Biomedical subjects

K Ohta

Publications and source records attributed to K Ohta.

At least 397 records · Page 22Linked to original sources

PubMed1995

Plexin: a novel neuronal cell surface molecule that mediates cell adhesion via a homophilic binding mechanism in the presence of calcium ions.

Plexin (previously referred to as B2) is a neuronal cell surface molecule that has been identified in Xenopus. cDNA cloning reveals that plexin has no homology to known neuronal cell surface molecules but possesses, in its extracellular segment, three internal repeats of cysteine clusters that are homologous to the cysteine-rich domain of the c-met proto-oncogene protein product. The exogenous plexin proteins expressed on the surfaces of L cells by cDNA transfection mediate cell adhesion via a homophilic binding mechanism, under the presence of calcium ions. Plexin is expressed in the receptors and neurons of particular sensory systems. These findings indicate that plexin is a novel calcium-dependent cell adhesion molecule and suggest its involvement in specific neuronal cell interaction and/or contact.

Amino Acid Sequence↗

PubMed1995

Favorable course of steroid-responsive nephrotic children with mild initial attack.

The course and prognosis of idiopathic nephrotic syndrome has thus far not been found to be predicted from the severity of the manifestations at the onset. Among 66 steroid-responsive nephrotic children, eight were asymptomatic without edema and identified by chance proteinuria on a urinary screening program. The selectivity index for proteinuria (a clearance ratio of IgG to transferrin) was 0.10 or less in all of the five children examined. All of the eight children responded quickly to the prednisolone therapy. Grades of proteinuria and hypoalbuminemia were lower in the asymptomatic children than in the symptomatic children who presented with edema. Median proteinuria levels were 2.0 versus 4.2 g/day/m2 (P < 0.01), respectively, and mean serum albumin levels were 2.2 +/- 0.3 versus 1.8 +/- 0.4 g/dl (mean +/- SD; P < 0.01), respectively. None of the eight asymptomatic children relapsed for at least one year after completion of the prednisolone treatment, while, in contrast, 30 of 58 symptomatic nephrotic children relapsed during the same one-year period (P < 0.01). These findings suggest that, among steroid-responsive nephrotic children, those with mild manifestations without edema may have a milder disease and show an extremely favorable clinical course.

Child↗

PubMed1995

Point mutations in the thyrotropin receptor in human thyroid tumors.

The mechanism of the impaired response to thyrotropin (TSH) in thyroid tumor cells was investigated by searching for structural changes in the TSH receptor (TSH-R) in neoplastic thyroid tissues in humans. Total RNA was prepared from 34 thyroid tissue samples (four normal, six adenoma, six follicular cancer, and 18 papillary cancer) and reverse- transcribed into single-stranded cDNA, which was then used as a template for the polymerase chain reaction and subjected to single-strand conformation polymorphism (SSCP) analysis. Two fragments, FRAG (468-692) (nucleotides 468 to 692, corresponding to the mid-portion of the receptor extracellular domain) and FRAG (2044-2295) (nucleotides 2044 to 2295, corresponding to the COOH-terminal, cytoplasmic domain of the TSH-R cDNA) showed differences in electrophoretic mobility among the various thyroid tissue samples. Direct sequencing revealed Phe197 (TTC) --> Ile(ATC), and Asp219 (GAT) --> Glu(GAG) substitutions in FRAG (468-692) from two papillary cancers. Three types of substitution were identified in FRAG(2044-2295): Asn715 (AAC) --> Asp(GAC) from one papillary cancer, Lys723 (AAG) --> Met(ATG) from one papillary cancer, and Asp 727 (GAC) --> Glu(GAG) from one normal tissue sample, one follicular cancer, and four papillary cancers. These results suggest that there exist structural changes in TSH-R in some cases of thyroid neoplastic tissue.

Adenoma↗

PubMed1995

Immunoblot analysis of cellular expression of Bcl-2 family proteins, Bcl-2, Bax, Bcl-X and Mcl-1, in human peripheral blood and lymphoid tissues.

The ability of Bcl-2 to inhibit apoptotic cell death is well established. Several homologues of the bcl-2 gene, such as bax, bcl-x or mcl-1, have recently been identified. Like Bcl-2, both Bcl-XL and Mcl-1 appear to function as repressors of apoptotic cell death, whereas Bax facilitates it, indicating possible interactions among them in the control of cellular survival. To investigate the in vivo role of expression of bcl-2 gene family products, immunoblot analysis using corresponding specific antisera was performed for peripheral blood cells and some lymphoid tissues in humans. We demonstrated that all Bcl-2 family proteins were expressed at various levels in hematolymphoid cell subpopulations isolated from peripheral blood, tonsil, spleen and thymus. Lymphoid expression of Bcl-2 family proteins tended to increase following activation, but declined with time in culture. Loss of Bcl-2 in cultured lymphoid cells was especially marked. Sole expression of Bax, but not other members of the Bcl-2 family, was observed on neutrophils, seemingly reflecting their shortest life-span among blood leukocytes. The results support the notion that a balance of expression of Bcl-2 family proteins may regulate the life and death of hematolymphoid cells at different stages of cell differentiation and activation.

Acute Disease↗

PubMed1995

Bilateral inguinal scrofuloderma during steroid therapy in a patient with bullous pemphigoid.

This report described a case of scrofuloderma that developed in the bilateral inguinal regions during treatment of bullous pemphigoid with systemic corticosteroid. Analysis of the literature on scrofuloderma between 1978-1993 disclosed that the number of cases with extracervical involvement are increasing. Immunosuppression could disseminate tuberculous focuses, resulting in extracervical involvement of SD connected with the underlying extrapulmonary tuberculous lesions.

Aged↗

PubMed1995

Delineation of producing ability of IgG and IgA subclasses by naive B cells in newborn infants and adult individuals.

Neonatal B cells with the naive (sIgD+) phenotype are able to generate IgG- and IgA-producing cells as well as IgM production in the presence of memory CD4+ T cells expressing L-selectin (CD62L) in pokeweed mitogen-stimulated cultures. We used this system to examine comparatively the ability of naive B cells to produce IgG and IgA subclasses in newborn infants and adult individuals. Naive B cells were enriched from both donors on the basis of sIgD positivity, and memory (CD45RO+) CD4+ T cells with CD62L expression were isolated from adults. We here demonstrate some differences in profiles of IgG and IgA subclass production between neonatal and adult naive B cells. In neonatal B cells, IgG1 and IgG3 were predominantly produced, but IgG2 and IgG4 production was virtually absent. Similar to neonatal B cells, adult naive B cells produced mainly IgG1 and IgG3, although memory (sIgD-) B cells from adults secreted all of the IgG subclasses. It should be noted that low but detectable levels of IgG2 and IgG4 were found in adults' naive B cell cultures. Although IgA produced by neonatal B cells was exclusively IgA1, IgA2-secreting cells were identifiable in adult naive B cells. The results suggest that further class switch of naive B cells to IgG2, IgG4 and IgA2 in addition to IgG1 and IgG3 may be controlled by their own age-dependent maturation process.

Adult↗

PubMed1995

Expression of sarcoplasmic reticulum Ca2+ -ATPase mRNA in the hypertrophied heart of young spontaneously hypertensive rats.

1. Recent evidence indicates that cardiac hypertrophy induced by pressure overload is associated with a decrease in sarcoplasmic reticulum (SR) Ca2+ -ATPase of myocytes, which may contribute to a diastolic dysfunction of the heart by causing intracellular Ca2+ overload. To elucidate whether or not this is also the case in genetic hypertension, we examined cardiac mRNA levels of SR Ca2+ ATPase in 11 week old spontaneously hypertensive rats (SHR) by northern blot analysis. 2. Furthermore, to test the effects of short-term inhibition of the renin-angiotensin system on its expression, we treated 10 week old SHR with angiotensin-converting enzyme inhibitors (alacepril and imidapril) or an AT1 receptor antagonist (SC-52458) for 7 days. 3. Though the left ventricular weight of SHR was significantly higher than that of Wistar-Kyoto (WKY) rats (277 +/- 6 vs 237 +/- 4 mg/100 g bodyweight, respectively, P < 0.05), the level of SR Ca2+ -ATPase mRNA showed no difference between SHR and WKY at this age. 4. Moreover, the aforementioned three drugs did not at all affect the SR Ca2+ -ATPase expression of SHR. 5. Thus, the expression of SR Ca2+ -ATPase was not down-regulated in the heart of 11 week old SHR, and seemed not to be mediated by angiotensin AT1 receptor at this age. Since some evidence on pressure-overloaded cardiac hypertrophy indicate that the decrease in SR Ca2+ -ATPase expression occur in prominent hypertrophy and in the failured heart, further studies on cardiac SR Ca2+ -ATPase expression in more aged SHR will be required.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

Suppression of vascular transforming growth factor-beta1 and extracellular matrix gene expressions by cilazapril and nifedipine in hypertensive rats.

1. We investigated the protective effects of an angiotensin-converting enzyme inhibitor (ACEI) and a Ca antagonist on vascular injury in hypertension. 2. Thirteen week old stroke-prone spontaneously hypertensive rats (SHRSP) were orally given cilazapril (ACEI 10 mg per kg day) or nifedipine (Ca antagonist 30 mg kg per day) for 12 weeks. After the treatment, the aorta and superior mesenteric artery were excised, and subjected to the extraction of RNA. mRNA levels for the transforming growth factor-beta1 (TGF-beta1) and extracellular matrix components such as fibronectin (FN), collagen type I (CoI), type III (CoIII) and type IV (CoIV) and laminin, were measured by northern blot analysis, using each specific cDNA probe. 3. In the mesenteric artery of SHRSP, TGF-beta1 mRNA levels were increased compared with Wistar-Kyoto (WKY) rats, being accompanied by a significant increase in mRNA levels for FN, CoI, CoIII, CoIV and laminin. In the aorta, only TGF-beta1 and fibronectin mRNAs were increased in SHRSP, but collagen and laminin were not increased. 4. Both cilazapril and nifedipine, to similar extents, suppressed the above mentioned increased gene expressions in both mesenteric artery and aorta, being associated with the improvement of vascular hypertrophy. 5. These results suggest that TGF-beta1 may be responsible for smooth muscle cell hypertrophy and the increased deposition of extracellular matrix in hypertensive blood vessels. Both cilazapril and nifedipine may lessen hypertensive vascular thickening, by suppressing the gene expression of TGF-beta1 and extracellular matrix.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

[Species and serovar-distribution, and drug-resistance of Shigella strains isolated from imported and domestic cases from 1990 through 1994 in Tokyo].

A total of 446 Shigella strains consisting of 336 imported and 110 domestic strains isolated in Tokyo from 1990 to 1994 were examined for their species and serovar-distribution, and their drug-resistance. In both imported and domestic strains, S. sonnei was found to be the most prevalent species, followed by S. flexneri. In imported strains, however, the isolation frequency of S. flexneri, S. boydii and S. dysenteriae were higher than that of domestic strains, and the serovar of each species was distributed in a wider range than that of the domestic strains. Provisional new serovar Shigella strains were isolated from 8 imported cases and 2 domestic cases. The drug-resistance-test using 9 drugs (CP, TC, SM, KM, ABPC, ST, NA, FOM, and NFLX) showed that 82.7% of the imported strains and 89.1% of the domestic strains were resistant to any drugs examined. Drugs of a high resistant rate were SM, TC, ST for the both groups. Drug-resistance-patterns of the resistant isolates varied to 21 types. Among those, a triple drug-resistance-type with TC SM ST was found the most frequently in both groups. None of the strains were resistant to FOM or NFLX.

Anti-Bacterial Agents↗

PubMed1995

[Regarding the Shigella flexneri 4 strains isolated in recent years].

A total of 38 strains of Shigella flexneri 4, 14 of which were subserotype 4a but 24 of which were of an undecided subserotype, isolated in recent years, were studied for their biochemical and serological characteristics, and drug susceptibility. Among the biochemical characteristics examined, 21 of the 38 strains (55.3%) were mannitol negative biotype and utilized sodium acetate, meanwhile, 17 of the mannitol positive strains did not utilize sodium acetate. The results of serological tests showed that 22 of the 24 strains, were of an undecided subserotype, basically subserotype 4a. Drug susceptibility was tested for nine drugs (CP, TC, SM, KM, ABPC, ST, NA, FOM and NFLX). Fifteen of the 17 mannitol positive strains (88.2%) and 12 of the 21 mannitol negative ones (57.1%), were found to be resistant to the 5 drugs, such as CP, TC, SM, ABPC or ST. None of the strains were resistant to KM, NA, FOM or NFLX.

Anti-Bacterial Agents↗

PubMed1995

Quantitation of hepatitis C viral RNA in liver and serum samples using competitive polymerase chain reaction.

AIMS: To investigate whether the amount of hepatitis C viral RNA (HCV-RNA) in liver and serum can predict the effectiveness of interferon treatment in patients with chronic hepatitis C. METHODS: The amount of HCV-RNA in frozen liver tissues and sera of 22 patients with chronic hepatitis C was determined before and after interferon alfa treatment by the competitive reverse transcriptional polymerase chain reaction method. RESULTS: Patients with small amounts of HCV-RNA in serum before treatment showed a significantly more effective response to interferon treatment. After treatment, HCV-RNA disappeared from both the liver and serum of all patients who sustained complete response (n = 11); in contrast, HCV-RNA decreased but persisted in the liver of all those who relapsed after cessation of treatment (n = 11). CONCLUSIONS: The elimination of hepatitis C virus from the liver as well as from the serum seems to be essential for sustained remission. The quantitation of HCV-RNA in liver biopsy specimens obtained after treatment would be a highly accurate predictor of whether relapse is likely to occur.

Base Sequence↗

PubMed1995

Induction of eosinophil cytokine generation by chemoattractants.

Recent studies have shown that eosinophils are capable of generating and releasing cytokines, illustrating a novel biologic aspect of eosinophils in regulating allergic inflammation by either autocrine or paracrine mechanisms. The effect of chemotactic agonists on eosinophil cytokine generation was examined by determination of interleukin-8 (IL-8) as a main parameter. Both complement C5a and N-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulated eosinophils to release IL-8, but platelet activating factor (PAF) did not exert any significant effects. The generation of IL-8 by chemoattractants was absolutely dependent on the presence of cytochalasin B. Pertussis toxin completely attenuated C5a- and FMLP-induced IL-8 production, indicating the involvement of pertussis toxin-sensitive G proteins in the signal transduction process. In situ hybridization showed that both C5a and FMLP promoted eosinophil IL-8 production via transcriptional gene activation. Furthermore, C5a and FMLP, but not PAF, induced significant secretion of granulocyte-macrophage colony-stimulating factor from eosinophils. These results indicate that C5a and FMLP stimulate eosinophils to elaborate cytokines, which could be an important mechanism in the regulation of allergic inflammation.

Actin Cytoskeleton↗

PubMed1995

Angiotensin II induces cardiac phenotypic modulation and remodeling in vivo in rats.

Cardiac phenotypic modulation and remodeling appear to be involved in the pathophysiology of cardiac hypertrophy and heart failure. We undertook this study to examine whether angiotensin II (Ang II) in vivo, independent of blood pressure, contributes to cardiac phenotypic modulation and remodeling. A low dose (200 ng/kg per minute) of Ang II was continuously infused into rats by osmotic minipump for 24 hours or 3 or 7 days to examine the effects on the expression of cardiac phenotype-related or fibrosis-related genes. This Ang II dose caused a small and gradual increase in blood pressure over 7 days. Left ventricular mRNAs for skeletal alpha-actin, beta-myosin heavy chain, atrial natriuretic polypeptide, and fibronectin were already increased by 6.9-, 1.8-, 4.8-, and 1.5-fold, respectively, after 24 hours of Ang II infusion and by 6.9-, 3.3-, 7.5-, and 2.5-fold, respectively, after 3 days, whereas ventricular alpha-myosin heavy chain and smooth muscle alpha-actin mRNAs were not significantly altered by Ang II infusion. Ventricular transforming growth factor-beta 1 and types I and III collagen mRNA levels did not increase at 24 hours and began to increase by 1.4-, 2.8-, and 2.1-fold, respectively, at 3 days. An increase in left ventricular weight occurred 3 days after Ang II infusion. Treatment with TCV-116 (3 mg/kg per day), a nonpeptide selective angiotensin type 1 receptor antagonist, completely inhibited the above-mentioned Ang II-induced increases in ventricular gene expressions and weight. Hydralazine (10 mg/kg per day), which completely normalized blood pressure, did not block cardiac hypertrophy or increased cardiac gene expressions by Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

PubMed1995

Transforming growth factor-beta 1 expression and phenotypic modulation in the kidney of hypertensive rats.

We have previously reported that renal mRNA levels for transforming growth factor-beta 1, fibronectin, and collagens were increased in 32-week-old stroke-prone spontaneously hypertensive rats (SHRSP) with severe nephrosclerosis. To elucidate the mechanism of hypertension-induced nephrosclerosis, we examined gene expression and localization of transforming growth factor-beta 1 and cellular phenotype in the kidney of 25-week-old SHRSP with moderate renal damage. Renal mRNA was measured by Northern blot analysis. The localization of transforming growth factor-beta 1 and cellular phenotype was determined by immunohistochemistry. In the kidney of 25-week-old SHRSP, renal transforming growth factor-beta 1 mRNA was elevated compared with Wistar-Kyoto rats (WKY), whereas renal collagen mRNAs of SHRSP were not increased. Immunoreactive transforming growth factor-beta 1 in SHRSP was mainly localized in glomerular cells. Furthermore, alpha-smooth muscle actin and desmin were significantly expressed in SHRSP glomerular cells, in contrast to negligible expression of these proteins in WKY. alpha-Smooth muscle actin staining was also observed in interstitial cells, and vimentin, another phenotypic marker, was expressed in atrophic tubular cells of SHRSP, despite no staining of these proteins in WKY. Furthermore, all these phenotypic changes in SHRSP were associated with increased cell proliferation, as shown by the increased number of proliferating cell nuclear antigen-positive cells. Treatment of SHRSP with cilazapril and nifedipine (from the age of 13 to 25 weeks) prevented the increase in transforming growth factor-beta 1 expression and the cellular phenotypic modulation and was accompanied by a reduction of urinary albumin excretion and inhibition of cell proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

PubMed1995

Immunohistochemical identification and characterization of smooth muscle-like cells in idiopathic pulmonary fibrosis.

The interstitium of the fibrotic lung possesses a contractile capability that is unusual for nonmuscle tissue. An abundance of actin filament-laden cells have been demonstrated in animal and human studies of fibrotic lung tissue and have frequently been termed myofibroblasts. The origin and significance of these cells remain unclear. Proliferation of cells with the capability to contract and thereby generate force within the parenchyma is potentially a significant contribution to the increased lung elastic recoil of advanced pulmonary fibrosis. In the present study, we immunohistochemically examined these intermediate phenotypes of filament-laden cells with a focus on those expressing smooth muscle-associated isoforms of actin. The monoclonal antibody HHF35 was used to study the presence and distribution of cells expressing alpha and gamma smooth muscle actin in idiopathic pulmonary fibrosis (IPF). Adjacent sections of tissue from open lung biopsies of eight patients with IPF were stained with a pentachrome stain and with multiple antibodies (HHF35, polyclonal anti-actin, anti-vimentin, anti-keratin, anti-procollagen I, and anti-von Willebrand Factor VIII) to identify specific cell types. In addition, anti-laminin antibody was used to stain basement membrane. Many tightly packed, HHF35-reactive cells were found to be architecturally dissociated from airways and blood vessels in all eight patients with IPF. Some HHF35-reactive bundles were composed of loosely associated cells, and single smooth muscle cell types (SMC) were distributed in the fibrotic interstitium. Interestingly, some of the SMC were distinctly negative for anti-laminin and stained atypically with pentachrome. Moreover, some single SMC were found to be anti-procollagen type I reactive with double staining technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

PubMed1995

Cardiac hypertrophy-related gene expression in spontaneously hypertensive rats: crucial role of angiotensin AT1 receptor.

Angiotensin converting-enzyme inhibitors (alacepril and imidapril) or an AT1-receptor antagonist (SC-52458) was administered to 10-week-old spontaneously hypertensive rats (SHR) for 7 days, and cardiac mRNA levels for contractile proteins and atrial natriuretic polypeptide (ANP) were comprehensively measured. The expression of skeletal alpha-actin and ANP was selectively enhanced in the heart of vehicle-treated SHR compared with Wistar-Kyoto rats (WKY), thereby suggesting that the phenotypic modulation of myocytes occurred at the early stage of hypertension. The above-mentioned three drugs similarly suppressed these enhanced gene expressions, nearly to the control levels. In contrast, although the treatment with hydralazine lowered the blood pressure of SHR similarly, hydralazine did not suppress ANP expression at all and only partially suppressed skeletal alpha-actin. Moreover, alacepril did not affect these gene expressions in WKY. Thus, AT1 receptor may be crucial for phenotypic modulation in the heart of SHR.

Angiotensin Receptor Antagonists↗

PubMed1995

Cerebral sparganosis mansoni--case report.

An 80-year-old male with paresis of the right upper extremity underwent surgery for a suspected metastatic brain tumor. A live Sparganum mansoni worm was removed from the parietal lobe through a left parietal craniotomy. Retrospective evaluation of magnetic resonance (MR) images revealed ipsilateral ventricular dilatation, despite the presence of a mass lesion resembling a metastatic brain tumor. This interesting MR imaging finding is an important point for differentiating between a brain tumor and cerebral sparganosis.

Aged↗

PubMed1995

Immunohistochemical investigations of parvalbumin localization in the skeletal muscle fibers of rats.

Parvalbumin (PA) is a water soluble, low-molecular weight, calcium-binding protein which has been thought to be involved in the relaxation of skeletal muscle fibers. Although it is well known that PA concentrations are higher in fast twitch fiber than slow twitch fiber, the localization of PA within the cytoplasm of single muscle fibers is still unknown. The present study, therefore, was undertaken to clarify the PA localization by immunohistochemical methods using the confocal laser scanning microscope (CLSM) and transmission electron microscope (TEM). Wistar strain male rats were fixed by vascular perfusion with 4% paraformaldehyde solution, and the extensor digitorm longus muscle was dissected out. For fluorescent antibody examination, these specimens were quickly frozen in melting isopentan and sections were cut using a cryostat at -25 degrees C. These sections were incubated in anti-PA and anti-Troponin (TR) respectively, and then exposed to Texas-Red- and FITC-labelled secondary antibodies. For TEM study, the pre-embedding method was used. Fluorescent immunohistochemical study has clearly shown that both PA and TR are located intimately in the I-band of the skeletal muscle fibers. The finding by the immunofluorescent study correlated well with those which have been seen at the ultrastructural level. The fact that PA is located in close proximity to TR is considered to be very reasonable when we consider it in terms of the muscular contraction-relaxation cycle.

Animals↗