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The aim of this study was to test the effectiveness of an occupational therapy program to promote well-being in people with experiences of mental illness. The method was a multicentre collaborative...

Microstructure change and helium release due to tensile loading on 304SS specimens implanted with low energy helium ions have been investigated. Specimens are irradiated with 8 keV helium ions at RT, 573 K and 873 K up to the fluence of 3 × 1021 He/m2. Tensile tests are performed at RT on unirradiated and irradiated specimens at a strain rate of 3.33 × 10−3/s. In every irradiation condition, specimens were tested to failure, and were elastically strained, yield point and plastically strained to 10%, 20% and 40% (total strain). After the tensile test, surface modification and microstructure change are observed with a scanning electron microscope (SEM) and a transmission electron microscope (TEM), respectively. It is shown that surface morphology and microstructure of irradiated specimens after the tensile test are drastically different from that of unirradiated specimens. The tensile loading also influences behavior of thermal desorption of helium and trap sites.

We report anesthetic management of patients undergoing single-lumen tracheal tube ventilation with artificial pneumothorax in thoracolaparoscopic esophagectomy in prone position. No adverse effect against respiratory and circulatory management was found during esophagectomy. Single-lumen tracheal tube ventilation with artificial pneumothorax potentially is a feasible method for thoracolaparoscopic esophagectomy in prone position.

Mechanical properties of low energy He irradiated 304SS have been investigated by means of tensile test and nano-identation hardness tests. Specimen size is 2.8 mm × 5.4 mm × 0.1 mm in gauge and 12.4 mm in total length. Specimens are irradiated with 8 keV helium ions at R.T., 573 K and 873 K up to the fluence of 3 × 10 21 He/m 2 . Tensile tests are performed on unirradiated and irradiated specimens at a strain rate of 3.33 × 10 −3 s −1 . In every irradiation condition, one specimen is tested to failure and the other two specimens are strained plastically to 10% and 20%. Formation of blisters with a diameter of about 500 nm is observed on the surface of tensile-tested specimens after R.T. irradiation. Some exfoliation of the blisters is also observed. When the irradiation temperature increases, a large number of cracks with a size of about several micrometers are formed on the surface together with exfoliation during the tensile test. The yield stress of specimens irradiated at R.T. and 573 K increases about 10% in comparison with that of the unirradiated specimen. The result of nano-indentation tests indicate that hardness near the surface increases depending on the irradiation temperature.

Mutations in the B-raf gene have been reported in a number of human cancers, including melanoma and lung cancer. More than 80% of the reported B-raf mutations were V599E; however, non-V599E mutations have been frequently found in non-small cell lung cancers as compared with melanoma. Some non-V599E mutations have been found surrounding Thr439, which is thought likely to be one of the three Akt phosphorylation sites in the B-raf protein. However, as a previous report indicated that Thr439 was not phosphorylated by Akt, the functional consequences of these mutations have been unclear. Here, we examined the effects of cancer-related B-raf mutations surrounding Thr439 on the activation of the mitogen-activated protein/ extracellular signal-regulated kinase kinase (MEK)/extracellular signal-regulated kinase (Erk) pathway and the transformation of NIH 3T3 fibroblasts. Among the three reported mutations (K438Q, K438T, and T439P) found in non-small cell lung carcinoma and melanoma, none elevated the activity of the MEK/Erk cascade as determined by in vitro kinase assays, immunoblots using antibody specific for phosphorylated Erk, or Elk1-dependent reporter assays. The inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt signaling by LY294002 increased the Erk activation induced by the mutant B-raf proteins, as well as by wild-type B-raf. Furthermore, the B-raf mutants did not have increased NIH 3T3-transforming activities, as determined by colony-formation assays. These results suggest that the B-raf mutations surrounding Thr439 found in human cancers are unlikely to contribute to increased oncogenic properties of B-raf.

Recently, mutations in the B-Raf gene have been identified in a variety of human cancers, such as melanoma and colorectal carcinoma, and more than 80% of the B-Raf mutations have been V599E. Although other mutations have been reported, their functional consequences are poorly understood. In our earlier study, we demonstrated that colon tumor-associated B-Raf mutations within the kinase activation segment are not necessarily associated with an increase in mitogen-activated protein/extracellular signal-regulated kinase kinase/extracellular signal-regulated kinase (MEK/Erk) or nuclear factor κB (NFκB) signaling activity or in NIH3T3-transforming ability [T. Ikenoue et al., Cancer Res., 63: 8132–8137, 2003]. In this study, we examined the effect of colon tumor-associated mutations within the B-Raf glycine-rich loop (G loop) on MEK/Erk and NFκB signaling and on the transformation of NIH3T3 fibroblasts or IEC-6 intestinal epithelial cells. Of the six G loop mutations examined, only the B-Raf G468A significantly increased MEK/Erk and NFκB signaling and NIH3T3 transformation. Only this mutation induced transformed phenotypes of IEC-6 cells. In contrast, the B-Raf G468E mutation significantly decreased MEK/Erk signaling and NIH3T3 transformation and had no effect on NFκB signaling. The B-Raf F467C mutation moderately elevated MEK/Erk signaling and NIH3T3 transformation. The other three B-Raf mutations, R461I, I462S, and G463E, did not increase MEK/Erk or NFκB signaling or NIH3T3 transformation. Except for F467C, none of the tumors with B-Raf mutations examined in this study had K-Ras mutations. These results suggest that some of the B-Raf G loop mutations reported in colorectal tumors do not increase kinase or transforming activities but might contribute to carcinogenesis via other mechanisms or be irrelevant to carcinogenesis.

Understanding the function of the hepatitis B virus X protein (HBx) is fundamental to elucidating the underlying mechanisms of hepatitis and hepatocarcinogenesis caused by hepatitis B virus (HBV) infection. We identified heat shock protein 60 (Hsp60) as a novel cellular target of HBx by the combination of affinity purification and mass spectrometry. Physical interaction between HBx and Hsp60 was confirmed by standard immunoprecipitation and immunoblot methods. Analysis of HBx deletion constructs showed that amino acids 88–117 of HBx were responsible for the binding to Hsp60. Confocal laser microscopy demonstrated that HBx and Hsp60 colocalized in mitochondria. Furthermore, terminal deoxynucleotidyl transferase-mediated dUTP end labeling (TUNEL) revealed that the introduction of Hsp60 into cells facilitated HBx-induced apoptosis. These findings suggest the importance of the molecular chaperon protein Hsp60 to the function of HBV viral proteins.

NEDD8/Rub1 is a ubiquitin (Ub)-like post-translational modifier that is covalently linked to cullin (Cul)-family proteins in a manner analogous to ubiquitylation. NEDD8 is known to enhance the ubiquitylating activity of the SCF complex (composed of Skp1, Cul-1, ROC1 and F-box protein), but the mechanistic role is largely unknown. Using an in vitro reconstituted system, we report here that NEDD8 modification of Cul-1 enhances recruitment of Ub-conjugating enzyme Ubc4 (E2) to the SCF complex (E3). This recruitment requires thioester linkage of Ub to Ubc4. Our findings indicate that the NEDD8-modifying system accelerates the formation of the E2-E3 complex, which stimulates protein polyubiquitylation.

It has recently been determined that the proteolytic destruction of IkappaB (inhibitor of NF-kappaB) by the ubiquitin-proteasome system plays a key role in the immediate elimination of IkappaB from the IkappaB-(NF-kappaB) complex which allows nuclear translocation of free NF-kappaB, thus leading to activation of a multitude of target genes. The SCF(Fbw1) (composed of Skp1, Cul-1, Roc1, and Fbw1) complex, identified as an IkappaBalpha-E3 ligase, binds and ubiquitylates IkappaBalpha phosphorylated by IkappaB kinase that has been activated in response to extracellular signals. The generating poly-ubiquitin chain is finally recognized by the 26S proteasome for ultimate degradation. In this NF-kappaB signalling pathway, it becomes clear that the SCF(Fbw1) activity is enhanced by a ubiquitin-like protein NEDD8 (equivalent to Rub1) that modifies Cul-1 in a manner analogous to ubiquitylation, and consequently, IkappaBalpha proteolysis is induced. NEDD8 is a new regulator of the SCF ubiquitin-ligase, functioning as a covalent modifier for proteolytic targeting at a physiological level.

SUMO-1 is a ubiquitin-like protein functioning as an important reversible protein modifier. To date there is no report on a SUMO-1 hydrolase/isopeptidase catalyzing the release of SUMO-1 from its precursor or SUMO-1-ligated proteins in mammalian tissues. Here we found multiple activities that cleave the SUMO-1 moiety from two model substrates, (125)I-SUMO-1-alphaNH-HSTVGSMHISPPEPESEEEEEHYC and/or GST-SUMO-1-(35)S-RanGAP1 conjugate, in bovine brain extracts. Of them, a major SUMO-1 C-terminal hydrolase had been partially purified by successive chromatographic operations. The enzyme had the ability to cleave SUMO-1 not only from its precursor but also from a SUMO-1-ligated RanGAP1 but did not exhibit any significant cleavage of the ubiquitin- and NEDD8-precursor. The activity of SUMO-1 hydrolase was almost completely inhibited by N-ethylmaleimide, but not by phenylmethanesulfonyl fluoride, EDTA, and ubiquitin-aldehyde known as a potent inhibitor of deubiquitinylating enzymes. Intriguingly, the apparent molecular mass of the isolated SUMO-1 hydrolase was approximately 30 kDa, which is significantly smaller than the recently identified yeast Smt3/SUMO-1 specific protease Ulp1. These results indicate that there are multiple SUMO-1 hydrolase/isopeptidases in mammalian cells and that the 30-kDa small SUMO-1 hydrolase plays a central role in processing of the SUMO-1-precursor.

The deubiquitinylating enzymes (DUBs), that release free ubiquitin (Ub) from its precursors or ubiquitinylated proteins, are known to comprise of a large protein family in eukaryotes, but those in mammalian tissues remain largely unknown. Here we report the existence of unexpectedly large species of DUBs in both soluble and membrane-bound fractions of bovine brain, based on their ability to cleave (125)I-labeled Ub-fused alphaNH-MHISPPEPESEEEEEHYC (designated as Ub-PESTc). Two cytosolic enzymes, tentatively called sDUB-1 and sDUB-2, with molecular masses of about 30 kDa were purified to near homogeneity by Ub-Sepharose affinity chromatography. sDUB-1 and sDUB-2 corresponded to UCH-L3 and UCH-L1/PGP 9.5, respectively. Intriguingly, the particulate fraction of the brain homogenate was found to also contain strong activities against (125)I-Ub-PESTc, which can be solubilized by treatment with 5% n-heptyl-beta-D-thioglucoside and 1% Nonidet P-40, but not by washing with 1 M NaCl. From the solubilized material, two new 30-kDa, membranous DUBs (called mDUB-1 and mDUB-2) were purified to apparent homogeneity by Ub-Sepharose chromatography. Two other Ub-aldehyde sensitive DUBs, designated as mDUB-3 and mDUB-4, were also partially purified by conventional chromatographic operations. These mDUBs differed from each other in substrate specificity and exhibited different characteristics from the sDUBs, revealing that they are a new type of membrane-bound DUB. These results indicate the presence of divergent DUBs in mammalian brain, which may contribute to regulation of numerous pivotal cellular functions mediated by the covalent modification of Ub.

BACKGROUND/AIMSGastric cancer is one of the most prevalent forms of cancer in East Asia. Point mutation of the p53 gene has been reported in more than 60% of cases of gastric cancer and can lead to genetic instability and uncontrolled cell proliferation. The purpose of this investigation was to evaluate the potential of p53 gene therapy for gastric cancer.METHODSThe responses of human gastric cancer cell lines, MKN1, MKN7, MKN28, MKN45, and TMK-1, to recombinant adenoviruses encoding wild type p53 (AdCAp53) were analysed in vitro. The efficacy of the AdCAp53 treatment for MKN1 and MKN45 subcutaneous tumours in nude mice was assessed in vivo.RESULTSp53-specific growth inhibition was observed in vitro in two of four gastric cancer cell lines with mutated p53, but not in the wild type p53 cell line. The mechanism of the killing of gastric cancer cells by AdCAp53 was found, by flow cytometric analysis and detection of DNA fragmentation, to be apoptosis. In vivo studies showed that the growth of subcutaneous tumours of p53 mutant MKN1 cells was significantly inhibited by direct injection of AdCAp53, but no significant growth inhibition was detected in the growth of p53 wild type MKN45 tumours.CONCLUSIONSAdenovirus mediated reintroduction of wild type p53 is a potential clinical utility in gene therapy for gastric cancers.

A new device structure based on microstrip line (MSL) is proposed to realize the MMW liquid crystal phase shifter. Fundamental characteristics for various device structures are evaluated by using FDTD Method. Here, we investigate in detail about the influence of "through hole" to the MMW propagation, which is the key component of the new device.

A 63-year-old man visited our hospital with complaints of the chest pain and loss of appetite. A computed tomography of chest showed wall thickening in the lower portion of the esophagus and carinal and para-aorta lymph node swelling. Upper gastrointestinal endoscopy revealed an irregular ulcerated lesion in the middle portion of the esophagus, which was pathologically diagnosed as small cell carcinoma. A computed tomography of the abdomen showed multiple liver metastases and para-aortic, cardiac, and common hepatic arterial lymph node swelling. One course of combined chemotherapy with CPT-11 and CDDP, then 3 courses of chemotherapy with CPT-11 showed clinical complete remission.

The graft-versus-tumor (GVT) effect that occurs following allogeneic bone marrow transplantation (BMT) and donor lymphocyte infusion (DLI) is currently being subjected to intensive investigation because of clinical evidence for GVT efficacy against leukemia. In this report, we investigate the efficacy and molecular mechanisms of GVT against solid tumors, using a modification of the mouse parent-to-F1 BMT model. Mouse Colon26 cells in which tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptor expression was stably knocked down were transplanted to investigate the role of the TRAIL-TRAIL receptor system in the GVT effect. In addition, Fas ligand-(FasL) deficient mice on a C57BL6 (B6) background were used as donors, to determine the significance of the Fas-FasL system for the antitumor effect. The group that received B6 DLI followed by preconditioning with 950 rad irradiation underwent tumor reduction associated with the induction of IFN-γ, TRAIL and tumor-cell apoptosis. In vitro cultured Colon26 cells were resistant to TRAIL but susceptible to the combination of IFN-γ and TRAIL in a TRAIL-dose-dependent manner. The infusion of lymphocytes from FasL-defective donors reduced the tumor progression, although efficacy was decreased in the TRAIL receptor knockdown tumors but not in wild-type ones, compared with infusion of B6-derived lymphocytes. The findings indicate that GVT activity against subcutaneous colon tumors is efficiently induced by preconditioning with irradiation and allogeneic DLI, and that TRAIL and IFN-γ act cooperatively in the antitumor effect. © 2005 Wiley-Liss, Inc.

Comparative proteomic analysis was used to search for characteristic alterations in the sera of hepatocellular carcinoma (HCC) patients who had undergone curative radiofrequency ablation treatment. Serum samples collected from eight patients before and after treatment were subjected to 2-DE. Eighty-eight protein spots differentially expressed with the treatment were selected by clustering analysis, and the proteins were identified by MS based on MALDI-TOF/TOF analysis and public database searches. The statistical analysis suggested that four proteins decreased after treatment (pro-apolipoprotein, alpha2-HS glycoprotein, apolipoprotein A-IV precursor, and PRO1708/PRO2044, which is the carboxy terminal fragment of albumin) and that seven proteins were increased after treatment, including leucine-rich alpha2-glycoprotein and alpha1-antitrypsin. These data facilitate the identification of differentially expressed proteins that are involved in HCC carcinogenesis and provide candidate biomarkers for the development of diagnostic and therapeutic tools.

Syringe swap is an important problem in anesthetic care, causing harm to patients. We examined the effect of colored syringe and a colored sheet on the incidence of syringe swaps during anesthetic management.We determined the color code. The blue-syringe contains local anesthetics; yellow-syringe, sympathomimetic drugs; and white-syringe with a red label fixed opposite the scale, muscle relaxants. The colored sheet displays the photographs of the syringe with drug name, dose and volume. The colored syringe and colored sheet were supplied for use from February 2004. We compared the incidence of syringe swaps during the period from February 2004 to January 2005 with that from February 2003 to January 2004.Although five syringe swaps were recorded from February 2003 to January 2004, in 5901 procedures, we encountered no syringe swaps from February 2004 to January 2005, in 6078 procedures. The colored syringe and colored sheet significantly decreased the incidence of syringe swaps during anesthetic management (P0.05).The use of the sheet together with colored syringes can prevent syringe swaps during anesthesia.

The transforming growth factor-beta (TGF-beta)-Smad signaling pathway inhibits the growth of human epithelial cells and plays a role in tumor suppression. The Smad4 gene is mutated or deleted in 50% of pancreatic cancers. In this study, we succeeded in establishing Smad4 knockdown (S4KD) pancreatic cancer cell lines using the stable RNA interference (RNAi) method. Smad4 protein expression was reduced dramatically and TGF-beta-Smad signaling was markedly inhibited in the S4KD cell lines. The S4KD and control cells were stimulated with TGF-beta and analysed using a cDNA microarray that contained 3756 genes, in order to screen for target molecules downstream of TGF-beta. The microarray analysis revealed that 187 S4KD genes and 155 genes in the control cells were regulated immediately upon TGF-beta stimulation. Quantitative RT-PCR analysis on several of these genes produced results that corroborated the outcome of the microarray analysis. Most of the genes in the S4KD and control cells identified by the array differed, which suggests signaling pathways that differ according to Smad4 status. Of the identified genes, 246 have not been reported previously as genes that lie downstream of TGF-beta. Genes that are involved in cell proliferation, adhesion, and motility were found to be regulated differentially with respect to S4KD and control cells. Cell migration induced by TGF-beta was inhibited in the S4KD cells, which might be associated with a different regulation of integrin beta7. The knock down of a specific gene using stable RNAi appears to be a promising tool for analysing endogenous gene function.

Recently, mutations in the B-Raf gene have been identified in a variety of human cancers, such as melanoma and colorectal carcinoma, and more than 80% of the B-Raf mutations have been V599E. Although other mutations have been reported, their functional consequences are poorly understood. In our earlier study, we demonstrated that colon tumor-associated B-Raf mutations within the kinase activation segment are not necessarily associated with an increase in mitogen-activated protein/extracellular signal-regulated kinase kinase/extracellular signal-regulated kinase (MEK/Erk) or nuclear factor kappaB (NFkappaB) signaling activity or in NIH3T3-transforming ability. In this study, we examined the effect of colon tumor-associated mutations within the B-Raf glycine-rich loop (G loop) on MEK/Erk and NFkappaB signaling and on the transformation of NIH3T3 fibroblasts or IEC-6 intestinal epithelial cells. Of the six G loop mutations examined, only the B-Raf G468A significantly increased MEK/Erk and NFkappaB signaling and NIH3T3 transformation. Only this mutation induced transformed phenotypes of IEC-6 cells. In contrast, the B-Raf G468E mutation significantly decreased MEK/Erk signaling and NIH3T3 transformation and had no effect on NFkappaB signaling. The B-Raf F467C mutation moderately elevated MEK/Erk signaling and NIH3T3 transformation. The other three B-Raf mutations, R461I, I462S, and G463E, did not increase MEK/Erk or NFkappaB signaling or NIH3T3 transformation. Except for F467C, none of the tumors with B-Raf mutations examined in this study had K-Ras mutations. These results suggest that some of the B-Raf G loop mutations reported in colorectal tumors do not increase kinase or transforming activities but might contribute to carcinogenesis via other mechanisms or be irrelevant to carcinogenesis.

Smad4 is a tumor-suppressor gene that is lost or mutated in 50% of pancreatic carcinomas. Smad4 is also an intracellular transmitter of transforming growth factor-beta (TGF-beta) signals. Although its tumor-suppressor function is presumed to reside in its capacity to mediate TGF-beta-induced growth inhibition, there seems to be a Smad4-independent TGF-beta signaling pathway. Here, we succeeded in establishing Smad4 knockdown (S4KD) pancreatic cancer cell lines using stable RNA interference. Smad4 protein expression and TGF-beta-Smad4 signaling were impaired in S4KD cells, and we compared the proteomic changes with TGF-beta stimulation using two-dimensional gel electrophoresis (2-DE) and mass spectrometry. We identified five proteins that were up-regulated and seven proteins that were down-regulated; 10 of them were novel targets for TGF-beta. These proteins function in processes such as cytoskeletal regulation, cell cycle, and oxidative stress. Introducing siRNA-mediated gene silencing into proteomics revealed a novel TGF-beta signal pathway that did not involve Smad4.

A 50-year-old woman underwent tonsillectomy under general anesthesia. She developed progressive hoarseness two month after the tonsillectomy, and a large granuloma of the larynx was found. Surgical removal of the granuloma was performed by laryngo-microsurgery. We should keep in mind that postintubation granuloma of the larynx might develop after tracheal intubation, and careful airway manipulation is needed to avoid this potential complication.

Mutations in the B-Raf gene have been reported in a number of human cancers, including colorectal carcinoma. More than 80% of the B-Raf mutations were V599E. Although other mutations have been reported, their functional consequences were unclear. Here, we examined the effect of colon tumor-associated B-Raf mutations within the kinase activation segment, including V599E, on extracellular signal-regulated kinase (Erk) and nuclear factor kappaB (NFkappaB) signaling, and on the transformation of NIH3T3 fibroblasts. Among the six mutations examined, only the B-Raf V599E and K600E mutations greatly increased Erk and NFkappaB signaling, and the transformation of NIH3T3 cells. The B-Raf F594L mutation moderately elevated Erk signaling and NIH3T3 transformation, but did not significantly increase NFkappaB signaling. Although the basal kinase activity of the B-Raf T598I mutant was comparable with that of wild-type, its oncogenic Ras-induced kinase activity was decreased to 60% of wild-type activity. The B-Raf D593V and G595R mutants showed severely reduced kinase activity and affected neither NFkappaB signaling nor NIH3T3 transforming activity. These results suggest that the B-Raf activation segment mutations other than V599E reported in colorectal tumors do not necessarily contribute to carcinogenesis by increasing kinase and transforming activities.

We did an obstetric management of a parturient, aged 32 years, with a history of local anesthetic hypersensitivity. The results of histamine release test, and cellular antigen stimulation test with lidocaine, mepivacaine, bupivacaine and preservative-free lidocaine during her pregnancy showed that all local anesthetics studied were positive. We used diphenhydramine as an alternative local anesthetic for episiotomy to the parturient during the delivery. Infiltration with diphenhydramine provided adequate analgesia without noticeable adverse reaction. One month after the delivery, we performed provocative challenge test with local anesthetics, and confirmed she had positive tests to lidocaine, mepivacaine and preservative-free lidocaine, and negative test to bupivacaine. Diphenhydramine is an adequate alternative of local anesthetics in patients with history of hypersensitivity to local anesthetics.

A planar-type electrically tunable phase shifter is demonstrated in the microwave region by using liquid crystal (LC) materials. A novel planar waveguide structure based on the microstrip line, which can convert the normal microstrip line to the inverted one, is designed. The new conversion circuit enables us to introduce LC materials on the microstrip line as easily as in the case of using the coplanar waveguide type of liquid crystal phase shifters. Larger phase shifting properties are confirmed empirically up to approximately 10 GHz with the application of a driving voltage of less than 10 V.

Prospective Study on Usefulness of Hood Attached to the Tip of Colonoscope Shintaro Kondo, Miki Ohta, Hirotsugu Watabe, Tsuneo Ikenoue, Takayuki Kawakami, Yutaka Yamaji, Makoto Okamoto, Haruhiko Yoshida, Takao Kawabe, Masao Omata Background: A hood attached to the tip of a colonoscope theoretically makes it possible to keep distance between lens of colonoscope and colonic mucosa and to obtain a better view. Recently, a variety of hoods have become commercially available. However, their usefulness has not been fully evaluated. Patients ,d Methods: A total of 294 patients were enrolled into this study. They were randomly allocated to transparent hood group, conventional hood group and non-hood group. Evaluated outcomes were completeness of the examination to the cecum, insertion time to the cecum and complications. No sedative medicine was administrated. PCF230I or PCF240I (Olympus, Tokyo, Japan) were used. Colonoscopists were all trainees who had experienced less than 1000 examinations. Results: Out of eligible 279 patients, 93, 91 and 95 patients were allocated to the transparent hood group, the conventional hood group and the non-hood group, respectively. No significant difference was found in patient’s background between the groups. Total colonoscopy were successful in 259 cases (92.8%). Failure were 5 cases (5.4%) in the transparent hood group, 6 cases (6.6%) in the conventional hood group and 9 cases (9.5%) in the non-hood group. No significant difference was found in unsuccessful rate between the groups. The median insertion time to the cecum was 11.0 minutes in the transparent hood group, 13.0 minutes in the conventional hood group and 12.0 minutes in the non-hood group (p Z 0.10). In the analysis of female cases, however, median insertion time was significantly shorter in the transparent hood group (11.0 minutes, 34 cases) than in the conventional hood group (16.0 minutes, 34 cases, p ! 0.05) and in the non-hood group (17.5 minutes 26 cases, p ! 0.05). No serious complications have occurred. Conclusion: A transparent hood may contribute to facilitate total colonoscopy for female patients.

Liver samples exhibited strong staining in portal tract lymphocytes, Kupffer cells and endothelinm. Lymphocytes in all gastrointestinal tissues stained strongly. Tissues not incubated with anti-hENT1 mAb were not stained. Conclusion: We report a novel immunohistoebemical assay and the first known immunohistochemieal localization of hENT 1 in human gastrointestinal tissues. This localization supports functional studies that eqinlibrative NT proteins are predominately found on the basolateral aspect of epithehal cells. As the absence of hENT1 confers high level nucleoside analogue drug resistance, this assay may serve as an important predictive tool in nucleoside analogue based gastrointestinal cancer therapies. CKWW is the recipient of an AHFMR Clinical Fellowship.