胰岛素样生长因子-Ⅰ对软骨细胞凋亡的抑制

目的:探讨胰岛素样生长因子-Ⅰ(IGF-Ⅰ)对软骨细胞增殖及白细胞介素-1(IL-1)诱导软骨细胞凋亡的影响,揭示其抗损伤作用机制,为关节软骨损伤治疗提供理论依据。方法:分离培养人胚胎关节软骨细胞,采用四氮甲基唑蓝(MTT)法测定不同含量软骨细胞增殖活性的变化,利用光镜、电镜、DNA电泳及流式细胞仪测定作为凋亡检测指标。结果:IGF-Ⅰ呈剂量依赖式促软骨细胞增殖,当IGF-Ⅰ含量达50μg/L时,促软骨细胞增殖作用达最大值。IL-1组光镜、电镜下可见典型的细胞凋亡形态学改变,琼脂糖凝胶电泳示特征性的DNA梯状条带,IGF-Ⅰ处理组未见明显凋亡征象。流式细胞仪检测发现,IGF-Ⅰ处理后软骨细胞凋亡率显著降低。结论:IGF-Ⅰ能促进软骨细胞增殖,对IL-1诱导的软骨细胞凋亡具有保护作用。     

新生儿听力筛查研究及其评价

我国每年有两千万新生儿出生，约有2万～6万新生儿患有听力障碍，远高于目前已开展的两病筛查（先天性甲状腺功能低下1：7000，苯丙酮尿症1：16500）。开展新生儿听力筛查，是一项社会意义重大的优生工程。本院已将新生儿听力筛查作为重点工作，由专职听力筛查的儿科医生和主管护师共同承担此项工作，并对患儿进行追踪随访，为早诊断、早干预提供帮助，同时调查家长对筛查结果的评价。现介绍如下。     

寄语新一代妇产科医生

作为一名从事妇产科工作多年的老同志，想借此机会和年轻的同志、同行们谈谈心。     

界定需要急诊入院的高危人群单纯依据既往的入院率会造成误导

预测哪些人可能因急性发病而需要急诊入院，已成为英国国家医疗卫生服务体系（NHS）的一个重要话题。卫生部门将那些患有复杂的慢性疾病，经常不定期地去二级医疗机构就医的人们视为高危人群。确定这些人之后，社区护理员或其他卫生人员将通过“个案管理”的方法照顾他们。“个案管理”此前被定义为“对疾病尚未控制或所需费用昂贵的患者进行加强医疗计划”。社区护理人员可来自任何护理部门，但一般认为社区护士更能胜任这一角色。此方法能够减少可避免的急诊入院患者数量，并有助于实现到2008年3月减少5％急诊住院床位日的公共医疗服务目标。但是，如何才能界定需要急诊入院的高危人群呢？     

经肝动脉介入治疗并发胆囊坏死(2例报告并文献复习)

目的 :探讨经肝动脉介入治疗并发胆囊坏死的发生原因和防治措施。方法 :报告 2例经肝动脉介入治疗并发胆囊坏死的病例 ,均经手术病理证实。并结合文献资料分析这一并发症发生的机率、原因 ,以及为了减少并发症的发生需要注意的一些问题。结果 :近 8年来我院共做经肝动脉介入治疗 6 80例次 ,并发胆囊坏死 2例 (0 3% )。其发生原因是多方面的。超选择插管不到位是该并发症发生的主要原因。结论 :胆囊坏死是经肝动脉介入治疗比较常见的严重并发症之一 ,在今后工作中应引起足够的重视 ,尤其对肝血管瘤的介入治疗更应慎重 ,使这一并发症的发生率降至最低限度。     

椎管内原发性孤立性纤维性肿瘤临床病理观察(附2例报告)

目的探讨椎管内孤立性纤维性肿瘤的临床病理特征、诊断和鉴别诊断,以期提高对该肿瘤的诊断水平。方法复习2例椎管内原发性孤立性纤维性肿瘤的临床资料,并观察其组织学特征和免疫组化标记。结果2例患者男、女各1例,年龄分别为23岁和32岁,临床表现为局部神经压迫症状。MRI示椎管内髓外硬膜内占位。组织学特征为梭形、卵圆形细胞呈束状、波浪状或旋涡状排列,富于胶原纤维及伴有分支状薄壁血管。细胞未见异型性和核分裂像。免疫组化示瘤细胞Vimentin( ),CD34( ),CD99( ),Bcl-2( ),AACT(-),Actin(-),S-100(-),EMA(-),GFAP(-),CD68(-),CD117(-),SMA(-),NF(-)。结论椎管内原发性孤立性纤维性肿瘤是一种罕见的肿瘤,诊断主要依靠病理形态学及免疫组化,并应与椎管内的其他梭形细胞肿瘤鉴别。     

中蒙医结合治疗胆囊切除术后综合征62例临床观察

目的：通过临床观察，探讨胆囊切除术后综合征的发生、发展及治疗效果。方法：通过对胆囊切除术后综合征的诱发因素、首发症状、ERCP诊断结果调查。探讨其发生发展规律以及中蒙医结合综合治疗的临床效果。结果：通过临床发现：①情绪不稳定引起本病主要诱发因素。②ERCP发现：胆管内残留结石，泥沙样结石的残留、残留胆囊结石、炎性梗阻为主要因素。结论：中蒙医结合治疗胆囊切除术后综合征疗效满意。     

Creatinine kinase kinetics studied by phosphorus-31 nuclear magnetic resonance in a canine model of chronic hypertension-induced cardiac hypertrophy.

To determine whether cardiac hypertrophy secondary to chronic renovascular hypertension is associated with altered in vivo myocardial metabolism, phosphorus-31 nuclear magnetic resonance saturation transfer techniques were used to study creatine kinase (CK) kinetics in six chronically hypertensive dogs with moderate cardiac hypertrophy and eight control dogs. The forward rate constant of CK and the flux of phosphocreatine to adenosine triphosphate were determined in both groups of dogs before and during norepinephrine administration (1 microgram/kg per min), used to increase heart rate x systolic blood pressure (rate-pressure product), cardiac output and oxygen consumption. Baseline and norepinephrine-induced changes in rate-pressure product, cardiac output and oxygen consumption were similar in both groups of dogs, as were baseline forward rate constant and flux of phosphocreatine to adenosine triphosphate. However, the norepinephrine-induced changes in forward rate constant and flux were significantly less in hypertensive than in control dogs (p less than 0.05) even though changes in hemodynamic and functional variables were similar in both groups. These data demonstrate that moderate myocardial hypertrophy is associated with altered CK kinetics, which do not appear to affect the heart's ability for global mechanical recruitment at this stage in the hypertensive process. It is possible that the changes in myocardial enzyme kinetics may contribute to diastolic dysfunction previously reported in this model and may be a precursor for ultimate development of heart failure if hypertension is maintained for prolonged periods.(ABSTRACT TRUNCATED AT 250 WORDS)     

The first case of Pseudallescheria boydii meningjitis in China — Electron microscopic study and antigenicity analysis of the agent

Summary Reported in this paper is the first case of isolation ofPseudalle-Scheria boydii from cerebral spinal fluid of a boy with meningitis in China. Morphology and culture were observed by light microscopy, electron scanning microscopy and transmission electron microscopy. In addition, mycelium antigen prepared by SDS-PAGE was compared with that of the other strain of Scedosporium apiospermum. Both of the strains showed more than 40 peptide lines. Their molecular weight was very similar. On the CS-930 Dual-Wavelength TLC Scanner the peaks of both antigens showed to lie in nearly the same position. It could be concluded thatPseudallescheria boydii andScedosporium apiospermum belong to the same genus, but they are of different strains and reproductive phases.     

Effects of immobilization stress on hippocampal monoamine release: Modification by mivazerol, a new α2-adrenoceptor agonist

Mivazerol is a new and selective α₂-adrenoceptor agonist which has demonstrated anti-ischemic effects, both in animals and in patients with myocardial ischemia. In the present study, mivazerol was evaluated for its ability to inhibit the release of catecholamines and serotonin (5-HT) in the hippocampus of freely moving rats, and also was compared to clonidine. In vivo microdialysis in combination with high-performance liquid chromatography (HPLC) was employed. Intravenous administration of mivazerol (8.0 μg/kg) had no effect on basal outflow of norepinephrine (NE), dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC). In contrast, clonidine (8.5 μg/kg, i.v.) attenuated the basal release of DOPAC, which has been proposed to reflect NE biosynthesis, suggesting that clonidine has an inhibitory effect on NE synthesis. In addition, both mivazerol and clonidine decreased the spontaneous release of 5-HT, which provided further evidence that α₂-adrenoceptors in the hippocampus modulate 5-HT. Sixty-min immobilization stress significantly increased the release of NE (177 ± 28%), DA (209 ± 46%) and DOPAC (337 ± 72%). Mivazerol (2.5, 8.0 and 25 μg/kg, i.v.) completely prevented the immobilization stress-induced enhancement of NE, DA and DOPAC, which was equi-effective to clonidine at a dose of 8.5 gmg/kg, i.v. These findings demonstrate that mivazerol has a profound modulatory effect on stress-induced neurotransmitter release in the hippocampus, at dose levels reported to protect against myocardial ischemia.