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Biomedical subjects

H Hashida

Publications and source records attributed to H Hashida.

At least 37 records · Page 2Linked to original sources
PubMed1999

Serum creatinine level underestimates hypertensive renal involvement in elderly patients with essential hypertension.

It is well recognized that serum creatinine level provides a quick general assessment of renal function. However, we frequently encounter elderly hypertensive patients with renal involvement whose serum creatinine levels are within normal limits. The aim of this study was thus to determine whether serum creatinine level is a sensitive indicator of renal function in elderly hypertensive patients. Study groups were classified according to age: 82 elderly patients (aged 65 yr or older) and 98 middle-aged patients (aged 40-65 yr) with essential hypertension. To assess hypertensive renal involvement, serum creatinine and serum uric acid levels were measured. We also measured the left ventricular mass (LVM) index by using echocardiography as a marker of hypertensive target organ damage. There was no age-related difference in the LVM index, but the serum creatinine level in elderly hypertensive patients was significantly lower than that in middle-aged hypertensive patients. There was no significant difference in serum uric acid level between the two groups. In addition, the LVM index was correlated with the serum uric acid level (r = 0.46, p = 0.0001) but not with the serum creatinine level in elderly hypertensive patients. In middle-aged hypertensive patients, the LVM index was related to both serum uric acid level (r = 0.41, p = 0.007) and serum creatinine level (r = 0.43, p = 0.003). In conclusion, serum creatinine level may underestimate hypertensive renal involvement in elderly hypertensive patients. In contrast, serum uric acid level may be a sensitive indicator of hypertensive target organ damage irrespective of age.

Adult↗
PubMed1999

Serial changes in sarcoplasmic reticulum gene expression in volume-overloaded cardiac hypertrophy in the rat: effect of an angiotensin II receptor antagonist.

This study was designed to clarify whether gene expression in the cardiac sarcoplasmic reticulum [sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, ryanodine receptor and calsequestrin] changes in accordance with left ventricular functional alterations in the volume-overloaded heart. Further, the effect of the angiotensin II type 1 receptor antagonist, TCV-116, on the expression of these genes was also evaluated. Left ventricular fractional shortening was significantly increased at 7 days, had returned to control levels at 21 days, and had significantly decreased at 35 days after the shunt operation, compared with sham-operated rats. The level of SERCA mRNA was significantly decreased at both 21 days and 35 days after the shunt operation. The levels of ryanodine receptor and phospholamban mRNAs were significantly decreased at 35 days in shunt-operated rats. The decrease in the SERCA mRNA level preceded the development of cardiac dysfunction. The levels of SERCA and ryanodine receptor mRNAs were correlated positively with left ventricular fractional shortening (r=0.73, P<0.0001 and r=0.61, P<0.01 respectively). Attenuation of the decrease in left ventricular fractional shortening occurred on treatment with TCV-116. After the treatment with TCV-116, the levels of SERCA and phospholamban mRNAs were restored to the respective values in sham-operated rats. Ryanodine receptor mRNA levels remained unchanged after treatment with TCV-116. These results indicate that the down-regulation of SERCA and ryanodine receptor mRNA levels may be related to cardiac dysfunction in the volume-overloaded heart. In addition, treatment with an angiotensin II receptor antagonist may restore the altered sarcoplasmic reticulum mRNA levels to control levels, and this may result in attenuation of the functional impairment in the volume-overloaded heart.

Angiotensin II↗
PubMed1999

Hypertrophic cardiomyopathy with mid-ventricular obstruction and splenic infarction associated with paroxysmal atrial fibrillation: a case report.

A 54-year-old woman had been treated for hypertrophic cardiomyopathy and paroxysmal atrial fibrillation since 1992. She was admitted with paroxysmal atrial fibrillation which was resolved by medical treatment. However, on the next day, left lateral chest pain appeared. Computed tomography disclosed a low density area in the spleen. She received anticoagulant therapy under a diagnosis of splenic infarction, and the pain disappeared. Echocardiography showed hypertrophic cardiomyopathy with mid-ventricular obstruction. She was treated with cibenzoline to prevent paroxysmal atrial fibrillation attack and attenuate the hemodynamic load. After treatment, the pressure gradient decreased from 41 to 7 mmHg. This patient with hypertrophic cardiomyopathy suffered a rare isolated splenic infarction associated with paroxysmal atrial fibrillation.

Anti-Arrhythmia Agents↗
PubMed1998

Cloning and mapping of ZNF231, a novel brain-specific gene encoding neuronal double zinc finger protein whose expression is enhanced in a neurodegenerative disorder, multiple system atrophy (MSA).

A novel brain-specific gene, neuronal double zinc finger protein (ZNF231), was cloned and mapped. We used the high-density cDNA filter method to analyze the gene-expression profile in brains with multiple system atrophy (MSA). MSA is a sporadic progressive neurodegenerative disease characterized clinically by cerebellar symptoms, parkinsonism, autonomic dysfunction, or their various combinations, but its pathogenesis has yet to be clarified. In total, 8300 cDNA clones were screened, and a novel gene, ZNF231, was identified, whose expression was elevated in cerebella of patients with MSA. Its transcript is approximately 16 kb long and encodes an open reading frame of 3926 amino acid residues that has several interesting motifs; two glycine-proline dipeptide repeats (aa 22-32 and aa 61-74), a pair of homologous C8 double zinc finger motifs (aa 169-226 and aa 465-521), a leucine zipper motif (aa 561-582), a SH3 domain-binding motif (aa 825-831), two nuclear targeting signals (aa 1011-1028 and aa 1071-1091), two glutamine-rich domains (aa 2428-2473 and aa 3775-3804), and a histidine-rich domain (aa 3597-3682). These features suggest that the new gene encodes a nuclear protein or transcription regulator. Northern blot and RT-PCR analyses showed that its expression is specific to the brain and apparently restricted to the neurons. Elevation of ZNF231 expression may be involved in the pathogenesis of multiple system atrophy. The gene for ZNF231 is located on chromosome 3p21.

Amino Acid Sequence↗
PubMed1998

Transmembrane 4 superfamily as a prognostic factor in pancreatic cancer.

Several members of the transmembrane 4 superfamily (TM4SF) have been reported to be related to tumor progression and metastasis. The aims of our study were to clarify the relationship between TM4SF and pancreatic cancer and to determine the prognostic significance of TM4SF in human pancreatic cancer. The mRNA levels for MRP-1/CD9, KAI1/CD82 and ME491/CD63, which belong to the TM4SF gene family, were evaluated in 40 resectable pancreatic adenocarcinomas using reverse transcriptase-PCR. MRP-1/CD9 gene expression was associated with lymph node status, and with pathological status. Moreover, MRP-1/CD9 expression was inversely associated with histo-pathological grading. KAI1/CD82 gene expression was inversely associated with tumor status. ME491/CD63 gene expression, however, was conserved in all pancreatic cancers. The overall survival rate for the 22 patients whose tumors had decreased MRP-1/CD9 gene expression was strikingly lower than that for the 18 patients with MRP-1/CD9-positive tumors. The overall survival rate of the 15 patients who were KAI1/CD82-positive was significantly higher than that of the 25 patients with decreased KAI1/CD82 gene expression. In a multivariate analysis using the Cox proportional hazards model, MRP-1/CD9 and KAI1/CD82 status was found to be the most significant.

Adenocarcinoma↗
PubMed1998

Increased contraction of myocytes isolated from the young spontaneously hypertensive rat: relationship between systolic and diastolic function.

This study was designed to assess heart performance in young (10-week-old) spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, in terms of whole heart function in vivo and mechanics of isolated ventricular myocytes in vitro. The data suggest that left ventricular pressure (LVP) generation is greater, and the maximal velocities of LVP generation and decline are faster in SHR than in WKY. Two-dimensional morphologic measurements show that SHR myocytes are hypertrophied and that augmented contractile function is also present in isolated cells as determined by the extent of shortening and velocity of shortening. Relaxation is also faster at the myocyte level as determined by velocity of relengthening. However, the slope of the relationship between myocyte peak shortening and velocity of relaxation was similar in both groups. These results suggest that hyperdynamic myocyte relengthening may reflect changes in elastic recoil from increased shortening rather than intrinsic changes in cellular mechanisms, which are independent of shortening.

Animals↗
PubMed1998

Left ventricular geometry as an independent predictor for extracardiac target organ damage in essential hypertension.

Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor. It has not been established, however, whether left ventricular geometry is an independent predictor of extracardiac target organ damage in essential hypertension. Study groups were classified according to relative wall thickness: 27 patients with concentric LVH and 50 patients with eccentric LVH. Age and left ventricular mass indexes of two groups were matched. As indexes of extracardiac target organ damage, retinal funduscopic grade, and serum creatinine level were measured. The severity of hypertensive retinopathy and the renal involvement were more severe in patients with concentric LVH than in patients with eccentric LVH. Extracardiac target organ damage was consistently higher in patients with concentric LVH than in those with eccentric LVH. Systemic hemodynamics paralleled ventricular geometric patterns, with higher peripheral resistance and lower aortic compliance in patients with concentric LVH, whereas end-diastolic volumes and stroke volumes were higher in patients with eccentric LVH than in patients with concentric LVH. In addition, total peripheral resistance was related to retinal fundoscopic grade (r = 0.41, P < .01), and serum creatinine level (r = 0.28, P < .05). Even in the presence of an identical degree of LVH, echocardiographically determined left ventricular geometry may provide a further independent stratification of extracardiac target organ damage in essential hypertension.

Aged↗
PubMed1998

Beneficial hemodynamic effects of oral prostacyclin (PGI2) analogue, beraprost sodium, on a patient with primary pulmonary hypertension--a case report.

A 65-year-old woman was admitted to our hospital because of exertional dyspnea in 1987. A diagnosis of primary pulmonary hypertension was confirmed by right heart catheterization. She had received conventional therapy in the outpatient clinic. She was readmitted with the deterioration of exertional dyspnea in 1995. Stabilization of pulmonary hemodynamics, while not achieved with conventional therapy, was achieved with additive administration of an oral prostacyclin (PGI2) analogue, beraprost sodium.

Administration, Oral↗
PubMed1998

Relation between coronary blood flow and left ventricular mass in hypertension: noninvasive quantification of coronary blood flow by thallium-201 myocardial scintigraphy.

This study was conducted to quantify coronary blood flow (CBF) noninvasively according to the fractionation principle and to elucidate the relation between CBF and left ventricular hypertrophy. CBF/cardiac output (CO), estimated on the basis of the ratio of myocardial uptake/total injected dose of thallium-201 (% cardiac uptake), was determined in 14 control subjects and 40 patients with essential hypertension. CBF and CBF per 100 g of myocardium (unit CBF) were calculated according to the following formulas: CBF= % cardiac uptake x CO, and unit CBF = (CBF/LVM) X 100, where CO and left ventricular mass (LVM) are echocardiographically determined. There was good reproducibility of % cardiac uptake (r = 0.983, p < 0.0001). Percent cardiac uptake was greater in hypertensive patients (4.65+/-1.44%) than in control subjects (3.64+/-0.64%), and there was a positive correlation between % cardiac uptake and LVM. CBF (ml/min) was greater in hypertensive patients (240.7+/-80.5) than in control subjects (194.9+/-36.9), but unit CBF (ml/min/100 g) was less in hypertensive patients (102.2+/-26.7) than in control subjects (150.3+/-30.5). Multiple regression analyses showed that LVM was the most potent independent predictor of resting CBF in hypertension. Our results indicate that CBF, determined by thallium-201 myocardial scintigraphy, increases parallel to the increase in LVM, but unit CBF decreases even in the resting condition in patients with essential hypertension.

Adult↗
PubMed1998

Marked attenuation of mitral regurgitation by stent implantation: a patient with unstable angina.

A 69-year-old woman was admitted because of increase of chest pain and dyspnea. Systolic murmur of Levine III/VI was heard. Electrocardiography showed ST depression caused by ischemia. Echocardiography revealed severe mitral regurgitation (MR) and inferoposterior hypokinetic wall motion. Left ventriculography revealed the presence of MR (II/IV). Coronary angiography showed severe organic stenosis of the right coronary artery. Based on these findings, the diagnosis was severe papillary muscle dysfunction caused by unstable angina. The lesion of the right coronary artery was successfully stented with a Palmaz-Schatz stent. During balloon inflation, the v wave of the pulmonary capillary pressure curve was greatly elevated. After the stent implantation, ST depression was normalized and MR improved dramatically. Therefore, we suppose that acute MR was induced by temporary papillary muscle dysfunction, and could be relieved with coronary angioplasty.

Aged↗
PubMed1997

Brain regional differences in the expansion of a CAG repeat in the spinocerebellar ataxias: dentatorubral-pallidoluysian atrophy, Machado-Joseph disease, and spinocerebellar ataxia type 1.

Three autosomal dominant spinocerebellar ataxias, dentatorubral-pallidoluysian atrophy (DRPLA), Machado-Joseph disease (MJD), and spinocerebellar ataxia type 1 (SCA1), are associated with the expansion of a CAG repeat in the respective genes. To investigate the association between CAG repeat expansion and neuropathological findings, we analyzed several brain regions from 9 cases of DRPLA, 3 cases of MJD, and 1 case of SCA1. We found that the expanded alleles were smaller in the cerebellar cortex than in other brain regions, such as the frontal cortex, in these three diseases. The discrepancy in the expanded CAG repeat length between cerebellar cortex and other tissues was most prominent in DRPLA, and especially in cases of adult-onset DRPLA. A significant correlation was found between the age at onset of DRPLA and the size of the CAG repeat expansion. Cerebella of DRPLA patients were microscopically dissected into three layers, the molecular and granular layers and the white matter, which were analyzed separately. The lower level of CAG repeat expansion in DRPLA cerebella was representative of CAG repeat expansion in the granule cells. The microdissected samples of the granular layer of the hippocampal formation, which is densely packed with neuronal cells, revealed that the degree of CAG repeat expansion in this layer was similar to that in the cerebellum. These observations suggest that granule cells in the cerebellum and hippocampus have low levels of CAG repeat expansion, and that other types of cells exhibit a higher level of CAG repeat expansion, in spinocerebellar ataxias.

Adolescent↗
PubMed1997

Alterations in expression of sarcoplasmic reticulum gene in Dahl rats during the transition from compensatory myocardial hypertrophy to heart failure.

OBJECTIVES: To clarify whether the functional changes during the transition from compensatory myocardial hypertrophy to failure are associated with changes in sarcoplasmic reticulum gene expression. METHODS: We examined the gene expression of sarcoplasmic reticulum proteins [sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, calsequestrin and ryanodine receptor] in Dahl salt-sensitive (Dahl-S) rats fed a high-salt (8%) diet from the age of 6 weeks. In-vivo contractile functioning was evaluated using echocardiography, and gene expression of sarcoplasmic reticulum proteins in the left ventricle was analyzed by Northern blotting for each stage of left ventricular hypertrophy. RESULTS: SERCA messenger RNA (mRNA) levels in Dahl-S rats with compensatory hypertrophy did not change significantly, whereas phospholamban mRNA levels were increased by 61% (P < 0.01), and calsequestrin mRNA levels were increased by 130% (P < 0.01) compared with those in Dahl salt-resistant (Dahl-R) rats. SERCA mRNA levels in Dahl-S rats with decompensated dilatation were decreased by 32% (P< 0.05), whereas levels of phospholamban and calsequestrin mRNA remained unchanged. Ryanodine receptor mRNA levels did not change either with compensatory hypertrophy or with decompensated dilatation. CONCLUSIONS: Alterations in expression of sarcoplasmic reticulum gene may be related to changes in systolic and diastolic properties in compensatory hypertrophy and heart failure.

Animals↗
PubMed1997

[Mitral prosthetic valve replaced twice due to repeated prosthetic valve endocarditis: a case report].

A 38-year-old man was admitted to our hospital for detailed examination of fever, cough and yellow sputum. At the age of 32, be had mitral prosthesis for the first time, because of mitral regurgitation due to mitral valve prolapse. Four years previously, he had again undergone mitral prosthetic valve replacement due to prosthetic valve endocarditis due to staphylococcus epidemidis. This occasion, staphylococcus aureus was isolated by arterial blood culture. Transesophageal echocardiography detected vegetation attached to the mitral prosthetic valve and paravalvular leakage. The diagnosis was prosthetic valve endocarditis. He underwent a third mitral prosthetic valve replacement. Detection of the source of infection was difficult only by transthoracic echocardiography, and immediate transesophageal echocardiography seemed mandatory to diagnose bacterial endocarditis.

Adult↗
PubMed1996

Regional and cellular expression of the Machado-Joseph disease gene in brains of normal and affected individuals.

Machado-Joseph disease (MJD) is an autosomal dominant disorder characterized pathologically by spinocerebellar degeneration. Recently, an expansion of CAG repeat in a gene located at the chromosome 14q32.1 was found to be responsible for the disease. Here, we investigated in situ the expression of the MJD gene (MJD1) in the central nervous systems of normal and affected individuals and in rat brains. This gene was expressed in all regions of rat and human normal brains with certain regional variations. MJD1 was transcribed preferentially in neurons, although low levels of MJD1 mRNA were also observed in glial cells. Neurons susceptible to degeneration in MJD expressed MJD1 but not selectively. In the affected brains, the MJD1 mRNA distribution and amount in all the areas examined were similar in patients and controls. In addition, the cellular MJD1 mRNA level correlated neither with clinical severity nor expanded length. Our study showed that the expression levels of trinucleotide repeats in MJD patients and normal controls did not differ, indicating that the pathogenesis of MJD may involve direct toxicity to vulnerable subsets and/or region-specific cofactors of MJD proteins.

Adolescent↗
PubMed1996

A clinical profile of corticobasal degeneration presenting as primary progressive aphasia.

We report a patient with primary progressive aphasia who first presented with amnesic aphasia that developed over the course of 3 years into nonfluent aphasia with buccofacial apraxia, followed in the next year by cognitive impairment and parkinsonism. Pathological findings were typical for corticobasal degeneration except for the distribution of cortical atrophy. This case suggests that corticobasal degeneration should be included in the differential diagnosis of primary progressive aphasia, especially in association with parkinsonism.

Aphasia, Primary Progressive↗
PubMed1996

[Familial hypertrophic cardiomyopathy generating a marked left ventricular pressure gradient in an 82-year-old woman].

Familial nonobstructive hypertrophic cardiomyopathy in 78-year-old woman was diagnosed in 1988. Since then she has been treated with a beta-blocking drug and a calcium antagonist. Her clinical condition was NYHA I or II for several years. Echocardiography revealed asymmetric septal hypertrophy in 1988 (interventricular septal thickness = 21 mm, posterior wall thickness = 10 mm). Systolic anterior motion of the mitral valve was first observed at the end of 1992. The left ventricular pressure gradient also gradually increased; it was about 138 mmHg in 1993 (age 82 yrs). The left ventricular ejection time index increased from 376 msec in May, 1992 to 459 msec in May, 1994. In September, 1994, the patient's condition gradually deteriorated (NYHA IV), and she was admitted to our hospital. To attenuate the left ventricular pressure gradient, 150 mg of disopyramide was administered. Her condition markedly improved: the left ventricular pressure gradient decreased from 180 mmHg to 76 mmHg, and the left ventricular ejection time index decreased from 485 msec to 419 msec. These results indicate that a left ventricular pressure gradient can be generated rapidly even in a very old patient, and that disopyramide may be useful to attenuate the left ventricular pressure gradient.

Aged↗
PubMed1996

[A 66-year-old woman with a patent ductus arteriosus and no significant progression of pulmonary arterial pressure over 17 years].

We report the case of a 66-year-old woman with a patent ductus arteriosus and no significant progression of pulmonary arterial pressure over 17 years. She was admitted to our hospital in 1978 because of palpitations on exertion and chest discomfort. Cardiac catheterization was done, and she was given a diagnosis of patent ductus arteriosus. Because the left-to-right shunt was small (15%) and because there was no evidence of pulmonary hypertension (38/18 mmHg), she was treated medically. In 1995 she was admitted again, to determine the cause of a cerebral infarction. The cerebral infarction was believed to have been caused by an embolism due to atrial fibrillation. She underwent cardiac catheterization again. The left-to-right shunt had increased to 41%, but the pulmonary artery pressure had not changed (27/14 mmHg). Intravascular ultrasound imaging was used to evaluate the ductus arteriosus. The diameter of the ductus was 4.4 mm and calcification was not observed. During the 17 years of follow-up, heart size increased slightly, but pulmonary artery pressure did not change. In addition, intravascular ultrasound was very useful for evaluating the condition of the ductus arteriosus.

Aged↗