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关键词： pancreas   exocrine   acini   development   mesenchyme  

摘要： To understand causes of developmental abnormalities of the pancreas, it is essential to understand its normal embryonic development. Current understanding of the development of pancreatic exocrine tissue is that it develops solely from embryonic epithelium, while the role of the surrounding mesenchyme is to signal to this epithelium and form connective tissue. Recent work in our laboratory has shown that pancreatic bud mesenchyme can contribute cells to islets during embryonic development. However, no published studies have investigated in detail whether mesenchyme contributes cells to the exocrine structures of the pancreas. The aim of this study was to investigate whether cells from foregut mesenchyme can contribute to pancreatic acini during embryonic development. Chick-quail chimera recombinant organs were constructed using pancreatic epithelium and mesenchyme from either the pancreas (n=12) or stomach (n=25). These were cultured for 7 days in 3-D collagen gels. The resulting specimens were analysed using morphological criteria and fluorescent immunocytochemistry against pancreatic amylase, insulin, and the quail-specific nucleolar antigen QCPN. Two independent observers determined the origins of acini as either solely epithelial, solely mesenchymal, or of mixed origin. Results are expressed as percentages of total acini identified in each group. Statistical analysis was performed using chi(2) tests (P < 0.01 was considered statistically significant). Recombinations of pancreatic epithelium and pancreatic mesenchyme yielded 11 acini, of which 45% were derived from epithelium only, 45% from mesenchyme only, and 10% of mixed origin. Recombinations of pancreatic epithelium and stomach mesenchyme yielded 78 acini, of which 40% were derived from epithelium only, 32% from mesenchyme only, and 28% of mixed origin. When acini with any mesenchymal cellular contribution were considered as a group, there was no significant difference between stomach and pancreatic mesenchy

关键词： hepatic undifferentiated sarcoma   adult   p53   hTERT   beta-catenin   genetic analysis  

摘要： Background/Aims: Hepatic undifferentiated (embryonal) sarcoma (HUS) is an exceptional hepatic malignant tumor in adults. Genetic studies were never reported in adult cases. Methods: In this study concerning three cases of HUS occurring in adult, we studied the three classical ways of carcinogenesis i.e. the TP53 (p53), Wnt (CTNNB1/beta-catenin and AXIN1) and telomerase (hTERT) pathways. We studied the expression of p53, beta-catenin and telomerase catalytic subunit hTERT by immunohistochemistry in the three cases;we determined TP53 gene mutation in two cases and the genome-wide allelotype, AXIN1, and CTNNB1/beta-catenin gene mutation in one case. Results: Immunohistochemistry showed an overexpression of p53 in more than 80 % of tumoral cells;furthermore, mutations of TP53 were observed in two cases, involving the sequence-specific DNA binding domain. In contrast, no mutation was found in CTNNB1/beta-catenin and AXIN1 genes. Tumoral cells did not show hTERT staining nor nuclear expression of beta-catenin. In addition, allelotype analysis in one case showed loss of heterozygosity of chromosome 7p, 11p, 17p, 22q, and allelic imbalance of 1p, 8p, 20q. Conclusions: In this report of HUS in three adult patients, we emphasize the role of TP53 pathway in carcinogenesis of this rare tumor. This point could be of interest for therapeutic strategies. (c) 2004 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

关键词： phenytoin   hERG   delayed rectifier potassium channel   I-Kr   embryonic arrhythmia   teratogenicity   hypoxia-reoxygenation damage   mouse  

摘要： BACKGROUND: The antiepileptic drug phenytoin (PHT) is a human and animal teratogen. The teratogenicity has been linked to PHT-induced embryonic cardiac arrhythmia and hypoxic damage during a period when regulation of embryonic heart rhythm is highly dependent on a specific K+ ion current (I-Kr). PHT has been shown to inhibit I-Kr. The aims of this study were to investigate whether teratogenic doses cause embryonic hypoxia during and after the I-Kr susceptible period and to further characterize PHT effects on embryonic heart rhythm. METHODS: Pregnant C57BL mice were administered the hypoxia marker pimonidazole followed by PHT or saline (controls) on GD 10 or GD 15. The embryos were fixed and sectioned, and the immunostained sections were analyzed with a computer assisted image analysis. Effects of PHT (0-250 mu M) on heart rhythm in GD 10 embryos cultured in vitro were videotaped and then analyzed by using a digitalization technique. RESULTS: PHT dose-dependently increased the hypoxia staining (6- and 11-fold after maternal dosing of 100 and 150 mg/kg, respectively) during the period I-Kr is expressed and functional (GD 10). In contrast, there were no differences between the PHT doses in hypoxia staining, and much less pronounced hypoxia after this period (GD 15). With increasing PHT concentrations, increased length of the interval (bradycardia) and large variations in length between individual heartbeats (arrhythmia) were recorded. CONCLUSIONS: PHT induced brady-cardia/arrhythmia and severe embryonic hypoxia during the I-Kr susceptible period, supporting the idea of an I-Kr-arrhythmia-hypoxia-related teratogenic mechanism. (c) 2005 Wiley-Liss, Inc.

关键词： heart development   embryonic cardiac outflow   truncus arteriosus development  

摘要： The normal development of the ventricular outlets and proximal region of the great arteries is a controversial subject. It is known that the conus, truncus arteriosus (truncus), and aortic sac participate;however, there are some doubts as to the actual prospective fate of the truncus. Some authors propose that it gives origin to the proximal region of the great arteries and that the myocardial cells of its wall become smooth muscle. Nevertheless, others think that the truncus only forms the arterial valve apparatus and that therefore the myocardial cells transform into fibroblasts. As a first approach to beginning to elucidate which process occurs, the aim of this article was to study the histological changes in the wall of these components of the developing heart in chick embryos whose hearts had been labeled at the truncoconal boundary at stage 22HH, tracing the changes up to stage 36HH. Also, the histological constitution of the wall of the pulmonary arterial trunk and its valve apparatus were studied in the posthatching and adult hearts of chickens and rats. The conus and truncus walls were always encircled by a myocardial sleeve from the outset of their development. Between stages 26HH to 28HH, the truncal myocardial cells adjacent to the mesenchymal tissue of the ridges began to lose cell-to-cell contacts and invaded the extracellular matrix. At stage 24HH, the aortic sac began to project into the pericardial cavity and became divided into two channels by the aortic-pulmonary septum at stage 26HH. The wall of the aortic sac is mostly constituted by a compact mesenchymal tissue. Initially, it does not have smooth muscle but this starts to appear at stage 30HH. The insertion ring of the valves, a broad structure, was formed by mesenchymal tissue. Both structures were always covered by a myocardial sleeve. The leaflets developed from the truncal ridges, the segment immediately proximal to the aortic sac. Our results indicate that the proximal region of the pulmon

关键词： CELL-SHAPE CHANGES   MYOSIN PHOSPHATASE   SIGNALING PATHWAY   EXCHANGE FACTOR   DORSAL CLOSURE   RHO-GTPASE   MELANOGASTER   PROTEIN   CELLULARIZATION   GASTRULATION  

摘要： Morphogenesis of the Drosophila melanogaster embryo is associated with a dynamic reorganization of the actin cytoskeleton that is mediated by small GTPases of the Rho family. Often, Rho1 controls different aspects of cytoskeletal function in parallel, requiring a complex level of regulation. We show that the guanine triphosphate (GTP) exchange factor DRhoGEF2 is apically localized in epithelial cells throughout embryogenesis. We demonstrate that DRhoGEF2, which has previously been shown to regulate cell shape changes during gastrulation, recruits Rho1 to actin rings and regulates actin distribution and actomyosin contractility during nuclear divisions, pole cell formation, and cellularization of syncytial blastoderm embryos. We propose that DRhoGEF2 activity coordinates contractile actomyosin forces throughout morphogenesis in Drosophila by regulating the association of myosin with actin to form contractile cables. Our results support the hypothesis that specific aspects of Rho1 function are regulated by specific GTP exchange factors.

关键词： FAS-INDUCED APOPTOSIS   SMOOTH-MUSCLE-CELLS   IN-VITRO ISCHEMIA   GENE-EXPRESSION   FACTOR VEGF   ERYTHROPOIETIN PROTECTS   SIGNAL-TRANSDUCTION   TUMOR ANGIOGENESIS   PROGENITOR CELLS   SPLICE VARIANTS  

摘要： Vascular endothelial growth factor (VEGF) is best known for its angiogenic activity on endothelial cells, but it also affects neurons, pneumocytes, and other mature cell types as well as endothelial, neural, and hematopoietic progenitors. Here, we examined its effect on pluripotential embryonic stem (ES) cells under hypoxic stress. ES cells were found to produce VEGF and to express VEGF receptor-2 and neuropilin-1 (Nrp-1), a VEGF(165) isoform-specific receptor. During hypoxia, expression levels of VEGF, Flk-1, and Nrp-1 were elevated. Inhibition or targeted gene inactivation of VEGF increased ES cell apoptosis during prolonged hypoxia (48 h) by about 10-fold. The survival activity of VEGF was specific since inhibition of other growth factors (including basic fibroblast growth factor, epidermal growth factor, insulin-like growth factor, platelet-derived growth factor, and placental growth factor) had no effect. Neuropilin-1 was involved in the VEGF-survival activity since overexpression of Nrp-1 decreased hypoxia-induced apoptosis about 3-fold. The hypoxia-response element, via which hypoxia-inducible transcription factors up-regulate VEGF expression under hypoxic conditions, was critical since targeted deletion of this element in the VEGF promoter enhanced hypoxia-induced ES cell apoptosis to the same extent as VEGF inhibition or gene inactivation. Thus, VEGF plays a critical role in survival of ES cells during prolonged hypoxia.

关键词： 组织学与胚胎学   教学图库   数字化   计算机多媒体技术   教学过程  

摘要： 介绍应用计算机多媒体技术构建一个内容丰富的组织学与胚胎学数字化教学图库的方法和要求,以及图库在教学过程中的多方面应用.

关键词： 医学专业知识   冶疗   医学基础课   考核合格者   组织胚胎学   人道主义情怀   临床课   儿科学   妇产科学   口译  

摘要： 当你面对患者痛苦的身躯、患者家属信任的表情,以及患者因你成功的冶疗而痊愈时那感激的目光时,你意识到了医生神圣的职责吗?你收获纠的将不只是成功的喜悦,更是对生命的理解和珍惜。通过临床医学专业知识的学习,你能够领略到生命的美丽与动人……

关键词： Sema4C   Wholemount   组织芯片   原位杂交  

摘要： 目的研究Sema4C基因在小鼠不同发育阶段的表达情况,为探讨其生物学功能提供相关线索。方法用地高辛进行标记并制备Sema4C特异性RNA探针。对于不同胎龄的胎鼠,用胚胎整体原位杂交(Wholemount)的方法检测Sema4C在不同发育阶段的表达,用组织芯片结合原位杂交的方法对Sema4C在成年小鼠不同组织中的表达进行检测。结果Sema4C基因在E11.5小鼠胚胎的前脑,眼原基,背根神经节,动脉弓中均有表达,E13.5小鼠胚胎除以上部位以外在上肢肢芽中也有部分表达。在成年小鼠的大脑皮层,小脑蒲肯野纤维层,视网膜视神经节细胞层和肾小管上皮细胞层中均有较高表达,而在肌肉,心脏,肺,脾脏,肝脏等组织中表达量比较低或未检测到表达。结论小鼠Sema4C基因除了在神经系统发育过程中持续高表达外,还在成年小鼠肾小管上皮中高表达,提示其可能在神经系统和肾脏生理功能方面发挥某种作用。

关键词： 组织学   胚胎学   实验   计算机辅助教学  

摘要： 组织学与胚胎学(以下简称组胚)是医学形态学科,实验教学是组胚教学的重要环节.为了提高实验教学质量,充分发挥多媒体教学的优势,我校于2002年组建了形态学实验中心(组胚与病理教研室共用),实现了实验教学的多媒体化.下面就组胚实验教学中引人多媒体技术进行教学改革的情况进行总结.