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Biomedical subjects

J Minami

Publications and source records attributed to J Minami.

At least 37 records · Page 2Linked to original sources
PubMed2000

Urinary excretions of albumin and type IV collagen in normotensive and hypertensive subjects.

Plasma albumin leaks into urine as a result of glomerular hypertension and basement membrane injury, while urinary type IV collagen derives from mesangial matrix and glomerular basement membrane. The purpose of this study was to elucidate the pathophysiological significance of these urinary microproteins as an indicator of cardiovascular organ injuries in hypertension. In health-checkup participants without diabetes, proteinuria, or microhematuria, and who were not being treated for hypertension or any other disease at the time of enrollment, urinary albumin and type IV collagen were measured and their relations to organ injuries and cardiovascular risk factors were evaluated. Of 1,079 subjects (40- to 65-year-old; 256 men and 823 women) enrolled in the study, 120 (11.1%) had untreated hypertension exceeding 140/90 mmHg. Urinary albumin was positively correlated with both age (r=0.16, p<0.001) and systolic blood pressure (r=0.27, p<0.001). Urinary type IV collagen was not only positively correlated with age (r=0.12, p<0.001) and diastolic blood pressure (r=0.14, p<0.001) but also negatively correlated with blood hemoglobin (r=-0.12, p<0.001). Urinary albumin, but not type IV collagen, had a significant relation to electrocardiographic signs of left ventricular hypertrophy (p=0.012) and retinal arteriosclerosis on fundoscopy (p <0.001). Thus both albumin and type IV collagen would seem to have increased in association with age and hypertension in this cohort. It is suggested that urinary albumin is an indicator not only of renal injury, but also possibly of development of cardiac hypertrophy and arteriosclerotic changes. Urinary type IV collagen, on the other hand, may be associated with renal tissue injuries that affect erythrokinetics.

Adult↗
PubMed1999

Promoter upstream bent DNA activates the transcription of the Clostridium perfringens phospholipase C gene in a low temperature-dependent manner.

The phospholipase C gene (plc) of Clostridium perfringens possesses three phased A-tracts forming bent DNA upstream of the promoter. An in vitro transcription assay involving C.perfringens RNA polymerase (RNAP) showed that the phased A-tracts have a stimulatory effect on the plc promoter, and that the effect is proportional to the number of A-tracts, and more prominent at lower temperature. A gel retardation assay and hydroxyl radical footprinting revealed that the phased A-tracts facilitate the formation of the RNAP-plc promoter complex through extension of the contact region. The upstream (UP) element of the Escherichia coli rrnB P1 promoter stimulated the downstream promoter activity temperature independently, differing from the phased A-tracts. When the UP element was placed upstream of the plc promoter, low temperature-dependent stimulation was observed, although this effect was less prominent than that of the phased A-tracts. These results suggest that both the phased A-tracts and UP element cause low temperature-dependent activation of the plc promoter through a similar mechanism, and that the more efficient low temperature-dependent activation by the phased A-tracts may be due to an increase in the bending angle at a lower temperature.

Binding, Competitive↗
PubMed1999

Amlodipine, a long-acting calcium channel blocker, attenuates morning blood pressure rise in hypertensive patients.

1. The effects of once-daily calcium channel blockers with different plasma half-lives on diurnal blood pressure changes were examined in hypertensive patients. 2. Patients with essential hypertension, nine men and 13 women aged 61 +/- 2 years, were treated with amlodipine or nitrendipine in a random cross-over design for 12-16 weeks each. The study drugs were given once daily as monotherapy (n = 8) or in combination with other classes of antihypertensive drugs (n = 14). The plasma half-life of amlodipine is as long as 36 h, while that of nitrendipine is 10 h. At the end of each treatment period, 24 h ambulatory blood pressure and pulse rate were monitored. 3. Average office blood pressure was comparably controlled below 140/90 mmHg by either amlodipine or nitrendipine, both in the monotherapy and the combination therapy groups; however, pulse rate was greater in nitrendipine than in amlodipine either in the monotherapy (by 6 b.p.m., P < 0.05) or in the combination therapy (by 5 b.p.m., P < 0.01). 4. In 24 h blood pressure monitoring, morning (05.30-09.00 h) blood pressure was higher in nitrendipine than in amlodipine by 6/4 mmHg in the monotherapy (P < 0.05) and by 7/5 mmHg in the combination therapy (P < 0.03), although the blood pressure in the remainder of the 24 h did not differ between the two treatment periods. In addition, pulse rate in the daytime (09.30-18.00 h) was greater in nitrendipine than in amlodipine by 6 b.p.m. in the monotherapy (P < 0.01) and by 7 b.p.m. in the combination therapy (P < 0.02). 5. These results suggest slow pharmacokinetics of amlodipine provides an advantage in controlling morning blood pressure and mitigating reflex activation of the sympathetic nervous system.

Amlodipine↗
PubMed1999

A Clostridium perfringens hem gene cluster contains a cysG(B) homologue that is involved in cobalamin biosynthesis.

The hem gene cluster, which consists of hemA, cysG(B), hemC, hemD, hemB, and hemL genes, and encodes enzymes involved in the biosynthetic pathway from glutamyl-tRNA to uroporphyrinogen III, has been identified by the cloning and sequencing of two overlapping DNA fragments from Clostridium perfringens NCTC8237. The deduced amino acid sequence of the N-terminal region of C. perfringens HemD is homologous to those reported for the C-terminal region of Salmonella typhimurium CysG and Clostridium josui HemD. C. perfringens CysG(B) is a predicted 220-residue protein which shows homology to the N-terminal region of S. typhimurium CysG. Disruption of the cysG(B) gene in C. perfringens strain 13 by homologous recombination reduced cobalamin (vitamin B12) levels by a factor of 200. When grown in vitamin B12-deficient medium, the mutant strain showed a four-fold increase in its doubling time compared with that of the wild-type strain, and this effect was counteracted by supplementing the medium with vitamin B12. These results suggest that C. perfringens CysG(B) is involved in the chelation of cobalt to precorrin II as suggested for the CysG(B) domain of S. typhimurium CysG, enabling the synthesis of cobalamin.

Base Sequence↗
PubMed1999

Gene duplication and multiplicity of collagenases in Clostridium histolyticum.

Clostridium histolyticum collagenase contains a number of different active components. Previously we have shown that colH encodes a 116-kDa collagenase (ColH) and a 98-kDa gelatinase. We purified a different 116-kDa collagenase (ColG) from the culture supernatant and sequenced its gene (colG). We also identified four other gelatinases (105, 82, 78, and 67 kDa) and determined their N-terminal amino acid sequences, all of which coincided with that of either ColG or ColH. Hybridization experiments showed that each gene is present in a single copy and each gene is transcribed into a single mRNA. These results suggest that all the gelatinases are produced from the respective full-length collagenase by the proteolytic removal of C-terminal fragments. The substrate specificities of the enzymes suggest that colG and colH encode class I and class II enzymes, respectively. Analysis of their DNA locations by pulsed-field gel electrophoresis and nucleotide sequencing of their surrounding regions revealed that the two genes are located in different sites on the chromosome. C. histolyticum colG is more similar to C. perfringens colA than to colH in terms of domain structure. Both colG and colA have a homologous gene, mscL, at their 3' ends. These results suggest that gene duplication and segment duplication have occurred in an ancestor cell common to C. histolyticum and C. perfringens and that further divergence of the parent gene produced colG and colA.

Amino Acid Sequence↗
PubMed1999

Identification of metal ligands in the Clostridium histolyticum ColH collagenase.

A Clostridium histolyticum 116-kDa collagenase has an H415EXXH motif but not the third zinc ligand, as found in already characterized zinc metalloproteinases. To identify its catalytic site, we mutated the codons corresponding to the three conserved residues in the motif to other amino acid residues. The mutation affecting His415 or His419 abolished catalytic activity and zinc binding, while that affecting Glu416 did the former but not the latter. These results suggest that the motif forms the catalytic site. We also mutated the codons corresponding to other amino acid residues that are likely zinc ligands. The mutation affecting Glu447 decreased markedly both the enzymatic activity and the zinc content, while that affecting Glu446 or Glu451 had smaller effects on activity and zinc binding. These mutations caused a decrease in kcat but no significant change in Km. These results are consistent with the hypothesis that Glu447 is the third zinc ligand. The spacing of the three zinc ligands is the same in all known clostridial collagenases but not in other known gluzincins, indicating that they form a new gluzincin subfamily. The effects of mutations affecting Glu446 and Glu451 suggest that the two residues are also involved in catalysis, possibly through an interaction with the two zinc-binding histidine residues.

Amino Acid Sequence↗
PubMed1999

Effects of smoking cessation on blood pressure and heart rate variability in habitual smokers.

We investigated the effects of 1-week of smoking cessation on ambulatory blood pressure, heart rate, and heart rate variability in 39 normotensive male habitual smokers (mean+/-SEM, 32.5+/-1.0 years). The ambulatory blood pressure, heart rate, and ECG R-R intervals were measured during a 24-hour period with a portable recorder (TM-2425) on the last day of 1-week smoking and nonsmoking periods. The order of the 2 periods was randomized. In the smoking period, the subjects were instructed to smoke cigarettes according to their usual smoking patterns. A power-spectral analysis of R-R intervals was performed to obtain the low-frequency (LF) and high-frequency (HF) components. The percentage of differences between adjacent normal R-R intervals >50 milliseconds (pNN50) was used as a time-domain measure of heart rate variability. The 24-hour ambulatory blood pressure was significantly lower in the nonsmoking period than in the smoking period, by 3.5+/-1.1 mm Hg systole [P<0. 01] and by 1.9+/-0.7 mm Hg diastole [P<0.05], whereas the nighttime blood pressure did not differ significantly between the 2 periods. The 24-hour heart rate was significantly lower in the nonsmoking period than in the smoking period, by 7.3+/-1.0 beats/min (P<0.0001). The pNN50 and the 24-hour HF component were significantly higher in the nonsmoking period than in the smoking period (P<0.0001 for each). The plasma norepinephrine and epinephrine concentrations were significantly lower in the nonsmoking period than in the smoking period (P<0.05 for each). These results demonstrate the substantial and immediate benefits of smoking cessation on these cardiovascular indices.

Adult↗
PubMed1999

Acute and chronic effects of a hypocaloric diet on 24-hour blood pressure, heart rate and heart-rate variability in mildly-to-moderately obese patients with essential hypertension.

We examined the acute and chronic effects of a nutritionally balanced, moderately hypocaloric diet on 24-hour ambulatory blood pressure, heart rate and heart-rate variability in mildly-to-moderately obese patients with essential hypertension. We enrolled 16 obese patients with essential hypertension [age: 51-76 years, body mass index (BMI): 26-32 kg/m2]. For the initial week, a standard diet of 2,000 kcal/day was given, followed by a 3-week of a hypocaloric diet of 850 kcal/day. In the last period of the standard diet and in the first and the last periods of the hypocaloric diet, each subject's 24-hour ambulatory blood pressure, heart rate and R-R intervals of the electrocardiogram were recorded, and electrolytes and catecholamines in 24-hour urine samples were also measured. A power spectral analysis of the heart-rate variability was performed over a 24-hour period based on the autoregressive method. The subjects lost 3.7+/-0.3 kg (mean +/- s.e.m.) of body weight during the 3-week hypocaloric diet period. The 24-hour blood pressure did not differ between the last period of the standard diet and the first period of the hypocaloric diet; however, it showed a significant reduction after 3 weeks of the hypocaloric diet. The decrease in the 24-hour blood pressure during the study period was 10.5+/-1.5 mm Hg systole and 4.3+/-1.8 mm Hg diastole. In contrast, the 24-hour heart rate was significantly reduced in the first period of the hypocaloric diet, although the body weight and blood pressure did not change, and the rate was maintained even in the last period of the hypocaloric diet. The decrease in the 24-hour heart rate during the study period was 2.8+/-0.9 beats per minute. The hypocaloric diet did not change any autonomic indices obtained from a power spectral analysis of the heart-rate variability. In conclusion, different responses to a hypocaloric diet were observed between the blood pressure and the heart rate in obese hypertensive patients. The changes in power spectral parameters of the heart-rate variability were less apparent than those found with the blood pressure or the heart rate.

Blood Pressure↗
PubMed1998

A study of the collagen-binding domain of a 116-kDa Clostridium histolyticum collagenase.

The Clostridium histolyticum 116-kDa collagenase consists of four segments, S1, S2a, S2b, and S3. A 98-kDa gelatinase, which can degrade denatured but not native collagen, lacks the C-terminal fragment containing a part of S2b and S3. In this paper we have investigated the function of the C-terminal segments using recombinant proteins. Full-length collagenase degraded both native type I collagen and a synthetic substrate, Pz-peptide, while an 88-kDa protein containing only S1 and S2a (S1S2a) degraded only Pz-peptide. Unlike the full-length enzyme, S1S2a did not bind to insoluble type I collagen. To determine the molecular determinant of collagen binding activity, various C-terminal regions were fused to the C terminus of glutathione S-transferase. S3 as well as S2bS3 conferred collagen binding. However, a glutathione S-transferase fusion protein with a region shorter than S3 exhibited reduced collagen binding activity. S3 liberated from the fusion protein also showed collagen binding activity, but not S2aS2b or S2b. S1 had 100% of the Pz-peptidase activity but only 5% of the collagenolytic activity of the full-length collagenase. These results indicate that S1 and S3 are the catalytic and binding domains, respectively, and that S2a and S2b form an interdomain structure.

Catalysis↗
PubMed1998

Effects of potassium supplementation on office, home, and 24-h blood pressure in patients with essential hypertension.

An increase in potassium (K) intake may lower blood pressure (BP), but inconsistent results have been obtained in clinical trials. We studied the effects of K supplementation in hypertensive patients with monitoring of home and ambulatory BP. Fifty-five patients with essential hypertension (26 men, 29 women, 36-77 years old) participated in this study. A 4-week K supplementation period and 4-week control period were assigned in a randomized crossover manner. During the K period, the subjects were given 64 mmol/day of K as slow-release KCl tablets. Office, home, and 24-h BP, as well as serum and urinary electrolytes, were measured at the end of each period. In the control period, office, home, and 24-h BP were 151 +/- 2/88 +/- 1 (mean +/- SE), 138 +/- 1/83 +/- 1, and 137 +/- 1/81 +/- 1 mm Hg, respectively. Serum K increased from 4.15 +/- 0.04 to 4.42 +/- 0.05 mmol/L, and urinary K increased from 54 +/- 2 to 96 +/- 3 mmol/day with the K supplementation. Office, home, and 24-h BP were significantly lower in the K period than in the control period, although the differences were small (2.7 +/- 1.1/1.4 +/- 0.6, 3.6 +/- 0.9/1.7 +/- 0.5, 3.4 +/- 1.0/1.2 +/- 0.5 mm Hg, respectively). Changes in home and 24-h systolic BP with K supplementation were highly significant (P < .001), compared with office BP (P < .05). The change in 24-h systolic BP was correlated negatively with baseline BP and urinary Na/K ratio, and positively with baseline urinary K excretion. The changes in daytime and nighttime BP were comparable. These results indicate that increasing K intake lowers BP in hypertensive subjects, especially in those with higher BP and lower K intake. Our study supports the usefulness of K supplementation in the treatment of hypertension, although its antihypertensive effect may be small.

Administration, Oral↗
PubMed1998

Blood pressure and other risk factors before the onset of myocardial infarction in hypertensive patients.

To investigate blood pressure (BP) as well as other risk factors before the onset of myocardial infarction in hypertensive patients, we analysed the BP and metabolic variables in 94 hypertensive patients who had been followed up in our out-patient clinic before the first onset (M1 group; n = 42, 69 +/- 1 years, mean +/- s.e.) or the recurrent onset (M2 group; n = 52, 69 +/- 1 years) of myocardial infarction. Ninety-four hypertensive outpatients who had no history of serious cardiovascular diseases (C group) were also recruited for an age- and sex-matched case-control study. The majority of the patients were taking anti-hypertensive drugs (M1: 90%; M2: 98%; C: 90%). The average BP values for 1 year before the onset of myocardial infarction were used for the analysis. The BPs before the onset of myocardial infarction were 147 +/- 2 mm Hg systole and 81 +/- 2 mm Hg diastole in the M1 group, and 141 +/- 2 mm Hg systole and 78 +/- 1 mm Hg diastole in the M2 group, while those of the C group were 146 +/- 1 mm Hg systole and 84 +/- 1 mm Hg diastole. The diastolic BP of the M2 group was significantly lower than that of the C group (P < 0.0001). In patients aged > or =69 years, the diastolic BP of the M1 and M2 groups (M1: 77 +/- 1 mm Hg; M2: 75 +/- 1 mm Hg) were significantly lower than that of the C group (83 +/- 1 mm Hg). The fasting blood glucose of the M1 and M2 groups was higher than that of the C group. The serum HDL cholesterol of the M1 group was lower than that of the other groups. These results suggest that, in addition to glucose and lipid metabolism disorders, low diastolic BP is associated with the onset of myocardial infarction, especially in reinfarction and in elderly hypertensive patients.

Aged↗
PubMed1998

Comparison of 24-hour blood pressure, heart rate, and autonomic nerve activity in hypertensive patients treated with cilnidipine or nifedipine retard.

We compared the effects of cilnidipine and nifedipine retard on 24-h blood pressure (BP), heart rate (HR), and autonomic nerve activity in patients with essential hypertension. Cilnidipine is a novel and unique 1,4-dihydropyridine calcium antagonist that has the L-type and N-type voltage-dependent calcium channel-blocking action. Fourteen hypertensive outpatients (four men and 10 women; aged 64 +/- 2 years, mean +/- SEM) were enrolled in this study. Their ambulatory BP and electrocardiogram were monitored for 24 h at intervals of 30 min with a portable recorder after a 4-week drug-free period, after a 4-week treatment period with cilnidipine (5 or 10 mg once daily), and after a 4-week treatment period with nifedipine retard (10 or 20 mg twice daily). The order of the three periods was randomized. Autonomic nerve activity was evaluated by a power spectral analysis of HR variability, by using the high-frequency (HF) component as an index of parasympathetic nerve activity and the ratio of the low-frequency (LF) component to the HF component (LF/HF) as an index of sympathovagal balance. Cilnidipine and nifedipine retard significantly reduced the 24-h BP of these patients to similar extents (cilnidipine, -11 +/- 3/-6 +/- 1 mm Hg; nifedipine retard, -15 +/- 3/-6 +/- 2 mm Hg). Cilnidipine did not change the 24-h average HR, whereas nifedipine retard significantly increased it (+3.3 +/- 1.4 beats/min; p < 0.05). Nifedipine retard significantly increased the LF/HF ratio in the daytime and the nighttime. Such changes were limited to the daytime in the treatment period with cilnidipine. These results suggest that cilnidipine is effective as a once-daily antihypertensive agent and had less influence on autonomic nervous system and HR than did nifedipine retard.

Autonomic Pathways↗
PubMed1998

Putative heat shock protein 70 gene from Actinobacillus actinomycetemcomitans: molecular cloning and sequence analysis of its gene.

We have cloned and sequenced two overlapping fragments of chromosomal DNA from Actinobacillus actinomycetemcomitans. The nucleotide sequence contained two open reading frames. The deduced amino acid sequences of the two open reading frames showed significant homology with the heat shock proteins hsp70 and hsp40 of other organisms respectively. The upstream open reading frame consisted of 1902 bp, corresponding to 634-amino-acid residues. The CAA codon for glutamines was frequently seen in hsp70, i.e., in 30 of 32 glutamines (93.8%). The spacing region between the two open reading frames was unusually long compared with other prokaryotic organisms. A number of unique and distinguishing features of the sequences in the hsp70 family were verified, and it was found that a particular spacing sequence between the hsp70 and hsp40 gene loci can be used to identify A. actinomycetemcomitans from the periodontal pocket.

Aggregatibacter actinomycetemcomitans↗
PubMed1998

Neurotoxicity of Clostridium perfringens epsilon-toxin for the rat hippocampus via the glutamatergic system.

The neurotoxicity of epsilon-toxin, one of the major lethal toxins produced by Clostridium perfringens type B, was studied by histological examination of the rat brain. When the toxin was injected intravenously at a lethal dose (100 ng/kg), neuronal damage was observed in many areas of the brain. Injection of the toxin at a sublethal dose (50 ng/kg) caused neuronal damage predominantly in the hippocampus: pyramidal cells in the hippocampus showed marked shrinkage and karyopyknosis, or so-called dark cells. The dark cells lost the immunoreactivity to microtubule-associated protein-2, a postsynaptic somal and dendric marker, while acetylcholinesterase-positive fibers were not affected. Timm's zinc staining revealed that zinc ions were depleted in the mossy layers of the CA3 subfield containing glutamate as a synaptic transmitter. The cerebral blood flow in the hippocampus was not altered significantly before or after administration of the toxin, as measured by laser-Doppler flowmetry, excluding the possibility that the observed histological change was due to a secondary effect of ischemia in the hippocampus. Prior injection of either a glutamate release inhibitor or a glutamate receptor antagonist protected the hippocampus from the neuronal damage caused by epsilon-toxin. These results suggest that epsilon-toxin acts on the glutamatergic system and evokes excessive release of glutamate, leading to neuronal damage.

Animals↗