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Biomedical subjects

M Kurabayashi

Publications and source records attributed to M Kurabayashi.

At least 145 records · Page 8Linked to original sources
PubMed1985

Studies on the placental transport mechanism for iron.

Transferrin (Tf) and ferritin (Fr), the proteins which participate in iron transport, were examined to determine their fluctuation during pregnancy and their localization in human placental tissue, and the iron transport mechanism between mother and fetus was discussed. The main results are as follows: Maternal serum ferritin (SFr) decreased remarkably and the maternal total iron binding capacity (TIBC) increased gradually as pregnancy progressed. Maternal serum iron (SI), SFr and TIBC at delivery were 59.8 +/- 26.2 micrograms/dl, 9.6 +/- 7.2 ng/ml and 495.2 +/- 100.3 micrograms/dl, and cord blood SI, SFr and TIBC were 161.5 +/- 42.1 micrograms/dl, 160.5 +/- 67.2 ng/ml and 177.7 +/- 33.9 micrograms/dl, respectively. Peroxidase conjugating antibody method revealed the localization of Tf on the microvillous surface of syncytiotrophoblasts, and the localization of Fr in all layers of trophoblasts, especially in the neighborhood of the surface. Ferritin content of the placenta in the 1st, 2nd and 3rd trimesters was 0.07 +/- 0.03, 0.18 +/- 0.03 and 0.25 +/- 0.09 (micrograms/mg protein), respectively. These results indicate that iron is transferred from the mother to the fetus by the placental active function, and Tf receptor and Fr on trophoblasts participate in the adequate placental iron transport.

Biological Transport↗
PubMed1984

Distribution of myosin isozymes in human atrial and ventricular myocardium: comparison in normal and overloaded heart.

We have prepared monoclonal antibodies specific for either atrial or ventricular myosin and defined the isomyosin composition of myocardium in normal and overloaded human hearts. In the atrial myocardium, normal isozymic pattern was V1 dominant which converted to being V3 dominant in an overloaded condition. In contrast, normal isomyosin pattern of the ventricular myocardium was exclusively V3 dominant, and only a small change in the proportion of isomyosin was observed in an overloaded condition. From this, we conclude that isozymic changes in cardiac myosin could occur in the human heart to meet increased work induced by cardiac overload. However, the physiological importance of these isomyosin redistributions in human myocardium seems to be much greater in the atrium than in the ventricle, since larger amounts of V1 isomyosin which could be transformed to V3 isomyosin were present in the atrial myocardium.

Adenosine Triphosphatases↗
PubMed1980

[Clinical observation of serous ferritin levels in obstetrics and gynecology--relation between maternal, fetal and neonatal sera (author's transl)].

a. By the 2-site radioimmunoassay, maternal, umbilical and neonatal sera of human were measured. b. Non-heme iron contents of some organs of maternal, fetal and neonatal mice were analysed and each segment was measured. The results were as follows. 1) The serous ferritin levels of early, mid and late pregnancy were 34.1 +/- 19.0 ng/ml, 22.9 +/- 12.2 ng/ml and 19.4 +/- 11.7 ng/ml respectively in non-anemic group, while 15.1 +/- 7.8 ng/ml, 10.2 +/- 6.7 ng/ml and 5.2 +/- 2.2 ng/ml in anemic group, both decreasing in the course of the pregnancy. 2) The serous ferritin levels of umbilical cords were significantly higher than those of mothers, and no relationship was found between them. According to the maternal serous ferritin levels, grouped into (a) less than 15 ng/ml, (b) over 15 ng/ml and less than 30 ng/ml, (c) more than 20 ng/ml, significant difference of umbilical serous ferritin levels was found between in (a) (b) and in (c). 3) Serous ferritin levels of neonate increased to peak on the 4th to 5th day after birth, as the serous bilirubin levels did. 4) Non-heme iron contents of some organs of pregnant mice varied a great deal, but the SII (containing the ferritin) segment increased in the course of pregnancy and during the puerperium.

Animals↗
PubMed1980

[Studies on iron metabolism and iron deficiency anemia in pregnant women--theoretical discussion on the relation between serum iron level and iron dose to be administrate, and clinical result after iron therapy (author's transl)].

Animal and clinical studies were performed in order to establish a criterion for diagnosis of iron-deficiency anemia and a standard dose of the intravenous iron treatment, based on properties of serum transferrin (Tr) in ironmetabolism during gestation. And the following results were obtained. 1) 59Fe-labelled large molecular colloid iron-solution (CSA-Fe) was injected in pregnant rats: the iron transferring to the fetuses originated from the mothers' serum iron isolated from CSA-Fe. 2) There was no difference of iron supplying abilities of Tr across to maternal and fetal tissues of rat, in anemia in the latter stage of gestation (A) and in non-pregnant iron-deficiency anemia (B), although there was significant difference in nature of Tr between rat and woman. 3) Tr of rat in A and in B: There was no difference in 59Fe-uptake into the rat reticulocytes from Tr between the two statuses. 4) In the clinical study, iron utilization rate was correlated with serum iron saturation rate both in A and B. 5) CSA-Fe was clinically given for A and B according to the original formulas, and utility of the formulas were confirmed.

Anemia, Hypochromic↗
PubMedDate not supplied

Effect of long-term hormone replacement therapy on angiotensin-converting enzyme activity and bradykinin in postmenopausal women with essential hypertension and normotensive postmenopausal women.

OBJECTIVE: Hormone replacement therapy (HRT) reduces the incidence of cardiovascular disease in postmenopausal women. Three-month short-term HRT in postmenopausal women with essential hypertension increased the plasma concentrations ofbradykinin with decreased serum angiotensin-converting enzyme (ACE) activity, which may be partially responsible for the cardioprotective effects of HRT. The objective was to determine whether 12-month long-term HRT in postmenopausal women with essential hypertension would maintain the decreased ACE activity and increased bradykinin levels and whether long-term HRT would increase the plasma bradykinin concentrations of normotensive postmenopausal women who had shown no significant changes in the 3-month HRT study, despite their decreased serum ACE activity. DESIGN: Twenty hypertensive and 15 normotensive postmenopausal women were treated with conjugated estrogens (0.625 mg/day) and medroxyprogesterone (2.5 mg/day) for 12 months. Twenty hypertensive and 15 normotensive postmenopausal women were used as controls. The controls were not treated with HRT. Serum ACE activity and plasma bradykinin concentrations were measured at baseline and at 12 months. RESULTS: Long-term HRT in both hypertensive and normotensive postmenopausal women significantly decreased serum ACE activity from 15.5+/-0.7 IU/L and 16.0+/-0.9 IU/L, respectively, at baseline to 13.3+/-0.5 IU/L and 14.2+/-0.9 IU/L, respectively, 12 months after the start of HRT (p < 0.05 and p < 0.05, respectively). Long-term HRT in both hypertensive and normotensive postmenopausal women also significantly increased plasma bradykinin concentrations from 22.1+/-4.4 pg/mL and 19.2+/-3.0 pg/mL, respectively, at baseline to 86.7+/-21.2 pg/mL and 73.5+/-23.0 pg/mL, respectively, 12 months after the start of HRT (p < 0.01 and p < 0.05, respectively). No significant changes in serum ACE activity or plasma bradykinin concentrations were observed in the control groups. CONCLUSIONS: Long-term HRT in hypertensive and normotensive postmenopausal women decreases their serum ACE activity and increases their plasma bradykinin concentrations. Thus, maintenance of elevated bradykinin with decreased serum ACE activity by HRT may be useful in reducing the risk of cardiovascular disease in both hypertensive and normotensive postmenopausal women.

Administration, Oral↗
PubMedDate not supplied

Mechanism of doxorubicin-induced inhibition of sarcoplasmic reticulum Ca(2+)-ATPase gene transcription.

Doxorubicin (DOX)-induced cardiomyopathy has been found to be associated with impaired Ca(2+) handling in the sarcoplasmic reticulum (SR), leading to reduced cardiac function. We have recently demonstrated that expression of mRNA encoding sarco(endo)plasmic reticulum Ca(2+)-ATPase 2 (SERCA2), a major Ca(2+) transport protein in SR, is markedly decreased in DOX-treated hearts. To extend this observation, we have dissected the molecular mechanisms by which DOX downregulates SERCA2 gene transcription. Using cultured rat neonatal cardiac myocytes, we found that the antioxidant N-acetylcysteine blocked the DOX-induced decrease in SERCA2 mRNA levels, as well as the DOX-induced increase in H(2)O(2) concentration; thus, H(2)O(2) is an intracellular mediator of DOX activity. Using a luciferase reporter assay, we found that the sequence from -284 to -72 bp in the 5' flanking region of the SERCA2 gene has a DOX-responsive element. Although several transcription factors have putative binding motifs in this region of the SERCA2 gene, only the expression of Egr-1 mRNA and the binding of Egr-1 protein to the 5' regulatory sequence of SERCA2 gene increased markedly after DOX administration. We also found that overexpression of Egr-1 was associated with a significant reduction in SERCA2 gene transcription. In addition, Egr-1 antisense oligonucleotides blocked the DOX-induced reduction in SERCA2 mRNA, suggesting that Egr-1 is a transcriptional inhibitor of the SERCA2 gene in DOX-induced cardiomyopathy. We observed activation of 3 mitogen-activated protein kinases (MAPKs), p44/42 MAPK, p38 MAPK, and stress-activated MAPK/Jun N-terminal kinase, by DOX, but only a specific inhibitor of the p44/42 MAPK kinase suppressed the effects of DOX on Egr-1 and SERCA2 mRNA expression. These findings indicate that reactive oxygen intermediates, the transcription factor Egr-1, and p44/42 MAPK are critical elements in the transcriptional regulation of the SERCA2 gene in response to DOX.

Animals↗
PubMedDate not supplied

Role of blood pressure in the progression of microalbuminuria in elderly Japanese type 2 diabetic patients: a 7-year follow-up study.

This 7-year retrospective longitudinal study was carried out in order to clarify the clinical features of elderly type 2 diabetic patients with microalbuminuria. Elderly Japanese type 2 diabetic patients (n = 22; age 50 - 73 years) with microalbuminuria were studied retrospectively. Patients whose urinary albumin excretion rate (UAER) decreased 7 years were considered 'nonprogressors' (n = 8) whereas those whose UAER increased were considered 'progressors' (n = 14). The mean 7-year level of glycosylated haemoglobin (HbA1c) did not differ significantly between non-progressors and progressors but the mean 7-year blood pressure (BP) of progressors (101 +/- 8 mmHg) was significantly higher than that of non-progressors (92 +/- 7 mmHg). In progressors who received no anti-hypertensive drugs, systolic BP was above the BP goal of 130/85 mmHg but mean BP and diastolic BP were below this goal. The results are consistent with the view that hypertension affects the progression of microalbuminuria; raised systolic BP may be a factor in this progression in elderly type 2 diabetic patients.

Aged↗
PubMedDate not supplied

Recurrent pyogenic vertebral osteomyelitis associated with type 2 diabetes mellitus.

We report a case of recurrent pyogenic vertebral osteomyelitis associated with type 2 diabetes mellitus. A 51-year-old male was admitted to our hospital because of lumbago and general fatigue, with multiple ulcers on the soles of his feet. Staphylococcus aureus was isolated from peripheral blood and the foot ulcers, and 67Gallium scintigram showed abnormal isotope uptake, accumulated at the lower thoracic spine. Antibiotics were administered and the patient underwent intensive insulin therapy. Magnetic resonance imaging (MRI), performed after the levels of C-reactive protein decreased to 0.0 mg/dl, indicated old inflammatory changes at the Th8-Th9 spine and antibiotics were stopped. Unexpectedly, 8 days later the patient complained of lumbago with fever again, and MRI showed acute inflammatory changes at the same lesion site. This case report suggests that it is important for complementary antibiotic therapy to continue after signs of inflammation have disappeared in cases of pyogenic vertebral osteomyelitis.

Diabetes Mellitus, Type 2↗
PubMedDate not supplied

Atrioventricular nodal re-entrant tachycardia with two functionally discrete fast pathways.

We present a case with two forms of atrioventricular nodal re-entrant tachycardia (AVNRT) that revealed similar H-A-V sequences, but could be differentiated only by their retrograde atrial activation sequences. Both tachycardias were induced following anterograde slow pathway conduction, suggesting the slow pathway as the anterograde limb of the re-entry circuit. The earliest atrial activation site of one form was in the same region of the bundle of His as that of the common type of AVNRT, while that of the other form was the ostium of the coronary sinus. Properly timed extra-stimuli delivered from the atrium or ventricle during the latter tachycardia penetrated through the fast pathway without resetting the tachycardia cycle length. These rare phenomena suggest the existence of two functionally discrete fast pathways, of which the alternative pathway alters to become the more predominant retrograde limb according to time and circumstances.

Adult↗
PubMedDate not supplied

Angiotensin-converting enzyme insertion/deletion polymorphism and polyneuropathy in type 2 diabetes without macroalbuminuria.

Angiotensin-converting enzyme (ACE) gene polymorphism is thought to be a potent risk factor for nephropathy and retinopathy in diabetes. We investigated the association between polyneuropathy and gene polymorphisms of both the ACE insertion/deletion (I/D) and angiotensinogen (AGT) M235T genes in 84 type 2 diabetic patients without macroalbuminuria (21 with polyneuropathy and 63 without). ACE genotype distribution did not differ significantly between patients with and without polyneuropathy, but the frequency of the I allele was significantly higher in those with polyneuropathy than in those without. In contrast, neither the genotype distribution nor the allele frequencies of the AGT gene differed between the two groups. In logistic regression analysis using a D-additive model, the D allele had a protective effect on polyneuropathy (odds ratio [OR], 0.34; 95% confidence interval [CI], 0.13-0.88). A D-dominant model hypothesis also gave a significant OR (0.28; 95% CI, 0.09-0.90). ACE I/D polymorphism, but not AGT M235T polymorphism, may affect polyneuropathy development in type 2 diabetes without macroalbuminuria.

Aged↗
PubMedDate not supplied

Angiotensin-converting enzyme gene polymorphism as a potent risk factor for developing microalbuminuria in Japanese patients with type 2 diabetes mellitus: a 9-year follow-up study.

To clarify the risk factors for developing microalbuminuria in patients with type 2 diabetes mellitus, a longitudinal observational study was performed. Fifty patients with normoalbuminuria were recruited and treated conventionally for 9 years. Polymorphisms of the angiotensin-converting enzyme (ACE) gene and the angiotensinogen M235T polymorphism were examined. During the study period, 12 of the 50 patients developed microalbuminuria; no patients progressed to macroalbuminuria. Multiple logistic regression analysis was performed using age, duration of diabetes, body mass index, haemoglobin A1c' blood pressure, serum lipid profile and genetic polymorphisms as independent variables and development of microalbuminuria as the dependent variable. The D allele of the ACE gene was an independent and significant variable. We conclude that the ACE gene D allele polymorphism is a potent risk factor for developing microalbuminuria in type 2 diabetic patients.

Adult↗
PubMedDate not supplied

Interleukin-6-induced reciprocal expression of SERCA and natriuretic peptides mRNA in cultured rat ventricular myocytes.

We investigated the effect of interleukin-6 (IL-6) expression on sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) mRNA levels in cultured rat neonatal ventricular myocytes. IL-6 plays a key role in regulating cardiac hypertrophy and the development of heart failure, and SERCA, ANP and BNP are all cardiac hormones with regulatory properties. Compared with baseline measurements, treatment with 50 U/ml IL-6 significantly decreased SERCA gene expression, but significantly increased ANP and BNP gene expression in the cardiac myocytes. These results suggest that the clinical overproduction of IL-6 in response to infection, autoimmune disease and cancer might be responsible for cardiac hypertrophy. Cardiac hypertrophy may result from the imbalance of both natriuretic peptides and SERCA transcription levels, caused by elevated IL-6 expression.

Animals↗
PubMedDate not supplied

Plasma adiponectin levels in post-menopausal women receiving hormone replacement therapy.

This study aimed to evaluate the correlation between plasma adiponectin levels and plasma lipid and lipoprotein levels in post-menopausal women (PMW) receiving hormone replacement therapy (HRT). Various clinical and biochemical parameters, including plasma lipid and lipoprotein concentrations and adiponectin levels, were measured in 54 healthy PMW before and after 3 and 6 months of HRT. Control groups consisted of women aged < 40 years (n = 20) or > 60 years (n = 17). PMW had significantly lower baseline adiponectin levels compared with the younger or older control groups, but adiponectin concentrations were not significantly altered after 3 or 6 months of HRT. Adiponectin levels in PMW were positively correlated with plasma high-density lipoprotein-cholesterol levels and were negatively correlated with body mass index and triglyceride levels. Our data suggest that circulating adiponectin may contribute to lipid homeostasis in PMW. Further studies are needed to elucidate the effects of HRT and oestrogen on adiponectin levels.

Adiponectin↗
PubMedDate not supplied

Clinical features associated with circulating concentration of soluble leptin receptor in patients with diabetes.

We aimed to determine if there were any clinical features that were significantly associated with the circulating concentration of soluble leptin receptor (OB-Re) in 67 Japanese subjects with diabetes mellitus. The characteristics evaluated included age, height, body weight, body mass index (BMI), systolic and diastolic blood pressure, duration of diabetes, haemoglobin A1C and blood lipid concentrations, urinary albumin excretion rate, circulating concentrations of leptin, tumour necrosis factor-alpha (TNF-alpha), TNF-alpha receptor 1 and genotypes of the angiotensin-converting enzyme (ACE) gene. We found statistically significant negative correlations between circulating OB-Re concentration and body weight, BMI, diastolic blood pressure, concentrations of leptin and TNF-alpha receptor 1. Serum OB-Re concentration was not associated with any of the other clinical characteristics that were measured, or with the different ACE genotypes. Our results suggest that OB-Re might have an important influence on the biological activity of leptin in diabetic subjects.

Diabetes Mellitus↗