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Yuko Ono

Publications and source records attributed to Yuko Ono.

At least 37 records · Page 2Linked to original sources
PubMed2004

Proton MRS of the peritumoral brain.

Long-echo (TR: 2000 ms, TE: 136 ms) proton MRS of the cerebral tissue in the vicinity to intracranial lesion was done in 15 patients, mainly with parenchymal brain tumors. Significant decrease of N-acetylaspartate (NAA) (P<0.001) and more frequent presence of lactate (P<0.01) comparing with distant normal white matter were found in the perilesional brain tissue. The level of NAA in the perilesional brain tissue had negative associations with presence of lactate in the lesion (P<0.05), excess of lactate in the lesion compared to perilesional brain (P<0.01), grade of the perilesional edema (P<0.01) and patient's age (P<0.05). Multivariate analysis disclosed that identification of lactate in the lesion is associated with lower relative NAA content in the perilesional brain tissue, independently on the presence or absence of any other factor, including brain edema (P<0.001). In patients with lobar lesions who had at least one epileptic seizure during course of their disease the relative NAA content in the perilesional brain was significantly lower, comparing with those who were seizure-free (P<0.05). Therefore, lactate diffused from the tumor, or other metabolites secreted by lactate-producing neoplasm, should be considered as important contributors to the neuronal dysfunction in the surrounding brain. Decrease of NAA in the vicinity to intracranial lesions may reflect neuronal alteration responsible for associated epilepsy.

Adult↗
PubMed2004

Glomerulonephritis in a patient with chronic active Epstein-Barr virus infection.

Renal involvement is rare in chronic active Epstein-Barr virus (EBV) infection. We report an 11-year-old girl who had focal mesangial proliferative glomerulonephritis with cellular crescents and renal tubular atrophy with foam cells in the lumen at the time of the first admission. However, the patient was not diagnosed with chronic active EBV infection until the third admission, 18 months later, because she did not exhibit typical clinical manifestations of infectious mononucleosis, i.e., fever, lymphadenopathy, hepatomegaly, or increased atypical lymphocytes. We performed in situ hybridization of EBV in renal biopsy and renal autopsy tissue and found EBV genome-positive cells in the enlarged vascular areas surrounding the renal tubules in both specimens. The relationship between mesangial proliferative glomerulonephitis with crescents and chronic active EBV infection is unknown.

Child↗
PubMed2004

Aldosterone antagonism ameliorates proteinuria and nephrosclerosis independent of glomerular dynamics in L-NAME/SHR model.

BACKGROUND: The renin-angiotensin-aldosterone system participates importantly in the progression of hypertensive renal disease. Angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists have been demonstrated to afford renoprotection in L-NAME-exacerbated nephrosclerosis in SHR rats. This study was designed to examine the effects of the aldosterone antagonist eplerenone on systemic and renal hemodynamics, glomerular dynamics, renal function and histopathology in L-NAME/SHR, and determine whether aldosterone antagonism would enhance the effectiveness of ACE inhibition. METHODS: Six groups of 20-week-old SHR were studied using renal micropuncture and histopathological techniques after 3 weeks of treatment: SHR control (tapwater, n = 10); SHR + eplerenone (101 +/- 8.3 mg/kg/day, n = 10); SHR + L-NAME (5.0 +/- 0.12 mg/kg/day, n = 9); SHR + L-NAME + eplerenone (n = 8); SHR + L-NAME + lisinopril (3 mg/kg/day, n = 9), and SHR + L-NAME + eplerenone + lisinopril (n = 9). RESULTS: L-NAME-treated SHR developed massive proteinuria, severe hypertensive nephrosclerosis, and tubulointerstitial damage. Eplerenone significantly reduced proteinuria (127.4 +/- 26.5 vs. 51.9 +/- 16.7 mg/24 h, p < 0.01), improved glomerular and arteriolar injuries (65 +/- 9 vs. 29 +/- 9 score/100 glomeruli, p < 0.01; 116 +/- 18 vs. 41 +/- 13 score/100 arterioles, p < 0.01, respectively), and decreased tubulointerstitial damage index (1.43 +/- 0.07 vs. 0.39 +/- 0.07, p < 0.01) without altering mean arterial pressure or glomerular dynamics. Combined therapy of eplerenone with lisinopril produced no further benefits than lisinopril alone. CONCLUSION: The aldosterone antagonist eplerenone significantly ameliorated proteinuria and nephrosclerosis in the L-NAME/SHR model, independent of hemodynamic effects.

Animals↗
PubMed2004

Early metabolic changes in metastatic brain tumors after Gamma Knife radiosurgery: 1H-MRS study.

Evaluation of early metabolic changes in metastatic brain tumors after Gamma Knife radiosurgery was performed by long-echo (TR, 2000ms; TE, 136ms; 128-236 acquisitions) volume-selected single-voxel proton magnetic resonance spectroscopy (MRS). Eighty-five brain metastases in 81 patients were investigated before treatment and 16-18h thereafter. Standard metabolic ratios, namely N-acetylaspartate (NAA)/creatine (Cr), phosphorylcholine/glycerophosphorylcholine (Cho)/Cr, NAA/Cho, lactate (Lac)/Cr, and mobile lipids (Lip)/Cr, were calculated, and comparison of their values before and after irradiation was done. No volumetric changes of any neoplasm were found in any case on the next day after treatment. At the same time, significant reduction of Cho/Cr (P < 0.001) and NAA/Cr (P < 0.01) ratios on the proton MRS of the tumor was disclosed. Reduction of Cho/Cr ratio was significantly more prominent in neoplasms with higher pretreatment Cho/Cr ratios (P < 0.001) and heterogeneous contrast enhancement (P < 0.01). Reduction of NAA/Cr ratio was predominantly determined by its pretreatment value (P < 0.001). The observed decrease of Cho/Cr ratio probably reflects inhibition of proliferative activity and early apoptotic cell loss, whereas reduction of NAA/Cr may result from radiation-induced modulation of neuronal activity in the peritumoral brain tissue. Serial proton MRS represents a valuable diagnostic tool for evaluation of metabolic changes in intracranial neoplasms after radiosurgical treatment.

Aged↗
PubMed2004

Imidapril improves L-NAME-exacerbated nephrosclerosis with TGF-beta 1 inhibition in spontaneously hypertensive rats.

OBJECTIVE: This study was designed to investigate whether chronic angiotensin-converting enzyme (ACE) inhibition prevents hypertensive glomerular injury and inhibits increases in the mRNA levels and immunohistological expression of the apoptosis inducer caspase-3, and transforming growth factor (TGF)-beta 1 during prolonged nitric oxide synthase (NOS) inhibition with N-nitro-L-arginine methyl ester (L-NAME) in spontaneously hypertensive rats (SHR). METHODS AND RESULTS: For 3 weeks, we studied three groups of 20-week-old male SHR: a control group, a l-NAME group, and a group treated with L-NAME and the ACE inhibitor imidapril. L-NAME rats developed severe hypertensive nephrosclerosis with significantly elevated blood pressure, markedly increased urinary protein excretion and serum creatinine levels, and more severe glomerulosclerosis and tubulo-interstitial changes. Levels of TGF-beta 1 mRNA in the renal tissue was also significantly increased in L-NAME rats compared with control SHR. Addition of imidapril significantly lowered blood pressure, inhibited nephrosclerosis and attenuated the mRNA level of TGF-beta 1 in comparison with L-NAME/SHR. Histologically, the glomerular cell apoptosis labeling index, terminal doxynucleotidil transferase-mediated dUTP nick-end labeling of fragmented DNA (TUNEL) and active caspase-3, and TGF-beta 1 positive areas were also reduced by imidapril. CONCLUSION: These data suggest that imidapril prevents glomerular and arteriolar damages and renal functions, through inhibiting both TGF-beta 1 production and apoptosis induction.

Animals↗
PubMed2004

Diffusion-weighted magnetic resonance imaging of organized subdural hematoma--case report.

A 59-year-old male presented with a left organized subdural hematoma. The hematoma appeared as a homogeneous low density area on brain computed tomography and as hyperintense and isointense area on both fluid-attenuated inversion recovery and T2-weighted magnetic resonance (MR) imaging. Echo-planar diffusion-weighted MR imaging showed a crescent hyperintense area under the dura mater and an irregular hypointense area over the brain surface in the left subdural space. The apparent diffusion coefficient (ADC) values of the solid and liquid hematoma were 0.86 +/- 0.32 x 10(-3) and 2.56 +/- 0.39 x 10(-3) mm2/sec, respectively. The ADC value of the solid hematoma was similar to acute subdural or intraparenchymal hematoma, and that of the liquid was similar to cerebrospinal fluid. Burr-hole surgery failed to remove all the hematoma, and he complained of persistent headache. The hematoma was removed through a craniotomy without further neurological deficits. Organized subdural hematoma often requires craniotomy for evacuation because of its solid content. Diffusion-weighted MR imaging and measurement of ADC values can differentiate solid from liquid hematoma, so are useful for selection of the surgical procedure.

Craniotomy↗
PubMed2004

Inhibitory effects of etodolac, a selective COX-2 inhibitor, on the occurrence of tumors in colitis-induced tumorigenesis model in rats.

Ulcerative colitis (UC)-associated neoplasia is one of the complications seen in patients with long-standing UC. Based on many epidemiological studies, colitis is assumed to promote colon tumorigenesis. Tumorigenesis is known to be suppressed in rodents and humans by selective cyclooxygenase-2 inhibitors. However, whether these drugs would serve as protective agents against UC-associated neoplasia remains unclear. Therefore, using a colitis-induced tumorigenesis rat model, we investigated the effects of etodolac, a selective cyclooxygenase-2 inhibitor, on tumorigenesis. The following 4 groups were examined: group A, administered trinitrobenzene sulfonic acid and 1,2-dimethylhydrazine; group B, in addition to the treatment in group A, also received etodolac; group C, administered etodolac alone; and group D, did not receive any agent throughout the study and served as an untreated control. The rats were sacrificed 163 days after the start of experiment, and the number of aberrant crypt foci and tumors in the intestine were counted using a stereoscopic microscope following methylene blue staining. The mean number of aberrant crypt foci was 52.4 in group A, 18.9 in group B, 0 in group C and 0.5 in group D. A total of 9 tumors were observed in group A alone, with none in the remaining groups. The numbers of aberrant crypt foci and tumors in group B were significantly lower than in group A. Etodolac, a selective cyclooxygenase-2 inhibitor, suppresses the occurrence of aberrant crypt foci and tumors in colitis-induced tumorigenesis in rats.

Animals↗
PubMed2004

[Significance of the Yamamoto-Kohama mode of invasion in the prognosis of esophageal squamous cell carcinoma: relationship with reduced expression of involucrin protein].

The Yamamoto-Kohama (Y-K) mode of invasion is a useful indicator of the prognosis of squamous cell carcinoma (SCC) of the oral cavity. We have previously reported that the Y-K mode of invasion is related to lymph node metastasis in esophageal SCC. Therefore, to clarify the relationship between the Y-K mode of invasion and survival rate, we histologicaly evaluated specimens obtained by esophagectomy from patients who had not received induction therapy. The results indicated that the overall survival rate of patients with esophageal SCC was significantly lower in the Y-K 4D group. In addition, significantly lower expression of involucrin protein was observed in pStage III cases than in pStage II cases. As a consequence of the poor prognosis of pStage III SCC, it was suggested that involucrin expression was correlated with survival rate. In conclusion, the Y-K mode of invasion and involucrin expression are considered to be informative prognostic indicators in patients with esophageal SCC.

Carcinoma, Squamous Cell↗
PubMed2004

[A case of organized chronic subdural hematoma presented with transient neurologic deficits].

A 59-year-old diabetic male presented with transient motor aphasia and monoparesis of the right upper limb. Brain CT scan showed a low density area in the left subdural space with a mild midline shift. Magnetic resonance (MR) T2-weighted and fluid-attenuated inversion recovery (FLAIR) imagings revealed homogenous hyperintensity with a hypointense web-like structure in the subdural hematoma. Cervical MR angiography showed no abnormal lesion at the bifurcation of the bilateral common carotid arteries. Conventional cerebral angiography showed an avascular, crescent, space-occupying mass over the left hemisphere without an etiologic lesion of cerebral ischemia. CT perfusion imagings indicated reduced cerebral blood flow (CBF) and prolonged mean transit time (MTT) in the left middle cerebral artery territory underneath the subdural hematoma. No epileptic discharge was found in electroencephalogram. Operative findings indicated that the hematoma was encapsulated with thickened outer and inner membranes including paste-like materials, and the brain surface was intact. Postoperative CT perfusion imagings revealed normal CBF and MTT. The pathophysiological mechanism which the chronic subdural hematoma produces the transient neurological deficit is still uncertain. The mechanical pressure of the hematoma on the neighboring cerebral vessels may cause impairment of blood flow leading to cerebral ischemia and paralysis of function. Our case indicated the transient neurological deficits attributed to a decreased CBF around the subdural hematoma and a change in pressure exerted by the hematoma during changes of head position and increased blood viscosity.

Cerebrovascular Circulation↗
PubMed2004

[Angiotensin type 1 receptor blocker reduced proteinuria in patients of focal glomerular sclerosis].

We report three cases of focal glomerular sclerosis (FGS) with proteinuria that improved with the administration of angiotensin type 1 receptor blocker (ARB, losartan or valsartan). These three patients were a 41-year-old male (case 1), a 22-year-old male (case 2) and a 47-year-old male (case 3), who showed proteinuria, renal dysfunction, and hyperlipidemia. In case 1, proteinuria and renal dysfunction were improved by losartan administration and low protein diet therapy. In case 2, losartan with steroid and immunosuppressant led to the complete remission of proteinuria, improvement of renal dysfunction and reduction of the glomerular injury score from repeat biopsy specimen by approximately 20%. In case 3, proteinuria was reduced by valsartan administration with steroid and immunosuppressant therapy. ARB treatment with steroid and immunosuppressant might be more effective on the reduction of proteinuria in FGS patients.

Adult↗
PubMed2003

Renoprotective effects of omapatrilat are mediated partially by bradykinin.

AIM: To investigate the effects of omapatrilat on systemic and renal hemodynamics, glomerular dynamics, renal function, and histopathological changes as well as the participation of the bradykinin B2 receptor in WKY, SHR, and L-NAME/SHR rats. METHODS: Eight groups of 17-week-old rats were examined using renal micropuncture techniques and histopathological analyses after 3 weeks of treatment: group 1, WKY control; group 2, WKY+omapatrilat (40 mg/kg/day); group 3, SHR control; group 4, SHR+omapatrilat; group 5, SHR+L-NAME (50 mg/l); group 6, SHR+L-NAME+omapatrilat; group 7, SHR+L-NAME for 3 weeks followed by omapatrilat for a subsequent 3 weeks, and group 8, SHR+L-NAME+omapatrilat+bradykinin antagonist icatibant (500 microg/kg/day). RESULTS: In WKY and SHR, omapatrilat significantly reduced the mean arterial pressure, increased effective renal blood flow and single nephron plasma flow associated with reduced glomerular arteriolar resistances. Furthermore, omapatrilat prevented and reversed L-NAME induced urinary protein excretion, glomerular and arteriolar injuries, glomerular morphometric alterations, and glomerular apoptosis (at least, p < 0.05). Icatibant partially inhibited these beneficial effects of omapatrilat. CONCLUSION: Omapatrilat provided potent antihypertensive and renoprotective actions, which were mediated, in part, by bradykinin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Cystic partially differentiated nephroblastoma, embryonal rhabdomyosarcoma, and multiple congenital anomalies associated with variegated mosaic aneuploidy and premature centromere division: a case report.

A rare association of embryonal genitourinary tumor(s) with cerebral malformations has been reported in eight infants with variegated mosaic aneuploidy (VMA) and premature centromere division. The authors report a new case of cystic partially differentiated nephroblastoma and embryonal rhabdomyosarcoma associated with VMA, premature centromere division, microcephalus, Dandy-Walker malformation, and cataracts. Nonrandom involvement of the chromosomes was found in VMA of the lymphocytes and the skin fibroblasts. In the cultured nephroblastoma cells, hyperdiploidy involving the same group of chromosomes involved in VMA of the somatic cells was observed, suggesting their derivation from the aneuploid population of the somatic cells.

Abnormalities, Multiple↗
PubMed2002

Pathological issues of gastric and lower esophageal cancer: helicobacter pylori infection and its eradication.

Gastric carcinoma is thought to develop via the actions of inducers and promoters of carcinogenesis. Tryptophan in charred fish or animal meat, ultraviolet rays, and irradiation, which damage genes of normal cells, have long been regarded as inducers of carcinoma, and agents such as alcohol, tobacco, aflatoxin, and nitrosoamine as promoters, with tobacco having both activities. The interaction between these environmental factors, principally diet, and Helicobacter pylori (Hp) is important in the genesis of gastric carcinoma. In this report, the histopathological feature of the Hp gastritis-carcinoma sequence is outlined, and the pathological characteristics of gastroesophageal reflux disease (GERD) and endoscopically negative reflux disease (ENRD) and the risk factors for lower esophageal carcinoma after Hp eradicated status in particular are discussed regarding aspects of cell cycle-associated factors. We conclude that (1) Infection with Hp increases the risk of gastric cancer in two histological phenotypes (i.e., diffuse undifferentiated type and intestinal differentiated type). Excessive cell replication and interrupting the mucus secretion mechanism may result in a large proportion of cells with genetic abnormalities. (2) Genetic alterations in gastric carcinogenesis may differ from those in colonic carcinogenesis. (3) The degree of GERD in Japanese patients is milder than that in patients from Western countries, although the incidence of GERD increases the status after successful eradication of Hp. It is also possible that accumulation of genetic abnormalities increases the number of cardiac and lower esophageal cancers. Investigation of cell cycle factors in GERD including ENRD can be expected to reveal the risk of carcinogenesis.

Esophageal Neoplasms↗