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Biomedical subjects

S Seto

Publications and source records attributed to S Seto.

At least 73 records · Page 4Linked to original sources
PubMed1991

[The relationship between the aortic pulse wave velocity and osteoporosis in elderly women].

The relationship between arteriosclerosis and osteoporosis (OP) was assessed in 20 elderly women. The aortic pulse wave velocity (PWV) was used as the index of arteriosclerosis and bone mineral content (BM) of the vertebral body, which was measured by quantitative computed tomography, was used as an index of OP. PWV and BM showed a significant correlation with aging (PWV and age: r = 0.466, p less than 0.05, BM and age: r = -0.487, p less than 0.05). In the group in which the serum alkaline phosphatase (ALP) was higher than 180 IU/l (n = 11), there was a significant inverse correlation between PWV and BM (r = -0.728, p less than 0.02). On the other hand, there was no correlation between PWV and BM in the group in which ALP was lower than 180 IU/l (n = 9). These results suggest that in cases with OP and high levels of ALP, calcium (Ca) seems to be released from the bone system and transferred to the wall of the aorta. The mechanism and pathogenesis of this Ca transference is unknown and should be investigated.

Aged↗
PubMed1991

Relationship between blood pressure and left ventricular mass in male patients with essential hypertension.

We performed retrospective study of the relationship between the severity and duration of hypertension and echocardiographically-detected left ventricular hypertrophy (echo-LVH) in patients with untreated essential hypertension. The subjects consisted of 92 untreated essential hypertensives who were observed for more than 5 years from the onset of diastolic hypertension (greater than or equal to 95 mmHg), and whose left ventricular (LV) mass index was measured at the end of the observation period. On the basis of the frequency of diastolic hypertension during the observation period, the population was categorized in 3 groups. In Group I (32 cases), diastolic hypertension was observed in more than 80% of blood pressures obtained throughout the entire observation period. In Group II (38 cases), diastolic hypertension was observed in 33 to 80% of the observation period. In Group III (22 cases), diastolic hypertension was observed in less than 33% of the observation period. The average diastolic blood pressure during the entire observation period in each group were 101.0, 96.0, and 90.7 mmHg in groups I, II, and III, respectively. The LV mass index was significantly higher in groups I (114.6 g/m2) and II (105.3 g/m2) than in group III (90.7 g/m2) (p less than 0.01). The prevalence of echo-LVH (more than 121 g/m2) was 34.4%, 18.4%, and 4.8% in groups I, II, and III, respectively. The average diastolic blood pressure in patients with echo-LVH (99.3 +/- 5.1 mmHg) was significantly higher than in patients without echo-LVH (95.7 +/- 4.7 mmHg). We concluded that the degree and duration of diastolic pressure elevation are closely correlated to the LV mass index.

Blood Pressure↗
PubMed1990

[Paradoxical response of blood pressure to salt loading in renovascular hypertension].

We studied the effect of high salt intake on blood pressure in two cases with renovascular hypertension. They had hypertension with hyperreninemia and marked difference in plasma renin activity between both renal veins. Blood pressure significantly decreased after single oral administration of captopril. Renal arteriogram revealed significant stenosis in the main artery to the left (case 1) and right (case 2) kidney. Blood pressure response was evaluated after seven (case 1) and five (case 2) days of low salt and seven days (both cases) of high salt intake. Mean blood pressure in two patients was significantly decreased (case 1; 118 +/- 5.5 to 108 +/- 6.1 mmHg and case 2; 150 +/- 3.8 to 138 +/- 3.1 mmHg). Plasma renin activity was also decreased (case 1; 6.25 to 0.77 ng/ml/hr and case 2; 22.8 to 6.3 ng/ml/hr). In case 2, blood pressure elevated markedly during low salt intake, compared with blood pressure level during normal salt intake. The results suggest that excessive salt intake in patients with unilateral renovascular hypertension produces blood pressure reduction because of suppression of renin-angiotensin system. We concluded that in patients with unilateral renovascular hypertension dietary sodium depletion may be harmful, whereas salt supplement may have a beneficial effect.

Adult↗
PubMed1989

Expanded phenotype and ethnicity in Setleis syndrome.

Setleis syndrome, an autosomal recessive disorder characterized by "coarse" face, temporal cutis aplasia, double upper eyelashes, absent lower eyelashes, chronic conjunctivitis, and prominent thick lips, was reported previously in 8 Puerto Rican children. We report on 3 unrelated children (one mentally retarded) with Setleis syndrome who are not of Puerto Rican descent. Two of our patients had imperforate anus, which has not previously been reported. The evolution of the phenotype over time is illustrated.

Abnormalities, Multiple↗
PubMed1989

Central effect of aprotinin, a serine protease inhibitor, on blood pressure in spontaneously hypertensive and Wistar-Kyoto rats.

We examined the effect of centrally administered aprotinin, a serine protease inhibitor, on blood pressure (BP) in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Twenty-two gauge needles and polyethylene catheters were implanted into lateral cerebroventricle and femoral artery, respectively, at 48 hours before the experiments. In Group 1 (8 SHR, 6 WKY), rats received a bolus intracerebroventricular injection (i.c.v.) of aprotinin (1,000 KIU/kg/10 microliters). A prompt increase of BP was observed in SHR after aprotinin and this elevation of BP was persisted for over 30 minutes (mean BP: 158.8 +/- 2.9 mmHg at control to 168.7 +/- 3.2 at 15 min., p less than 0.01; to 168.3 +/- 3.4 at 30 min., p less than 0.01). On the other hand, BP of WKY decreased gradually after aprotinin (mean BP: 143.0 +/- 3.3 at control to 136.8 +/- 2.7 at 15 min., n.s.; to 134.2 +/- 5.1 at 30 min., p less than 0.05). The intravenous injection (i.v.) of aprotinin (Group 2: 7 SHR, 5 WKY) and the i.c.v. of artificial cerebrospinal fluid (CSF) (Group 3: 5 SHR, 6 WKY) did not affect BP in both SHR and WKY except for the minor transient increase of BP in WKY immediately after artificial CSF i.c.v.. We performed additional experiments to study the contributions of sympathetic nervous system and vasopressin to these changes in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of blood pressure changes on development and regression of electrocardiographic left ventricular hypertrophy: a 26 year longitudinal study.

At the Radiation Effects Research Foundation, medical examinations have been conducted biennially since 1958 on a fixed population of approximately 20,000 individuals. Blood pressure measurements and electrocardiographic (ECG) recordings are available for 6,569 individuals who were monitored for at least 11 of the 13 2 year intervals between 1958 and 1984. Data from 601 individuals who had satisfied the Foundation's ECG diagnostic criteria of left ventricular hypertrophy ("Kagan-Yano code") on at least one occasion were reviewed. Both the development and the regression of ECG left ventricular hypertrophy were ascertained in 61 subjects (17 men and 44 women). During the course of development of ECG left ventricular hypertrophy, hypertension (including borderline cases) was noted in 83.3% of the subjects. The most common pattern of ECG left ventricular hypertrophy development was high voltage, followed by ST-T changes. In about half of these cases, the condition of hypertrophy regression was associated with lowering of blood pressure, marked by the disappearance of high voltage ECG readings.

Blood Pressure↗
PubMed1987

Prevention of adriamycin-induced interphase death by 3-aminobenzamide and nicotinamide in a human promyelocytic leukemia cell line.

Adriamycin caused significant interphase death in HL-60 cells during six hours of incubation, which was abolished by the poly(ADP-ribose) polymerase inhibitors, 3-aminobenzamide or nicotinamide. Neither agent changed adriamycin uptake by HL-60 cells. Although 3-aminobenzamide did not alter the number of DNA strand breaks caused by adriamycin, it prevented adriamycin-induced depletion of intracellular NAD+ and ATP, and maintained energy charge. These findings suggest that the activation of poly(ADP-ribose) synthesis plays an important role in the adriamycin-induced interphase death of proliferating HL-60 cells.

Benzamides↗
PubMed1987

Pyridine nucleotide cycling and poly(ADP-ribose) synthesis in resting human lymphocytes.

NAD is a critical cofactor for the oxidation of fuel molecules. The exposure of human PBL to agents that cause DNA strand breaks to accumulate can deplete NAD pools by increasing NAD consumption for poly(ADP-ribose) formation. However, the pathways of NAD synthesis and degradation in viable PBL have not been carefully documented. The present experiments have used radioactive labeling techniques to trace the routes of NAD metabolism in resting PBL. The cells could generate NAD from either nicotinamide or nicotinic acid. PBL incubated with [14C]nicotinic acid excreted [14C]nicotinamide into the medium. Approximately 50% of a prelabeled [14C]NAD pool was metabolized during 6 to 8 hr in tissue culture. Basal NAD turnover was prolonged threefold to fourfold by 3-aminobenzamide (3-ABA), an inhibitor of poly(ADP-ribose) synthetase. Supplementation of the medium with 3-ABA also prevented the accelerated NAD degradation that ensued after exposure of PBL to deoxyadenosine plus deoxycoformycin at concentrations previously shown to cause DNA strand break accumulation. These results demonstrate that quiescent human PBL continually produce NAD and utilize the nucleotide for poly(ADP-ribose) synthesis.

Deoxyadenosines↗
PubMed1987

Short-term prednisolone for inducing seroconversion from hepatitis B e antigen to antibody along with clinical improvement in patients with chronic active hepatitis type B.

Short-term prednisolone therapy was instituted on 27 patients with chronic active hepatitis (CAH) type B, in an attempt to induce seroconversion from hepatitis B e antigen (HBeAg) to the corresponding antibody (anti-HBe). Patients with CAH received a four-week regimen of prednisolone with daily dosage tapering from 40 to 10 mg (total 700 mg). Within one year after the withdrawal of prednisolone, 19 (70%) lost HBeAg and 11 of them (41% of the total) developed anti-HBe, at rates significantly higher than 3 (12%) and 1 (4%) who spontaneously showed respective serological changes among 26 matched controls during one year (p less than 0.001). Within two years after the withdrawal, 21 (78%) lost HBeAg and 19 (70%) developed anti-HBe, in contrast to 6 (23%) and 2 (8%) of controls who showed respective changes during that period (p less than 0.001). Seroconversion to anti-HBe was invariably accompanied by clinical and biochemical improvements along with loss of DNA polymerase from circulation. Elevation in transaminase levels, reflecting the rebound of steroid withdrawal, always heralded and appeared to be required for the seroconversion, but serious aggravation of hepatitis was not encountered in any of the patients.

Adult↗
PubMed1987

Effect of propranolol and indomethacin on the depressor action of captopril in patients with essential hypertension.

The contribution of the renin-angiotensin system (RA) and of prostaglandins (PG) to the acute depressor effect of captopril (Capt) was studied in 13 hypertensive patients suppressing either RA by propranolol (Prop) or PG by indomethacin (Indo). Four patients showed abolition of the depressor effect of Capt by pretreatment with both Prop and Indo (Group 1). Indo, but not Prop, cancelled the depressor effect in another 4 patients (Group 2). In the remaining 5 patients, either Prop or Indo did not alter the depressor response to Capt (Group 3). Patients in Group 3 were older than patients in Group 1 and 2 and showed lower plasma volume value. Several mechanisms might contribute to the acute depressor effect of Cap, including not only the suppression of RA and the enhancement of PG, but perhaps other undetermined factor(s), especially in older patients.

Adult↗
PubMed1986

Inhibition of DNA repair by deoxyadenosine in resting human lymphocytes.

Profound lymphopenia is characteristic of immunodeficient children who lack adenosine deaminase (ADA). When ADA is inactive, deoxyadenosine (dAdo) is phosphorylated by immature T lymphoblasts and inhibits cell division. However, dAdo also causes the slow accumulation of DNA strand breaks in nondividing, mature human peripheral blood lymphocytes. To explore the basis for this phenomenon, we have assessed the effects of dAdo and other deoxynucleosides on the repair of gamma-radiation induced DNA strand breaks in resting normal lymphocyte cultures. As measured by a sensitive DNA unwinding assay, most DNA strand breaks were rejoined within 2 hr after exposure of lymphocytes to 500 rad. In medium supplemented with deoxycoformycin, a tight binding ADA inhibitor, dAdo retarded DNA rejoining in a dose and time dependent manner. The inhibition required dAdo phosphorylation. Over an 8-hr period, 10 microM dAdo gradually rendered peripheral blood lymphocytes incompetent for DNA repair. Among several other compounds tested, 2-chlorodeoxyadenosine, an ADA resistant dAdo congener with anti-leukemic and immunosuppressive activity, was the most powerful inhibitor of DNA repair, exerting significant activity at concentrations as low as 100 nM. Both dAdo and 2-chlorodeoxyadenosine blocked unscheduled DNA synthesis in irradiated resting lymphocytes, as measured by [3H]thymidine uptake. On the basis of this and other data, we suggest that quiescent peripheral blood lymphocytes break and rejoin DNA at a slow and balanced rate. The accumulation of dATP progressively retards the DNA repair process and thereby fosters the time-dependent accretion of DNA strand breaks. By inhibiting DNA repair, dAdo, 2-chlorodeoxyadenosine and related compounds may substantially potentiate the toxicity of DNA damaging agents to normal and malignant lymphocytes.

Cells, Cultured↗
PubMed1986

Lymphocyte dysfunction after DNA damage by toxic oxygen species. A model of immunodeficiency.

The metabolic causes for immune impairment in patients with severe chronic inflammatory diseases have not been clearly defined. Recently, the overproduction of poly(ADP-ribose) in resting lymphocytes with unrepaired DNA strand breaks has been suggested to contribute to immune dysfunction in adenosine deaminase-deficient patients. Our experiments have determined to what extent DNA damage and poly(ADP-ribose) synthesis might also explain the impaired mitogen responsiveness of PBL exposed to toxic oxygen species. Treatment of normal resting human lymphocytes with xanthine oxidase and hypoxanthine dose-dependently induced DNA strand breaks and triggered the rapid synthesis of poly(ADP-ribose). Subsequently, NAD+ and ATP pools decreased precipitously. Lymphocytes exposed previously to the enzymatic oxidizing system did not synthesize DNA after stimulation with PHA. However, if the medium was supplemented with 3-aminobenzamide or nicotinamide, two compounds that inhibit poly(ADP-ribose) formation, cellular NAD+ and ATP pools were preserved, and the lymphocytes responded vigorously to a mitogenic challenge. Excessive poly(ADP-ribose) synthesis, provoked by DNA strand breakage, may represent a common pathway that connects the immunodeficiency syndromes associated with (a) exposure of lymphocytes to toxic oxygen species during chronic inflammatory states, (b) adenosine deaminase deficiency, and (c) certain DNA repair disorders.

DNA↗
PubMed1986

Effect of sodium restriction and corticosteroids on glandular kallikrein in plasma and in the submandibular gland.

We investigated whether sodium restriction or mineralocorticoid influence the release of submandibular kallikrein into the blood and/or the concentration of kallikrein in glandular tissue. For this we measured submandibular gland blood flow, arterial and submandibular gland venous kallikrein, and kallikrein in glandular homogenates of male Sprague-Dawley rats after one week of either low sodium or deoxycorticosterone acetate (DOCA) treatment. We also studied the effect of dexamethasone on the concentration of kallikrein in gland tissue and peripheral plasma. Kallikrein in plasma and in homogenates was measured by radioimmunoassay. Blood flow was determined by timed collections of venous outflow. Kallikrein release was calculated as the arteriovenous difference in kallikrein times the rate of submandibular gland plasma flow. The concentration of kallikrein in arterial plasma, the basal submandibular kallikrein release into blood, and the concentration of kallikrein in submandibular gland tissue were all higher during low sodium than during normal sodium intake (20.1 +/- 3.6 ng/ml vs 10.7 +/- 0.5, p less than 0.05; 0.40 +/- 0.09 ng/min/100 g bw vs 0.18 +/- 0.02, p less than 0.05, and 81.6 +/- 5.5 micrograms/mg protein vs 65.1 +/- 4.0, p less than 0.05, respectively). In contrast, DOCA treatment did not affect the concentration of kallikrein in arterial plasma, the basal release of kallikrein from the submandibular gland into blood, or the concentration of kallikrein in the gland. Dexamethasone in doses that did not affect the normal growth of the animals had no significant effect on the concentration of kallikrein either in submandibular gland tissue or in peripheral plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1986

DNA strand breaks, NAD metabolism, and programmed cell death.

An intimate relationship exists between DNA single-strand breaks, NAD metabolism, and cell viability in quiescent human lymphocytes. Under steady-state conditions, resting lymphocytes continually break and rejoin DNA. The balanced DNA excision-repair process is accompanied by a proportional consumption of NAD for poly(ADP-ribose) synthesis. However, lymphocytes have a limited capacity to resynthesize NAD from nicotinamide. An increase in DNA strand break formation in lymphocytes, or a block in DNA repair, accelerates poly(ADP-ribose) formation and may induce lethal NAD and ATP depletion. In this way, the level of DNA single-strand breaks in the lymphocyte nucleus is linked to the metabolic activity of the cytoplasm. The programmed removal of lymphocytes (and perhaps of other cells) with damaged DNA, may represent a novel physiologic function for poly(ADP-ribose)-dependent NAD cycling.

Aphidicolin↗
PubMed1986

Changing pattern of age-specific prevalence of hepatitis B surface antigen and corresponding antibody in Japan.

During the period 1978-1984 in Japan, the prevalence of hepatitis B surface antigen (HBsAg) in age groups below age 15 years was 18/2,550 (0.7%), and it was particularly low in the group below age 5 years (2/706 (0.3%)). The low prevalence of HBsAg in children under 15 years of age contrasted sharply with the much higher prevalence in persons age 15 years and older (36/2,050 (1.8%)). In accord with this, the prevalence of antibody to hepatitis B surface antigen (anti-HBs) was much lower in children below age 15 years than that in persons 15 years of age and older (29/2,550 (1.1%) vs. 242/2,050 (11.8%)). Furthermore, the prevalence of hepatitis B viral markers in 1978-1984 was lower than that during the period from 1972-1977 in every age group. A total of 13 (81%) of 16 mothers of carrier children, identified in 1978-1984, were positive both for HBsAg and hepatitis B e antigen in their sera. Now that mother-to-baby transmission appears to be the main route for establishing the persistent carrier state, its interruption should reduce the reservoir of hepatitis B virus, toward its eventual eradication, in Japan.

Adolescent↗