[Studies of sleep disorders in the aged and middle aged using polysomnography].
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Biomedical subjects
Publications and source records attributed to N Yamaguchi.
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Clinical effects of the monotherapy with ceftazidime (CAZ) were evaluated in patients with severe infections associated with febrile granulocytopenia in hematological disorders in 10 institutions. CAZ (4-6g/day) was administered intravenously by drip infusion divided into 2 to 4 doses. 83% of the underlying diseases were hematological malignancies. Infections mainly consisted of documented sepsis (10%), presumed sepsis (60%). Overall efficacy rate was 65%, and that of septic patients was 83.3%. Adverse reactions were minimal, and this study revealed safety of CAZ.
A role of pancreatic glucagon in hemorrhage induced hyperglycemia was studied in anesthetized dogs with or without functional adrenalectomy (ADRX), surgical hepatic denervation (HNX), and surgical pancreatectomy (PCX). Plasma epinephrine, norepinephrine, and glucose concentrations were determined in both hepatic venous and aortic blood. Plasma glucagon (IRG) and insulin (IRI) levels were determined in aortic blood. All dogs were bled until aortic systolic pressure dropped to approximately 50% (64.8 +/- 1.6 mmHg, n = 25) of its control value (136.7 +/- 4.4 mmHg, n = 25), and the hypotension was maintained for 5 min. In control dogs (n = 10), hemorrhage markedly increased aortic epinephrine and hepatic venous norepinephrine. Similarly, aortic IRG, hepatic venous glucose and aortic glucose rose significantly during hemorrhage. In dogs with HNX combined with ADRX (n = 10), aortic epinephrine and hepatic venous norepinephrine remained unchanged during hemorrhage. Aortic IRG concentration, however, increased to a level similar to that observed in the control group. Aortic glucose increased significantly along with significant increases in hepatic venous glucose. In dogs with PCX combined with HNX and ADRX (n = 5), the increases in aortic IRG, hepatic venous glucose and aortic glucose observed in the first two groups in response to hemorrhage were virtually abolished. The results indicate that the increase in aortic IRG during hemorrhage is of pancreatic origin. We conclude that the pancreatic glucagon may be involved in the hyperglycemic response to hemorrhage, most likely through glucose mobilization by the liver during the early phase of hemorrhagic hypotension.
Chest X-ray findings in two infants with Chlamydia trachomatis pneumonia were reported. Both cases showed bilateral interstitial infiltrates and hyperinflation. These findings are not specific to this pneumonia. Chlamydia trachomatis pneumonia should be considered as one possibility when we find such findings on chest X-ray in infants.
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We studied the phenotype of megakaryoblasts (MKB) in two patients with blastic crisis of chronic myeloid leukemia by simultaneous detection of platelet peroxidase (PPO) activity and platelet glycoproteins (GP) with monoclonal antibodies at the ultrastructural level. When 227A (anti-GPIb) was used, the finding of GP correlated well with the presence of PPO in the majority of MKB, and a few MKB were found to express PPO but lack GP. When 224B (anti-GPIIb/IIIa) was applied, we found a few MKB of a further type, which expressed GP but lacked PPO. These results indicate that the expression of platelet markers is partially aberrant in neoplastic MKB, and that MKB are heterogenous in their phenotypic expressions. Thus, the detection of PPO or GP alone may miss some MKB. For the accurate identification of MKB and the demonstration of aberrant expression of platelet markers, simultaneous detection of the markers seems to useful.
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A 76-year-old woman, who had suffered from liver cirrhosis, was referred to our hospital because of pancytopenia. Her peripheral leukocyte count was 2,500/microliters with 43% myeloblasts, hemoglobin at 9.0 g/dl and platelet count of 0.9 x 10(4)/microliters. Aspirate from bone marrow showed hypercellular marrow with 52% myeloblasts. No chromosomal abnormality was detected. She was diagnosed as acute myelogenous leukemia (AML, M2). The diagnosis of liver cirrhosis was confirmed by laboratory data and findings of abdominal sonography. Moreover, she had valvular aortic stenosis. These complications made it difficult to treat her with combined chemotherapy containing anthracycline antibiotics, so she was given a small dose of cytosine arabinoside (Ara-C, 10 mg/body/12 hr) for 18 days. After severe myelosuppression, complete remission was achieved. The highest serum concentration of Ara-C was obtained at 15 min after subcutaneous injection of Ara-C; thereafter the Ara-C concentration decreased immediately within 60 min in a pattern similar to that observed in patients without liver cirrhosis. Thus, low-dose Ara-C regimen might be a useful treatment for aged patients with AML, even complicated with liver cirrhosis.
A case of familial juvenile Alzheimer's disease with apallic state at the relatively early stage and various neurological features was reported. A 33-year-old woman showed a progressive dementia followed by apallic state at the relatively early stage, and died of cardiac failure at the age of 45. Neurological examination disclosed chorea, myoclonus, rigidity, pyramidal sign, and generalized convulsion. Neuropathologically, extensive senile changes such as senile plaques, neurofibrillary tangles, and granurovascular degenerations were observed in the brain, chiefly in the cerebral cortex and limbic system. The present case was characterized by a severe neuronal loss in the subcortical gray matter such as the caudate nucleus, dentate nucleus, substantia nigra, and thalamus as well as a marked myelin loss and axonal damages in the cerebral white matter. This case suggested a combination of multisystemic degeneration and a primary degeneration of the cerebral white matter. The additional peculiar aspects in this case were the senile plaques and amyloid angiopathy in the cerebellar cortex, and the senile plaques and grumose degeneration in the cerebellar dentate nucleus. In the clinicopathological standpoint, the apallic state in this case could be attributed to a severe degeneration of the cerebral white matter in addition to the cerebral cortical deterioration. Furthermore, the occurrence of chorea and myclonus might be contributed to the severe degeneration of the caudate nucleus and to the degeneration of the dentate nucleus, particularly to the grumose degeneration, respectively.
A female patient what M3 was seen to incur marked hemorrhagic diathesis during therapy. Heparin infusion was performed to inhibit disseminated intravascular coagulation (DIC). However, oozing from the puncture site of the r-subclavian vein was observed. Her data on coagulation were as follows: AT-3 greater than 100%, fibrinogen 69.0 mg, XIII less than 40%, FPA 2.9 ng/ml and FDP-D dimer 256 ng/ml. The alpha-2-plasmin inhibitor (alpha 2-PI) was 44% and FDP 160 microgram/ml. These results suggested DIC with activated fibrinolysis. Thus, epsilon aminocaproic acid in conjunction with heparin, fibrinogen, and concentrated XIII was administered. The abnormal bleeding improved with an increase of alpha 2-PI and XIII. This clinical response indicated that an activated fibrinolysis and a decreased XIII might have been responsible for provoking the bleeding of the patient.
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A case of muscular ventricular septal defect shown by the phase image derived from Fourier analysis of gated equilibrium radionuclide angiocardiography is presented. The diagnostic feature of the defect on the phase image was a marked phase delay localized mainly in the trabecular portion of the right ventricle. This characteristic finding seemed to be caused by the left to right shunt flow through the defect located in the muscular portion of the interventricular septum.
We describe a patient with adult T cell Leukemia to whom alpha-interferon therapy was highly effective. Although a combination chemotherapy (ACVP) first introduced was effective in reducing total leukocyte counts, the percentage of leukemic cells relative to total leukocyte counts was decreased first after the institution of alpha-interferon therapy. The patient is now under complete remission for four years. It was noted in this patient that circulating alpha-interferon, measured by a sensitive radioimmunoassay, was consistently low as compared with the value found in the age-, sex-matched healthy control (p less than 0.001). Since adult T cell leukemia is pathogenetically related to the retrovirus infection, low levels of circulating alpha-interferon of the patient may be important from both pathogenetic and therapeutic standpoints. Alpha-interferon therapy may be an useful additive for the chemotherapy of adult T cell leukemia.
Changes in circulating plasma catecholamine (CA: E, epinephrine; NE, norepinephrine; and DA, dopamine) concentrations in aortic (AO) blood were investigated in relation to variable rates of CA secretion from both adrenal (ADR) glands in response to bilateral carotid artery occlusion (BLCO) in vagotomized dogs anesthetized with sodium pentobarbital. During BLCO (3 min), AO systolic pressure (AP) increased along with significant increases in ADR-CA output, renal venous (RV) CA output, as well as in AO-E and NE concentrations. A ratio of NE:E in ADR venous and AO blood did not exceed 0.42 +/- 0.09 and 1.09 +/- 0.24 upon BLCO, respectively. In contrast, the NE:E ratio in RV blood increased significantly from 5.39 +/- 0.91 to 9.78 +/- 1.31. Following adrenalectomy (ADRX), the increase in AO-NE in response to BLCO was significantly attenuated by approximately 56%, but the increase in RV-NE output was not affected by ADRX. The results show that in vagotomized dogs, NE is co-released with E from the adrenal glands upon BLCO. The data also indicate that the increase in AO-NE concentration was dependent to a similar extent on the simultaneous increases in ADR-NE output and neuronal NE release. We conclude that under conditions where the sympathoadrenal system is activated, circulating plasma NE concentration may be significantly affected by an increase in ADR-NE output. Sympathetic neuronal contributions would, thereby, be overestimated in assessing overall sympathetic nerve activity by measuring circulating NE. NE concentrations in local venous effluent from individual organs may be more reliable estimates of the sympathetic nerve activity.
This study reports on the effects of yohimbine and clonidine on the release of adrenal and renal catecholamines (epinephrine, E; norepinephrine, NE; and dopamine, DA) in response to bilateral carotid occlusion (BCO, 3 min) in vagotomized dogs anesthetized with sodium pentobarbital. The model used allowed us to simultaneously compare adrenal catecholamine secretion with neuronal NE release in the kidney. In control dogs, the net output (ng/min/g tissue) of adrenal E (70.5 +/- 19.7), NE (22.2 +/- 5.9) and DA (2.6 +/- 0.8) increased markedly (P less than 0.01) during BCO to a maximum level of 265.1 +/- 87.9, 97.4 +/- 30.6 and 10.5 +/- 3.2, respectively. Similarly, the net output (ng/min/g tissue) of renal NE (0.66 +/- 0.06) and DA (0.09 +/- 0.02) increased significantly (P less than 0.01) to 1.00 +/- 0.11 and 0.15 +/- 0.04, respectively. Aortic systolic pressure (mm Hg) (140.8 +/- 8.0) and heart rate (beats/min) (162.7 +/- 5.1) also increased (P less than 0.01) to 212.5 +/- 19.3 and 179.5 +/- 5.4, respectively. In dogs treated with yohimbine (0.3 mg/kg, i.v.), the net increase in adrenal catecholamine output was diminished by approximately 47% (P less than 0.05). In contrast, the net increase in renal NE output was potentiated by 41% (P less than 0.05). The net increase in heart rate was also enhanced significantly (P less than 0.01) in the presence of yohimbine. In dogs receiving clonidine (15 micrograms/kg, i.v.) the increases in net output of both adrenal and renal catecholamine were abolished. Similarly, pressor and heart rate responses were abolished in the presence of clonidine. The results indicate that yohimbine exerted a differential effect on renal sympathetic nerves (increase) and adrenal medullae (decrease) in modulating catecholamine release in response to BCO, while clonidine abolished both neural NE release and adrenal catecholamine secretion. This study suggests that a presynaptic alpha 2-adrenoceptor-mediated mechanism, the blockade of which enhances neural NE release at peripheral sympathetic nerve terminals in many tissues, may not be involved in the modulation of adrenal catecholamine secretion during BCO.
This study investigated congenital anomalies occurring in the middle and the inner ears, with particular attention to their features, localizations, and frequencies. One hundred human temporal bones obtained from 73 individuals, aged 31 gestational weeks to 39 years, each of whom had anomalies of the middle ear and/or inner ear, were used for this study. The temporal bones had been removed at autopsy, fixed, dehydrated, embedded in celloidin, and sectioned horizontally or vertically at 20 microns. Every 10th horizontal section or every 20th vertical section was stained with hematoxylin and eosin, mounted and studied under a light microscope. In the middle ear the structure most often found to be anomalous was the facial nerve; in the inner ear it was the lateral semicircular canal. The implications of the anomalies observed are discussed as they relate to fetal development, dysfunction of the ear, and clinical interpretation of diagnostic radiological studies.
The relationship between lymphocyte activation by purified plant glycoside and the suppression of antibodies against sheep erythrocytes was investigated by an adoptive cell transfer system. Glycosides are one of the main components of Shôsaikotô--famous hematopoietic remedies of oriental medicine. In earlier reports, BALB/c mice treated with these drugs, suppressed the plaque-forming cell (PFC) response to T-dependent antigens. In contrast, the PFC response was enhanced for T-independent antigens. In this communication, an experiment was designed to determine the nature of the suppressive factor(s) produced in treated mice. Mice were orally or intraperitoneally administered 1 mg/kg of five types of purified SS derivatives every other day on five consecutive occasions. Spleen cells and serum were prepared from SS-treated mice and were then passively transferred to recipient mice. On the spleen cells (and not any of the sera) from drug-treated hosts effectively suppressed the PFC in recipients. The spleen cells of treated mice were further divided into adherent and non-adherent cells; each cell type was transferred into recipient animals. The observed suppressive activity was clearly detected in the non-adherent cell population. A subsequent analysis of the lymphocyte subpopulation revealed that Lyt.1.1 negative and Lyt.2.2 positive cells were responsible for this suppression. It was concluded that some SS derivatives elevate the activities of the major immunocyte population, with suppressor cell activity predominating.
A unicellular algae, Chlorella pyrenoidosa, was used as a biological response modifier. In C57BL/6(B6), C3H/He and DDD/1 mice, both intraperitoneal or oral administrations of autoclaved Chlorella cells or heat-extracted substance were carried out every other day for 10 days before mouse mammary carcinoma (MM-2) or Ehrlich ascites cells were transplanted into the peritoneal cavity. In case of mouse leukemia cells (EL-4), subcutaneous transplantation was carried out. All control mice died within 20 days after each tumor cell transplantation, while 73.3-80% of the treated groups survived over 60 days in the combination of MM-2 vs. C3H/He and EL-4 vs. B6, respectively. The cytotoxic activities against tumor cells, that were abolished by treatment with anti-Thyl.2 monoclonal antibody plus complement, were evidenced in the experimental host. Since Chlorella cells and derivatives showed no indication of direct in vitro cytotoxicity to either tumor or mouse spleen cells, the antitumor effects documented may be mediated by host immune response.