Search PubMed⌕ Search

Biomedical subjects

Y Hinuma

Publications and source records attributed to Y Hinuma.

At least 73 records · Page 4Linked to original sources

[Effects of hyperoxia, glycerol and ventricular drainage on ICP and CBF in patients with increased ICP due to CSF circulatory-absorbance disturbance].

The effects of hyperoxia, glycerol and ventricular drainage on intracranial pressure (ICP) and cerebral blood flow (CBF) were studied in cases with cerebrospinal fluid (CSF) circulatory-absorbance disturbance due to subarachnoid hemorrhage (SAH) or intraventricular hematoma. Ventricular fluid pressure (VFP) was monitored through a controlled ventricular drainage (CVD) tube using a Statham P-50 pressure transducer. CBF was measured by the 10mCi133Xe intravenous injection method using a Valmet BI-1400 rCBF analyzer. ISI (initial slope index) was used for the CBF value. Studied cases were 19 SAH patients and 2 hypertensive intracerebral hematoma cases with intraventricular hematoma. Hyperoxia included hyperbaric oxygen (HBO), reduced ICP and CBF. During pure oxygen inhalation at atmospheric pressure (1ATA . O2), there was a tendency toward a relationship showing that the higher the resting state ICP, the lesser the likelihood of a CBF decrease. This may indicate that increased ICP impairs cerebral vascular reactivity to hyperoxia in relation to the degree of elevation. The effects of hyperoxia on ICP and CBF were temporary and they promptly returned to the resting state after cessation of oxygen inhalation. In some cases, there was a rebound phenomenon in ICP after HBO. Glycerol administration reduced ICP and increased CBF. There was no clear correlation between resting state ICP and CBF increase after glycerol administration. The effects of glycerol were also temporary. ICP control by opening CVD increased CBF. There was a correlation between the level of resting state ICP and the CBF increase after the opening of CVD. In cases with CSF circulatory-absorbance disturbance, elevated ICP reduced CBF and may further worsen the cerebral damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

High- and low-affinity interleukin 2 receptors: distinctive effects of monoclonal antibodies.

We previously established several mouse hybridoma cell lines producing monoclonal antibodies against the human interleukin 2 (IL 2) receptor molecule. As they bind to both high- and low-affinity IL 2 receptors, their effects on binding of 125I-labeled IL 2 to high- and low-affinity receptors were examined by Scatchard plot analysis. Two of these monoclonal antibodies, HIEI and H-47, reduced the IL 2 binding affinity of high-affinity receptors from a Kd of 14 to 20 pM to a Kd of 110 to 140 pM, but slightly raised that of low-affinity receptors. These two antibodies scarcely affected the numbers of high- and low-affinity receptors. On the other hand, H-31 completely blocked IL 2 binding to both high- and low-affinity receptors, and H-A26 slightly reduced the affinities of both high- and low-affinity receptors, from 17 pM to 28 pM and from 28 nM to 54 nM, respectively. H-48 had little affect on IL 2 binding to high- or low-affinity receptors. By use of these monoclonal antibodies, the inhibitory effect of IL 2 on growth of an HTLV-I-immortalized T cell line was demonstrated to be transmitted from high-affinity, but not low-affinity, receptors.

Animals↗

HTLV-I carriers among migrants from an ATL-endemic area to ATL non-endemic metropolitan areas in Japan.

The prevalence of antibodies against HTLV-I among Kyushu natives aged 16 to 39 years who moved from Nagasaki and Kagoshima prefectures to Aichi prefecture (a non-endemic area for ATL) was compared by their cities or counties of birth. The positive rate of anti-HTLV-I antibody was 2.4% (II/400) among Nagasaki natives, 6.4% (20/312) among Kagoshima natives and 4.0% (31/772) for both combined. There was a slight difference in the positive rate of anti-HTLV-I antibody between Kyushu natives from cities (3.3%) and from counties (4.5%). In county areas, the prevalence of anti-HTLV-I antibodies among migrants from areas of relatively higher mortality for malignant lymphomas (7.5%) was significantly higher (p less than 0.01) than among persons from lower mortality areas (1.9%). Most "positive" persons had moved from Kyushu to Aichi prefecture between the ages of 15 and 18 years. The results of the present study suggest that: there is a considerable number of HTLV-I carriers among Kyushu natives who have settled in ATL non-endemic areas, especially among those born in regions of Kyushu district which have a high mortality rate for malignant lymphomas; and that Kyushu natives who had settled in metropolitan areas might have been exposed to HTLV-I during childhood in their birthplace.

Adolescent↗

Interleukin 2 (IL-2) rapidly induces phosphorylation of a cellular protein, pp67, in an IL-2 dependent murine cell line.

We have investigated interleukin 2 (IL-2)-induced protein phosphorylation in an IL-2 dependent murine cell line by the two-dimensional gel electrophoresis. IL-2 rapidly and markedly induced phosphorylation of a cellular protein distinct from the IL-2 receptor, with a molecular weight of 67,000 daltons and an isoelectric point of 5.8, named pp67. IL-2 dose-responses of pp67 phosphorylation and cell proliferation were well correlated. Phosphoamino acid analysis showed that the phosphorylation site of pp67 was a serine residue. Further, when the cells were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) instead of IL-2, similar increase of pp67 phosphorylation was observed. Such IL-2 dependent protein phosphorylation was also detected in various human IL-2 receptor bearing T cells. Thus we speculate that the phosphorylation of pp67 could be regulated by protein kinase C and it could be a common feature in an early event of the intracellular growth signaling from the IL-2 receptor.

Amino Acids↗

High-affinity receptor-mediated internalization and degradation of interleukin 2 in human T cells.

Receptor-mediated internalization and degradation of IL-2 were investigated in cell lines carrying human T cell leukemia/lymphoma (lymphotrophic) virus type I (HTLV-I) and PHA-treated normal PBL. The HTLV-I-carrying cell lines ILT-Yan and TL-Mor, and the PBL expressed both high- and low-affinity IL-2-R. However, another HTLV-I-carrying T cell line, MT-1, expressed mainly low-affinity receptors. Greater than 50% of the IL-2 bound to high-affinity receptors was internalized within 10 min when these cells were incubated at 37 degrees C. The internalized IL-2 was rapidly degraded and the products were excreted into the culture fluid. The t1/2 of IL-2 degradation in these cells was estimated as 60-80 min at 37 degrees C. The internalization and degradation of IL-2 were both temperature dependent. Light-microscopic autoradiography with 3H-labeled IL-2 confirmed the internalization of IL-2, and suggested that some IL-2 might be carried to the nucleus.

Cell Compartmentation↗

Antigens related to three core proteins of HTLV-I (p24, p19 and p15) and their intracellular localizations, as defined by monoclonal antibodies.

Three distinct monoclonal antibodies (MAbs) specific for human T-cell leukemia virus type-I (HTLV-I) core proteins with molecular weights of 24 kDa (p24), p19 or p15 were produced, characterized and compared. These antibodies were named NOR-1 (anti-p24, IgG2a), GIN-7 (anti-p19, IgG2b) and FR-45 (anti-p15, IgG2a). Immunofluorescence assay showed that they reacted specifically with methanol-fixed cells of virus-bearing cell lines, and that only GIN-7 bound, albeit weakly, to the surface of a small percentage of viable cells. Like natural antibodies to HTLV-I in human serum, GIN-7 stained the fixed cells brightly and diffusely, and gave more intense fluorescence than NOR-1 and FR-45, which stained restricted areas of the cells. NOR-1, GIN-7 and FR-45 specifically precipitated core proteins p24, p19 and p15, respectively, from a lysate of HTLV-IMT-2 labelled with 35S-cysteine. NOR-1 precipitated p53, p36, and p24, GIN-7 precipitated p53, p32, p28 and p19, and FR-45 precipitated p53, p36, and p15 from a lysate of 35S-cysteine-labelled MT-2 cells. GIN-7 also precipitated p32, p28 and p19 from a lysate of MT-2 cells, labelled by surface iodination, but NOR-1 and FR-45 did not detect any proteins in this lysate. GIN-7 also detected p28 in 3H-glucosamine-labelled MT-2 cells. Antibody binding competition assay showed that the sera of ATL patients significantly interfered with the binding of NOR-1 and GIN-7 but not with that of FR-45, to antigens of disrupted virus of MT-2 cells. This complete set of MAbs against the HTLV-I gag gene products is useful for biological and functional studies of the HTLV-I core proteins.

Animals↗

Primary infection of Japanese infants with adult T-cell leukaemia-associated retrovirus (ATLV): evidence for viral transmission from mothers to children.

Primary infection with adult T-cell leukemia virus (ATLV) was investigated by follow-up studies on 16 ATLV-seropositive mothers and their breastfed infants in an ATLV-endemic area of Japan. Maternal antibody to ATLV decreased in all the infants, and was detectable in only three of 12 infants tested 6 months after birth. Reappearance of the antibody 9-18 months after birth was observed in only four of the 16 infants. The ATLV-bearing cells in peripheral blood were detected in all 16 mothers after delivery. None of the 16 infants showed ATLV-bearing cells in peripheral or cord blood sampled at birth, or 1, 3 or 6 months after birth. However, virus-bearing cells in the blood became detectable 9-18 months after birth in 13 of the 16 infants. Maternal antibody and virus-bearing cells were never detected in a control group of seven infants of ATLV-seronegative mothers. These findings provide evidence for the high incidence of primary ATLV infection during early infancy among infants born to ATLV-seropositive mothers and suggest maternal viral transmission. Furthermore, samples of breast milk from all 12 seropositive mothers examined contained cell-associated ATLV capable of being transmitted to peripheral leucocytes of neonates. This finding suggests that one of the possible maternal transmission routes of ATLV is via breast milk.

Adult↗

A field study of infection with human T-cell leukemia virus among African primates.

African non-human primates were surveyed seroepidemiologically for natural infection of human T-cell leukemia virus type I (ATLV/HTLV-I) or its closely related virus(es). Materials from three genera (Cercopithecus, Papio, and Theropithecus), four species (grivet monkey, Anubis baboon, Hamadryas baboon, and gelada), totalling 983 animals under natural conditions, were obtained in a field study in Ethiopia. Virus infection was determined by the indirect immunofluorescence test using HTLV-I specific antigens. Animals seropositive for HTLV-I were found among grivet monkeys and Anubis baboons including the hybrid offspring between Anubis and Hamadryas baboons but not pure-Hamadryas baboons and geladas. From these results, the HTLV-I family was proved to be widespread on the African continent and was regarded as a common retrovirus among catarrhines.

Animals↗

New monoclonal antibodies that define multiple epitopes and a human-specific marker on the interleukin 2 receptor molecules of primates.

Twelve hybridoma cell lines producing monoclonal antibodies to the human interleukin 2 (IL-2) receptor (IL-2R) molecule were prepared. These antibodies were characterized by competitive antibody-binding assay and sequential immunoprecipitation assay with four known monoclonal antibodies to the human IL-2R molecule. The twelve new monoclonal antibodies were divided among the four known antibody types, the HIEI-, H-A26-, H-31-, and anti-Tac-type, and an additional new type, the H-48-type. The H-48 antibody did not compete with any other antibodies in the competitive binding assay. The binding of 125I-IL-2 to MT-2 cells and the IL-2-dependent growth of normal activated T-cells were both strongly inhibited by all the H-31- and anti-Tac-type antibodies, and partially or slightly inhibited by HIEI- and H-A26-type antibodies, but were not inhibited by the H-48 antibody. Thus, the same type of monoclonal antibodies had a similar effect on the function of IL-2R. These results suggest that epitopes for the same type of antibodies could be single identical epitopes or epitopes closely associated with each other. On the other hand, these antibodies also reacted variously with a panel of various human and simian lymphoid cell lines immortalized with human T-cell leukemia virus type-I (HTLV-I): the H-45 antibody reacted only with the human cell lines, the H-C1 and H-44 and H-47 antibodies reacted with human and ape cell lines, and the other antibodies reacted with cell lines of humans, apes and Old and New World monkeys. These differences in the reactivity of the antibodies with the primate cell lines suggest that the antigenic structure of the IL-2R molecule changed during evolutionary divergence of the primates.

Animals↗

Budding process and fine structure of lymphadenopathy-associated virus (LAV).

The budding process and fine structure of lymphadenopathy-associated virus (LAV), were studied by indirect immunofluorescence (IF) and electron microscopy (EM). By IF, LAV antigen was seen to be distributed focally within infected CCRF-CEM cells. Consistent with this finding, electron micrographs showed that LAV particles occurred in a focally aggregated state in a restricted area of the surface of the infected cells. LAV particles possessed bar-shaped, dense and central or eccentric cores. In addition, two or more cores were occasionally observed in one virus particle, or the cores were sometimes absent when thin sections were examined. The envelope of the virus particles had an irregular structure, although LAV particles were approximately spherical.

Antigens, Viral↗

Sporadic cases of carriers of human T-lymphotropic virus type 1 in Southeast Asia.

Sera obtained from 3,472 persons in Malaysia, Thailand, Philippines and Indonesia were tested for the presence of antibody to adult T-cell leukemia-associated antigen by the gelatin particle agglutination test and indirect immunofluorescence. Among these, only two seropositives were identified. One was a 30-year-old male Malaysian of Indian origin. The other was a 42-year-old female Thai who resided in Bangkok. These results suggested that the infection of human T-lymphotropic virus type 1 might not be endemic in these countries.

Adolescent↗

Seroepidemiology of the human retrovirus (HTLV/ATLV) in Okinawa where adult T-cell leukemia is highly endemic.

A survey of carriers of antibodies to HTLV-specific antigens was made in 11 islands among 60 Okinawan islands to examine the regional variation in the prevalence of HTLV carriers. The overall seropositive rate was 21% among 7,545 adults aged 40 years or more. The incidence of virus carriers was low in only one of the 11 islands (1-6%), while it was 14-31% in the other 10 islands.

Adult↗

Prevention of HTLV-I transmission through the breast milk by a freeze-thawing process.

Fifteen human breast milk samples obtained from mothers seropositive for human T-cell lymphotropic virus type-I (HTLV-I) antigen were kept frozen overnight at -20 degrees. Each milk sample was then co-cultivated with cord lymphocytes obtained from 15 anti-HTLV-I antibody-negative mothers. No HTLV-I antigen-positive cells were detected among the cord lymphocytes subjected to co-cultivation. These results suggest that thawing of frozen breast milk may prevent HTLV-I transmission from mother to child via breast milk.

Antigens, Viral↗

Seroepidemiology of adult T-cell leukemia virus (HTLV-I/ATLV): origin of virus carriers in Japan.

There are two large clusters of HTLV-I/ATLV carriers in the world. One large endemic area could be Africa, but available information is not yet sufficient to prove this. The other definitely large endemic area is Japan. Much smaller endemic areas and sporadic cases of the virus-carriers have been found in many parts of the world, including the Caribbean basin and Taiwan. Where did ATL virus carriers in Japan come from? From seroepidemiological studies, it is postulated that the carriers originated among Jomon people, who were the earliest inhabitants of Japan in 300 to 10,000 B.C. or earlier.

Carrier State↗

Seroepidemiology of adult T-cell leukemia virus infection and analysis of sero-positive cases in Taiwan.

For a seroepidemiologic study of adult T-cell leukemia virus (ATLV) infection in Taiwan, the gelatin particle agglutination technique and the indirect immunofluorescence method were used for anti-ATLV titration. Sporadic sero-positive cases were found all over the Taiwan districts except among the aborigines (0/947). Sero-positive rates ranged from 0 to 5.6% (except ATL family) and a total of 48 cases were found in 3682 Han-Chinese. Among them 9 cases were newly found in family surveys, and 39 cases were observed in random samples. As an average positive rate was 1.0%, by calculation about 80,000 sero-positive cases are supposed to be present in Taiwan. A most remarkable feature of the sero-positive cases was the high rate in couples. Various patterns of sero-positive cases existed in pedigrees. Anti-ATLV positive sera of Chinese living in Taiwan and Japanese were compared by immunoprecipitation and there was no difference between them. The possible infection route from Japan to Taiwan is discussed.

Adult↗

Impairment of T-cell control of Epstein-Barr virus infected B-cells in patients with adult T-cell leukemia.

The abilities of peripheral blood lymphocytes from 9 patients with adult T-cell leukemia (ATL) and 14 healthy control adults to cause regression of proliferating B-cell foci induced by Epstein-Barr virus (EBV) were examined. Marked regression of EBV-transformed B-cell foci was observed in lymphocytes from all 10 EBV-seropositive donors but with none of those of the 4 EBV-seronegative donors in the control group. The lymphocyte of all 9 patients with ATL, who were EBV-seropositive, caused little or no regression of B-cell foci like those of EBV-negative healthy donors. These results suggest that the absence of regression of EBV-induced B-cell proliferation observed in ATL patients is due to impairment of EBV-specific killer T-cell activities.

Adult↗