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

No abstract available.
Child* ; Humans ; Infant*

No abstract available.

No abstract available.

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

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

The purpose of this study is to evaluate the effects of Woohwangcheongsim-won on reperfusion following the MCA occlusion in rats. To evaluate the effect of Woohwangcheongsim-won on reperfusion following the MCA occlusion, the volume of cerebral ischemia and edema was measured. The volume of the control group, which was ischemic-damaged was 23.6%, and that of the sample group was 13.5%. The voluminal ratio of the right/left hemisphere was 116 in the control group, and that of the sample group was 107.
Animals ; Brain Edema ; Brain Ischemia* ; Edema ; Infarction, Middle Cerebral Artery* ; Middle Cerebral Artery* ; Neuroprotective Agents* ; Rats ; Reperfusion

The cerebral artery spasm is a phenomenon frequently present in cases of subarachnoid hemorrhage (SAH). Previous reports indicated that vasospasm could be produced primarily by muscle contraction and constricted vessels that exhibit myonecrosis and subendothelial changes. Pharmacological studies have shown that vasospastic arteries decrease in contractility but increase the spontaneous tone and stiffness compared to normal cerebral arteries. We carried out electron microscopic to observe the morphological changes of the basilar artery following the experimental SAH. We examined changes in the size of the lumen and thickness of the basilar artery in SAH. Morphological changes of cerebral basilar artery following SAH : (1) The size of the lumen of basilar artery decreased about 47%, while its thickness increased about 170%. (2) The shape of the endothelial cell transformed to a cuboidal type and its thickness increased, while the length of the smooth muscle cell shortened and the thickness increased.
Arteries ; Basilar Artery* ; Cerebral Arteries ; Endothelial Cells ; Hemorrhage* ; Muscle Contraction ; Myocytes, Smooth Muscle ; Subarachnoid Hemorrhage ; Vasospasm, Intracranial