No abstract available.
Body Weight* ; Humans ; Infant, Low Birth Weight* ; Infant, Newborn

No abstract available.
Child* ; Humans ; Infant*

No abstract available.

No abstract available.

Ulcerative colitis is recognized as important causes of gastrointestinal diseases in children and adults. I observed the fine structural changes of goblet cell regeneration after experimental ulcerative colitis induced by dextran sulfate sodium (DSS) in rats. Experimental colitis was induced with 5% DSS in the drinking water for 5 days, and the healing groups were fed with pure water for 7 days thereafter. In the early stage of goblet cell regeneration (repair 3 days group), granular endoplasmic reticulums were developed around the nucleus, and some mucigen granules were observed around the nucleus. In the middle stage of goblet cell regeneration (repair 5 days group), Golgi complexes were well developed in the upper region to the nucleus, and many mucous granules were observed. In the matured goblet cell regeneration (repair 7 days group), many mucous granules appeared in the upper region of the cell, and cell organelles were located in the base and periphery of the cell. These results suggest that the goblet cell was completely reconstructed within 7 days after ulcerative colitis.
Adult ; Animals ; Child ; Colitis* ; Colitis, Ulcerative ; Dextran Sulfate* ; Dextrans* ; Drinking Water ; Endoplasmic Reticulum, Rough ; Gastrointestinal Diseases ; Goblet Cells* ; Golgi Apparatus ; Humans ; Organelles ; Rats ; Regeneration* ; Water

Inflamatory bowel disease is the general medical terminology on chronic inflammatory illness of unknown origin, but it is considered that environmental, genetical, immunological factors may develop this chronic disease. I examined the histological changes on the experimental ulcerative colitis induced by dextran sulfate sodium(DSS) in rats. Experimental colitis was induced with 5% DSS in the drinking water for 5days in rats (experimental group). And the repair group were treated with 5% DSS for 5days and with pure water after 7days in rats. In experimental group, there are many inflammatory finding in colon of rat which contained loss of body weight, crypt erosion, recruitment of inflammatory cells, submucosal edema. In repair group, the inflammation was recovered that the body weight was incerased, the crypt was recovered. And Ki 67 immunoreaction were restricted lower 1/3 crypt in normal group but positive Ki 67 reaction appeared in the repaired all region. In this study, DSS was induced experimental colitis and the colitis was repaired when we stoped DSS supply. And the Ki 67 during repaired period were overproduction.
Animals ; Body Weight ; Chronic Disease ; Colitis* ; Colitis, Ulcerative ; Colon ; Dextran Sulfate* ; Dextrans* ; Drinking Water ; Edema ; Immunologic Factors ; Inflammation ; Rats ; Water

The experimental ulcerative colitis is chronic inflammatory illness in colon, which didn't reveal the exact reason and pathophysiological situation. In this study, the colitis was induced by 3% DSS (mw; 40,000) for 5 days in mouse which was resemble to inflammatory bowel disease in human, and immunohistochemical changes were observed in the mucosa. In inflammatory group, thickness of the colon was increased and the length of colon was shorter than that of the normal group and the body weight decreased. In microscopic aspect, the crypt erosion, many inflammatory cells and submucosal edema were occurred. In immunohistochemical study, the immunity of COX1 in the inflammatory group was not changed to comparing the normal group, but COX2 immunoreactivity was increased than the normal group, HSP70 immunoreactivity were also increased than the normal group. MAC387 which used to detect the macrophage was increased than the normal group and PCNA immunoreactivity were increased along to the mucal layer. And the number of apoptosis cells detected by TUNEL was increased. In these results, the experimental colitis revealed the tissue defense mechanism as well as inflammatory system and observed the stuffs related to the regeneration.
Animals ; Apoptosis ; Body Weight ; Colitis ; Colitis, Ulcerative* ; Colon ; Edema ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Inflammation ; Inflammatory Bowel Diseases ; Macrophages ; Mice ; Mucous Membrane ; Proliferating Cell Nuclear Antigen ; Regeneration ; Ulcer*

Dehydration induced an increase in plasma osmotic pressure that causes the release of the neurohypophysial hormone (Vasopresin, Oxytocin) which are synthesized in neurons of the paraventricular (PVN) and supra optic (SON) nuclei in the hypothalamus. On the other hand, PVN which plays an important role as an integration site for the neuroendocrine and autonomic nervous system neurons responded to osmotic stimulation. In this experiment, we studied that the change of several neuropeptidies (AVP: arginine vasopressin, CRF: cor-ticotrophin releasing factor, GAL: galanin, NT: neurotensin. NPY: neuropeptide Y) immunoreactivity in the PVN according to the dehydration. The body weight of the rats decreased during dehydration and various changes were detected in hypothalamic neuropeptidies immunoreactivity.Our results show that: 1. Dehydration significantly increased AVP, CRF and GAL immunoreactivity in the PVN. 2. Dehydration slowly decreased NT immunoreactivity in the PVN. 3. NPY immunoreactive cell bodys were appeared during dehydration which did not observed in PVN at normal group.
Animals ; Arginine Vasopressin ; Autonomic Nervous System ; Body Weight ; Dehydration* ; Galanin ; Hand ; Hypothalamus ; Immunohistochemistry ; Neurons ; Neuropeptides* ; Neurotensin ; Osmotic Pressure ; Plasma ; Rats

Neurons are very sensitive to various injuries such as ischemia, hypoxia, hypoglycemia, etc. Frequently, the hippocampal CA1 area has been used as a region for studying ischemic delayed neuronal death, which is induced by middle cerebral artery occlusion (MCAO). However, it is still controversial whether the delayed neuronal death is necrotic or apoptotic. In this study, we investigated the neuronal death in hippocampal CA1 areas by TUNEL stain and electron microscopic observation using a rat MCAO and reperfusion model. RESULTS: 1. The TUNEL positive reaction occurred only within the CA1 area ipsilateral to MCAO. 2. In EM images, many features that imply necrosis were found in the CA1 pyramidal neurons ipsilateral to MCAO. These results indicate that both necrotic and apoptotic features coexist in the delayed neuronal death of the hippocampal CA1 area after MCAO.
Animals ; Anoxia ; Hypoglycemia ; In Situ Nick-End Labeling* ; Infarction, Middle Cerebral Artery ; Ischemia ; Necrosis ; Neurons* ; Rats* ; Reperfusion

In order to study damages on brain cells upon occlusion and reperfusion, brain infarction was induced by insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. After occlusion of 1 hr and reperfusion for variable duration, brain slices were used to observe changes in the brain morphology and in the pyramidal neurons of the himppocampal formation. In this study we found following results. 1) The operation took 20~30 min and about 30% of the operated animals were suitable for studying neurological aspects. 2) The TTC stain showed that about 23.9% of the total brain area was damaged in the 72 hr-reperfusioned sample. 3) The degree of brain edema was larger in the left hemisphere (damaged side) than in the right one (contralateral undamaged side). 4) Pyramidal cells of the damaged hippocampal formation showed features of necrosis such as shrinkage, large vacuole, swelling, and cell debris. 5) The numbers of survived cells per mm2 of the hippocampal formation were 93 in the undamaged animal, and 23 and 3 in the 3 and 7 days after reperfusion, respectively.
Animals ; Brain ; Brain Edema ; Brain Infarction ; Carotid Artery, Internal ; Hippocampus* ; Ischemia ; Middle Cerebral Artery* ; Necrosis ; Neurons ; Nylons ; Pyramidal Cells* ; Reperfusion ; Vacuoles