No abstract available.
Education* ; Humans ; Students, Medical*

No abstract available.
Family Practice* ; Humans ; Outpatients* ; Thyroid Diseases* ; Thyroid Gland*

For the study on the effect of retinoic acid on the formation of palatal rugae and the cleft palate, retinoic acid was administered orally 150mg/kg of body weight by gastric tube at GD 10.5 to Sprague-Dawley rats. The pregnant rats were sacrificed on GD 17.5 under ether anesthesia, and laparatomized. After removal of uterus, the number of pregnant sacs and fetuses were counted. The fetuses weighed, the MEE (medial edge epithelium) thickness measured and the mitotic figures counted after routine processing and H·E stain. All the palates were photographed, and the number of rugae & the rugal pattern analysed. TEM photographs of MEE cells were observed after routine processing. The results were as follows ; 1. Rat fetus body weight after retinoic acid treatment increased significantly compared with the control group. 2. Mitotic figures in the retinoic acid treated group increased significantly compared with control group. 3. In the retinoic acid treated group, 79.3% of fetuses had cleft palates. Among fetuses with cleft palates, complete cleft palates were 10.6%, incomplete cleft palate 89.4%. Incomplete clefts were of two types ; median type (cleft palate at the intermolar region) and soft palate type (cleft posterior to the 8th rugae). Median type was 64.6% and the soft palate type 35.4%. 4. 2.3% of the fetuses had the numerical anomaly of the palatal rugae in the control group, but that of retinoic acid treated group 87.7%. 5. 17.4% of palatal rugae of the control group was disrupted, but 100% of the retinoic acid treated group disrupted. 6. Rugal papillae were observed in the 15.1% of fetuses of the control group and 63.1% of fetuses of the retinoic acid treated group. 7. Longitudinal rugae were observed in 19% of fetuses of the retinoic acid treated group, but not in the control group. 8. In TEM photographs, cytoplasmic processes, intercellular space, and desmosomes decreased. Swelling of mitochondria & ER were also found in the retinoic acid treated groups. According to the above results, it appears that there is close relationship between palatal rugae and cleft palates, and that excess retinoic acid induces disruption of pattern and numerical variations of rat fetus palate rugae. Also retinoic acid has an inhibitory effect on the proliferation of medial edge epithelial cells of palatal shelves. The cleft palates may be induced by the above mentioned retinoic acid effects. But, the exact mechanisms of retinoic acid on cleft palate formation is not thoroughly known and should be further studied.
Anesthesia ; Animals ; Body Weight ; Cleft Palate* ; Cytoplasm ; Desmosomes ; Epithelial Cells ; Ether ; Extracellular Space ; Fetus ; Mitochondria ; Palate ; Palate, Soft ; Rats ; Rats, Sprague-Dawley ; Tretinoin* ; Uterus

OBJECTIVES: The authors have intended to know the drug interaction of fluoxetine and haloperidol when coadministering two drugs to the chronic schizophrenics by assessing the changes of positive, negative symptoms and extrapyramidal symptoms. METHOD: We selected 38 patients, the chronic schizophrenics with no physical problems. they are randomly assigned to placebo group and drug group. And then, placebo or fluoxetine 20mg were administered to the subjects of each group during 8 week period. We have assessed their psychopathology and extrapyramidal symptoms using positive and Negative Syndrome Scale(PANSS), Clinical Global Impression(CGI), Simpson-Angus Scale at o, 2, 4, 6, 8 week during the period. RESULTS: 38 patients have completed the study during 8 week. 1) PANSS, CGI : no significant difference between groups and no significant change according to the times. 2) Simpson-Angus Scale : no significant changes. CONCLUSION: When co-administering fluoxetine and haloperidol, there were no significant changes of psychopathology and extrapyramidal symptoms. There results suggest that it is safe to coadminister fluoxetine to schizophrenic with haloperidol treatment.
Drug Interactions ; Fluoxetine* ; Haloperidol* ; Humans ; Psychopathology*

A case of pulmonary alveolar proteinosis is reported. Most of the alveolar spaces were filled with amorphous deep eosinohilic material which revealed strong positive reaction to periodic acid-Schiff staining. Electron microscopic observation of this material showed numerous lamellar bodies in the alveolar spaces and cytoplasms of alveolar macrophages. A part of them were concentric multilamellated type A lamellar bodies and the other were finger printlike type B bodies. Combined type A and type B lamellar bodies were rarely present. From the above features it is suggested that both type A and B lamellar bodies could be transformed one another and those lamellar bodies may be originated from pulmonary surfactant.

Carcinoma of the breast can produce cutaneous metastases which sbow highly diversified clinical pictures. The cutaneous metastases produce four definite clinical types: inflammatory carcinoma, telangiectatic carcinoma, nodular carcinoma, and carcinoma, en cuirasse. We present a case of 78-year-old nulliparous woman who had several painful dark purplish colored zosteriform papulovesicular eruptions, suggestive of herpes zoster, on the right breast, right axilla, scapular area, and upper arm for three month. Two month later, well dermacated linearly arranged erysipeloid eruptions appeared around the previous skin lesions and the right chest wall. Histopathological findings showed metastatic ductal carcinoma with massive vascular permeation but the primary focus was undetermined.
Female ; Humans ; Neoplasm Metastasis

No abstract available.
Vascular Access Devices*

No abstract available.

Although the mechanism of the development of hypertension has not been fully elucidated, abnormal ion transport across the cardiovascular musle membrance may play some role in this mechanism. The elevation of intraceular sodium by inhibition of the Na(+), K(+)-ATPase diminshes the sodium gradient for calcium extrusion and/or increase Na(+)/Ca(++) exchange across the cell membrance. In any event, contractility and vascular tone of cardiovascular system can be incresed as reslut of an increase of intracellular calcium. Recently it is reported that the defects of Na(+), K(+)-ATPase occur in spontaneously hypertensive rat(SHR) hearts, compared to control normotensive Spargue Dawley(SD) rat hearts. However, one missing, unresolved question arose in the previous reports in whether the reduced Na(+)-pump activity in the heart of SHR is associated with the development of hypertension itself in these animals or is a consequence of inhertied pathological features that later reslut in a reduced pump activity. In order to clearify this question it is attempted to measured to measure the change of the Na(+), K(+)-ATPase activities in cardiac sarcolemma purified from both the normotensive SD rats and SHR rats during growth ; Simultaneously the charge of cation concentration in both intracellular space(RBC) and extracelluar space(ECF) are measured to the erythrocyte test(Garay and Meyer) applied to the clinical investiation of hypertension. The results obtained are summarized as follows ; 1) The systolic blood pressure of 7 week old SHR was 120-130mmHg, which was not significantly different from that of the age-matched SD rats. However, the blood pressure was elevated to 160-170mmHg in 13-15 week old SHR, even elevated to 190mmHg in one of 19 week old SHR. On the other hand, SHR, in which hypertension was well established had pronounced cardiac hypertrophy. 2) The Na(+), K(+)-ATPase activities in cardiac sarcolemma of the SHR rats were decreased gradually as hypertension established.The decrease of Na(+), K(+)-ATPase was well associated with the increase of intracellular potassium concentration.By contrast, thr Na(+), K(+)-ATPase activities and cation transports og the normotensive SD rats were not significanlty chaged during growth. 3) The charges of Na(+), K(+)-ATPase activities in SHR were specific because the activities of Ca(++)-ATPase which is one of the membrance bound enzyme were not changed during growth appeared to be a major fator which generated hypertension in SHR rats. However, question on how the Na(+), K(+)-ATPase activities are decreased and which event is initiative between reduction of Na(+), K(+)-ATPase and development of hypertension are still remained unclear. Recent literature suggests the there might be a genetic factor, so-called Na(+)-pump inhibitor, involved in the meachanism.
Animals ; Blood Pressure ; Calcium ; Cardiomegaly ; Cardiovascular System ; Erythrocytes ; Hand ; Heart ; Hypertension ; Ion Transport ; Potassium ; Rats ; Rats, Inbred SHR* ; Sarcolemma ; Sodium

Beta-lapachone (beta-Lap; 3,4-dihydro-2, 2-dimethyl-2H-naphthol[1, 2-b]pyran-5,6-dione) is a novel anti-cancer drug under phase I/II clinical trials. beta-Lap has been demonstrated to cause apoptotic and necrotic death in a variety of human cancer cells in vitro and in vivo. The mechanisms underlying the beta-Lap toxicity against cancer cells has been controversial. The most recent view is that beta-Lap, which is a quinone compound, undergoes two-electron reduction to hydroquinone form utilizing NAD(P)H or NADH as electron source. This two-electron reduction of beta-Lap is mediated by NAD(P)H:quinone oxidoreductase (NQO1), which is known to mediate the reduction of many quinone compounds. The hydroquinone forms of beta-Lap then spontaneously oxidizes back to the original oxidized beta-Lap, creating futile cycling between the oxidized and reduced forms of beta-Lap. It is proposed that the futile recycling between oxidized and reduced forms of beta-Lap leads to two distinct cell death pathways. First one is that the two-electron reduced beta-Lap is converted first to one-electron reduced beta-Lap, i.e., semiquinone beta-Lap (SQ).- causing production of reactive oxygen species (ROS), which then causes apoptotic cell death. The second mechanism is that severe depletion of NAD(P)H and NADH as a result of futile cycling between the quinone and hydroquinone forms of beta-Lap causes severe disturbance in cellular metabolism leading to apoptosis and necrosis. The relative importance of the aforementioned two mechanisms, i.e., generation of ROS or depletion of NAD(P)H/NADH, may vary depending on cell type and environment. Importantly, the NQO1 level in cancer cells has been found to be higher than that in normal cells indicating that beta-Lap may be preferentially toxic to cancer cells relative to non-cancer cells. The cellular level of NQO1 has been found to be significantly increased by divergent physical and chemical stresses including ionizing radiation. Recent reports clearly demonstrated that beta-Lap and ionizing radiation kill cancer cells in a synergistic manner. Indications are that irradiation of cancer cells causes long-lasting elevation of NQO1, thereby sensitizing the cells to beta-Lap. In addition, beta-Lap has been shown to inhibit the repair of sublethal radiation damage. Treating experimental tumors growing in the legs of mice with irradiation and intraperitoneal injection of beta-Lap suppressed the growth of the tumors in a manner more than additive. Collectively, beta-Lap is a potentially useful anti-cancer drug, particularly in combination with radiotherapy.
Animals ; Apoptosis ; Benzoquinones ; Cell Death ; Electrons ; Humans ; Hydroquinones ; Injections, Intraperitoneal ; Leg ; Mice ; NAD ; Naphthoquinones ; Necrosis ; Radiation Tolerance ; Radiation, Ionizing ; Reactive Oxygen Species ; Recycling ; Substrate Cycling