No abstract available.
Erythropoietin*

No abstract available.
C-Reactive Protein* ; Female ; Obstetric Labor, Premature* ; Pregnancy

Melanosis coli is characterized by a dark brownish discoloration of the colonic mucosa. Its pathogenesis is still unknown. Recently it was proposed that the apoptosis of mucosal epithelium due to habitual use of laxatives play an important role for induction of melanosis coli. We studied clinicopathologic aspects of 12 cases of melanosis coli and analysed the histochemical and immunohistochemical characteristics of them. Results are as follows. : Mean patient's age was 53.5, and the male:female ratio was 4:8. Nine patients had a history of constipation, and all of these had administrated various kinds of laxatives. The severity of discoloration was correlated with the duration of constipation and age. There was no difference of anatomical distribution in colon. Other remarkable mucosal lesions were not accompanied. On pathologic examination, all cases showed frequent yellow-brown pigment laden cells in lamina propria. These pigments were positive for periodic acid Schiff stains, Fontana Masson stains, and Victoria blue stains, however they were negative for prussian blue stain. On immunohistochemical stainings pigmented cells were positive for CD68, and negative for S-100 protein and neuron specific enolase. These results indicate that they are macrophages. On ultrastructural examination pigmented cytoplasms were filled with variable sized electron dense granules including irregulary round deformed membranous structures, lipid vacuoles. Apoptosis of mucosal epithelium was noted in 5 cases. These findings suggest that apoptosis is the significant pathologic process in the progression of some cases of melanosis coli.
Female ; Male ; Humans

No abstract available.
Mandibulofacial Dysostosis*

No abstract available.
Agenesis of Corpus Callosum

Apoptosis (or programmed cell death) is defined by morphologic changes induced by a spectrum of physical and chemical agents. resulting in non-pathologic cell loss, which is relevant to a range of biological processes, including differentiation, development, maturation, and injury of cells as well as immunologic function. In this study, we examined the frequency of apoptotic bodies and mitoses (apoptotic and mitotic indices) in the tissue samples of 35 patients of prostatic carcinoma, which were grouped according to the Gleason scores, and 5 cases of benign prostatic hyperplasia. The indices were determined as the numbers of apoptotic and mitotic bodies per 100 tumor cells in hematoxylin eosin stained section. The apoptotic bodies were confirmed by the in situ nick end labelling method. The apoptotic and mitotic indices were observed more frequently in prostatic carcinoma than the benign hyperplastic prostatic tissues with a positive correlation between the frequency of apoptotic bodies and Gleason scores in prostatic cancer. In conclusion, an increased programmed cell death was correlated with the increasing malignant potential (higher Gleason scores) in prostatic cancer.
Apoptosis ; Biological Processes ; Cell Death ; Eosine Yellowish-(YS) ; Hematoxylin ; Humans ; In Situ Nick-End Labeling ; Mitosis ; Mitotic Index ; Neoplasm Grading ; Prostatic Hyperplasia ; Prostatic Neoplasms*

Sialosyl Tn mucin antigen (STn) is a carbohydrate antigen of tumor associated mucin formed by the premature 2~6 sialation of N-acetylgalactosamine. STn has been expressed in several tumor types and showed prognostic significance in colonic carcinoma. The authors evaluated the expression of STn immunohistochemically and correlated its expression with clinicopathologic variables in 100 gastric cancers. In early gastric cancer, STn was expressed in 24 cases out of 50 cases (48%). In advanced gastric cancer, STn was expressed in 48 of 50 (96%). The difference in STn expression between advanced gastric cancer and early gastric cancer was statistically significant. The difference in STn expression between tumors with lymph node metastasis and those without lymph node metastasis, between tubular adenocarcinoma and signet ring cell carcinoma, and between intestinal type and diffuse type adenocarcinoma was statistically insignificant in early or advanced gastric adenocarcinoma. These results suggest that the STn expression plays a role in the tumor progression in both early and advanced gastric adenocarcinomas.
Adenocarcinoma* ; Carcinoma, Signet Ring Cell ; Colon ; Lymph Nodes ; Mucins* ; Neoplasm Metastasis ; Stomach ; Stomach Neoplasms

No abstract available.
Decompression* ; Facial Nerve* ; Melkersson-Rosenthal Syndrome*

Taxol is an active chemotherapeutic agent against a variety of solid tumors and a potentially useful drug for augmenting the cytotoxic action of radiotherapy against certain cancers. Taxol blocks cells in the mitotic phase of cell cycle. The aim of this study was to define the in vivo response of rapidly dividing cells of the small intestinal mucosa to taxol. We studied the numbers of apoptotic and mitotic cells and the expression of bcl-2 and p53 in rat jejunal crypt cells at 1, 2, 4, 8, 12, 16, and 24 hours and 3 and 5 days after intraperitoneal injection of taxol. Mitosis peaked at 2 and 4 hours and 12 and 16 hours. Apoptosis peaked at 16 hours and returned to normal after five days. The glands in crypts showed marked distortion with atypical lining cells after three days, which returned to normal at 5 days. bcl-2 expression was markedly decreased at 8 to 24 hours and subnormally recovered after three to five days. p53 showed no significant changes throughout. The histopathological changes in small intestine due to taxol were transient with complete recovery. bcl-2 expression was inversely corresponded to numbers of apoptosis. The changes were p53 independent. Further studies to understand the conditions that maximize the cell-cycle modulating effects of taxol cl-may greatly enhance its anti-tumor effectiveness.
Animals ; Apoptosis ; Cell Cycle ; Injections, Intraperitoneal ; Intestinal Mucosa ; Intestine, Small* ; Mitosis ; Paclitaxel ; Radiotherapy ; Rats*

BACKGROUND AND PURPOSE: Many clinical and experimental studies showed that in global ischemic encephalopathy, hyperglycemia consistently excacerbate ischemic brain damages with high mortality and morbidity. In contrast, the results of experiments on focal ischemic lesions were controversial or contradictory to each other according to various conditions. In addition, there have been few studies on the effects of hyperglycemia on delayed neuronal necrosis of hippocampus, which is one of characteristic patterns of selective neuronal necrosis. METHODS: Mongolian gerbils were used and divided into 4 groups ; control(group 1) with 4ml of intraperitoneal(ip) saline injection, hypoglycemia(group 2) was induced by 36-hour of starvation, marked hyperglycemia(group 3) was induced by 20ml/kg ip injection of 50% dextrose solution, and moderate hyperglycemia (group 4) was induced by 5ml/kg ip injection of 50% dextrose solution. Each hyperglycemia group was devided into 2 subgroups (A&B) according to the injection time, either 15 minutes before or after the ligation of arteries, respectively. Focal ischemic lesions were induced by 4-hour ligation of left common carotid artery (CCA) followed by 24 hour reperfusion. Global ischemic encephalopathy was induced by 10 min occlusion of bilateral CCAs followed by reperfusion for 1 or 3 days. RESULTS: In this study, hyperglycemia groups showed high incidence of mortality. Hypoglycemia group showed slightly less damages than control group and the damages were significantly decreased in group 3A. The gerbils in group 4 showed significantly aggravated damages than group 2 and 3. Timing of injection did not show significant difference. The thalamus was the only area showing significant differences among experimental groups. The gerbils with 10-min occlusion of bilateral CCAs with 1 or 3 days of reperfusion showed typical bilateral delayed neuronal damages in control group. In contrast, the hyperglycemia groups showed high incidence of infarction and mortality as well as unilateral delayed neuronal damages. CONCLUSION: This study showed different effects of hyperglycemia on focal cerebral ischemia according to blood glucose level and the difference in thalamus suggests the possibility of effects of glucose on local physicochemical factors. Mechanism of decreased delayed neuronal damages in group 4A with global ischemia was not clear and further studies would be helpful.
Arteries ; Blood Glucose* ; Brain Ischemia ; Brain* ; Carotid Artery, Common ; Gerbillinae* ; Glucose ; Hippocampus ; Hyperglycemia ; Hypoglycemia ; Incidence ; Infarction ; Ischemia ; Ligation ; Mortality ; Necrosis ; Neurons ; Reperfusion ; Starvation ; Thalamus