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Biomedical subjects

H Hamaguchi

Publications and source records attributed to H Hamaguchi.

At least 109 records · Page 6Linked to original sources
PubMed1996

Further association study on dopamine D2 receptor variant S311C in schizophrenia and affective disorders.

The dopamine D2 receptor gene is a candidate gene for schizophrenia because the potency of certain neuroleptics correlates with their affinity for this receptor. Case-control studies in 291 schizophrenics, 78 patients with affective disorders, and 579 controls on an association of a molecular variant of S311C of the dopamine D2 receptor with psychiatric disorders were conducted. The frequency of individuals with S311C was significantly higher in schizophrenics with the absence of negative symptoms (17.1%, P < 0.00001), but similar in schizophrenics with the presence of negative symptoms (5.7%, P = 0.46) when compared with the controls (4.1%). The frequency of S311C was significantly higher in familial schizophrenics from one local area but not in those from other areas. It was significant that S311C was frequently present in patients with mood-incongruent psychotic affective disorders (33.3%, P < 0.0001), but not in those with other affective disorders. These data suggest that S311C might be one of the genetic factors for symptomatic dimensions of delusions and hallucinations and might be involved in underlying clinical heterogeneity in schizophrenia and affective disorders.

Adult↗
PubMed1996

Prolonged survival of rat hepatic allografts pretreated with a single donor-specific blood transfusion: the distribution of donor cells expressing class I major histocompatibility complex antigens in the recipient.

We previously reported that a pretransplant transfusion of either ACI strain rat donor blood or PVG.r1 strain blood, which shares only the RT1.A class I major histocompatibility complex (MHC) region with an ACI donor, significantly prolonged the survival of ACI-to-LEW rat hepatic allografts, suggesting that the class I MHC antigens can be immunosuppressive in rat hepatic allografts. The distribution of the donor cells expressing RT1.Aa class I MHC antigens in the recipients was investigated using a MN4-91-6 mouse anti-rat class I (RT1.Aa) MHC monoclonal antibody. The donor class I MHC-positive cells accumulated mainly in the splenic white pulp and lymph nodes at 12 and 24 hr after blood transfusion, while very few cells were seen in the thymus, liver, lungs, and kidneys. The number of cells began to decrease in the splenic white pulp and lymph nodes at 24 hr after transfusion. This may indicate the destruction of donor cells by the recipient cells. Within 48 hr after transfusion, most cells disappeared from the recipient tissue. In an attempt to study the role of the spleen in inducing immunological unresponsiveness, a splenectomy was performed at the time of transplantation and this abrogated the prolongation of hepatic allograft survival in the recipients which received the donor blood. These findings suggest that the presence of class I MHC-positive cells in the splenic white pulp, a T-dependent area, may play an important role in inducing immunological unresponsiveness.

Animals↗
PubMed1996

Suppression of hepatic allograft rejection in the rat by mitomycin C-treated donor splenocytes: in situ splenic distribution of donor class I major histocompatibility complex antigen-positive cells in the recipient.

A single intravenous injection of 3 x 10(6) donor splenocytes treated with mitomycin C (MMC) 7 days before hepatic transplantation prolongs survival of hepatic allografts in the ACI(RT1a) to LEW(RT1(1)) rat combination. This effect is donor specific. The in situ distribution in the recipient of the donor cells administered preoperatively was investigated using intracellularly fluorescence-labeled donor splenocytes. The donor cells were accumulated mainly in the splenic white pulp and lymph nodes at 12 and 24 hr after injection. Contrarily, very few cells were seen in the thymus, liver, kidney, and lung. The number of cells with dull and weak fluorescence began to increase in the splenic white pulp and lymph nodes at 24 hr after injection. This may indicate the breakdown of donor cells by recipient cells. In contrast, a number of donor cells could be detected even after 48 hr and a few cells at 7 days after splenocyte injection in the LEW-to-LEW isogeneic combination. As we previously revealed the role of class I major histocompatibility complex (MHC) antigens in prolonging hepatic allograft survival in the rat, the splenic distribution of donor class I MHC-positive cells in the recipient after intravenous administration of MMC-treated donor splenocytes was studied using immunostaining with a MN4-91-6 mouse anti-rat RT1.Aa class I MHC monoclonal antibody. The donor class I-positive cells accumulated mainly in the splenic white pulp at 12 and 24 hr after injection. This is similar to that observed in the fluorescence study. Within 48 hr after injection, most cells had disappeared from the recipient tissue. These findings suggest that the splenic white pulp, a T-dependent area, may play an important role in inducing immunological unresponsiveness.

Animals↗
PubMed1996

Apolipoprotein(a) and pentanucleotide repeat polymorphisms are associated with the degree of atherosclerosis in coronary heart disease.

To evaluate whether a high level of lipoprotein(a) (Lp(a)) is a risk for the development of coronary heart disease (CHD), 94 Japanese patients and 64 age-matched Japanese controls, diagnosed after coronary angiography (CAG), were analyzed with special reference to the relations between the degree of atherosclerosis, Lp(a) levels and the apolipoprotein(a) (apo(a)) genotypes. the degree of atherosclerosis was evaluated based on CAG findings in the following three ways: the number of diseased vessels, the Gensini score, and the presence or absence of vascular ulcers and/or irregular outlines of coronary stenotic lesions. Apo(a) protein sizes and the pentanucleotide (TTTTA) repeat polymorphism in the 5' control region of the apo(a) gene were analyzed. Multivariate predictors for the number of diseased vessels were, in decreased order of significance, plasma Lp(a) levels, history of smoking, hypertension, diabetes mellitus, and body mass index (BMI). Independent factors associated with the Gensini score were Lp(a) levels, BMI, hypertension, and diabetes mellitus. A negative association of Lp(a) levels with apo(a) protein sizes, and higher Lp(a) levels in those homozygous for an allele with 8 8 (TTTTA)-repeats, was found in both the controls and patients. In decreasing order of significance, apo(a) protein sizes, the degree of atherosclerosis, the genotype of the pentanucleotide repeat, and gender were independent predictors of Lp(a) levels in stepwise regression models. Apo(a) protein sizes were a significant predictor, and the genotype homozygous for the 8 (TTTTA)-repeats was a possible predictor, for the degree of atherosclerosis in CHD. These findings support the notion that a high Lp(a) level is a risk for the development of atherosclerosis in CHD.

Alleles↗
PubMed1996

Plasma soluble interleukin-2 receptor level in patients with primary myelodysplastic syndromes: a relationship with disease subtype and clinical outcome.

To assess the hypothesis that the plasma soluble interleukin-2 receptor (sIL-2R) level may have predictive value for morbidity/mortality in patients with myelodysplastic syndromes (MDS), we determined in plasma sIL-2R level of 80 MDS patients and examined their subsequent clinical course. Compared with low-risk MDS (refractory anaemia (RA) and RA with ringed sideroblasts) patients and normal subjects, the plasma sIL-2R level was significantly elevated in high-risk MDS (three other MDS subtypes and acute leukaemia following MDS) patients (high-risk MDS versus low-risk MDS, P < 0.01; high-risk MDS versus normal subjects, P < 0.01). 14/40 low-risk MDS patients developed at least one of the following during the follow-up period: erythrocyte transfusion dependence, infections requiring hospitalization, disease progression or MDS-related death. The plasma sIL-2R level was higher in these eventful subjects than in event-free low-risk subjects (P < 0.0001), and all of 10 low-risk subjects with a plasma sIL-2R level > 540 U/ml experience at least one event. By logistic regression analysis of various parameters in these 40 low-risk subjects, the plasma sIL-2R level was identified as the strongest independent parameter for predicting eventful subjects (P < 0.0047). The plasma sIL-2R level did not show a predictive value in high-risk MDS. This study revealed that the plasma sIL-2R level is significantly elevated in high-risk MDS and suggested that the plasma sIL-2R level is a valuable predictive factors for the clinical outcome in low-risk MDS.

Adult↗
PubMed1996

Failure to find associations of the CA repeat polymorphism in the first intron and the Gly-63/Glu-63 polymorphism of the neurotrophin-3 gene with schizophrenia.

This study aimed to replicate positive associations between polymorphisms of the neurotrophin-3 gene and schizophrenia. The reported associations, which were the results of searching for mutations in the locus in schizophrenics under the hypothesis of neurodevelopmental etiology of schizophrenia, are that the states carrying the (CA)23 allele of the CA repeat in the first intron have a 2.56-fold increased risk of schizophrenia and those carrying the allele Glu-63 instead of Gly-63 have a 2.6-fold increased risk of schizophrenia with onset before 25 years and with duration of the illness of more than 10 years. We analyzed these polymorphisms in 80 schizophrenics with onset before 25 years of age and with duration of illness of more than 10 years and 80 age-matched psychosis-free controls. With our sample size, there was a 90% chance of detecting odds ratios observed in initial positive reports. We found similar allele and genotype frequencies of both polymorphisms between the schizophrenic and control groups. We failed to support associations between the polymorphisms of the neurotrophin-3 gene analyzed and schizophrenia.

Adult↗
PubMed1996

Sequestration of the short and long isoforms of dopamine D2 receptors expressed in Chinese hamster ovary cells.

The short (D2S) and long (D2L) isoforms of dopamine D2 receptors were stably expressed in Chinese hamster ovary cells, and dopamine-induced sequestration was examined by measuring the loss of binding of the hydrophilic ligand [3H]sulpiride from the cell surface. Dopamine treatment of Chinese hamster ovary cells expressing D2S for 30 min at 37 degrees caused a 43.8 +/- 3.4% decrease in [3H]sulpiride binding activity measured by incubation of the treated cells with [3H]sulpiride at 4 degrees for 4 hr after the dopamine was washed out. The half-life of the decrease in binding was estimated to be 18.7 +/- 1.6 min, and the concentration of dopamine giving a half-maximal effect (EC50) was estimated to be 180 +/- 90 nM. The decrease was reversible, and the binding activity was recovered by washing out the dopamine and incubating the cells at 37 degrees for 30 min but was not reversible when the cells were incubated at 4 degrees. The binding activity of [3H]spiperone, a hydrophobic ligand, was not affected by the dopamine treatment under the same experimental conditions. These results indicate that approximately one half of the D2S receptors undergo agonist-induced sequestration, probably endocytosis, in a reversible and temperature-dependent manner. Sequestration of D2L receptors was not as apparent as that of D2S receptors; the decrease in [3H]sulpiride binding activity was 21.6 +/- 0.9% and the rate of the decrease was delayed, with a half-life of 33.2 +/- 7.8 min, although effective concentrations of dopamine were similar, with EC50 = 170 +/- 50 nM. A D2S receptor variant containing a missense mutation changing Ser311 in the third intracellular loop to cysteine was found to be sequestered to a significantly lesser extent than with wild-type D2S receptors. This finding was discussed with respect to the report that this variant gene is found more frequently in schizophrenic patients than in control subjects.

Animals↗
PubMed1996

Wound healing effect of the new imidazole antimycotic lanoconazole in rats.

The wound healing effect of cream preparations of lanoconazole (CAS 101530-10-3, NND-318), an antimycotic imidazole compound, was examined using an excisional open skin-wound model produced on the back of rats. The rapid decrease in the size of wounded areas showed that 0.5% and 1% lanoconazole creams accelerated spontaneous healing. The effectiveness was almost similar to that of an ointment containing 5% deproteinized calf blood extract (DCBE), a wound healing agent on the market. In contrast, neither 1% clotrimazole cream nor 1% bifonazole cream, both of which are imidazole antimycotics, showed an accelerative effect. The wound healing effect of lanoconazole was further confirmed by histological evaluation; a thicker and more cellular granulation tissue was formed, and epidermal regeneration was more stimulated by lanoconazole than by non-treatment or vehicle alone. The effect of lanoconazole on the formation of granulation tissue in rats was also studied using a cotton pellet implantation method. Lanoconazole accelerated the formation of this tissue in terms of dry weight in a dose dependent manner (0.5-4 mg/pellet), and collagen content and angiogenesis also increased in the stimulated tissue, indicating that these accompany the compound-induced acceleration of tissue formation. These results suggest that lanoconazole has a distinctive wound healing effect which is a feature no other imidazole antimycotic is known to possess to date.

Administration, Topical↗
PubMed1996

Wound healing effect of malotilate in rats.

The wound healing effect of malotilate (CAS 59937-28-9, NKK-105) was investigated by using an excisional skin-wound model produced on the back of normal and healing-impaired (induced by prednisolone pretreatment) rats. The rapid decrease in the square measure of wound areas and the improvement in the histological evaluation clarified that 0.3% and 1% cream preparations of malotilate were obviously effective in accelerating spontaneous healing in the normal rats. The accelerative effect of malotilate cream preparations was likely superior to that of an ointment containing 5% deproteinized calf blood extract used as a reference agent. The same effect was also observed in the healing-impaired rats. The histological findings revealed that a thicker and more cellular granulation tissue, which in turn created an adequate bed for rapid re-epithelization, was formed in the malotilate-treated animals. Acceleration of granulation tissue formation by malotilate was also supported by the cotton pellet implantation method. It is concluded from these results that malotilate seems to be a promising agent for topical wound therapy.

Administration, Topical↗
PubMed1995

Fluorescence spectra of bacteriorhodopsin and the intermediates O and Q at room temperature.

An unequivocal answer is given to the question of why the reported fluorescence spectra of bacteriorhodopsin (bR568) have been different from one another. The inconsistency is shown to arise from the accumulation of the fluorescent intermediates O and Q (KN) by cw excitation light. Their fractions in the photo-stationary states depend on the excitation power and the suspension pH. We report the intermediate-free fluorescence spectrum of bR568 obtained with a weak excitation source (632.8 nm, 5.3 x 10(15)-1.9 x 10(16) photons cm-2.s-1) and a near-IR sensitive intensified photodiode array system. The fluorescence maxima of the spectra, F(lambda) and f(nu), are located at 755 +/- 10 nm and 12700 +/- 200 cm-1, respectively. The spectrum of O is identical to that of the deionized purple membrane bR605 (Fmax = 750 +/- 5 nm, fmax = 13,000 +/- 100 cm-1). Q (KN) exhibits a blue-shifted spectrum more than that of bR568 (Fmax < 720 nm, fmax > 13,400 cm-1).

Bacteriorhodopsins↗
PubMed1995

Mid-trimester fetal sex determination from maternal peripheral blood by fluorescence in situ hybridization without enrichment of fetal cells.

To determine the fetal sex on 30 women who were 16-20 weeks pregnant, about 100,000 maternal blood nucleated cells were analysed by means of fluorescence in situ hybridization (FISH) with a Y-chromosome-specific DNA probe. Cells with the hybridization signal were detected in 12 of the 30 women. All the 12 mothers gave birth to a male child. Of the other 18 women who had no Y-positive cells in the peripheral blood, 14 gave birth to a female child and four gave birth to a male child. These false-negative results probably occurred because the number of cells examined was inadequate. The data obtained in this study suggest that fetal sex determination using maternal peripheral blood with FISH is possible and that this diagnostic method will be clinically useful when more cells are analysed.

Blood Cells↗
PubMed1995

Characterization of hepatic allograft infiltrates in rats pretreated with donor-specific blood transfusion (DST).

A single intravenous injection of 1 ml freshly heparinized donor blood given 7 days prior to transplantation prolonged significantly the survival of subsequent hepatic allografts in fully allogeneic ACI(RT1a)-to-LEW(RT1(1)) rats. The cellular identity of allograft infiltrates was investigated at various times after transplantation using OX8 (CD8) and W3/25 (CD4) monoclonal antibodies. The number of CD8+ cells increased rapidly and reached a peak on Day 3 after transplantation of the untreated allografts. Similarly, the number of CD8+ cells in the allografts from DST-treated rats was maximum on Day 3 and decreased gradually thereafter. The maximum number of CD4+ cells was found on Day 3 in untreated allografts. In contrast, no significant infiltration of CD4+ cells occurred during the first 7 days after transplantation in DST-treated allografts. Thereafter, the number of CD4+ cells increased rapidly and reached a peak on Day 14. CD4+ cells remained persistently elevated in hepatic allografts of rats pretreated with DST, but did not become functionally competent or initiate rejection. These findings suggest that persistent infiltration by CD4+ cells is a characteristic feature of long-surviving hepatic allografts in rats pretreated with DST.

Animals↗
PubMed1995

Serum lipoprotein(a) concentrations and apolipoprotein(a) phenotypes in the families of NIDDM patients.

We studied the quantitative and qualitative characteristics of lipoprotein(a) [Lp(a)] as a function of apolipoprotein(a) [apo(a)] phenotype in 87 members (42 males, 45 females) of 20 diabetic families, 26 of whom were diagnosed with non-insulin-dependent diabetes mellitus (NIDDM) with moderate glycaemic control (HbA1c 7.1 +/- 1.2%). Apo(a) phenotyping was performed by a sensitive, high-resolution technique using SDS-agarose/gradient PAGE (3-6%). To date, 26 different apo(a) phenotypes, including a null type, have been identified. Serum Lp(a) levels of NIDDM patients and non-diabetic members of the same family who had the same apo(a) phenotypes were compared, while case control subjects were chosen from high-Lp(a) non-diabetic and low-Lp(a) nondiabetic groups with the same apo(a) phenotypes in the same family. Serum Lp(a) levels were significantly higher in NIDDM patients than in non-diabetic subjects (39.8 +/- 33.3 vs 22.3 +/- 19.5 mg/dl, p < 0.05). The difference in the mean Lp(a) level between the diabetic and non-diabetic groups was significantly (p < 0.05) greater than that between the high-Lp(a) non-diabetic and low-Lp(a) non-diabetic groups. An analysis of covariance and a least square means comparison indicated that the regression line between serum Lp(a) levels [log Lp(a)] and apo(a) phenotypes in the diabetic patient group was significantly (p < 0.01) elevated for each apo(a) phenotype, compared to the regression line of the control group. These data together with our previous findings that serum Lp(a) levels are genetically controlled by apo(a) phenotypes, suggest that Lp(a) levels in diabetic patients are not regulated by smaller apo(a) isoforms, and that serum Lp(a) levels are greater in diabetic patients than in non-diabetic family members, even when they share the same apo(a) phenotypes.

Apolipoproteins↗