Retinoic acid induced heparin-binding protein expression and localization during gastrulation,neurulation, and organogenesis

Retinoic acid induced heparin-binding protein (RIHB) is a highly basic, soluble polypeptide of the chick embryonic extracellular matrix. We have examined the expression and localization of RIHB during very early embryogenesis by in situ hybridization and immunohistochemistry. RIHB mRNA is very weakly detectable above background in the blastodiscs of unincubated eggs. The expression increases greatly over the first 24 hours of incubation, and is observed throughout the blastodisc in all three of the germ layers following gastrulation. As neurulation occurs, the expression becomes more restricted to certain areas, notably the ectoderm, the neural folds, and especially the notochord. After the neural tube has formed the expression in the tube itself decreases dramatically, whereas the expression in the head ectoderm and the notochord persists. After 72 hours of incubation expression remains relatively high throughout most of the embryo, with higher levels of expression in regions undergoing organogenesis and lower levels in organs which have already differentiated. RIHB protein is also weakly detectable in unincubated eggs as patches of immunoreactive material between the blastodisc and the vitelline. After 6 hours of incubation small regions of basement membrane are immunoreactive. RIHB is detected in this matrix, apparently before even fibronectin. The amount of RIHB protein increases dramatically over the first 24 hours of incubation. It is found in basement membrane separating the epiblast from the hypoblast, then later in that separating the ectoderm from the mesoderm. It is also detected surrounding individual cells, especially of the ectodermal layer. During neurulation RIHB is observed in the basement membrane surrounding the neural fold and the notochord, and in the lamina separating the ectodermal, mesodermal, and endodermal layers. Later in development, RIHB is detected in the basement membrane under the epidermis, throughout the developing limbs, and in the lamina of various developing organs, such as the eye, the pulmonary bud, the intestine, and the mesonephros. These results demonstrate that RIHB is highly expressed during the early embryonic period, by all three germ layers, and is an important and very early component of the embryonic extracellular matrix. Its very broad expression and localization argue for a more general role in development than its demonstrated weak neurotrophic activity. © 1994 Wiley-Liss, Inc.     

Effects of cadaver dissection on the attitudes of medical students

Summary: Summary. A study was conducted to determine whether the attitudes of medical students to death and caring changed during the 3 months following exposure to cadaver dissection. All first-year students were invited to complete a questionnaire immediately before their initial cadaver dissection experience, after 6 weeks, and after a further 3 months. The questionnaire reflected attitudes to death, violent death, death of someone known to the respondent and caring when someone known to the respondent is seriously injured. Ethnicity and previous exposure to dying has no effect on responses, but overall men students' reactions were significantly less than for women ( P < 0.001). The responses given on the final part of the questionnaire after 3 months were significantly lower than those to most questions in the first part of the questionnaire. The exceptions were those questions where the subject in the given scenario was known to the respondent, where reactions were rated significantly greater ( P < 0.001) in the follow-up questionnaire and can be explained on the basis that they were a personal referent.
Students rapidly develop a coping mechanism which enables them to view cadaver dissection as an occupation quite divorced from living human beings. During these early months of training solicitude decreases for those who die who are unknown to them, but concern for personal referents increases. Educators should be aware of the dramatic change of attitudes among students and the process of professionalization which might influence their caring of future patients.     

19例SARS死亡病例临床分析

为分析严重急性呼吸综合征(SARS)死亡患者的临床特征、治疗及死亡相关因素,对2003年5月6日至6月27日收治的220例SARS患者中19例死亡患者的临床、实验室、影像学资料、临床治疗及死亡相关因素进行回顾性分析。结果19例死亡SARS患者年龄24～86岁,平均(57.63±16.76)岁。大于45岁13例(68.4%)。男性15例(78.9%),女性4例(21.1%)。有明确接触史19例(100%)。并存基础病13例(68.4%)。死亡距发病时间14～54d,平均(35.37±11.66)d。临床表现主要有发热19例(100%),咳嗽12例(63.2%),畏寒5例(26.3%),气促10例(52.6%),胸闷11例(57.9%),肌痛5例(26.3%),腹泻6例(31.6%)。实验室检查血常规中早期白细胞总数正常或降低,淋巴细胞降低。血气分析低氧血症16例(84.2%);心肌酶肌酸激酶心肌型同工酶(CKMB)、乳酸脱氢酶(LDH)、α羟丁酸脱氢酶(HBDH)随病情的严重程度而进行性升高。T细胞亚群CD3、CD4、CD8绝对值随病情的严重程度而进行性降低。胸部X线双侧、肺病变面积>1/3者19例(100%)。临床诊断继发混合感染(细菌、真菌)19例(100%)。采用综合治疗,其中激素18例(94.7%)、机械通气15例(78.9%)。死于呼吸衰竭18例(94.7%)。提示年龄、合并基础病、肺部病变程度、低氧血症、T细胞亚群CD3、CD4绝对值降低、激素剂量、混合感染等是影响S     

37例创伤死亡病例分析

本文对住院因外伤致死者进行了一般分析，说明创伤造成死亡占总死亡人数之６３。７％，而其中６５％均为青壮年和中年，并着重对颅脑损伤的死亡情况加以分析，提出对特重型颅脑外伤当非手术疗法无效时，应行手术探查减压，另外对腹部挫伤和烧伤及开放性骨折引起死亡的病例进行了讨论。     

Diethylnitrosamine-induced metastasizing hepatocellular carcinomas in New Zealand white rabbits

Summary The aim of this study was to produce large liver tumors reliably, and to diagnose the tumors during development. Therefore, New Zealand white rabbits were treated withN-nitrosodiethylamine orally three times per week by gavage and were examined by clinical-chemical assay at regular intervals during the average treatment period of 14 months. The total cumulative dose was 1200 mgN-nitrosodiethylamine over 14 months. After a short treatment period the initial dose of 3 mg/kg had to be reduced to 1.5 mg/kg. In all 11 treated animals (100%) liver tumors were seen at the end of the study. Four control animals did not show any neoplastic changes. Clinical parameters investigated were for an assessment of liver function, total protein, urea, creatinine, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, albumin and neuraminic acid as well as some serum electrolytes. The in vivo diagnosis of liver tumors based on changes in these parameters proved to be relatively unreliable. The liver enzyme tests and urea concentration only yielded significant changes when the liver tumors were very large. Changes in neuraminic acid levels were the most reliable indicator for the presence of a liver tumor in this animal model. In the 11 treated animals, serum values of this marker increased towards the end of the study'by an average of 300 mg/dl. The induced tumors were mainly hepatocellular carcinomas. Only in 1 animal was a hepatocellular adenoma found. Further primary tumors diagnosed were six adenomas in the kidneys and two uterus adenomas, as well as nasal cavity tumors (two papillomas, one carcinoma, one adenoma and one adenocarcinoma). In 70% of the treated rabbits the hepatocellular carcinomas had metastasized to the lungs.     

Cellular degeneration and synaptogenesis in the developing retina of the rat

We have investigated the time course and magnitude of cellular degeneration in the ganglion cell layer and the presumptive amacrine and bipolar regions of the inner nuclear layer during the development of the retina in the rat. Pyknotic profiles are present in the ganglion cell layer during the first 2 postnatal weeks, reaching peak numbers during the first 4 postnatal days (corresponding to the time of greatest loss of ganglion cells and their axons: Potts et al., '82; Lam et al., '82; Perry et al., '83). Two observations suggest that the majority of pyknotic profiles present in the ganglion cell layer during the second postnatal week are not ganglion cells. First, following injection of kainic acid into one superior colliculus, degenerating ganglion cells in the contralateral retina are cleared within 24-48 hours. Therefore, since most ganglion cell and axon loss occurs within the first postnatal week, few of the pyknotic profiles present in the second week are likely to be ganglion cells. Second, the time course of cellular degeneration in the ganglion cell layer during the second postnatal week follows a very similar pattern to that seen in the presumptive amacrine sublayer of the inner nuclear layer. Such a correspondence suggests that two phases of cell death occur in the ganglion cell layer: during the first postnatal week the majority of dying cells are ganglion cells, and in the second, most cell death is due to a loss of displaced amacrine cells. In the inner nuclear layer pyknotic profiles are most numerous in the presumptive amacrine region on postnatal days 6 and 7, and in the presumptive bipolar region on day 10. Synaptogenesis in the inner plexiform layer occurs later but reflects the order of cell death. Thus, conventional (presumed amacrine) synapses were first observed on day 11 and synaptic ribbons (indicative of bipolar synapses) on day 13. These observations suggest that amacrine and bipolar cells initiate synapses only after their numbers have stabilized.     

Post-mortem analysis for two prevalent β-oxidation mutations in sudden infant death

BACKGROUND: Fatty acid oxidation disorders may cause sudden and unexpected infant death and are associated with the histological hallmark of hepatic steatosis. The goal of the present study was to assess the value of post-mortem molecular analysis for medium-chain acyl-coenzyme A dehydrogenase (MCAD) and mitochondrial trifunctional protein (MTP) defects in unexplained sudden infant death (SID) associated with fatty infiltration of the liver. MCAD catalyzes the first step of medium-chain fatty acid oxidation while MTP catalyzes the last three steps of long-chain fatty acid oxidation. METHODS: In a retrospective study, 220 consecutive cases of sudden and unexplained infant death certified by medical examiners at Wake Forest University Medical Center were assessed for hepatic steatosis. Subjects with evidence of hepatic steatosis were screened for mutations in MCAD and MTPalpha-subunit using DNA isolated from paraffin-embedded liver tissue, single-strand conformation variance, and nucleotide sequence analyses. RESULTS: Sixteen cases (7.3%) were associated with diffuse micro-vesicular or mixed micro- and macro-vesicular hepatic steatosis. Two of these 16 cases (12.5%) had disease-causing mutations. One was homozygous for the prevalent MCAD A985G mutation. The second was a compound heterozygous for the prevalent MTP G1528C mutation and a novel 1 bp deletion in exon 18 of the MTPalpha-subunit gene. CONCLUSIONS: A significant proportion (7.3%) of SID is associated with hepatic steatosis. The present data support post-mortem molecular analysis for the MCAD A985G and MTP G1528C prevalent mutations in cases of sudden and unexplained infant death associated with hepatic steatosis.     

An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immuno-reactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.     

急性心肌梗塞猝死的诱因及抢救(附13例报告)

本文报告了急性心肌梗塞猝死13例。分析猝死的诱因主要有血清钾浓度降低,严重心律失常,包括室内传导阻滞、室性并行心律、室性早搏等。近年来急性心肌梗塞的发病率日趋增高,心源性猝死也随之增多,有必要对猝死的诱因进行探讨,以采取有效的抢救措施。