Progressive idiopathic atrophoderma of Pasini and Pierini: the evaluation of cutaneous atrophy by 13-MHz B-mode ultrasound scanning method.
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Adolescent↗
Biomedical subjects
I Abe
Publications and source records attributed to I Abe.
Improvement of blood pressure control in a hypertension clinic: a 10-year follow-up study.
The objective of the study was to assess whether the publication of new guidelines, such as JNC VI 1997 and WHO/ISH 1999, and the development of new antihypertensive drugs have improved blood pressure (BP) control. A total of 150 patients (age 29-88, mean 66+/-11 years in 2001) who were followed at our hypertension clinic during 1991-2001 were retrospectively investigated. We compared the clinical characteristics of the patients in 2001 to those in 1991 and 1996, using the averaged BP determined at two occasions each year for our analysis. The average BP decreased during the 10 years between 1991 and 2001. When good BP control was defined as <140/90 mmHg, the rate of patients with good BP control increased from 31% in 1991 to 43% in 1996, and to 57% in 2001 (P<0.001 vs 1991). Both younger (< or =64 years) and older (> or =65 years) patients showed similar improvement during these 10 years. In 2001, satisfactory BP control (<130/85 mmHg) was achieved in 24% of younger patients, which was significantly higher than the achievement in 1991 (10%, P=0.02). This improvement occurred at the same time as an increase in the prescription of Ca antagonists and angiotensin II antagonist. The patients with improved BP control during these 10 years (n=50) showed lower body mass index (BMI) and serum total cholesterol levels in 2001 compared to persistently uncontrolled patients (n=54). Furthermore, the change in BMI during these 10 years was significantly less in the patients with improved BP control than in the persistently uncontrolled patients. In conclusion, BP control improved in the 10 years studied, and it seems to be attributable to the more frequent use of the newer drugs such as angiotensin II antagonists and Ca antagonists, to lifestyle modification and also to the growth in awareness of the importance of strict BP control.
Adult↗
[Guidelines on Treatment of Hypertension in the Elderly--2002 Revised Version].
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Aged↗
Molecular cloning, expression, and site-directed mutations of oxidosqualene cyclase from Cephalosporium caerulens.
A cDNA for oxidosqualene:lanosterol cyclase (OSLC) was cloned and sequenced from the fungus Cephalosporium caerulens, that produces a steroidal antibiotic, helvolic acid. A 2280 bp open reading frame encoded an M(r) 87078 protein with 760 amino acids. The cDNA was functionally expressed in the OSLC-deficient mutant GIL77 strain of Saccharomyces cerevisiae. A truncated recombinant enzyme (Delta49N) starting from the second methionine (M50) residue was completely inactive, suggesting that ca. 30 additional hydrophilic amino acid residues at the N-terminal are essential for the folding of the enzyme. Furthermore, the active site residues, H234 and D456 (numbering in S. cerevisiae OSLC), were chosen for site-directed mutagenesis experiments; H234E, H234Y, H234F, D456E, D456N, and D456H mutants were inactive, while H234W and H234K mutants retained lanosterol-forming activity.
Acremonium↗
Comparative actions of insulin sensitizers on ion channels in vascular smooth muscle.
Thiazolidinedione and isoxazolidinedione insulin sensitizers activate peroxisome proliferator-activated receptor gamma (PPAR gamma). Some thiazolidinediones modify ion channels in smooth muscles; however, the mechanism by which their actions occur has not been clarified. We, thus, examined the effects of three thiazolidinediones (troglitazone, pioglitazone, and rosiglitazone) and isoxazolidinedione (JTT-501), as well as an intrinsic ligand for PPAR gamma, 15-deoxy-Delta(12,14) prostaglandin J(2) (prostaglandin J(2)), on voltage-operated Ca(2+) currents (I(Ca)), voltage-dependent K(+) currents (I(Kv)), and Ca(2+)-activated K(+) currents (I(Kca)), to clarify whether a thiazolidinedione structure or PPAR gamma activation is related to their actions on ion channels. The whole-cell patch clamp method was used to record currents in smooth muscle cells from guinea-pig mesenteric arteries. Thiazolidinediones inhibited I(Ca) in a dose-dependent manner (troglitazone>pioglitazone=rosiglitazone). Troglitazone (> or =1 microM) and rosiglitazone (100 microM), but not pioglitazone, inhibited I(Kv). Rosiglitazone (> or =10 microM) enhanced, troglitazone (> or =1 microM) inhibited, and pioglitazone did not affect I(Kca). A high concentration of JTT-501 (100 microM) inhibited I(Ca), I(Kv), and I(Kca) to a similar extent. Prostaglandin J(2) enhanced I(Kca), but affected neither I(Ca) nor I(Kv). In summary, the three thiazolidinediones and isoxazolidinedione act differently on Ca(2+) and K(+) channels in vascular smooth muscle. The action of thiazolidinediones on I(Ca) could be attributed to specific regions of the molecules and not to activation of PPAR gamma. Involvement of PPAR gamma activation in the stimulation of I(Kca) is possible but should be tested further.
Analysis of Variance↗
Green tea polyphenols as potent enhancers of glucocorticoid-induced mouse mammary tumor virus gene expression.
The effect of natural and synthetic galloyl esters on glucocorticoid-induced gene expression was evaluated by using rat fibroblast 3Y1 cells stably transfected with a luciferase reporter gene under the transcriptional regulation of the mouse mammary tumor virus promoter. The glucocorticoid-induced gene transcription was strongly suppressed by synthetic alkyl esters; n-dodecyl gallate showed the most potent inhibition (66% inhibition at 10 microM), which was far more potent than that of crude tannic acid. n-Octyl and n-cetyl gallate also showed good inhibition, while gallic acid itself was not so active, suggesting that the presence of hydrophobic side chain is important for the suppressive effect. On the other hand, surprisingly, green tea gallocatechins, (-)-epigallocatechin-3-O-gallate and theasinensin A, potently enhanced the promoter activity (182 and 247% activity at 1 microM, respectively). The regulation of the level of the glucocorticoid-induced gene expression by the antioxidative gallates is of great interest from a therapeutic point of view.
Animals↗
Ellagitannins and hexahydroxydiphenoyl esters as inhibitors of vertebrate squalene epoxidase.
Ellagitannins isolated from various plant sources as well as newly synthesized n-alkyl (C(1)-C(18)) esters of hexahydroxydiphenyl (HHDP) dicarboxylic acid were evaluated as enzyme inhibitors of recombinant rat squalene epoxidase, a rate-limiting enzyme of cholesterol biosynthesis. Among the ellagitannins tested, pedunculagin (IC(50) = 2.0 microM) and eugeniin (IC(50) = 1.6 microM), both containing (S)-HHDP ester group(s), showed remarkable inhibition, which was more potent than those of previously reported substrate analogue inhibitors. Furthermore, ellagic acid (IC(50) = 2.0 microM), a bislactone formed by hydrolytic release of a HHDP group from ellagitannins, was also a good inhibitor of the enzyme. On the other hand, the synthetic HHDP esters with C(6) (IC(50) = 0.93 microM) and C(8) alkyl side chains (IC(50) = 0.83 microM) showed potent enzyme inhibition at the submicromolar concentration range, while esters with shorter chain lengths (C(1)-C(4)) and a C(18) ester exhibited moderate inhibition (IC(50) = 8-47 microM).
Animals↗
Benzalacetone synthase. A novel polyketide synthase that plays a crucial role in the biosynthesis of phenylbutanones in Rheum palmatum.
Benzalacetone synthase (BSA) is a novel plant-specific polyketide synthase that catalyzes a one step decarboxylative condensation of 4-coumaroyl-CoA with malonyl-CoA to produce the C6-C4 skeleton of phenylbutanoids in higher plants. A cDNA encoding BAS was for the first time cloned and sequenced from rhubarb (Rheum palmatum), a medicinal plant rich in phenylbutanoids including pharmaceutically important phenylbutanone glucoside, lindleyin. The cDNA encoded a 42-kDa protein that shares 60-75% amino-acid sequence identity with other members of the CHS-superfamily enzymes. Interestingly, R. palmatum BAS lacks the active-site Phe215 residue (numbering in CHS) which has been proposed to help orient substrates and intermediates during the sequential condensation of 4-coumaroyl-CoA with malonyl-CoA in CHS. On the other hand, the catalytic cysteine-histidine dyad (Cys164-His303) in CHS is well conserved in BAS. A recombinant enzyme expressed in Escherichia coli efficiently afforded benzalacetone as a single product from 4-coumaroyl-CoA and malonyl-CoA. Further, in contrast with CHS that showed broad substrate specificity toward aliphatic CoA esters, BAS did not accept hexanoyl-CoA, isobutyryl-CoA, isovaleryl-CoA, and acetyl-CoA as a substrate. Finally, besides the phenylbutanones in rhubarb, BAS has been proposed to play a crucial role for the construction of the C6-C4 moiety of a variety of natural products such as medicinally important gingerols in ginger plant.
Amino Acid Sequence↗
Novel polyketides synthesized with a higher plant stilbene synthase.
The physiological function of the stilbene synthase (STS) from groundnut (Arachis hypogaea) is the formation of resveratrol. The enzyme uses 4-coumaroyl-CoA, performs three condensations with malonyl-CoA, and folds the resulting tetraketide into a new aromatic ring system. We investigated the capacity for building novel and unusual polyketides from alternative substrates. Three types of products were obtained: (a) complete reaction (stilbene-type), (b) three condensations without formation of an aromatic ring (CTAL-type pyrone derailment), and (c) two condensations (BNY-type pyrone derailment). All product types were obtained from 4-fluorocinnamoyl-CoA and analogs in which the coumaroyl moiety was replaced by furan or thiophene. Only type (b) and (c) products were synthesized from other 4-substituted 4-coumaroyl-CoA analogs (-Cl, -Br, -OCH3). Benzoyl-CoA, phenylacetyl-CoA, and medium chain aliphatic CoA esters were poor substrates, and the majority of the products were of type (c). The results show that minor modifications can be used to direct the enzyme reaction to form a variety of different and new products. Manipulation of the biosynthesis of polyketides by synthetic analogs could lead to the development of a chemical library of pharmaceutically interesting novel polyketides.
Acyl Coenzyme A↗
Lack of association between QT dispersion and blood pressure response during dental surgery.
1. It is well known that dental surgery induces increases in blood pressure. However, the factors influencing this increase are not yet fully understood. We have determined the relationship between QTc (= QT/RR(1/2), with RR being the R-R interval in seconds) dispersion, measured with a 12-lead surface electrocardiogram, and changes in blood pressure during tooth extraction. 2. Both QTc dispersion and the power spectrum of R-R variability were determined before the dental surgery was undertaken. The low-frequency (LF; 0.041-0.140 Hz), high- frequency (HF; 0.140-0.500 Hz) and total spectral powers (TF; 0.000-4.000 Hz) were calculated and the ratio of LF to HF and the percentage of HF relative to TF (%HF; HF/TF x 100) were used as indices of sympathovagal balance and parasympathetic activities, respectively. 3. In the present study, QTc dispersion failed to correlate with LF/HF and %HF. Systolic blood pressure and pulse rate increased significantly during tooth extraction; however, changes in these variables failed to correlate with QTc dispersion. 4. These results suggest that QTc dispersion is not associated with the power spectrum of R-R variability and that it does not affect the blood pressure response during tooth extraction.
Adult↗
Myocardial imaging with 123I-metaiodobenzylguanidine in essential hypertension and renovascular hypertension.
Iodine-123 metaiodobenzylguanidine (MIBG) myocardial imaging is considered to reflect cardiac sympathetic function. We performed myocardial MIBG scintigraphy and echocardiography in 27 patients with essential hypertension (EHT), 7 patients with renovascular hypertension (RVHT), and 8 normotensive subjects (NT) to investigate alterations in MIBG myocardial imaging in the presence of hypertension and left ventricular hypertrophy (LVH). EHT were divided into two groups based on LV wall thickness; EHT with LVH group (> or = 13 mm, n = 15) and EHT without LVH group (< 13 mm, n = 12). The delayed uptake of MIBG was decreased, and the washout rate of MIBG was greater in the EHT with LVH group than EHT without LVH group or NT group. The washout rate was correlated with LV mass and LV diastolic function (as assessed by mitral flow). In RVHT group, the MIBG washout rate increased even without LVH, compared with NT and EHT without LVH groups. In summary, the washout rate of MIBG increased in parallel with the development of LVH in EHT and increased independently of the LV mass in RVHT. Cardiac sympathetic function could be altered in hypertensive LVH and in renovascular hypertension.
3-Iodobenzylguanidine↗
Association of body mass index with blood pressure in 80-year-old subjects.
OBJECTIVE: Little data are available on the association between obesity and high blood pressure in elderly individuals, particularly in subjects over 80 years of age. The aim of the present study was to determine the association between body mass index (BMI) and blood pressure in 80-year-old subjects. METHODS: This study was part of the 8020 Data Bank Survey, which was designed to collect the baseline data of systemic and dental health conditions in 80-year-old subjects. We studied the cross-sectional association of BMI with blood pressures in 645 Japanese (258 men and 387 women), who were 80 years old. RESULTS: Mean systolic blood pressure rose from 146.6 mmHg in the first quintile of BMI to 147.5 mmHg in the second, 150.3 mmHg in the third, 151.6 mmHg in the fourth, and 156.4 mmHg in the fifth quintiles (test for trend, P = 0.006). Mean diastolic blood pressure rose from 75.8 mmHg in the lowest quintile of BMI to 81.8 mmHg in the highest (test for trend, P = 0.002). We performed multiple regression analysis, controlling for factors known to influence blood pressure values, such as sex, alcohol intake, current smoking status and serum glucose, total cholesterol and creatinine concentrations. The association between BMI and systolic and diastolic blood pressure, respectively, was highly statistically significant in all analyses. CONCLUSION: These results show that a close relationship is present between obesity and high blood pressure, even in very old subjects.
Aged↗
Magnesium decreases arterial pressure and inhibits cardiovascular responses induced by N-methyl-D-aspartate and metabotropic glutamate receptors stimulation in rostral ventrolateral medulla.
OBJECTIVE: Magnesium sulfate (MgSO4) is widely used for the treatment of eclampsia. However, effects of Mg2+ in central cardiovascular regulation remain unclear. In the present study, the role of Mg2+ on cardiovascular regulation in the rostral ventrolateral medulla (RVLM) of rats was examined. METHODS: Adult male Wistar rats were anesthetized with urethane, and artificially ventilated. The ventral surface of the medulla was exposed, and the RVLM was identified by microinjection (50 nl) of l-glutamate (l-Glu; 2 nmol). Then, MgSO4 (1, 3, 10 nmol, n = 7 for each dose) and magnesium chloride (MgCl2; 10 nmol, n = 7) were microinjected into the RVLM. l-Glu (2 nmol), N-methyl-D-aspartate (NMDA; 20 pmol), alpha-amino-3-hydroxy-5-methyl isoxazole-4-propionic acid (AMPA; 5 pmol) and (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD, metabotropic glutamate receptor agonist; 1 nmol] were also microinjected with or without pretreatment of MgSO4 (10 nmol; n = 7 for each drug). RESULTS: MgSO4 dose-dependently decreased mean arterial pressure (MAP) and heart rate (HR). The high dose of MgSO4 (10 nmol) significantly decreased MAP and HR (-25 +/- 4 mmHg and -43 +/- 6 bpm). Similarly, MgCl2 decreased MAP and HR (-27 +/- 4 mmHg and -30 +/- 6 bpm). The pressor response evoked by NMDA or (1S,3R)-ACPD was significantly attenuated by the pretreatment with MgSO4. In contrast, pressor response caused by l-Glu or AMPA was not affected by pretreatment with MgSO4. CONCLUSIONS: These results suggest that Mg2+ has an inhibitory role on the RVLM neurons, and inhibits cardiovascular responses induced by NMDA and metabotropic glutamate receptor agonists.
Animals↗
Osteonecrosis in patients with systemic lupus erythematosus develops very early after starting high dose corticosteroid treatment.
OBJECTIVES: To investigate the actual time of onset of osteonecrosis (ON) after high dose corticosteroid treatment in systemic lupus erythematosus (SLE). METHODS: 72 patients with active SLE, who received high dose corticosteroid for the first time, for the development of ON at hips and knees were monitored by magnetic resonance imaging for at least 12 months. RESULTS: ON lesions were detected in 32/72 patients (44%) between one and five months (3.1 months on average) after starting high dose corticosteroid treatment. No osteonecrotic lesion was newly detected from the sixth month of treatment until the end of the follow up period. CONCLUSION: The findings suggested that the actual time of onset of ON in SLE is within the first month of high dose corticosteroid treatment.
Adolescent↗
Impaired beta-adrenergic hyperpolarization in arteries from prehypertensive spontaneously hypertensive rats.
Stimulation of beta-adrenoceptors leads to vascular smooth muscle hyperpolarization, presumably through the beta-adrenoceptors/Gs protein/adenylate cyclase/ATP-sensitive K(+)-channels (KATP) signaling cascade, which may play an important role in the sympathetic control of membrane potential. beta-Adrenoceptor-mediated hyperpolarization has been shown to be impaired in the established stage of experimental hypertension. The present study tested the hypothesis that beta-adrenergic hyperpolarization may be defective before the development of hypertension in some forms of genetic hypertension. We evaluated beta-adrenoceptor-mediated hyperpolarization using microelectrodes in mesenteric resistance arteries from 5-week-old, prehypertensive, spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY). Isoproterenol-induced hyperpolarization was significantly smaller in SHR than in WKY (10(-7) mol/L: -4.6+/-0.6 versus -7.8+/-0.8 mV, P<0.01; 10(-6) mol/L -7.8+/-0.5 versus -9.8+/-0.6 mV, P<0.05; n=9). Furthermore, hyperpolarization to cholera toxin, a direct activator of Gs protein, was also impaired in SHR. On the other hand, hyperpolarization to forskolin, an adenylate cyclase activator, and to levcromakalim, a KATP opener, was comparable between groups. These findings suggest that beta-adrenoceptor-mediated hyperpolarization is defective in SHR before the development of hypertension, presumably because of an abnormality at the Gs protein site. Considering the importance of membrane potential in the control of vascular tone, altered beta-adrenergic control of membrane potential might play a role in the development of hypertension in SHR.
Animals↗
Central orexin-A augments sympathoadrenal outflow in conscious rabbits.
We determined the cardiovascular and neurohormonal responses to intracerebroventricular administration of orexin-A in conscious rabbits. Intracerebroventricular injection of orexin-A elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 100 pmol of orexin-A (14.0+/-0.7 mm Hg and 55.4+/-14.9%, respectively) were obtained at 40 and 25 minutes after injection, respectively. Plasma epinephrine and glucose concentrations were significantly increased at 60 and 90 minutes after intracerebroventricular injection of orexin-A (control versus 90 minutes; for epinephrine, 38.0+/-12.8 versus 167.5+/-42.5 pg/mL, P<0.01; for glucose, 6.66+/-0.18 versus 7.75+/-0.14 mmol/L, P<0.01). Plasma norepinephrine and insulin concentrations increased at 60 and 90 minutes but did not attain significant values. Intracerebroventricular injection of orexin-A also caused significant increases in plasma vasopressin concentrations. However, pretreatment with an intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, abolished these cardiovascular and neurohormonal responses. On the other hand, intravenous injection of the same dose of orexin-A (100 pmol) used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular orexin-A acts in the central nervous system and activates sympathoadrenal outflow, resulting in increases in arterial pressure and plasma glucose levels in conscious rabbits.
Animals↗
Central human cocaine- and amphetamine-regulated transcript peptide 55-102 increases arterial pressure in conscious rabbits.
We determined cardiovascular and neurohormonal responses to intracerebroventricular administration of human cocaine- and amphetamine-regulated transcript (CART) peptide 55-102 in conscious rabbits. Intracerebroventricular injection of CART 55-102 elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 1 nmol of CART 55-102 (+5.0+/-2.6 mm Hg and +72.5+/-20.8%) were obtained 40 and 60 minutes after injection, respectively. Plasma epinephrine and glucose concentrations significantly increased 30 and 60 minutes after intracerebroventricular injection of CART 55-102 (control versus 60 minutes for epinephrine, 77.0+/-62.4 versus 1067.5+/-329.3 pg/mL, P<0.01; for glucose, 6.25+/-0.33 versus 11.57+/-0.93 mmol/L, P<0.01). Plasma norepinephrine concentrations also significantly increased at 30 minutes. Plasma insulin, vasopressin, and cortisol concentrations increased at 60 minutes but did not attain significant values. However, pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular and neurohormonal responses. In contrast, intravenous injection of the same dosage of CART 55-102 (1 nmol) as that used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular human CART 55-102 acts in the central nervous system and activates sympathoadrenal outflow, which results in increases in arterial pressure and plasma glucose levels in conscious rabbits.
Animals↗
The influence of chronic antihypertensive treatment on the central pressor response in SHR.
UNLABELLED: We examined the influence of chronic antihypertensive treatment on the central pressor response in SHR. Adult male SHR were divided into 5 groups, i.e., those receiving 1) enalapril (Enal: 25 mg/kg/day in drinking water, n=12); 2) losartan (Los: 40 mg/kg/day, n=11); 3) candesartan (Cand: 4 mg/kg/day, n=12); 4) hydralazine+hydrochlorothiazide (H&H: 50+7.5 mg/kg/day, n=9); 5) vehicle ( CONTROL: n=9). At 4 weeks of treatment, hypertonic saline (0.25, 0.5 M) was intracerebroventricularly (i.c.v.) injected into conscious rats. Plasma catecholamines were measured before and after i.c.v. injection. On completion of the experiment, heart weight was measured, and angiotensin-converting enzyme (ACE) activity of the cerebrum was determined. All antihypertensive drugs elicited comparable reductions in systolic blood pressure, while heart rate was significantly higher in the H&H group than in the other groups during treatment. Pressor response to i.c.v. hypertonic saline (0.5 M) was significantly smaller in the Enal (12 +/- 3 mmHg) and Cand (11 +/- 2 mmHg) groups than in the Los (22 +/- 2 mmHg), H&H (16 +/- 2 mmHg), and CONTROL (29 +/- 5 mmHg) groups. Plasma catecholamines did not differ among the groups. Heart weight was lowest in the Enal group, followed by the Los and Cand groups. ACE activity of the cerebrum was significantly decreased in the Enal group. The results suggest that chronic treatment with various antihypertensive drugs differentially alters the central pressor response in SHR, and enalapril and candesartan are effective in attenuating this response.
Angiotensin-Converting Enzyme Inhibitors↗