芳香烃受体与肿瘤的关系

芳香烃受体是一个配体依赖性激活的转录因子,外源性芳香烃化合物能与其结合并使其激活,从而引起多种代谢酶升高,活性增强,致癌性代谢产物增多,最终导致肿瘤的发生.现就芳香烃受体的基本概念及其与肿瘤的关系作简要综述.     

经乳头根部小切口盐水假体隆乳术-30例临床回顾

目的：选择合适的皮肤切口入路,操作方便,组织损伤小,术后瘢痕不明显是未来隆乳术的发展方向。基于这一原则,笔者选择经乳头根部小切口行盐水假体隆乳术,旨在观察术后的效果。方法：全麻或局麻下,于乳头下侧缘距基底部2mm处设计半环形切口。对于乳头过小者,可向两侧乳晕水平方向延长5mm,总长度小于2．5cm。沿此切口切开皮肤全层,沿乳腺导管走行方向分离,在乳腺下或胸大肌下制造腔穴,将充注式盐水袋假体置入腔穴。再将200ml～300ml盐水通过阀门注入。观察双侧乳房大小、形状、对称性均满意后分层缝合和包扎。结果：从2000年1月～2007年12月,我们用此种方法行隆乳术30例。术后早期5例患者出现乳头感觉暂时减退,1～3月后均恢复正常。10例乳房表面出现局部轻微褶皱塌瘪,2例假体破裂,取出后再次置入新假体。无乳头畸形、包膜挛缩、双侧不对称,所有患者对切口瘢痕感到满意。结论：经乳头根部小切口置入盐水充注式假体手术,操作简便,安全性高,损伤乳腺组织少,愈后切口瘢痕隐蔽。该术式是可行的,值得在临床上推广应用。     

血管生成素与妊娠

血管生成素(Angs)是一类新发现的促血管生成因子,具有调节血管生成、退化及血管稳定性的作用,参与胚胎血管的发育、肿瘤血管的生成及转移等过程.目前研究较多的是Ang-1和Ang-2,二者结构相似而功能各异,共同受体为酪氨酸激酶-2受体(Tie-2).Angs及其受体存在于胎盘组织及胎儿体内,在妊娠整个过程中均可表达,对于妊娠全过程起重要作用.妊娠疾病中Angs/Tie系统基因表达失控,可能与子痫前期、胎儿生长受限等妊娠疾病的发病过程有关,深入研究Angs在妊娠疾病中的作用,将为临床上妊娠疾病的诊断和治疗提供重要的理论依据.     

AII amacrine cells in the mammalian retina show disabled-1 immunoreactivity

Disabled 1 (Dab1) is an adapter molecule in a signaling pathway, stimulated by Reelin, which controls cell positioning in the developing brain. It has been localized to AII amacrine cells in the mouse and guinea pig retinas. This study was conducted to identify whether Dab1 is commonly localized to AII amacrine cells in the retinas of other mammals. We investigated Dab1-labeled cells in human, rat, rabbit, and cat retinas in detail by immunocytochemistry with antisera against Dab1. Dab1 immunoreactivity was found in certain populations of amacrine cells, with lobular appendages in the outer half of the inner plexiform layer (IPL) and a bushy, smooth dendritic tree in the inner half of the IPL. Double-labeling experiments demonstrated that all Dab1-immunoreactive amacrine cells were immunoreactive to antisera against calretinin or parvalbumin (i.e., other markers for AII amacrine cells in the mammalian retina) and that they made contacts with the axon terminals of the rod bipolar cells in the IPL close to the ganglion cell layer. Furthermore, all Dab1-labeled amacrine cells showed glycine transporter-1 immunoreactivity, indicating that they are glycinergic. The peak density was relatively high in the human and rat retinas, moderate in the cat retina, and low in the rabbit retina. Together, these morphological and histochemical observations clearly indicate that Dab1 is commonly localized to AII amacrine cells and that antiserum against Dab1 is a reliable and specific marker for AII amacrine cells of diverse mammals.     

Citrin缺陷所致新生儿肝内胆汁淤积症研究进展

Citrin缺陷所致新生儿肝内胆汁淤积症(NICCD)是近年来新发现的一种遗传代谢缺陷病,是由于SLC25A13基因突变引起citrin蛋白合成障碍所致.其临床表现复杂多样,确诊需要依赖基因诊断,目前尚缺少特异性的治疗方法.该文介绍了NICCD的国内外研究进展及发展趋势,以促进国内对NICCD的认识和进一步研究.     

Citrin缺陷所致新生儿肝内胆汁淤积症研究进展

Citrin缺陷所致新生儿肝内胆汁淤积症(NICCD)是近年来新发现的一种遗传代谢缺陷病,是由于SLC25A13基因突变引起citrin蛋白合成障碍所致.其临床表现复杂多样,确诊需要依赖基因诊断,目前尚缺少特异性的治疗方法.该文介绍了NICCD的国内外研究进展及发展趋势,以促进国内对NICCD的认识和进一步研究.     

Tid1 functions as a tumour suppressor in head and neck squamous cell carcinoma

Human tumourous imaginal disc (Tid1), a human homologue of the Drosophila tumour suppressor protein Tid56, is involved in multiple intracellular signalling pathways such as apoptosis, cell proliferation, and cell survival. Here, we investigated the anti‐tumourigenic activity of Tid1 in head and neck squamous cell carcinoma (HNSCC) in vitro and in vivo. Firstly, the clinical association between Tid1 expression and progression of HNSCC was explored. It was found that expression of Tid1 was negatively associated with tumour status, recurrence, and survival prognosis using immunohistochemical analysis of primary HNSCC patient tumour tissue. Secondly, ectopic expression of Tid1 in HNSCC cells was shown to significantly inhibit cell proliferation, migration, invasion, anchorage‐independent growth, and xenotransplantation tumourigenicity. Thirdly, we showed that overexpression of Tid1 attenuated EGFR activity and blocked the activation of AKT in HNSCC cells, which are known to be involved in the regulation of survival in HNSCC cells. On the other hand, ectopic expression of constitutively active AKT greatly reduced apoptosis induced by Tid1 overexpression. Together, these findings suggest that Tid1 functions as a tumour suppressor in HNSCC tumourigenesis. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.