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Biomedical subjects

T Kanda

Publications and source records attributed to T Kanda.

At least 127 records · Page 7Linked to original sources
PubMed2000

Assessment of in vivo oxidative stress in hypertensive rats and hypertensive subjects in Tanzania, Africa.

Oxidative stress has been reported to be involved in not only cardiovascular diseases but in hypertension, which is a major risk for cardiovascular diseases. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) has been recognized as a sensitive biomarker of oxidative DNA damage and also of oxidative stress. In the present study, we assessed the oxidative stress in human subjects with hypertension and in hypertensive rats. In stroke-prone spontaneously hypertensive rats at the age of 14 weeks, the excretion of urinary 8-OHdG was significantly (p < 0.05) increased compared with that in age-matched normotensive Wistar-Kyoto rats. Next, we investigated the relationship between oxidative DNA damage and cardiovascular risk factors among Tanzanians aged 46-58 years in a population study carried out in 1998 in at Dar es Salaam, Tanzania, according to the WHO-CARDIAC Study Protocol. Sixty subjects (male/female, 28/32) were selected by SPSS Base 8.0 from those who completed a 24-h urine collection. The 24-h urinary 8-OHdG of the hypertensive subjects (SBP > or =140 mmHg and/or DBP > or =90 mmHg) was significantly (p < 0.05) higher than that of the normotensive subjects (SBP <140 mmHg and DBP <90 mmHg) after adjusting for age and gender (Hypertensives: 17.31 +/- 2.0 ng/mg creatinine, n=38; Normotensives: 10.10 +/- 2.64 ng/mg creatinine, n=22). Oxidative stress was thought to be involved in hypertensive subjects and in hypertensive rats.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2000

Pathological changes of human unmyelinated nerve fibers: a review.

In the cutaneous nerves, unmyelinated nerve fibers outnumber the myelinated ones but are scarcely analyzed, especially at autopsy. This indifference toward the pathology of unmyelinated nerve fibers may be due to the necessity of electron microscopic analyses and, more importantly, the obscurity of pathological alteration of unmyelinated nerve fibers in aging as well as in peripheral nerve disorders. The aim of this article is to review (1) the normal appearance including postmortem changes, (2) the age-related changes, and (3) the pathological alteration in various neuropathic and non-neuropathic conditions, of unmyelinated nerve fibers in the sural nerve. For the complete analyses of sural nerve, qualitative and quantitative estimation of unmyelinated nerve fibers in all specimens should be recommended and it sometimes has an important diagnostic value.

Aging↗
PubMed2000

Antipituitary antibodies as pathogenetic factors in patients with pituitary disorders.

Our previous reports showed detection of antipituitary antibodies (APA) by immunoblot analysis and enzyme linked immunosorbent assay (ELISA) by using rat pituitary tissue as antigen in patients with certain endocrine disorders. In the present report, we evaluated APA by using our immunoblot and ELISA technique in 76 patients with various pituitary disorders. The prevalence of a 22 kDa band of APA detected by immunoblot was found to be significantly higher (P<0.01) in patients with pituitary disorders (20 of 76, 26%) than in the controls (3 of 209, 1%). APA levels detected by ELISA were significantly higher in patients with GH deficiency, isolated ACTH deficiency, acromegaly, and idiopathic panhypopituitarism compared with control (mean +/- SD; 2.40+/-2.66, 2.36+/-1.87, 2.09+/-1.87, 3.10+/-1.96 versus 1.42+/-0.64 (C.I.) P<0.05, respectively). APA levels detected by ELISA in 7 patients with GH deficiency showed a statistically significant decrease (p<0.05) after administration of GH replacement therapy. APA detection by immunoblot is useful in examining as pathogenesis, while ELISA may be useful as an objective index of pathological state in patients with autoimmune-related pituitary disorders.

Adolescent↗
PubMed2000

Involvement of circulating interleukin-6 and its receptor in the development of euthyroid sick syndrome in patients with acute myocardial infarction.

OBJECTIVE: In patients with acute myocardial infarction (AMI), low triiodothyronine (T(3)) levels with normal or subnormal levels of thyrotropin (TSH), the euthyroid sick syndrome (ESS), have been reported, however, the mechanism of altered thyroid hormone metabolism is unknown. Recent reports have shown that interleukin-6 (IL-6) plays a key role in the pathogenesis of AMI and ESS. This preliminary study investigates the relationship between thyroid states and plasma levels of IL-6, the soluble IL-6 receptor (sIL-6R), and the soluble transducing 130kDa glycoprotein (sgp130) in AMI. DESIGN AND METHODS: We measured the concentration of TSH, free T(3) (FT(3)), free thyroxine (FT(4)), IL-6, sIL-6R and sgp130 in plasma from 24 patients with AMI and 20 normal controls. RESULTS: All 24 AMI patients showed significantly lower concentrations of FT(3) with normal or subnormal levels of TSH, and higher concentrations of IL-6 and sIL-6R than controls. IL-6 level was correlated with creatine phosphokinase (CPK) and FT(3) levels but not with FT(4 )or TSH levels in patients with AMI. The time course of IL-6 and FT(3 )concentration seemed to be closely linked. sIL-6R level was correlated with CPK and sgp130 levels, but not with FT(3), FT(4) or TSH levels. FT(4 )level was correlated with sgp130 level. CONCLUSION: Patients with AMI develop ESS through activation of IL-6 and its receptor system.

Aged↗
PubMed2000

Augmented responses of angiotensin I and II in patients with ischemic heart disease: relation to left ventricular function.

To evaluate the effects of left ventricular (LV) dysfunction upon the sympathetic nervous and renin-aldosterone-angiotensin systems, neurohormonal factors were measured in patients with ischemic heart disease. Eleven patients were divided into two groups by their LV ejection fraction based on previous catheterization; preserved (EF > or = 60%) and impaired (EF < 60%) LV systolic function groups. They performed supine ergometer exercise and blood samples were drawn at rest and at peak exercise. After dynamic exercise, plasma norepinephrine was significantly (p < 0.05) increased in patients with preserved LV function, whereas it was not altered in patients with impaired LV function (norepinephrine 20.8 +/- 20.5 vs 45.8 +/- 41.9, respectively). We observed no differences in basal or peak levels of neurohormonal factors, including plasma renin activity, aldosterone, and brain natriuretic peptide (BNP), between the groups. Although the plasma levels of angiotensin I and II were not different in the two groups at rest or at peak exercise, their increasing ratios from rest to peak exercise were significantly higher in patients with impaired LV function compared to those with preserved LV function (angiotensin I; -18.6 +/- 31.0% vs 64.8 +/- 66.5%, p < 0.05, angiotensin II; -5.9 +/- 41.2% vs 60.7 +/- 40.4% , p < 0.05). These results suggest that the increasing ratios of angiotensin I and II are superior to BNP as predictors of LV dysfunction, and that the sympathetic nervous system has already been activated even at rest and did not respond to dynamic exercise in patients with LV dysfunction in ischemic heart disease.

Aged↗
PubMed2000

Effects of antihypertensive therapy on blood pressure and left ventricular hypertrophy in patients with severe hypertension.

The mechanisms responsible for regression of left ventricular (LV) mass with antihypertensive therapy in patients with severe hypertension remain unclear. This study was designed to examine whether systolic and diastolic blood pressures are associated with changes in LV mass. Eighteen patients with essential hypertension whose average seated diastolic blood pressure was >or = 110 mm Hg were enrolled in the study. All patients were administered antihypertensive therapy and underwent M-mode echocardiography before and after 6 months of treatment. In all patients, antihypertensive treatment significantly reduced systolic blood pressure from 175 +/- 21 mm Hg at baseline to 143 +/- 22 mm Hg at 6 months (p < 0.001), and diastolic blood pressure from 116 +/- 7 mm Hg at baseline to 92 +/- 20 mm Hg at 6 months (p < 0.001). LV mass index at 6 months was significantly reduced compared to its baseline value (p < 0.05). Change (value at 6 months-value at baseline) in systolic and diastolic blood pressures correlated positively with the change in LV mass index (r = 0.61, p < 0.01 and r = 0.71, p < 0.001, respectively). The patients were divided into responders. whose LV mass regressed by > or = 10% (n = 9), and nonresponders, whose LV mass regressed by < 10% (n = 9). Systolic (p < 0.001) and diastolic (p < 0.001) blood pressures. interventricular septal thickness (p< 0.05), posterior wall thickness (p < 0.001), and LV mass index (p < 0.001) were significantly decreased in the responders, but not in the nonresponders, at 6 months compared with those at baseline. Systolic (p < 0.05) and diastolic (p < 0.05) blood pressures in nonresponders were significantly higher than those in the responders at 6 months. The changes in systolic and diastolic blood pressures did not correlate with the change in LV mass index in the responders or the nonresponders. The regression of LV mass is strongly affected by reducing blood pressure. This is the first study using antihypertensive therapy to demonstrate that a change in blood pressure correlates positively with changes in LV mass index in severely hypertensive patients.

Adult↗
PubMed2000

C-reactive protein as a prognostic marker in lymphocytic myocarditis.

The prognosis of patients with lymphocytic myocarditis (LM) is poor with the combined endpoint of death or transplant in the Myocarditis Treatment trial being 56% at 5 years. Physicians often have difficulty determining the prognosis in an individual patient. Patients with LM may have ongoing myocardial inflammation. We evaluated the ability of a serum marker of inflammation to predict prognosis in patients with LM. Serum concentrations of C-reactive protein (CRP) were measured in patients with LM. Thiry-one patients with clinical and histologic evidence of LM were evaluated. Patients with coronary artery disease, and idiopathic dilated and secondary cardiomyopathies were excluded. Overall mortality and morbidity from congestive heart failure was assessed at 28 days. The mean plasma CRP concentrations in the five patients who died within the 28-day follow-up period were significantly higher than in those patients who survived (17.4 +/- 5.6 vs 5.9 +/- 3.3 mg/ml, p < 0.05). The CRP concentration was positively correlated with plasma levels of lactic dehydrogenase and the New York Heart Association functional class. Routine measurement of CRP may be a useful tool for determining the prognosis in patients with LM.

Adolescent↗
PubMed2000

Prolongation of QT interval and ventricular septal hypertrophy.

Long QT syndrome (LQTS) is a prime example of interplay between molecular biology, cellular physiology, and organ physiology. Both the congenital and acquired forms of LQTS are due to intrinsic and/or acquired abnormalities of the ionic currents responsible for cardiac repolarization. We analyzed the QTc interval, QRS axes and interventricular septal thickness (IVST) in 41 patients who had a prolonged QT interval on routine electrocardiography (ECG) (5 females and 36 males, mean age 65+/-13 years). The QRS axis of patients in the LQTS group (27+/-49 degrees) was significantly lower (p < 0.05) than in the control group (46+/-26 degrees). However, the IVST in the LQTS group (10+/-2 mm) was significantly thicker than in the control group (9+/-1 mm) (p < 0.05), while the WTd was not significantly different. The QTc interval in patients with ventricular septal hypertrophy (IVST > or = 12 min, 478.8+/-7.9 msec) was significantly longer (p < 0.05) than in the normal group (IVST < 12 mm, 472.1+/-17.5 msec). In conclusion, the results of this preliminary study suggest that prolongation of the QT interval on ECG should prompt screening for electrocardiographic evidence of ventricular hypertrophy in patients with this disease.

Adult↗
PubMed2000

Therapy with the nonpeptide endothelin receptor antagonist 97-139 in a murine model of congestive heart failure: reduction of cardiac mass and myofiber hypertrophy.

Endothelin-1 (ET-1) is a potent vasoconstrictor. This peptide exerts numerous effects on the heart, including regulation of cardiomyocyte growth during hypertrophy. The effects of the structurally novel, nonpeptide, ET-1-selective, competitive antagonist (ETA) 97-139 were investigated in mice with congestive heart failure (CHF) and myocardial hypertrophy. Morphological and microscopical analyses were conducted on day 56 after viral inoculation following 28 day treatment with 99-139. Eight week-old DBA2 mice were intraperitoneally inoculated with encephalomyocarditis virus at a dose of 500 pfu/mouse. The 30 mice were divided into two groups--an ETA treated group and an untreated group. Heart weight (HW) in the infected group was significantly (p < 0.05) increased compared to that in the uninfected group. HW and the HW/body weight (BW) ratio were significantly (p < 0.05) reduced in the ETA treated group compared with the untreated group (HW; 127.7 +/- 6.2 mg vs 144.3 +/- 4.2 mg, HW/BW; 4.9 +/- 0.9 x 10(-3) vs 5.4 +/- 0.5 x 10(-3)). Myofiber diameter in the ETA treated group was significantly reduced compared with the untreated group (12.1 +/- 1.5 microm vs 14.3 +/- 1.9 microm). These results suggest the ET-1 receptor antagonist 97-139 has an effect on the reduction of cardiac mass and myofiber hypertrophy, and that 97-139 may be a useful agent for CHF due to viral myocarditis.

Animals↗
PubMed2000

Portal systemic encephalopathy presenting with dressing and constructional apraxia.

We report a case with portal systemic encephalopathy who presented with dressing and constructional apraxia and subtle weakness of the left hand. We initially suspected a cerebrovascular attack in the right cerebral hemisphere, but brain T1-weighted magnetic resonance (MR) imaging revealed high intensity in the basal ganglia and hyperammonemia was detected. We performed abdominal MR angiography, which visualized an intrahepatic portal systemic shunt. Cerebral blood flow, measured by xenon-enhanced computed tomography, was decreased in the bilateral, but more dominantly right-sided, parietal watershed regions. We speculate that these boundary territories might be susceptible to damage by toxic metabolites of hepatic encephalopathy.

Aged↗
PubMed2000

QT dispersion is increased in diabetic patients with foot ulcer.

QT dispersion, a measure of inhomogenous ventricular repolarization, was measured in diabetic patients with foot ulcer. We recruited 75 patients with non insulin-dependent diabetes mellitus: patients with neuropathic ulcer (n=15, NU group), with ischemic ulcer (n=20, IU group), with previous myocardial infarction (n=20, MI group) and without any diabetic microangiopathies (n=20, DC group). We also studied normal control subjects (n=15, NC group). The interlead variability of rate corrected QT interval (QTc dispersion) was calculated. QTc interval in the MI group was significantly higher than that in the NC or DC but showed no difference in the NU and IU groups. QTc dispersion in the IU (54+/-15 msec) as well as MI (60+/-21 msec) group were significantly higher than the NC (36+/-18 msec) or DC group (39+/-14 msec). This may be due to complicated coronary artery disease in the IU group. Furthermore, QTc dispersion was also increased (49+/-14 msec) in the NU group in which cardiac autonomic nervous dysfunction was suggested. Patients with both types of diabetic ulcer demonstrated increased QT dispersion due to atherosclerosis or neurological disorder.

Aged↗
PubMed2000

[Studies on circulating interleukin-6 and thyroid functions in acute myocardial infarction].

The euthyroid sick syndrome is reported to exist in acute myocardial infarction(AMI). Previous reports showed serum levels of triiodothyronine(T3) are low and thyroid stimulating hormone(TSH) is normal or subnormal levels in patients with AMI. However, the mechanism of altered thyroid hormone metabolism is unknown. Interleukin-6(IL-6) is reported to be a key role in the pathogenesis of AMI and euthyroid sick syndrome. We measured circulating TSH, free T3(FT3), free thyroxine (FT4), IL-6, soluble IL-6 receptor, soluble transducing 130-kD glycoprotein, atrial natriuretic peptide(ANP) and brain natriuretic peptide in 25 patients and 32 healthy subjects. Circulating FT3 levels in patients with AMI became lower than in control group(p < 0.05). IL-6 levels were significantly(p < 0.05) higher than those of healthy subjects. The peak levels of IL-6 was 30.5 +/- 46.9 pg/ml at 25-27 hours(the first peak) and 64.4 +/- 24.6 pg/ml at 70-72 hours(the second peak). FT3 was negatively related to IL-6(p < 0.05) and hANP(p < 0.05) in patients with AMI. These results indicate that the lower levels of FT3 show the greater severity of AMI. We conclude that euthyroid sick syndrome occurs in patients with AMI and euthyroid sick syndrome may regulated by IL-6 through suppressed of thyroid function.

Aged↗
PubMed2000

[Effects of cholinergic drugs and noradrenaline on the activity of neurons in the rat nucleus raphe magnus in vitro].

The nucleus raphe magnus (NRM) is considered to be an important descending inhibitory system in the pain transmission. Both noradrenergic and cholinergic inputs to NRM have an important role in the modulation of pain. Microinjection of cholinergic agonists or noradrenergic antagonist into the NRM produces antinociception. In order to investigate effects of carbachol (a cholinergic agonist) and epibatidine (a nicotinic cholinergic agonist) on the activity of NRM neurons, we recorded the activity of NRM neurons using extracellular recording technique in the rat brainstem slice preparation and analyzed the changes of the activity by application of carbachol and epibatidine. Further, we studied whether these cholinergic agonists and noradrenaline modulate the activity of the identical NRM neurons. Carbachol increased firing frequencies (FF) in 34 (33%) spontaneously active neurons and decreased FF in 56 (54%). In 19 (50%) silent neurons, carbachol induced firing activity. Epibatidine increased FF in 30 (62.5%) spontaneously active neurons. In 3 (25%) silent neurons, epibatidine induced firing activity. Noradrenaline increased FF in 44 (67.5%), decreased FF in 14 (21.5%) spontaneously active neurons. In 9 (64%) silent neurons, noradrenaline induced firing activity. Carbachol, epibatidine and noradrenaline had effects on a substantial number of the identical NRM neurons. All spontaneously active neurons inhibited by noradrenaline were also inhibited by carbachol. The correlative effects between carbachol and epibatidine, and between epibatidine and noradrenaline were both unremarkable. Carbachol increased or decreased the firing activity of a substantial number of NRM neurons. Carbachol may facilitate or reduce the outflow of the descending inhibitory pathway. Epibatidine increased the firing activity of a substantial number of NRM neurons. Epibatidine may facilitate the outflow of the descending inhibitory pathway. Combinations of carbachol and epibatidine, carbachol and noradrenaline, or epibatidine and noradrenaline may modulate the pain transmission through a part of the same pathway from NRM neurons.

Action Potentials↗
PubMed2000

A case of probable acute interstitial pneumonia with a dramatic response to pulse corticosteroid administration.

A 38-year-old Japanese male without any significant respiratory risk factors was admitted to our hospital because of an acute onset of fulminant pneumonia refractory to intravenous antibiotics administration and an unexplained creatine kinase elevation. He was intubated and under ventilator support on the second hospital day, but responded dramatically to i.v. pulse methylprednisone treatment. After exclusion of secondary etiologies including collagen diseases, we concluded this case as a probable acute (idiopathic) interstitial pneumonia, or Hamman-Rich syndrome, responding dramatically to the corticosteroid pulse administration.

Acute Disease↗
PubMed2000

Markers of undiagnosed incidental cancer in comparison with clinical prostatic cancer.

We propose that carcinoembryonic antigen (CEA) may be a tumor marker for prostatic cancer in addition to prostate specific antigen (PSA), gamma-seminoprotein and prostate acid phosphatase (PAP). The tests were done on 15 sera and autopsy specimens of prostatic cancer. Eight of them were clinical cancers and the remaining seven were incidental ones. We measured serum PAP, PSA, CEA and CA 19-9 and immunohistochemically evaluated these specimens. In clinical cancers, serum PAP, PSA, CEA and CA 19-9 were 1272.9 +/- 3094.4, 146.7 +/- 233.6, 36.3 +/- 36.0 and 80.4 +/- 92.0. Immunohistochemically, all were positive for PAP, PSA, CEA and CA 19-9. In incidental cancers, serum PAP, PSA, CEA and CA 19-9 were 2.4 +/- 1.5, 7.9 +/- 16.9, 128.1 +/- 182.7 and 201.8 +/- 416.1. We conclude that the patients with higher levels of plasma PAP or PSA should go through CEA and CA 19-9 measurement in order to diagnose clinical prostatic cancer.

Acid Phosphatase↗
PubMed2000

Non-invasive diagnosis of a Schwannoma by ultrasonography: a case study.

A 52-year-old female came to this institution complaining of a right leg mass lesion. Ultrasonography showed a 16 x 12 x 20mm hypoechoic solid mass lesion in the right leg. The patient underwent surgery during the diagnosis of Schwannoma. Preoperative diagnosis of Schwannoma is difficult by examination. Computerized tomography and magnetic resonance imaging, showed the origin of Schwannoma. However, the lesion was noted to be in a direct continuity with the cord-like echogenic structure consistent with a nerve by echography. We prefer to conduct preoperative examination by ultrasonography in patients with Schwannoma. In conclusion, we have reported a case of Schwannoma diagnosed by non-invasive ultrasonography.

Female↗