No abstract available.
Embryonic Structures ; Fetus ; Humans* ; Kidney*

A study was made of the differences in clinical features and immunological aspects between herpes zoster patients with malignancies and those without malignant tumors. The results obtained from the retrospective review of medical records are as follows: Herpes zoster occurred more frequently in younger patients(less than twenty) with malignanciee as compared with the control group of the same ages,' Male was dominant among zoster patients with malignancies as is the contrary to contral group; Tihere were no marked differences in primarilly involved dermatomes between the two groups; Generalized varicelliform eruptiona were more common in zoster pa,tients with malignaneies than in control group, It seemed that zoster patients with malignancies complained of milder degree of pain. Zoeter patienta associated with malignancies were more frequently DNCB-negative and had decreased OKT3+ pan T cells, OKT4+ helper/inducer T cells as compared with control group, which suggest impaired cell mediated immunity in the former.
Herpes Zoster* ; Humans ; Immunity, Cellular ; Male ; Medical Records ; Retrospective Studies ; T-Lymphocytes

Since the first report by Drury and Szent-Gyorgyi in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. A lot of investigations on the working mechanisms of adenosine have been focused mainly on the effects on the coronary blood flow. However, the cellular mechanisms underlyiag the inhibitory action of adenosine on the SA node are not well understood yet. Furthe-rmore, the physiological role of adenosine in the regulation of the heart beat remains still to be explored. Thus, this study was undertaken to examine the behavior of the rabbit SA node ander the influence of adenosine, and the interactions between adenosine and aminophylline on the SA node, and then to compare these results with those of acetylcholine. At the same dosage range, adenosine suppressed the sinus rate and atrial contractility even in the reserpinized preparation. The spontaneous firing rate of the SA node at 35degrees C (mean+/-SEM, n=16) was 154+/-3.3 beats/min. The parameters of action potential were: maximum diastolic potential(MDP), -73+/-1,7 mV; overshoot(OS), 9+/-1.4 mV; slope of pacemaker potential(SPP), 94+/-3.0 mV/sec. Adenosine suppressed the firing rate of the SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of 10(-4)M and was potentiated in parallel with the increase in adenosine concentration. Changes in the action potential by adenosine were dose-dependent as show by the increase of MDP and the decrease of SPP until 10(-4)M. Above this concentration, however, the amplitude of the action potential decreased markedly due to the simultaneous decrease of both MDP and OS. Dipyridamole, which is known to block the adenosine transport aross the cell membrane, definately potentiated the action of adenosine. The effects of adenosine on the SA node were inhibited by aminophylline. However, the similar effects of acetylcholine to those of adenosine were not reversed by aminophylline. These results suggest that adenosine suppressed the pacemaker activity by acting dire-ctly on the membrane of the SA node, and the effects of adenosine on SA node are sele-ctively inhibited by aminophylline.
Acetylcholine ; Action Potentials ; Adenosine ; Aminophylline ; Cell Membrane ; Dipyridamole ; Fires ; Heart ; Humans ; Membranes ; Research Personnel

No abstract available.

Malignant rhabdoid tumor (MRT) is a rare and highly aggressive neoplasm of infancy and childhood. Although it was originally described and most frequently reported in the kidney, it may occur in various extra-renal sites such as the liver, thymus, and soft tissue. In the last decade primary central nervous system (CNS) MRTs have been reported in both the supra- and infratentorial compartments. Patients with CNS MRT were generally below the age of two and reports in adults are extremely rare. This is a case of primary cerebellar MRT in a 24-year-old woman, who had presented with intermittent headache, vocal cord palsy, and cerebellar dysfunctions such as abnormal finger to nose test and tandem gait. By magnetic resonance imaging scan, a well-enhancing solid mass was demonstrated at the posterior fossa filling the 4th ventricle, which extended into the medulla and cervical cord via the foramen of Magendie. Histologically, the monotonous polygonal tumor cells were arranged in diffuse sheet with occasional hemorrhagic necrosis. The nuclei were vesicular and eccentrically located due to eosinophilic, PAS-positive, intracytoplasmic inclusions with prominent nucleoli. They were diffusely or focally immunoreactive for vimentin, neurofilament, cytokeratin, GFAP, synaptophysin, and smooth muscle actin, while epithelial membrane antigen and desmin were negative. Ultrastructurally, the polyhedral tumor cells were densely packed with primitive intercellular junctions. Scanty fibrillar intermediate filaments were intermingled with cellular organelles. Postoperatively, craniospinal irradiation and systemic chemotherapy have been done and she has been free of tumor recurrence during the 13 months' follow-up periods.
Actins ; Adult* ; Central Nervous System ; Cerebellar Diseases ; Cerebellum* ; Craniospinal Irradiation ; Desmin ; Drug Therapy ; Eosinophils ; Female ; Fingers ; Follow-Up Studies ; Gait ; Headache ; Humans ; Intercellular Junctions ; Intermediate Filaments ; Keratins ; Kidney ; Liver ; Magnetic Resonance Imaging ; Mucin-1 ; Muscle, Smooth ; Necrosis ; Nose ; Organelles ; Recurrence ; Rhabdoid Tumor* ; Synaptophysin ; Thymus Gland ; Vimentin ; Vocal Cord Paralysis ; Young Adult

No abstract available.
Captopril* ; Child* ; Humans ; Hypertension*

No abstract available.
Child* ; Humans ; Purpura, Thrombocytopenic, Idiopathic*

It is known that the cardiovascular system is extremely sensitive to the effect of both exogenous and endogenous opiates. In rabbits, less than 1% of the usual morphine dose necessary to produce antinociception results in significant hypotension and bradycardia. The endozenous opiate, beta-endorphin, is stored along with pitulatary adrenocorticotorphin(ACTH), and the action of stressors seems to result in the release of both peptides. Therefore it seems likely that beta-endorphin is released during stress such as shock and that it might contribute to the hypotension. In order to probe this hypothesis, hypovolemic and endotoxin shock model were produced in rabbits. If these hemorrhage and endotoxin induced hypotension were mediated through the beta-endorphin release, the blockade of beta-endorphin should reverse such hypotension. Using the specific opiate antagonist, Naloxone-HCl, these hypotensions could be reversed and prevented as following results show, 1) As compared with the saline control, the hypovolemic shock experiment had a 36.49+/-14.44% increase in mean arterial pressure(MAP) within 2 to 3 minutes and the endotoxin shock had a 52.43+/-23.66% increase in MAP within 5 to 6 minutes after naloxone treatment (0.4mg/kg). 2) AS compared with the saline control, in both hypovolemic and endotoxin shock naloxone pretreatment(0.4mg/kg) could prevent the decrease of MAP significantly. 3) No significant difference were seen in heart rate between the control and both experimental groups. And plasma bets-endorphin was measured by radioimmunoassay(RIA), using beta-endorphin kit(Immunonucler corportion, Stillwater, Minnesota, USA) and Beckman 8,000 tau-Counter, in these shock model with following results. 1) Hemorrhage and endotoxin induced shock produced a significant increase in plasma beta-endorphin to about 3 times control and reversed by naloxone treatment(0.4mg/kg) significantly as compared with saline control. 2) AS compared with the saline control, in both hypovolemic and endotoxin experiments naloxone pretreatment(0.4mg/kg) could prevent the increase of plasma beta-endorphin significantly.
Rabbits ; Animals

Lithium salts are being used increasingly to treat patient with affective disorders, especially acute mania, or bipolar manic-depressive illness. For therapeutic effect the lithium content must be maintained at or above a particular level. Lithium poisoning due to overdosage may be seen occasionally, and its course is determined primarily by the rate of renal lithium elimination. A search is therefore indicated for procedures that could raise the lithium clearance. In a number of reports renal lithium excretion has been studied in relation to the excretion of water, sodium, potassium and hydrogen, but effects of sodium or water on the lithium excretion has not yet been clarified. Hence the present study was undertaken to investigate the effects of corticosteroid on the excretion of lithium ion. The female rat (Sprague-Dowley), weighing from 200 to 300g, was injected with 50mg/kg of lithium chloride intraperitoneally, and then injected with graded dosage of fludrocortisones and dexamethasone in each group. During the injected rats were incubated in metabolic cage, 24 hour urine of rats were collected. At 24 hours after injection, the rats were sacrificed with guillotine, the blood were collected. And then the concentrations of Na⁺, K⁺, Li⁺ of collected urine and serum were checked by Flame photometer. The results are summarized as follows 1. Fludrocortisone decreased the serum concentration of lithium and increased the urinary excretion of lithium. 2. In the group treated with low dose of dexamethasone (0.1 mg/kg), the serum concentration of lithium was decreased and high dose of dexamethasone (1 mg/kg) increased the urinary excretion of lithium. 3. Fludrocortisone increased the urinary [Na⁺]/[K⁺] in serum and decreased [Na⁺]/[K⁺] inurine, but opposite effects were occurred in dexamethasone. By above results, it may be concluded that corticosteroid increased the urinary excretion of lithium and decreased the serum concentration of lithium, but it seems to be there in no relationship between these effects of corticosteroid and of the renal Na⁺ or K⁺ transport.
Adrenal Cortex Hormones* ; Animals ; Bipolar Disorder ; Dexamethasone ; Female ; Fludrocortisone ; Humans ; Hydrogen ; Lithium Chloride ; Lithium* ; Mood Disorders ; Poisoning ; Potassium ; Rats ; Renal Elimination* ; Salts ; Sodium ; Water

To evaluate the possible therapeutic effects of growth hormone and vitamin C on multiorgan failure, a rat model was developed for LPS-induced sepsis. Using this model, the effects of growth hormone and vitamin C on tissue damages, catalase and i-NOS activities, and MDA levels were examined in the lung and liver. The level of TNF-in plasm was also examined. Male, Sprague-Dawley rats were injected with LPS intraperitoneally then divided into 3 groups : positive controls injected with LPS only, the ones injected with growth hormone or vitamin C immediately after the LPS injections. The lung and the liver were then isolated, blood samples were collected at 24 or 48 hours after the LPS injection, then examined for histopathological and biochemical changes. The results obtained were as follows. 1. LPS induced sinusoid vasodilation and mild destruction of lobular structure in the liver. In the lung, alveolar structure appeared to be thickened and interstitial edema was observed. The levels of MDA in the liver and the lung was increased by LPS, while the activity of catalase was decreased. The activity of i-NOS of those tissues was also increased, which was more pronounced at 24 hr. The level of TNF-in plasm was increased by LPS 2. In the lung, vitamin C suppressed lymphocyte and neutrophil infiltration, alveolar wall thickening and interstitial edema. In the liver, vitamin C protected against the destruction of the lobular structure. The activity of catalase reduced by LPS was reversed partly by vitamin C. The activity of i-NOS enhanced by LPS was also reversed by vitamin C. The level of TNF-in plasm reduced in some animals by vitamin C, which however was not significant statistically (P<0.05). 3. Growth hormone showed similar protective effects against inflammation and damages in the liver and lung tissues. Growth hormone reversed partly the LPS effects on the level of MDA, the activity of catalase and i-NOS induction in the liver and the lung. Growth hormone reduced plasma level of TNF-alpha substantially, which contrasted from vitamin C. Besides this, overall protective effects of growth hormone against LPS-induced experimental sepsis were similar to those of vitamin C. From this results, the mechanism of growth hormone on suppression of LPS-induced tissue damage might be associated with production of antioxidative enzyme and suppression of plasma TNF level.
Animals ; Ascorbic Acid ; Catalase ; Edema ; Growth Hormone ; Human Growth Hormone* ; Humans* ; Inflammation ; Liver ; Lung ; Lymphocytes ; Male ; Models, Animal* ; Neutrophil Infiltration ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Sepsis* ; Tumor Necrosis Factor-alpha ; Vasodilation