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Biomedical subjects

I Kondo

Publications and source records attributed to I Kondo.

At least 37 records · Page 2Linked to original sources
PubMed2001

Vitamin D deficiency and risk of hip fractures among disabled elderly stroke patients.

BACKGROUND AND PURPOSE: Risk of hip fracture after stroke is 2 to 4 times that in a reference population. Osteomalacia is present in some patients with hip fractures in the absence of stroke, while disabled elderly stroke patients occasionally have severe deficiency in serum concentrations of 25-hydroxyvitamin D (25-OHD) (</=5 ng/mL). To determine the effects of vitamin D status on hip fracture risk, we prospectively studied a cohort of patients with hemiplegia after stroke who were aged at least 65 years. METHODS: We compared baseline serum indices of bone metabolism, bone mineral density, and hip fracture occurrence in stroke patients with serum 25-OHD </=25 nmol/L (</=10 ng/mL; deficient group, n=88) with findings in patients from the same cohort who had 25-OHD levels 26 to 50 nmol/L (10 to 20 ng/mL; insufficient group, n=76) or >/=51 nmol/L (>/=21 ng/mL; sufficient group, n=72). RESULTS: Over a 2-year follow-up interval, hip fractures on the paretic side occurred in 7 patients in the deficient group and 1 patient in the insufficient group (P<0.05; hazard ratio=6.5), while no hip fractures occurred in the sufficient group. The 7 hip fracture patients in the deficient group had an osteomalacic 25-OHD level of <5 ng/mL. Higher age and severe immobilization were noted in the deficient group. Serum 25-OHD levels correlated positively with age, Barthel Index, and serum parathyroid hormone. CONCLUSIONS: Elderly disabled stroke patients with serum 25-OHD concentrations </=12 nmol/L (</=5 ng/mL) have an increased risk of hip fracture. Immobilization and advanced age cause severe 25-OHD deficiency and consequent reduction of BMD.

Aged↗
PubMed2001

Contrast harmonic power Doppler imaging of congenital ventricular diverticulum--a case report.

A case of an 81-year-old woman with a left ventricular diverticulum who underwent myocardial contrast echocardiography is reported. After administration of the contrast agent, a pulsed Doppler flow measurement clearly revealed the biphasic waveform of the ejection flow in the pre-systolic and systolic phase at the ostium of the diverticular cavity. A harmonic power Doppler image showed that part of the diverticulum wall had similar acoustic properties to the ventricular septal wall. Intracardiac blood flow and myocardial perfusion could be clearly evaluated and a ventricular diverticulum was correctly diagnosed using contrast echocardiography.

Aged↗
PubMed2001

Suppression of fatty acid metabolism after exercise stress in patients with no electrocardiographic ST segment shift during balloon angioplasty.

Although ST segment shift is a marker of myocardial ischemia, some patients have no ST segment shift during percutaneous transluminal coronary angioplasty (PTCA). The aim of this study is to investigate myocardial perfusion and metabolism in adaptation for ischemia using 201TI and 123I-BMIPP dual exercise stress myocardial single photon emission computed tomography (SPECT) (dual stress SPECT). In 28 patients with coronary artery disease, dual stress SPECT was performed 3 weeks before PTCA. Early and delayed images were obtained at 5 minutes and at 3 hours after termination of ergometer stress, respectively. During PTCA, 12-lead ECG was recorded, and a significant ST segment shift was defined as more than 1 mm elevation or a depression of the J-point at the first ballooning. No collateral circulation on the coronary angiogram or 201TI filling on the delayed images were observed on any of the target regions of PTCA. Patients were divided into 2 groups: with (Group A: n = 15) and without (Group B: n = 13) significant ST segment shift during PTCA. A redistribution of TI was observed in 14 (93%) of Group A and 10 (77%) of Group B patients. Incidence of BMIPP redistribution was significantly higher in Group B (11 [85%]) than in Group A (3 [20%]) (p < 0.05). Redistribution of BMIPP means suppression of fatty acid metabolism during exercise stress. Augmentation of glucose metabolism is speculated to be an energy source in ischemic preconditioning.

Angioplasty, Balloon, Coronary↗
PubMed2001

[Cherubism].

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Cherubism↗
PubMed2001

Identification of autoreactive T cells in Vogt-Koyanagi-Harada disease.

PURPOSE: To determine the finer specificity and immunologic features of autoreactive T cells in Vogt-Koyanagi-Harada (VKH) disease. METHODS: T-cell clones (TCCs ) specific to tyrosinase family proteins were raised from the peripheral blood mononuclear cells (PBMCs) of patients with VKH disease, and the response of the TCCs to 30-mer peptides was determined. The TCCs that were reactive to the peptides with strong binding sites for HLA DRB1*0405 were initially tested. Then, a finer specificity of these TCCs against 12- to 14-mer peptides was determined. The cytokine production of these clones was measured by ELISA. RESULTS: A total of 62 stable TCCs were established from the PBMCs of five patients with VKH (28 clones against tyrosinase, 34 clones against tyrosinase-related protein [TRP]1). Five of 28 TCCs for tyrosinase and 2 of 34 for TRP1 were reactive to the 30-mer peptides with strong binding sites for HLA DRB1*0405. These seven clones showed proliferative responses to one or more of the 12- to 14-mer peptides that match the motif of the strong binding site for HLADRB1*0405. Five of seven of the TCCs may be T-helper (Th) type 1, one of the remaining TCCs may be Th0, and the other may be Th2. CONCLUSIONS: The autoreactive T cells against tyrosinase and/or TRP1 may contribute to the development of VKH disease.

Adult↗
PubMed2001

[A family of hereditary spastic paraplegia with dementia, ataxia, and dystonia].

We reported three siblings with complicated hereditary spastic paraplegia. The striking features in these patients were characterized by early onset of gait disturbance, mental deficiency, and dystonia. The most likely diagnosis was Mast syndrome. Patient 1: A 44 years-old woman. She first developed gait disturbances at age of 8. She was admitted in our hospital because of progressive spastic paraplegia. Neurological examination revealed mental deficiency, saccadic pursuit eye movement, speech disturbance of cerebellar type, ataxia, and spastic paraplegia. She showed also dystonia in the face, tongue, and trunk. MRI showed cerebellar atrophy. Patient 2: A 51 years-old brother of the patient 1. He had mentally retarded. Late teens he developed gait disturbance. Gradually he manifested spastic paraplegia, dysarthria, dysphasia, mental deficiency, and ataxia. He also showed incontinence of urine and feces. Then he became bedridden, apathetic, and showed forced crying. MRI showed diffuse brain atrophy. Patient 3: A 48 year-old woman. This woman, a sister of the patient 1, showed progressive gait disturbance and dysarthria. She also developed incontinence, apathy, and dystonia. She became bedridden, responding to simple questions with only occasional single-word answers. Her speech was slurred, and spastic paraplegia was noted. MRI showed diffuse brain atrophy including marked atrophy of the cerebellum.

Brain↗
PubMed2000

Tyrosinase family proteins are antigens specific to Vogt-Koyanagi-Harada disease.

Vogt-Koyanagi-Harada (VKH) disease (and sympathetic ophthalmia) is an ocular inflammatory disease that is considered to be a cell-mediated autoimmune disease against melanocytes. The purpose of this study was to determine the Ags specific to VKH disease and to develop an animal model of VKH disease. We found that exposure of lymphocytes from patients with VKH disease to peptides (30-mer) derived from the tyrosinase family proteins led to significant proliferation of the lymphocytes. Immunization of these peptides into pigmented rats induced ocular and extraocular changes that highly resembled human VKH disease, and we suggest that an experimental VKH disease was induced in these rats. We conclude that VKH disease is an autoimmune disease against the tyrosinase family proteins.

Adult↗
PubMed2000

Identification and characterization of 5' extension of mammalian agrin cDNA, the exons and the promoter sequences.

Agrin, which is secreted from motor neurons, is essential for the formation and maintenance of the vertebrate neuromuscular junctions. Here we show the complete N-terminal sequence of the mammalian cDNA required for the expression and secretion as well as the intron/exon structure and the 5'-flanking sequence required for basal promoter activity. The 5'-flanking region and the first exon are extremely GC rich and contain a CpG island. These features may account for hindrance in identification of the 5' end of the cDNA and the promoter region of the mammalian agrin gene.

Agrin↗
PubMed2000

P2-purinergic receptor antagonists reduce the minimum alveolar concentration of inhaled volatile anesthetics.

In the central nervous system (CNS), adenosine triphosphate (ATP) is reported to serve as a fast excitatory neurotransmitter via P2X receptor. To examine possible involvement of inhibition of ATP signal-transmission in anesthetic mechanism, the effect of intracerebroventricular (ICV) administration of P2 receptor antagonists on the minimum alveolar concentration (MAC) of sevoflurane and isoflurane was studied in rat. ICV administration of P2 receptor antagonists, suramin and pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), significantly reduced MAC of both anesthetics. The reduction of the MAC by both suramin and PPADS was dose-dependent and reached plateau at 150 microgram/rat. These results suggest that the inhibition of ATP-signal transmission may be involved in analgesic or anesthetic effect in brain.

Adenosine Triphosphate↗
PubMed2000

Effect of cibenzoline on regional left ventricular function in hypertrophic obstructive cardiomyopathy.

BACKGROUND: Cibenzoline, a class Ia antiarrhythmic drug, can be used to relieve left ventricular (LV) outflow obstruction in hypertrophic obstructive cardiomyopathy (HOCM). However, the mechanism of this agent in HOCM has been controversial. HYPOTHESIS: This study was designed to investigate the effect of cibenzoline on regional LV function and the acoustic properties in HOCM using ultrasonic integrated backscatter. METHODS: Ten patients with HOCM and 16 healthy volunteers were examined. In patients with HOCM, wall thickening (%WT) and the magnitude of cyclic variation of integrated backscatter (mag-CVIBS) in the interventricular septum (IVS) and LV posterior wall were measured before and after oral administration of cibenzoline. To assess asynchrony of contractile elements, the phase difference between CVIBS and %WT were measured from the LV posterior wall. Pressure gradients at the LV outflow tract were estimated using continuous-wave Doppler echocardiography. RESULTS: Although %WT decreased significantly in the LV posterior wall, %WT and mag-CVIBS remained unchanged in the IVS. The phase difference in the LV posterior wall was significantly greater in patients with HOCM than in healthy volunteers (HOCM:healthy volunteers, 1.57 +/- 0.23:1.00 +/- 0.03, p < 0.001) at baseline. After administration of cibenzoline, the phase difference shifted to normal value (from 1.57 +/- 0.23 to 1.28 +/- 0.27, p = 0.0382), and pressure gradients at the LV outflow tract decreased (from 109 +/- 55 to 58 +/- 48 mmHg, p = 0.0063). Changes in pressure gradients at the LV outflow tract and the phase difference were closely related. CONCLUSIONS: Regional function and the acoustic properties of myocardium in HOCM were altered by cibenzoline in the LV posterior wall but remained unchanged in the IVS. The normalization of the phase difference in the LV posterior wall was closely related to the decrease in pressure gradients at the LV outflow tract. These findings suggest that negative inotropic action and the improvement of asynchrony in the LV posterior wall rather than in the IVS may contribute to the reduction of pressure gradients at the LV outflow tract in HOCM.

Acoustics↗
PubMed2000

Ocular and extraocular inflammation induced by immunization of tyrosinase related protein 1 and 2 in Lewis rats.

Vogt-Koyanagi-Harada (VKH) disease is an ocular inflammatory disease and is considered to be a cell-mediated, autoimmune disease against melanocytes. To learn more about the mechanisms involved in VKH disease, the identification of the antigens specific to the disease and the development of an animal model are critically important. We have expressed and purified the melanocyte specific proteins, tyrosinase-related protein 1 (TRP1) and 2 (TRP2). Lewis rats developed an ocular and extraocular inflammatory disease 12 days after immunization with TRP1 or TRP2 that was characterized clinically by the infiltration of inflammatory cells and accumulation of massive fibrin in the anterior and posterior chambers of the eye. Histologically, inflammatory cells were found in the anterior and posterior chambers, iris, ciliary body, the choroid, subretinal space and vitreous body. In severe cases, a serous detachment of the retina was observed. In mild cases, focal inflammatory lesions surrounded by normal chorioretinal architecture were observed and the inflammation persisted for more than 42 days after the injection. Some eyes showed accumulation of epithelioid cells in the choroid or the retinal pigment epithelium which were similar to the Dalen-Fuchs nodules found in patients with VKH disease. The alterations of the photoreceptor outer segment and the outer nuclear layer were less severe than in experimental autoimmune uveitis induced by retinal antigens. Extraocular manifestations such as skin lesions and meningitis were also observed. The clinical course and histological findings in these rats resembled the changes in patients with VKH disease.

Animals↗
PubMed2000

A novel color M-mode Doppler echocardiographic index for left ventricular relaxation: depth of the maximal velocity point of left ventricular inflow in early diastole.

Color M-mode Doppler echocardiography (CMD) has been utilized in assessing left ventricular (LV) filling dynamics. We tested a novel CMD index, the depth of the spatiotemporal maximum of early diastolic inflow (D-maxV) in the left ventricle, to clarify its significance in assessing LV diastolic function. In 26 normal subjects and 32 patients with ischemic heart disease, D-maxV was determined with CMD as the distance from the mitral valve opening point to the center of the aliasing area in early diastole. Transmitral flow velocity was measured with pulsed Doppler. During routine catheterization, high-fidelity LV pressure measurements yielded diastolic variables in patients. D-maxV was significantly lower in the patients than the normals (13.0+/-7.0 vs 23.4+/-6.8 mm, P < 0.0001). D-maxV exhibited significant linear correlations with the minimal first derivative of LV pressure (r = 0.72, P < 0.01), the time constant of isovolumic relaxation (r = -0.67, P < 0.01), and LV minimal pressure (r = -0.53, P < 0.02) in the patients with wide ranges of peak early to late inflow velocity ratio (0.43-3.9) and deceleration time of early filling (79-293 ms). D-maxV showed an inverse correlation with LV end-diastolic pressure (r = -0.53, P < 0.02) and no significant correlation with mean pulmonary capillary wedge pressure. Moreover, Kaplan-Meier analysis focusing on the patients with myocardial infarction revealed that the group with D-maxV < 10.4 mm (n = 13) exhibited a lower cumulative cardiac event-free rate than that with D-maxV > or = 10.4mm (n = 14) (49.4% vs 92.9% at 5 years, P < 0.05). The depth of the spatiotemporal maximum of early diastolic LV inflow velocity reflects LV relaxation and is free of pseudonormalization. Evaluation of the LV relaxation separately from preload may have a prognostic value for myocardial infarction.

Adult↗
PubMed2000

Identification of two novel mutations in the SLC25A13 gene and detection of seven mutations in 102 patients with adult-onset type II citrullinemia.

Adult-onset type II citrullinemia (CTLN2) is characterized by a liver-specific deficiency of argininosuccinate synthetase (ASS) protein. We have recently identified the gene responsible for CTLN2, viz., SLC25A13, which encodes a calcium-binding mitochondrial carrier protein, designated citrin, and found five mutations of the SLC25A13 gene in CTLN2 patients. In the present study, we have identified two novel mutations, 1800ins1 and R605X, in SLC25A13 mRNA and the SLC25A13 gene. Diagnostic analysis for the seven mutations in 103 CTLN2 patients diagnosed by biochemical and enzymatic studies has revealed that 102 patients had one or two of the seven mutations and 93 patients were homozygotes or compound heterozygotes. These results indicate that CTLN2 is caused by an abnormality in the SLC25A13 gene, and that our criteria for CTLN2 before DNA diagnosis are correct. Five of 22 patients from consanguineous unions have been shown to be compound heterozygotes, suggesting a high frequency of the mutated genes. The frequency of homozygotes is calculated to be more than 1 in 20,000 from carrier detection (6 in 400 individuals tested) in the Japanese population. We have detected no cross-reactive immune materials in the liver of CTLN2 patients with any of the seven mutations by Western blot analysis with anti-human citrin antibody. From these findings, we hypothesize that CTLN2 is caused by a complete deletion of citrin, although the mechanism of ASS deficiency is still unknown.

Adolescent↗
PubMed2000

An exfoliative toxin A-converting phage isolated from Staphylococcus aureus strain ZM.

Exfoliative toxin A (ETA) causes staphylococcal scalded-skin syndrome in children. The gene for ETA was believed to be coded by the chromosomal DNA. We isolated temperate phages from an ETA-producing strain, ZM, using a restriction minus strain, 1039, as an indicator. One of the prophages, designated phi-ZM-1 mediated lysogenic conversion of ETA. The polymerase chain reaction assay of the eta gene revealed that phage phi-ZM-1 carries the structural gene for ETA.

Exfoliatins↗
PubMed2000

Sensitive detection of myocardial contraction abnormality in chronic hemodialysis patients by ultrasonic tissue characterization with integrated backscatter.

Since acoustic properties of the myocardium are sensitive to the myocardial structure and the contractile conditions of myocyte, the authors evaluated cardiac dysfunction based on the integrated ultrasonic backscatter in 18 hemodialysis (HD) patients (duration: 102 +/- 84 months, mean age: 57.6 +/- 9.7 years) and 11 age-matched normals. The cyclic variation of integrated backscatter (CV-IB) at interventricular septum (IVS) and left ventricular posterior wall (PW) was measured and compared with percent fractional shortening (%FS) and percent wall thickening (%Th). The CV-IB of HD patients was smaller than that of control subjects (IVS: 6.2 +/- 1.1 dB vs 8.2 +/- 1.1 dB, p = 0.0003 and PW: 8.4 +/- 2.2 vs 10.3 +/- 1.3, p= 0.025). No significant difference was observed in %FS and %Th between HD patients and control subjects. In HD, the ratio of velocities of early diastolic inflow (E) to late atrial inflow was decreased (0.7 +/- 0.2 vs 1.1 +/- 0.7, p = 0.049) and deceleration time of E was prolonged significantly (200 +/- 28 msec vs 159 +/- 30 msec, p = 0.0082). In the absence of overt cardiac systolic dysfunction, myocardial damage indicated as a decrease in CV-IB and diastolic dysfunction identified on transmitral velocity waveform were detected, which may reflect from the myocardial fibrosis. As a mechanism, pressure overload, hyperparathyroidism, and anemia were neglected, and the other humoral factors may contribute to the myocardial damage in chronic renal failure.

Aged↗