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Yuko Sato

Publications and source records attributed to Yuko Sato.

69 records · Page 4Linked to original sources
PubMed2002

Regulation of cerebral cortical blood flow by the basal forebrain cholinergic fibers and aging.

This article reviews the study of neural vasodilator mechanisms of the cerebral cortex by basal forebrain cholinergic nerve fibers and their age-related function in rats. During the last decade, we have demonstrated a neural regulatory system of cerebral blood flow in rats involving intracerebral cholinergic vasodilator nerve fibers originating in the basal forebrain and projecting to the cerebral cortex. Activation of these cholinergic vasodilator fibers results in the release of acetylcholine (ACh) within the cortex, activation of both nicotinic and muscarinic ACh receptors, and vasodilatation without coupling to glucose metabolic rates. This cholinergic vasodilator system has been shown to decline with age in rats mainly due to age-related declines of nicotinic ACh receptor activity. However, muscarinic ACh receptor activity and the release of ACh into the extracellular space in the cortex are well maintained during aging. The present age-related decline of the intracerebral cholinergic vasodilator system found in rats seems to affect cognitive function during aging, although this cholinergic vasodilator system has not yet been demonstrated in humans.

Aging↗
PubMed2002

Expression of the TEL/EVI1 fusion transcript in a patient with chronic myelogenous leukemia with t(3;12)(q26;p13).

The t(3;12)(q26;p13) translocation is a recurrent chromosomal aberration observed in myeloid malignancies. It has been shown that the translocation results in the fusion of the TEL (ETV6) gene at 12p13 and the EV11 gene at 3q26. We report the first case with Philadelphia (Ph)-positive chronic myelogenous leukemia (CML) expressing the TEL/EVI1 fusion transcript. A 26-year-old man was initially diagnosed as having the chronic phase of Ph-positive CML. The t(3;12)(q26;p13) emerged 16 months prior to the myeloid blastic crisis. Reverse transcriptase-polymerase chain reaction detected the TEL/EVI1 transcript without the intervening 5' non-coding exon of EVI1, suggesting that inappropriate expression of the EVI1 protein driven by the TEL promotor could play a critical role in progression to the blast crisis of CML.

Adult↗
PubMed2002

t(1;3)(p36;p21) is a recurring therapy-related translocation.

Chromosome bands 1p36 and 3p21 are known to be recurring breakpoints in therapy-related (t-) leukemia. We identified a recurring translocation, t(1;3)(p36;p21), in eight patients with various hematologic malignancies: three patients with ALL, one with chronic myelogenous leukemia (CML) in accelerated phase (AP), two with MDS, and two with AML(M3). Five of the eight patients had a history of chemotherapy, including alkylating agents in three, before the translocation was detected. In two of these five patients, the t(1;3)(p36;p21) emerged only at relapse or in the accelerated phase of CML. The karyotypes of the patients were complex, including -7 and structural abnormalities of 5q, 6q, 7q, 9p, and 11q23. Survival time varied among patients (25 days to more than 16 years). Using FISH with 13 1p35-36 cosmid probes (tel-FB12-CA5-G7-FD2-CB1-ED8-FD9-G32-AE3-G50-AD8-GG4-G43-cen), we delineated the 1p36 breakpoint in two patients with MDS and ALL as lying between FB12 and FD2 (between BAC47P3 and PAC963K15), with a small deletion near the breakpoint in both cases. In the patient with MDS, there was also a deletion at 3p21.3, as detected with the cosmid probe cosNRL9. The results of the present study suggest that t(1;3)(p36;p21) in hematologic diseases is associated with prior exposure to mutagens, including alkylating agents.

Adult↗
PubMed2002

Identification of the breakpoints at 1p36.2 and 3p21.3 in an AML(M3) patient who had t(1;3)(p36.2;p21.3) at the third relapse.

Recently, we reported that a recurrent translocation, t(1;3)(p36;p21) is closely associated with prior chemotherapy including alkylating agents, assessing eight patients with various hematologic malignancies (Genes, Chromosomes and Cancer 34:186-192), 2002). Furthermore, we delineated the 1p36 breakpoint in two patients lying between RP11-BAC47P3 and RP5-PAC963K15 at 1p36.3 with a small deletion near the breakpoint. In one of them, we also found deletion at 3p21.3 with cosNRL9 probe, which is included in a 370-kb lung cancer homologous deletion region. However, due to scantiness of the patient materials at that time, we could not determine the precise breakpoint at 1p36 or 3p21 in any of the patients. In this report, we identified the 1p36 and 3p21 breakpoints of an AML (M3) patient who is included in the previous patient series. The patient showed t(1;3)(p36;p21) together with t(15;17) at the third relapse. With FISH using BAC/PAC probes, we determined the 1p36 breakpoint within RP11-295B1 at 1p36.2 and the 3p21 breakpoint between RP11-3B7 and RP11-901L6 at 3p21.3. There was no deletion around the two breakpoints in this patient. To the best of our knowledge, this is the first report that has identified the precise breakpoint of t(1;3)(p36;p21) translocation. It is obvious that the 1p36.2 and 3p21.3 breakpoints of this patient are different from those of the previous patients, suggesting that the genes and the molecular event is different from those of the previous patients. The patients with t(1;3)(p36;p21) should be subclassified according to the precise breakpoints or the genes involved.

Adult↗
PubMed2002

Pyramidal and extrapyramidal involvement in experimental infection of cynomolgus monkeys with enterovirus 71.

Among the enteroviruses, polioviruses and enterovirus 71 (EV71) are two major neurotropic viruses causing serious neurological manifestations. While polioviruses are being eradicated globally by vaccination, EV71 still has the potential to cause a large outbreak such as that in Taiwan in 1998, in which there were many fatalities. In this study, we determined the neurovirulence of EV71 by neuropathological analysis of cynomolgus monkeys after experimental infection with five EV71 strains, which were isolated from individual patients with fatal encephalitis; meningitis; and hand, foot, and mouth disease. After intraspinal inoculation, the monkeys developed neurological manifestations within 1-6 days post-inoculation, irrespective of the inoculated strains. These manifestations included not only pyramidal tract signs such as flaccid paralysis, but also extrapyramidal tract signs such as tremor and ataxia. Histological and viral examinations confirmed virus replication in the spinal cord, brainstem, cerebellar cortex, and dentate nuclei, and cerebrum. The strains isolated during the 1970s and 1990s showed no particular differences with respect to neurotropism. Thus, it is clear that EV71 has a wider neurotropism than that of polioviruses.

5' Untranslated Regions↗
PubMed2002

The human prefrontal and parietal association cortices are involved in NO-GO performances: an event-related fMRI study.

One of the important roles of the prefrontal cortex is inhibition of movement. We applied an event-related functional magnetic resonance imaging (fMRI) technique to observe changes in fMRI signals of the entire brain during a GO/NO-GO task to identify the functional fields activated in relation to the NO-GO decision. Eleven normal subjects participated in the study, which consisted of a random series of 30 GO and 30 NO-GO trials. The subjects were instructed to press a mouse button immediately after the GO signal was presented. However, they were instructed not to move when the NO-GO signal was presented. We detected significant changes in MR signals in relation to the preparation phases, GO responses, and NO-GO responses. The activation fields related to the NO-GO responses were located in the bilateral middle frontal cortices, left dorsal premotor area, left posterior intraparietal cortices, and right occipitotemporal area. The fields of activation in relation to the GO responses were found in the left primary sensorimotor, right cerebellar anterior lobule, bilateral thalamus, and the area from the anterior cingulate to the supplementary motor area (SMA). Brain activations related to the preparation phases were identified in the left dorsal premotor, left lateral occipital, right ventral premotor, right fusiform, and the area from the anterior cingulate to the SMA. The results indicate that brain networks consisting of the bilateral prefrontal, intraparietal, and occipitotemporal cortices may play an important role in executing a NO-GO response.

Adult↗
PubMed2002

Performance of nanofiltration for arsenic removal.

Performance of rapid sand filtration inter-chlorination system was compared with nanofiltration (NF) to reduce the arsenic health risk of drinking water. It was found that rapid sand filtration with inter-chlorination is not effective in removing arsenic. If total arsenic concentration in raw water is below 50 microg/L regardless of the turbidity of raw water, arsenic can be removed below WHO guideline value of 10 microg/L by conventional coagulation (polyaluminum chloride dosage is about 1.5 mg Al/L). However, if the raw water arsenic concentration exceeds 50 microg/L, more coagulant dosage or enhanced coagulation is needed. To adopt optimum coagulant dosage for arsenic removal, it needs to monitor raw water arsenic concentration, but it is difficult because arsenic measurement is time consuming. In addition, if raw water contains As(III), it is difficult for rapid sand filtration inter-chlorination system to meet an arsenic maximum contaminant level of 2 microg/L, which would achieve reduction of cancer risk below 10(-4). On the other hand, the NF membrane (NaCl rejection 99.6%) could remove over 95% of As(V) under relatively low-applied pressure (< 1.1 MPa). Furthermore, more than 75% of As(III) could be removed using this membrane without any chemical additives, while trivalent arsenic could not be removed by rapid sand filtration system without pre-oxidation of As(III) to As(V). Because both As(V) and As(III) removals by NF membranes were not affected by source water composition, it is suggested that NF membrane can be used in any types of waters.

Arsenic↗
PubMed2002

Hepatitis B and C virus infection and p53 mutations in human hepatocellular carcinoma in Harbin, Heilongjian Province, China.

To clarify the importance of hepatitis B (HBV) and C virus (HCV) infection and p53 gene mutation in the genesis of hepatocellular carcinoma (HCC), we investigated DNA samples of formalin-fixed paraffin-embedded HCC tissue specimens from patients in the North China area of Harbin, Heilongjian province. Fifty-eight DNA samples from 43 cases obtained during surgery and the remaining 15 autopsy materials were analyzed by polymerase chain reaction (PCR) about HBV and HCV. The p53 gene (exon 7) mutant testing, in addition, was performed by PCR-direct sequencing. Histopathologically, we determined the histological grade of HCC in all specimens. Forty-five (77.6%) of 58 cases were HBV DNA-positive; only two (3.4%) HCV RNA-positive cases were found. Two of 37 samples screened showed a point mutation (AGG to AGT) at codon 249, the exon 7 hot spot of the p53 gene. The fact implies that HBV plays a very important role, but aflatoxin B1 is not an important factor in the genesis of HCC in Harbin, Heilongjian district, People's Republic of China.

Journal Article↗
PubMed2002

Role of CCK-A receptor for pancreatic function in mice: a study in CCK-A receptor knockout mice.

INTRODUCTION: The cholecystokinin (CCK) family of peptides and receptors is present throughout the brain and gastrointestinal tract. The CCK receptors can be pharmacologically subdivided into two subtypes: CCK-A and CCK-B. CCK-A receptor is enriched in the pancreas of mice. AIMS: To determine pancreatic functions in a CCK-A receptor deficient mouse mutant generated by gene targeting in embryonic stem cells. The targeting vector contained lacZ and neo insertions in exon 2. METHODOLOGY: To examine exocrine functions, amylase release from the dispersed acini in vitro was examined. In the in vivo study, the mixture of bile-pancreatic juice was collected, and amylase, bicarbonate, and bile acid outputs were determined after the administration of various stimulants. The cystic duct of the gallbladder and the pylorus were ligated to exclude the involvement of gallbladder contraction and gastric acid. Pancreatic enzyme content was measured, and histologic examinations by HE and lacZ staining were conducted. To examine endocrine functions, oral glucose tolerance test (2 g/kg) was determined. RESULTS: The body weight, pancreatic wet weight, and enzyme content in the pancreas were similar among the three genotypes. Amylase release in vivo and in vitro and bicarbonate secretion in vivo were not stimulated by CCK-8 in CCK-AR (-/-) mice, whereas the responses to other stimulants were substantial in (-/-) mice. Administration of secretin did not increase bicarbonate secretion regardless of genotype. A normal glucose tolerance was observed in (-/-) mice. Acinar cells, islets, and duct cells were stained by lacZ, and HE staining revealed no pathologic findings. CONCLUSION: The CCK-A receptor is important for pancreatic exocrine secretion, but not essential for maintaining glucose concentration and pancreatic growth in mice.

Amylases↗
PubMed2002

Comparison of neuropathogenicity of poliovirus in two transgenic mouse strains expressing human poliovirus receptor with different distribution patterns.

In order to determine the influence of poliovirus receptor (PVR) expression on poliovirus cell tropism and neuropathogenesis, two transgenic (tg) mouse models were produced in which PVR was expressed under the transcriptional control of the human PVR gene promoter (hg-PVR mice) and the CAG promoter (CAG-PVR mice). Then the pathogenicity of poliovirus after intracerebral inoculation of the type 1 Mahoney strain was compared. These showed completely different clinical and pathological changes. In the former, the expression of PVR in neurons in the central nervous system (CNS) conferred susceptibility to poliovirus, and a paralytic disease that resembled the human poliomyelitis occurred. In the latter, PVR expression was detected in glial and ependymal cells in addition to the neurons. Paralysis of the limbs and death were rarely observed and mice survived without showing substantial clinical abnormality. Histopathological examination revealed that glial and ependymal cells also became susceptible to poliovirus infection. Poliovirus antigens were mainly detected in ependymal and glial cells and hippocampal neurons near the lateral ventricles in the brain, but were not frequently detected in neurons in the brainstem unlike in the hg-PVR mice. The levels of viral antigens and virus recovered from the CNS of CAG-PVR mice began to decrease as early as 2 days after inoculation, which suggested induction of a fast immune response. These results suggest that the neuropathogenicity of poliovirus changes markedly depending on the specific expression of the PVR molecule in the CNS.

Animals↗
PubMed2002

Increased lymphatic lipid transport in genetically diabetic obese rats.

Otsuka Long-Evans Tokushima fatty (OLETF) rats are a model for noninsulin-dependent diabetes mellitus (NIDDM), which is first manifested at 18 wk of age. We assessed age-related changes in lymphatic lipid transport in the intestine of OLETF rats and compared them with those of control Long-Evans Tokushima Otsuka (LETO) rats. Olive oil was infused into the rats with a mesenteric lymph fistula, which was created under ethrane anesthesia. A significant increase in lymphatic triglyceride (TG) transport in OLETF rats was observed at 18-19 wk compared with under 17 wk, but no age-related change was observed in LETO rats. Food restriction, exercise training, or troglitazone treatment in OLETF rats prevented the age-related increase in lipid transport. Biliary phosphatidylcholine concentration was higher in OLETF rats than in LETO rats, but no difference was seen in bile acid concentrations or the activity of microsomal TG transfer protein between the two strains. This study shows that increased lipid transport in the intestine may occur in NIDDM.

Animals↗
PubMed2001

Targeted integration of foreign DNA into a defined locus on chromosome 19 in K562 cells using AAV-derived components.

Targeted integration of foreign DNA is ideal for gene therapy, particularly when target cells such as hematopoietic cells actively divide and proliferate. Adeno-associated virus (AAV) has been shown to integrate its genome into a defined locus, AAVS1 (19q13.3-qter). The inverted terminal repeat (ITR) and Rep proteins are responsible for this site-specific integration, and a system has been developed that delivers a gene preferentially into AAVS1 by using these components of AAV. We examined whether this system could be applied to gene transfer into K562 cells. Two rep expression plasmids were tested, 1 driven by the cytomegalovirus (CMV) promoter (pCMVR78) and the other under the translational control of an internal ribosome entry site (pMGiR78) with mouse mammary tumor virus promoter. K562 cells were cotransfected with a rep plasmid and a plasmid containing a neo gene flanked by the ITRs. G418-resistant clones were isolated and analyzed by Southern blot analysis and fluorescence in situ hybridization (FISH). Southern blot analysis suggested AAVS1-specific integration of the neo gene in 6 (35%) of 17 clones when K562 cells were transfected with pMGiR78 by lipofection. FISH located the neo gene on chromosome 19 in 5 of these 6 clones (29%). Eight (32%) of 25 clones obtained by electroporation with pCMVR78 had the neo gene at AAVS1, according to Southern blot analysis, and 4 of these 8 clones (16%) were positive according to FISH analysis. These results suggest that site-specific integration of foreign DNA can be achieved at a significantly high rate in human hematopoietic cells using the AAV components.

Chromosomes, Human, Pair 19↗
PubMedDate not supplied

High telomerase activity correlates with the stabilities of genome and DNA ploidy in renal cell carcinoma.

Malignant tumors have telomerase activity, which is thought to play a critical role in tumor growth. However, the relation between telomerase activity and genomic DNA status in tumor cells is poorly understood. In the present study, we examined telomerase activity in 13 clear cell type renal cell carcinomas (CRCCs) with similar clinicopathologic features by telomeric repeat amplification protocol assay (TRAP). Based on TRAP assay results, we divided the CRCCs into two groups: a high telomerase activity group and a low/no telomerase activity group. We then analyzed genomic aberration, DNA ploidy, and telomere status in these two groups by comparative genomic hybridization (CGH), laser scanning cytometry (LSC), and telomere-specific fluorescence in situ hybridization (T-FISH), respectively. CGH showed the high telomerase activity group to have fewer genomic changes than the low/no telomerase activity group, which had many genomic aberrations. Moreover, with LSC, DNA diploid cells were found more frequently in the high telomerase activity group than in the low/no telomerase activity group. In addition, T-FISH revealed strong telomere signal intensity in the high telomerase activity group compared with that of the low/no telomerase activity group. These results suggest that telomerase activity is linked to genomic DNA status and that high telomerase activity is associated with genomic stability, DNA ploidy, and telomere length in CRCC.

Adult↗