治疗剂量的~(131)Ⅰ对甲亢患者淋巴细胞染色体影响的研究

本文随机选择６０例服１３１Ⅰ治疗的甲亢（甲状腺机能亢进）患者对其服１３１Ⅰ前１天、服１３１Ⅰ后第６天、２个月和６个月分别进行ＳＣＥ频率和染色体畸变率的检测。结果是服１３１Ⅰ前１天、服１３１Ⅰ后第６天、２个月和６个月患者的淋巴细胞ＳＣＥ频率和染色体畸变率分别为：４４５±０７２,０２８±００９;７６１±１２４,０７７±０１８;６９４±１１８,０３７±０１３;４５３±０６２,０３４±０１１。经过统计分析（ｔ检验）服１３１Ⅰ前１天和服１３１Ⅰ后第６天ＳＣＥ频率和染色体畸变率均有非常显著性差异,服１３１Ⅰ２个月后ＳＣＥ频率和染色体畸变率有所下降,与服１３１Ⅰ前一天比较ＳＣＥ频率仍具有显著性差异,染色体畸变率无显著性差异;服１３１Ⅰ６个月后ＳＣＥ频率和染色体畸变率恢复到服１３１Ⅰ前一天的水平,两者之间均无显著性差异。因此我们认为治疗剂量（平均为２２２ＭＢｑ）的１３１Ⅰ对甲亢患者的染色体具有一定的损伤,但这种损伤可在６个月内得到恢复。     

Glial cell line-derived neurotrophic factor protects against delayed neuronal death after transient forebrain ischemia in rats

Glial cell line-derived neurotrophic factor, a member of the transforming growth factor-beta superfamily, is a potent neurotrophic factor, which has a variety of biological activities that affect several types of neurons in both the central and peripheral nervous systems. In this study, we examined the effects of glial cell line-derived neurotrophic factor on delayed neuronal death in the hippocampal CA1 region of rats after transient forebrain ischemia. In the control rats pretreated with the vehicle, transient forebrain ischemia-induced delayed neuronal death in the hippocampal CA1 region was observed seven days after reperfusion. Pretreatment with glial cell line-derived neurotrophic factor (1.0 microg), which was directly microinjected into the right hippocampal CA1 region, gave significant protection against the delayed hippocampal neuronal death. On the contralateral side of the hippocampus, which was not injected with glial cell line-derived neurotrophic factor, delayed neuronal death similar to that seen in vehicle-treated control animals was observed. Intracerebroventricular glial cell line-derived neurotrophic factor (2.5 microg) injection also protected against delayed neuronal death. In addition, pretreatment with glial cell line-derived neurotrophic factor gave significant protection against apoptotic cell death induced by brain ischemia in the hippocampal CA1 region, as determined by in situ staining for DNA fragmentation. These findings suggest that glial cell line-derived neurotrophic factor plays an important role in delayed neuronal death induced by brain ischemia.     

IL-12 is dispensable for innate and adaptive immunity against low doses of Listeria monocytogenes

We have studied IL-12p35-deficient (IL-12p35(-/-)) mice to evaluate the role of IL-12 in resistance against Listeria monocytogenes. In the absence of bioactive IL-12p75, mutant mice acquired higher bacterial organ burden than wild-type mice and died during the first week following infection with normally sublethal doses of Listeria. Moreover, blood IFN-gamma levels were strikingly reduced in mutant mice at day 2 post-infection. These results suggest that in IL-12p35-deficient mice impaired production of IFN-gamma which is crucial for activation of listericidal effector functions of macrophages leads to defective innate immunity against Listeria. In contrast to mice deficient for IFN-gamma or IFN-gamma receptor which are unable to resist very low infection doses of Listeria, IL-12p35(-/-) mice resisted up to 1000 c.f.u. and were able to eliminate Listeria. Spleen cells from mutant mice re-stimulated with heat-killed Listeria produced considerable amounts of IFN-gamma, suggesting that at low dose infection sufficient IFN-gamma is produced independently of IL-12. Subsequent challenge of these immunized mice with high doses of L. monocytogenes resulted in sterile elimination demonstrating efficient memory responses. These results demonstrate for the first time that at low doses of Listeria IL-12 is neither critical for innate immunity nor for the development of protective T cell-dependent acquired immunity.     

Genetic dissection of the complex pathological manifestations of collagen disease in MRL/lpr mice

An MRL strain of mice bearing a Fas-deletion mutant gene, lpr, MRL/MpJ-lpr/lpr (MRL/lpr) develops collagen disease involving vasculitis, glomerulonephritis, arthritis and sialoadenitis, each of which has been studied as a model for polyarteritis, lupus nephritis, rheumatoid arthritis and Sjögren’s syndrome, respectively. Development of such lesions seems dependent on host genetic background since the congenic C3H/HeJ-lpr/lpr (C3H/lpr) mice rarely develop them. To identify the gene loci affecting each lesion, a genetic dissection of these complex pathological manifestations was carried out. First, histopathological features in MRL/lpr, C3H/lpr, (MRL/lpr × C3H/lpr) F1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr) F1 backcross mice were analyzed. Genomic DNA of the backcross mice were subjected to association studies by Chi-squared analysis for determining which polymorphic microsatellite locus occurs at higher frequency among affected compared to unaffected individuals for each lesion. As a result, gene loci recessively associated with each lesion were mapped on different chromosomal positions. We concluded that each of these lesions in MRL/lpr mice is under the control of a different set of genes, suggesting that the complex pathological manifestations of collagen disease result from polygenic inheritance.     

Effect of passive immunotherapy on murine gut-derived sepsis caused by Pseudomonas aeruginosa.

The effect of passive immunotherapy with antisera against heat-killed Pseudomonas aeruginosa and three of its exo-enzymes (elastase, alkaline protease and exotoxin A) in gut-derived P. aeruginosa sepsis was evaluated. Mice were given a suspension of P. aeruginosa strain D4 in their drinking water, together with ampicillin (200 mg/kg) to disrupt the normal bacterial flora. Cyclophosphamide was then administered to induce translocation of P. aeruginosa that had colonised the gastrointestinal tract so that gut-derived septicaemia was produced. In this model, intraperitoneal administration of antiserum against heat-killed bacteria, 100 microl/mouse, twice a day for 3 consecutive days significantly increased the survival rate over that of mice treated with normal rabbit serum. Antiserum against elastase, alkaline protease, or a combination of these two antisera, failed to provide significant protection. In contrast, antiserum against exotoxin A significantly increased the survival rate over that of mice treated with normal rabbit serum. These results indicate that passive immunisation with antiserum against heat-killed bacteria and exotoxin A, but not with antiserum against either elastase or alkaline protease, protects mice against gut-derived sepsis caused by P. aeruginosa.     

Thymidine phosphorylase expression in progression of cervical cancer: correlation with microvessel count, proliferating cell nuclear antigen, and apoptosis

AIMS: To determine how epithelial and stromal thymidine phosphorylase expression affects angiogenesis, rapid tumour growth, and decreased apoptotic activity in cervical cancer at varying stages of progression. METHODS: Epithelial and stromal thymidine phosphorylase expression, the microvessel count (reflected by factor VIII related antigen), and proliferating cell nuclear antigen (PCNA) were assessed immunohistochemically in 25 specimens of normal cervical epithelium, 35 of carcinoma in situ (CIS), 34 of microinvasive carcinoma, and 34 of invasive cervical squamous cell carcinoma. Apoptosis was evaluated by the terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labelling (TUNEL) method. The relation of epithelial and stromal thymidine phosphorylase expression to microvessel count, PCNA index, and apoptotic index was examined. RESULTS: Epithelial and stromal thymidine phosphorylase expression progressively increased along a continuum from normal epithelium to invasive squamous cell carcinoma. Epithelial and stromal thymidine phosphorylase expression showed a significant positive correlation with microvessel counts. Within each histological stage, CIS cases with high stromal thymidine phosphorylase expression, invasive squamous cell carcinoma cases with high epithelial thymidine phosphorylase expression, and microinvasive carcinoma cases with high thymidine phosphorylase expression in both epithelium and stroma had a significantly higher microvessel count. High epithelial thymidine phosphorylase expression was associated with a significantly higher PCNA index in CIS and microinvasive carcinoma, but not in invasive squamous cell carcinoma. No significant correlation was seen between apoptotic index and either epithelial or stromal thymidine phosphorylase expression or microvessel count. CONCLUSIONS: Epithelial and stromal thymidine phosphorylase expression may combine to promote angiogenesis during progression of cervical cancer, and epithelial thymidine phosphorylase expression may stimulate tumour cell proliferation in the early stages.     

Prostatic signet-ring cell carcinoma: Case report and literature review

Signet-ring cell carcinoma (SRCC) of the prostate is a very rare neoplasm and there have been only 38 cases reported to date. Here the 39th case of prostatic SRCC containing a small amount of neutral mucin, prostatic specific antigen (PSA) and prostatic specific acid phosphatase (PSAP) in the signet-ring cells is reported. It was also found that some intracytoplasmic lumina were derived from the shallow or deep invagination of luminal membranes of cancer cells that formed the neoplastic glands. Using immunohistochemistry, a combination of monoclonal antibodies against cytokeratins 7 and 20 as well as PSA and PSAP may be useful in differentiating prostatic primary SRCC from metastatic SRCC originating in the gastrointestinal tract.     

人工关节磨损颗粒诱导钛合金植入物松动的实验研究

为比较不同人工关节微小磨损颗粒诱导假体周围骨吸收及假体松动生物效应的差异。方法：本实验采用Ｘ线摄片骨密度灰度值测定以及植入物推出力学强度测试等手段,对Ｔｉ－６Ａｌ－４Ｖ,Ｃｏ－Ｃｒ－Ｍｏ与ＵＨＭＷＰＥ三种微小颗粒诱导的假体周围骨结构改变及假体松动作定量分析。结果统计分析显示,直径２．５微米的Ｔｉ－６Ａｌ－４Ｖ颗粒诱导植入物旁骨吸收与植入物松动的程度明显低于相同直径的Ｃｏ－Ｃｒ－Ｍｏ颗粒或ＵＨＭＷＰ     

遗传性脊髓小脑型共济失调的CAG三核苷酸突变检测

目的 评价ＳＣＡ１、ＳＣＡ２、ＳＣＡ３／ＭｊＤ、ＳＣＡ６、ＳＣＡ７和ＤＲＰＬＡ的ＣＡＧ三核苷酸异常扩增突变「（ＣＡＧ）ｎ」,在中国人遗传性脊髓小脑型共济失调（ｓｐｉｎｏｃｅｒｅｂｅｌｌａｒ ａｔａｘｉａ,ＳＣＡ）患者的分布频率。方法 经聚合酶链反应、变性聚丙烯酰按凝胶电泳和银染显带技术,检测分析了８５个中国人常染色体显性遗传ＳＣＡ家系（其中患者１６７例）和３７例散发ＳＣＡ患者的ＳＣＡ１、ＳＣＡ２、     

实验性应激对STZ昆明小鼠血糖水平影响的对照研究

目的 :了解慢性实验性应激对 STZ昆明小鼠血糖水平的影响和作用特点。方法 :取 STZ鼠 4 0只 ,正常昆明小鼠 2 0只 ,按血糖、性别配对后分为四组。实验性应激方法为限制、旋转和拥挤 ,为时六周 ,实验后每两周复查一次血糖。结果 :慢性应激可使雄性 STZ昆明小鼠血糖明显升高。药物、应激与性别单一因素对血糖的作用均不明显 ,药物与应激的交互作用对第 4、 6周血糖作用明显 ,药物、应激与性别三者的交互作用对第 6周血糖作用明显。结论 :慢性实验性应激刺激能使 STZ鼠血糖显著升高 ;雄鼠对应激的血糖反应性比雌鼠敏感。