The distribution of GABA-containing neurons in the anterior horn of L_(4～5) segments of rat spinal cord and their relationship with somatic efferent were studied by combined method of HRP and immunocytochemistry and immunoelectron microscopic method. The results showed that under light microscope, the GABA-immunoreactive cell bodies and terminals were seen in all layers of the anterior horn including Rexed′s layer IX which located in the anterolateral part of the anterior horn. The GABA-positive neurons had round or triangle cell body with many processes and could be divided into two (large and medium) types. Under electron microscope, GABA-immunoreactive products appeared as small granular deposits located in perikarya, dendrite and axon. In axon terminals the immunoreactive products located at periphery of the synaptic vesicles and on the outer membrane of the mitochondria. The GABA-positive dendrites received symmetrical afferent synapses from GABA-positive or negative axon terminals. The combined method of HRP and immunocytochemistry showed that in Rexed′s layer IX there were HRP single labeled neurons, GABA single labeled neurons and HRP/GABA double labeled neurons. The double labeled neurons accounted for 79% of total HRP labeled cells. Above mentioned results first identified the neurons in Rexed′s layer IX of the anterior horn contain GABA which participate in somatic efferent and receive autoregulation from GABA-neurons and nonGABA-neurons at synaptic level.

Using immunoelectron microscopic technique the SPergic autoregulatory synapses in the nucleus raphe magnus were studied. The results showed that there were SPlike perikarya and nerve fibers. The positive perikarya mainly were large polypolar cells. The positive fibers appeared as beaded-like and formed axodendritic synapses with SP-positive dendrites besides synapses formed with SP-negative structures. In the autoregulatory synapses the pre- and postsynaptic element were both labeled with immunoreactive products which precipitated at the periphery of small clear synaptic vesicles and the dendritic tubes, on the outer membrane of mitochondria, and in the cytoplasmic matrix. The pre- and postsynaptic membrane were symmetrical, and the synaptic vesicles aggregated near the presynaptic membrane. The synaptic cleft was about 20 nm in width and contained electron dense materials. The generality, structural characteristics and functional significance of the autoregulatory sysnapses were discussed.

The distribution of neurotensin (NT) and neuropeptide Y (NPY) in the rat hypothalamic arcuate nucleus has been studied ultrastructurally by means of double labeling preembedding immunoelectron microscopic PAP technique. First, the NPY immunoreaction was demonstrated by chromogen DAB, and second, the NT immunoreaction was demonstrated by ammonium molybdate-TMB method. After being stabilized by DAB-cobalt chloride, the vibratome sections were processed for electron microscopic study. The results showed that in the arcuate nucleus the NPY immunoreactive products appeared as high electron-dense granular or flocculent materials deposited diffusely in the organelles and matrix of perikaryon, around the dendritic microtubules and axonic small clear vesicles. Whereas the NT immunoreactive products were dense needle- or mass-like deposits distributed dispersively in the perikaryon, dendrites and axon terminals. They can easily be distinguished although being intermingled together. The NPY-containing dendrites and axons formed synaptic connections with immuno-negative axon terminals, NT-containing somata and dendrites formed also synaptic conections with negative axon terminals. In addition, NPY-positive axon terminals formed symmetrical axodendritic synapses with NT-positive dendrites. The present results provided another new ultrastructural evidence for the peptidergic synaptic regulation of NT neurons in hypothalamus.

The protective effect of vitamin E and the change in activity of enzymes at hepatic injury by carbon tetrachloride(CCl_4) were studied with histochcmical methods. 60 rats were devided into three groups(A,B,C). The group A was untreated control; the animals of group B and C were injected(i. m.) with 0.9% NaCl 1 ml/100g or vitamin E 1 ml/100g body weight qd for 7 days respectively and then treated with 30% CCl_4 0.05ml/l00g by adding to the solution of NaCl or vitamin E from 8th to 14th days. On the 15th day, rats were sacrificed for histochemical study of the liver parenchyma. The results showed that the activity of SDH, G-6-Pase, ATPase, 5-NT or AcP in liver lobules of groups B and C animals were changed conspicuously after treatment with CCl_4. The quantitative histochemistry of SDH and G-6-Pase was also consistent with these results. The activity of SDH, G-6-Pase, ATPase and 5-NT were inhibited, but of AcP was elevated. As compared with those in the rats of group A, the changes however in group B appeared more obviously than those in group C. The results indicated that CCl_4 of the given dose induced acute damage in liver cells, while vitamin E had important protective effect against acute liver damag induced by CCl_4.

In order to explore the roles of different neurotransmitters in epileptic pathogenesis,the synaptic connections between glutamic acid (Glu) neurons and GABA neurons in normal rat hippocampus were studied by pre-embedding double labeling immunoelectron microscopy. The GABA immunoreaction was first demonstrated by chromogen DAB, then the Glu immunoreaction was demonstrated by molybdic acid-TMB method. After being stabilized by DAB-cobalt chloride,the sections were processed for electron microscopic embedding. Under electron microscope, there were many Glu immunoreaction-positive neurons in the pyramidal layer of hippocampal CA1 area and some GABA immunoreaction-positive neurons with pyramidal or polygonal perikarya in the pyramidal, polymorphic and radiant layer of CA1 area. There were also symmetric dendro-axonic synapses formed by GABA-positive dendrites and Glu-positive axons in the polymorphic layer and symmetric axo-dendritic synapses formed by GABA-positive axons and Glu-positive dendrites in the radiant layer. In addition, there were symmetric autoregulatory axo-dendritic synapses between Glu-positive axons and dendrites and autoregulatory axo-axonic synapses (both symmetric and asymmetric) between GABA-positive axons. Above mentioned results, for the first time,showed that there were complex synaptic regulatory relationships between excitatory Glu neurons and inhibitory GABA neurons in the hippocampal CA1 area, thereby, providing ultrastructural evidence for different neurotransmitters participating in epileptic pathogenesis.

In order to explore the roles of different neurotransmitters in epileptic pathogenesis,the synaptic connections between glutamic acid (Glu) neurons and GABA neurons in normal rat hippocampus were studied by pre-embedding double labeling immunoelectron microscopy. The GABA immunoreaction was first demonstrated by chromogen DAB, then the Glu immunoreaction was demonstrated by molybdic acid-TMB method. After being stabilized by DAB-cobalt chloride,the sections were processed for electron microscopic embedding. Under electron microscope, there were many Glu immunoreaction-positive neurons in the pyramidal layer of hippocampal CA1 area and some GABA immunoreaction-positive neurons with pyramidal or polygonal perikarya in the pyramidal, polymorphic and radiant layer of CA1 area. There were also symmetric dendro-axonic synapses formed by GABA-positive dendrites and Glu-positive axons in the polymorphic layer and symmetric axo-dendritic synapses formed by GABA-positive axons and Glu-positive dendrites in the radiant layer. In addition, there were symmetric autoregulatory axo-dendritic synapses between Glu-positive axons and dendrites and autoregulatory axo-axonic synapses (both symmetric and asymmetric) between GABA-positive axons. Above mentioned results, for the first time,showed that there were complex synaptic regulatory relationships between excitatory Glu neurons and inhibitory GABA neurons in the hippocampal CA1 area, thereby, providing ultrastructural evidence for different neurotransmitters participating in epileptic pathogenesis.

BACKGROUND:In recent years, based on high-throughput molecular imaging, integration of genomics, proteomics and computer aided design and the application of correlative “technical chains” have achieved great achievements in the research of breast cancer, lung cancer, gastric cancer, colon cancer, ovarian cancer and melanin tumor. However, there are few researches on oral squamous cel carcinoma. OBJECTIVE:To detect the gene expression profile of the oral squamous cel carcinoma tissue and normal paracarcinoma tissue using DNA chip-based gene expression profile. METHODS:Two samples of oral squamous cel carcinoma tissue and normal paracarcinoma tissue of patients who received treatment at Stomatological Hospital of Guangdong Province of China in 2013 were included in this study. The gene expression profiles of oral squamous cel carcinoma and normal paracarcinoma tissue were determined by the Roche NimbleGen gene expression microarrays. RESULTS AND CONCLUSION: According to screening criteria of differential genes, 7 872 out of 32 448 detected genes were differentialy expressed genes of oral squamous cel carcinoma, which accounts for 24% of the total number of the screening genes. 3 800 genes were up-regulated, and 4 072 were down-regulated. The results confirm that through detection with the help of gene expression profile clip, 7 872 differentialy expressed genes were obtained through DNA chip-based gene expression profiles according to the screening criteria. Thus it can be concluded that the occurrence and development of the tumors are not a result of single or several genes. Previous experiments based on a single or several genes have great limitations. These findings also suggest that the occurrence of tumor is a result of mutual regulatory effects of many genes forming a network, moreover, the interactions of the network is quite complicated.

Gingival recession is one of the common oral symptoms. Periodontal soft tissue defects caused by gingival recession and problems related to aesthetics, prosthetics and orthodontic treatment have garnered increasing attention. This article reviews the etiology, classification and treatment of gingival recession to provide a reference for the diagnosis and treatment of gingival recession. Anatomical characteristics of teeth, bacterial and viral infection, Occlusion trauma, Improperbrushing methods and other daily behaviors and iatrogenic factors may lead to gingival recession. Miller classification is the most commonly used classification standard. It is divided into 4 degrees according to the relationship between gingival recession and the association between the gingival membrane and the loss of adjacent alveolar bone or interdental papilla. Gingival surgeries, such as coronally advanced flap, laterally positioned flap, subepithelial connective tissue graft for Miller Ⅰ degrees and Ⅱ gingival recession retreat, obtain a more satisfactory success rate. Regarding the Ⅲ degree gingival recession, the postoperative curative effect is poor and can only cover part of the root. Regarding Ⅳ degrees gingival recession, surgery cannot reach the root surface coverage. For patients with Miller Ⅳgingival recession caused by severe periodontitis, the surgical treatment is poor, and repair methods, such as sputum, can also be considered. In recent years, a variety of biological materials have been jointly applied to gingival surgery, such as tooth enamel matrix derivative (EMD), allograft acellular dermal matrix (ADM), porcine collagen matrix (PCM) and platelet-rich fibrin (PRF). The use of these biomaterials can improve root coverage, increase gingival thickness and keratinized gingival width, avoid the requirement of palatal flap removal, reduce the surgical risk and increase patient compliance.

Objective:To observe the recovery of exercise tolerance among stroke survivors using the cardiopulmonary exercise test (CPET) and analyze the factors influencing it.Methods:A total of 81 stroke survivors hospitalized in the Department of Rehabilitation Medicine of our hospital in year 2018 and 2019 were selected. The general clinical data of all patients were collected retrospectively and combined with the data from CPET to establish a data set. Version 25.0 of the SPSS software was used for multiple linear regressions analysis, with the peak oxygen uptake as the dependent variable, and the age, Brunnstrom stage, peak power, peak heart rate, peak respiratory exchange ratio, peak breathing reserve, peak ventilation per minute, the slope of the VE-VCO 2 curve (ΔVE/ΔVCO 2) and peak end tidal partial pressure of carbon dioxide as independent variables. Results:Stroke survivors at Brunnstrom stage III Ⅲ, Ⅳ and Ⅴ or higher decreased sequentially with their age, but their peak oxygen uptake increased gradually. The multiple linear regression model constructed by " stepwise method" showed that the fitted multiple linear regression equation was statistically significant ( F=100.228, P<0.001). Moreover, the average peak power, peak heart rate, peak ventilation per minute and the slope of the VE-VCO 2 curve were all found to be significant independent predictors of peak oxygen uptake in these stroke survivors. Conclusions:Skeletal muscle power, cardiac function, pulmonary ventilation and ventilation efficiency are useful independent predictors of the exercise tolerance of stroke survivors.