Search PubMed⌕ Search

Biomedical subjects

S Asai

Publications and source records attributed to S Asai.

At least 37 records · Page 2Linked to original sources
PubMed2001

Screening for acetaldehyde dehydrogenase 2 genotype in alcohol-induced asthma by using the ethanol patch test.

BACKGROUND: We have previously reported that alcohol-induced asthma in Japanese patients is caused by increased blood acetaldehyde concentration resulting from abnormalities of acetaldehyde dehydrogenase 2 (ALDH2) enzyme activity on the basis of ALDH2 genotype differences. OBJECTIVES: The purpose of the present study was to determine whether the ethanol patch test could predict the ALDH2 genotype in Japanese asthmatic subjects. METHODS: An ethanol patch test on the upper arm and a questionnaire survey addressing the past history of alcohol-induced asthma were administered to 148 adult Japanese asthmatic subjects. The ALDH2 genotypes in these 148 subjects were also determined by means of PCR. RESULTS: The genotype distribution of ALDH2 determined by PCR in 68 subjects with positive ethanol patch test results was 4 (5.9%), 56 (82.4%), and 8 (11.8%) for genotypes NN (normal homozygote), NM (mutant heterozygote), and MM (mutant homozygote). The ALDH2 genotype in 80 subjects with a negative test result was only NN. The distribution of ALDH2 genotype in 78 (52.7%) subjects who had experienced alcohol-induced asthma symptoms on the basis of the questionnaire was 27 (34.6%), 44 (56.4%), and 7 (9.0%) for genotypes NN, NM, and MM, respectively. On the other hand, 70 subjects had never experienced alcohol-induced asthma symptoms. In these subjects the ALDH2 genotype was NN in 51 (72.9%), NM in 18 (25.7%), and MM in 1 (1.4%). CONCLUSIONS: Our results indicate that the results of ethanol patch testing correlate well with ALDH2 genotype, as determined by means of PCR, suggesting that the ethanol patch test is useful for the screening of alcohol-induced asthma.

Adult↗
PubMed2001

High correlation between results of the [1-13C]-phenylalanine breath test and phenylalanine hydroxylase (EC 1.14.16.1) activity of the liver in rats.

BACKGROUND: (13)CO(2) is decreased in patients with end-stage liver disease by the [1-(13)C]-phenylalanine breath test. Decreased (13)CO(2) is supposed to be caused by the decreased ability of the liver to oxidize phenylalanine. However, no direct evidence has been reported. METHODS: The [1-(13)C]-phenylalanine breath test was performed in galactosamine hepatitis rats (n = 14) and control rats (n = 8). Plasma phenylalanine concentration before intravenous administration of [1-(13)C]-phenylalanine, the elimination rate of phenylalanine and the phenylalanine hydroxylase (PAH; EC 1.14.16.1) activity of the whole liver were examined. RESULTS: Increase of (13)CO(2) in the breath [Delta(13)CO(2) ( per thousand)] of galactosamine hepatitis rats 2 min after administration of [1-(13)C]-phenylalanine was only 1/5 of that in control rats. The concentration of plasma phenylalanine and the elimination rate of plasma phenylalanine in hepatitis rats did not show significant differences compared to control rats. On the other hand, a clear difference in the activity of PAH was observed between hepatitis rats and control rats. Delta(13)CO(2) ( per thousand) 2 min after administration of [1-(13)C]-phenylalanine was highly correlated to the PAH activity of the whole liver (r = 0.917). CONCLUSION: It was strongly indicated that decreased Delta(13)CO(2 ) in hepatitis rats was the result of decreased activity of PAH.

Animals↗
PubMed2001

Ultrasonographic differentiation between tuberculous lymphadenitis and malignant lymph nodes.

OBJECTIVE: To assess the usefulness of ultrasonography in the differential diagnosis of cervical tuberculous lymphadenitis versus malignant lymph nodes. METHODS: Ultrasonography of cervical lymph nodes was performed with a real-time linear scanner using a 7.5- or 11-MHz probe or both. Ultrasonographic findings were retrospectively reviewed in 73 patients: 49 with malignant lymphoma, 15 with tuberculous lymphadenitis, and 9 with metastatic lymph nodes. RESULTS: Ultrasonographic features specific to cervical tuberculous lymphadenitis were strong echoes (33.3%) and an echogenic thin layer (86.7%). When the lymph nodes had at least 1 of these 2 features, tuberculous lymphadenitis was diagnosed with a sensitivity of 100% and a specificity of 100%. CONCLUSIONS: Ultrasonographic evaluation of cervical lymph nodes can be useful in the diagnosis of cervical tuberculous lymphadenitis.

Adolescent↗
PubMed2001

[Validity of reticulocyte count testing in reimbursement practice: a cost-effectiveness analysis].

Recently reticulocyte count testing has markedly decreased in Japan. We studied the current status of the reduction of reimbursement for reticulocyte count testing and the cost-effectiveness of the test in an academic hospital. The orders of complete blood counts(CBC) accompanied by reticulocyte count testing in Tokai University Hospital declined from 58.9 to 13.3% during the last decade. Among a total of 15,538 test orders for reticulocyte count in outpatients, full reimbursement was refused in 123(0.79%) during a one year period from April 1999 to March 2000. The cost-effectiveness of reticulocyte count testing was evaluated in 719 new outpatients who visited Tokai University Hospital during this period. A useful result(UR) of testing was defined as that which contributed to a change in a physician's diagnosis- or decision-making, relating to a "tentative initial diagnosis" obtained from patient history and physical examination alone. Cost-effectiveness for either CBC alone or in combination with reticulocyte count testing was evaluated by calculating clinical effectiveness(the number of URs yielded by a test per patient), economic efficiency(cost required for a test per UR generated), and the cost-effectiveness values(cost required for additional test(s) per additional UR generated). There was a wide disparity in the clinical effectiveness of reticulocyte count twisting among the hospital departments, ranging from 0.53 UR/patient(Gastroenterology-2) to 0(Oral Surgery, Neurology, Urology). Poor clinical effectiveness shown in particular hospital departments endorsed the increasing percentages in reimbursement rejection by the payer of health insurance. The test should be ordered more carefully in consideration of reimbursement and in regard to its cost-effectiveness among different patients groups.

Cost-Benefit Analysis↗
PubMed2001

A scoring system for ultrasonographic differentiation between cervical malignant lymphoma and benign lymphadenitis.

The purpose of our study is to assess the usefulness of a scoring system for ultrasonography using a high-frequency transducer as a non-invasive examination in the differential diagnosis of cervical malignant lymphoma from benign lymphadenitis. Ultrasonography was performed with a real-time linear scanner using 7.5 and/or 11 MHz probes in 66 patients who were presented with cervical lymphadenopathy and were suspected to have malignant lymphoma. Thereafter, a surgical biopsy was performed for histopathological diagnosis, revealing 49 cases of malignant lymphoma and 17 cases of benign lymphadenitis. Ultrasonographic findings were reviewed retrospectively. The incidence of following ultrasonographic features was found to be significantly higher in malignant lymphoma than in benign lymphadenitis. These were; (1) longitudinal and transverse diameter ratio(L/T) < 2.0, (2) a delineation of multiple nodes, (3) a tendency of fusion, (4) an irregular margin, (5) hypoechoic masses with heterogeneous internal echoes, (6) a presence of line echoes and (7) an absence of hilum. These 7 ultrasonographic features were used in combination for a scoring system to discriminate malignant lymphoma from benign lymphadenitis. When ultrasonographic findings of lymph nodes fulfilled more than 3 of the 7 features, malignant lymphoma was diagnosed with a sensitivity of 98.0% and a specificity of 76.5%. Ultrasonographic evaluation of swollen cervical lymph nodes using a high-frequency transducer would be informative and should be performed prior to a surgical biopsy.

Adolescent↗
PubMed2000

The heart is a source of circulating cardiotrophin-1 in humans.

Cardiotrophin-1 (CT-1) is a new member of the interleukin (IL)-6 family of cytokines and one of the endogenous ligands for gp130 signaling pathways in the heart, which has potent hypertrophic and survival effects on cardiac myocytes. However, the clinical significance of CT-1 is poorly understood, mainly because there is no widely applicable specific and sensitive assay system for measuring plasma levels of circulating CT-1. We therefore developed a competitive radioimmunoassay (RIA) for human CT-1 with rabbit antiserum recognizing the N-terminus region of human CT-1 and using recombinant human CT-1 as a calibrator. The assay displays no cross-reactivities with any of the IL-6 family of cytokines including IL-11, leukemia inhibitory factor, ciliary neurotrophic factor, and oncostatin M. The lower detection limit in buffer was found to be 43 fmol/ml, and the working range was 120-8300 fmol/ml (CV < 15%). This RIA directly recognizes CT-1-like immunoreactivity in human plasma with a mean value of 571 +/- 75 fmol/ml (mean +/- SD) in healthy volunteers. The RIA coupled with gel filtration chromatographic analyses showed that the major molecular form of circulating CT-1 corresponds to recombinant full-length human CT-1. Moreover, there is a significant increase in the plasma CT-1 concentration from the aorta and coronary sinus, which clearly indicates that the heart secretes CT-1 via the coronary sinus into the peripheral circulation. This RIA should serve as a powerful tool for investigating the clinical significance of CT-1.

Adult↗
PubMed2000

Two distinct components of initial glutamate release synchronized with anoxic depolarization in rat global brain ischemia.

Numerous reports have suggested that anoxic depolarization is a critical event in the pathogenesis of cerebral ischemia. Extracellular glutamate concentration ([Glu]e) is closely related to the pathogenesis of ischemia. Therefore, these pathogenic mechanisms merit study, especially the relationship between [Glu]e elevation and the ionic basis of early changes in membrane potential after ischemic insult in vivo. It is often presumed from electrophysiological studies that a causal relationship exists between impaired glutamate uptake and/or progressive glutamate increase and anoxic depolarization, but few in vivo reports have found any sign of a progressive increase of [Glu]e elevation preceding anoxic depolarization. Recently, we reported the application of an oxygen-independent real-time technique for monitoring glutamate levels in the extracellular space during in vivo ischemia, and demonstrated that the massive glutamate release during ischemia is biphasic. In the present study, using this real-time monitoring system, we carried out a more detailed analysis of the initial events in the first phase of glutamate release during ischemia-induced anoxic depolarization. The shape of the rising slope that forms the peak of the first phase suggested two components. The second component was approximately 10 times steeper than the first, with two different components of the rise on the way to the peak of the biphasic [Glu]e elevation. This is the first report to demonstrate these components of the initial glutamate peak, and suggests a progressive second component of the [Glu]e increase preceding Ca2+-dependent release from synaptic vesicles with anoxic depolarization, in vivo.

Animals↗
PubMed2000

Biochemical characterization of casein kinase II as a protein kinase responsible for stimulation of HIV-1 protease in vitro.

The physiological significance of casein kinase II (CK-II) on the protease (PR) activity of recombinant HIV-1 PR (rPR) was biochemically investigated in vitro. We found that (i) the purified rPR (p11) functions as a phosphate acceptor of CK-II; (ii) the PR activity of rPR is stimulated approximately 2.9-fold after its full phosphorylation by recombinant human CK-II (rhCK-II) in a manner similar to that observed for recombinant HIV-1 reverse transcriptase (rRT); and (iii) this stimulation is completely inhibited by two polyphenol-containing anti-oxidant compounds [quercetin and epigallo-catechin gallate (EGCG)] at 0.1 microM or a glycyrrhetinic acid derivative (oGA) and catechin at 10 microM without significant effect on the PR activity of rPR. These results suggest that (i) CK-II may be a host mediator responsible for stimulation of PR and RT in HIV-1-infected cells; and (ii) the selective inhibition of the CK-II-mediated stimulation of HIV-1 PR and RT by potent CK-II inhibitors may be involved in their anti-HIV-1 effects at the cellular level.

Amino Acid Sequence↗
PubMed2000

Quantitative evaluation of extracellular glutamate concentration in postischemic glutamate re-uptake, dependent on brain temperature, in the rat following severe global brain ischemia.

Changes in brain temperature are known to modulate the marked neuronal damage caused by an approximately 10-min intra-ischemic period. Numerous studies have suggested that the extracellular glutamate concentration ([Glu](e)) in the intra-ischemic period and the initial postischemia period is strongly implicated in such damage. In this study, the effects of intra-ischemic brain temperature (32, 37, 39 degrees C) on [Glu](e) were investigated utilizing a dialysis electrode combined with ferrocene bovine serum albumin (BSA), which allows oxygen-independent real-time measurement of [Glu](e). This system allowed separate quantitative evaluation of intra-ischemic biphasic glutamate release from the neurotransmitter and metabolic pools, and of postischemic glutamate re-uptake in ischemia-reperfusion models. The biphasic [Glu](e) elevation in the intra-ischemic period did not differ markedly among intra-ischemic brain temperatures ranging from 32 to 39 degrees C. Intra-ischemic normothermia (37 degrees C) and mild hyperthermia (39 degrees C) markedly inhibited [Glu](e) re-uptake during the postischemic period, although the intra-ischemic [Glu](e) elevation did not differ from that during intra-ischemic hypothermia (32 degrees C). It was assumed that normothermia or mild hyperthermia in the intra-ischemic period influences intracellular functional abnormalities other than the intra-ischemic [Glu](e) elevation, thereby inhibiting glutamate re-uptake after reperfusion rather than directly modulating intra-ischemic [Glu](e) dynamics.

Animals↗
PubMed2000

The high level of hCDC10 gene expression in neuroblastoma may be associated with favorable characteristics of the tumor.

BACKGROUND: The biological behavior of neuroblastomas detected through mass screening (MS, </=1 year of age) and that of mass screening-negative later-presenting (MSN, >1 year of age) neuroblastomas have been reported to differ in many studies. To investigate the biological differences between these two groups, we analyzed the differences in mRNA profiles. MATERIALS AND METHODS: We analyzed the mRNA profiles of MS and MSN neuroblastomas using differential display, and cloned and sequenced the bands differentially expressed between these two groups. Using the RNA analysis by polymerase chain reaction (RNA-PCR) method, the relative amount of mRNA in tumor tissue in each sample was measured. Associations between relative amount of mRNA and clinical and genetic variables related to patient prognosis and the effect of the level of mRNA expression on survival probability were investigated using statistical methods. RESULTS: Using differential display and RNA-PCR, we found that the mRNA for the human homologue of the yeast cdc10 gene (hCDC10) identified in Saccharomyces cerevisiae was expressed at a higher level in the MS group of patients than in the MSN group of patients (0.554 +/- 0.197 for MS neuroblastoma, n = 24 and 0.244 +/- 0.179 for MSN neuroblastoma, n = 10, P < 0.01), and this difference was suggested to be independent of the histologic subtype of tumor. A high level of hCDC10 mRNA expression in neuroblastomas (relative amount of hCDC10 mRNA > 0.35) was also suggested to be associated with younger age at diagnosis (</=1 year of age, P < 0.01), favorable clinical stage (I, II, and IVs, P < 0. 01), and favorable histology in the Shimada classification (P < 0. 01), whereas a low level of hCDC10 mRNA expression (relative amount of hCDC10 mRNA </=0.35) was suggested to be associated with the progression of clinical stage (P < 0.01) and N-myc gene amplification (>1 copy, P < 0.05). Patients with neuroblastomas with a high level of hCDC10 mRNA expression were suggested to have a better prognosis than those with a low level of hCDC10 mRNA expression (P < 0.01). CONCLUSIONS: A high level of hCDC10 mRNA expression in neuroblastomas may be associated with favorable clinical and biological characteristics, and the expression of hCDC10 mRNA in neuroblastomas may affect the clinical and biological characteristics of this type of tumor.

Cell Cycle Proteins↗
PubMed2000

Detection of aberrations of 17p and p53 gene in gastrointestinal cancers by dual (two-color) fluorescence in situ hybridization and GeneChip p53 assay.

We performed dual (two-color) fluorescence in situ hybridization (FISH) using direct fluorescent labeling probes for p53 and chromosome 17 in six gastrointestinal (3 stomach and 3 colon) cancers. In three of these (1 stomach and 2 colon) the interphase cell nuclei showed an imbalance of signals for the p53 and chromosome 17; that is, the p53 signal count was lower than the chromosome 17 signal count, indicating deletion of the p53 gene. Moreover, metaphase FISH analysis demonstrated that those nuclei actually had a chromosome 17 with deletion of the p53 gene. Interestingly, these three cases had an abnormal chromosome 17 copy number, that is, chromosome 17 aneusomy. Furthermore, to investigate the possibility of p53 mutation in tumors with an imbalance of signals for chromosome 17 and p53 per nucleus, we performed a GeneChip p53 assay which has recently been developed. GeneChip p53 assay demonstrated that a primary tumor sample from one colon cancer case had a heterozygous point mutation of CGT (Arg) to CAT (His) at codon 273 in exon 8. In addition, a sample of metastatic tumor in the liver from the same case revealed two heterozygous point mutations. One of them was the same mutation as that is the primary tumor; the other was GTG (Val) to GGG (Gly) at codon 217 in exon 6. In conclusion, we found that the combination of dual-color FISH and GeneChip p53 assay offered reliable results and important information concerning not only deletion of the p53 gene and chromosome 17 aneusomy but also p53 mutations. Using these techniques, we demonstrated that an imbalance of signals for chromosome 17 and p53 per nucleus, chromosome 17 aneusomy, and accumulation of p53 mutations had occurred during carcinogenesis and development of gastrointestinal cancers.

Centromere↗
PubMed2000

Effects of sodium cromoglycate on cytokine production following antigen stimulation of a passively sensitized human lung model.

BACKGROUND: Interleukin-5 (IL-5) and tumor necrosis factor-alpha (TNF-alpha) play key roles in bronchial asthma. Sodium cromoglycate (DSCG) and dexamethasone (Dex) are used in the treatment of asthma as anti-inflammatory agents. OBJECTIVE: We investigated whether DSCG inhibited the expression of IL-5 and TNF-alpha mRNA and proteins from isolated human lungs, and compared these findings with those of Dex. METHODS: Human lung specimens were passively sensitized with sera from atopic patients, then preincubated in the presence of DSCG (10(-3), 10(-4), 10(-5) M) or Dex (10(-6) M) for 2 hours. The specimens were stimulated with Dermatophagoides antigen, then cultured for 48 hours. The supernatant was collected 1, 2, 4, 8, 24, and 48 hours to measure IL-5 and TNF-alpha by enzyme-linked immunosorbent assay. mRNA expression was examined by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Tumor necrosis factor-alpha protein reached a peak level at 4 hours (156.57 +/- 18.29 pg/mL). Dex decreased TNF-alpha protein to 31.86 +/- 4.67 pg/mL (P < .001). There was also a decrease of TNF-alpha protein to 107.43 +/- 14.25 pg/mL by 10(-4) MD SCG (P < .001). Antigenic stimulation also increased the release of IL-5 protein at 4 hours and the peak level was observed at 24 hours (150.29 +/- 19.12 pg/mL). Dex decreased IL-5 protein to 28.57 +/- 5.27 pg/mL (P < .0001), 10(-4) M DSCG also decreased to 111.57 +/- 15.28 pg/mL (P < .05). RT-PCR analysis showed persistence of IL-5 and TNF-alpha mRNA expression from 1 to 24 hour after antigen stimulation. Dex but not DSCG inhibited IL-5 and TNF-alpha mRNA levels. CONCLUSION: Our results showed that DSCG significantly inhibited IL-5 and TNF-alpha production by human lung specimens, suggesting that it acts as an anti-inflammatory agent.

Aged↗
PubMed2000

Age-related changes of cornu ammonis 1 pyramidal neurons in gerbil transient ischemia.

This study reports that postischemic apoptotic cell death of the hippocampal cornu ammonis (CA) 1 neurons is delayed in aged gerbils. Age-related changes in the process of CA1 neuronal death following transient ischemia was studied. Two groups of Mongolian gerbils were used in this study, which compared adult (4-month-old) and aged (24-month-old) animals by hematoxylin-eosin stain, in situ nick-end labeling (TUNEL method) and electron microscopy. In the process of neuronal death, neuronal loss of the aged group was histologically less severe than that of the adult group. TUNEL-positive cells were found on days 3-5 after ischemia in the adult group, while they were still found on day 7 in the aged group. The apoptotic process of the aged group was delayed compared to the adult group. Furthermore, lipofuscin was ultrastructurally observed inside the apoptotic body 5 days after ischemia in CA1 pyramidal neurons of the aged group. It is likely that colocalization of lysosomal enzyme cathepsin D with lipofuscin might be associated with the age-related alteration of lysosomal system in the neurons. Altogether these data suggest that age-related lysosomal changes might affect the apoptotic cascade process in postischemic CA1 neurons.

Aging↗
PubMed2000

Oxygen-independent real-time monitoring of distinct biphasic glutamate release using dialysis electrode in rat striatum during anoxia: in vivo evaluation of glutamate release and reversed uptake.

Using a dialysis electrode, previous studies showed a clear biphasic release of glutamate during anoxia and ischemia. In this study, we examined two hypotheses: (1) glutamate is of vesicular origin and its release is thus Ca2+- and ATP-dependent in the first phase, while in the second phase glutamate is derived primarily from the metabolic pool, and (2) reversed glutamate uptake, due to electrogenic stoichiometry, produces the second phase during anoxic insult in the rat brain. A dialysis electrode continuously perfused with glutamate oxidase and ferrocene-conjugated bovine serum albumin (BSA) optimized the time resolution of monitoring, allowing quantitative oxygen-independent, real-time measurement of the extracellular glutamate concentration ([Glu]e) during anoxia. [Glu]e dynamics were analyzed during anoxia by combining the dialysis electrode with focal microinjection of substances inducing glutamate release. Following anoxia in the rat brain, a sharp and rapid [Glu]e elevation took place (first phase). The [Glu]e elevation then shifted, continuing a gently sloping rise throughout the anoxic period (second phase). This first phase disappeared with intracranial administration of either Co2+ or omega-conotoxin. The second phase rise increased with focal microinjection of KCl (300 mM, 1 microL) and decreased with NaCl (300 mM, 1 microL), ultimately reaching a plateau in both cases. Preloading with a novel glutamate transporter inhibitor (tPDC) decreased both the first and second phases of [Glu]e elevation. This dialysis electrode system provides data supporting in vivo evidence that the peak of the first phase of [Glu]e elevation is derived from the "neurotransmitter pool," while the second phase is derived from the neuronal and glial "metabolic pool," which is, at least, partly related to a "reversed uptake" mechanism in the anoxic rat brain.

Animals↗
PubMed2000

[An imported case of primary pulmonary coccidioidomycosis].

Coccidioides immitis is a causative agent of coccidioidomycosis, which is one of the most dreadful mycosis because of its infectious and pathogenic nature. The endemic areas are in the southwestern parts of the United States and other semi-arid regions throughout the Western Hemisphere. During the early 1990s, the incidence of coccidioidomycosis in California increased dramatically, resulting in recognition for this mycosis as a reemerging infectious disease in the United States. The patients included a large number of non-informed visitors from non-endemic countries. Our report is on an imported case of primary pulmonary coccidioidomycosis. A 35-year-old Japanese male, after living in the United States for nine months, suffered from a combination of headache and fever. He was given a serological examination, and a chest radiograph in Phoenix, Arizona in the United States and was diagnosed as coccidioidomycosis. A daily dosage of 400 mg of fluconazole was administered and he returned to Japan. His headache and skin rash persisted and he was admitted to our hospital to evaluate the severity of his disease. There were no fungi cultured from neither bronchoalveolar nor cerebrospinal fluid and he was discharged. The patient had been treated with fluconazole and his symptoms, high-resolution CT and serological antibody titer were monitored. After 18 months, his clinical and radiological evolution was favorable and his serological IgM titer was below its sensitivity medication was stopped and there were no relapses.

Adult↗
PubMed2000

[1-(13)C]Galactose breath test for quantitative measurement of liver function in a short period.

BACKGROUND: Using a rat model of hepatectomy, we investigated whether the severity of hepatopathy could be quantitatively measured from changes in expiratory (13)CO(2) levels after intravenous administration of [1-(13)C]galactose. MATERIALS AND METHODS: Under nembutal anesthesia, 100 mg/kg [1-(13)C]galactose was administered to rats via the femoral vein, and expiratory (13)CO(2) levels were measured for 60 min. Then, 30, 70 or 90% hepatectomy was performed. In the control group, simple laparotomy was performed. Breath test was conducted 20 min after laparotomy. We examined the correlation of total (13)CO(2) output (S) or single point (13)CO(2) level (SP) every 5 min until 30 min, and at 45 and 60 min with liver weight/body weight (LW/BW) (%). RESULTS: In the control group, the breath test graph reached a plateau level, but in all groups undergoing hepatectomy a plateau level was not reached during measurement. The correlation coefficient between S(30) after [1-(13)C]galactose administration and LW/BW was 0.889 (p< 0.0001). The correlation coefficient between SP(25) after [1-(13)C]galactose administration and LW/BW was highest, 0.923 (p< 0.0001). CONCLUSION: In the breath test with intravenously administered [1-(13)C]galactose, hepatopathy could be evaluated by measuring S(30) and hepatopathy could be more accurately quantitatively evaluated by measuring SP(25) over a short period.

Animals↗
PubMed2000

Thymidylate synthase expression correlates closely with E2F1 expression in colon cancer.

Thymidylate synthase (TS) is thought to be one of the target genes that the E2F1 transcription factor binds to and regulates. However, the relationship between the expressions of TS and E2F1 in primary colon cancer specimens remains unclear. The aim of this study was to define the relation of TS and E2F1 gene expressions in tumor samples from 23 colon cancer patients. TS and E2F1 gene expressions were measured by TaqMan reverse transcription-PCR assay using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an internal standard and expressed as a TS:GAPDH or E2F1:GAPDH mRNA ratio. A close relationship was found between TS gene expression and E2F1 gene expression (r2 = 0.598, P < 0.001) in 23 tumor samples analyzed. Surprisingly, a high correlation between TS gene expression and E2F1 gene expression was observed even in advanced tumors from stage IV colon cancer patients. These results suggest that transcription of the TS gene may be regulated by E2F1 in primary colon cancer specimens and that this gene-regulatory pathway from E2F1 to TS may be highly conserved during malignant progression. Four of the 23 patients showed TS overexpression with increased E2F1 expression. These results suggest that the ability of a tumor to increase TS expression may possibly be due to an overexpression of E2F1. Although the number of patients was relatively small, our study provides new insights into the molecular mechanisms underlying the regulation of TS expression in colon cancers.

Adult↗