No abstract available.
Humans ; Hyalin* ; Hyaline Membrane Disease* ; Infant, Newborn

PURPOSE: DNA mismatch repair gene is responsible for hereditary nonpolyposis colorectal cancer. But it is not well known its role in sporadic colorectal cancer patients. We analysed normal hMSH2, hMLH1 protein expression in colorectal adenocarcinoma tissues and corresponding normal tissues to find out the role of mismatch repair gene in sporadic colorectal cancer by Western blotting. METHODS: Normal hMSH2 and hMLH1 protein expression was studied on 25 colorectal cancer and corresponding normal tissue by Western blot with hMSH2 and hMLH1 monoclonal antibody. Normal protein band was expressed on 100 kD in hMSH2 and 87 kD in hMLH1. SW480 and LoVo cell line was used as positive and negative control for hMSH2 and LoVo and SW480 as positive and negative for hMLH1. And we analysed the relation between the hMSH2, hMLH1 protein expression and clinicopathological parameters. RESULTS: It was 2 cases (8%) that both hMSH2 and hMLH1 protein expression was not observed. Three cases (12%) were negative for hMSH2 and 2 cases (8%) for hMLH1. One or both hMSH2, hMLH1 protein expression was not observed in 7 cases (28%) in total. There was no correlation for proximal occurrence (25% vs 35%), young age (37.5% vs 23.5%) and lymph node metastasis (50% vs 47%). But poorly and mucinous differentiation was regarded as having relation with negative expression of hMSH2 and hMLH1 (50% vs 17.6%) but not significant statistically. CONCLUSION: Sporadic colorectal cancer with negative expression of normal hMSH2 and hMLH1 protein showed no relation to younger age, proximal site preference and lymph node metastasis. But it was suggested that mismatch repair gene protein was involved in cancer cell differentiation in sporadic colorectal cancer.
Adenocarcinoma ; Blotting, Western ; Cell Differentiation ; Cell Line ; Colorectal Neoplasms* ; Colorectal Neoplasms, Hereditary Nonpolyposis ; DNA Mismatch Repair ; Humans ; Lymph Nodes ; Mucins ; Neoplasm Metastasis

No abstract available.
Polyhydramnios*

No abstract available.
Infant, Newborn ; Meconium Aspiration Syndrome* ; Meconium*

To determine the incidence of prenatal brain damage, and evaluate the clinical and neurosonographical characteristics, we prospectively examined 508 newborn infants with intracranial ultrasound within the first day of life who admitted to the NICU of Severance Hospital from June 1990 to January 1992 and reviewed maternal or neonatal medical records. We found 12 cases (2.4%) of fetal brain lesions and ten of which had antenatal periventricularintraventricular hemorrhage and posthemorrhagic hydrocephalus. One of 10 infants had focal parenchymal hemorrhage, 1 had diffuse parenchymal hemorrhage with a porencephalic cavity, 1 had multicystic periventricular leukomalacia with spongiform cerebromalacia, and 1 had multicystic periventricular leukomalacia. Another 2 infants showed multicystic periventricular leukomalcia and multicystic encephalomalacia with ventriculomegaly respectively. Of 12 infants with prenatal brain damage, 7 were full-term, 5 were preterm, 9 were appropriate-for-gestational age, 2 were small-for-gestational-age, 7 were male, and 9 were delivered vaginally. Ten of 12 infants had perinatal asphyxia and five of which showed severe asphxia. Ten of 12 cases had significant materanl histories (three of which had preterm labor, three had premature rupture of amniotic membrane, one had preeclampsia, one had frequent upper respiratory tract infection and influenza, one had herb medication, and one had mental retardation). Only one infant with prenatal brain damage was asymptomatic and ll infants exhibited a few clinical signs during the neonatal period (all 5 infants had respiratory distress symptom, 4 infants had multiple congenital anomalies, 2 infants showed janudice and one infant had seizure). Of 9 infants who were taken electroencephalogram, 7 infants showed abnormal findings and four of 9 infants taken brainstem auditory evoked potential test exhibited abnormal response. Cerebral palsy and mental retardation were documented in two infants, 5 infants were lost on follow-up examination, and 5 infants were discharged against doctor's advices and died. This study confirms that some drain damage is prenatal and these lesions are associated with the development of cerebral palsy. therefore, prenatal brain damage can not be attributed to obstetrical events and neonatal care, We recommend that a fetal neurosonographic examination should be done in the last trimester of all pregnancies, especially in the presence of significant obstetric history or suspected fetal malformations and neonatal brain sonogaraphy be done within the first week of life. These examination are justified because they would allow early intervention to help offset possible neurologic deficits, would help prepare parents and pediatricians for possible limitations, and would prevent lawsuits and protect against malpractice allegations. But, it is not clear that every newborn infants need an ultrasound scan, since detection of prenatal brain damage would be of little benefit to the patients and enormous cost of routinely examining all pregnancies would be required.
Amnion ; Asphyxia ; Brain* ; Cerebral Palsy ; Early Intervention (Education) ; Electroencephalography ; Encephalomalacia ; Evoked Potentials, Auditory, Brain Stem ; Female ; Follow-Up Studies ; Hemorrhage ; Humans ; Hydrocephalus ; Incidence ; Infant* ; Infant, Newborn ; Influenza, Human ; Intellectual Disability ; Leukomalacia, Periventricular ; Male ; Malpractice ; Medical Records ; Neurologic Manifestations ; Obstetric Labor, Premature ; Parents ; Pre-Eclampsia ; Pregnancy ; Pregnancy Trimester, Third ; Prospective Studies ; Respiratory Tract Infections ; Rupture ; Ultrasonography

No abstract available.
Anti-Bacterial Agents* ; Sepsis*

No abstract available.
Ileum*

No abstract available.
Fetus* ; Nuchal Translucency Measurement* ; Pregnancy*

Rectus sheath hematoma of the abdominal wall is a well-recognized, but uncommon condition, caused by a tear in an epigastric vessel and characterized by sudden onset of severe abdominal pain and palpable mass. In most cases, a precipitating cause can be demonstrated. Causes include external trauma, strenuous activities, coughing, lifting, sneezing, vomiting, straining while urinating or defecating, golfing, pregnancy and the puerperium, anticoagulation therapy, infection, chronic diesase, arteriosclerosis, hypertension, prior paracentesis or laparotomy, inadequate hemostasis or excessive retraction in surgery, and idiopathy. Unfortunately, the correct diagnosis often is missed, and the hematoma is found only during an exploratory laparotomy. Treatment should be conservative in most instances. Although the mortality rate for patients with rectus sheath hematoma is low, the condition may be fatal if the volume of the hemorrhage is large and if treatment is delayed. Hence, it should be included in the differential diagnosis of any patient who presents to the emergency department with acute onset of abdominal pain. Our purpose is to familiarlize emergency physicians with the pathophysiology, the diagnosis, and the treatment of rectus sheath hematoma. We describe a patient with fatal rectus sheath hematoma presenting to the emergency department and give a review of the literature.
Abdominal Pain ; Abdominal Wall ; Arteriosclerosis ; Cough ; Diagnosis ; Diagnosis, Differential ; Emergencies ; Emergency Service, Hospital ; Golf ; Hematoma* ; Hemorrhage ; Hemostasis ; Humans ; Hypertension ; Hypovolemia* ; Laparotomy ; Lifting ; Mortality ; Paracentesis ; Postpartum Period ; Pregnancy ; Shock* ; Sneezing ; Vomiting

PURPOSE: Bile acids (especially deoxycholate) was known to be toxic and mutagenic on colon epithelium. They proposed at least four mechanisms for the bile acid toxicity. It is the one of these mechanisms that bile acid inhibits the xenobiotic metabolizing enzyme activity (esp glutathione S-transferase, GST). So we measured the cytosolic GST level of colon carcinoma cell lines after deoxycholate exposure whether or not the deoxycholate lowered the cytosolic GST activity. METHODS: Three colon cancer cell lines (LoVo, SW480, HT29) were used for this study. We calculated the cellular toxicity by MTS method. And cytosolic GST activity was measured according to the method as Habig described. For total GST activity, 2.5 mM 1-chloro-2,4-dinitrobenzene was used for substrate, and measured as absorbance in 340 nm. RESULTS: Basal cytosolic GST level for LoVo, SW480, HT29 cell line was 514.59+/-27.01, 291.63+/-38.44 and 344.58+/-47.92 nmol/min/mg cytosol protein. GST level did not changed significantly after 5 days culture without DCA. But GST level was decreased significantly to 128.63+/-21.35, 134.33+/-41.76 and 163.10+/-22.73 nmol/min/mg cytosol protein each cell line after 5 days deoxycholate exposure (p<0.005). CONCLUSION: Cytosolic GST level was lowered significantly after deoxycholate exposure for 5 days. One of the mechanisms of bile acid toxicity for colon cancer cell is proposed to inhibit cytosolic GST activity.
Bile ; Bile Acids and Salts ; Cell Line* ; Colon* ; Colonic Neoplasms* ; Cytosol* ; Deoxycholic Acid* ; Dinitrochlorobenzene ; Epithelium ; Glutathione Transferase* ; Glutathione* ; HT29 Cells ; Humans