The neuroendoerine cells (NE cell) of the lung have been studied in 61 human fetuses by silver stain, immunocytochemical method and electron microscopic technique. The NE cells are mainly located in epithelium of conducting portion with various appearance. Some NE cells are neuron like with several processes. The 5-HT positive NE cells are often found in the epithelium of the primitive alveoli with pyramidal, squamous and tadpole-like appearance. Based upon their ultrastructure, the NE cells are rich in organelles and dense core vesicles (DCV). The NEB is often covered by a layer of cuboidal cells, but no nerve fibers are found among the cells in the NEB.The argyrophil cells usually appear in the 12th week, and reach the maximum number by 20th week. Before the 19th week, the argyrophil cells in the upper segment of the conducting portion are more numerous than those in the lower segment, while after 19th week the condition is just reverse. A regression curve made from the number of argyrophil cells and the thickness of intrapulmonary arteries in different fetal ages shows positive correlation.

Objective The diolistic assay has been modified to make it simpler and more efficient in labeling neurons and glia. Methods CNS neurons and glial cells were labeled with DiI diolistic assay in fixed tissue and living brain slices of C57/B6J mice. Results The method allowed the visualization of the fine structure of neurons and glia including synaptic structures such as dendritic spines. Conclusion With the method, the labeling efficacy of cell's fine structure is improved, making it preferable for the analysis of dendritic spine. In addition, the ability to label the living neuron and glia will extend its application vastly.

The methods and experiences of anatomy,histology and embryology teaching in English for foreign students are discussed in this article to exchange experiences with each other and progress together.

BACKGROUND: The augmenter of liver regeneration (ALR) is a kind of important secondary liver regeneration factors, and it can particularity promote the liver regeneration. OBJECTIVE: To clone the RNA extracted from neonatal rat liver to ALR gene, and to analyze the gene using the bioinformatics. DESIGN, TIME AND SETTING: The study, gene molecule in vitro experiment, was performed at the Laboratory of Neurobiology, College of Life Science of Henan University between March 2008 and May 2008. MATERIALS: The liver tissues were harvested from 3-day-old Wistar rat of SPF grade. METHODS: Total RNA was exacted from rat liver tissues using guanidinium isothiocyanate-phenol-chloroform extraction method. According to the guideline of molecular biology experiment, the target fragment was amplified using reverse transcription-polymerase chain reaction. Alter purified, the target gene was recovered with gel recovery kit and subcloned to pGEM-T easy, and then was transformed to E.coli. The extracted piasmid was sequenced by Shanghai Sangon Biological Engineering Technology And Service Co., Ltd. The sequence was analyzed with molecular biological software. MAIN OUTCOME MEASURES: Polymerase chain reaction amplification band; analysis of gene sequence; sedne, threonine and tyrosine phosphorylation predictions; phytogenetic analysis of ALR. RESULTS: The potymerase chain reaction product was in concordance with target fragment. The analysis of the gene sequence proved it is the ALR gene. The overall length of the ALR gene was 378 bp, it was highly conservative in many species, for instance the Homo sapiens, the Mus musculus, the Bos Taurus and the Danio redo. CONCLUSION: In this experiment, we have cloned the ALR gene successfully.

Objective To study the effects of matrine on inducing autophagy and autophagic death in BEL-7402 cells. Methods BEL-7402 cells were cultured in RPMI1640 alone or exposed to different concentration of matrine. Cell growth inhibition was assessed by MTT assay. Apoptosis was evaluated by flow cytometry. Autophagosome marker LC3 was examined by immunofluorescence microscopy. The ultrastructure change of cells was analyzed by transmission electron microscope. Results The cell proliferation was inhibited by matrine in a dose dependent manner. Its IC50 value was 1.1 mg/mL at 48 h. Treatment with 0.6-1.6 mg/mL matrine for 12 h induced apoptosis of BEL-7402 cells and the apoptosis rate reached (44.88?0.78)% at concentration of 1.2 mg/mL. The autophagy positive cells were greatly increased after 1.2 mg/mL matrine treated in BEL-7402 cells and the number of cells reached (63.16?0.29)%. Morphological features of typical autophagic death were apparent in the cytoplasm at the ultrastructural level. Conclusion Matrine could induce autophagy and autophagic death of BEL-7402 cells in vitro.

Objective To study ethanol-induced the neuroapoptosis of visual cortex in offspring mice. Methods Pregnant female mice were fed by intubating alcohol daily,beginning on E5(embryonic,E) and continuing through the pup's birth.The neuroapoptosis in P0,P7 and P14 visual cortex was visualized by Caspase-3 activity immunohistochemistry and Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling(TUNEL) staining. Results Usually,the pup's birth days would delay one or two days after ethanol exposure.Moreover,ethanol induced reabsorption of fetus and malformations,such as microcephaly,anencephaly and myeloschisis with spinabifida and so on,were found in the study.Apoptosis index in ethanol treatment groups was obviously higher than that in control at either P0,P7 or P14(P

Aim To study ethanol-induced changes in the development and neuronal number of visual cortex in C57BL /6 mice. Methods Female mice were fed with ethanol during pregnancy . The neuron density (ND) and cortical thickness (CT) in visual cortex of off spring mice were measured at either P0, P7 and P14 with hematoxylin and eosin (H.E) and Nissl staining. Results Embryonic death and malformationswere found in the ethanol-treated groups. Malformations, such as microcephaly,anencephaly and myeloschisis with spinabifida, etc were found in late-term embryos. The malformation rate was 12%. Compared with control group, the development of visual cortex in ethanol-treated groups was delayed, and its lamination was in disorder. The neuron polarity was disturbed. Neuron loss was found after ethanol exposure. At various ages, the neuron density in ethanol-treated groups was lower than that in control group(P

Objective In order to investigate the influence of reelin deficiency on the hippocampal development, the histochemical characteristics of hippocampal pyramidal cells and granule cells of reeler mice were analyzed, therefore, reelin's function would be better understood with more morphological evidences. Methods With immunofluorescent double labeling, the pyramidal cells, granule cells and mossy cells in hippocampi between wild type and reeler mice were labeled. Results The development and lamination of hippocampal cortical plate were in disorder. Pyramidal cells and granule cells dispersed, and moreover, granule cells proliferated rapidly and migrated into hilus, so that the bound between granule layer and hilus disappeared. Conclusion As a stop signal and regulatory signal, reelin plays important roles in neuronal migration of developing cortical plate, especially in the regulation of granule cell proliferation.

Objective In order to make a epileptic model in organotypic slice culture and to further investigate the epileptic pathology. Methods Immunohistochemistry, Fluoro-Jade B staining and BrdU labeling were carried out in the hippocampal slices with domoic acid treatment after 7 days of culture.Results Domoic acid could induce a series of pathological changes, such as, dispersion of granule cells(0.105±0.063) mm vs (0.057±0.012) mm, t = 4.8, P<0.01), neurogenesis in granular layer and cell loss of pyramidal cell and Mossy cell as well. Conclusions In hippocampal organotypic slices, domoic acid induced such pathological changes as human temporal lobe epilepsy and epileptic animal model. It is an ideal epileptic model for pathological, pharmacological and electronic physiological studies with great applicable prospect.

In order to understand the alcohol's toxicity to the quantitative alternations of synapses in mouse visual cortex, the expression of synaptophysin after prenatal alcohol exposure was investigated. In present study, the experimental mice at P0, P7, P14 and P30 were grouped, as control, 2 g x kg(-1) alcohol treatment and 4 g x kg(-1) alcohol treatment. The pre-synaptic elements which were used to represent synapses were marked with synaptophysin (a synaptic vesicle associated protein) by immunocytochemistry technique. The synaptophysin positive boutons in layer VI of visual cortex were imaged under laser confocal microscope. With stereological methods, the number cal density of synapse in visual cortex was calculated in different groups at various ages. Moreover, Western blotting was carried out to detect the expression of synaptophysin in visual cortex. The results showed that prenatal alcohol exposure could cause synaptic loss with long-term effect and in a dose dependent manner. For instance, there were significant difference among the different treatment groups of P0, P14 and P30 as well (P < 0.05). Western blotting supported the results of immunofluorescent labeling. In conclusion, prenatal alcohol exposure can induce the synaptic loss dose dependently and with long-term effect. Our findings implicate that the synaptic loss with long-term effect in CNS probably contributes to the lifelong mental retardation and memorial lowliness associated with childhood FAS.