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Biomedical subjects

M Matsunaga

Publications and source records attributed to M Matsunaga.

At least 163 records · Page 9Linked to original sources
PubMed1987

[Light and electron microscopic observations of cysts in the brain from an autopsy case of cryptococcus meningitis].

We gave some considerations to the significance of cyst formation in a case of cryptococcus meningitis by examining the cysts themselves and comparing the organisms in the cysts with those disseminated throughout the subarachnoid space by light and electron microscopy. An 18-year-old girl had complained of headache, stiffneck and fever at the onset. These symptoms worsened into confusion without any definite diagnosis, then resulted in an arrest of spontaneous respiration which led to use of respirator for 12 days. The patient died 40 days after the onset. The brain weighed 1440 g and showed moderate swelling with opacity of the leptomeninges, which was very evident over the convexity and around the basal side of the pons. Subarachnoid fresh hemorrhage was also observed around the basal side of the brain stem. Microscopic examination of the subarachnoid space revealed widely disseminated Cryptococcus neoformans varied in size, whose cell wall showed a positive staining reaction to PAS. The organisms had characteristic spicules positively stained with cresyl violet radiating out of the cell body, and were associated with infiltration of lymphocytes, macrophages and polymorphonuclear leukocytes throughout the subarachnoid space. Some portions of arachnoid membrane, dura mater and vessel walls in the subarachnoid space especially the adventitia of the basilar artery were replaced by multiple cysts. The cysts were tightly filled with large numbers of small uniformly sized organisms which often showed budding. These cysts showed no histological evidence for inflammation. Further studies to demonstrate those differences were carried out with electron microscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

[Akinetic mutism from recurrent hydrocephalus: successful treatment with levodopa, bromocriptine and trihexyphenidyl].

A case of akinetic mutism was reported with reference to a marked improvement by levodopa, bromocriptine and trihexyphenidyl. A 39-year-old male, first seen on February 2, 1981, had an occipitalgia, accompanied by nausea and vomiting. For several months before this consultation, the patient had suffered from asthenopia. Brain CT scan and cerebral angiogram demonstrated internal hydrocephalus due to aqueduct stenosis of unknown etiology. After a ventriculoperitoneal shunt operation on February 20, 1981, he completely recovered. Two years and a half after the shunt insertion he had no difficulty in his daily life. He reentered the hospital on December 21, 1983, because of personality change, mental deterioration and bradykinesia. Brain CT scan showed recurrent hydrocephalus resulting from shunt blockage. Following the shunt revision, hydrocephalus was resolved. Nevertheless, the patient did not return to his previous state. And he became bed-ridden, incontinent of urine, and unable to take fluids or foods, following which he went into a state of akinetic mutism. Other neurological findings were as follows: upward gaze palsy, impaired convergence, convergence nystagmus, plastic rigidity of neck and all four limbs, and diffuse hyperreflexia with right Babinski's sign. Abnormal involuntary movement was not seen. On March 27, 1984, levodopa therapy was instituted and on April 2, trihexyphenidyl was combined with levodopa. Shortly after administration of levodopa and trihexyphenidyl, akinetic mutism began to improve, but upward gaze palsy was not affected. He began to speak and could walk unassisted by the end of July.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Dynamic changes in plasma inactive renin levels in Bartter's syndrome after administration of captopril and angiotensin II.

Changes in plasma active and inactive renin concentration (ARC and IRC) after captopril administration and angiotensin II (AII) infusion were studied in six patients with Bartter's syndrome. A single oral dose of captopril (8-25 mg) lowered the blood pressure and increased both ARC and IRC. AII infusion elevated blood pressure, suppressed ARC and increased IRC. In this syndrome of high renin levels, infused AII appeared to increase inactive renin secretion by reducing its conversion to active renin. On the other hand, an acute fall in AII levels and/or renal perfusion pressure by captopril increased both active and inactive renin. This indicates that the increase in the secretion of inactive renin, stimulated by captopril, might exceed any increase in its conversion to active renin in patients with Bartter's syndrome, in whom the production of renin is accelerated, and conversion of inactive renin to active renin probably already operates near its maximum.

Adolescent↗
PubMed1986

Pure dysarthria due to anterior internal capsule and/or corona radiata infarction: a report of five cases.

Five cases with a sudden onset of dysarthria in the setting of hypertension are presented. No case had limb weakness or other neurological deficits. Computed tomographic scan demonstrated a small low density lesion in the anterior part of the internal capsule or the adjacent corona radiata. All cases showed a good recovery from dysarthria within two to four weeks.

Afferent Pathways↗
PubMed1986

Class II major histocompatibility complex antigen expression and cellular interactions in thyroid glands of Graves' disease.

Class II major histocompatibility complex (MHC) antigens have been demonstrated on the surface of thyroid epithelial cells (thyrocytes) from patients with autoimmune thyroid disease. The present study was designed to investigate how the expression of class II MHC antigens is involved in autoimmune processes in Graves' disease by studying cellular interactions among thyrocytes, lymphocytes within thyroid glands (TG), and peripheral blood (PB) lymphocytes. Thyrocytes were prepared by collagenase digestion, and T or non-T cells were separated by E-rosette formation. Thyrocytes were cocultured in the presence or absence of interferon-gamma, and the expression of HLA-DR antigens on cultured thyrocytes was examined by an indirect immunofluorescence method using monoclonal anti-HLA-DR antibody and monoclonal anti-HLA-DQ antibody. The cellular interactions were assessed as the proliferative response of T cells to autologous stimulators, such as thyrocytes or lymphocytes. Expression of HLA-DR antigens on thyrocytes after culture for 18 h in the absence of interferon-gamma was found in two thirds of the patients with Graves' disease studied (n = 18). Interferon-gamma induced and maintained the expression of HLA-DR antigens on thyrocytes. The percentages of HLA-DR+T cells were significantly higher among TG-T cells than among PB-T cells [32.6 +/- 12.4% (+/- SD) vs. 12.2 +/-5.0%; n = 18; P less than 0.01]. Thyrocytes from Graves' patients induced proliferation of both autologous PB-T cells and TG-T cells, and TG-T cells stimulated proliferation of autologous PB-T cells. In conclusion, interferon-gamma induces HLA-DR antigen expression on thyrocytes from patients with Graves' disease, and these cells induce proliferation of autologous T cells, which may, in turn, act on thyrocytes to perpetuate the process.

Adolescent↗
PubMed1986

Serum from patients with autoimmune diseases induces in vitro production of disease-associated antibodies by peripheral blood mononuclear cells from normal subjects.

Antibodies present in serum of patients with rheumatoid arthritis (RA), autoimmune thyroid diseases, and myasthenia gravis are preferentially cytotoxic to suppressor T lymphocytes from normal subjects induced by Concanavalin A. The aim of this study was to determine whether the lymphocytotoxic antibodies found in patients with these diseases also react with regulatory T cells to facilitate production of the autoantibodies responsible for each disease. Peripheral blood mononuclear cells (PBMC) from normal subjects were treated with serum from patients and complement. After washing, residual viable cells were cultured with pokeweed mitogen for 7 days. Immunoglobulin M rheumatoid factor and antihuman thyroglobulin antibody (anti-hTgAb) in the culture supernatants were measured by RIA. Anti-hTgAb was produced in culture supernatants of PBMC treated with serum samples from patients with autoimmune thyroid diseases, whereas serum samples from patients with RA, myasthemia gravis, or normal subjects did not stimulate production of detectable anti-hTgAb. In contrast, Immunoglobulin M rheumatoid factor was produced by normal PBMC treated only with serum from patients with RA. When normal T cells treated with serum were cultured with autologous untreated non-T cells in the presence of pokeweed mitogen, autoantibodies also were produced. Furthermore, the production of anti-hTgAb was suppressed by adding untreated T cells to the mixture of treated T cells and untreated non-T cells. These results suggest that lymphocytotoxic antibodies found in patients with autoimmune disorders may cause disease-associated suppressor T cell dysfunction.

Adolescent↗
PubMed1986

Prevention of nephrosclerosis and cardiac hypertrophy by captopril treatment of spontaneously hypertensive rats.

The relationship between hypertension and cardiovascular damage was assessed in three groups of spontaneously hypertensive rats (SHR): 1. stroke prone SHR (SHR-SP) treated orally with an angiotensin I converting enzyme inhibitor (captopril) (100-400 mg/L in the drinking water) from 6 to 35 weeks of age, 2. SHR-SP maintained on tap water until 30 weeks of age, 3. stroke resistant SHR (SHR-SR) maintained on tap water. The controls were Wister Kyoto rats (WKY) maintained on tap water. Captopril-treated SHR-SP showed blood pressure lower than that of untreated SHR-SP, similar to SHR-SR. The ratio of heart weight to body weight was 0.55% in SHR-SP, 0.39% in captopril-treated SHR-SP, 0.46% in SHR-SR, and 0.39% in WKY. The kidneys of SHR-SP showed glomerular sclerosis, glomerular fibrosis, tubular casts, interstitial cell infiltration and vascular wall thickening or hyperplasia of the small arteries and arterioles. The severe glomerular sclerosis was mostly distributed in the inner and middle portions of cortex. Immunohistological study showed IgG, C3 and fibrinogen in the glomeruli and arterioles in SHR-SP. In captopril-treated SHR-SP, similar to SHR-SR, only minor histological changes were seen and there was no deposition of IgG, C3 or fibrinogen. No changes were seen in WKY. Thus, it was concluded that nephrosclerosis and cardiac hypertrophy in SHR-SP are prevented by captopril. The role of the renin-angiotensin and kallikrein-kinin systems in organ pathogenesis in SHR-SP is discussed.

Animals↗
PubMed1986

[Histydyl-proline diketopiperazine (HPD), a metabolite of thyrotropin-releasing hormone (TRH), improves the ataxic gait in 3-acetylpyridine (3-AP) treated rats].

Histidyl-proline diketopiperazine (HPD) is the active metabolite deriving from thyrotropin-releasing hormone (TRH). However, its regional distribution in the central nervous system is quite different from TRH. Above all, it is to be noted that cerebellum is one of the richest region of HPD. In rat cerebellum, for example, the concentration of HPD is 20 times higher than that of TRH. This indicates the probable action of HPD within cerebellar system. Recently, a fascinating hypothesis has been proposed by Prasad et al that some activities of TRH are based on its conversion to HPD. The purpose of this experiment is to clarify whether the hypothesis may also be appropriate for the action in the cerebellar system. Twenty four Wistar rats treated with 3-acetylpyridin (3-AP) intraperitoneally were used in our experiment. Before 3-AP administration, those rats were conditioned by electric stimulation to run forward. The 3-AP treated rat is established so as to make an ataxic rat along with a selective degeneration of the inferior olive nucleus. Those ataxic rats were divided into 3 groups according to the test drugs, that is, the group of HPD, TRH (5 mumole/kg each), and saline [the same volume (3.6 ml/kg)] control. Eight rats of each group received an intraperitoneal injection once a day from 5th to 9th day after 3-AP treatment. The behavioral tests were carried out at the 5th, 7th, and 9th day after 3-AP treatment. The ataxic gaits were observed every 30 minutes over 4 hours in succession.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effects of probes of membrane potential on metabolism in synaptosomes.

Effects of three probes for measuring membrane potential, tetraphenylphosphonium (TPP+), rhodamine 6G and 3,3'-dipropylthiocarbocyanine (diS-C3-(5)) on energy metabolism in synaptosomes were investigated. None of the three probes had any effect on lactate production in synaptosomes. TPP+ and rhodamine 6G did not inhibit the respiration of synaptosomes with pyruvate and succinate as exogenous substrate and were only weakly inhibitory with endogenous substrates. In contrast, diS-C3-(5) markedly inhibited the respiration of synaptosomes with glucose, pyruvate and endogenous substrates. All three probes reduced ATP content in synaptosomes and depolarized the membrane potential in synaptosomes with increasing concentrations of the probes. It is, therefore, preferable to estimate membrane potential with TPP+ or rhodamine 6G at their low concentrations where their effect on metabolism is negligible.

Adenosine Triphosphate↗
PubMed1985

N-Acetylneuraminyllactosylceramide, GM3-NeuAc, a new influenza A virus receptor which mediates the adsorption-fusion process of viral infection. Binding specificity of influenza virus A/Aichi/2/68 (H3N2) to membrane-associated GM3 with different molecular species of sialic acid.

Agglutinates of native chicken erythrocytes caused by influenza virus A/Aichi/2/68 (H3N2) at 4 degrees C were potently fused and lysed at low pH (optimum pH 5.3) at 37 degrees C. Exogenous gangliosides GM3 (Sia alpha 2-3Gal beta 1-4Glc beta 1-ceramide) and GM2 (GalNAc beta 1-4(Sia alpha 2-3)-Gal beta 1-4Glc beta 1-ceramide) were integrated into the membranes of chicken asialoerythrocytes within 5-min incubation at 37 degrees C. We found that the incorporation of ganglioside GM3 containing N-acetylneuraminic acid into asialoerythrocytes restored the biological responsiveness to the virus as established by agglutination at 4 degrees C and fusion and hemolysis at 37 degrees C at pH 5.3. Biological responsiveness of GM3-NeuAc-erythrocytes to the virus was considerably higher than that of GM3-NeuGc-erythrocytes under the same experimental conditions. Treatment of the GM3-NeuAc-erythrocytes with neuraminidase again resulted in the complete abolishment of the response to the virus. Erythrocytes containing GM2-NeuAc showed no detectable biological responses toward the virus. The above results indicate that the hemagglutinin of influenza virus A/Aichi/2/68 (H3N2) recognizes the sialyloligosaccharide chain of ganglioside GM3 as its receptor which mediates the adsorption and fusion process on the virus entry into the host cells and has more preferential specificity for binding to N-acetylneuraminic acid-containing GM3 than that to N-glycolyl type in the target cell membranes.

Adsorption↗
PubMed1985

Chromosomal characteristics of chronic and blastic phases of Ph-positive chronic myeloid leukemia.

To evaluate the appearance of chromosome changes, in addition to the Philadelphia (Ph) chromosome, as predictive and diagnostic parameters of transformation in chronic myeloid leukemia (CML), such changes were analyzed in the chronic phase (CP) and compared with those of the blastic phase (BP) of CML. The common chromosome changes observed in the CP were loss of a Y (-Y), trisomy 8 (+8), an isochromosome for the long arm of chromosome #17 [i(17q)], a double Ph (+Ph), reciprocal translocations, and partial deletions. In most patients with chromosome changes in addition to the Ph, the percentage of abnormal clones increased steadily during the CP and was accompanied by other chromosome changes shortly before or at the onset of the BP, except for cases with -Y or i(17q) clones. In general, most chromosome changes observed shortly before or at the BP were complex. These facts suggest that complex chromosome changes could be utilized as predictive and diagnostic parameters of blastic transformation in CML.

Adult↗
PubMed1985

Ganglioside GM1b as an influenza virus receptor.

Receptor activity toward influenza virus A/Aichi/2/68 (H3N2) of a pair of gangliosides, GM1b (NeuAc alpha 2-3 Ga1 beta 1-3 GalNAc beta 1-4 Gal beta 1-4 GLc beta 1-1'-ceramide) and GM1a (Gal beta 1-3 GalNAc beta 1-4 (NeuAc alpha 2-3) Ga1 beta 1-4 Glc beta 1-1'-ceramide) is described. Receptor activity was monitored by an assay system including incorporation of gangliosides into chicken asialoerythrocytes which had lost the biological response for the virus, and subsequent estimation of recovery of virus-mediated haemagglutination and haemolysis. GM1a and GM1b were incorporated in similar amounts into chicken asialoerythrocytes. It was found that GM1b-erythrocytes revealed distinct recovery of influenza virus A/Aichi-mediated agglutination at 4 degrees C and subsequent haemolysis at 37 degrees C at pH 5.3. However, restoration of biological responsiveness of the erythrocytes to the virus by incorporation of GM1a was very low under the same conditions. The above results indicate that the haemagglutinin of the influenza virus A/Aichi/2/68 (H3N2) recognizes the saliosyl residue linked to nonreducing 'terminal' galactose rather than 'inner' galactose in the ganglio-tetraose core of gangliosides. GM1b could be one of the functional receptors to the influenza virus.

Animals↗