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Biomedical subjects

T Ohashi

Publications and source records attributed to T Ohashi.

At least 109 records · Page 6Linked to original sources
PubMed1998

Oral administration of human T-cell leukemia virus type 1 induces immune unresponsiveness with persistent infection in adult rats.

The major route of human T-cell leukemia virus type 1 (HTLV-1) infection is mother-to-child transmission caused by breast-feeding. We investigated the host immune responses to orally established persistent HTLV-1 infection in adult rats. HTLV-1-producing MT-2 cells were inoculated into immunocompetent adult rats either orally, intravenously, or intraperitoneally. HTLV-1 proviruses were detected in the peripheral blood and several organs for at least 12 weeks. Transmission of HTLV-1 to these animals was confirmed by analysis of HTLV-1 flanking regions. Despite persistent HTLV-1 presence, none of the orally inoculated rats produced detectable levels of anti-HTLV-1 antibodies, whereas all intravenously or intraperitoneally inoculated rats showed significant anti-HTLV-1 antibody responses. T-cell proliferative responses against HTLV-1 were also absent in orally inoculated rats. Our findings suggest that gastrointestinal exposure of adult rats to HTLV-1-infected cells induces persistent HTLV-1 infection in the absence of both humoral and cellular immune responses against HTLV-1. This immune unresponsiveness at primary infection may subsequently affect the host defense ability against HTLV-1.

Administration, Oral↗
PubMed1998

Downward gaze palsy caused by bilateral lesions of the rostral mesencephalon.

A 55-year-old man with diabetes mellitus developed diplopia and experienced difficulty in moving his eyes in the vertical plane, especially downward. Horizontal movement of each eye was normal with exotropia. Magnetic resonance imaging revealed small and high signals on both sides of the midbrain near the interstitial nucleus of Cajal (INC). Based upon the recent experimental evidence, we speculate that bilateral lesions involving the INC may have caused downward gaze palsy in our patient.

Blepharoptosis↗
PubMed1998

Expression of cytokine genes in a patient with conjunctival melanoma compared with other pigment cells.

Conjunctival melanomas, which have a relatively good prognosis as compared to other mucosal melanomas, have been investigated morphologically and pathologically. We examined the gene expression of several cytokines in a patient with conjunctival melanoma and compared them to those of other pigment cells of the eye, because no reports have discussed cytokine expression in melanoma of the eye. Samples were collected from a 64-year-old woman with conjunctival melanoma and mRNAs were extracted and reverse-transcriptase polymerase chain reaction was performed. We found that potent inhibitors of tumor cell growth such as interleukin 2, 4, 6 and gamma-interferon were expressed in the tumor. These inhibitors were not expressed in other pigment cells of the eye, in blood, in conjunctival melanosis or in choroidal melanomas. The basic fibroblast growth factor gene, which has also been known to stimulate melanoma cell growth, was not expressed in the conjunctival melanoma, and it showed +/- or weak expression in choroidal melanomas, but it was expressed in the pigment cells in the eye and in conjunctival melanosis. Although only limited cytokine expression was examined here, these results may suggest an influence of these cytokines to the growth of conjunctival melanoma.

Adult↗
PubMed1998

[The effects of high-dose steroid therapy on sudden deafness].

The effect of high-dose steroid therapy on sudden deafness were investigated in 19 cases. A daily intravenous administration dose of hydrocortisone sodium succinate was tapered from 800 mg to 200 mg as follows; 800 mg 800 mg, 600 mg, 600 mg, 400 mg, 400 mg, 300 mg, and 200 mg. Another 19 cases, the control group, were treated with intravenous application of prednisolone, tapered from 50 mg to 10 mg in 10-mg steps and each dose applied for 3 days. There were no significant differences in the effect on hearing between the two groups as measured by three different analyses: criteria proposed by the Committee on Sudden Deafness of the Japan Health Ministry; magnitudes of improvement of mean thresholds at five frequencies from 250 Hz to 4 kHz in affected side; and the ratio of the magnitudes of improvement of mean thresholds in affected side to magnitudes of difference between the initial mean thresholds in affected side and those in contralateral side. These findings suggest that high-dose steroid therapy for sudden deafness is not so effective as it is for idiopathic facial palsy. This may be due to the difference in the mechanisms of development between the two conditions. No critical side effects were observed in our study, which would argue for the safety of our method of high-dose steroid therapy for routine clinical use. It might be advisable to conduct additional clinical studies to determine the effect of high-dose steroid therapy for sudden deafness, because our study was conducted on a small number of patients and was not double-blind or randomized.

Adolescent↗
PubMed1998

[Combination chemotherapy with cis-platinum and ifosfamide for hormone unresponsive prostate cancer].

PURPOSE: There is no effective therapy against hormone refractory prostate cancer. This led us to evaluate the effectiveness and toxicity of cis-platinum (CDDP) and ifosfamide (IFM) combination chemotherapy in the patients with hormone-unresponsive carcinoma of the prostate. METHODS: Patients with hormone-unresponsive prostate cancer were scheduled to receive CDDP 70 mg/m2 intravenously on day 1 and IFM 1.2 g/m2/day intravenously on day 1 through day 5 of 28-day cycle. RESULTS: Twenty seven patients with hormone unresponsive prostate cancer were enrolled onto this trial. Of these patients, seven (26%) demonstrated a partial objective response (PR), and ten (37%) a stable disease (ST). The response duration of PR cases lasted from 6 to 49 months with a median of 16 months and the response duration of PR + ST cases lasted from 3 to 36 months with a median of 10 months. Subjective improvement was obtained in 11 patients (41%). Survival duration of all cases were 4 to 89 months with a median of 23 months and probabilities of survival at 3 years and 5 years were 36% and 24%, respectively. The toxicity of this treatment was mostly mild to moderate, anemia (96%), leukocytopenia (89%), anorexia (81%), alopecia (67%), thrombocytopenia (44%), hematuria (38%), renal dysfunction (19%) and liver dysfunction (7%) were noticed. Severe toxicity was observed in two cases, one acute renal failure and one endotoxin shock. CONCLUSION: We conclude that CDDP and IFM combination chemotherapy was active regimen for hormone unresponsive prostate cancer.

Aged↗
PubMed1998

Central nervous system effects of the novel antiallergic agent HSR-609 and typical antiallergic agents using behavioral and electroencephalographic analyses in dogs.

We studied the central nervous system (CNS) effects of 3-[4-(8-fluoro-5, 11-dihydrobenz[b] oxepino[4, 3-b]pyridin-11-ylidene)piperidino]propionic acid dihydrate (HSR-609), a novel amphoteric antiallergic agent having antihistaminic activity. Its effects on gross behavior, spontaneous electroencephalograms (EEG) and some pharmacological parameters of unanesthetized, unrestrained dogs with chronic indwelling brain electrodes after oral administration were compared with typical antiallergic agents and 8-fluoro-5, 11-dihydro-11-(1-methyl-4-piperidylidene)benz[b] oxepino[4,3-b]pyridine (PY-608), a non-amphoteric basic compound having a similar chemical structure to HSR-609. HSR-609 (1, 10 and 100 mg/kg) and terfenadine (100 mg/kg) had no effect on the behavior, EEG patterns, sleep-wakefulness cycles or EEG power spectrum. Cyproheptadine (10 mg/kg), ketotifen (30 mg/kg) and PY-608 (10 mg/kg) increased slow waves with high amplitude in all EEG leads and caused dissociation between the slowing of EEG and waking behavior. Both azelastine (30 mg/kg) and oxatomide (100 mg/kg) caused generalized seizure discharges accompanied by agitation with the former and sedation with the latter. These findings suggest that observations of behavior and EEG in conscious dogs can be useful for clarifying the pharmacological characteristics of various antiallergic agents on the CNS. We were able to show that HSR-609 has no effect on the behavior and EEG of dogs because of its amphoteric chemical structure.

Animals↗
PubMed1998

Ocular tilt reaction with vertical eye movement palsy caused by localized unilateral midbrain lesion.

A 60-year-old man developed diplopia and experienced difficulty moving his eyes. Vertical movement of each eye, including vestibulo-ocular reflex and smooth pursuit, was extremely limited. Horizontal eye movements were normal. His head position was tilted toward his left. There was 10 prism diopters of exotropia and 10 prism diopters of right hypertropia. Fundus photographs revealed a clockwise torsion of both eyes. These signs indicate leftward ocular tilt reaction. Magnetic resonance imaging showed a small area of an increased signal intensity localized in the midbrain dorsomedial to the red nucleus on the right side. Based on recent experimental evidence, it may be assumed that the unilateral lesion involving the right interstitial nucleus of Cajal most probably caused leftward ocular tilt reaction in our patient.

Cerebral Hemorrhage↗
PubMed1997

Two oligomeric forms of plasma ficolin have differential lectin activity.

Ficolins are plasma proteins with binding activity for carbohydrates, elastin, and corticosteroids. The ficolin polypeptide has a collagen-like domain that presumably brings three subunits together in a triple helical rod, a C-terminal fibrinogen-like domain (fbg) similar to that of tenascin, which presumably has the binding activities, and a small N-terminal domain that we find to be the primary site for forming the ficolin oligomer. By sedimentation equilibrium we determined that the main plasma form, which we call big ficolin, had mass of 827,000 Da, consistent with 24 subunits. Little ficolin, about half this size, was obtained after binding to a GlcNAc affinity column. Electron microscopy of little ficolin showed a parachute-like structure, with a small globe at one end, corresponding to the 12 N-terminal domains, and the fbg domains clustered together at the ends of the collagen rods. Big ficolin was formed by the face to face fusion of the fbg domains of two little ficolins, leaving the rods and N-terminal domains projecting at opposite ends. Little ficolin maintained a high affinity for the GlcNAc column, and big ficolin had a low affinity or none. The binding sites for ligands may be obscured in this big ficolin oligomer, providing a regulation of their activity.

Animals↗
PubMed1997

Adenovirus-mediated gene transfer and expression of human beta-glucuronidase gene in the liver, spleen, and central nervous system in mucopolysaccharidosis type VII mice.

Mucopolysaccharidosis type VII (Sly syndrome) is a lysosomal storage disease caused by inherited deficiency of the lysosomal enzyme beta-glucuronidase. A murine model of this disorder has been well characterized and used to study a number of forms of experimental therapies, including gene therapy. We produced recombinant adenovirus that expresses human beta-glucuronidase and administered this recombinant adenovirus to beta-glucuronidase-deficient mice intravenously. The beta-glucuronidase activities in liver and spleen were elevated to 40% and 20%, respectively, of the heterozygote enzymatic level at day 16. Expression persisted for at least 35 days. Pathological abnormalities of these tissues were also improved, and the elevated levels of urinary glycosaminoglycans were reduced in treated mice. However, the beta-glucuronidase activity in kidney and brain was not significantly increased. After administration of the recombinant adenovirus directly into the lateral ventricles of mutant mice, the beta-glucuronidase activity in crude brain homogenates increased to 30% of heterozygote activity. Histochemical demonstration of beta-glucuronidase activity in brain revealed that the enzymatic activity was mainly in ependymal cells and choroid. However, in some regions, the adenovirus-mediated gene expression was also evident in brain parenchyma associated with vessels and in the meninges. These results suggest that adenovirus-mediated gene delivery might improve the central nervous system pathology of mucopolysaccharidosis in addition to correcting visceral pathology.

Adenoviridae↗
PubMed1997

The change in tenascin expression in mouse uterus during early pregnancy.

PURPOSE: Our aim was to examine the changes in spatiotemporal tenascin (TN) expression in mouse uterus during early pregnancy, when the uterine tissue undergoes a tremendous restructuring. METHODS: Using immunohistochemistry and in situ hybridization, the changes in distribution of TN protein in mouse uterine tissues in pregnancy Day 0 through Day 5 were analyzed. RESULTS: Immunoreactive TN and TN mRNA were expressed in the basement membrane of the epithelium as well as in the smooth muscle layer, and their distribution shifted from the subbasement region on Day 0-3 to the smooth muscle layer on Days 4 and 5. CONCLUSIONS: These results indicate that TN expression in the uterus during early pregnancy is spatiotemporally different and may be regulated by a different mechanism.

Animals↗
PubMed1997

TSC-36 (follistatin-related polypeptide) gene expression in estrogen receptor positive osteoblastic cell line, CDO7F.

Using an osteoblastic cell line (CDO7F) that was selected as an estrogen receptor positive cell by immunocytochemical detection and reverse transcription-polymerase chain reaction (RT-PCR) subtractive cDNA cloning using oligo(dT)30-Latex and PCR was performed to isolate a gene that is induced by estrogen. A cDNA clone was isolated and its nucleotide sequence identified it as TSC 36, previously called follistatin-related polypeptide. Northern blot analysis showed that the TSC-36 gene expression was certainly upregulated by estrogen. Tamoxifen also upregulated this gene expression. These findings indicate that TSC-36 may be one of the estrogen-regulated genes in osteoblastic cells.

Animals↗
PubMed1997

Immunohistopathological characterization of pig pneumonia caused by a combined Aujeszky's disease virus and Actinobacillus pleuropneumoniae infection.

Nine pigs were inoculated endobronchially with Actinobacillus pleuropneumoniae serotype 1 (App-1) 6 days after infection with Aujeszky's disease virus (ADV); four died within 3 days and the remainder were killed after 1-6 days. Immunohistopathologically, there were two types of pneumonic lesion: pleuropneumonia, characterized by coagulative necrosis, oedema and fibrinous thrombosis; and necrotizing interstitial pneumonia, characterized by bronchitis, bronchiolitis and alveolitis. The former type of lesion was associated with App-1 antigen, and the latter with ADV antigen. These results indicated that a combined ADV and App-1 infection produced severe haemorrhagic pleuropneumonia; and that ADV and App-1 each produced a characteristic pneumonic lesion.

Actinobacillus pleuropneumoniae↗
PubMed1997

A dimeric form of soluble recombinant sheep LFA-3(CD58) inhibits human T-cell proliferation by generating regulatory T cells.

We recently observed that the soluble recombinant from of sheep LFA-3, termed sLFA-3 is biologically active as determined by E-rosette inhibition and inhibition of human T-cell proliferation in response to the recall antigen. In the present study, we examined the immunosuppressive properties of a derivative of sLFA-3, a dimeric form of the first domain (D1) of sLFA-3, named sD1Hcys dimer which was made by oxidative binding of the two D1 molecules through disulfide bonds formed between the SH side chains of a cysteine which was added to the C-terminal of the D1 domain. By investigating the suppressive properties of the sD1Hcys dimer, we obtained evidence that antigen-stimulated T-cell proliferation was inhibited by the suppressor T cell, mainly CD4 + CD45RA - CD45RO + and CD8 + CD45RA - CD45RO + T cells, generated by incubating PBLs with a low dose (0.5 microgram/ml) of sD1Hcys dimer in the presence of a low dose of IL-2 and GM-CSF. Flow cytometric analysis showed that the expression of some surface molecules on T cells were modulated by a high dose (5 micrograms/ml) of sD1Hcys dimer such as downregulation of CD3 and upregulation of IL-2R, but were not modulated by a low dose (0.5 microgram/ml) of the sD1Hcys dimer. These findings suggest that the sD1Hcys dimer exerts its suppressive effects on the antigen-induced proliferation assay by generating suppressor T cells. The sD1Hcys dimer might therefore have potential as an immunotherapeutic agent to inhibit and/or anergize antigen-specific T-cell responses.

Animals↗
PubMed1997

Molecular cloning and functional expression of equine interleukin-1 receptor antagonist.

Equine interleukin-1 receptor antagonist (IL-1ra) was molecularly cloned to establish a basis for cytokine therapy of acute and chronic inflammatory diseases in the horse. cDNA clones encoding the whole coding sequence of equine IL-1ra were isolated from equine peripheral blood mononuclear cells (PBMC) that had been stimulated with lipopolysaccharide (LPS). The equine IL-1ra cDNA obtained in this study contained an open reading frame encoding 177 amino acid residues. The predicted amino acid sequence of equine IL-1ra shared 75.7, 75.3 and 76.3% similarity with sequences of human, murine and rabbit IL-1ras, respectively. An N-glycosylation site and five cysteine residues conserved in human, murine and rabbit IL-1ras were also found at the corresponding positions in equine IL-1ra. Recombinant glutathione S-transferase (GST)-equine IL-1ra fusion protein produced by Escherichia coli was purified. This protein was shown to inhibit the cytostatic or cytotoxic activity of IL-1 on A375S2 cells, indicating that the equine IL-1ra cDNA obtained in this study encodes biologically active equine IL-1ra.

Amino Acid Sequence↗
PubMed1997

Increased coronary heart disease mortality after the Hanshin-Awaji earthquake among the older community on Awaji Island. Tsuna Medical Association.

OBJECTIVES: To investigate the characteristics of earthquake (EQ)-induced coronary heart disease (CHD) deaths. SETTING AND PARTICIPANTS: On January 17, 1995, the south part of Hyogo Prefecture in Japan was struck by a major EQ (Hanshin-Awaji EQ) measuring 7.2 on the Richter scale. We investigated the characteristics of EQ-induced CHD deaths (myocardial infarction and sudden death) in the Tsuna region, which is a community with a large older population (31% of the total of 64,000 residents are 60 years of age or older) and includes the epicenter and one of the most heavily damaged areas. MEASUREMENTS: EQ-related CHD mortality on the basis of direct access to records of physicians who were able to continue services for the EQ victims without interruption by this disaster situation. RESULTS: Coronary heart disease deaths increased for a few months after the EQ, and the total number from January 17 to April 30, 1995, was 45, which was significantly (1.5 times) higher than the 31 deaths during the same period of the previous year (1994). The CHD deaths after the EQ all occurred in individuals more than 60 years of age and had a positive correlation with EQ-induced damages. Concerning the onset time, CHD deaths occurred 1.8 times more often (P < .05) in the nighttime (11 PM to 5 AM) and 1.4 times as often during the morning (5 AM to 11 AM), whereas their occurrence did not vary during a 12-hour period from 11 AM to 11 PM. CONCLUSION: Deaths of older individuals from CHD persisted for a few months after the EQ and were especially prominent during the nighttime and morning. Reduction of stress and related coronary risk factors in this period may suppress CHD deaths after a major EQ.

Aged↗
PubMed1997

Abrogation of in vitro suppression of human immunodeficiency virus type 1 (HIV-1) replication mediated by CD8+ T lymphocytes of asymptomatic HIV-1 carriers by staphylococcal enterotoxin B and phorbol esters through induction of tumor necrosis factor alpha.

CD8+ T lymphocytes of asymptomatic human immunodeficiency virus type 1 (HIV-1) carriers (AC) suppress HIV-1 replication in vitro. Failure of host defense mechanisms and increased virus proliferation are associated with disease progression. The exact mechanisms inducing these changes at the advanced stage of the disease are still obscure. In this study, we searched for experimental conditions favoring the abrogation of the suppression of viral replication in peripheral blood mononuclear cells (PBMC) of AC by using various pharmacological and biological probes modifying cell activation. Among such agents, staphylococcal enterotoxin B (SEB) and phorbol 12-myristate 13-acetate (PMA) markedly increased otherwise low levels of HIV-1 replication in cultures of phytohemagglutinin-stimulated AC PBMC following in vitro HIV-1 LAI infection. A similar but less pronounced virus induction was also observed in macrophage-tropic HIV-1. Individual pretreatment of CD4+ and CD8+ PBMC fractions with these agents caused a reduction in CD8+ cell proliferation and enhanced HIV-1 replication in CD4+ cells. SEB- and PMA-mediated augmentation of HIV-1 replication in AC PBMC was significantly blocked by neutralizing antibody to tumor necrosis factor-alpha (TNF-alpha), although recombinant TNF-alpha alone failed to reproduce the effects of SEB or PMA. Our results suggest that the induction of TNF-alpha may be one of the mechanisms that overcomes the CD8+-induced suppression of HIV-1 replication in AC and that it may induce HIV-1 replication.

Antibodies↗