Search PubMed⌕ Search

Biomedical subjects

T Okada

Publications and source records attributed to T Okada.

At least 721 records · Page 40Linked to original sources
PubMed1991

Major histocompatibility complex controls clonal proliferation of CD5+ B cells in H-2-congenic New Zealand mice: a model for B cell chronic lymphocytic leukemia and autoimmune disease.

By employing H-2-congenic NZB, NZW and (NZB x NZW)F1 mice with either the homozygous H-2d/H-2d, H-2z/H-2z or heterozygous H-2d/H-2z haplotype, we found that in the spleen of all the congenic strains homozygous for H-2z, there were extremely high frequencies of CD5+ B cells. These cells eventually proliferated in an oligoclonal or even monoclonal fashion, and B cell-chronic lymphocytic leukemia (B-CLL) developed in some cases. Because this feature was not observed in H-2d/H-2d homozygotes or H-2d/H-2z heterozygotes, the high CD5+ B cell frequencies are apparently controlled by the homozygosity of a locus or cluster of loci closely linked to H-2z complex of NZW strain. As the CD5+ B cell frequencies in the peritoneal cavity did not differ among the H-2-congenic strains, the frequencies of these cells in the peritoneal cavity and in the spleen appear to be at least in part under separate control. Flow cytometry and Southern blot analyses using an immunoglobulin gene JH probe revealed that the H-2z/H-2z homozygotes, there was a propagation of distinct clonal populations between the spleen and the peritoneal cavity, a finding which suggested that in the major histocompatibility complex (MHC)-related microenvironments for CD5+ B cell propagation differ between the two compartments. All our findings taken together imply that certain different but related MHC haplotypes may predispose either to B-CLL or to autoimmune disease, in close relatives.

Animals↗
PubMed1991

Possible mapping of the gene for transient myeloproliferative syndrome at 21q11.2.

The parental origin of the extra chromosome 21 was studied in 20 patients with trisomy 21-associated transient myeloproliferative syndrome (TMS) using chromosomal heteromorphisms as markers; this was combined with a study of DNA polymorphisms in 5 patients. Of these, 10 were shown to result from duplication of a parental chromosome 21, viz., maternal in 8 and paternal in 2. A patient with Down syndrome-associated TMS had a paracentric inversion in two of his three chromosomes 21 [47,XY,-21,+inv(21)(q11.2q22.13)mat,+inv(21)(q11.2 q22.13)mat]. These findings support our hypothesis of "disomic homozygosity" of a mutant gene on chromosome 21 in 21-trisomic cells as being a mechanism responsible for the occurrence of TMS. The finding also suggests that the putative TMS gene locus is at either 21q11.2 or 21q22.13, assuming that the gene is interrupted at either site because of the inversion. The study of 5 TMS patients using DNA polymorphic markers detected a cross-over site on the duplicated chromosomes 21 between 21q11.2 (or q21.2) and 21q21.3 in one patient, and a site between 21q21.3 and q22.3 in another patient, evidence that confined the gene locus to the 21cen-q21.3 segment. These findings suggest that the putative TMS gene is located at 21q11.2. The extra chromosome 21 in the latter two TMS patients probably resulted from maternal second meiotic non-disjunction, in view of the presence of recombinant heterozygous segments on their duplicated chromosomes 21.

Chromosome Aberrations↗
PubMed1991

Hypoxia-induced change in prostanoids production and coronary flow in isolated rat heart.

The contribution of prostanoids to the change in coronary flow induced by hypoxia was examined in Langendorff-perfused rat heart. In the coronary effluent, 5 prostanoids, i.e., prostaglandins (PGs) D2, E2, and F2 alpha, 6-keto PGF1 alpha and thromboxane (TX) B2, were quantified by GC/MS, whereas PGA2, B2, and E1 were not detected under any conditions. During hypoxia, coronary flow initially increased to 189.5 +/- 17.8% of the control, and at the same time release of all PGs, except for TXB2, increased significantly (6-keto PGF1 alpha: from 3.57 +/- 0.98 to 5.54 +/- 1.25 pmol/min.g, D2: from 1.47 +/- 0.26 to 2.22 +/- 0.26 pmol/min.g, E2: from 0.27 +/- 0.08 to 0.96 +/- 0.21 pmol/min.g, F2 alpha: from 0.23 +/- 0.09 to 0.48 +/- 0.13 pmol/min.g, TXB2: from 0.61 +/- 0.10 to 0.58 +/- 0.15 pmol/min.g). During the later phase (10-20 min) of hypoxia, coronary flow decreased without concomitant decrease in the release of PGs. The administration of indomethacin (10 microM) and aspirin (1 mM) did not affect the normoxic coronary flow. However, during the early phase of hypoxia, they significantly suppressed the increase in coronary flow. Administration of arachidonic acid (1 mg/l) increased PG release 6.4-12.5-fold and increased coronary flow to 176.1 +/- 6.5% of the control level. In the presence of arachidonic acid, there was a good correlation between the coronary flow and the amount of released vasodilative PGs (PGE2 and 6-keto PGF1 alpha), suggesting the contribution of these PGs to coronary vasoregulation. On the other hand, when hearts were made hypoxic in the presence of arachidonic acid, percentage increase in PG release was much reduced, and similarly, coronary flow was not elevated. These results indicate that the increase in coronary flow during the early phase of hypoxia is mediated, at least in part, by the increased release of vasodilative PGs.

Animals↗
PubMed1991

CD5+ B cells in autoimmune disease and lymphoid malignancy.

Evidence is accumulating that CD5+ B cells belong to a developmental lineage distinct from that of conventional B cells and mainly participate in natural immunity. They have attracted attention because of their involvement in autoimmunity and lymphoid malignancy in both mice and humans. Patients with rheumatoid arthritis and Sjögren's syndrome were found to show a striking increase in the number of CD5+ B cells. B cell-chronic lymphocytic leukemia cells frequently express CD5. However, there are arguments against the role for CD5+ B cells in autoimmune disease, particularly in murine and human systemic lupus erythematosus (SLE). Whereas most IgM anti-DNA antibodies are produced by CD5+ B cells, high-affinity, pathogenic IgG antibodies are produced mainly by CD5- B cells. Either of two possibilities can explain the failure of CD5 expression of B cells responsible for producing IgG anti-DNA antibodies: either the cells are conventional B cells or the cells are CD5+ B cells that lack CD5 expression. In studies using SLE-prone NZB x NZW F1 mice and their H-2-congenic progeny, we discussed herein the possibility that CD5+ B lineage cells are also responsible for the pathogenic IgG autoantibody production by phenotypic switching from CD5+ to CD5-, probably under a particular genetic background. A line of H-2-congenic NZB x NZW F1 progeny failed to produce IgG anti-DNA antibodies, but in turn, showed a marked clonal proliferation of CD5+ B cells. Thus, it appears that genetically determined signals for either proliferation or differentiation would lead CD5+ B cells to cause distinct disease, i.e., autoimmune disease or lymphoid malignancy. Further studies using H-2-congenic New Zealand mice may provide insights into the correlation between autoimmunity and related lymphoid malignancy.

Animals↗
PubMed1991

Analysis of immunoregulatory activity of a choriocarcinoma-derived factor: specific suppression of proliferative process of cell-mediated immune responses including LAK cell generation.

The immunosuppressive activity of a JEG-3 choriocarcinoma-derived factor in human IL-2-dependent T cell responses has been studied, together with its effect on IL-2-independent T cell responses induced by 10 nM TPA. The factor completely suppressed the IL-2-independent proliferative responses of T cells but failed to suppress antigenic expression of activation-associated CD 25 molecules. Further studies examined the effect of the factor on LAK cell generation induced by rIL-2. Recombinant IL-2-induced LAK cell proliferation was observed on Day 4 and Day 5, but not on Day 3. As the factor suppressed the responses of LAK cell proliferation, we tested whether it blocked the generation of Day 3, Day 4 and Day 5 LAK cells. The addition of the factor failed to suppress the generation of Day 3 LAK cells, while it partially suppressed the lytic activity of Day 4 LAK cells and completely suppressed that of Day 5 LAK cells. The data suggest the presence of a heterogeneous pattern for LAK cell generation; one without proliferation, but the other requiring proliferation, to acquire killer activity. Taken together with the evidence that the factor failed to suppress NK activity, the choriocarcinoma-derived factor suppressed only the proliferative events of immunocompetent cells, but inhibited neither their activation nor the differentiation events. This immunosuppressive factor might be involved in the prevention of host-mediated rejection of choriocarcinoma cells or maternal rejection of the fetus.

Choriocarcinoma↗
PubMed1991

High incidence of sleep apnea syndrome in a male diabetic population.

In order to study the possible relationship between sleep apnea syndrome (SAS) and diabetes mellitus, we first examined the prevalence of SAS among 12,787 general patients (6554 males and 6233 females) who visited Katsumata Hospital at Nagoya, Japan. Among them, thirty-five males and five females were diagnosed as having SAS. The male patients were statistically analysed by the corrected Mantel-Haenszel chi-square test taking the body type into account, and it was found that the prevalence of SAS was significantly high both in a diabetic population and in a hypertensive one. Among 40 SAS patients of both sexes, 34 were given a glucose tolerance test (GTT) with oral administration of 75 g glucose. Thirteen showed a diabetic pattern, 12 a borderline pattern and only 9 had a normal pattern. All 13 diabetic patients had non-insulin-dependent type diabetes (NIDDM). The present results showed that SAS has a close relationship not only to hypertension but also to NIDDM.

Adolescent↗
PubMed1991

Tc-99m(V) DMSA uptake in cardiac amyloidosis.

Tc-99m(V) DMSA scintigraphy was performed on two patients with primary cardiac amyloidosis. Scintigraphy performed (after radionuclide administration) showed accumulation in the myocardium.

Amyloidosis↗
PubMed1991

C3 deposition in IgA nephropathy in children and adolescents.

The aim of this study was to assess the significance of C3 deposition in IgA nephropathy in children and adolescents. One hundred and two patients aged 5-21 years (57 male and 45 female) were studied. The findings of C3 deposition were classified into 8 groups by immunofluorescent (IF) pattern and intensity as follows: group MC3+ (N = 12): mesangiocapillary pattern and 3+ in intensity; group MC2+ (N = 13): mesangiocapillary and 2+; group MC1+ (N = 4): mesangiocapillary and 1+; group M3+ (N = 11): mesangial and 3+; group M2+ (N = 24): mesangial and 2+; group M1+ (N = 18): mesangial 1+; group S (N = 12): only segmentally positive; and group N (N = 8): negative. Histological changes were scored semiquantitatively as an activity index (cellular proliferation, necrosis, interstitial cell infiltration, and cellular crescents) and a chronicity index (mesangial sclerosis, segmental and global glomerular sclerosis, fibrous crescents, adhesion and tubulo-interstitial change). IF findings were scored semiquantitatively and laboratory findings were also studied. The following results were obtained: 1) The scores of total activity index in MC groups were higher than in the M, S or N groups, and the greater the degree of C3 deposition, the higher the score; 2) Such result was not evident in the chronicity index; 3) High IF scores of IgG and IgM were found in the MC3+ and MC2+ groups; 4) Hematuria was more severe in MC3+ and MC2+ than in other groups, and proteinuria was more prominent in the MC than other groups. Thus the degree of C3 deposition was parallel with histological activity and urinary findings.

Adolescent↗
PubMed1991

C3 deposition in serially biopsied children with IgA nephropathy.

Twenty-five children with IgA nephropathy were studied by serial renal biopsy to investigate C3 deposition. The children were classified into three groups according to the immunofluorescent (IF) course of C3 deposition: group I (N = 9): unchanged or slightly decreased; group II (N = 4): changed to segmental deposition; and group III (N = 12): changed to negative deposition. Histological changes were scored semiquantitatively as an activity index (cellular proliferation, necrosis, interstitial cell infiltration and cellular crescents) and a chronicity index (mesangial sclerosis, segmental and global glomerular sclerosis, adhesion, fibrous crescents and tubulo-interstitial change). The IF findings were scored semiquantitatively and laboratory data were also studied. The following results were obtained: 1. Normal urinalysis was often observed in group III; 2. The IF scores of IgA and IgG were decreased at the second biopsy in all groups, most notably in group III; 3. The activity indices at second biopsies were decreased in all groups, most notably in groups II and III, consistently with our previous study which showed that C3 deposition increases in accordance with histological activity; 4. The chronicity index was unchanged in all groups and C3 deposition did not reflect histological chronicity. Thus, this study indicates that C3 deposition occurs as the disease progresses and reflects histological activity.

Adolescent↗
PubMed1991

Long-term follow-up of electrocochleogram in Ménière's disease.

Serial electrochochleogram (ECochG) recordings were obtained over a long time span from 24 patients with Ménière's disease showing dominant negative SP. The long-term fluctuation of responses (especially SP) was evaluated. Dominant -SP or abnormally increased SP/AP ratio has been unchanged over long periods in most operated or nonoperated patients. It is assumed that the generation of -SP dominance may chiefly result from the malfunction of hair cells, which may be caused by abnormal changes in inner ear fluids associated with endolymphatic hydrops or by other unknown disturbances in the cochlea. The mechanical factor of basilar membrane displacement can hardly be considered as a main cause of SP abnormality.

Audiometry, Evoked Response↗
PubMed1991

Effect of cardiac sympathetic nerve stimulation on acutely ischemic myocardium--a comparison with the response to exogenous noradrenaline.

To assess the integrity of an adrenergic nervous function in acute myocardial ischemia, the contractile response of the ischemic region to cardiac sympathetic nervous stimulation (CSNS) was measured in comparison that with to exogenous noradrenaline (NA) infusion. In 13 anesthetized open chest mongrel dogs, haemodynamic changes, segmental wall motion, and the concentration of NA in the efferent coronary vein were measured. CSNS was performed by electrically stimulating the left ansa subclavia. Data concerning baseline values, values during CSNS, and those obtained during NA infusion both before and up to 5 h after coronary occlusion were compared. Regional myocardial blood flow of the ischemic region was also measured using the H+ clearance method. Systolic expansion with coronary occlusion was not changed or augmented by CSNS. However, improvement was observed in all experiments when NA infusion was used. The percent change of systolic shortening, indicating the response of segmental wall motion to CSNS, decreased soon after occlusion, recovered temporarily within 30 min after occlusion, but did not improve throughout the period after 60 min. The decrease of NA overflow into the efferent vein by CSNS showed a biphasic pattern; reduction occurring immediately after occlusion and again 3-5h after occlusion. Throughout these experimental studies it was considered that the preserved responses to the exogenous injected NA represented the contribution of presynaptic factor.

Animals↗
PubMed1991

A case of epicardial cyst.

A rare case of epicardial cyst diagnosed at surgery was presented. A 64-year old woman was admitted for evaluation of a mediastinal mass shown by echocardiography to be adjacent to both ventricles. Computed tomography (CT) and magnetic resonance imaging (MRI) studies were performed. On CT, there was evidence of an abnormal mass lesion at the lateral side of the outlet of the right ventricle. The CT number of the mass was 24.7, suggesting cystic lesion. MRI revealed that the intensity of the lesion signal was higher than that of subcutaneous fat on the T2 weighted image. On the T1 weighted image, a low intensity was identified in the same region. During operation a mass originating from the epicardium was diagnosed as an epicardial cyst.

Echocardiography↗
PubMed1991

Differential roles of the adrenal gland in the suppression of morphine antinociceptive tolerance development by alpha- and beta-adrenergic blockers.

Concomitant treatment with phentolamine, an alpha-blocker, or with propranolol, a beta-blocker, suppressed the development of morphine tolerance in sham-operated (Sham) mice. In adrenalectomized (ADX) mice, daily morphine developed tolerance as well as in the Sham group, and concurrent phentolamine suppressed the development of tolerance, whereas such suppression by propranolol was abolished. Supplemental treatment of ADX mice with dexamethasone did not restore the suppressive effect of propranolol. These results suggest that different mechanisms underlie the prevention of tolerance development by alpha- and beta-blockers, and that adrenal cortex does not seem to participate in the suppression by beta-blockers.

Adrenal Glands↗
PubMed1991

Morphometrical changes in the apical surface of the colonic absorptive cells in perinatal rats with special reference to the effect of fetal oral administration of milk in utero.

Perinatal changes in the apical surface of the colonic absorptive cells in the rat were studied morphometrically. Cell microvilli length increased from day 20 through neonatal day 3, during which a maximum incremental growth rate was noted between fetal day 22 and neonatal day 1. Microvilli width remained almost constant throughout the period. Enlargement of the apical surface of the microvilli showed a similar developmental pattern as was seen from the measurement of length and surface area of any one of the microvilli. Fetal oral administration of milk in utero caused incremental growth in length and surface area, as well as an associated apical surface enlargement. The present study indicates that the function of the colonic absorptive cells, which is acquired later on in utero, is activated by ingestion of maternal milk after birth.

Administration, Oral↗
PubMed1991

Retinal ganglion cells projecting to the nucleus of the optic tract in the rat.

The nucleus of the optic tract (NOT) has been identified as the link between the retina and the premotor nuclei in the pathway mediating the optokinetic nystagmus (OKN). However, it is still unclear from what parts of the retina and what kinds of retinal ganglion cells the NOT receives visual inputs related to OKN. In the present study, horseradish peroxidase conjugated with wheatgerm agglutinin (WGA-HRP) was injected into the NOT of hooded rats to investigate retrogradely labeled cells in the retina. A solution of WGA-HRP was injected into the NOT through a glass micropipette. Injection sites of the brain and the retina were processed by tetramethyl benzidine protocol and Hanker-Yates method. The labeled cells were observed in the whole area of the retina contralateral to the injection site, while located only in the ventral region of the retina ipsilateral to the injection site. In the retina contralateral to the injection site, a large number of small-sized cells and a few medium-sized cells were labeled diffusely except for surroundings of the optic disc, whereas in the ipsilateral retina there were small and medium-sized cells in the ventral part, being about 8 times greater than those in the contralateral retina. The present study indicates that visual signals responsible for OKN are conducted through the retinal ganglion cells mainly contralaterally, and only from the ventral area of the retina ipsilateral to the injection site.

Animals↗
PubMed1991

Ultracytochemical localization of acid phosphatase and trimetaphosphatase activities in the transitional epithelium of the rat urinary bladder.

Acid phosphatase and trimetaphosphatase activities have been demonstrated cytochemically in the transitional epithelium of the rat urinary bladder. Acid phosphatase activity was examined by the method of Robinson and Karnovsky (1983), and trimetaphosphatase activity was examined by the method of Kobayashi et al. (1988). Intense positive reaction for acid phosphatase activity was observed with both beta-glycerophosphate and p-nitrophenyl phosphate as substrates, in lysosomes, Golgi complex, GERL, multi-vesicular bodies and wrapping lysosomes. The reaction product of the trimetaphosphatase activity was visualized as fine particulated deposits along the limiting membrane of some lysosomes, and of tubular structures located in the basal cytoplasm. There seems to be a fine distinction and reciprocal complementary functional relationship between two kinds of lysosomes containing either acid phosphatase or trimetaphosphatase activity.

Acid Anhydride Hydrolases↗
PubMed1991

Identification of colony-stimulating factor activity in patients with malignant tumors associated with excessive leukocytosis.

We have tried to demonstrate and identify colony-stimulating factor (CSF) activity in the plasma, pleural fluid, ascites or culture supernatant of tumor cells in 11 patients with malignant tumors associated with unexplained persistent leukocytosis. The specimens were treated with anti-granulocyte (G)-CSF or anti-granulocyte/macrophage (GM)-CSF monoclonal antibodies, then added to GM-progenitor (CFU-GM) cultures without exogenous CSFs. In all patients, untreated specimens generated CFU-GM-derived colonies, and colony formation was clearly inhibited by only one of the two antibodies, indicating the presence of either G-CSF or GM-CSF in the specimens. Furthermore, we measured the concentrations of G-CSF or GM-CSF in the specimens using an enzyme-linked immunosorbent assay, and confirmed the results by CFU-GM assay. Two patients were shown to have GM-CSF-producing tumors, while the other patients were G-CSF-producing. These assays are useful in identifying CSF activity in patients with CSF-producing tumors.

Aged↗