胰岛素样生长因子1对新生大鼠缺氧缺血性脑损伤保护机制的研究

目的　建立单侧缺氧缺血性脑损伤 (HIBD)动物模型 ,研究胰岛素样生长因子 1(IGF 1)对HIBD的影响和可能机制。　方法　选择健康 7日龄Wistar大鼠 12 0只 ,建立HIBD模型 ,随机分成假手术组、HIBD组、HIBD后 0 .2mg/kg人基因重组IGF 1干预组 (RH IGF 1组 )、0 .0 6 6mg/kg人基因重组IGF 1干预组 (SRH IGF 1组 )及盐水对照组 (对照组 )。各组按观察时段进一步分为 2 4、4 8、72h组 ,每组 8只。各组于规定时刻观测脑形态学改变、谷氨酸 (Glu)含量、凋亡细胞计数、Bcl 2蛋白表达。　结果　 (1)HIBD 4 8h组Glu(116 2 .2± 10 8.1)mg/kg ,较假手术组(75 0 .9± 5 3.4 )mg/kg明显升高 (P <0 .0 5 ) ;HIBD组凋亡细胞计数 [2 4h :(7.6± 1.9) % ,4 8h(12 .6±1.2 ) % ,72h :(13.8± 0 .9) % ],较假手术组 [2 4h(2 .0± 0 .2 ) % ,4 8h(2 .0± 0 .3) % ,72h(2 .0±0 .2 ) % ]明显增加 (P均 <0 .0 5 )。 (2 )与对照组相比 ,RH IGF 1组脑组织病变减轻 ;干预 4 8h组Glu[SRH IGF 1组 (781.4± 5 4 .2 )mg/kg ,RH IGF 1组 (74 0 .5± 4 6 .6 )mg/kg],较对照组 (112 6 .6± 4 8.0 )mg/kg明显降低 (P均 <0 .0 5 ) ;RH IGF 1组凋亡细胞计数 [2 4h :(3.6± 0 .9) % ,4 8h(8.2± 2 .2 ) % ,72h(9.4± 1.4 ) % ],较对     

Female patients complaining about hair loss: documentation of defective scalp hair dynamics with contrast-enhanced phototrichogram

BACKGROUND: The complaint of chronic hair loss frequently affects female subjects and there is little or no objective technology available in the general dermatology or even in the hair clinics to guide the observer in the management of the patient. The purpose of this report is to share the results of refined hair growth measurements that were collected in 92 female subjects complaining about hair loss. METHODS: Clinically they were classified as having a patterned hair loss according to Ludwig (L; n=50), diffuse hair loss (D; n=13) or no visible hair loss but complaining of hair shedding (N; n=29). Two scalp sites on the top of the head and one occipital site were investigated after clipping by close-up photography before and after a hair dye (contrast enhancement, CE). Forty-eight hours later a new photograph was taken after CE in view of phototrichogram analysis (CE-PTG). Finally a last hair clip was performed 30 days later and hair thickness and length determined for linear growth measurements (LHGR). RESULTS: Herein we confirm that the top of the head shows usually a higher hair density than occipital sites, a physiological observation that applies both to men and women. From the technological perspective, we also document that CE improves hair detection in all sites. Interestingly, in affected patients (L and D) the relative increase of hair counts after CE was much higher (range +22.4% to +28.3%) compared with apparently unaffected females (N; range +8.2% to +9.7%). This increase in hair counts was only due in part to the presence of less pigmented thinning hair (thickness less than 40 microm). Such thin hairs were found in statistically significantly higher proportions in younger patients with mildly severe (grade I) patterned alopecia (Ludwig: L). In other patients with hair loss and in more severe forms of patterned alopecia - especially in older patients - the thin hair is not detected in abnormal proportions. In all sites slower growth rates and decreased anagen percentages indicate a defective hair replacement programme distinguishing L patterns from diffuse hair loss and from apparently unaffected patients complaining of chronic hair loss. Globally, we also noted that increasing age is associated with significant regression of scalp hair (decreased hair counts, thinner hair and slower LHGR). CONCLUSION: On the basis of the present data together with female data from the literature and our own studies in male subjects, we suggest a three-step mechanism leading to hair loss 1.Shortening of growth phase the hair cycle with maintained thick hair, i.e. more frequent hair cycling that leads to more hair shedding. 2.Intermittent production of short thin hair, i.e. morphological evidence of miniaturisation. 3.Very occasional or almost no hair production, i.e. dormant follicles or irreversible follicular atrophy. Depending on the genetic background, hormonal microenvironment in the scalp and conditioning of individual hair follicle bio-responses, female and male patterned hair loss may end up into different phenotypes.     

Attempts to make models for Alzheimer''s disease

Profound reductions in cortical acetylcholine levels together with degeneration of cholinergic neurons in the basal forebrain have been reported in patients with Alzheimer's disease. A similar loss of the cholinergic neurons of the basal forebrain and impairment of learning and memory occur in animals injected with a nerve growth factor-diphtheria toxin conjugate, suggesting that this animal model is suitable to analyze cholinergic roles on learning and memory processes, and also the pathogenesis of Alzheimer's disease. In addition, animal models constructed by electrolytic or neurotoxic lesioning of the basal magnocellular nucleus, and models made by transgenetic technology were described.     

表皮生长因子及其受体与流产关系的探讨

采用放射免疫竞争抑制饱和分析法，检测４７例难免流产患者，６５例人工流产及２０例健康非孕妇女血清表皮生长因子（ＥＧＦ）水平；同时采用免疫组织化学法检测流产者胚胎组织中表皮生长因子受体（ＥＧＦＲ）表达程度。结果：人工流产组血清ＥＧＦ水平高于自然流产及非孕妇女，而自然流产与非孕妇女差异无显著性；胚胎组织中ＥＧＦＲ阳性表达率人工流产组明显高于自然流产组。提示：ＥＧＦ通过与其受体结合对妊娠维持、胚胎及胎儿的     

Chronic parasite infection in mice induces brain granulomas and differentially alters brain nerve growth factor levels and thermal responses in paws

Schistosoma mansoni infection, both in humans and in animal models, is known to induce granulomas in the liver and intestine. It has also been reported that in humans the eggs of this parasite can reach the brain, causing psychiatric and neuropathological disorders. Whether this also occurs in rodents is unknown. To answer this question, mice were infected with this parasite and the central nervous system (CNS) examined at various time intervals. The results show that schistosomiasis induced granulomas in several regions of the CNS and increased nerve growth factor (NGF) levels in the cortex, hypothalamus and brain stem, but not in the hippocampus. The infection also caused paw hyperalgesia, as determined by the hot-plate test, and a local increase in NGF, but not in substance P. These findings indicate that the murine model of infection can be used for studying mechanisms leading to human neuroschistosomiasis and suggest that the neuropathological disorders and the sensory deficits observed in human schistosomiasis are associated with impaired levels of NGF in the peripheral and central nervous system. Received: 18 January 1996 / Revised, accepted: 16 April 1996     

CT增强扫描在评价NSCLC血管生成中的临床意义

目的　探讨非小细胞肺癌 (NSCLC)血管内皮生长因子 (VEGF)的表达水平与CT增强程度的关系 ,从影像学角度评价肿瘤血管生成在肺癌诊断、治疗及淋巴结转移中的临床价值。方法　对 30例NSCLC病人进行动态螺旋CT扫描 (SCT) ,测量病灶增强幅度 ,并利用免疫组化技术检测VEGF。对病灶增强值、VEGF阳性表达及淋巴结转移情况进行统计学分析。结果　 30例肺癌病人CT增强值均数为 (36 .2 8± 6 .41 )HU ,VEGF阳性表达 2 1例 ,阴性表达 9例。VEGF在中晚期的阳性表达高于早期病人 (Ρ<0 .0 5) ,淋巴结转移组高于非淋巴结转移组 (Ρ <0 .0 5) ;癌灶增强值与VEGF阳性表达、肿瘤分期及淋巴结转移亦呈正相关。结论　NSCLC的CT增强程度能够反映肿瘤的血管生成 ,并与淋巴结转移密切相关 ,有助于肺癌的诊断、TNM分期 ,而且可以从肿瘤分子生物学行为方面补充目前肺癌分期方法的不足     

Nerve conduction as a means of estimating early post-mortem interval

Summary Methods in current practice for ascertaining time of death are largely based on the cooling of the body after death and are somewhat unreliable. A theoretica relationship is known to exist between the decline in the properties defining nerve conduction and time after death caused by the gradual cessation of metabolic activity in nerves. A number of such properties were measured in rats during life and after death. In most cases the relationship was found to be inconsistent. The chronaxie of the strength duration curve for the sciatic nerve was, however, found to increase consistently and reproducibly in a linear fashion over the first 90 min after death to a plateau value which was maintained beyond 135 min. These findings are discussed as the possible basis of a forensic method of determining the duration of the “post mortem interval” within the first few hours after death.      

小儿氨基酸注射液治疗胎儿宫内发育迟缓的探讨

经临床鉴定静脉内注射小儿氨基酸对治疗胎儿宫内发育迟缓具有肯定效果。在Ｂ超监视下，使用小儿氨基酸的孕妇组于用药期间，胎儿生长参数ＢＰＤ和ＨＣ显著高于使用成人氨基酸的孕妇组。１０例足月娩出胎儿体重均达到甚至超过２．５ｋｇ。由此得出结论：使用小儿氨基酸注射液对于改善胎儿宫内发育迟缓优于成人氨基酸。