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Biomedical subjects

J Kubota

Publications and source records attributed to J Kubota.

At least 19 recordsLinked to original sources
PubMed2006

Improved search for nu(mu) --> nu(e) oscillation in a long-baseline accelerator experiment.

We performed an improved search for nu(mu) --> nu(e) oscillation with the KEK to Kamioka (K2K) long-baseline neutrino oscillation experiment, using the full data sample of 9.2 x 10(19) protons on target. No evidence for a nu(e) appearance signal was found, and we set bounds on the nu(mu) --> nu(e) oscillation parameters. At Deltam(2)=2.8 x 10(-3) eV(2), the best-fit value of the K2Knu(mu) disappearance analysis, we set an upper limit of sin(2)2theta(mue) < 0.13 at a 90% confidence level.

Journal Article↗
PubMed2005

Search for coherent charged pion production in neutrino-carbon interactions.

We report the result from a search for charged-current coherent pion production induced by muon neutrinos with a mean energy of 1.3 GeV. The data are collected with a fully active scintillator detector in the K2K long-baseline neutrino oscillation experiment. No evidence for coherent pion production is observed, and an upper limit of is set on the cross section ratio of coherent pion production to the total charged-current interaction at 90% confidence level. This is the first experimental limit for coherent charged pion production in the energy region of a few GeV.

Journal Article↗
PubMed2005

Evidence for muon neutrino oscillation in an accelerator-based experiment.

We present results for nu(mu) oscillation in the KEK to Kamioka (K2K) long-baseline neutrino oscillation experiment. K2K uses an accelerator-produced nu(mu) beam with a mean energy of 1.3 GeV directed at the Super-Kamiokande detector. We observed the energy-dependent disappearance of nu(mu), which we presume have oscillated to nu(tau). The probability that we would observe these results if there is no neutrino oscillation is 0.0050% (4.0 sigma).

Journal Article↗
PubMed2002

Effects of diode laser therapy on blood flow in axial pattern flaps in the rat model.

Axial pattern skin flaps are a very important reparative tool for the plastic and reconstructive surgeon in the reconstruction of tissue defects. From whatever unfortunate reason, part or all of such flaps occasionally suffers from irreversible ischaemia with loss of the flap. Infrared diode laser therapy has been shown to improve local and systemic circulation. The present study was designed to assess the effect of an 830 nm diode laser (power density, 18.5 W/cm(2), energy density 185 J/cm(2)) on the blood flow of axial pattern flaps in the rat model and their survival, compared with unirradiated controls. The flaps were raised in all animals ( n=40), and blood flow assessed with laser speckle flowmetry (LSF). In the experimental groups (3 groups, n=10 per group), the flaps were irradiated either directly over the dominant feeder vessel (iliolumbar artery), at the proximal end or at the distal end of the flap itself and blood flow assessed during irradiation. Flowmetry was performed again in all animals at 5 and 10 min postirradiation, and the flaps sutured back in position. The unirradiated controls were handled in exactly the same way, but the laser was not activated. The survival rate of the flaps was assessed on the fifth postoperative day. LSF demonstrated significant increased blood flow in the flaps at 5 and 10 min postirradiation in all experimental groups compared with the control animals. At five days postirradiation, there was significantly better survival of the flaps in all the experimental groups compared with the controls ( p<0.01), but no significant difference was seen between any of the experimental groups. We conclude that laser therapy increases the blood flow and perfusion of transferred flaps, and that this has significant effects on the survival of the flaps. One possible mechanism of modulation of the autonomic nervous system is discussed.

Animals↗
PubMed2000

Nitric oxide mediates inhibitory effect of losartan on angiotensin-induced contractions in hamster but not rat aorta.

We investigated a possible contribution of nitric oxide (NO) and prostaglandins to the inhibitory effect of losartan on contractions to Ang I (10(-6) M) and Ang II (10(-7) M) with or without L-NAME (10(-4) M) or indomethacin (10(-5) M) in the aorta of WKY, SHR and hamster (n=7 each). Rings of thoracic aorta (2-mm long) were placed in a myograph (5 ml). Endothelium-dependent vasodilations were evaluated with acetylcholine (10(-8) to 10(-6) M). After a 45-minute incubation with L-NAME under a resting tension of 2 g, only hamster aorta contracted (p<0.01). The SHR aorta showed impaired relaxations to acetylcholine compared with the WKY and hamster aorta (p<0.05). Despite the difference in the stimulated NO release, losartan completely abolished the responses to Ang I and Ang II both in WKY and SHR vessels irrespective of the presence of L-NAME. In contrast to the rat aorta, the inhibitory effect of losartan was attenuated in the presence of L-NAME in the hamster aorta (78% vs 99% inhibition, p<0.05). Indomethacin did not alter the effect of losartan in any vessels. Our results suggest that the presence of NO, particularly a basal secretion of NO, is necessary for the full expression of the inhibitory effect of losartan in the hamster, but not in WKY or SHR, aorta. Unlike NO, prostaglandins do not appear to play a role in the effect of losartan.

Angiotensins↗
PubMed2000

Immunohistochemical analysis of CA125, CA19-9, and Ki-67 in stage III or IV endometriosis: positive correlation between serum CA125 level and endometriotic epithelial cell proliferation.

BACKGROUND: Serum levels of CA125 and CA 19-9 are often elevated in patients with endometriosis, but the clinical or biological significance of this is not well established. The aim of the present study was to compare serum and tissue levels of CA125 and CA19-9, and to examine the correlation between these levels and cell proliferation using immunohistochemical analysis in stage III or IV endometriosis. METHODS: Forty-five cases diagnosed histologically as endometriosis were analyzed (26 cases were stage III and 19 were stage IV using the revised American Fertility Society classification). The preoperative serum levels of CA125 and CA19-9 were measured by immunoradiometric assay. Immunohistochemical analysis was performed using antibodies against CA125, CA199, and Ki-67 (a representative marker of cell proliferation). RESULTS: The serum levels of CA125 and CA19-9 were elevated (over the cutoff values) in 25 cases and 21 cases, respectively. There was no significant correlation between serum CA125 and serum CA19-9 levels (correlation coefficient [q]=0.19). The serum CA19-9 level correlated well with the degree of immunostaining for CA19-9 (q=0.57), but not with the Ki-67 labeling index. The serum CA125 level did not show a strong correlation with CA125 staining (q=0.41), but it correlated well with the Ki-67 labeling index (q=0.53). CONCLUSIONS: The present study indicates that the serum CA125 level may correlate with the proliferative activity of epithelial cells in endometriotic lesions.

Adult↗
PubMed1999

Alternative angiotensin II formation in rat arteries occurs only at very high concentrations of angiotensin I.

Contrary to previous reports, recent enzymatic assays showed the predominance of chymase-like activity in rat arteries. We determined the existence and significance of such alternative pathways in rat carotid arteries by measuring contraction of arterial rings in organ baths and blood pressure in conscious rats. Hamster aorta served as a positive control for chymase. Temocapril (30 micromol/L) inhibited the contractions to angiotensin (Ang) I (10(-9) to 10(-5) mol/L) except at high concentrations of Ang I (>10(-7) mol/L). Addition of chymostatin (100 micromol/L) to temocapril exerted a synergistic inhibitory effect. Hamster aorta gave similar results, except that temocapril was 30-fold less effective than in rat arteries. [Pro(11), D-Ala(12)]Ang I (10(-8) to 10(-5) mol/L), a chymase-specific substrate, provoked similar responses in rat and hamster arteries; chymostatin, but not temocapril, attenuated the responses. CV 11974 (30 micromol/L), an Ang II type 1 receptor antagonist, abolished the responses to both peptides. In conscious rats, Ang I (0.03 to 30 microg/kg) and [Pro(11),D-Ala(12)]Ang I (7 to 700 microg/kg) produced similar pressor responses. Not only CV 11974 (1 mg/kg) but also temocapril (2 mg/kg) abolished Ang I-induced responses in vivo. CV 11974, but not temocapril, inhibited responses to [Pro(11), D-Ala(12)]Ang I. Our results showed the presence of the alternative pathway in rat arteries, but it did not play a major role. Arteries with the opposing characteristics of chymase responded equally to [Pro(11),D-Ala(12)]Ang I. These findings suggest that biochemical and [Pro(11),D-Ala(12)]Ang I-derived results may not reflect the functional significance of chymase.

Angiotensin I↗
PubMed1998

Cardioprotective effects of quinapril after myocardial infarction in hypertensive rats.

Although angiotensin-converting enzyme inhibitors are beneficial for patients with congestive heart failure, the appropriate timing and dosage in acute myocardial infarction are still controversial. We examined the hemodynamic effects of quinapril administered before acute myocardial infarction in spontaneously hypertensive rats (SHR). Quinapril (10 mg/kg per day in drinking water) was started 1 week before infarction and continued for 4 weeks after infarction (total duration 5 weeks). The hemodynamic parameters were evaluated by cardiac catheterization 4 weeks after coronary ligation. Sham-operated SHR served as controls. After infarction, left ventricular end-diastolic and right atrial pressures were increased (P < 0.01) and blood pressure and cardiac index were decreased (P < 0.01); the magnitude of blood pressure reduction was similar in the treated and untreated rats with infarction. Quinapril improved these hemodynamic parameters significantly and decreased left and right ventricular weight. These results suggest that a prior treatment with quinapril in SHR with acute myocardial infarction is hemodynamically beneficial.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Transesophageal echocardiographically guided atrial transseptal catheterization in patients with normal-sized atria: incidence of complications.

The incidence of cardiac complications from atrial transseptal catheterization has never been quantified in patients with normal-sized atria. Series defining the complication rate are derived from diseased hearts with structural changes that may alter the complication rate of the procedure. The generation of a standardized incidence of perforation in a population of structurally normal atria has important implications. A total of 46 atrial transseptal catheterizations guided by transesophageal echocardiography (TEE) for radiofrequency ablation of left-sided accessory pathways was performed in 42 patients during a 3-year period (1990-1993). Clinical and echocardiographic data were analyzed, with special attention given to TEE reports pre- and post-transseptal catheterization. Only one complication occurred in the 46 procedures (2.2%): a perforation of the left atrium that led to pericardial effusion and cardiac tamponade. In a small series of patients with normal sized atria, we have demonstrated that TEE-guided transseptal catheterization in a procedure with a low complication rate.

Adult↗
PubMed1995

Fee-for-service versus capitation-based reimbursement: how the payment method affects utilization of echocardiographic services by referring physicians.

Historically, health insurance carriers (HIC) have reimbursed physicians on a fee-for-service basis for echocardiographic studies. With the emergence of managed care, the HIC now may have the option of paying on a capitation basis. To determine whether the method of reimbursement had any bearing on the types of patients referred for echocardiographic services, we conducted a two-phase (retrospective) study. In Phase One, we assessed two groups of ambulatory patients with regard to patient characteristics, medical reason for referral, and echocardiographic results. Group A (4,066 patients) had insurance plans that stipulated reimbursement for echocardiographic services as part of capitation for cardiology services. Group B (3,061 patients) had plans that reimbursed for echocardiographic services on a fee-for-service basis. In Phase Two, we assessed a total of 5,947 patients (3,833 from Group A and 2,114 from Group B) over a period of 40 months to determine the frequency of referral for a second echocardiogram within 2 years of a normal one and the repeat normalcy rate. The results showed that the capitation reimbursement group included younger, predominantly female patients who were referred more often for a more benign reason and who more frequently were diagnosed echocardiographically with less severe disease, higher rates of normalcy, and repeat normalcy. These findings suggest that in our geographic area the capitation method of reimbursement permitted more liberal utilization of echocardiographic services. In this era of cost awareness, the study suggests the need for better screening of patients referred for echocardiographic services.

Capitation Fee↗
PubMed1995

Comparable effects of angiotensin II and converting enzyme blockade on hemodynamics and cardiac hypertrophy in spontaneously hypertensive rats.

Angiotensin-converting enzyme inhibitors may regress left ventricular hypertrophy (LVH) without decreasing blood pressure (BP). The aim of the present study was to compare the effects of low and high doses of lisinopril and the angiotensin II receptor antagonist TCV116 (TCV) on LVH and hemodynamics in spontaneously hypertensive rats (SHR). Lisinopril (0.5 and 3 mg/kg per day) and TCV (0.3 mg/kg per day) were given to 8-week-old male SHR daily for 2 weeks. Untreated SHR and Wistar-Kyoto rats (WKY) served as controls. Untreated SHR had a greater left ventricular (LV) weight than WKY (p < 0.01). Lisinopril (3 mg/kg per day) decreased both LV weight and BP. Lisinopril (0.5 mg/kg per day) significantly decreased LV weight, but not BP. In contrast, although TCV significantly decreased BP, LVH was not suppressed. Renal blood flow (RBF) in untreated SHR was less than that in WKY (p < 0.05), but was increased with either lisinopril (3 mg/kg per day)-treated rats (p< 0.05). These findings suggest that factors other than afterload reduction play a role in the regression of LVH with lisinopril, whereas a longer duration of treatment and/or a higher dose may be necessary with TCV. Despite the decrease in BP, TCV normalized RBF in SHR, perhaps due to the blockade of renal angiotensin II.

Angiotensin II↗
PubMed1995

[A case of adenomyelolipoma].

We report case of adenomyelolipoma. CT and MRI revealed a large, capsulated, septated adrenal mass with abundant fat tissue. However, enhancing components were demonstrated at the capsule and septations on angiography. On the pathological study, the capsule and septations consisted of adrenal adenoma and the tumor contained various forms of myelolipomatous tissues. These myelolipomatous tissues were classified into 4 groups. Type I: Scattering of fat cells and hematopoietic elements without coalescence. Type II: Collection of myelolipomatous tissue with unclear margin or small myelolipomatous tissue that cannot be classified as type I or III. Diameter of the lesion is less than 1 cm. Type III: Collection of myelolipomatous tissue with clear margin or replacement of cortical nodule. Diameter of the lesion is less than 1 cm. Type IV: Collection of myelolipomatous tissue. Diameter of the lesion is equal to or greater than 1 cm. We defined adenomyelolipoma as a lesion combining adrenal adenoma (or hyperplasia) and various forms of myelolipomatous tissues (type I-IV) in view of the strong relationship between adrenal adenoma (or hyperplasia) and myelolipomatous tissue.

Adenoma↗
PubMed1994

Converting enzyme inhibition improves congestion and survival in hypertensive rats with high-output heart failure.

The effects of angiotensin-converting enzyme (ACE) inhibitors in high-output heart failure have not yet been well established. We evaluated the effects of lisinopril (3 mg/kg/day) on hemodynamics, neurohormones, and survival in 10-week-old spontaneously hypertensive rats (SHR) with aortocaval fistula. Sham-operated treated and untreated SHR served as controls. Cardiac output (CO) was determined by thermodilution method, and renal blood flow (RBF) was assessed by laser-Doppler flowmetry. In sham-operated SHR, 2-week treatment with lisinopril decreased blood pressure (BP), left ventricular (LV) weight, and total peripheral resistance (TPR) (p < 0.01 each) and increased RBF and plasma renin activity (PRA) (both p < 0.05); CO and LV end-diastolic pressure (LVEDP) were unchanged. Fistula creation induced biventricular hypertrophy and high-output heart failure [increased LVEDP, CO, pulse pressure, and plasma norepinephrine (NE) and decreased RBF] with congestive signs (ascites, tachypnea). Lisinopril decreased LVEDP (p < 0.01), increased RBF, prolonged survival (both p < 0.05), and prevented ascites (0 vs. 46%) and increased PRA (p < 0.05) and attenuated the increase in plasma NE. Heart weight, BP, and CO were not affected by lisinopril. Thus, lisinopril ameliorated congestion and improved survival in SHR with fistula without compromising cardiorenal hemodynamics. Venous and renal dilatation and attenuation of vasoconstrictive systems may have contributed to the beneficial effects.

Animals↗
PubMed1994

Left ventricular function of the heart regressed by nifedipine in spontaneously hypertensive rats.

Left ventricular (LV) performance of the pharmacologically regressed heart in hypertension is still unclear. We compared LV function of the heart regressed by nifedipine with that of the hypertrophied heart in spontaneously hypertensive rats (SHR). Nifedipine (30 mg/kg/day in food) was given to 15-week-old male SHR for 20 weeks (n = 12). Age- and sex-matched SHR served as controls (n = 12). LV catheterization was performed using a micromanometer and cardiac output was determined by the thermodilution method. Hemodynamic studies were performed after washout of nifedipine (24 h), when blood pressure had returned to the untreated level. Peak pumping ability was assessed during acute volume loading with saline. Nifedipine significantly decreased blood pressure in conscious animals (222 +/- 11 to 201 +/- 12 mmHg, p < 0.01) and reduced LV weight (1.20 +/- 0.07 to 1.07 +/- 0.05g, p < 0.01). After washout of nifedipine, LV systolic and end-diastolic pressures, dp/dtmax and cardiac output determined under pentobarbital anesthesia were similar in the treated and untreated groups. Peak pumping ability during acute preload elevation was also similar in the 2 groups. Plasma norepinephrine was unaltered, and plasma renin activity was significantly lower in the treated rats (p < 0.05). These results indicate that nifedipine regressed LVH with a minimal reduction of blood pressure and without evidence of neurohumoral activation or volume retention. In conclusion, LV function of the heart regressed by nifedipine was preserved after a spontaneous rise in blood pressure and during acute preload elevation.

Animals↗
PubMed1993

Lisinopril reduces cardiac hypertrophy and mortality in rats with aortocaval fistula.

We evaluated the effects of lisinopril (1 mg/kg per day) on hemodynamics, cardiac hypertrophy, and neurohumoral factors in Wistar rats with an abdominal aortocaval fistula. After 4 weeks of treatment, the results were compared with values obtained for untreated rats with a fistula and for sham-operated rats. Volume loading induced biventricular hypertrophy, hemodynamic signs of high-output heart failure (increased cardiac output, left ventricular end-diastolic pressure, and pulse pressure), and impaired renal function (decreased renal blood flow and kidney weight; increased blood urea nitrogen). Lisinopril did not affect these cardiorenal hemodynamics, but decreased left ventricular mass and mortality rate (both P < 0.05). Lisinopril attenuated the increase in plasma norepinephrine, and increased plasma renin activity (both P < 0.05). Thus, lisinopril reduced left ventricular mass and mortality in rats with high-output heart failure without changing the cardiorenal hemodynamics. Neurohumoral inhibition may play a role in the beneficial effects of lisinopril.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Deficiency of holo-, but not apo-, ceruloplasmin in genetically copper-intoxicated LEC mutant rat.

Long-Evans Cinnamon(LEC) mutant rats exhibited less than 5% of normal levels of serum ceruloplasmin oxidase activity, but immunoblot analysis showed normal levels of immunologically detectable ceruloplasmin protein in sera from the mutant rats. Immunostaining of cryosections from the liver tissues with anti-ceruloplasmin antibody showed no significant difference between normal and LEC rats. Results from pulse labeling of ceruloplasmin for 3 hours with [35S]methionine in primary hepatocyte culture, followed by immunoprecipitation, SDS-PAGE and fluorography, showed only minor changes in ceruloplasmin protein synthesis and secretion. These results suggest that the mutation(s) does not affect ceruloplasmin gene expression, but results in a failure in the mechanism whereby copper is incorporated into newly synthesized apoceruloplasmin to produce oxidase active holoform.

Animals↗
PubMed1993

Haemodynamic and neurohumoral changes in spontaneously hypertensive rats with aortocaval fistulae.

1. Our aim was to evaluate the effects of an aortocaval fistula (1 mm) on cardiorenal haemodynamics, cardiac hypertrophy and neurohumoral factors in spontaneously hypertensive rats and to compare the results with those observed in Wistar rats at 2 weeks after fistulae placement. Sham-operated spontaneously hypertensive rats and Wistar rats served as controls. 2. Heart weight was significantly increased in spontaneously hypertensive rats (34%) and in Wistar rats (43%) at 2 weeks after fistula creation. Left ventricular systolic pressure and dp/dtmax. were significantly decreased (both P < 0.01) in spontaneously hypertensive rats with fistulae which had higher left ventricular end-diastolic pressure than Wistar rats with fistulae (P < 0.01). Signs of circulatory congestion (ascites, tachypnoea, prostration) were observed only in the overloaded spontaneously hypertensive rats (45%). Cardiac index was comparably increased in both fistulae groups due to an increase in stroke index, since heart rate was not increased. 3. Fistulae placement decreased renal blood flow and kidney weight, and increased blood urea nitrogen to a greater degree in spontaneously hypertensive rats (all P < 0.05); serum creatinine levels were unaltered. Plasma noradrenaline concentration was increased in spontaneously hypertensive rats with fistulae (P < 0.05), whereas plasma renin activity was not changed. 4. Thus, spontaneously hypertensive rats with fistulae developed overt haemodynamic signs of high-output heart failure with frequent ascites and dyspnoea, whereas most of these findings were milder or absent in Wistar rats. This model provides an opportunity to evaluate the pathophysiological and pharmacological responses in high-output heart failure.

Animals↗