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Biomedical subjects

S Hino

Publications and source records attributed to S Hino.

At least 73 records · Page 4Linked to original sources
PubMed1995

Exercise-induced changes in the expression of surface adhesion molecules on circulating granulocytes and lymphocytes subpopulations.

This study examined the relationship between exercise-induced changes in the concentration of circulating immunocompetent cells and their surface expression of adhesion molecules: L-selectin (CD62L) and three beta 2-integrins [LFA-1(CD11a/CD18), Mac-1 (CD11b/CD18), and p150/95(CD11c/CD18)]. Eight young male volunteers exercised on a cycle ergometer for 60 min at 60% maximal oxygen uptake. Peripheral blood samples, collected every 30 min throughout exercise and during the 2-h recovery period, were used for flow-cytometric analysis. The experimental results were compared with control data obtained ever 60 min at corresponding times of the nonexercise day. The exercise regimen induced a granulocytosis and a lymphocytosis, mainly due to an elevation of CD8+ and CD16+ cells. During recovery, a further granulocytosis occurred but accompanied by a lymphopenia. The increased CD8+ cell-count during exercise was characterized by a selective mobilization of the CD62L- and CD11ahigh cells, i.e. primed CD8+ cells. A postexercise suppression of CD4+ cell-count was derived only from CD62L+ cells. The CD11b+ and CD11c+ lymphocytes also increased during exercise, largely attributable to an increase in CD16+ cells which co-expressed CD11b and CD11c molecules. The CD62L surface density of granulocytes increased significantly during recovery. This resulted from a selective influx of CD62Lhigh granulocytes into the circulation. There were no significant changes in per-cell density of the three beta 2-integrins on granulocytes and lymphocytes throughout the experimental period. These results suggest that the cell-surface expression of CD62L (and CD11a) molecules is associated with the differential mobilization of CD8+ cells during exercise, the postexercise suppression of CD4+ cell-counts and the granulocytosis following exercise.

Adult↗
PubMed1995

Two independent outbreaks of measles in partially vaccinated junior high schools in Tottori, Japan.

We analyzed retrospectively a relative risk of measles attacks in vaccinated vs. unvaccinated students using two independent outbreaks in Japan. The first involved 33/328 (10%) students where 64% students and 30% measles cases had been vaccinated. The second involved 27/241 (11%) students where 81% students and 48% measles cases had been vaccinated. The attack rates of vaccinated vs. unvaccinated students were significantly low (p < 0.001), but they accounted 25% in both episodes. The statistically significant clinical features among vaccinated and unvaccinated cases included the average duration of fever, 5.16 +/- 1.71 vs. 6.67 +/- 2.19 days (p = 0.01) and the incidence of complications, 0 vs. 25%, respectively. These results suggested that the measles in vaccinated cases were mostly due to secondary failures.

Adolescent↗
PubMed1995

Dependency of antibody titer on provirus load in human T lymphotropic virus type I carriers: an interpretation for the minor population of seronegative carriers.

To evaluate the prevalence of seronegative carriers of human T lymphotropic virus type I (HTLV-I), buffy coat samples from 1015 Okinawan high school students were tested by immunoassays and nested polymerase chain reaction (PCR). Among 17 HTLV-I carriers, 1 person who was seronegative and 1 who was PCR-negative were identified. gag and tax/rex PCR titers correlated with each other (r = .92; P < .001). Of the 17 carriers, 14 (82%) had high virus loads (geometric averages, 522 gag and 703 tax/rex copies/micrograms of DNA; 95% confidence intervals, 38-7260 and 75-6594, respectively). Carriers with low virus loads had < or = 2.2 gag copies. In the high-virus-load group, the gag PCR titers correlated with the antibody titers (r = 0.88; P < .001). The regression line intersected the minimum antibody detection level at 35 gag copies/micrograms of DNA. These results suggest that a small percentage of carriers may be seronegative.

Adolescent↗
PubMed1995

Association between maternal antibodies to the external envelope glycoprotein and vertical transmission of human T-lymphotropic virus type I. Maternal anti-env antibodies correlate with protection in non-breast-fed children.

Vertical transmission of human T-lymphotropic virus type I (HTLV-I) depends primarily on breast-feeding; substitution of bottle-feeding has reduced the transmission rate from 20% in breast-fed children to 3% among bottle-fed. To determine the correlates of transmission for long breast-feeding (> or = 6 mo), short breast-feeding (< 6 mo), and bottle-feeding mothers, the antibody titers of transmitter (T) mothers and non-transmitter (nT) mothers were analyzed by using synthetic and recombinant epitopes representing the immunodominant epitopes of gag (Gag1a, r24), env (Env1/5, MTA1, RE3), and tax (Tax8/22-24) proteins. Seroreactivity to gag and tax epitopes was not significantly different except for anti-r24 antibody titer, which was significantly higher among T-mothers (geometric mean 134) when compared with nT-mothers (62) in the long-feeding group (P < 0.001). Profiles of antibody titers against env epitopes were different. Within the long-feeding group, Env1/5, MTA1, and RE3 titers were significantly higher among T-mothers (258, 1,476, and 738, respectively) when compared with nT-mothers (106, 279, and 320, respectively) (P < 0.01 for all three epitopes). In contrast, within the bottle-feeding group, antibody titers to Env1/5 (269) and RE3 (418) among nT-mothers were significantly higher than those among T-mothers (80 and 113, respectively) (P < 0.01). These data confirm that high-titered anti-HTLV-I antibodies in the long-feeding group correlate with milk-borne transmission of HTLV-I and, more importantly, imply that maternal anti-env antibodies may reduce the risk of non-milkborne infection.

Amino Acid Sequence↗
PubMed1994

HTLV-I proviral DNA in umbilical cord blood of babies born to carrier mothers.

Human T-lymphotropic virus type I (HTLV-I) in cord blood raises the possibility of intrauterine transmission as an alternative pathway to transmission via breast milk. However, none of 7 children with HTLV-I proviral DNA positive cord blood had seroconverted by 24-48 months. Contamination of cord blood by maternal blood was precluded on the basis of viral load and IgA concentration. Thus cord blood proviral DNA is not a hallmark of intrauterine infection. Moreover, none of the cord blood samples of 9 formula-fed children later confirmed to be infected was positive for HTLV-I, indicating that intrauterine infection is not a likely candidate as an alternative pathway.

Breast Feeding↗
PubMed1994

Altered expression of a novel cellular gene as a consequence of integration of human T cell lymphotropic virus type 1.

By analysing a genomic DNA clone derived from the human T cell lymphotropic virus type 1 (HTLV-1)-infected cell line, TL-Su, we found that an integrated HTLV-1 provirus interrupted the poly(A) signal-containing exon of a novel gene, RY-1. Nucleotide sequence analysis of a cDNA derived from Jurkat cells revealed that the normal RY-1 mRNA could encode a novel protein that has an unique primary structure, suggesting that a nucleic acid binding property was involved. Proviral integration led to an accumulation of aberrant RY-1 mRNA species in the cells. All the aberrant RY-1 cDNAs derived from TL-Su cells terminated at the poly(A) site of the R region of the HTLV-1 long terminal repeat and initiated in the intron, approx. 800 bp upstream from the putative second exon. Furthermore, another intron, downstream from this position, remained unspliced in some of the cDNAs. In addition to the activation by the integrated viral elements of cryptic promoters located upstream, mechanisms involving altered rates of degradation or transport from the nucleus to the cytoplasm of intron-containing RNA were suggested.

Amino Acid Sequence↗
PubMed1994

Expression of human T lymphotropic virus type 1 (HTLV-1) tax/rex gene in fresh bronchoalveolar lavage cells of HTLV-1-infected individuals.

Accumulating evidence has suggested the involvement of HTLV-1 in the inflammatory lesions of various organs, including the lung. However, the causal relationship between HTLV-1 and inflammatory responses in the organs remains to be elucidated. In order to evaluate the expression of HTLV-1 and its effects in the lung, we examined the expression of mRNA for the HTLV-1 tax/rex gene in fresh bronchoalveolar lavage cells (BALC) and peripheral blood mononuclear cells (PBMC) of 23 seropositive individuals, including six patients with HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), by use of an improved method of reverse transcription-polymerase chain reaction (RT-PCR). The tax/rex mRNA was more frequently detected in BALC than in PBMC. All the HAM/TSP patients and eight of 17 carriers without neurological symptoms showed the expression of tax/rex mRNA in the BALC. IgM class antibodies to HTLV-1 were preferentially detected in sera of the tax/rex mRNA-positive individuals. The detection of tax/rex mRNA correlated closely with the presence of lymphocytosis accompanied by an elevated proportion of IL-2 receptor-bearing T cells in the BALC. Our findings indicate the crucial role of viral expression in the inflammatory response in the lung in HTLV-1-infected individuals.

Adolescent↗
PubMed1994

The target antigen of anti-tubular basement membrane antibody-mediated interstitial nephritis.

Our previous studies showed that 54 kD and 48 kD tubular basement membrane (TBM) proteins were the major form of the target antigen involved in anti-TBM antibody-mediated tubulo-interstitial nephritis in humans. In those studies, we isolated the 54 kD glycoprotein (named gp54) from collagenase-digested bovine TBM. NH2-terminal amino acid sequencing indicated that gp54 represented a newly defined glycoprotein. In this study, we further characterized the target antigen, using mouse monoclonal antibodies to gp54 and polyclonal anti-gp54 peptide antibody. Two monoclonal antibodies (H79 and H80) were established, and they reacted, by immunofluorescence, predominantly with the proximal TBM of humans, rabbits, and Wistar, Sprague-Dawley, and Brown-Norway rats, but not with that of Lewis rats. They were also fixed by blotting intensely to the 54 kD component and weakly to the 48 kD component of collagenase-digested human TBM. In vivo transfer of H79 to Wistar rats showed extensive linear binding of mouse IgG to the TBM and the basal membrane of the small intestine; however, no pathologic changes were seen by light microscopy. The anti-gp54 peptide antibody reacted with both the 54 kD and 48 kD TBM components of human TBM. mRNA was prepared from rabbit kidneys, and fractionated to enrich mRNA encoding the 54 kD and 48 kD peptides. On in vitro translation experiments with the mRNA fraction, the 54 kD and 48 kD peptides were immunoprecipitated with anti-gp54 antibodies. These findings indicate that the 54 kD and 48 kD components are encoded with different mRNA, but that they share the same antigenic epitope.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Combined therapy in children and adolescents with IgA nephropathy.

We retrospectively evaluated renal outcome in a total of 38 children and adolescents with IgA nephropathy who were selected for 6-month therapy for clinical (proteinuria > 1 g/m2/24 hour) and pathologic (mesangial proliferation, crescent formation, and tubulo-interstitial changes) features suggestive of progressive renal failure. Seventeen patients (group A) were treated with a combination of prednisolone, cyclophosphamide and dipyridamole, and the remaining patients (21; group B) were treated with the same drugs plus warfarin. All the patients were followed-up for more than 2 years (range 2-10 years, mean 4.8). In both groups, the mean urinary protein excretion value was significantly reduced after the therapy, compared with that at entry into the therapy. The significant reduction continued for up to 6 years in group A and up to 5 years in group B. Creatinine clearance was stable until 5-6 years after the trial in both groups, but 4 patients progressed to end-stage renal failure after that period. Post-therapy biopsy was performed in 14 patients, and was compared with the pre-therapy biopsy. The activity score had improved in both groups, but the chronicity score did not. These results indicate that there was a temporary effect and limited benefit with this treatment of combined drugs for children and adolescents with IgA nephropathy. The additive effect of warfarin was not substantiated.

Adolescent↗
PubMed1994

Intervention of maternal transmission of HTLV-1 in Nagasaki, Japan.

Seroepidemiological and laboratory virological evidences strongly suggested that endemicity of HTLV-1 in Nagasaki Japan depends on maternal infant infections via breast milk. The most obvious way to prove this concept was an intervention study with refraining from breast-feeding by carrier mothers. Most infected babies seroconverted by the age of 12 months, which made it possible to diagnose the infection at the age of 12 months for the statistical purpose. Serology and PCR on both adults and children were consistent each other, suggesting the absence of seronegative carriers. The intervention study revealed that approximately 80% of maternal infection was prevented by refraining from breast feeding by carrier mothers. The remaining fraction of infections in formula-fed babies suggested an alternative infection pathway. Although intrauterine infections has been suggested by others to explain the PCR-positive cord blood samples. However, groups of cord blood-positive children and seroconverted children were distinct each other. Therefore, the presence of HTLV-1 provirus in the cord blood can not be a marker of intrauterine infection. Mothers who infected a child has approximately 10 times higher risk of another infection for the next baby than those who did not.

Breast Feeding↗
PubMed1994

Type IV collagen alpha 5 chain. Normal distribution and abnormalities in X-linked Alport syndrome revealed by monoclonal antibody.

Although the evidence indicates that mutation of the gene for the alpha 5 chain of type IV collagen, alpha 5-(IV), is the primary defect in X-linked Alport syndrome, protein data for the alpha 5(IV) chain with regard to its normal distribution and its distribution in patients with Alport syndrome is lacking. We produced a rat monoclonal antibody (H51) by immunizing rats with a synthetic peptide corresponding to the nonconsensus amino acid sequence of alpha 5(IV) NC1 domain. H51 reacted by Western blotting with 26-kd cationic monomers and associated dimers of human type IV collagen NC1 domain. Immunohistochemical studies demonstrated that in normal human kidney alpha 5(IV) was present in the glomerular basement membrane and basement membranes of the Bowman's capsule and in some tubules (collecting ducts). The alpha 5(IV) chain was also detected in the basement membranes of normal skin, eye, and lung. Male patients with X-linked Alport syndrome revealed no reactivity of renal and epidermal basement membranes with H51, whereas alpha 5(IV) staining was normal in the glomerular basement membrane of patients with other types of glomerular diseases, including benign familial hematuria. The staining was also normal in the skin of nonaffected males in X-linked Alport families. Female heterozygous for Alport syndrome exhibited a discontinuous or mosaic pattern in the immunofluorescent staining of the epidermal basement membrane. These findings confirm that in patients with X-linked Alport syndrome there are abnormalities in alpha 5(IV) in renal and epidermal basement membranes at the protein level. Immunofluorescent staining of skin biopsies with this antibody may be of value in making a diagnosis of Alport syndrome, and, furthermore, may aid in detecting carrier females in whom urinary abnormalities are often mild or silent.

Adolescent↗
PubMed1993

Amplification and detection of a single molecule of human immunodeficiency virus RNA.

Detection of plasma viremia in human immunodeficiency virus type 1 (HIV-1)-infected people is indispensable for the diagnosis of seronegative infection as well as for the evaluation of virus activities in vivo. The direct detection of HIV-1 RNA in circulation has been performed by means of reverse transcription followed by polymerase chain reaction (RT-PCR). As an attempt to establish a highly sensitive assay, we evaluated the effects of two-step amplification with nested primers and double priming of reverse transcription on the sensitivity of RT-PCR. The sensitivity of two-step amplification was 100 times higher than that of one-step amplification. The double priming of reverse transcription further increased the sensitivity of the following two-step amplification 100 times, which appeared to be enough to detect HIV-1 RNA from as little as a 2.2 x 10(-4) TCID50 unit equivalent of culture supernatant of HIV-1-infected cells and a single molecule of HIV-1 gag complementary RNA synthesized by in vitro transcription. By use of this most sensitive assay, we successfully detected HIV-1 RNA in serum or plasma from all 22 patients with acquired immune deficiency syndrome (AIDS) or AIDS-related complex (ARC) and 13 out of 14 untreated asymptomatic carriers. Of 43 asymptomatic carriers under the treatment with interferon-alpha or azidothymidine, 17 cases showed negative results, indicating that the virus activity was suppressed by the therapeutics. We also noted the inhibitory effect of heparin on RT-PCR.

Base Sequence↗
PubMed1993

Triathlon competition induced a transient immunosuppressive change in the peripheral blood of athletes.

This study was designed to determine whether or not physical and psychological stress of triathlon competition causes an immunosuppressive change in the peripheral blood of athletes, if it does occur, how long does it take to recover. Fifteen healthy men, aged 19 to 40, volunteered for this study. Peripheral blood was drawn four times at approximately the same time on the following days; one day before the race, immediately after, one day and eight days after, and served for determining circulating leucocyte and lymphocyte subset counts, in vitro lymphocyte proliferative response and natural killer activity. The results showed that triathlon competition caused considerable changes in the cell counts of peripheral blood leucocyte and lymphocyte subsets, and a transient reduction in vitro lymphocyte proliferative response and natural killer activity, all of which returned to pre-race levels in one to eight days after the race.

Adult↗
PubMed1993

[Focal glomerular sclerosis in a sibling].

We described here one sibling with focal glomerular sclerosis. Proteinuria was noticed at the age of five in brother and four in sister. Both of them developed nephrotic syndrome shortly after the discovery of proteinuria. The nephrotic syndrome was resistant to corticosteroid, immunosuppressive agents or the combination of these drugs. Percutaneous renal biopsy in them revealed morphological and immunohistological features compatible to focal glomerular sclerosis. HLA typing in HLA-A, B, C and DR loci was identical to both. This observation suggests that genetic factors is associated with the pathogenesis of focal glomerular sclerosis.

Adolescent↗
PubMed1993

Transforming growth factor-beta protein and mRNA in glomeruli in normal and diseased human kidneys.

BACKGROUND: Evidence indicates a key role for transforming growth factor-beta (TGF-beta) in the accumulation of pathologic extracellular matrix in experimental glomerular injury. The aim of this study was to elucidate the expression of TGF-beta and its role in human glomerulonephritis. EXPERIMENTAL DESIGN: Expression of TGF-beta 1 in normal and diseased human kidneys was examined by immunohistochemical staining with two antibodies (Ab1 and Ab2), and by in situ hybridization with an oligonucleotide probe. RESULTS: Staining with Ab1, which mainly recognizes mature TGF-beta 1 and the latency-associated peptide (LAP) of natural TGF-beta 1, was linearly positive along the glomerular basement membrane (GBM) and weakly so in the mesangium of normal tissues and those of various glomerular diseases which were pretreated with acid-urea to unmask a hidden epitope. Ab2, which reacts mainly with TGF-beta-LAP, bound to the mesangium and sclerotic areas of the tissues untreated with acid-urea. Immunoelectron microscopy showed that Ab1 was localized to the GBM and the mesangial matrix, and that Ab2 was distributed in subepithelial, or mesangial/paramesangial electron-dense deposits. The presence of mature TGF-beta 1 and TGF-beta-LAP in normal kidneys was confirmed by immunoblotting using guanidine-extracted fractions of glomeruli and GBM isolated from normal human kidneys. Mesangial staining of TGF-beta 1 with Ab2 was significantly correlated with the mesangial matrix increase in mesangial proliferative types of nephritis. In situ hybridization revealed TGF-beta 1 mRNA expression in glomerular cells. Cells with positive mRNA signals were evident in glomeruli that were increased in both mesangial cells and TGF-beta 1 protein expression. The glomerular cells with positive signals were numerous, compared with the number of infiltrating monocyte-macrophages identified with a monoclonal antibody. CONCLUSIONS: These results indicate that mature TGF-beta and TGF-beta-LAP are localized in association with the matrix components of GBM or mesangium, and with immune deposits in human glomeruli. Glomerular expression of TGF-beta is enhanced in human glomerular diseases, and may contribute to the mesangial matrix increase.

Adolescent↗