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Biomedical subjects

H Tsujimoto

Publications and source records attributed to H Tsujimoto.

At least 253 records · Page 14Linked to original sources
PubMed1987

Structural abnormality and over-expression of the myc gene in feline leukemias.

Tumor cells of feline leukemia were examined for structural abnormality and expression of the myc gene. Four of 12 spontaneous leukemia cases showed structural abnormalities of the myc gene detected by Southern blotting analysis. Of these 4 cases, one (Case 1) showed a DNA rearrangement in the 5' portion of the c-myc locus associated with integration of feline leukemia virus (FeLV) genome. Another case had a newly inserted myc gene which was transduced by FeLV. In the 2 other cases, no relation of abnormalities of the myc gene to FeLV was detected. One case of experimental leukemia induced by inoculation of a cell line, FT-1, established from Case 1 showed a c-myc gene rearrangement similar to that observed in Case 1. Expression of myc RNA was examined in 3 leukemia T-cell lines, FT-1, FL74 and F422, by Northern blotting analysis. A high level of myc transcript was detected in all 3 cell lines. The size of myc RNAs in FT-1 and FL74 was the same as that of normal myc RNA, while in F422 which had myc-containing FeLV (myc-FelV), the full genome and spliced form of myc-FeLV viral RNA were detected.

Animals↗
PubMed1987

Protection of cynomolgus monkeys against infection by human T-cell leukemia virus type-I by immunization with viral env gene products produced in Escherichia coli.

Protection against human T-cell leukemia virus type-I (HTLV-I) infection in cynomolgus monkeys, achieved by immunizing the animals with env gene products of HTLV-I produced in Escherichia coli, was evaluated. Four monkeys that had been immunized with the env product produced antibody against HTLV-I gp68 and gp46, and their sera were found to cause strong inhibition of syncytium formation of a cat fibroblast cell line induced by HTLV-I. Immunized and non-immunized monkeys were challenged with live MT-2 cells, a high HTLV-I-producer cell line. After challenge, all the control non-immunized monkeys were infected with HTLV-I, as judged by the frequent detection of HTLV-I-antigens in cultures of their peripheral blood mononuclear cells (PBMC), whereas no antigens were recovered from PBMC of immunized monkeys. These results indicate that humoral immunity against HTLV-I-envelope protein elicited by immunization with the polypeptides synthesized in bacteria protected the monkeys against primary infection with HTLV-I.

Animals↗
PubMed1987

Serological survey and virus isolation of simian T-cell leukemia/T-lymphotropic virus type I (STLV-I) in non-human primates in their native countries.

Infection with a simian retrovirus (STLV-I) closely related to human T-lymphotropic virus type I (HTLV-I) was investigated in non-human primates living in their native countries in Africa and Asia. Serum antibodies cross-reacting with HTLV-I antigens were detected in 85 of 567 non-human primates of 30 species. Seropositive animals were found among African green monkeys, olive baboons, Sykes' monkeys, mandrills and patas monkeys in several countries in Africa, and cynomolgus monkeys, Celebes macaques and siamangs in Indonesia. The frequency of seropositivity was much higher in adult than in young African green monkeys, cynomolgus monkeys and Celebes macaques. STLV-Is were isolated by establishing II lines of virus-producing lymphoid cells in the presence of interleukin-2 from 5 species of seropositive non-human primates, i.e. the African green monkey, Sykes' monkey, Celebes macaque, cynomolgus monkey and siamang. All these cell lines had T-cell markers and Tac antigen, and the cell lines from the African green monkey and Sykes' monkeys were Leu2a+ while those from other species were Leu3a+. These cell lines expressed viral antigens reacting with human sera from adult T-cell leukemia (ATL) patients and monoclonal antibodies (MAbs) against p19 and p24 of HTLV-I core proteins, and produced virus particles having RNA-dependent DNA polymerase activity. Cellular DNAs from these cell lines contained provirus sequences homologous to HTLV-I, shown by Southern blot hybridization. The restriction patterns of these provirus genomes were different from those of HTLV-I and were also dissimilar in the different species.

Age Factors↗
PubMed1987

Development of adult T-cell leukemia-like disease in African green monkey associated with clonal integration of simian T-cell leukemia virus type I.

Proviral integration of a simian retrovirus highly homologous to human T-cell leukemia virus type I was examined in cellular DNAs extracted from primary peripheral blood lymphocytes of 31 adult African green monkeys (Cercopithecus aethiops) that were seropositive for simian T-cell leukemia virus type I (STLV-I). Among these monkeys, one case with overt leukemia, showing pleomorphic leukemia cells similar to those in human adult T-cell leukemia (ATL), and five cases in a preleukemic state of ATL-like disease were found. Judging from the integration site of the provirus genome, primary lymphocytes of these leukemic or preleukemic cases contained monoclonally proliferated STLV-I-infected cells, whereas lymphocytes of other seropositive monkeys without hematological abnormalities were polyclonal, and those of seronegative monkeys did not contain the provirus. The restriction patterns with PstI ans SstI of most STLV-I proviruses were identical to those of the previous isolate from this species, but in three monkeys there was a deletion of one PstI site. From the correlation of the development of simian ATL-like disease with the monoclonal integration of the STLV-I provirus genome, it should be indicated that STLV-I has similar leukemogenicity to human T-cell leukemia virus type I, and so STLV-I infection in African green monkeys will be useful as an animal model of human ATL.

Animals↗
PubMed1987

Human T-cell leukemia virus type I isolates from Gabon and Ghana: comparative analysis of proviral genomes.

Two isolates of human T-cell leukemia virus type I (HTLV-I) were obtained from lymphocyte cultures of a healthy carrier in Gabon and another in Ghana. Their proviruses were analyzed by Southern blot hybridization and compared with prototypical HTLV-I isolated in Japan and the United States. The provirus genomes of both strains were highly homologous to the prototype HTLV-I along the whole viral genome. The restriction endonuclease sites of the Ghanian isolate were almost identical with those of the prototype HTLV-I, but 10 of 26 sites of the Gabonese isolate were different from those of the prototype. Furthermore, the restriction map of the Gabonese isolate resembled those of a simian T-cell leukemia virus (STLV-I) isolated from a chimpanzee from Sierra Leone and a variant of HTLV-I from Zaire (HTLV-Ib) more closely than those of any other known HTLV-I. These results indicated the existence of some unique strains of HTLV-I transmitted among African people, and the importance of clarifying the origin and transmission of HTLV group viruses.

Biological Evolution↗
PubMed1987

Infection of feline lymphoid cells with feline leukemia virus in culture.

An in-vitro system for infection of cat T lymphocytes with feline leukemia virus (FeLV) was developed. For establishment of this system, FeLV was inoculated in vitro into concanavalin-A stimulated primary lymphoid cells and long-term cultured T cells grown with interleukin-2 (IL-2) from various feline lympho-hematopoietic organs. During serial cultivation with IL-2, FeLV group-specific antigen (GSA) was detected 5-6 weeks after infection in the primary cultures, and 1 week after infection in the long-term cultures of T cells. The percentage of FeLV-GSA-positive cells gradually increased with passages and reached more than 80% in several cultures of lymphoid cells, that became persistently infected and produced FeLV. These FeLV-infected lymphoid cells expressed T-cell markers, but showed no obvious differences in growth or cytological characteristics from FeLV-free feline lymphoid cells during the observation period of 60 weeks.

Animals↗
PubMed1986

Experimental inoculation of monkeys with autologous lymphoid cell lines immortalized by and producing human T-cell leukemia virus type-I.

Cynomolgus monkeys and squirrel monkeys were inoculated with autologous lymphoid cell lines immortalized by and producing human T-cell leukemia virus type-I (HTLV-I) in order to serve as an animal model of adult T-cell leukemia (ATL). The autologous cell lines were established from peripheral blood mononuclear cells (PBMC) from each monkey by co-cultivation with lethally irradiated MT-2 cells producing HTLV-I. All of these cell lines, which had monkey karyotypes, grew continuously without addition of interleukin-2 (IL-2) and expressed virus-specific proteins of HTLV-I and IL-2 receptor. After inoculation with the autologous cell lines, specific antibodies against HTLV-I proteins could be detected in their plasma, and transformed HTLV-I-infected cells could be recovered from their peripheral blood for at least 6 months. However, no signs of ATL have been observed to data, i.e. 2 years after inoculation.

Animals↗
PubMed1986

Detection of the X gene product of simian T-cell leukemia virus.

The gene product of the X region was examined in simian lymphoid cell lines producing simian T-cell leukemia virus (STLV), which is closely related to human T-cell leukemia virus (HTLV). By use of specific antibodies against pX peptides of HTLV-I, a protein of 41 kDa was identified as a pX product of STLV.

Animals↗
PubMed1986

Hematologic abnormalities similar to the preleukemic state of adult T-cell leukemia in African green monkeys naturally infected with simian T-cell leukemia virus.

Studies were made of the hematologic features of 23 adult African green monkeys (Cercopithecus aethiops) naturally infected with simian T-cell leukemia virus (STLV), which is closely related to human T-cell leukemia virus type I. None of the STLV-infected monkeys showed any clinical signs, but their absolute lymphocyte count and percentage of atypical lymphocytes were significantly higher than those of uninfected monkeys. Three STLV-infected monkeys had especially high percentages of atypical lymphocytes. Most of the atypical lymphocytes were small- or medium-sized lymphocytes with a lobulate or convoluted nucleus, and were very similar to the leukemic cells in human cases of adult T-cell leukemia (ATL), while other atypical cells were large lymphoblastoid cells. Both types of atypical cells were positive for Leu2a and Tac antigens, and expressed STLV antigen after short-term culture. These findings suggested the presence of a preleukemic state in these STLV-infected monkeys similar to that seen in human ATL, and indicated the value of this natural infection system as an animal model of ATL in humans.

Animals↗
PubMed1986

Conventional and immunocolloidal gold electron microscopy of eight simian retroviruses closely related to human T-cell leukemia virus type I.

Simian retroviruses closely related to human T-cell leukemia virus type I (HTLV-I) were isolated from 8 species, examined by both conventional and thin section immunocolloidal gold electron microscopy, and compared with HTLV-I. Mature forms of simian viruses were found in extracellular aggregates and within cytoplasmic vacuoles. They were morphologically similar to each other and to HTLV-I. They consisted of a seemingly smooth envelope and a centrally located nucleoid. Their size varied considerably among species and also within the same species; this is characteristic of this group of retroviruses. No budding particles of simian viruses were observed. Thin section immunocolloidal gold electron microscopy using various human and simian sera showed that simian viruses were antigenically related to each other and to HTLV-I. One drawback of this otherwise very useful technique was the difficulty in identifying virions because of the poor preservation of their fine structure by fixation with glutaraldehyde alone. This was overcome by using materials prepared for conventional electron microscopy, in which virions showed weak but specific reactions with gold particles after deosmification and antigen restoration with sodium metaperiodate.

Animals↗
PubMed1985

Sequence homology of the simian retrovirus genome with human T-cell leukemia virus type I.

A retrovirus highly related to human T-cell leukemia virus type I (HTLV-I) was isolated from a T-cell line established from a seropositive pig-tailed monkey and the provirus genome was molecularly cloned using HTLV-I as a probe. The monkey virus (STLV) had the genomic structure of the LTR-gag-pol-env-pX-LTR. Analysis of the env-pX-LTR region revealed the 90% homology of the nucleotide sequence with that of HTLV-I in each region. This high homology of the sequence indicates that STLV is a member of the HTLV family, but apparently different from HTLV-I. This suggests that the possibility of recent interspecies transmission from monkeys to humans in the endemic area is very small. From its similarity to HTLV, STLV should be useful as an animal model in studies on natural HTLV infection and leukemogenesis of HTLV in humans.

Animals↗
PubMed1985

Isolation of simian retroviruses closely related to human T-cell leukemia virus by establishment of lymphoid cell lines from various non-human primates.

Simian retroviruses closely related to human T-cell leukemia virus (HTLV) were isolated by establishing virus-producing lymphoid cell lines from 7 species of non-human primates. By co-cultivation with human umbilical cord-blood cells and/or in the presence of interleukin-2, lymphoid cell lines were successfully established from the chimpanzee. African green monkey, pig-tailed macaque, red-faced macaque, Formosan monkey, Japanese monkey and bonnet monkey that had antibodies against HTLV antigens. These cell lines reacted with human sera of ATL patients and monoclonal antibodies against p19 and p24 of HTLV antigens. Cellular DNAs contained the provirus sequences homologous to HTLV-I by Southern blot hybridization. Moreover, they produced extracellular type-C virus particles and RNA-dependent DNA polymerase. All of these lymphoid line cells had Tac antigen, interleukin-2 receptor, and those of chimpanzee and red-faced macaque had helper/induced T-cell markers, while those derived from African green monkey had suppressor/cytotoxic T-cell markers. Furthermore, simian HTLV-related viruses of pig-tailed macaque, red-faced macaque and Japanese monkey were transmitted to human lymphocytes on co-cultivation.

Animals↗
PubMed1985

Adult T-cell leukemia-like disease in monkey naturally infected with simian retrovirus related to human T-cell leukemia virus type I.

Spontaneous T-cell leukemia similar to human adult T-cell leukemia (ATL) was found in an African green monkey naturally infected with simian retrovirus closely related to human T-cell leukemia virus type I (HTLV-I). Monoclonal integration of the simian retrovirus was detected in the primary leukemic cells, suggesting an association of the retrovirus with ATL-like leukemia in the monkey.

Animals↗
PubMed1984

Detection and characterization of simian retroviruses homologous to human T-cell leukemia virus type I.

Lymphoid cell lines were established from five different species of monkeys which were positive in antibodies cross-reactive with human T-cell leukemia virus type I (HTLV-I) and were shown to contain provirus sequences homologous to HTLV-I. Gene-specific probes of HTLV-I, gag, pol, env, pX, and LTR, hybridized efficiently with monkey DNAs from these cell lines under stringent conditions, indicating that the proviruses are very similar to HTLV-I along with whole viral genomes. However, the preliminary restriction mapping turned out the difference between simian retroviruses and HTLV-I and also among simian retroviruses. These findings suggest a common ancestor of simian and human retroviruses, but exclude the recent interspecies transmission between monkeys and humans.

Animals↗
PubMed1984

Meal feeding schedule and ventromedial hypothalamic lesions do not affect rhythm of pineal serotonin N-acetyltransferase activity in rats.

Effects of meal feeding schedule and bilateral lesions of the ventromedial hypothalamus (VMH) on the circadian rhythm of pineal serotonin N-acetyltransferase (SNAT) activity were examined in rats, under LD (12:12) condition. Neither meal feeding nor VMH lesions affected the phase of the circadian rhythm of pineal SNAT activity, but the VMH lesions reduced the level. Meal feeding caused a shift of the phases of the daily rhythms of phosphoenolpyruvate carboxykinase and tyrosine aminotransferase activities in the liver. These findings suggest that the circadian rhythm of pineal SNAT activity is not entrained by the food intake, and that the VMH does not function as a master oscillator of the rhythm.

Acetyltransferases↗
PubMed1984

Shift of metabolism in rats with ventromedial hypothalamic lesions with respect to changes in daily rhythms of enzyme activity.

Metabolic alterations in ventromedial hypothalamus (VMH)-lesioned rats were investigated by examining daily changes of enzyme activities and urea concentrations three weeks after the operation. VMH-lesions in female adult rats caused a significant elevation in the activity of acetyl-CoA carboxylase in the liver and parametrial adipose tissue. These changes suggest an increased lipogenesis. VMH-lesions also elicited an increase in activities of glucokinase (GK), pyruvate kinase (PK) and fructose 1,6-bisphosphatase (FBPase), and a decrease in activities of phosphofructokinase (PFK), glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) in the liver. The apparently inconsistent changes in activities of key glycolytic enzymes, GK, PK and PFK, and key gluconeogenic enzymes, G6Pase, PEPCK and FBPase in the liver may be explained by the fact that they were favorable for glucose oxidation through pentose phosphate cycle and provide NADPH for lipogenesis in the liver. Furthermore, VMH-lesions induced an increase in urea contents of the liver and serum, and elicited an increase in activity of liver tyrosine aminotransferase (TAT) and a decrease in activity of liver histidase. These changes suggest an accelerated amino acid and protein catabolism, and favor an increment in the supply of the substrate for lipogenesis. Daily rhythms of TAT, histidase activities and serum urea concentration observed in the control rats were abolished by VMH-lesions. These findings suggest that VMH-lesions elicit the loss of these daily rhythms, probably through the disturbance of the circadian rhythm of feeding behavior at this dynamic phase (three weeks after operation) of obesity.

Acetyl-CoA Carboxylase↗