Prenatally diagnosed neuroblastomas have been reported in increasing numbers over the past several years. The vast majority are in favorable stages of the disease (stage I, II, IV-S). The authors experienced one case of stage IV-S neuroblastoma of the adrenal gland with liver metastasis, which regressed spontaneously after removal by adrenalectomy. This patient was noticed to have an abdominal mass at prenatal ultrasonography performed at 36weeks of gestation. This tumor was a neuroblastoma of the left adrenal gland with multiple liver metastases. Left adrenalectomy and liver biopsy were performed at 3 months of age. Thirty-eight months after surgery, an MRI demonstrated that the hepatic metastatic lesions had completely regressed without chemotherapy or radiation.
Adrenal Glands ; Adrenalectomy* ; Biopsy ; Drug Therapy ; Humans ; Liver* ; Magnetic Resonance Imaging ; Neoplasm Metastasis* ; Neuroblastoma* ; Pregnancy ; Prenatal Diagnosis ; Ultrasonography, Prenatal

BACKGROUND: N-acetylcysteine(ACE) is used both orally and intravenously in a variety of experimental pathologies resembling human disease states which exhibit endothelial toxicity as a result of oxidative stress, including acute pulmonary oxygen toxicity, septicemia and endotoxin shock. Despite these observations in vivo, it is not certain how this thiol drug produces its protective effects. ACE is a cysteine derivative which is able to directly react with oxygen radicals and may also act as a cysteine and glutathione(GSH) precursor following deacetylation. In this paper, we tried to know whether the therapeutic doses of ACE can modify the inflammatory function of the neutrophils and can increase the glutathione level of plasma in chronic obstructive pulmonary disease(COPD) patients. In addition, the effect of ACE to the purified neutrophil in terms of superoxide release and glutathione synthesis were observed. METHOD: Firstly, we gave 600mg of ACE for seven days and compare the release of superoxide, luminol-enhanced chemiluminescence from the neutrophils, neutrophil chemotaxis, and plasma GSH levels before and after ACE treatment in COPD patients. Secondly, we observed the dose dependent effect of ACE to the purified neutrophil's superoxide release and GSH levels in vitro. RESULTS: 1) Usual oral therapeutic doses(600mg per day) of ACE for seven days did affect neither on the neutrophils superoxide release, chemiluminescence, chemotaxis, nor on the plasma GSH concentration in the COPD patients. 2) ACE decreases the purified neutrophil's superoxide release and increase the GSH production in dose dependent fashion in vitro. CONCLUSION: Despite the fact that oral ACE treatment did not affect on the neutrophil's inflammatory function and plasma GSH concentration in COPD patients in usual therapeutic doses, it decreases the superoxide release and increases the GSH production from the isolated neutrophils in high molar concentrations. These findings suggest that to obtain an antioxidative effects of ACE, it might be needed to increase the daily dosage of ACE or therapeutic duration or change the route of adminisration in COPD patients.
Acetylcysteine* ; Chemotaxis* ; Cysteine ; Glutathione* ; Humans ; Luminescence ; Molar ; Neutrophils* ; Oxidative Stress ; Oxygen ; Pathology ; Plasma* ; Pulmonary Disease, Chronic Obstructive ; Reactive Oxygen Species ; Sepsis ; Shock ; Superoxides*

No abstract available.
Humans

Acardiac twinning affects 1 in 100 monozygotic twin pregnancies and 1 in 35,000 pregnancies overall. This condition is characterized by the absence or rudimentary development of fetal heart, and associated with various anomaly. The presence of an acardiac twin requires the normal (or "pump") twin to provide circulation for itself, as well as the acardiac sibling. The acardiac malformations are uniformly fatal in the affected twin, and mortality in the co-twin is as high as 55%. The principal perinatal problems associated with acardiac twinning are pump-twin congestive heart failure, maternal hydramnios, and preterm delivery. We recently experienced a case of acardius anceps associated with a normal male infant, so present with a brief review of the literature.
Fetal Heart ; Heart Failure ; Humans ; Infant ; Male ; Mortality ; Polyhydramnios ; Pregnancy ; Siblings ; Twins, Monozygotic

Estrogenic hormone in various doses and durations was administered to adult male white rats to study the hormonal effect on the prostatic gland. In this study 48 rats. weighing approximately 250 gm. were divided into 8 groups of six rats. Group 1: Control for 2 weeks experiment Group 2: Control for 4 weeks experiment Group 3. Administration of estradiol 0.5 mg., 7 doses Group 4: Administration of estradiol 0.5 mg., 14 doses Group 5. Administration of estradiol 0. 25 mg., 7 doses Group 6: Administration of estradiol 0. 25 mg., 14 doses Group 7: Administration of estradiol 0. 125 mg., 7 doses Group 8: Administration of estradiol 0. 125 mg., 14 doses Estradiol was administered every other Day as scheduled. One day after the final injection, the animals were sacrificed. Body weight and weight of the prostatic gland, both the ventral and the dorsal lobes, were obtained. The effect of estradiol in various doses on the prostatic size was observed to be almost the same throughout the experimental groups. But estradiol administered for longer periods has slightly more effect than when administered for shorter periods. The effect of estrogen administered to the rats with intact gonads did not antagonize or neutralize the endogenous testicular androgen, but did suppress the release of pituitary gonadotrophin, resulting in less production of testicular androgen. A large dosage of estrogen does not necessarily cause a marked reduction in the prostatic weight.
Adult* ; Animals ; Body Weight ; Estradiol ; Estrogens* ; Gonads ; Humans ; Male* ; Prostate ; Rats*

Androgenic and estrogenic hormones were administered to adult male white rats with intact gonads and adult male white castrate rats to study their effects on citric acid concentration of the prostate gland. In this study 30 male rats, 14 to 16 weeks of age, weighing approximately 250 to 300 gm., were divided into 5 groups of six rats: Group 1: Control Group 2: Administration of testosterone propionate 0.5 mg., 7 doses Group 3: Administration of estradiol 0.2 mg., 7 doses Group 4: Castration and administration of testosterone propionate 0.5 mg., 7 doses Group 5: Castration and administration of both testosterone propionate 0.5 mg. and estradiol 0.2 mg., 7 doses each. One day after the final injection with sex hormones, the animals were sacrificed and the prostatic citrate was determined using the Kim-Tesar modification of the Taylor's method. Estrogen administration to the male rats with intact gonads caused an increase in the prostatic citrate concentration. Testosterone propionate administration after castration returned the citrate concentration to normal, but estradiol administration along with testosterone propionate after castration caused a rise in the prostatic concentration of citric acid. Hypophysectomized white rats purchased from the Hormone Assay Laboratory were castrated and were administered androgen and estrogen to study their effects on the prostatic concentration of citric acid, 36 rats were divided into 6 groups of six rats: Group 1: Control (no hypophysectomy) Group 2: Hypophysectomy and castration Group 3: Hypophysectomy, castration and administration of testosterone propionate 0.5 mg., 7 doses Group 4: Hypophysectomy, castration and administration of both testosterone propionate 0.5 mg, and estradiol 0.5 mg., 7 doses each Group 5: Hypophysectomy castration and administration of both testosterone propionate 0.5 mg. and estradiol 0.25 mg., 7 doses each Group 6: Hypophysectomy, castration and administration of both testosterone propionate 0.5 mg. and estradiol 0.125 mg., 7 doses each. Hypophysectomy and castration caused a marked increase in the prostatic concentration of citric acid. When testosterone propionate was administered to hypophysectomized castrate, the ciric acid value returned to normal. Administration of estradiol along with testosterone propionate to hypophysectomized castrate caused changes in the prostatic citrate concentration according to the dosage of estradiol administered, the more the dosage, the more the concentration of the prostatic citrate. Concentration of the prostatic citrate can not be taken as an index of androgenic activity.
Adult ; Animals ; Castration ; Citric Acid* ; Estradiol ; Estrogens ; Gonadal Steroid Hormones* ; Gonads ; Humans ; Hypophysectomy ; Male* ; Prostate ; Rats* ; Testosterone Propionate

Normal diet, high protein high fat diet and high carbohydrate diet were prepared and given to young male white rats to study the effects of the diets on the prostatic concentration of citric acid. Also, the effects of exogenous testosterone propionate, castration and exogenous testosterone propionate and on sexual activity were studied. The first experiment was a 60 day observation. In the controls and among the animals administered testosterone propionate, the prostate-body weight ratio was higher in the high protein, high fat diet group than in the groups fed high carbohydrate and normal diets. The prostatic citrate, however, was higher in the high carbohydrate diet group. By administration of testosterone propionate, citric acid concentration of the prostate was higher in the high protein, high fat diet group and sexual activity in this group caused a more marked increase in the prostatic citrate concentration. The second experiment was continued for 203 days. The high protein, high fat diet caused an increase in the prostate-body weight ratio and a relatively higher but insignificant concentration of prostatic citrate. Sexual activity did not cause an increase in the prostatic citrate concentration. Concentration of the prostatic citrate can not be taken as an index of androgenic activity.
Animals ; Castration ; Citric Acid* ; Diet ; Diet, High-Fat ; Humans ; Male ; Prostate ; Rats ; Sexual Behavior ; Testosterone Propionate

Young adult male rats were injected with carbon tetrachloride along with cortisone acetate simultaneously and the effect of cortisone acetate on the damage of the liver and the liver's effect on the reproductive gland and its accessories were studied. The following results were obtained: Cortisone acetate given rats with damaged livers caused a very remarkable decrease in the weights of the accessory glands of reproduction, while the liver was restored to normal hepatic architecture. Judging from the marked weight decreases of the glands, cortisone acetate is thought to be responsible for enhancing the estrogenic effect through liver dysfunction despite the return to normal hepatic histology. Citric acid concentration in the prostatic tissue was not altered greatly by cortisone acetate administration. The concentration of the prostatic citrate can not be taken as an index of androgenic activity.
Animals ; Carbon Tetrachloride ; Citric Acid ; Cortisone* ; Estrogens ; Humans ; Liver Cirrhosis ; Liver Diseases ; Liver* ; Male* ; Rats* ; Reproduction ; Weights and Measures ; Young Adult

Young adult male white rats were castrated to remove the main source of production of sex hormones in the body. Carbon tetrachloride was injected to induce damage to the liver in two groups of animals. The effect of hepatic damage on the histological and biological activity of exogenous sex hormones on the accessory glands of reproduction was observed. Castration causes a very remarkable decrease in the weight of the accessory glands of reproduction. Exogenous androgen restored the glands to normal. Hepatic damage did not lay a role in the inactivation of exogenous androgen. A direct antagonism between the exogenous androgen and the exogenous estrogen seemed to be present and the hepatic damage did not play role to accelerate or suppress this action. Citric acid concentration in the prostatic tissue showed a sharp rise following castration but restoration of the gland by giving exogenous sex hormones returned the citric acid concentration to hormonal levels. The hepatic damage did not cause a rise in the citric and content when both androgens and estrogens were together. The concentration of the prostatic citrate can not be taken as an index of androgenic activity.
Androgens ; Animals ; Carbon Tetrachloride ; Castration ; Citric Acid ; Estrogens ; Gonadal Steroid Hormones* ; Humans ; Liver ; Liver Cirrhosis ; Male* ; Rats* ; Reproduction ; Young Adult

Young adults male rats were injected with carbon tetrachloride to induce damage to the liver in order to study the influence of this damage on the effects of exogenous estrogens and androgens on the reproductive glands and their accessories. The liver damage by the toxin caused a marked decrease in the weights of the prostate and the seminal vesicles of the rat whereas there was no great alteration in testicular effect of exogenous androgen seemed not be significant whereas the effect of exogenous estrogen was greatly increased by the condition. Histological findings in the reproductive glands following hepatic damage are chiefly those of atrophic changes. Citric acid concentration in the prostatic tissue was not influenced by liver damage but estrogen administration caused a marked increase and estrogen with liver damage caused a sharper rise in the concentration. Citric acid content of prostatic tissue can not be taken as an index of androgenic activity.
Androgens ; Animals ; Carbon Tetrachloride ; Citric Acid ; Estrogens ; Gonadal Steroid Hormones* ; Humans ; Liver ; Liver Cirrhosis ; Male* ; Prostate ; Rats* ; Seminal Vesicles ; Weights and Measures ; Young Adult