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Y Ueda

Publications and source records attributed to Y Ueda.

At least 505 records · Page 28Linked to original sources

Coexpression of trk family members and low-affinity neurotrophin receptors in rat dorsal root ganglion neurons.

We examined the colocalization of trk family and low-affinity neurotrophin receptor (LANR) mRNAs by means of in situ hybridization histochemistry in rat dorsal root ganglion (DRG) neurons. About 35-40%, 5%, and 15-20% of DRG neurons were positive for trkA, trkB, and trkC mRNAs, respectively. Each member of the trk family was coexpressed with LANR. The trkB mRNA-expressing neurons essentially lacked trkA and trkC mRNAs, and most of trkA and trkC mRNAs-expressing neurons (85-90%) belonged to different subpopulations, suggesting that they are involved in different functions.

Animals↗

Role of amino acids in salivation and the localization of their receptors in the rat salivary gland.

The distribution of gamma-aminobutyric acid (GABA) receptor subunits such as GABAAR-gamma 1 and GABAAR-gamma 2, and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) type receptor subunits such as GluR-1, GluR-2/3 and GluR-4, and N-methyl-D-aspartic acid (NMDA) type subunits such as NR1 were investigated by immunocytochemistry. Furthermore, the roles of these amino acids, GABA and glutamate, on salivation were analyzed in the rat submandibular and sublingual glands. Some similarities were observed in the distribution patterns of GABAA type receptors and AMPA receptors. In the submandibular ganglion cells, collecting ducts and striated ducts, these subunits were expressed strongly; however, there were some differences in their expression patterns between the submandibular and sublingual gland acinar cells. Since these receptor subunits were expressed in the acinar cell bodies of the submandibular gland, they were not expressed in the acinar cells but were expressed in the myoepithelial cells in the sublingual gland. On the other hand, no NR1 expression was observed. To examine the roles of GABA and glutamate in salivation, the submandibular and sublingual glands were perfused partially with Ringer's solution via a facial artery to avoid systemic influence, and substrates were infused into the perfusion solution. No salivary secretion was evoked by GABA or glutamate infusion in the absence of electrical stimulation (2-3 V, 5 ms, 20 Hz). Salivary flow evoked by electrical stimulation of the chorda-lingual nerve caused significant inhibition by GABA (10(-6), 10(-5), 10(-4) and 10(-3) M) and the GABAAR agonist muscimol 10(-3) and 10(-6) M) (n = 6, P < 0.05). Such GABA-induced inhibition was antagonized by the GABAAR antagonists bicuculline (BCC; 10(-6) and 10(-3) M) and picrotoxin (PTX; 10(-6) and 10(-3) M). On the other hand, salivary flow evoked by electrical stimulation (8-10 V, 5 ms, 20 Hz) of the superior cervical ganglion (SCG) was not affected by GABA. While high doses of glutamate (10(-1) M) and NMDA (10(-1) M) showed no effects on salivary flow despite application of electrical stimulation, AMPA at a high concentration (10(-1) M) significantly inhibited salivary secretion (n = 6, P < 0.05). These studies revealed that inhibitory and excitatory amino acid receptors such as GABAA and AMPA type receptors are coexpressed in the rat salivary glands, and that GABA inhibits salivary secretion via GABAA receptors which may act with acetylcholine. However, the role of glutamate in salivation remains unclear despite the presence of AMPA type receptors. The present findings suggest that glutamate does not act alone but with other substances such as peptides and/or other amino acids.

Animals↗

Simultaneous monitoring of the seizure-related changes in extracellular glutamate and gamma-aminobutyric acid concentration in bilateral hippocampi following development of amygdaloid kindling.

We simultaneously monitored the seizure-related changes in extracellular hippocampal glutamate (Glu) and gamma-aminobutyric acid (GABA) concentration in brain dialysates in order to clarify the role of Glu and GABA in the development of kindling. Brain dialysates were collected every 5 min from 10 min prior to 80 min after stimulus in the three developing conditions consisting of pre-kindling state, stage 3 (C-3), and five consecutive stage 5 (5*C-5) following kindling in the same rat. Extracellular Glu level increased rapidly, lasting for only 5 min after stimulus. The post-stimulus ratio of Glu increase in partially kindled rats (C-3) was 2.5-3.5 times of the baseline, and in fully kindled rats it was about 5 times of the baseline. Extracellular GABA concentration enhanced gradually, reaching a plateau level at 15-20 min and lasting for several hours after stimulus at each stage. The enhancement of GABA level was about 1.5 times of the baseline in partially kindled stage, and was about 2.5 times of the baseline in fully kindled stage. There was no significant difference between the two hemispheres with respect to either the time-course or the magnitude of Glu and GABA increase respectively. These data show that progressive, transient and stimulus-induced enhancement of extracellular Glu levels combined with long-lasting elevation of extracellular GABA levels in the bilateral ventral hippocampi results in imbalance between the excitatory and inhibitory neuronal systems, causing excessive propagation of seizure activity, culminating in the secondary generalized seizure of amygdaloid kindling.

Amygdala↗

Neurofibromatosis 1 gene (NF1) mutation is a rare genetic event in myelodysplastic syndrome regardless of the disease progression.

Neurofibromatosis 1 gene (NF1) is a tumor suppressor gene and the product of which down-regulates Nras protein by its GTPase activating protein-related domain (NF1-GRD). Although the incidence of NF1 mutation was reported to be rare in the chronic phase of myelodysplastic syndrome (MDS), there have been no previous reports on its configuration in patients showing the disease progression. We examined NF1 in 50 patients with MDS including 9 who had progressed to more advanced stages and 16 to acute leukemia. Six patients had an Nras mutation. We carried out allele specific restriction analysis (ASRA) to detect a mutation at the first nucleotide A of codon 1423 (AAG), a mutational hot spot. We also employed a polymerase chain reaction mediated single strand conformation polymorphism (PCR-SSCP) method to confirm the result of ASRA and to detect a point mutation in other sequences of FLR exon. In consequence, ASRA disclosed wild type configuration and PCR-SSCP showed no aberrant band in any sample examined whether the samples harboured an Nras mutation or not. We conclude that NF1 mutation does not play a crucial role in the development and the progression of MDS.

Base Sequence↗

Double mutations of the N-ras gene in a patient with acute myelomonocytic leukemia.

We report a patient with acute myelomonocytic leukemia (AMMoL) who showed two independent point mutations of the N-ras gene at codons 12 and 13. Longitudinal analysis revealed that one mutation at codon 13 was detectable throughout his disease course and the other at codon 12 emerged as a second mutation 14 months after the diagnosis was made, at the refractory stage. Cloning to vector and subsequent sequencing confirmed that these mutations occurred in different alleles. Chromosome findings showed a simple abnormal karyotype at presentation and further karyotypic aberrations during his disease course, concomitantly with the second mutation of the N-ras gene. These findings revealed a close relationship among the disease progression, karyotypic evolution and a newly-appearing N-ras mutation.

Aclarubicin↗

Coexistent myelodysplastic syndrome and non-Hodgkin lymphoma. Report of a case and review of the literature.

The patients with a hematopoietic neoplasm can develop myelodysplastic syndrome following chemotherapy. We report herein a case of non-Hodgkin B-cell lymphoma and refractory anemia with ringed sideroblasts. Absence of the preceding chemotherapy establishes the true coincidence of the two disorders. We review 25 similar cases reported in the last 11 years and discuss the possible etiology of coexistence.

Aged↗

Early and late results of repair of tetralogy of Fallot with subarterial ventricular septal defect. A comparative evaluation of tetralogy with perimembranous ventricular septal defect.

Between November 1966 and December 1990, 511 pediatric patients with tetralogy of Fallot underwent corrective operation at Tenri Hospital. There were 78 patients with subarterial ventricular septal defect. Mean age at repair was 5.6 +/- 3.3 years. The method of right ventricular outflow tract reconstruction was simple infundibulectomy in 14 patients, right ventricular ventricular outflow patch in 36, and transannular patch in 28. There were 7 (9.0%) early deaths as a result of low cardiac output syndrome and acute renal failure. The pressure ratio of the right ventricle to the left ventricle was 0.62 +/- 0.18 during the early postoperative catheterization. Follow-up was achieved for 442.6 patient-years and ranged from 0.5 to 27 years, with an average of 8.5 +/- 6.7 years. There were three late deaths (2 cardiac and 1 noncardiac). Actuarial survival was 94.8% +/- 4.0% at 20 years. Catheterization during late follow-up (6.8 +/- 4.7 years after repair) was done in 53 patients and the pressure ratio of the right ventricle to the left ventricle was 0.48 +/- 0.21. Fifteen patients underwent subsequent operation because of residual lesions, including ventricular septal defect in four patients, pulmonary stenosis in nine, combined ventricular septal defect and pulmonary stenosis in one, and pulmonary regurgitation in one, with no mortality. Actuarial rate of freedom from reoperation was 71.1% +/- 8.0% at 10 years and 58.8% +/- 16.8% at 20 years. Patients with tetralogy and subarterial ventricular septal defect were more likely to have the development of residual obstruction at the level of the pulmonary valve anulus after repair than were those with tetralogy and perimembranous ventricular septal defect.

Abnormalities, Multiple↗

New aspects of cell biology in osteosarcoma.

Among the solid tumors of childhood and adolescence, osteosarcoma (OS) represents the most prominent example of efficient aggressive chemotherapy with secondary surgical therapy. A specific subclassification of the tumor is indispensable and must include recent results of cell biology. The co-distribution of different collagen types I-VI reflects the diverse differentiation of osteosarcoma cells, supporting the concept of a pluripotent mesenchymal cell to be the stem cell of the tumor. In contrast, osteonectin (SPARC) may not be considered as a reliable marker for osteosarcoma. The experience of special proteins being secreted by osteosarcoma cells is rather limited. Detailed molecular biological studies are still lacking. A loss of alleles on chromosome 17, particularly in the defined region 17p 13, can be observed in more than 75% of all OS, suggesting the contribution of a tumor suppressor gene, p53, located in that region. It is a 53 kd nucleophosphoprotein binding the major transforming protein, the large T antigen of Simian Virus 40. Immunohistological results showed positive staining with the antibody Pab 240 in 13 of 18 cases. In one osteoblastic OS, a novel splice mutation resulting in a fusing of exon 5 directly to exon 7 was detected. RB1 gene is also of major importance for the tumorigenesis of OS. The multidrug resistance (mdr) is associated with a membrane-bound channel-forming transport protein, the P-glycoprotein. It is a conserved plasma membrane component of about 170 kd. Both the human isoforms mdr 1 and mdr 3 are localised in the long arm of chromosome 7.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Neoplasms↗

Continuous retrograde cerebral perfusion aids repair of aortic laceration during sternal re-entry.

We successfully repaired an anticipated large laceration of the ascending aorta occurring during sternal re-entry in a 68-year old woman undergoing replacement of a prosthetic aortic valve. Cerebral protection was ensured by using continuous retrograde cerebral perfusion via femoro-femoral bypass with deep hypothermia. The cooling time was 20 minutes. The minimum nasopharyngeal temperature was 15 degrees C and the duration of the retrograde perfusion was 11 minutes at a rate of 600 ml per minute. The postoperative course was uneventful and no neurological deficits occurred.

Aged↗

Establishment and characterization of an antihuman thyrotropin (TSH) receptor-specific CD4+ T cell line from a patient with Graves' disease: evidence for multiple T cell epitopes on the TSH receptor including the transmembrane domain.

From the peripheral lymphocytes of a patient with Graves' disease, we established a T cell line using its reaction to a pool of 49 synthetic peptides corresponding to the entire human thyrotropin receptor (TSHR) sequence. This T cell line showed a specific response to the pool of peptides in a microproliferation assay (stimulation index: 4.8). Flow cytometry analysis revealed that the cell surface markers were CD4+ CD8-, T cell receptor (TcR) alpha beta+, and Tcr gamma delta-. To investigate T cell epitopes on TSHR, the T cell line reacted well against three groups: the N-terminal (amino acids 31-169) and C-terminal (338-420) regions of the extracellular domain and the N-terminal half (441-661) of the transmembrane domain of the receptor. This suggests a multiplicity of T cell epitopes on the TSHR, and was further supported by analysis of TcR gene expression in the cell line that showed the expression of 5 V alpha genes; V alpha-1, 2, 10, 20, and w25. In conclusion, the results of the present study indicated multiple T cell epitopes on the TSHR molecule including the transmembrane domain.

Adult↗

CD28 ligands CD80 (B7-1) and CD86 (B7-2) induce long-term autocrine growth of CD4+ T cells and induce similar patterns of cytokine secretion in vitro.

The interaction of CD28 and its ligands is critical for antigen-induced T cell activation. Recent studies have demonstrated the existence of at least two members of the B7 receptor family. In this report, the co-stimulatory signals provided by CD80 (B7-1) or CD86 (B7-2) were compared to CD28 ligation by mAb. We demonstrate that the kinetics of induction of T cell proliferation after anti-CD3 stimulation was similar regardless of the form of co-stimulation. Similarly, B7-1 and B7-2 could both maintain long-term expansion of CD4 cells. The co-stimulatory effects of both B7-1 and B7-2 were dependent on CD28 cross-linking, based on complete inhibition of proliferation by CD28 antibody Fab fragments. Co-stimulation with B7-1 and B7-2 induced high levels of cytokine secretion by resting T cells, and the effects of B7-1 and B7-2 could not be distinguished. This conclusion is based on analysis of the initial activation of CD28+ T cells, as well as T cell subpopulations consisting of CD4+ and CD8+ T cells. Both B7-1 and B7-2 could elicit IL-4 secretion from CD4+ T cells while anti-CD28 antibody induced substantially less IL-4 secretion. Furthermore, both B7-1 and B7-2 could stimulate high levels of IFN-gamma and IL-4 from CD4+CD45RO+ cells, while neither B7 receptor could co-stimulate IFN-gamma and IL-4 secretion from CD4+CD45RA+ T cells. B7-1 and B7-2 could, however, co-stimulate CD4+CD45RA+ T cells to secrete IL-2. By contrast, when previously activated T cells were tested, re-stimulation of CD4+ T cell blasts with B7-1 or B7-2 resulted in higher secretion of IL-4 and IL-5 than anti-CD28, while re-stimulation with anti-CD28 antibody maintained a higher level of secretion of IL-2 and IFN-gamma than B7-1 or B7-2. These observations may have important implications because they suggest that the manner of CD28 ligation can be a critical determinant in the development of cytokine secretion that corresponds to Th1- and Th2-like patterns of differentiation. Together these observations suggest that there are no intrinsic differences between B7-1 and B7-2 in their ability to co-stimulate the populations of cells that we have tested.

Animals↗

Both CD28 ligands CD80 (B7-1) and CD86 (B7-2) activate phosphatidylinositol 3-kinase, and wortmannin reveals heterogeneity in the regulation of T cell IL-2 secretion.

In this report, the co-stimulatory signals provided by CD80 (B7-1) or CD86 (B7-2) were compared to CD28 ligation by mAb. We demonstrate that while both anti-CD3 and anti-CD28 antibodies induced activation of phosphoinositide (PI) 3-kinase, the kinetics of activation differed. Anti-CD28 produced a sustained activation of PI 3-kinase while anti-CD3 induced activation was transient. Both B7-1 and B7-2 could induce prolonged activation of PI 3-kinase. The co-stimulatory effects of B7-1 and B7-2 were dependent on CD28 cross-linking, based on complete inhibition of PI 3-kinase activation by CD28 antibody Fab fragments. While Jurkat T cells co-stimulated with anti-CD3 and B7-1 or B7-2 secreted high levels of IL-2, there were distinct effects of anti-CD28 mAb and B7-1 or B7-2 on IL-2 secretion in conjunction with protein kinase C activation. To assess functional effects of CD28 ligation, pharmacologic inhibitors of PI 3-kinase were evaluated. In Jurkat cells, efficient inhibition of PI 3-kinase activation after B7-2 stimulation was achieved using wortmannin; however, we observed a surprising increase in IL-2 secretion after B7 or anti-CD28 stimulation. The effect of wortmannin was concentration dependent. Moreover, the effect was specific for receptor-mediated activation as wortmannin did not enhance phorbol ester plus ionomycin-induced IL-2 secretion. Another inhibitor of PI 3-kinase, LY294002, also resulted in augmentation of anti-CD28-induced IL-2 secretion by Jurkat cells. The effects of wortmannin on IL-2 secretion were also examined in primary T cells. In marked contrast, wortmannin resulted in a potent inhibition of anti-CD3 plus B7-1 or anti-CD28-induced IL-2 secretion while phorbol ester plus ionomycin-induced IL-2 secretion was wortmannin resistant. Together these observations demonstrate that signal transduction by both B7-1 and B7-2 involves PI 3-kinase, and that PI 3-kinase or other wortmannin-sensitive targets are important for IL-2 secretion. Finally, treatment of Jurkat cells with PI 3-kinase inhibitors alone was sufficient to induce low levels of IL-2 secretion. This is consistent with the notion that a wortmannin-sensitive target such as PI 3-kinase may down-regulate IL-2 secretion in Jurkat cells.

Androstadienes↗

Isolation and characterization of Rhodovulum strictum sp. nov. and some other purple nonsulfur bacteria from colored blooms in tidal and seawater pools.

Several strains of phototrophic purple nonsulfur bacteria were isolated from colored blooms occurring in tidal and seawater pools in Japan. All of these isolates had ovoid to rod-shaped cells that were motile by means of single polar flagella and contained vesicular intracytoplasmic membranes together with bacteriochlorophyll a and carotenoids of the spheroidene series. They produced ubiquinone 10 as the major quinone and contained straight-chain fatty acids, with C18:1 predominating. They were mesophilic, halophilic, and photoheterotrophic, utilized sulfide and thiosulfate as electron donors for phototrophic growth, and photoassimilated a wide variety of organic compounds as carbon sources. Our results suggested that all of these isolates are members of the recently described genus Rhodovulum. The isolates were classified into four groups (designated groups I through IV) on the basis of phenotypic and genotypic data. The group I isolates, which were the most abundant purple nonsulfur bacteria recovered from the blooms, grew in the presence of NaCl concentrations ranging from 0.5 to 3.0% (optimum NaCl concentration, 0.8%) and at pH values ranging from 7.5 to 9.0 (optimum pH, 8.0 to 8.5). On the basis of these unique physiological traits, together with genotypic and phylogenetic data, we propose that the group I isolates should be classified as members of a new species, Rhodovulum strictum. The group II isolates were identified definitely as Rhodovulum sulfidophilum, and the group III and IV isolates were phenotypically most similar to R. sulfidophilum and Rhodovulum adriaticum, respectively, but could be differentiated from these species by DNA-DNA pairing data.

Bacteria↗

Identification and characterization of the thymidine kinase gene of Yaba virus.

DNA of Yaba virus, a member of the poxviruses, was mapped by cross-hybridization between fragments of various restriction enzymes. The genome was approximately 135 kb in length and possessed two characteristic features of poxviruses: cross-links and inverted terminal repeats at both termini. Hybridization of fragments of Yaba virus DNA to known vaccinia virus DNA fragments indicated that the thymidine kinase (TK) gene mapped within the 0.9 kb XhoI-HincII fragment between 52.5 and 53.5 kb from the left end of the genome. The fragment could rescue the TK+ phenotype in TK- cells preinfected with a TK vaccinia virus mutant. Nucleotide sequencing of the fragment revealed an ORF capable of encoding 181 amino acids. The sequence TAAAAATGAAAAATTA upstream of the ORF was considered to be the promoter and the downstream sequence TTTTTAT to be the early transcription termination signal. These sequences are in good accord with the consensus regulatory sequences for the expression of early genes of other known poxviruses. The amino acid sequence similarity among the poxvirus TK genes suggests that Yaba virus is most closely related to swinepox virus and less similar to fowlpox virus.

Amino Acid Sequence↗

Detection of astroviruses from stool samples in Japan using reverse transcription and polymerase chain reaction amplification.

We developed a reverse transcription and polymerase chain reaction (RT-PCR) method for detecting astrovirus serotypes 1, 2, 3, 5, 6 and 7 (but not serotype 4). Furthermore, we developed the specific primers for detecting serotypes 1 and 2, the most predominant serotypes in the world. Sensitivity of the first PCR with serotype common primers was about 10 times higher than that of enzyme immunoassay with monoclonal antibody (EIA-MAb). Sensitivity of the second PCR with the serotype-specific primers was even higher. The RT-PCR method was useful for detecting astroviruses from clinical samples, especially serotypes 1 and 2.

Base Sequence↗

Elastic recoil and intimal thickening after coronary stenting.

In this study, the long-term elastic recoil of the stents and the intimal thickening over the stents were evaluated separately. Twenty-nine patients who received a Wiktor coronary stent were angiographically followed-up at 2 weeks, 3 months, and 6 months. The elastic recoil of the stent was evaluated by the changes in minimum stent diameter. The intimal thickness was evaluated by the difference between minimum stent diameter and minimum lumen diameter. Minimum stent diameter showed no significant change up to 6 months. The significant increase (P < 0.05) of the intimal thickness was detected only between 2 weeks and 3 months. In conclusion, the Wiktor stent prevented the elastic recoil up to 6 months, and was covered by the neointima which increased its thickness mainly between 2 weeks and 3 months after stenting. It was suggested that stent restenosis was not caused by the elastic recoil, but by the intimal thickening.

Aged↗

Resistance to glomerular injury in the diabetic biobreeding rat.

This study was designed to determine whether the diabetic BioBreeding rat develops significant renal injury following long-term moderate to severe hyperglycaemia. Diabetic and control rats were followed from the onset of diabetes (2-4 months) to 18 months of age. Frank proteinuria and/or albuminuria were always absent. Glomerular filtration rate, measured by inulin clearance (ml min-1 (100 g body weight)-1), was significantly higher in diabetic rats than in controls at 10, 12 and 18 months of age. Advanced glycosylation end-product cross-links assessed by percentage solubility of tail tendon collagen were moderately increased in diabetic compared with control animals. Urinary excretion of advanced glycosylation end-products in unfractionated urine and in urine fractionated for low molecular mass peptides (< 10 kDa) was 11-fold greater in the diabetic rats than in the control group. Urinary excretion of nitric oxide metabolites (nmol NO2- and NO3- (24 h)-1) were significantly (P < 0.05) greater in diabetic rats than in controls after 8 months of age. Mild histopathology resembling human diabetic nephropathy, including increased mesangial volume and glomerular basement membrane thickness, was detected at 18 months of age. The findings of hyperfiltration and mild glomerular morphological changes in diabetic BioBreeding rats are similar to the abnormalities seen in stage 2 human diabetic nephropathy. We hypothesize that two factors which may contribute to the resistance or tolerance to renal injury in the BioBreeding diabetic rat are increased nitric oxide production and the decreased accumulation of advanced glycosylation end-products.

Animals↗