产业的发展策略

经济全球化进程的加快，中国加入世贸组织，为我国医药产业国际化发展带来了机遇。     

Mechanisms of opioid-induced tolerance and hyperalgesia.

Opioid tolerance and opioid-induced hyperalgesia are conditions that negatively affect pain management. Tolerance is defined as a state of adaptation in which exposure to a drug induces changes that result in a decrease of the drug's effects over time. Opioid-induced hyperalgesia occurs when prolonged administration of opioids results in a paradoxic increase in atypical pain that appears to be unrelated to the original nociceptive stimulus. Complex intracellular neural mechanisms, including opioid receptor desensitization and down-regulation, are believed to be major mechanisms underlying opioid tolerance. Pain facilitatory mechanisms in the central nervous system are known to contribute to opioid-induced hyperalgesia. Recent research indicates that there may be overlap in the two conditions. This article reviews known and hypothesized pathophysiologic mechanisms surrounding these phenomena and the clinical implications for pain management nurses.