[The effect of VDT polarity and target size on pupil area].
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Biomedical subjects
Publications and source records attributed to T Kondo.
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Nine female and 20 male hypogonadotropic GH-deficient patients were studied for sexual development by hCG/hMG. In the female patients, gonadotropin therapy was started at the mean age of 22.7 +/- 2.1 years. The administration of progesterone induced withdrawal bleeding at an average of 2.77 +/- 1.94 years after the initiation of hMG/hCG therapy in 8 of the 9 patients studied. Of 6 patients who had been confirmed as positive in a gestagen test, induction of ovulation by hMG/hCG was observed in 5 patients at an average of 5.58 +/- 1.23 years after the onset of therapy, but not in the remaining patient who had been given estrogen and progesterone 4 years 9 months prior to the initiation of the gonadotropin therapy. In male patients, gonadotropin therapy was started at the mean age of 23.6 +/- 5.7 years. Seminal fluid was obtained by masturbation and brought to our clinic in the morning. Of the 20 patients, 19 patients could be observed once a month regularly. Of the 19 patients, spermatozoa could be detected at a mean period of 2.19 +/- 0.87 years after initiation of hCG/hMG therapy in 18, but not in the remaining patient, after 5 years of therapy, who did not receive hCG/hMG regularly. The sperm count exceeded 20 x 10(6)/ml and more in 12 and was lower than that in 8 patients after 3 years of the therapy. No side effects were observed in female patients, but gynecomastia developed in 2 of the 20 male patients. These data suggest that gonadotropin therapy for hypogonadotropic GH-deficient patients is effective in promoting ovulation and spermatogenesis despite the initial replacement therapy with sex hormones.
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The cytotoxicity of two types of nickel oxide particles was investigated in rat alveolar macrophages cultured in vitro. The trypan blue dye exclusion test and the release of lactate dehydrogenase into culture medium were used as cytotoxic indices. Although both types of nickel oxide particles were produced by the same manufacturer and were commercially sold under the same name of "nickel oxide", one type of the nickel oxide particles which had black color was much more cytotoxic than the other type of green color. The black nickel oxide particles were more soluble in various kinds of solutions than the green nickel oxide particles. Therefore, it appears that the difference in the cytotoxicity of the black and green nickel oxide particles may be attributable to the difference in the solubility of the particles.
Abscess formation is uncommon in eosinophilic lung disease. In this paper we present a case of chronic eosinophilic pneumonia in which bronchofiberoscopy revealed scattered small abscesses in the large airways. Pathological examination revealed the presence of inflammatory cells with eosinophilic infiltration in both the bronchial mucosa and lung parenchyma.
This is a report of a case of glomerular lipidosis with familial combined hyperlipidemia and panhypopituitarism. A 60-yr-old woman was admitted for evaluation of hyponatremia. Administration of hydrocortisone normalized the level of serum Na. A pituitary hormone-stimulating test and brain computed tomography revealed panhypopituitarism with an empty sella. Glucocorticoid deficiency due to secondary hypoaldosteronism was thought to have caused the Na loss. She had been treated for thyroid dysfunction and hyperlipidemia with replacement of thyroid hormone and a lipid-lowering drug. Hyperlipidemia changed from type V into IIa in 4 yr. Furthermore, one of her brothers and one of her sons were suspected to have type IV hyperlipidemia. Familial combined hyperlipidemia accompanied by secondary hypothyroidism was thought to have increased the levels of both total cholesterol and triglyceride. Two renal biopsies in 3 yr showed lipid deposits in the mesangial cells and indicated a positive correlation between the levels of serum lipids and lipid deposits in glomeruli, which suggested an important role of abnormal lipid metabolism in the progression of glomerular lipidosis.
To investigate the neural mechanism of the expiratory activity of the inspiratory muscles during a cough, EMG of the respiratory muscles were recorded in anesthetized and tracheostomized dogs. A laparoscope was used to minimize injury to the abdominal muscles for implantation of the electrodes into the costal diaphragm. During the expulsive phase of a cough, the diaphragm was active in 7 of 12 dogs and the external intercostal muscle was active in 3 of 6 dogs. During a cough, the expiratory activity of the diaphragm, after the termination of its inspiratory activity, started at 52.9 +/- 24.6 ms, and that of external intercostal muscle started at 51.1 +/- 20.5 ms. The expiratory activity of the internal intercostal muscle and of the transversus abdominis started at 34.3 +/- 13.0 and 27.8 +/- 15.2 ms, respectively. The onset of expiratory activity of the inspiratory muscles is significantly later than that of expiratory muscles. Continuous activity in the expiratory muscles evoked by airway occlusion, i.e., Hering-Breuer reflex, was suppressed during the inspiratory phase of a cough, but not suppressed during the expulsive phase even when the expiratory activity of the diaphragm was observed. We concluded that the expiratory activity of inspiratory muscles is controlled independently of both expiratory activity of the expiratory muscles and inspiratory activity of the inspiratory muscles.
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To investigate the role of calmodulin in stimulus-secretion coupling in pancreatic acinar cells, we studied the effects of W-7, a calmodulin inhibitor, and KN-62, a specific inhibitor of Ca2+/calmodulin-dependent protein kinase II (Ca2+/CaM kinase II), on amylase secretion from rat pancreatic acini. Calmodulin inhibitor (W-7, 100 microM) and Ca2+/CaM kinase II inhibitor (KN-62, 10 microM) reduced amylase secretion stimulated by cholecystokinin (CCK) or carbachol. W-7 and KN-62 also inhibited amylase secretion stimulated by both calcium ionophore (A23187) and phorbol ester (12-O-tetradecanoylphorbol-13-acetate, TPA). To clarify the role of calmodulin in the interaction of intracellular mediators, pancreatic acini were permeabilized with streptolysin O. Following permeabilization, amylase secretion was stimulated by submicromolar free Ca2+, and this Ca(2+)-dependent amylase secretion was enhanced by guanosine 5'-[gamma-thio]triphosphate (GTP gamma S), TPA or cyclic adenosine 3',5'-monophosphate (cAMP). W-7 and KN-62 had no effects on amylase secretion stimulated by Ca2+ alone, but inhibited the enhancement in Ca(2+)-dependent amylase secretion by GTP gamma S, TPA or cAMP. These data suggest that calmodulin plays an important role in Ca(2+)-dependent amylase secretion from pancreatic acinar cells and in the interaction between Ca2+ and other intracellular messengers.
This study is to clarify the ability of technetium-99m-Hexakis-2-methoxyisobutyl isonitrile(MIBI) myocardial scintigraphy for assessment of the effect of PTCR/PTCA as compared with conventional thallium-201 myocardial scintigraphy (201Tl). 99mTc-MIBI (740-888MBq) was injected before emergency PTCR/PTCA, and the initial imaging was performed immediately after PTCR/PTCA in 4 patients with acute myocardial infarction (AMI). On the other hand, in 2 patients with old myocardial infarction (OMI), 201Tl and MIBI myocardial imagings were performed before and one week after rescue PTCA. The defect area on the follow-up MIBI imaging was smaller than that on the initial MIBI imaging in 2 patients with successful emergency PTCR/PTCA. But in the other 2 AMI patients with unsuccessful reperfusion, the defect area did not significantly decrease after PTCR/PTCA. Reperfusion was successful in one of the two patients with OMI. In both the two patients with OMI, the MIBI defect area did not significantly decrease after rescue PTCA. MIBI myocardial scintigraphy is a useful noninvasive method for evaluating the effect of emergency PTCR/PTCA for myocardial salvage in patients with AMI, because MIBI is a kit type agent, and it does not redistribute.
Hemoglobin analysis by CO-oximeter is more easily and rapidly available method than other spectrophotometric or GC methods. In the present study, the possibility of diagnosis of asphyxia by CO-oximeter was examined experimentally using rabbits. When measured value of oxyhemoglobin (O2Hb) was lower than about 20% and that of deoxyhemoglobin (HHb) was, on the other hand, higher than about 80%, being accompanied by low measured values of both methemoglobin (MetHb) and CO-hemoglobin (COHb) (< 5%), asphyxia should be firstly considered as the cause of death. To the corpses found at the scene of fire, three chief factors causing death such as burns, suffocation due to oxygen deficiency and intoxication by poisonous gases may have occurred simultaneously, and through measuring the values of O2Hb, COHb, MetHb and HHb, the main lethal factor could be selected out among these three factors above and the cause of death could be examined much more closely. Because of easy and rapid analysis, it could be considered that CO-oximeter was useful for forensic practices and police activities.
We tested the hypothesis that the cardiopulmonary baroreflex control of forearm vascular resistance is impaired in patients with hypertrophic nonobstructive cardiomyopathy (HNCM). Forearm vascular responses to lower body negative pressures (LBNP) at -20 mmHg and -40 mmHg and to lower body positive pressure (LBPP) at +20 mmHg and +40 mmHg were compared between 11 patients with HNCM and 6 normal subjects. Forearm blood flow was measured with a strain gauge plethysmograph and forearm vascular resistance was calculated by dividing mean blood pressure by forearm blood flow. The left ventricular end-diastolic dimension and the left atrial dimension changed with the increases in LBNP and LBPP in patients with HNCM and in normal subjects. The ranges of these changes were similar in the 2 groups. Mean blood pressure and heart rate did not change during LBNP and LBPP. LBNP increased but LBPP decreased forearm vascular resistance in normal subjects, but neither LBNP nor LBPP changed the resistance in patients with HNCM. Increases in the resistance to cold pressor tests did not differ between the 2 groups. In patients with HNCM, there was a negative correlation between forearm vascular resistance at LBNP -20 mmHg and the left ventricular wall thickness (r = -0.81, p < 0.01). These results suggest that the cardiopulmonary baroreflex control of forearm vascular resistance is impaired in hypertrophic cardiomyopathy and that this impairment may be associated with left ventricular wall thickness.
Elevated levels of lipoprotein(a) [Lp(a)] have been associated with an increased risk of ischemic heart disease (IHD), and higher levels of Lp(a) are associated with lesions of significantly greater severity. We have examined Lp(a), total cholesterol (TC) and high density lipoprotein-cholesterol (HDL-C) levels in patients with IHD including those with normal coronary arteries with vasospastic angina. The study population consisted of 206 patients (166 males and 40 females) who underwent diagnostic coronary angiography for known IHD. Twenty-eight patients had effort angina, 36 rest angina, 8 unstable angina and 134 old myocardial infarction. IHD patients were categorized as zero vessel disease (0VD), single vessel disease (SVD) and multi-vessel disease (MVD). To investigate the relationship between atherosclerosis and IHD, these patients were further divided into 3 groups based on angiographic findings. Eighteen patients had entirely normal coronary arteries (normal group), 24 discretely diseased coronary arteries (discrete group) and 80 diffusely diseased coronaries (diffuse group). The results were compared with those obtained from 50 healthy individuals. Lp(a) levels for IHD patients (12.4 mg/dl) were significantly higher than those of controls (7.1 mg/dl, p < 0.05). However, there were no statistical differences between 0VD (13.1 mg/dl) and MVD (12.8 mg/dl). Similarly, no statistical differences of Lp(a) values were found among the normal group (13.3 mg/dl), discrete group (12.0 mg/dl) and diffuse group (12.9 mg/dl). Mean levels of HDL-C in 0VD (51.3 +/- 13.5 mg/dl) were significantly higher than those of SVD (42.9 +/- 11.5 mg/dl, p < 0.05). However, no significant differences were observed between controls (59.5 +/- 15.3 mg/dl) and 0VD (51.3 +/- 13.5 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
Inversion of chromosome 16 was found in a 73-year-old female with acute myeloblastic leukemia (FAB:M2). Complete remission was achieved by combined chemotherapy (DNR, Ara-C, 6-MP, Prednisolone), but she relapsed 6 months later without CNS involvement and died of respiratory failure presumably due to cerebrovascular accident during remission reinduction chemotherapy. Biphenotypic surface markers (CD2+ and CD13+) were observed on relapse. Eosinophilia was not observed throughout. Our patient and the other reported case suggest that biphenotypism and the lack of eosinophilia and monocytosis in inv (16) leukemia may be correlated with a poor prognosis.
Summaries of first drafts of Environmental Health Criteria (EHC), which were circulated for comments by IPCS in the period of 1991-1992, were presented. EHC drafts on 14 compounds and one methodology were received in this period.
Activity of the respiratory muscles during natural defecation was studied in two anesthetized and two decerebrate dogs. In anesthetized dogs, excitation of the abdominal muscles and an increase in gastric pressure were observed during defecation. However, pleural pressure was little influenced by such increase in abdominal pressure, maintaining the same rhythmic changes as observed during spontaneous respiration. The rhythmic changes in pleural pressure were associated with rhythmic activity of the diaphragm. When gastric pressure increased during defecation, the diaphragmatic activity also increased during both the inspiratory and expiratory phases. In a decerebrate dog, airflow and airway pressure changed similarly to during defecation. The diaphragm was continuously active, with superimposed rhythmic augmentation. In a paralyzed and artificially ventilated dog with open-chest, the phrenic nerve similarly developed discharges. We conclude that the non-respiratory activity and rhythmic augmentation of phrenic nerve discharge during defecation is pre-programmed in the command for defecation. The activity of phrenic motoneurons may be further modulated by changes in thoracic and abdominal pressure. These mechanisms may act together to coordinate respiration and defecation.
A 36-year-old male was admitted to the Ehime University Hospital with anemia, eosinophilia and hepatosplenomegaly. Peripheral blood examination demonstrated severe anemia (Hb 7.1g/dl), thrombocytopenia (Plt 6.8 x 10(4)/microliters) and increase of peripheral leukocyte counts (53,000/microliters) with 32.0% of eosinophils which had lobulated nuclei, abnormal distribution of eosinophilic granules and a few vacuoles. The level of serum IgE was low (< 5IU/ml), while that of serum vitamin B12 was elevated. A diagnosis of eosinophilic leukemia was made. He was noted to have spontaneous fluctuations in his eosinophil and total leukocyte counts. To analyze the mechanism of cyclic eosinophilic leukocytosis, we examined eosinophil colony stimulating activity of the serum and plasma of the patient. These examination showed that eosinophil colony-stimulating activity was not found in his serum and plasma, and cyclic eosinophilic leukocytosis was due to the hemopoietic stem cell disorder.
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