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Biomedical subjects

Ryuzo Ueda

Publications and source records attributed to Ryuzo Ueda.

At least 127 records · Page 7Linked to original sources
PubMed2003

Monoamine oxidase polymorphisms and smoking behaviour in Japanese.

Although nicotine dependence is one of the primary reasons why smokers cannot quit smoking, nicotine cannot explain all of the psychopharmacological effects of tobacco smoke. Accumulating evidence points to potent inhibition of monoamine oxidase (MAO) which metabolizes neurotransmitters relating to additive behaviour. We have therefore investigated the association between smoking behaviour and MAO ( variable number of tandem repeat in the promoter region and A644G) polymorphisms. The genotypes were examined in 504 Japanese outpatients (217 men and 287 women) who visited Aichi Cancer Centre Hospital. The age-adjusted odds ratios (aORs) were estimated by a logistic model. Among males, we did not find a significant association of the smoking habit with either of the polymorphisms. The median Fargastrom test for nicotine dependence (FTND) score among male current smokers was significantly higher with than without the 4-repeat allele (5.8 and 4.7, respectively). The aOR of FTND 6 versus FTND 6 was 2.72 (95% confidence interval 1.13-6.50) for males with the 4-repeat allele. Among females, the aOR of being current smokers compared to never smokers was 0.49 (0.26-0.93) for individuals with the 4-repeat allele. Our results indicate that the polymorphisms of influence the smoking habit for female, as well as the nicotine dependence and smoking initiation for male smokers. These findings among male smokers support the view that MAO affects a smokers' requirement for nicotine and may explain why some people are predisposed to tobacco addiction and why some individuals find it difficult to stop smoking.

Adolescent↗
PubMed2003

Extragonadal germ cell tumors in Japan.

Extragonadal germ cell tumors (EGCT) represent only 2-5% of adult germ cell malignancies. Some publications from Asia have reported inferior treatment outcomes compared to data from an international study group. To ascertain whether this is generally the case, here we analyze treatment outcomes for 30 Japanese patients with EGCT. The medical records of 30 patients (25 nonseminomas and 4 pure seminomas) treated from 1992 to 2002 were reviewed retrospectively. All patients with seminoma achieved long survival except one who died of chemotherapy-related sepsis. Ten and 11 patients with EGCT presented with mediastinal and retroperitoneal primary sites, respectively. The 5-year overall survival (OS) and progression-free survival (PFS) for nonseminoma was 71% and 42%, respectively. The 5-year OS and PFS was 60% and 44%, respectively, for 10 patients with mediastinal nonseminoma, and 91% and 48%, respectively, for patients with retroperitoneal nonseminoma. Tumor marker values on day 7 were available for 19 patients. Among the 19 patients in whom AFP or beta-HCG were measured on day 7, the values had declined in 12 patients and were transiently elevated in 7 patients compared to pretreatment values. The transient elevations of tumor markers were significantly associated with poor OS (P = 0.02) and PFS (P = 0.008). The treatment outcome of Japanese patients with EGCT seemed to be comparable to that reported from international studies, suggesting no difference between ethnic groups. Transient tumor marker elevations on day 7 predict poor survival in EGCT patients and may be a useful parameter for identifying patients requiring more aggressive treatment.

Adolescent↗
PubMed2003

Frequent occurrence of CCND1 deregulation in patients with early stages of plasma cell dyscrasia.

Chromosomal translocations involving the immunoglobulin heavy chain gene (IgH) and nonrandom protooncogene loci are the hallmark of genetic alterations found not only in multiple myeloma (MM), but also in premalignant stages of MM, including monoclonal gammopathy of undetermined significance (MGUS) and smoldering myeloma (SMM). We studied the frequency of IgH (14q32) rearrangements and their partner chromosomes in 16 Japanese patients with MGUS (13 cases), and SMM (3 cases) by means of interphase double-color fluorescence in situ hybridization (DCFISH) applied to purified plasma cells and using CD138-bead selection. IgH rearrangement was recognized in nine of the patients (56.3%). Protooncogene loci juxtaposed to IgH were identified in seven cases including CCND1 (11q13) in six cases and FGFR3 (4p16) in one. Four out of the six t(11;14)-positive cases showed nuclear staining of the cyclin D1 protein, whereas none of the seven t(11;14)-negative cases did. Moreover, neither MUM1(6p25)-IgH nor MAFB(20q11)-IgH fusion signals were observed. This suggests to us that cyclin D1 deregulation due to the presence of t(11;14) is involved in the early development of plasma cell neoplasms, and that this event alone is not enough for the development of symptomatic myeloma.

Adult↗
PubMed2003

Long-term effects of donepezil on P300 auditory event-related potentials in patients with Alzheimer's disease.

The P300, one of the cognitive event-related potentials (ERPs) of the cerebral cortex, reflects the functioning of the neurochemical system involved in cognitive processes. We investigated clinical significance of the components of auditory P300 ERPs, in comparison with neuropsychologic tests including the Mini-Mental State Examination and the Japanese version of the Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-J cog), for evaluating of the effect of donepezil (DPZ) (5 mg daily for 6 months), an acetylcholinesterase inhibitor, in patients with Alzheimer's disease (AD). Reduction of P300 latency associated with a parallel improvement of ADAS-J cog scores was observed after administration of 5 mg/day of DPZ in patients with AD. P300 latency gives very useful information on the progression of AD, especially in the longitudinal follow-up of patients with AD during treatment with DPZ acting on cholinergic pathways.

Aged↗
PubMed2003

Circulating thrombomodulin levels are related to latent progression of atherosclerosis in hypertensive patients.

The present study was designed to test the hypothesis that circulating levels of thrombomodulin are elevated in patients with hypertension in proportion to the severity of the vascular damage. A cross-sectional study was carried out using a population consisting of 96 patients with essential hypertension without clinically evident cardiovascular disease (mean age: 65 +/- 10 years) and 99 healthy normotensive control subjects (64 +/- 9 years). Blood was sampled and serum concentrations of soluble thrombomodulin were measured using an enzyme immunoassay method. We calculated the ratio of the concentration of thrombomodulin to that of creatinine, because soluble thrombomodulin is excreted by the kidney and the serum level of thrombomodulin was correlated with that of creatinine (p < 0.05). The association between the ratio and other clinical variables was investigated. The ratio of the thrombomodulin to creatinine concentrations was higher in hypertensive (29.3 +/- 10.9) than in control subjects (24.4 +/- 5.9; p < 0.0001). Systolic blood pressure was correlated with the ratio but the ratio showed no correlation with serum lipid levels when analyzed using data from all subjects. In hypertensive patients, the ratio correlated with the grade of sclerotic, but not hypertensive, changes in the fundus oculi (Scheie's classification, p < 0.001). Furthermore, the ratio correlated with brachial-ankle pulse wave velocity (p < 0.001). However, no correlation was detected between the ratio and blood pressure. These results suggest that circulating levels of thrombomodulin are elevated in hypertensive patients as compared to normotensive subjects and that the thrombomodulin level may be a molecular marker of the latent progression of atherosclerosis in hypertensive patients.

Aged↗
PubMed2003

Candesartan reduces oxidative stress and inflammation in patients with essential hypertension.

The present study was designed to test the hypothesis that blockade of angiotensin II type-1 receptors reduces oxidative stress and inflammation in patients with essential hypertension. The study population comprised 132 hypertensive patients, some receiving and others not receiving medical treatment. At enrollment their systolic and/or diastolic blood pressures were > or = 140 and/or > or = 90 mmHg, respectively. The serum concentration of C-reactive protein, and the urine concentrations of 8-epi-prostaglandin F2alpha and 8-hydroxydeoxyguanosine were measured at baseline and after 12 weeks of treatment either with an angiotensin II type-1 receptor blocker, candesartan (8 mg daily) (age 64 +/- 12 years; male/female 28/39; n = 67), or other antihypertensive agents that do not block the renin-angiotensin system (age 65 +/- 10 years, male/female 25/40, n = 65). Candesartan reduced the levels of C-reactive protein (from 0.07 +/- 0.04 [median value +/- median absolute deviation] to 0.06 +/- 0.03 mg/dl, p < 0.0001), 8-epi-prostaglandin F2alpha (from 210 +/- 92 to 148 +/- 59 pg/mg creatinine, p < 0.0001), and 8-hydroxydeoxyguanosine (from 5.7 +/- 1.9 to 4.0 +/- 1.3 ng/mg creatinine, p < 0.0001), while the levels of these markers were not altered after the treatment with other antihypertensive agents. Blood pressure decreased by a similar amount in both groups, and the reductions in the levels of the markers did not correlate with that of blood pressure. These results suggest that candesartan reduces oxidative stress and inflammation in hypertensive patients independently of its effects on blood pressure. This may provide useful information for determining therapeutic strategies to minimize tissue injury by inflammation and oxidative stress in hypertensive patients.

Adult↗
PubMed2003

Myofibroblasts proliferation of idiopathic and collagen vascular disorders associated nonspecific interstitial pneumonia.

Nonspecific interstitial pneumonia (NSIP) has been recognized as a separate histological classification of interstitial lung disease. Similar features are found not only in idiopathic NSIP, but also in NSIP associated with collagen vascular disorder (CVD-NSIP). We examined the clinical symptoms, laboratory findings, and prognosis of 13 cases of idiopathic NSIP and 11 cases of CVD-NSIP. Immunohistochemical staining was performed using the streptavidin/biotin/peroxidase method with anti-alpha-smooth muscle actin antibody. No differences in the distribution of clinical features, laboratory findings, and prognosis were observed between idiopathic NSIP and CVD-NSIP. In immunohistochemical staining of the fibrosing areas, myofibroblasts were observed in 7 of 13 idiopathic NSIP cases, but in 10 of 11 CVD-NSIP cases. With regards to intra-alveolar organization, myofibroblasts were observed in all 10 CVD-NSIP cases, but they were observed in only 2 of 9 idiopathic NSIP cases. We found a significantly higher myofibroblast proliferation in the intra-alveolar organization of CVD-NSIP compared to idiopathic NSIP. Clinically, idiopathic NSIP and CVD-NSIP are similar, but are pathologically different.

Aged↗
PubMed2003

[A case of sarcoidosis with rheumatic features (Löfgren's syndrome)].

Rheumatoid arthritis was diagnosed in a 30-year-old woman with erythema nodosum and arthritic symptoms since 1994, and she was treated with anti-rheumatic agents. Mediastinal and bilateral hilar lymphadenopathy and abnormal pulmonary shadows were detected in 1996, and she was admitted to our hospital in 1997. We also recognized the elevation of ACE and lysozyme, and found granulomas in a transbronchial lung biopsy and an arthrosis synovia biopsy. From these findings, sarcoidosis was diagnosed. Sarcoidosis demonstrating erythema nodosum, arthritis, and bilateral hilar lymphadenopathy is called Löfgren's syndrome. In Caucasians, Löfgren's syndrome is frequently encountered, but it is rare in Japanese. Our case had coexisting arthrosis symptoms, and satisfied the diagnosis criteria of rheumatic arthritis. Therefore, the differential diagnosis was important. We emphasize that it is necessary to consider Löfgren's syndrome when diagnosing patients with rheumatic features, even in Japan.

Adult↗
PubMed2003

Regression of esophageal papillomatous polyposis caused by high-risk type human papilloma virus.

Esophageal squamous papilloma is an uncommon benign squamous epithelial polypoid tumor and is usually identified as a solitary lesion in the lower esophagus. Chronic mucosal irritation and infection with human papilloma virus (HPV) are two proposed etiologies. However, the natural history of esophageal squamous papilloma is unknown, and whether it can develop to esophageal cancer is also controversial. The authors report a case of esophageal papillomatous polyposis in which the presence of high-risk HPV DNA was proven by type-specific polymerase chain reaction (PCR). The patient was an 83-year-old man referred to our hospital with complaints of nausea and dysphagia. Esophago-gastroduodenoscopy (EGD) was carried out, and diffuse polyposis of the entire length of the esophagus and stenosis in the antrum of the stomach were revealed. Histological examination of the tissue confirmed the diagnosis of squamous papilloma of the esophagus and poorly differentiated adenocarcinoma of the stomach. Furthermore, HPV type-specific PCR was carried out in the biopsied specimens, and HPV type-16 and type-33 were detected. One month after total gastrectomy performed for the treatment of gastric cancer, follow-up EGD was carried out, and complete regression of the esophageal polyps was noted. This case is rare and supports the evidence that esophageal squamous papilloma is caused by infection with HPV. Furthermore, this case also reflects a unique aspect of the natural history of esophageal papillomatous polyposis.

Adenocarcinoma↗
PubMed2003

Transforming growth factor beta1 gene polymorphism in patients with systemic sclerosis.

OBJECTIVE: To determine whether transforming growth factor beta1 (TGFbeta1) gene DNA polymorphism is associated with pathogenesis in the fibrosis of patients with systemic sclerosis (SSc). METHODS: Eighty-seven Japanese patients with SSc including 30 with diffuse type and 57 with limited type together with 110 unrelated controls were investigated. Pulmonary fibrosis was determined in 34 SSc patients using high-resolution chest computed tomography. TGFbeta1 genetic polymorphisms were analyzed in 2 loci; T869C (Leu10Pro) in codon 10 at exon 1, and C-509T in the promoter region using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: Neither the genotype of T/C polymorphism in T869C nor C/T polymorphism in C-509T revealed any difference in distribution between SSc and controls. In the group of SSc patients with pulmonary fibrosis, a weak but significantly high frequency (p = 0.05) of TC+CC (the presence of C allele) in T869C, and CT+TT (the presence of T allele) in C-509T was found. Compared with controls, the pulmonary fibrosis group showed no difference in the highly frequent alleles. CONCLUSION: Our results suggest that TGFbeta1 polymorphisms do not play a role in the pathogenesis of SSc, even though there remains the possibility of a risk factor for genetic susceptibility to pulmonary fibrosis.

Adult↗
PubMed2003

Increased endogenous endothelin-1 in coronary circulation is associated with restenosis after coronary angioplasty.

BACKGROUND: The relationship between vasoactive substances, including endothelin-1, nitric oxide, serotonin, angiotensin II and noradrenaline, and coronary restenosis after percutaneous transluminal coronary angioplasty (PTCA) is not clear. OBJECTIVE: To determine whether any vasoactive substance may be a marker of coronary restenosis after PTCA. METHODS: Twenty-nine patients with angina pectoris underwent elective PTCA. Three months after PTCA, coronary angiography was performed again to study the patency of the lesions. Seven patients had coronary restenosis (greater than 50% stenosis) (restenosis group) and the rest of the patients were without restenosis (patency group). Their blood samples were obtained from the coronary sinus before, immediately after and three months after PTCA. RESULTS: Endothelin-1 levels obtained immediately after PTCA (3.44+/-0.26 pg/mL) and three months after PTCA (3.57+/-0.29 pg/mL) were significantly higher than those obtained before PTCA (3.00+/-0.26 pg/mL) in the restenosis group, but not in the patency group (3.34+/-0.15 pg/mL, 3.02+/-0.17 pg/mL and 3.14+/-0.18 pg/mL, respectively). A transient decrease in nitrite/nitrate levels was observed immediately after PTCA in both groups. The serotonin levels three months after PTCA were significantly decreased in the patency group, but not in the restenosis group, and the levels of angiotensin II and noradrenaline did not change in either group throughout the study. CONCLUSIONS: Among several vasoactive substances, endothelin-1 seems to be associated with the process of coronary restenosis after PTCA. Increased endothelin-1 levels in the coronary circulation after PTCA may indicate an increased risk of coronary restenosis.

Aged↗
PubMed2003

[A case of bacteria-associated hemophagocytic syndrome induced by nosocomial pneumonia].

This study reviews the case of a 67-year-old man who initially presented with high fever and dyspnea. He was subsequently admitted for treatment of pneumonia. On admission, severe leucopenia and thrombopenia were observed in the peripheral blood, with significant phagocytosis of hematopoietic cells including erythroblasts and leukocytes by macrophages in the bone marrow. Following the administration of antibiotic therapy, an improvement in pneumonia and cytopenia symptoms was noted. Clinically, we diagnosed this case as bacteria-associated hemophagocytic syndrome (BAHS) with community-acquired pneumonia. In general BAHS is seen following severe hematologic disease or pneumonia, and so the treatment of BAHS is quite difficult. This particular case had no additional hematologic disorder, and all presenting symptoms of BAHS were resolved immediately following the improvement in pneumonia with post-antibiotic therapy.

Aged↗
PubMed2002

Mechanism of constitutive activation of FLT3 with internal tandem duplication in the juxtamembrane domain.

Internal tandem duplication (ITD) of the juxtamembrane (JM) domain of FLT3 is the most frequent mutation in human acute myeloid leukemia, and is significantly associated with leukocytosis and a poor prognosis. Previously we reported that FLT3 with ITD (FLT3/ITD) formed a homodimer and was autophosphorylated on tyrosine residues, while the mechanism remains unclear. In this study, we elucidated the role of the JM domain in FLT3 activation. Mutant FLT3 with not only ITD but also an elongating or shortening JM domain transformed murine IL3-dependent myeloid progenitor cell line 32D regardless of the tyrosine residues in the JM domain. These mutant FLT3s were constitutively tyrosine phosphorylated and activated signal-transduction molecules such as SHC, MAP kinase and STAT5a. Notably, co-transfection of the truncated FLT3/ITD lacking kinase and C-terminal domains with the wild type (Wt)-FLT3 into 32D cells resulted in the autonomous proliferation. In these cells, truncated FLT3/ITD generated a hetero-complex with Wt-FLT3 and Wt-FLT3 was constitutively tyrosine phosphorylated. These findings indicate that the FLT3 JM domain plays an important role in receptor activation, and that the length-mutated JM domain induces ligand-independent receptor activation but also activates Wt-FLT3 in a trans-manner.

Amino Acid Sequence↗
PubMed2002

De novo CD5+ diffuse large B-cell lymphoma: a clinicopathologic study of 109 patients.

De novo CD5+ diffuse large B-cell lymphoma (CD5+ DLBCL) is known to have phenotypically and genotypically different characteristics than CD5- DLBCL and mantle cell lymphoma (MCL). To further characterize CD5+ DLBCL, 109 patients with CD5+ DLBCL were reviewed, and the results were compared with those of 384 CD5- DLBCL and 128 cyclin D1+ MCL patients. Patients with CD5+ DLBCL showed a higher age distribution (median, 66 years; P =.0083) and a female predominance (male-female ratio, 49:60, P =.011) compared with those with CD5- DLBCL. CD5+ DLBCL was more closely associated with many aggressive clinical features or parameters than CD5- DLBCL: 69% older than 60 years (P =.039), 34% with performance status greater than 1 (P =.0016), 69% with serum lactate dehydrogenase level higher than normal (P <.0001), 62% with stage III/IV disease at diagnosis (P =.0023), 35% with more than one extranodal site (P =.023), and 40% with B symptoms (P =.0031). The overall International Prognostic Index score was thus significantly higher for the patients with CD5+ DLBCL than for those with CD5- DLBCL (P =.00005). The most frequent site of extranodal involvement was bone marrow (28%), a higher frequency than that for CD5- DLBCL (P <.0001) but lower than that for cyclin D1+ MCL (P =.0015). Histopathologically, CD5+ DLBCL showed centroblastic morphology except for 3 patients with immunoblastic disease, and interfollicular growth pattern (7%) and intravascular or intrasinusoidal infiltration (19%) were observed. Immunophenotypically, CD5+ DLBCL was characterized by a CD5+CD10-CD19+CD20+CD21-CD23- cyclin D1- phenotype and a predominance of surface IgMkappa. Of particular interest is that CD5+ DLBCL was characterized by a survival curve significantly inferior to that for patients with CD5- DLBCL (P =.0026). These findings suggest that CD5+ DLBCL may constitute a unique subgroup of DLBCL.

Adolescent↗
PubMed2002

Hepatitis B virus genotypes in Uzbekistan and validity of two different systems for genotyping.

Hepatitis B virus (HBV) has been classified into seven genotypes, designated A-G. The HBV genotype has a characteristic geographical distribution. The Republic of Uzbekistan is located in the heart of Asia and has been considered to be a region with high endemicity of hepatitis viruses. However, the present distribution of hepatitis virus infection in this region is unknown. The aim of this study was to investigate the distribution of HBV genotypes and to elucidate the validity of two genotyping systems in Uzbekistan. Fifty-four patients with hepatitis B surface antigen were investigated. HBV genotypes were determined by two methods: one based on restriction fragment length polymorphism (RFLP) targeting to S region, and another on enzyme-linked immunosorbent assay (ELISA), using monoclonal antibodies to pre-S2 region. Seven (13%) and 47 (87%) of the 54 subjects were classified into genotypes A and D, respectively. Dual infection of two viral populations of the same genotype was observed in one subject. No significant difference of ALT level (203.3 +/- 244.7 vs. 190.6 +/- 39.5) and HBeAg (42.9% vs. 42.6%) were found between genotypes A and D. In this study, the validity of the genotyping systems in this region was confirmed.

Base Sequence↗