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Biomedical subjects

H Tomiyama

Publications and source records attributed to H Tomiyama.

At least 19 recordsLinked to original sources
PubMed1995

Inhibition of gamma delta T cell recognition by receptors for MHC class I molecules.

NK cells have receptors for MHC class I molecules that inhibit cytotoxicity against target cells. We show that recognition of gamma delta CTL is negatively regulated by receptors for MHC class I molecules. Cytolysis of C1R cells by gamma delta CTL clones was inhibited by the expression of polymorphic HLA class I molecules on target cells and was restored by blocking with anti-HLA class I mAb, suggesting the presence of inhibitory receptors for HLA class I molecules. The receptors for HLA class I molecules on gamma delta T cells were heterogenous. The immune responses to various Ags may be regulated via these inhibitory receptors on T cells and NK cells.

Clone Cells↗
PubMed1995

Isolation of a human allo-peptide presented by HLA-B51 molecules.

Recent studies have demonstrated directly that alloreactive mouse CTL recognize peptides presented by MHC class I molecules. However, there is no direct evidence that human alloreactive CTL recognize peptides presented by HLA class I molecules. We have isolated an HLA-B51 alloreactive CTL clone, 2B3, that did not kill the TAP defective cell lines T2 and .174, whereas it killed the TAP-positive cell line T1 and .174 cells transfected with TAP genes. These findings suggested that this clone recognizes a TAP-dependent allo-peptide. We attempted to isolate the human allo-peptide recognized by the 2B3 clone from HLA-B51 molecules. A naturally occurring HLA-B*5101 binding peptide isolated from T1 cells was recognized by the 2B3 clone. The peptide was also isolated from HLA-B*5101 molecules purified from C1R-B*5101 cells. In the present study, we directly demonstrated that a human alloreactive CTL clone recognizes peptide presented by HLA class I molecules.

Antigen Presentation↗
PubMed1995

Changes in the E/A ratio induced by handgrip-exercise are related to changes in the plasma atrial natriuretic peptide level, but not to changes in brain natriuretic peptide in mild essential hypertension.

We investigated the relationship between changes in atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) and changes in cardiac function during mild exercise in patients with mild hypertension. The handgrip test (HGT) was performed by 21 untreated, mildly hypertensive patients, mean age 45 +/- 5 years. M-mode and pulse Doppler echocardiograms were recorded before and during HGT. In 7 patients (Group A), diastolic function, which was determined by the peak early velocity and peak atrial velocity (E/A) ratio using Doppler echocardiography was attenuated during HGT (1.19 +/- 0.21 TO 1.04 +/- 0.16, p < 0.05). There was no change in diastolic function in the remaining 14 patients, left atrial diameter, cardiac index, ejection fraction, plasma renin activity, plasma norepinephrine, blood pressure, nor heart rate were different between the two groups. While ANP was increased in Group A during HGT (from 41.0 +/- 18.2 to 54.0 +/- 24.1 pg/ml, p < 0.05) it was unchanged in Group B (36.8 +/- 16.3 to 33.5 +/- 11.9 pg/ml). BNP did not change in either Group (Group A: 2.9 +/- 3.1 to 3.0 +/- 3.4 pg/ml, Group B: 2.6 +/- 1.6 to 3.6 +/- 4.8 pg/ml). The percent change in ANP during HGT did not correlate with the percent change in BNP. Thus, the impairment of cardiac functional reserve appeared to influence ANP excretion in patients with mild hypertension.

Adult↗
PubMed1992

Blood pressure response to hyperinsulinemia in salt-sensitive and salt-resistant rats.

We investigated the role of insulin in salt-sensitive hypertension in Dahl salt-sensitive and salt-resistant rats. The rats were kept in metabolic cages, and sodium intake and urinary sodium excretion were measured. In salt-sensitive rats receiving a 0.3% NaCl diet, sodium retention was significantly greater at weeks 1 and 2 in rats that received an insulin infusion than in those receiving a saline infusion. Mean arterial blood pressure and plasma norepinephrine levels were significantly higher at week 3 in insulin-treated rats than in saline-treated rats (mean arterial pressure, 137 +/- 3 mm Hg versus 119 +/- 3 mm Hg, p < 0.05; plasma norepinephrine, 0.40 +/- 0.02 ng/ml versus 0.27 +/- 0.01 ng/ml, p < 0.05). Insulin did not influence sodium retention, mean arterial pressure, or plasma norepinephrine in salt-resistant rats. Coadministration of an alpha-blocker (bunazosin, 10 mg/kg per day for 3 weeks) in salt-sensitive rats abolished the insulin-induced elevations in mean arterial pressure and sodium retention. When salt-sensitive rats were fed a low salt diet (0.03% NaCl), insulin did not raise mean arterial pressure. Thus, insulin elevated blood pressure only in the salt-sensitive model. The sympathetic nervous system and sodium retention in the early phase of insulin overload may contribute to elevation of mean arterial pressure in this model.

Animals↗
PubMed1991

Role of sympathetic activity in blood pressure reduction with low calorie regimen.

To investigate the effects of a low calorie regimen on sympathetic function and its relation to blood pressure response, 22 untreated obese essential hypertensive patients (50 +/- 2 years, body mass index 29 +/- 1 kg/m2) were hospitalized and a diet was prescribed of 2,000 kcal/day for 5 days (control period) followed by 800 kcal/day for 21 days without changing salt intake (8-10 g/day). The dose of intravenous phenylephrine infusion needed to elevate systolic blood pressure 20 mm Hg (CD20) and the 24-hour urinary excretion of norepinephrine (UNE) were measured. During the low calorie period, blood pressure normalized in 14 patients (responder group, 124 +/- 3/79 +/- 4 mm Hg) and eight remained hypertensive (poor responder group, 158 +/- 6/103 +/- 3 mm Hg). At the control period, blood pressure and body mass index were similar, but the responder group had higher UNE (134 +/- 15 micrograms/day) and CD20 (127 +/- 11 micrograms) than the poor responder group (89 +/- 6 micrograms/day and 79 +/- 13 micrograms, respectively). During the low calorie period, both UNE (87 +/- 15 micrograms/day) and CD20 (74 +/- 10 micrograms) decreased in the responder group; no change was seen in the poor responder group. Changes in UNE and systolic blood pressure were correlated (r = 0.6, p less than 0.05). In conclusion, suppression of sympathetic activity plays a role in blood pressure reduction during moderate caloric restriction.

Blood Pressure↗
PubMed1990

Renal effects of Fab fragments of kinin antibodies on deoxycorticosterone acetate-salt-treated rats.

The role of the renal kallikrein-kinin system in the regulation of renal function is not completely understood. Intrarenal kinins can influence renal function by acting as paracrine hormones at basolateral, luminal, or both sites in the distal nephron. To examine the role of intrarenal kinins in deoxycorticosterone acetate-salt-treated rats, which have high renal kallikrein, Fab fragments of antibradykinin antibody or DArg[Hyp3Thi5,8DPhe7]bradykinin, a kinin antagonist, were used to block kinins. At the dose used, the antibody (25 mg) and kinin antagonist (10 micrograms/min/rat) inhibited the hypotensive effect of intra-arterially injected bradykinin (100 ng) by 70% and 52%, respectively. The antibody appeared in the urine within 30 minutes after administration. Urinary volume was lowered from 9.4 +/- 0.2 to 6.7 +/- 0.4 microliters/min/g kidney wt (p less than 0.001, paired t test) by the antibody and from 8.5 +/- 0.3 to 6.8 +/- 0.4 microliters/min/g kidney wt (p less than 0.004, paired t test) by the kinin antagonist. The antibody lowered urine sodium excretion from 1.11 +/- 0.04 to 0.88 +/- 0.06 mueq/min/g kidney wt (p less than 0.001, paired t test), whereas the kinin antagonist had no significant effect. Neither altered blood pressure, renal blood flow, or glomerular filtration rate. These data suggest that in deoxycorticosterone acetate-salt-treated rats, excretion of water and sodium is regulated in part by kinins. The antidiuretic effect of the antibody and kinin antagonist might be due to blockade of kinins in the vascular-interstitial space of the kidney, since the kinin antagonist is likely hydrolyzed in the proximal tubule and does not reach the lumen of the distal nephron.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Studies on evaluation of the oxygen transport system function with multistage treadmill stress testing: comparison between normal control subjects and patients with coronary heart disease].

The oxygen transport system (OTS) function was evaluated with multistage treadmill stress testing on 171 normal control subjects and 80 patients with coronary heart disease (CHD). After Bruce's definition, OTS function was expressed with functional aerobic impairment (FAI), left ventricular impairment (LVI) or myocardial aerobic impairment (MAI), heart rate impairment (HRI) or chronotropic reserve impairment (CRI) and peripheral circulatory impairment (PCI). All subjects were monitored on heart rate, blood pressure, electrocardiogram and endtidal O2 and CO2 before and every one minute during the symptom limited maximal stress testing. Seventy three of 80 coronary patients were subjected to the coronary arteriography and were classified into four groups; 31 with single vessel disease (SVD), 20 with double vessel disease (DVD), 15 with triple vessel disease (TVD) and 7 with A-C bypass surgery. Comparison between normal control subjects and the CHD patients with regard to the relation of age and VO2max derived from the linear regression analysis disclosed the identical age-related decrease in VO2max in both groups. The age corrected VO2max in the CHD patients, however, was 2.2 METS less than that of normal control subjects. Therefore, the level of VO2max in CHD patients was determined not only by disease, but also by ageing process itself. Comparisons among three CHD groups with regard to FAI, LVI, HRI and PCI clearly demonstrated different functional impairments paralleling to the severity of the disease process. On the other hand, the patients with A-C bypass surgery revealed almost identical functional impairment to the patients with SVD. In conclusion, these simple and noninvasive evaluations of the oxygen transport system could give us valuable informations reasonably differentiating the clinical status of the patients with CHD.

Adult↗
PubMed1989

[Dysplasia of the gallbladder].

Out of 2,027 resected gallbladders that were examined, 46 (2.2%) manifested dysplasia and, to study this further, step sections, 5 mm apart, were performed. The average age of these dysplastic cases was 63.8 years, with a male to female ratio of 1:3. The most frequent dysplastic sites in the gallbladder were in the fundus and the body. Excluding adenomas, polypoid lesions, the dysplasia appeared flat, granular, or irregular. As to diameter, 68.6% were within 1 cm, and 89% were no more than 2 cm. The majority of cases manifesting mild dysplasia had lesions of up to 5 mm in size while the lesions seen in moderate cases were within 2 cm. Stones were found in 80.4% of the cases, and incidences of intestinal metaplasia and pseudopyloric gland metaplasia were found in 80.4% and 100% of these cases, respectively. Incidences of dysplasia adjacent to the carcinoma was seen in 41.8% of the cases, and frequently found in early-stage lesions and well-differentiated carcinomas. Our findings have led us to believe that recognition of the intestinal metaplasia-dysplasia-carcinoma sequence is important.

Adult↗
PubMed1988

Prediction of the progression of cardiac hypertrophy in middle-aged mild hypertensives.

To investigate the predictive value of exercise tests and diastolic function measurements for the progression of left ventricular hypertrophy, symptom-limited treadmill stress testing and echocardiography were performed before and after a follow-up period of 3.5 years in 47 mild hypertensive men aged 42 +/- 2 years. The men were classified into three groups by the progression of the left ventricular mass index (%LVMI) during the observation, i.e. (LVMI after follow-up) - (LVMI before follow-up)/(LVMI before follow-up). The high-progression group (n = 13) had a %LVMI exceeding mean +/- 2/3s.d. of all subjects; the low-progression group (n = 21) had a %LVMI within mean +/- 2/3s.d. and the non-progression group (n = 13) had a %LVMI less than mean -2/3s.d. At the beginning of the observation, age, blood pressure at rest, LVMI, ejection fraction, mean velocity of circumferential fibre shortening, peak shortening rate and systolic time intervals (ET/PEP, ratio of ejection time to pre-ejection period) were similar among the three groups. However, the high-progression group showed a higher systolic pressure at peak exercise, a lower peak filling rate and a longer time to peak filling rate (TPFR) as corrected by the R-R interval of the ECG. These data suggest that systolic pressure at peak exercise and echocardiographically assessed diastolic function are useful in predicting the progression of cardiac involvement in mild hypertension.

Adult↗
PubMed1987

Interleukin-2 responses of MRL/lpr mouse splenocytes and lymph node cells induced by TPA and A23187.

Treatment of splenocytes and lymph node cells of 5 month-old MRL/lpr mice with TPA induced IL-2-dependent proliferation of the cells in the presence of CA++. The induced response was inhibited completely by a monoclonal antibody to IL-2 receptor. The combination of TPA and A23187 in the lpr cells induced both proliferation and production of IL-2 in a Ca++-dependent fashion. The proliferative response of the lpr cells was equivalent to that of congenic (MRL/+/+) or normal cells, but the quantity of IL-2 secreted from the lpr cells was significantly less than that of the controls. Actinomycin D, but not mitomycin C, blocked IL-2 secretion from the treated lpr cells indicating de novo synthesis of IL-2 mRNA in the cells. Thus the lpr lymphocytes can be activated to proliferate in response to IL-2, yet they do not secrete IL-2 at a normal level even if activation signals are transmitted into the cells.

Animals↗
PubMed1986

Paul-Bunnell antigen in murine T cell differentiation: abnormal expression in MRL/Mp-lpr/lpr mice.

Expression of Paul-Bunnell (P-B) antigen was studied on lymphoid cells of normal mice, autoimmune MRL/Mp-lpr/lpr (lpr), and congenic MRL/Mp-+/+(+/+) mice. Evidence was presented that the P-B antigen is a differentiation-associated antigen of murine T cells: Cells with high P-B pattern and density on normal T cells increased as their differentiation proceeded in the peripheral lymphoid tissues. In thymus, P-B antigen was predominantly expressed on hydrocortisone resistant and PNA nonagglutinable cells. The degree of P-B expression on T cells of peripheral lymphoid tissues correlated well with that of Lyt-1 and Lyt-2 antigens (r greater than 0.7). Similar studies on lymphocytes obtained from lpr and +/+ mice at different ages revealed that P-B antigen on the peripheral T cells of lpr mice began to decrease at 6 to 8 wk of age and that the majority of the cells became low P-B cells by 10 wk, accompanied by decrease in expression of Lyt-1 antigen. In contrast, its expression on lpr thymocytes did not differ from that of +/+ or normal mice. The lymph node cell population of lpr mice at the height of the lymphadenopathy was composed of 80% of low P-B and dull Lyt-1 cells and less than 15% of "normal" P-B and Lyt-1 positive cells. These results indicate distorted differentiation of the lpr peripheral lymphocytes that are responsible for the massive lymphadenopathy and the morbid processes.

Aging↗
PubMed1986

Differential effects of procaine and phenethyl alcohol on excision repair of DNA in u.v.-irradiated Escherichia coli.

Experiments were performed to investigate the involvement of the cell membrane in the excision DNA repair process in Escherichia coli. Two membrane-binding drugs, procaine and phenethyl alcohol (PEA), inhibited liquid-holding recovery (LHR) in u.v.-irradiated E. coli wild-type and recA strains. In uvrB and polA strains where, after u.v.-irradiation, LHR was absent the two drugs had no effect. Both drugs markedly reduced the removal of u.v.-induced thymine dimers in the DNA of wild-type cells (H/r30). Analysis by alkaline sucrose gradients revealed that PEA inhibited the incision step in excision repair. In contrast, procaine had no effect on incision but apparently inhibited the late steps in excision repair. PEA dissociated DNA from the cell membrane, whereas procaine did not. The results suggest that the two drugs PEA and procaine inhibit LHR and the excision repair process operating on u.v.-induced damage in E. coli by at least two different mechanisms each of which may involve the cell membrane.

Cell Membrane↗
PubMed1986

Intestinal metaplasia-dysplasia-carcinoma sequence of the gallbladder.

One thousand cases of resected gallbladders were histologically investigated by serial step sections. Intestinal metaplasia was found at rates of 4.0% and 30.6% in the cases without and with stone, respectively. It was found at rates of 69.8% and 61.1% in the cases of dysplasia and carcinoma, respectively. The goblet cells were found at rates of 34.5% and 26.3% in the lesions of carcinoma and dysplasia, respectively. On the other hand, the dysplasia and adenoma intermingled in the tumor tissue at the rates of 22.2% and 8.3% in 36 cases of carcinoma, respectively. Although normal epithelial cells of the gallbladder contain mainly sulfomucin, the goblet cells have sialomucin. The ratio of sialomucin-containing cells increased in the tissue of dysplasia and carcinoma. As to their location, intestinal metaplasia, dysplasia, and carcinoma showed a similar distribution in the gallbladder. Accordingly, it should be considered that the sequence of intestinal metaplasia-dysplasia-carcinoma is significant. Pseudo-pyloric glandular metaplasia was found at rates of 45.5% in the cases of cholecystitis without stone, 77.2% in those with stone, 100% in those with dysplasia, and 72.3% in those with carcinoma. However, it should be considered that pseudo-pyloric glandular metaplasia has less relationship for the bases of carcinogenesis as compared with intestinal metaplasia.

Adult↗