PubMed Health⌕ Search

Biomedical subjects

M Shida

Publications and source records attributed to M Shida.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Acute lymphocytic leukemia having surface phenotype of CD 2 and NKH-1 with rapid clinical course].

Abnormal expansion of large granular lymphocytes (LGLs) was observed in peripheral blood and bone marrow in a 28-year-old man. He had general lymphadenopathy and splenomegaly. Surface phenotypical analysis of LGLs showed that these LGLs express CD 2, Ia and NKH-1 but not express CD 3, CD 4, CD 8 and Leu 7. Cytochemical analysis of these LGLs revealed positive acid phosphatase and beta-glucuronidase reaction but negative alpha-naphthyl acetate esterase reaction. These LGLs showed very weak NK activity against only MOLT-4 but showed no cytotoxic activity against K 562. An beta-receptor gene rearrangement of human T-cell receptor was not found by Southern blot analysis. Rapid and fetal clinical course with the results of theses analytical studies showed that this case is highly suggestive of acute leukemia of LGLs which is committed to NK cell lineage.

Adult↗
PubMed1990

[Successful ATG and bolus methylprednisolone therapy towards severe aplastic anemia with splenomegaly].

A 22-year-old female patient with severe aplastic anemia was treated by ATG.bolus methylprednisolone therapy. After the therapy, anemia and thrombocytopenia began to recover within a month. The frequency of blood transfusion decreased thereafter. Since anemia due to splenomegaly was certified, bolus methylprednisolone therapy was performed in good response. Suppressor T-cells towards hemopoiesis were confirmed in this case, and hemopoietic potential was augmented by ATG.bolus methylprednisolone therapy. In spite of discontinuation of any therapy in 1986, she is being in good health more than five years.

Adult↗
PubMed1989

Role of adrenergic receptor systems in canine left ventricular hypertrophy.

Although the sympathetic nervous system and catecholamines have been postulated to play an important role in the development of myocardial hypertrophy, the precise mechanism is still ill-defined. We therefore investigated myocardial norepinephrine and the adrenergic receptor systems in two experimental canine models for cardiac hypertrophy; in 12 dogs with surgical cardiac denervation, and in 12 dogs with chronic infusion of a subhypertensive dose of norepinephrine at a rate of 0.04 mg/kg/day. After two months both models induced myocardial hypertrophy, indicated by significant increases in the heart weight, left ventricular wall thickness and cell diameter, as compared with 14 sham-operated control dogs. Cardiac denervation remarkably depleted myocardial norepinephrine while plasma norepinephrine remained unchanged. Both alpha 1- and beta-receptors were up-regulated, with Bmax increasing by 124% and 49%, respectively. The decrease in myocardial cyclic AMP content was relatively small as compared with the marked depletion in myocardial norepinephrine, probably compensated by augmentation of beta-receptor system activity. Chronic norepinephrine infusion also reduced myocardial norepinephrine content possibly due to stimulation of presynaptic alpha 2-receptor inhibiting norepinephrine synthesis and release. The number of alpha 1- and beta-receptors also increased by 97% and 30%, respectively, while myocardial cyclic AMP content remained unchanged. These observations indicate that neither direct stimulation of norepinephrine on the myocardial cell nor increased cyclic AMP is the mechanism for cardiac hypertrophy. A greater increase in the alpha 1-receptor, rather than in the beta-receptors, in both models implies that a disproportional augmentation of the alpha 1-receptor system may play an important role in the development of myocardial hypertrophy.

Animals↗
PubMed1989

[Role of adrenergic receptor system in canine left ventricular hypertrophy].

Although sympathetic nervous system and catecholamines have been postulated to play an important role in the development of myocardial hypertrophy, the precise mechanism is still ill-defined. We then developed two experimental canine models; 12 dogs with surgical cardiac denervation by the method of Geis et al, inducing up-regulation of myocardial adrenergic receptors, and 12 dogs with chronic infusion of subhypertensive dose of norepinephrine (NE) at a rate of 0.04 mg/kg/day. After two months, both models induced myocardial hypertrophy, as indicated by significant increases in left ventricular (LV) wall thickness and cell diameter as compared with 14 sham-operated control dogs. Cardiac denervation remarkably depleted myocardial NE contents, while plasma NE remained unchanged. Both alpha-1 and beta receptors were unregulated, Bmax increasing by 90% and 50% respectively. Decrease in myocardial cyclic-AMP content was relatively small as compared with the marked reduction in myocardial NE, probably by the compensatory augmentation of beta receptor system activity. Chronic NE infusion also reduced myocardial NE content possibly due to stimulation of presynaptic alpha-2 receptor inhibiting NE synthesis and release. Number of alpha-1 and beta receptors also increased by 90% and 30% respectively, while myocardial cyclic-AMP content remained unchanged. These observations indicate that neither direct stimulation of NE on the myocardial cell nor increased in cyclic-AMP is the mechanism for cardiac hypertrophy in both models.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[Hypertrophic cardiomyopathy with left ventricular dilatation].

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

On the molecular organization, diversity and functions of desmosomal proteins.

After a brief review of epithelial cell junctions, the authors describe a series of observations and experiments directed toward elucidating the molecular organization and functions of the proteins of desmosomes (maculae adherentes). Their immunofluorescence observations reveal differences between the proteins of junctional complex and other desmosomes of the same cells. Quantitative immuno-localization studies are described using protein A-colloidal gold markers and a series of monospecific, polyclonal antibodies directed against cytokeratins and four desmosomal protein families. It is shown that desmoplakin III (about 81 kDa) is restricted to the desmosomal cytoplasmic plaque, which possesses outer and inner dense zones. Desmoplakins I/II (about 240 kDa and 210 kDa) extend across the same range and beyond into the intermediate filament-rich cytoplasm. Two glycoprotein families, desmoglein I (DGI; about 150 kDa) and desmoglein II (DGII; about 97-118 kDa), extend from the desmosomal midline (or beyond) across the desmoglea (intercellular space), through the plasma membrane and across both layers of the plaque, terminating near its cytoplasmic border. Cytokeratins do not extend into the desmosome. With new procedures utilizing guanidine HCl for preparing and fractionating desmosomal proteins, DGII has been purified to homogeneity. DGII, DGI and a third protein are all shown to bind Ca2+, which is known to promote desmosome assembly.

Animals↗
PubMed1987

Mouse T-cell-dependent proliferative response to syngeneic serum modified with various agents used in root canal therapy.

Syngeneic sera modified with seven agents were used as the immunogens to induce lymph-node cell proliferation in C57BL/6 mice. Immunogenicity could be conferred upon tolerated syngeneic serum by modification with diluted tincture of iodine (J) or formocresol (FC). However, the synergistic action of formalin and cresol appeared to be an indispensable condition in acquiring immunogenicity of FC-modified syngeneic serum (FC-MS). Moreover, immunological tolerance to native serum was not terminated after injection of J-MS or FC-MS. These proliferative functions were dependent on Lyt-1 cells. The cells directed against J- or FC-modified syngeneic serum were specific for the immunizing hapten J or FC. However, they did not recognize the hapten per se, but rather, the conjugate-specific determinants, i.e. these contributed by both the hapten and the self-carrier.

Animals↗
PubMed1987

[Hypertrophic cardiomyopathy manifesting different modes of illness: report of three cases].

Three cases of hypertrophic cardiomyopathy (HCM) which presented with different modes of appearance of left ventricular hypertrophy are reported. Case 1: A 24-year-old man had three relatives with HCM. At 13 years of age, he showed no electrocardiographic or echocardiographic abnormalities characteristic of HCM. During the ensuing 11 years, he developed asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM), with right bundle branch block and T-wave inversion. Cardiac catheterization confirmed the diagnosis of hypertrophic obstructive cardiomyopathy by demonstrating an intraventricular pressure gradient of 25 mmHg. These observations indicate that this case developed abnormal hypertrophy during adolescence on the basis of genetic predisposition of an autosomal dominant trait. Case 2: A 51-year-old woman had three proven and three possibly affected relatives. At 35 years of age, she had a normal electrocardiogram, although the echocardiogram was not available. Now, 16 years later, she had developed ASH with abnormal Q-waves and was diagnosed as having non-obstructive HCM. These suggest that ASH can be manifested as late as during middle-age, even in those with genetic predisposition. Case 3: A 47-year-old woman was diagnosed as having hypertension and her blood pressure was 190/100 mmHg at 40 years of age, though she had no abnormal electrocardiographic findings and heart murmurs. Now, at 47 years of age, she had developed T-wave inversion, ASH, SAM, and an intraventricular pressure gradient of 50 mmHg. Thus, her ASH appeared during middle-age, and was probably provoked by hypertension, though a complete family survey could not be conducted. These three patients' findings indicate that there may be various modes of appearance of left ventricular hypertrophy in HCM. In the majority of patients with genetic predisposition, abnormal hypertrophy may develop during adolescence as in Case 1. In others, it may develop in middle-age, as it did in Case 2. The disease spectrum of HCM may additionally include those who develop abnormal hypertrophy during middle-age, following provocation by hypertension, as in Case 3.

Adult↗
PubMed1986

Elicited antibody nature of human monoclonal protein with anti-streptolysin O activity--analysis with monoclonal anti-idiotype antibody.

Sera from 7 patients with multiple myeloma having antistreptolysin O (ASO) activity in high titers were detected by a streptolysin O (SLO) inhibition assay. However, activity was in low titer when assayed by a passive agglutination assay. The discrepancy between these 2 assays raised some doubts as to whether these monoclonal proteins (M.protein) bond to SLO in the same manner as elicited antibodies. Immunochemical analysis and idiotope analysis using monoclonal antibody to one of these M.proteins strongly suggest that M.protein with ASO activity bind to SLO in a manner similar to elicited antibody. The discrepancy between the 2 assays might be due to differences in the antigenic structure of different forms of the SLO molecule.

Antibodies↗
PubMed1985

Comparison of beta-glucan structures in a cell wall mutant of Saccharomyces cerevisiae and the wild type.

A mutant of Saccharomyces cerevisiae defective in the cell wall beta-glucan structure was obtained. The mutant cells are extremely sensitive to (beta 1-3)-glucanase digestion and mild alkali treatment. Structural analysis revealed that the alkali-insoluble, skeletal glucan from wild type cells contains two components, a (beta 1-3) linked glucan with a laminated structure, and a highly branched glucan containing predominantly (beta 1-6) linkages. The mutant cells lack the latter component.

Cell Wall↗
PubMed1983

Unusual monoclonal DNA binding immunoglobulin.

The monoclonal antibodies directed against DNA were produced by somatic cell hybridization with parental cells (SP-2) and spleen cells from nonimmunized autoimmune MRL/lpr mice. The immunoglobulins were recovered from the culture supernatant from hybridoma by a solid immunoadsorbent and antibody immunoprecipitation. The results from the specificities of DNA binding monoclonal immunoglobulins suggest that the antibodies to DNA have the antibody combining sites for both epitope of double stranded helix and base of DNA and support the concept of the multiple antigen binding potentials of the hybridoma autoantibodies.

Animals↗
PubMed1982

Ultrastructural and biochemical identification of Con A receptors in the desmosome.

Correlated ultrastructural and biochemical methods were used to identify and localize Concanavalin A (Con A) receptors in the desmosomes of bovine epidermis. Specific carbohydrate residues were labeled with ferritin-Con A in thin sections of tissue embedded in a hydrophilic resin. Quantitative mapping of ferritin distribution in labeled desmosomes revealed that Con A receptors are localized in the intercellular zone and concentrated along the desmosomal midline or central dense stratum. Labeling was almost entirely absent when sections were treated with ferritin-Con A in the presence of 0.1 M alpha-methyl mannoside, a hapten-inhibitor of Con A. "Whole" desmosomes and desmosomal intercellular regions (desmosomal "cores") were purified from bovine muzzle epidermis. Sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis reveals a limited number of major desmosomal protein constituents. Certain of these are glycoproteins and are greatly enriched in the core fraction. Almost all the desmosomal glycoproteins are intensely labeled when electrophoretic gels of whole desmosome or core fractions are exposed to fluorescent Concanavalin A.

Animals↗