• Korean Journal of Fisheries and Aquatic Sciences
• /
• v.33 no.2
• /
• pp.129-136
• /
• 2000

Differentiation and development of the digestive organ of the black sea bream, AcanHepagus schlegeli were studied by means of histological methods. The hatched lawn if TL(total length) $2.0 mm (n=10)$ had a yolk sac of $1,000{\times}590 {\mu}m$ and simple straight digestive tract, which was composed of cuboidal epithelium. In the pre-larval stage of TL $3.5 mm$, digestive tract could be distinguished into esophagus, stomach and intestine, and the exocrine glands were appeared in the pancreas. In this stage mucosal folds, eosinophilic granule cells and brush border were observed in the posterior intestine. Yolky materials were completely absorbed and the brush border was recognized in the free surface of anterior intestine in TL $3.7 mm$. In the stomach mucosal folds began to appear from TL $4.0 mm$. In this time the zymogen granules were recognized in the cytoplasm of pancreatic exocrine cells. In the post-larval stage ranged from $4.5 to 5.0 mm$ in TL, hepatic cords started to develop, and the mucous secretory cells of PAS positivewere observed at esophagus and intestine. In the post-larval stage ranged from $6.3 to 7.0 mm$ in TL, histological layer of esophagus and intestine could be distinguished into serous membrane, muscular layer, submucosal layer and mucosal layer. From over TL $9.0 mm$, stomach could be distinguished into cardiac, fundic and pyloric portion, and the gastric gland began to appear at mucosal fold of fundic stomach. In the juvenile stage ranged from $10.0 to 11.0 mm$ in TL, histological structures of esophagus and intestine were similar to those of adult. From over TL $15.0 mm$, histological structures of stomach were similar to those of adult. Structural and functional digestive organ of black sea bream was present from the juvenile stage ranged from $15.0 to 17.0 mm$ in TL.

• Tuberculosis and Respiratory Diseases
• /
• v.46 no.3
• /
• pp.317-326
• /
• 1999

Background: Neural control of airway function is through parasympathetic, sympathetic and non-adrenergic, non-cholinergic mechanisms. The autonomic nervous system controls the airway smooth muscle tone, mucociliary system, permeability and blood flow in the bronchial circulation and release of mediators from the mast cells and other inflammatory cells. The cardiovascular and respiratory autonomic efferent fibers have a common central origin, so altered cardiovascular autonomic reflexes could reflect the altered respiratory autonomic status. Therefore, we performed this study to assess the autonomic abnormality and determine the correlating factors of severity of autonomic neuropathy in patients with chronic obstructive pulmonary disease(COPD) using easily reproducible cardiovascular autonomic reflex function test. Method: The study included 20 patients with COPD and 20 healthy persons obtained on Health Promotion Center in Yeungnam university hospital. All the patients had history and clinical features of COPD as defined by the American Thoracic Society. Any patients with myocardial ischemia, cardiac arrythmia, hypertension, central or peripheral nervous system disease, diabetes mellitus, or any other diseases known to produce autonomic neuropathy, has excluded. The autonomic nervous system function tests included three tests evaluating the parasympathetic system and two tests evaluating the sympathetic system. And also all subjects were subjected to pulmonary function test and arterial blood gas analysis. Results: Autonomic dysfunction was more commonly associated with patients with COPD than healthy person The parasympathetic dysfunction was frequent in patient with COPD, but sympathetic dysfunction seemed preserved. The severity of parasympathetic dysfunction in patients with COPD was correlated with the degree of duration of disease, smoking, reductions in the value of $FEV_1$ and FVC, and arterial hypoxemia but no such correlation existed for age, type of COPD, $FEV_1$/FVC, or $PaCO_s$. Conclusion: There is high frequency of parasympathetic dysfunction associated with COPD and the parasympathetic abnormality in COPD is increased in proportion to severity of airway disease. In COPD, parasympathetic dysfunction probably does not the cause of disease, but it may be an effect of disease progression.

• Tuberculosis and Respiratory Diseases
• /
• v.45 no.6
• /
• pp.1214-1222
• /
• 1998

Background : The intrapleural hypofibrinolysis is caused by mainly excessive concentration of pleural plasminogen activator inhibitor-1 antigen(PAI-1 Ag), which binds tissue type plasminogen activator. In pleural inflammation induced by sclerosing agents for pleurodesis, levels of pleural PAI-1 antigen increase in relation to decreasing D-dimer levels. It has been known that the pleural mesothelial cells have the capability of secreting PAI-1 Ag in response to inflammation in vivo. Therefore, we estimated whether pleural inflammation changes the balance between fibrinolytic and coagulative properties in exudative pleural effusions. Method : The thirty cases was included in our study. We determined the pleural levels of glucose, lactic dehydrogenase(LDH), pH and the counts of white blood cell(WBC), polymorpho leukocyte(PMN), lymphocyte as the parameters of pleural inflammation and cellular components of pleural fluid. The plasma level of fibrinogen in fluid and the neutrophil count in blood were determined. The levels of D-dimer, PAI-1 Ag and thrombinantithrombin III complex(TAT) were determined by ELISA(Behring, Marburg, Germany). Result : The causes of pleural effusion were as following : tuberculous in 14 cases, malignant in 10 cases and parapneumonic in 6 cases. The levels of pleural D-dimer, PAI-1 Ag and TAT was significantly higher than that of plasma(p<0..001). The severity of pleural inflammation did not correlated with pleural D-dimer, PAI-1 Ag, TAT and their plasma levels. But the level of pleural TAT correlated with pleural WBC and lymphocyte count. Conclusion : We found that the severity of pleural inflammations did not correlated with pleural D-dimer, PAI-1 Ag, TAT and the possibility of local production of PAI-1 antigen is present.