To evaluate the ultrastructural changes and the mechanism causing liver injury by lead, light and electron microscopic(LM and EM) examination using Timm sulphide silver method(TSM) was done. Sprague-Dawley rats were divided into a control and 3 experimental groups. The experimental groups were orally administered 0.5% lead acetate(LA). Group 1 received a one time dose of 10 ml of LA by gastric intubation. Groups 2 and 3 continuously received LA instead of drinking water. The control group was composed of 3 rats in each group which did not receive any treatment. Rats of group 1, 2 and 3 and control were sacrificed at 1/2, 1, 1 1/2 hours, 2 days, and at 1, 2, 4, 6 and 8 weeks later, except group 3. Before sacrifice, they were perfused with 0.1% sodium sulphide and 2.5% glutaraldehyde through the abdominal aorta for TSM. The liver was taken for LM and EM examinations. Blood lead concentration began to increase from the 2nd day up to 3.29 microgram/ml at 2nd week, and the urinary delta-ALA level showed a steady increase from the 2nd day. LM and EM examination of liver revealed that absorbed lead granules in group 1 were transported into sinusoidal spaces, Kupffer cells, and the hepatocytes within 1 hour and then disappeared 1/2 hour thereafter. In group 2 deposited lead was found in the hepatocytic cytosol bound to mitochondria. That in turn inhibited mitochondrial respiration with resultant mitochondrial swelling at the 1st week and thereafter at 6th week myelin figure formation and condensation of mitochondria, and peroxisomes were increased at 8th week. Based on these results it can be concluded that a transient intake of subletal dose of LA is biotransformed completely by periportal hepatocytes within 1 1/2 hours, but excessively accumulated lead can induce liver cell injury due to lipid peroxidation of membrane by direct toxic effect of lead and by products of lipid peroxidation. We postulate that lead acetate triggers presumably primarily mitochondrial membrane injury and then other organellar changes may play a role in disturbance of a network of interacting of key events capable of causing cell death.
Rats ; Animals

No abstract available.
Pneumothorax*

No abstract available.
Adrenocorticotropic Hormone* ; Animals ; Plasma* ; Rats*

No abstract available.
Axis, Cervical Vertebra* ; Estradiol* ; Testosterone*

BACKGROUND: Estrogen deficiency accelerates loss of bone mass and changes lipid profile in the postmenopausal women, so that the osteoporosis and astherosclerosis were developed. But it has not enough studies including the premenopausal women. So we have investigated about the differences of body mass index(BMI), lipid profile and bone mineral density (BMD) with pre- and postmenopausal women. METHODS: We have evaluated 201 premenopausal women and 322 postmenopausal women out of total 651 who had visited Health Screening Center in the hospital of Eul-Ji Medical College from November, 1995 to July, 1996. RESULTS: The mean age of total subjects, premenopausal women, postmenopausal women were 51.9, 43.9, 56.8 years, respectively. The mean period after menopause was 8.1 years. Significant difference was seen in BMI, lipid profile and BMD according to age and menopause(P<0.01). BMI was related to lipid profile(P<0.01), but not to BMD(P>0.1). In postmenopausal women BMI, BMD and lipid profile were related to postmenopausal period (P<0.05). In viewing their correlations BMD had strong adverse correlations with factors such as age, menopause, and postmenopausal period. Lipid profile had weak positive correlations with factors such as age, menopause, BMI(P<0.001). CONCLUSIONS: The lipid profile are related to factors such as age, BMI, menopause, and postmenopausal period. The BMD is related to above factors except BMI. Prospective study is needed to evaluate the influence of estrogen on BMD and lipid metabolism. Thus, it helps to the prevention and treatment of the osteoporosis and hyperlipidemia in the postmenopausal women.
Bone Density* ; Estrogens ; Female ; Humans ; Hyperlipidemias ; Lipid Metabolism ; Mass Screening ; Menopause ; Osteoporosis ; Postmenopause

OBJECTIVES: Phencyclidine(PCP) or PCP-like substances such as ketamine have been know to rekindle the cognitive dysfunction in schizophrenia. The aims of this study were to identify whether PCP-like substances can produce cognitive deficit in schizophrenia, to discuss relation with aging process, and finally to speculate underlying neurochemical mecha-nisms by various drug responses. METHODS: In experiment I, radial maze tests were done in 24 Sprague-Dawley rats for 3 days to get baseline data. Being divided into 4 groups(6 rats respectively) of normal aged, normal adult controls, atropine-treated and ketamine-treated, the radial maze tests were repeated on every week for 6 weeks, and then the rats were sacrificed by intracardiac perfusion with phosphate-buffered 10% formaldehyde solution for histology. The brain specimen was stained with hematoxylin-eosin to count cells in the prefrontal cortex and hippocampus. In experiment II, radial maze tests were done for 48 rats before any drug treatment and only after ketamine administration. Thereafter, haloperidol, bromocriptine, clonidine, nimodipine, tacrine, valproic acid, naloxone and fluoxetine were intramuscularly injected on every other day in addition to ketamine. Radial maze tests were repeated on every week for 6 weeks, and then rats were prepared by the same procedure for histology. RESULTS: 1) Reaction times of radial maze tests of atropine-treated rats were significantly prolonged than those of normal aged(p<0.05) or normal adult controls(p<0.05). Cell numbers of prefrontal cortex & hippocampus in ketamine-treated rats were significantly reduced than those in normal aged(p<0.05) or normal adult controls(p<0.005). 2) Reduced cell numbers by ketamine became significantly raised by tacrine administration in prefrontal cortex $ hippocampus(p<0.05), while there were no significant changes on radial maze test. Cell numbers also tended to be raised by nimodipine, fluoxetine and haloperidol administration. CONCLUSIONS: In conclusion, the visuospatial memory disorders in ketamine-induced psychotic rats might be partly associated with aging process. Furthermore, the responses to the various drugs suggested cholinergic system might have an important role in the neurochemical mechanism of the cognitive dysfunction in ketamine-induced psychosis. Otherwise, calcium metabolism as well as serotonergic and dopaminergic systems seemed to be possibly related.
Acetylcholine ; Adult ; Aging* ; Animals* ; Brain ; Bromocriptine ; Calcium ; Cell Count ; Clonidine ; Fluoxetine ; Formaldehyde ; Haloperidol ; Hippocampus ; Humans ; Ketamine ; Memory Disorders ; Metabolism ; Models, Animal* ; Naloxone ; Nimodipine ; Perfusion ; Prefrontal Cortex ; Psychotic Disorders ; Rats ; Rats, Sprague-Dawley ; Reaction Time ; Schizophrenia* ; Tacrine ; Valproic Acid

The use of recombinant DNA technology to produce human growth hormone has resulted in a marked increase in availability of Growth Hormone(GH) to treat short stature due to GH deficiency and other conditions, such as Turner syndrome, familial short stature, chronic renal insufficiency and intrauterine growth retardation (IUGR). But, the GH therapy may result in the adverse events such as sodium and water retention, pseudotumor cerebri, slipped capital femoral epiphysis, growth of nevi, recurrence of tumor. We experienced a case of severe hypertension associated with GH therapy in a 14-year-old male who presented high blood pressure up to 190/100 mmHg and normalized at 2-3 weeks after discontinuation of GH. Therefore, we think that the blood pressure should be carefully monitored during GH therapy.
Adolescent ; Blood Pressure ; DNA, Recombinant ; Fetal Growth Retardation ; Growth Hormone* ; Human Growth Hormone ; Humans ; Hypertension* ; Male ; Nevus ; Noonan Syndrome ; Pseudotumor Cerebri ; Recurrence ; Renal Insufficiency, Chronic ; Slipped Capital Femoral Epiphyses ; Sodium

No abstract available.
Cardiac Output* ; Ductus Arteriosus* ; Humans ; Infant, Newborn*

No abstract available.

We experienced nutiple brain abscess in two neonates. Diagnosis was made CT scan, Which revealed multiple ring-like enhancing leason in both frontoparietal and left posterior parietal cerebral parenchyme. Therapy was consisted of systemic antibiotic treatment and CSF V-P shunt operation due to complicated hydrocephalus. One neonate was died and the other neonate has been followed up due to convulsion and neurological sequale.
Brain Abscess* ; Diagnosis ; Humans ; Hydrocephalus ; Infant, Newborn* ; Rabeprazole ; Seizures ; Tomography, X-Ray Computed