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K Imai

Publications and source records attributed to K Imai.

At least 91 records · Page 5Linked to original sources

Suppression of hadrons with large transverse momentum in central Au+Au collisions at root square[s(NN)] = 130 GeV.

Transverse momentum spectra for charged hadrons and for neutral pions in the range 1 GeV/c<p(T)<5 GeV/c have been measured by the PHENIX experiment at RHIC in Au+Au collisions at root square[s(NN)] = 130 GeV. At high p(T) the spectra from peripheral nuclear collisions are consistent with scaling the spectra from p+p collisions by the average number of binary nucleon-nucleon collisions. The spectra from central collisions are significantly suppressed when compared to the binary-scaled p+p expectation, and also when compared to similarly binary-scaled peripheral collisions, indicating a novel nuclear-medium effect in central nuclear collisions at RHIC energies.

Journal Article↗

Overexpression of MUC1 reconfigures the binding properties of tumor cells.

Although it is known that adhesion and antiadhesion are essential to the metastatic spread of tumor cells, little is known about the molecules that regulate these processes. MUC1 is overexpressed and aberrantly glycosylated by a variety of tumor cells. Studies described here examined whether tumor-associated MUC1 conferred new binding properties on tumor cell lines. Flow cytometry analysis with soluble P-, E- and L-selectin/IgM chimeric proteins was performed on human pancreatic (S2-013 and Panc-1) and colon (Caco-2) tumor cells. S2-013 cells bound E- and P-selectin and Caco-2 cells bound P-selectin. Epitope-tagged MUC1 (MUC1F) expressed by S2-013, Panc-1 and Caco-2 tumor cells did not bind to P-, E- or L-selectin. Overexpression of MUC1F on the surface of S2-013 cells blocked the interactions of E-selectin to tumor-associated ligand(s) but did not affect accessibility of monoclonal antibodies to other cell surface glycoproteins (CD9, CD44). Cell aggregation assays revealed that MUC1F expressed by S2-013 cells was able to bind to intracellular adhesion molecule-1 expressed on B cells. Overexpression of MUC1F containing a targeted mutation (the tandem repeat domain entirely or partially deleted) did not block the binding of E-selectin to its S2-013-associated ligand. These results demonstrate for the first time that the heavily O-glycosylated tandem repeat domain of MUC1 can simultaneously mediate and block binding to adhesion molecules with some molecular specificity and further support the hypothesis that MUC1 plays a dual role in the metastatic spread of tumor cells.

Amino Acid Sequence↗

Observation of a (6)(LambdaLambda)He double hypernucleus.

A double-hyperfragment event has been found in a hybrid-emulsion experiment. It is identified uniquely as the sequential decay of ( 6)(LambdaLambda)He emitted from a Xi(-) hyperon nuclear capture at rest. The mass of ( 6)(LambdaLambda)He and the Lambda-Lambda interaction energy DeltaB(LambdaLambda) have been measured for the first time devoid of the ambiguities due to the possibilities of excited states. The value of DeltaB(LambdaLambda) is 1.01+/-0.20(+0.18)(-0.11) MeV. This demonstrates that the Lambda-Lambda interaction is weakly attractive.

Journal Article↗

Determination of bradykinin in rat urine by coupled-column high pressure liquid chromatography with precolumn derivatization with a water-soluble fluorogenic reagent.

Bradykinin (BK) in rat urine was determined by coupled-column HPLC with precolumn fluorogenic derivatization with a water-soluble reagent, 3-(7-fluoro-2,1,3-benzoxadiazole-4-sulfonamido)benzenesulfonic acid (m-BS-ABD-F). The derivatization of BK with m-BS-ABD-F was completed at 70 degrees C for 100 min and gave only a single peak of BK derivative in addition to the peaks of the blank. The hydrophilicity of the derivatization reagent effectively prevented the adsorption of BK during the sample pretreatment and improved the recovery of BK. Good linearity was shown between the amount of BK spiked in urine (0-10 pmol) and the peak area of the BK derivatives (correlation coefficients >0.999), and the detection limits of the BK derivative were 35 fmol (S/N = 3). The precisions (cv, %) of intra- and interday assay were not more than 5.5% and the accuracies were in the range of 95.3-111% (1 and 5 pmol of BK in urine, n = 3). Although the peak regarded as that of the BK derivative rapidly decreased after incubation at 37 degrees C, addition of urinary kininase inhibitors to the urine samples drastically suppressed the decrease of this peak, confirming that the identified peak was that of the BK derivative. The urinary kinin excretion in male SD rats (9-11 weeks old) determined by the present method was 56.0 +/- 22.1 pg/min/kg (mean +/- SE, n = 5).

Animals↗

Adenovirus-mediated transfection of caspase-8 augments anoikis and inhibits peritoneal dissemination of human gastric carcinoma cells.

Caspase-8 is a member of the cysteine protease family that modulates apoptosis induced by a variety of cell death signals and has recently been found to be activated during the process of anoikis, which is a form of apoptosis caused by loss of anchorage in epithelial cells. We previously demonstrated that the inhibition of anoikis promotes peritoneal dissemination of human gastric carcinoma MKN45 cells, which are anchorage dependent. This suggests that augmentation of anoikis may suppress dissemination of carcinoma cells. To determine whether extrinsic overexpression of caspase-8 can augment anoikis in MKN45 cells, we transfected them with the caspase-8 gene using an adenoviral (Adv) vector (Adv-caspase-8). Here we demonstrate that Adv-caspase-8 infection, at 15 multiplicity of infection (MOI), can augment anoikis in MKN45 cells and suppresses MKN45 peritoneal dissemination in SCID mice. The inhibitory effect on peritoneal dissemination resulted in a prolonged survival compared with that in control mice. In contrast, the Adv-caspase-8 (15 MOI) had no distinct effect on cell viability or growth either of attached MKN45 cells or of s.c. tumor growth in SCID mice. Thus, Adv-mediated overexpression of caspase-8 suppressed peritoneal dissemination mainly through augmentation of anoikis. In addition, Adv-caspase-8-mediated augmentation of anoikis was similarly observed in another gastric carcinoma MKN74 cell line. In contrast, Adv-p53 could not augment anoikis in MKN45 cells. These results imply that Adv-mediated gene transfer of caspase-8 can selectively induce apoptosis in detached carcinoma cells and, thus, shows potential as a novel cancer therapy against dissemination of gastric and probably other carcinoma cells originating from epithelial tissues.

Adenocarcinoma↗

Clinicopathologic and prognostic significance of matrilysin expression at the invasive front in human colorectal cancers.

Matrix metalloproteinases (MMPs) have been implicated in tumor progression. Matrilysin, one of the matrix metalloproteinases, is frequently overexpressed in gastrointestinal cancers. The aim of our study was to assess the validity of matrilysin as a prognostic marker of colorectal cancers. Matrilysin expression was immunohistochemically analyzed using formalin-fixed, paraffin-embedded specimens from 113 colorectal cancer patients who had undergone curative surgery. The lumenal surface of neoplastic glands in the superficial layer was apically stained, while the cytoplasm of cancer cells at the invasive front was diffusely stained for matrilysin. Sections with immunostaining signals in more than 30% of carcinoma cells at the invasive front, which were observed in 47 (42%) cases, were judged as being positive for matrilysin. Matrilysin positivity was significantly correlated with the depth of invasion, lymph node metastasis, lymphatic invasion, advanced Dukes' stage and poor outcome. Patients with matrilysin-positive cancer had a significantly shorter overall survival time than those with matrilysin-negative cancer. For patients with intermediate invasive tumor (T2 or T3), only matrilysin was a significant prognostic variable for predicting overall survival in multivariate analysis. Matrilysin expression at the invasive front could be an important marker, predicting an unfavorable prognosis after surgical treatment in patients with colorectal cancer.

Biomarkers, Tumor↗

Comparative study for histology, proliferative activity, glycoproteins, and p53 protein between old and recent colorectal adenomas in Japan.

The incidence of colorectal carcinoma is increasing in Japan. Malignant transformation in colorectal neoplasia is usually considered to be owing to adenoma-carcinoma sequence. Elucidation of the recent alteration in the biological properties of colorectal adenoma is sure to be useful to understand the recent increase of the colorectal carcinoma in Japan. We compared the histopathological feature, mitotic index, proliferative activity (Ki-67 labeling index), expression of glycoproteins such as MUC2 mucin, sialyl Lewis A (SLe(a)) and sialyl dimeric Lewis X (SLe(x)), and p53 protein overexpression, between 108 adenomas in the old period (Group A, from 1969 to 1985) and 140 adenomas in the recent period (Group B, from 1995 to 1998). The histological dysplasia, mitotic index and Ki-67 labeling index of the adenomas were significantly higher in Group B than in Group A. In contrast, the expression of MUC2 mucin, which is considered to be a differentiation factor of intestinal mucosal epithelium, was significantly reduced in Group B than in Group A. The SLe(a) and SLe(x) expressions showed no significant difference between them. The p53 expression showed no significant difference between them, except for the moderate dysplasia. These findings indicate that recent colorectal adenomas show more advanced degrees of histological dysplasia, more rapid growth, and reduced differentiation than colorectal adenomas, which developed at earlier times, and may be related with the recent high incidence of colorectal carcinoma in Japan.

Adenoma↗

Production of (4)(double Lambda)H hypernuclei.

An experiment demonstrating the production of double-Lambda hypernuclei in (K(-),K(+)) reactions on (9)Be was carried out at the D6 line in the BNL alternating-gradient synchrotron. The technique was the observation of pions produced in sequential mesonic weak decay, each pion associated with one unit of strangeness change. The results indicate the production of a significant number of the double hypernucleus (4)(double Lambda)H and the twin hypernuclei (4)(Lambda)H and (3)(Lambda)H. The relevant decay chains are discussed and a simple model of the production mechanism is presented. An implication of this experiment is that the existence of an S = -2 dibaryon more than a few MeV below the double Lambda mass is unlikely.

Journal Article↗

Cancer prevention with green tea and monitoring by a new biomarker, hnRNP B1.

The study of green tea polyphenols as a cancer preventative is approaching a new era, with significant results accumulating rapidly. This paper briefly reviews four topics related to mechanisms of action of tea polyphenols: (I) identification of the genes commonly affected by EGCG, as demonstrated by Clontech's Atlas cDNA Expression Array; (II) the significance of heterogeneous nuclear ribonucleoprotein B1 (hnRNP B1) as a new biomarker for early detection of lung cancer, and inhibition of its expression by EGCG; (III) the synergistic or additive effects of EGCG with the cancer preventive agents, sulindac and tamoxifen, on induction of apoptosis in PC-9 cells and on inhibition of intestinal tumor development in multiple intestinal neoplasia (Min) mice; (IV) the results of a 10 year prospective cohort study demonstrating the effectiveness of daily consumption of green tea in preventing cancer, and a prototype study for developing green tea beverage as cancer preventive.

Animals↗

Expression of angiomodulin (tumor-derived adhesion factor/mac25) in invading tumor cells correlates with poor prognosis in human colorectal cancer.

Angiomodulin (tumor-derived adhesion factor/mac25/insulin-like growth factor binding protein-7), a cell-adhesive glycoprotein, is secreted by cancer cells and vascular endothelial cells. It may be involved in angiogenesis and modulation of the vascular functions necessary for tumor development. Although angiomodulin is expressed in colon cancer, there is limited information on it concerning cancer progression. In the present immunohistochemical study, we examined expression of angiomodulin in human colorectal cancer and its relationship with prognosis. A group of 89 surgically resected colorectal cancers was investigated immunohistochemically. In 37 cases (41.6%), angiomodulin was expressed in invading cancer cells. Early recurrence within 12 months after surgery was higher in patients with angiomodulin-expressing cancer than in those without (p < 0.05). The Kaplan-Meier life table revealed that patients with angiomodulin-positive tumor cells had a shorter survival time than those with negative cells (p < 0.01). The prognosis of patients with Dukes' C and angiomodulin-positive cells was apparently worse than that of patients with Dukes' D and angiomodulin-negative cells. Multivariate analysis with logistic regression indicated that only angiomodulin expression in cancer cells, lymph node metastasis and age remained significant prognostic variables for survival (p < 0.05). Angiomodulin showed correlations with poor prognosis, indicating that it may be a useful prognostic marker in patients with colorectal cancer.

Adult↗

Measurement of the midrapidity transverse energy distribution from square root of [(s)NN] = 130 GeV Au + Au collisions at RHIC.

The first measurement of energy produced transverse to the beam direction at the Relativistic Heavy-Ion Collider at Brookhaven National Laboratory is presented. The midrapidity transverse energy density per participating nucleon rises steadily with the number of participants, closely paralleling the rise in charged-particle density, such that / remains relatively constant as a function of centrality. The energy density calculated via Bjorken's prescription for the 2% most central Au+Au collisions at square root[s(NN)] = 130 GeV is at least epsilon(Bj) = 4.6 GeV/fm(3), which is a factor of 1.6 larger than found at sqrt[s(NN)] = 17.2 GeV ( Pb+Pb at CERN).

Journal Article↗

The (CTG)n polymorphism in the NOTCH4 gene is not associated with schizophrenia in Japanese individuals.

BACKGROUND: The human NOTCH4 gene is a candidate gene for schizophrenia due to its chromosomal location and neurobiological roles. In a British linkage study, NOTCH4 gene polymorphisms were highly associated with schizophrenia. In a Japanese case-control association study, however, these polymorphisms did not show significant associations with schizophrenia. We conducted a case-control study with Japanese subjects to explore an association between the triplet repeat polymorphism in the NOTCH4 gene and schizophrenia, including subtypes of schizophrenia, longitudinal disease course characteristics, and a positive family history for psychoses. METHODS: We examined the (CTG)n repeat polymorphism in the NOTCH4 gene among 100 healthy Japanese individuals and 102 patients with schizophrenia (22 paranoid, 38 disorganized, 29 residual, 64 episodic, 31 continuous, 42 with prominent negative symptoms, and 46 with positive family histories) using a polymerase chain reaction-based, single-strand conformational polymorphism analysis. RESULTS: Five different alleles consisting of 6, 9, 10, 11, and 13 repeats of CTG (Leu) in patients with schizophrenia, and 4 alleles consisting of 6, 9, 10, and 11 repeats in controls were found. No significant differences in genotype or allele frequencies of repeat numbers were found between controls and patients. In addition, there were no associations between the polymorphism and schizophrenia subtypes, longitudinal disease course characteristics, or positive family history of the patients. CONCLUSIONS: Our data suggest a lack of association between the NOTCH4 gene triplet repeat polymorphism and schizophrenia in Japanese individuals.

Adult↗

Oxidative stress in the absence of inflammation in a mouse model for hepatitis C virus-associated hepatocarcinogenesis.

The mechanism of hepatocarcinogenesis in hepatitis C virus (HCV) infection is still undefined. One possibility is the involvement of oxidative stress, which can produce genetic mutations as well as gross chromosomal alterations and contribute to cancer development. We recently showed that after a long period, the core protein of HCV induces hepatocellular carcinoma (HCC) in transgenic mice with marked hepatic steatosis but without inflammation, indicating a direct involvement of HCV in hepatocarcinogenesis. To elucidate the biochemical events before the development of HCC, we examined several parameters of oxidative stress and redox homeostasis in a mouse model of HCV-associated HCC. For young mice ages 3-12 months, there was no significant difference in the levels of hydroperoxides of phosphatidylcholine (PCOOH) and phosphatidylethanolamine in liver tissue homogenates between transgenic and nontransgenic control mice. In contrast, the PCOOH level was increased by 180% in old core gene transgenic mice > 16 months old. Concurrently, there was a significant increase in the catalase activity, and there were decreases in the levels of total and reduced glutathione in the same mice. A direct in situ determination by chemiluminescence revealed an increase in hydroperoxide products by 170% even in young transgenic mice, suggesting that hydroperoxides were overproduced but immediately removed by an activated scavenger system in young mice. Electron microscopy revealed lipofuscin granules, secondary lysosomes carrying various cytoplasmic organelles, and disruption of the double membrane structure of mitochondria, and PCR analysis disclosed a deletion in mitochondrial DNA. Interestingly, alcohol caused a marked increase in the PCOOH level in transgenic mice, suggesting synergism between alcohol and HCV in hepatocarcinogenesis. The HCV core protein thus alters the oxidant/antioxidant state in the liver in the absence of inflammation and may thereby contribute to or facilitate, at least in part, the development of HCC in HCV infection.

Animals↗

A fluorogenic reagent, 4-mercapto-7-methylthio-2,1,3-benzoxadiazole for carboxylic acids, designed by prediction of the fluorescence intensity.

During the course of our studies of the development of fluorogenic reagents having a 4,7-disubstituted benzofurazan structure, we previously proposed 7-acetylamino-4-mercapto-2,1,3-benzoxadiazole (AABD-SH) as a fluorogenic reagent for carboxylic acids. Since then, progress has made it possible to estimate the fluorescence quantum yields of the 4,7-disubstituted benzofurazan compounds on the basis of the PM3 calculation of their S1-T2 energies. Subsequently, a new fluorogenic reagent, 4-mercapto-7-methylthio-2,1,3-benzoxadiazole (MTBDSH) was designed and synthesized. In the presence of condensation reagents, triphenylphosphine (TPP) and 2,2'-dipyridyl disulfide (DPDS), MTBD-SH readily reacted with n-caprylic acid within 1 min at room temperature. The derivatives of five carboxylic acids (n-caprylic acid, n-capric acid, lauric acid, myristic acid, and palmitic acid) were well-separated on a reversed-phase column and were fluorimetrically detected at 519 nm with excitation at 391 nm. The detection limits (S/N = 3) were 2.4-5.0 fmol. Thus, MTBD-SH had properties that were considered to be superior. For carboxylic acids, itwas superior not only to AABD-SH, but also to many other conventional reagents. The superiority was examined in terms of its reactivity and sensitivity and the avoidance of interfering peaks that were derived from the reagent itself or degradation products in the chromatogram.

Carboxylic Acids↗

Centrality dependence of charged particle multiplicity in Au-Au collisions at square root of (s)NN = 130 GeV.

We present results for the charged-particle multiplicity distribution at midrapidity in Au-Au collisions at square root of [s(NN)] = 130 GeV measured with the PHENIX detector at RHIC. For the 5% most central collisions we find dN(ch)/d eta(vertical line eta = 0) = 622+/-1(stat)+/-41(syst). The results, analyzed as a function of centrality, show a steady rise of the particle density per participating nucleon with centrality.

Journal Article↗

Nuclear BAG-1 localization and the risk of recurrence after radiation therapy in laryngeal carcinomas.

BAG-1 is a multifunctional chaperone modulator may contribute to p53-mediated cell cycle arrest. We attempted to investigate whether BAG-1 expression is correlated with prognosis of laryngeal carcinoma patients after radiotherapy. Immunohistochemical analyses revealed BAG-1 expression was present in all laryngeal carcinomas examined, and its expression pattern varied, i.e. cytoplasmic, nuclear and both these staining types. Patients whose tumors predominantly express nuclear BAG-1 have a significantly poor failure-free survival rate after radiotherapy. We thus propose that nuclear BAG-1 localization is a prediction of unfavorable outcome should radiation therapy be undertaken for laryngeal carcinoma patients.

Biomarkers, Tumor↗

Association of trypsin expression with recurrence and poor prognosis in human esophageal squamous cell carcinoma.

BACKGROUND: Overexpression of the matrix serine proteinase (MSP) trypsin has been implicated in tumor growth, invasion, and metastasis. The objective of this study was to clarify the clinicopathologic and prognostic significance of trypsin expression in esophageal squamous cell carcinomas (SCC). METHODS: Production of trypsin in tissue extracts was analyzed by immunoblotting and gelatin zymography. The authors analyzed the association between immunohistochemically detected trypsin expression in esophageal SCC and clinicopathologic characteristics, and they investigated whether trypsin is a predictor of recurrence and/or survival. RESULTS: Overproduction and activation of trypsin was observed in 6 of 10 tumor extracts. The trypsin immunoreactivities at the invasive front were more intense than those at the superficial layer. Sections with immunostaining signals in greater than 30% of carcinoma cells at the invasive front, which were observed in 52 (52%) cases, were judged to be positive for trypsin. Trypsin positivity was significantly correlated with the depth of invasion (P < 0.0001), lymph node metastasis (P = 0.0048), advanced pTNM classification (P = 0.0006), recurrence (P = 0.0003), and recurrence within the first postoperative year (P = 0.0005). Patients with trypsin positive carcinoma had significantly shorter disease free and overall survival times than did those with trypsin negative carcinoma (P < 0.0001 and P < 0.0001, respectively). Trypsin retained its significant predictive value for disease free and overall survival in multivariate analysis that included conventional clinicopathologic factors (P = 0.0029 and P = 0.0006, respectively). Patients with concomitant overexpression of trypsin and matrilysin at the invasive front, in which they often were colocalized, had the worst prognosis. CONCLUSIONS: The authors' results suggest that trypsin plays a key role in the progression of esophageal carcinoma. Detection of trypsin expression as well as matrilysin is useful for the prediction of recurrence and poor prognosis.

Carcinoma, Squamous Cell↗