Biomedical subjects
Y Doi
Publications and source records attributed to Y Doi.
[Factors that influence the serum of atrial natriuretic peptide and brain natriuretic peptide concentrations--is there a specific marker for senile patients?].
To evaluate factors that influence of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels in elderly people, we measured those levels in 54 men and 148 women (84.4 +/- 0.5 years old), and looked for associations of ANP and BNP with clinical factors and echocardiographic variables [left ventricular mass index and atrial to-early peak transmitral velocity ratio (A/E)]. ANP and BNP levels were 1.6 and 6.5 times higher than average. Sex was not a significant factor. We also looked for a link between cardiac rhythms and levels of ANP and BNP. Patients with atrial fibrillation had significantly higher levels of ANP and BNP than did patients with sinus rhythm. ANP and BNP levels were abnormally high in patients with left ventricular hypertrophy (LVH). We could measured A/E in 161 of 202 subjects; 154 of 157 subjects with normal LV systolic function had A/E > 1 which indicates abnormally low in LV diastolic function. Moreover, abnormally high LV diastolic stress might have been present, because 124 of 202 subjects had aortic regurgitation. We divided the patients into two groups: those 65 to 75 years old, and those over 75 years old. The older patients had significantly higher levels of ANP and BNP even without LVH and without a difference in renal function. Furthermore, the older patients had significantly higher levels of BNP even without LVH, with normal renal function, with sinus rhythm, with normal LV systolic function, and in NYHA Class I or II. These data indicate that ANP and BNP levels in people with senility may be associated with the cardiac rhythm and with abnormally low renal function, myocardial hypertrophy, abnormally high cardiac volume, and abnormally low diastolic function.
[Congenital aortic regurgitation complicated by infective endocarditis of tricuspid valve due to spontaneous closure of ventricular septal defect: a case report].
A 32-year-old woman presented with a rare case of tricuspid valve endocarditis causing inflammatory reopening of the spontaneously closed ventricular septal defect (VSD), associated with aortic valve malformation. She was admitted to our hospital because of fever lasting 4 weeks. Severe aortic regurgitation was revealed by color Doppler echocardiography. Blood culture identified Microccus faecalis. Antibiotics were administered over 3 weeks, but serial echocardiography showed a developing vegetation in the right ventricle and left-to-right shunt flow. The diagnosis was infective endocarditis complicated by aortic ring abscess and interventricular septal fistula. Surgery performed on the 22nd hospitalized day found a vegetation of the tricuspid valve, a membranous type of VSD, and aortic valve malformation. Aortic valve replacement, patch closure of VSD, and tricuspid valvuloplasty achieved a successful outcome.
[Sixty percent lidocaine tape alleviates pain on injection of propofol after diminishing venipuncture pain].
We evaluated the efficacy of the 60% lidocaine tape in alleviating pain associated with intravenous propofol administration in 71 gynecological patients. Thirty-eight women had the tape applied for 2.5 h before venipuncture, with the remaining patients acting as the control. A 20 gauge cannula was inserted into the cephalic vein. Propofol at room temperature was injected at a rate of 1200 ml.hr-1. The statistical significance of differences was established with the Mann-Whitney's U test and the chi 2 test. The median level of pain intensity resulting from venipuncture among the patients treated with the tape was smaller than that in the control group (16.5, vs 34, P = 0.006). Thereafter, cannulation was successfully achieved with reduced or no pain (VAS at cannulation < or = 25, n = 39), and only 16% of the treatment group complained of pain on injection as compared with 53.8% of the control group (P = 0.02). Moreover, the pain intensity was decreased with lidocaine tape (P = 0.006). The cost of the lidocaine tape is covered by medical insurance for reducing pain on venipuncture. Thus, as the tape also alleviates the pain on injection of propofol through its anesthetic action, it can be a safe, easy and cost-effective method as "it kills two pains with one tape".
Na+-dependent glucose uptake and collagen synthesis by cultured bovine retinal pericytes.
This study was performed to clarify the presence of sodium-dependent glucose uptake and its role in the synthesis of type IV and type VI collagen by cultured bovine retinal pericytes. The glucose uptake by retinal pericytes and retinal endothelial cells was measured using 3H-D-glucose in the presence or absence of sodium. Glucose uptake in the presence of sodium was twice as high as that observed in the presence of phlorizin and sodium or in the absence of sodium. Sodium-dependent glucose uptake was observed at different sodium concentrations, and its half-maximal stimulation occurred at 48 mM. These findings were not observed in retinal endothelial cells. Levels of type IV and type VI collagen produced by retinal pericytes were significantly increased at glucose concentrations higher than 20 mM. Phlorizin decreased both collagen synthesis and glucose consumption by retinal pericytes incubated with 30 mM of glucose to the levels observed with 5 mM of glucose. These data suggest that sodium-dependent glucose uptake is present in retinal pericytes and that excessive glucose entry into the cell is an important factor for overproduction of collagen. Phlorizin normalized the synthesis of type IV and type VI collagen with decreasing glucose consumption under high glucose conditions.
Quality of life of old people living in the community.
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ERM (ezrin/radixin/moesin)-based molecular mechanism of microvillar breakdown at an early stage of apoptosis.
Breakdown of microvilli is a common early event in various types of apoptosis, but its molecular mechanism and implications remain unclear. ERM (ezrin/radixin/moesin) proteins are ubiquitously expressed microvillar proteins that are activated in the cytoplasm, translocate to the plasma membrane, and function as general actin filament/plasma membrane cross-linkers to form microvilli. Immunofluorescence microscopic and biochemical analyses revealed that, at the early phase of Fas ligand (FasL)-induced apoptosis in L cells expressing Fas (LHF), ERM proteins translocate from the plasma membranes of microvilli to the cytoplasm concomitant with dephosphorylation. When the FasL-induced dephosphorylation of ERM proteins was suppressed by calyculin A, a serine/threonine protein phosphatase inhibitor, the cytoplasmic translocation of ERM proteins was blocked. The interleukin-1beta-converting enzyme (ICE) protease inhibitors suppressed the dephosphorylation as well as the cytoplasmic translocation of ERM proteins. These findings indicate that during FasL-induced apoptosis, the ICE protease cascade was first activated, and then ERM proteins were dephosphorylated followed by their cytoplasmic translocation, i.e., microvillar breakdown. Next, to examine the subsequent events in microvillar breakdown, we prepared DiO-labeled single-layered plasma membranes with the cytoplasmic surface freely exposed from FasL-treated or nontreated LHF cells. On single-layered plasma membranes from nontreated cells, ERM proteins and actin filaments were densely detected, whereas those from FasL-treated cells were free from ERM proteins or actin filaments. We thus concluded that the cytoplasmic translocation of ERM proteins is responsible for the microvillar breakdown at an early phase of apoptosis and that the depletion of ERM proteins from plasma membranes results in the gross dissociation of actin-based cytoskeleton from plasma membranes. The physiological relevance of this ERM protein-based microvillar breakdown in apoptosis will be discussed.
Clinical and electrocardiographic profiles producing exercise-induced U-wave inversion in patients with severe narrowing of the left anterior descending coronary artery.
To elucidate which clinical features produce U-wave inversion, 339 patients with severe narrowing of the left anterior descending artery were evaluated. In patients with anterior myocardial infarction, extensive coronary artery disease and protected left anterior descending arterial territory are essential in the development of U-wave inversion, whereas electrocardiographic changes at rest in addition to anterior lead ST depression, rather than coronary anatomy, are important in those without anterior myocardial infarction.
Cloning of the gene for poly(3-hydroxybutyric acid) depolymerase of Comamonas testosteroni and functional analysis of its substrate-binding domain.
A poly(3-hydroxybutyric acid) (PHB) depolymerase gene of Comamonas testosteroni YM1004 was cloned on Sau3AI fragment from genomic DNA into Escherichia coli DH5. Nucleotide sequence analysis dedicated a 1539 bp open reading frame encoding a protein 513 amino acid with a putative 25 residue signal peptide for secretion. The deduced amino acid sequence was very similar to that of PHB depolymerase of Comamonas sp. In order to understand the characteristics of substrate-binding domain of the depolymerase, we constructed its glutathione S-transferase (GST) fusion protein and investigated the ability of adsorption on PHB single crystals by using gold-conjugated antibody and transmission electron microscopy. The fusion protein adsorbed on PHB single crystals tightly and homogeneously, suggesting that binding domain contributes to the adsorption of enzyme on solid PHB without site specificity.
Home blood-pressure control in Japanese hypertensive population.
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Polymorphism of the angiotensin-converting enzyme (ACE) gene in patients with thrombotic brain infarction.
The relationship between cerebrovascular disease and an insertion/deletion (I/D) polymorphism in intron 16 of the angiotensin-converting enzyme (ACE) gene is still being debated. We examined its role as a risk factor in patients with thrombotic brain infarction. The association between ACE polymorphism and ischemic stroke was examined in 181 patients with thrombotic brain infarction and 271 controls without strokes. The I/D polymorphism was examined using the polymerase chain reaction. Distributions of the ACE genotypes and alleles did not differ between the infarcted patients and the controls. Both distributions in patients with onset at age 60 years or younger were significantly higher than those in younger controls (genotype: chi 2 = 7.6, P = 0.02; allele: chi 2 = 5.6, P = 0.02). There were no significant differences in the distributions of ACE genotypes and alleles between the patients with lacunar infarcts and with cortical infarcts in all ages. There were also significant differences in the distribution of ACE genotypes and alleles between the younger and the elderly subgroup of patients with brain infarction (genotype: chi 2 = 12.9, P = 0.002; allele: chi 2 = 11.1, P = 0.0009). Furthermore, there was a significant decline in the frequency of the ACE D allele with increasing age in all patients with thrombotic brain infarction. These observations demonstrated a significant association between the ACE gene polymorphism and thrombotic brain infarction in patients age 60 years or younger in a Japanese population. Furthermore, there may be an association between the ACE D allele and mortality after cerebral infarction.
CMO I deficiency caused by a point mutation in exon 8 of the human CYP11B2 gene encoding steroid 18-hydroxylase (P450C18).
Corticosterone methyloxidase I (CMO I) deficiency is an autosomal recessive disorder of aldosterone biosynthesis. To determine further the molecular genetic basis of CMO I deficiency, a patient of Turkish origin that suffered from CMO I deficiency was studied. Nucleotide sequencing of the PCR-amplified exons from the genomic DNA of this patient revealed a single point mutation CTG (leucine) CCG (proline) at codon 461 in exon 8 of CYP11B2, which is involved in the putative heme binding site of steroid 18-hydroxylase (P450(C18)). The expression study using a cDNA introducing the point mutation revealed that the amino acid substitution totally abolishes the P450(C18)p3 enzyme activities required for conversion of 11-deoxycorticosterone to aldosterone, even though the mutant product was detected in the mitochondrial fraction of the transfected cells. These results suggest that this point mutation causes CMO I deficiency.
Weibel-Palade bodies as a storage site of calcitonin gene-related peptide and endothelin-1 in blood vessels of the rat carotid body.
BACKGROUND: The vasculature of the carotid body has been considered to play a role in the regulation of blood flow into this organ. This light and electron microscope immunocytochemistry deals with endothelium-dependent vasomotion by vasodilatory calcitonin gene-related peptide (CGRP) and vasoconstrictive endothelin-1 (ET-1). METHODS: After adult male rats were perfused with a solution of periodate-lysine-paraformaldehyde through the left ventricle, the carotid artery bifurcations were isolated and utilized for light and electron microscope immunolabelings with CGRP and ET-1 primary antisera. RESULTS: By light microscope immunocytochemistry, immunoreactions to CGRP were seen along the endothelium of the carotid body artery (CBA) and its branches, and those of ET-1 were observed along the endothelium of the intralobular capillaries in addition to the above vessels. By immunoelectron microscopy, immunoreactive gold particles of CGRP and ET-1 were identified in the rough endoplasmic reticulum (rER) and in the Weibel-Palade (WP) bodies of endothelial cells of the CBA and its branches. Colocalization of both immunoreactive gold particles was observed in the same WP body. Immunoreactive gold particles of CGRP were also identified in the rER, Golgi apparatus, and specific granules of the dark glomus cells. CONCLUSIONS: Conceivably, CGRP and ET-1 are synthesized in the rER of these endothelial cells and are stored in the WP bodies for the autoregulation of blood flow.
Apical tubules in marginal cells of the differentiating stria vascularis.
BACKGROUND: Apical tubules (ATs) in marginal cells (MCs) of the stria vascularis appear in limited stages of differentiation of the MCs, but their origin and roles remain uncertain. The present study was designed to solve the problem of whether the ATs are intracellular compartments derived from the Golgi apparatus (GA). METHODS: The cochleae of Wistar rats at ages of postnatal days 1, 3, and 5 were prepared for electron microscopy and cytochemistry using thiamine pyrophosphatase (TPPase) and coenzyme A phosphatase (CoA-Pase) as marker enzymes of trans Golgi cisterns and fluorescent labelled lectin, griffonia simplicifolia agglutinin-I (GS-1). RESULTS: The ATs appeared in the apical cytoplasm of the MCs between postnatal days 1 and 5. Reaction products of TPPase and CoA-Pase activities were localized in the trans-Golgi cisterns and the ATs, which were occasionally in a close apposition to the GA. The reaction was found along the apical plasma membrane of the MCs only in case of TPPase. Heavy reactions to GS-1 were seen in the supranuclear region as well as along the apical plasma membrane of the MCs. CONCLUSIONS: The present ultrastructural and cytochemical studies indicate that the ATs, which appear in the MCs at limited perinatal stages, originate from the trans-Golgi cisterns. These ATs may be involved in the apical plasma membrane supply for the differentiation of the MCs prior to the generation of EP.
Increase or decrease of HDL-cholesterol concentrations during pravastatin treatment depending on the pre-treatment HDL cholesterol levels.
OBJECTIVE: The effect of pravastatin was evaluated using patient data accumulated in the data base of a hospital information system (HIS). METHODS: We selected 130 patients treated with pravastatin 10 mg per day, for a minimum period of 4 weeks. RESULTS: In the t test analysis, the reduction rates of total cholesterol (TC) and low-density lipoprotein (LDL) levels for pravastatin administration were 18%, and 27%, respectively. These values were similar to previous reports. The high-density lipoprotein (HDL) level, however, did not change significantly, although previous reports have shown an elevation of HDL levels. In an attempt to explain the origin of this difference, we studied the pretreatment value dependence of the cholesterol change using regression analysis. We found that pravastatin raised the HDL level in those cases where pretreatment values were lower than 58 mg.dl-1 and reduced it for higher values. We also showed that the reductions of TC, LDL and triglyceride (TG) levels correlated positively with their pretreatment values.
Molecular mass of poly[(R)-3-hydroxybutyric acid] produced in a recombinant Escherichia coli.
Poly[(R)-3-hydroxybutyric acid] (PHB) was produced at 37 degrees C by a recombinant Escherichia coli harboring the Alcaligenes eutrophus biosynthesis phb-CAB genes in Luria-Bertani media containing glucose at 10-30 g/l at different pH values and the time-dependent changes in the molecular mass of PHB were studied. PHB polymers accumulated within cells while glucose was present in the medium. The number-average molecular mass of PHB decreased with time during the course of PHB accumulation, and the values for PHB were markedly dependent on the cultivation conditions of the E. coli, ranging from 0.5 MDa to 20 MDa. Under specific conditions (pH 6.0), E. coli produced PHB with an extremely high molecular mass (20 MDa). It has been suggested that a chain-transfer agent is generated in E. coli cells during the accumulation of PHB.
Enzymatic preparation of pyridoxine 4'- and 5-alpha-D-glucosides.
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Reduced tissue oxygenation and its reversibility by glycemic control in diabetic patients.
Relationship of transcutaneous oxygen pressure (TcP(O2)) to glycemic control and diabetic complications was investigated in patients with non-insulin dependent diabetes mellitus. TcP(O2) was measured in 103 patients with non-insulin dependent diabetes mellitus. Correlation of TcP(O2) to HbA1c, fasting blood sugar (FBS), age, duration of diabetes, serum lipids, hypertension, and diabetic complications were examined. We divided the patients into three groups according to their glycemic control: good control group (HbA1c < 7.0%), fair control group (HbA1c, 7.0-8.9%) and poor control group (HbA1c > or = 9.0). We compared TcP(O2) of these three groups with 19 non-diabetic controls. In 103 patients, TcP(O2) at baseline correlated with HbA1c, FBS and age (P < 0.001, P < 0.01 and P < 0.05, respectively), but did not correlate with duration of diabetes mellitus, neuropathy, nephropathy or retinopathy. TcP(O2) of good and fair control group was not reduced comparing to the non-diabetic control (63 +/- 11, 59 +/- 10 and 64 +/- 12 mmHg, respectively). The poor control group had significantly reduced TcP(O2) (55 +/- 10 mmHg) comparing to non-diabetic control (P < 0.005) and good control group (P < 0.005). Furthermore, in an independent study, TcP(O2), arterial oxygen pressure (Pa(O2)), oxygen pressure of dorsal pedal vein (PV(O2)) and erythrocyte 2,3-diphosphoglycerate (2,3-DPG) in eight patients with poor glycemic control were followed prospectively. Six patients with improvement of glycemic control showed a significant increase of TcP(O2) and Pa(O2) (P < 0.001 and P < 0.005, respectively). However, two patients without improvement of hyperglycemia had no change in TcP(O2) and Pa(O2). PV(O2) and 2,3-DPG levels of erythrocytes were not changed in six patients. These findings suggest that tissue oxygenation in diabetic patients was deteriorated in relation to hyperglycemia and was reversed with glycemic control. Improvement of Pa(O2) might contribute partly to the increase of TcP(O2).