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  • 1
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Werner syndrome (WS) is a rare autosomal recessive disorder of humans characterized by the premature onset and accelerated rate of development of several major age-related disorders. An aberration in DNA replication or repair is suggested by the evidence of genome instability. Since the structural gene for DNA polymerase β maps within the region of the WS mutation on the short arm of chromosome 8 and is involved in both DNA repair and DNA replication, we evaluated its candidacy as the WS gene. Several independent lines of evidence did not support that hypothesis: (1) activity gels showed normal enzyme activity and electrophoretic mobility; (2) nucleotide sequence analysis of the entire coding region failed to reveal mutations (although indicated mistakes in the published sequence); (3) single-strand conformation polymorphism (SSCP) and heteroduplex analyses failed to reveal evidence of mutations in the promoter region; (4) a newly discerned polymorphism failed to reveal evidence of homozygosity by descent in a consanguineous patient; and 5) fluorescence in situ hybridization (FISH) analysis placed the DNA polymerase β gene centromeric to D8S135 at 8p11.2 and thus beyond the region of peak LOD scores for WS.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have studied linkage disequilibrium between CTG repeats and an Alu insertion/deletion polymorphism at the myotonin protein kinase gene (DMPK) in 102 Japanese families, of which 93 were affected with myotonic dystrophy (DM). All of the affected chromosomes are in complete linkage disequilibrium with the Alu insertion allele. Among the normal chromosomes, alleles of CTG repeats 5 and ≥ 17 are exclusively associated with the insertion allele. On the other hand, intermediate alleles of 11– 16 repeats show a significantly greater association with the deletion allele. A strikingly similar pattern of linkage disequilibrium observed in European populations suggests a common origin of the DM mutation in the Japanese and European populations.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have studied linkage disequilibrium between CTG repeats and anAlu insertion/deletion polymorphism at the myotonin protein kinase gene (DMPK) in 102 Japanese families, of which 93 were affected with myotonic dystrophy (DM). All of the affected chromosomes are in complete linkage disequilibrium with theAlu insertion allele. Among the normal chromosomes, alleles of CTG repeats 5 and ⩾ 17 are exclusively associated with the insertion allele. On the other hand, intermediate alleles of 11-6 repeats show a significantly greater association with the deletion allele. A strikingly similar pattern of linkage disequilibrium observed in European populations suggests a common origin of the DM mutation in the Japanese and European populations.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0827
    Keywords: Ipriflavone ; Calcitonin ; Bone mineral density ; Osteoporosis ; Serum calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effects of ipriflavone (7-isopropoxy-3-phenyl-4H-1-benzopyran-4-one) on bone mineral density (BMD) of the 3rd lumbar vertebra and on calcium (Ca)-related factors, including serum calcitonin (CT) levels before and after rapid calcium infusion (4 mg/kg for 5 minutes), were studied in 11 elderly female subjects (80 ± 2 years of age, mean ± SE). Ipriflavone (IP) administration (600 mg/day, 7 months) resulted in inhibition of BMD loss in 7 patients (responders, mean change of BMD value 2.2 ± 2.3%), whereas 4 patients showed a loss of BMD (nonresponders, mean change of BMD value -13.1 ± 2.6%) compared with pretreatment values. The responder group showed a significant increase in mean pretreatment serum CT levels (from 20 ± 2 pg/ml to 42 ± 7 pg/ml,P 〈 0.05) after treatment with IP, and a significant decrease in the mean basal serum level of corrected Ca (from 9.6 ± 0.2 mg/dl to 8.7 ± 0.1 mg/dl,P 〈 0.01) after treatment with IP; nonresponders did not show these changes. For responders, both the percentage of change and the maximal value of serum CT in response to Ca infusion were maintained at rather high levels, both before and after IP treatment; nonresponders showed almost no response to a stimulation test for CT. These findings suggest that IP inhibits bone loss in elderly female subjects possibly through the mechanism of increasing CT secretion.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. To examine whether an angiotensin-converting enzyme (ACE) inhibitor prevents left ventricular (LV) hypertrophy even in low-renin hypertension, we studied the effect of the administration of perindopril on cardiac hypertrophy induced by partial renal ablation in hypertensive rats.2. Rats that had undergone partial nephrectomy were randomly divided into four groups that received the following as drinking water: Group A, tap water; Group B, 1% sodium chloride (NaCl); Group C, NaCl + perindopril 3 mg/ kg per day; and Group D, NaCl + perindopril 1 mg/ kg per day. Plasma renin activity (PRA), angiotensin-II (AII) concentration and cardiac tissue AII were measured.3. Supplementation of NaCl following nephrectomy increased the blood pressure and cardiac weight compared with rats that had undergone nephrectomy alone (P〈0.05). Treatment with perindopril (3 mg/kg per day) did not affect the blood pressure and plasma AII but inhibited the increase of cardiac weight (P〈0.05). Left ventricular AII was decreased in cases of reduced renal mass hypertension, but was not changed by treatment with perindopril.4. These results demonstrate that perindopril may be able to prevent LV hypertrophy even in low-renin hypertension, which was not mediated by a reduction of blood pressure or suppression of the circulating and cardiac renin-angiotensin systems. Other mechanisms of ACE inhibitors may contribute to the cardioprotective effects.
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The role of the sympathetic nervous system in orthostatic and postprandial blood pressure reduction in patients with essential hypertension was studied in 13 hypertensive patients and 10 age-matched normotensive subjects.2. The blood pressure (BP), pulse rate, and plasma norepinephrine (NE) were measured: (i) every minute for 20 min in the upright position after overnight recumbency (ii) every 30 min after food intake for 3 h in the supine position.3. Orthostatic BP reduction (〉 13 mmHg in mean BP) was observed in eight hypertensive patients with a maximum after 4 min. Seven of these patients showed postprandial hypotension (〉 13 mmHg) with a maximum 90 min after eating, while none of the normotensives exhibited such BP reductions. Before and during the tests the plasma NE levels were higher in hypertensive patients than in the normotensives. The plasma NE level was increased from 370±80 to 790±110 pg/mL 4 min after standing (P〈0.01) in hypertensive patients and from 220±40 to 530±90 pg/mL (P〈0.01) in normotensive subjects. The plasma NE level was decreased 90 min after food intake from 390±90 to 260±80 pg/mL in hypertensives. Changes in plasma NE correlated with those in mean BP after standing for 4 min (r= 0.379, P〈0.05) and also with those 90 min after food intake (r= 0.457, P〈0.05).4. These findings suggest that patients with essential hypertension have abnormally increased basal sympathetic nerve activity at rest, and that their orthostatic and postprandial BP reductions may both be caused by impairment of the sympathetic nervous system and of cardiovascular reflexes.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. To investigate the role of transcriptional and post-transcriptional factors in increasing renin synthesis secondary to angiotensin-converting enzyme (ACE) inhibitors, we studied the changes in levels of renal renin mRNA, plasma renin and other hormonal factors.2. Spontaneously hypertensive rats were orally administered 10 mg/kg spirapril or vehicle daily for 3, 14 or 28 days.3. Plasma renin activity in the spirapril-treated group was significantly elevated compared with that in the vehicle group at any time (P〈0.01). However, there was no significant change in plasma angiotensin II concentration between the two groups. The ratio of renal renin mRNA to β-actin mRNA in the spirapril-treated group was higher than that in the control group (P〈0.01).4. At 28 days, plasma renin activity in the spirapril-treated group was significantly elevated compared with that at 14 days (P〈0.05). However, there was no change in renin mRNA between 14 and 28 days after ACE inhibitor administration.5. Plasma ACE activity in the treatment group was less than that in the control group at any time (P〈0.01).6. Our study demonstrated a non-proportional change in plasma renin and renal renin mRNA levels. It is suggested that the main determinant of the rate of renin synthesis after administration of an ACE inhibitor may be post-transcriptional factors, and that unknown mechanisms may be involved in the increase in plasma renin level after long-term administration of ACE inhibitor in addition to the short feedback mechanism brought about by the decrease in angiotensin II.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 16 (1989), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The possible interactions between the renal effects of atrial natriuretic peptide (ANP) and angiotensin II (All) were studied in normal sodium-replete human subjects. Recent investigations have suggested that ANP inhibits the pressor and volume-retaining effects of activation of the renin-angiotensin system. Thus, ANP may attenuate the effects of All on renal haemodynamics or tubular transport.2. ANP (0.1 μg/kg per min, 60 min) was intravenously infused into eight normal human subjects with and without pretreatment with enalapril (20 mg, per oral), an inhibitor of the converting enzyme, and during infusion of All (10 mg/kg per min).3. ANP infusion alone caused increases in the urine volume (from 96 ± 23 to 229 ± 44 mL/h, P 〈 0.05) and urinary sodium excretion (from 11.5 ± 1.6 to 20.9 ± 4.2 mEq/h, P 〈 0.05). These changes were accompanied by an increase in the glomerular filtration rate (from 127 ± 9 to 158 ± 9 mL/min, P 〈 0.05). ANP infusion after enalapril administration lowered the mean blood pressure (from 76 ± 2 to 71 ± 3 mmHg, P 〈 0.05) to a level similar to that observed during ANP infusion alone (from 84 ± 2 to 74 ± 2 mmHg, P 〈 0.01), but did not result in a significant diuresis (from 139 ± 23 to 174 ± 51 mL/h) or natriuresis (from 19.7 ± 2.5 to 14.3 ± 3.4 mEq/h, P 〈 0.05). This combined treatment with a converting enzyme inhibitor and ANP reduced both the glomerular filtration rate (160 ± 9 to 141 ± 10 mL/min) and the renal plasma flow (from 775 ± 49 to 570 ± 45 mL/min, P 〈 0.01).4. The antinatriuretic effects of exogenous All were reversed by superimposed ANP infusion (urinary sodium excretion: from 4.8 ± 1.0 to 24.3 ± 5.2 mEq/h, P 〈 0.01). Under these conditions, the glomerular filtration rate increased (from 114 ± 6 to 156 ± 7 mL/min, P 〈 0.05) to levels similar to those observed with ANP infusion alone. In addition the increased tubular sodium reabsorption induced by All was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 ± 3.5 to 80.3 ± 16.6%, P 〈 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 ± 9.8 to 87.6 ± 8.8%, P 〈 0.05).5. These results suggest that ANP interacts with endogenous All particularly in the glomerulus, to cause a diuresis and natriuresis, and also suggest that ANP inhibits All-induced tubular sodium reabsorption.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Deletion polymorphism, DD, of the angiotensin-converting enzyme (ACE) gene is reported to be related to cardiovascular disease, which is frequently based on insulin resistance.2. To clarify the relationship between the ACE genotype DD and plasma glucose increases after an oral glucose load, we performed 75 g oral glucose tolerance test (OGTT) in 301 non-diabetic men (age range 30–60 years) undergoing general check-up.3. Insertion/deletion (I/D) polymorphism of the ACE gene was explored using a polymerase chain reaction. The frequency of the II, ID and DD genotypes was 0.43, 0.43 and 0.14, respectively.4. There were no differences in baseline clinical characteristics between subjects with each ACE genotype.5. The mean (±SEM) plasma glucose level at 60 min of the OGTT was significantly higher in subjects with the DD genotype (170.8±6.9 mg/dL) than in subjects with either the II or ID genotype (mean value for two groups 156.6±2.7 mg/dL; P 〈 0.05). Moreover, the mean percentage change of plasma glucose after 60 min of the OGTT, a marker of plasma glucose increase, was significantly higher in individuals with the DD genotype than in individuals with either the II or ID genotypes.6. In contrast, the mean fasting plasma glucose level, the plasma glucose level at 120 min, the glucose response area and the fasting insulin level were not different between individuals with the DD genotype and individuals with other genotypes.7. In conclusion, subjects with the DD genotype showed transiently higher levels of plasma glucose after an oral glucose load than subjects with other genotypes. Further studies are required to determine whether the association between ACE genotype and postprandial hyperglycaemia influences the incidence of cardiovascular disease and diabetes mellitus.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 17 (1990), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of chronic oral administration of inhibitors of angiotensin converting enzyme (ACE) on the vascular renin–angiotensin system were studied.2. Male Sprague-Dawley rats were treated orally with five ACE inhibitors, captopril, enalapril, ramipril, cilazapril and CS-622 (10 mg/kg per day), for periods of 1–2 weeks. Their mesenteric arteries were then isolated and perfused in vitro with Krebs'-Ringer solution, and the angiotensin II (AII) released into the perfusate was measured under unstimulated and isoproterenol-stimulated conditions. The vascular renin activity was also determined after treatments with ACE inhibitors.3. Treatment with captopril for 1 week suppressed the isoproterenol-stimulated increase in All release, but had little effect on the baseline release. Oral treatment with captopril for 2 weeks or with other ACE inhibitors for 1 week markedly inhibited both the unstimulated and stimulated release of AII from the mesenteric vasculature.4. Both the vascular renin activity and the plasma renin activity increased on captopril treatment, but their changes with time were different.5. These results indicate that virtually complete inhibition of the vascular renin–angiotensin system can be achieved after prolonged treatment with ACE inhibitors, and suggest that the chronic antihypertensive action of ACE inhibitors is not solely due to inhibition of the plasma renin–angiotensin system.
    Type of Medium: Electronic Resource
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