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| 1 | Molecular diagnosis and therapy for occult peritoneal metastasis in gastric cancer patients显示文摘To apply an individualized oncological approach to gastric cancer patients,the accurate diagnosis of disease entities is required.Peritoneal metastasis is the most frequent mode of metastasis in gastric cancer,and the tumor-node-metastasis classification includes cytological detection of intraperitoneal cancer cells as part of the staging process,denoting metastatic disease.The accuracy of cytological diagnosis leaves room for improvement;therefore,highly sensitive molecular diagnostics,such as an enzyme immunoassay,reverse transcription polymerase chain reaction,and virusguided imaging,have been developed to detect minute cancer cells in the peritoneal cavity.Molecular targeting therapy has also been spun off from basic research in the past decade.Although conventional cytologyis still the mainstay,novel approaches could serve as practical complementary diagnostics to cytology in near future. | Shunsuke Kagawa Kunitoshi Shigeyasu Michihiro Ishida Megumi Watanabe Hiroshi Tazawa Takeshi Nagasaka Yasuhiro Shirakawa Toshiyoshi Fujiwara | 2014 | World Journal of Gastroenterology2014，20，47： | 11 |
| 2 | ARID1A expression in gastric adenocarcinoma:Clinicopathological significance and correlation with DNA mismatch repair status显示文摘AIM:To analyze the mismatch repair(MMR)status and the ARID1A expression as well as their clinicopathological significance in gastric adenocarcinomas.METHODS:We examined the expressions of MMR proteins and ARID1A by immunohistochemistry in consecutive 489 primary gastric adenocarcinomas.The results were further correlated with clinicopathological variables.RESULTS:The loss of any MMR protein expression,indicative of MMR deficiency,was observed in 38cases(7.8%)and was significantly associated with an older age(68.6±9.2 vs 60.4±11.7,P<0.001),a female sex(55.3%vs 31.3%,P=0.004),an antral location(44.7%vs 25.7%,P=0.021),and a differentiated histology(57.9%vs 39.7%,P=0.023).Abnormal ARID1A expression,including reduced or loss of ARID1A expression,was observed in 109 cases(22.3%)and was significantly correlated with lymphatic invasion(80.7%vs 69.5%,P=0.022)and lymph node metastasis(83.5%vs 73.7%,P=0.042).The tumors with abnormal ARID1A expression more frequently indicated MMR deficiency(47.4%vs 20.2%,P<0.001).A multivariate analysis identified abnormal ARID1A expression as an independent poor prognostic factor(HR=1.36,95%CI:1.01-1.84;P=0.040).CONCLUSION:Our observations suggest that the AIRD1A inactivation is associated with lymphatic invasion,lymph node metastasis,poor prognosis,and MMR deficiency in gastric adenocarcinomas. | Ryo Inada Shigeki Sekine Hirokazu Taniguchi Hitoshi Tsuda Hitoshi Katai Toshiyoshi Fujiwara Ryoji Kushima | 2015 | World Journal of Gastroenterology2015，21，7： | 7 |
| 3 | Glutamine depletion induces murine neonatal melena with increased apoptosis of the intestinal epithelium显示文摘AIM:To investigate the possible biological outcome and effect of glutamine depletion in neonatal mice and rodent intestinal epithelial cells.METHODS:We developed three kinds of artificial milk with different amounts of glutamine;Complete amino acid milk (CAM),which is based on maternal mouse milk,glutamine-depleted milk (GDM),and glutaminerich milk (GRM).GRM contains three-fold more glutamine than CAM.Eighty-seven newborn mice were divided into three groups and were fed with either of CAM,GDM,or GRM via a recently improved nipple-bottle system for seven days.After the feeding period,the mice were subjected to macroscopic and microscopic observations by immunohistochemistry for 5-bromo-2'deoxyuridine (BrdU) and Ki-67 as markers of cell proliferation,and for cleaved-caspase-3 as a marker of apoptosis.Moreover,IEC6 rat intestinal epithelial cells were cultured in different concentrations of glutamine and were subject to a 4-[3-(4-iodophenyl)-2-(4-nitrophenyl)2H-5-tetrazolio]-1,3-benzene disulfonate cell proliferation assay,flow cytometry,and western blotting to examine the biological effect of glutamine on cell growth and apoptosis.RESULTS:During the feeding period,we found colonic hemorrhage in six of 28 GDM-fed mice (21.4%),but not in the GRM-fed mice,with no differences in body weight gain between each group.Microscopic examination showed destruction of microvilli and the disappearance of glycocalyx of the intestinal wall in the colon epithelial tissues taken from GDM-fed mice.Intake of GDM reduced BrdU incorporation (the average percentage of BrdU-positive staining;GRM:13.8%,CAM:10.7%,GDM:1.14%,GRM vs GDM:P < 0.001,CAM vs GDM:P < 0.001) and Ki-67 labeling index (the average percentage of Ki67-positive staining;GRM:24.5%,CAM:22.4% GDM:19.4%,GRM vs GDM:P=0.001,CAM vs GDM:P =0.049),suggesting that glutamine depletion inhibited cell proliferation of intestinal epithelial cells.Glutamine deprivation further caused the deformation of the nuclear membrane and the plasma membrane,accompanied by chromatin degeneration and an absence of fat droplets from the colonic epithelia,indicating that the cells underwent apoptosis.Moreover,immunohistochemical analysis revealed the appearance of cleaved caspase-3 in colonic epithelial cells of GDM-fed mice.Finally,when IEC6 rat intestinal epithelial cells were cultured without glutamine,cell proliferation was significantly suppressed after 24 h (relative cell growth;4 mmol/L:100.0% ± 36.1%,0 mmol/L:25.3% ± 25.0%,P < 0.05),with severe cellular damage.The cells underwent apoptosis,accompanied by increased cell population in sub-G0 phase (4 mmol/L:1.68%,0.4 mmol/L:1.35%,0 mmol/L:5.21%),where dying cells are supposed to accumulate.CONCLUSION:Glutamine is an important alimentary component for the maintenance of intestinal mucosa.Glutamine deprivation can cause instability of the intestinal epithelial alignment by increased apoptosis. | Takayuki Motoki Yoshio Naomoto Junji Hoshiba Yasuhiro Shirakawa Tomoki Yamatsuji Junji Matsuoka Munenori Takaoka Yasuko Tomono Yasuhiro Fujiwara Hiroshi Tsuchita Mehmet Gunduz Hitoshi Nagatsuka Noriaki Tanaka Toshiyoshi Fujiwara | 2011 | World Journal of Gastroenterology2011，17，6： | 4 |
| 4 | CD14 upregulation as a distinct feature of non-alcoholic fatty liver disease after pancreatoduodenectomy显示文摘AIM:To investigate the pathogenesis of non-alcoholic fatty liver disease(NAFLD)after pancreatoduodenectomy(PD).METHODS:A cohort of 82 patients who underwent PD at Okayama University Hospital between 2003 and 2009 was enrolled and the clinicopathological features were compared between patients with and without NAFLD after PD.Computed tomography(CT)images were evaluated every 6 mo after PD for follow-up.Hepatic steatosis was diagnosed on CT when hepatic attenuation values were 40 Hounsfield units.Liver biopsy was performed for 4 of 30 patients with NAFLD after PD who consented to undergo biopsies.To compare NAFLD after PD with NAFLD associated with metabolic syndrome,liver samples were obtained from 10 patients with NAFLD associated with metabolic syndrome [fatty liver,n = 5;non-alcoholic steatohepatitis(NASH),n = 5] by percutaneous ultrasonography-guided liver biopsy.Double-fluorescence immunohistochemistry was applied to examine CD14 expression as a marker of lipopolysaccharide(LPS)-sensitized macrophage cells(Kupffer cells)in liver biopsy specimens.RESULTS:The incidence of postoperative NAFLD was 36.6%(30/82).Univariate analysis identified cancer of the pancreatic head,sex,diameter of the main pancreatic duct,and dissection of the nerve plexus as factors associated with the development of NAFLD after PD.Those patients who developed NAFLD after PD demonstrated significantly decreased levels of serum albumin,total protein,cholesterol and triglycerides compared to patients without NAFLD after PD,but no glucose intolerance or insulin resistance.Liver biopsy was performed in four patients with NAFLD after PD.All four patients showed moderate-to-severe steatosis and NASH was diagnosed in two.Numbers of cells positive for CD68(a marker of Kupffer cells)and CD14(a marker of LPSsensitized Kupffer cells)were counted in all biopsy specimens.The number of CD68+ cells in specimens of NAFLD after PD was significantly increased from that in specimens of NAFLD associated with metabolic syndrome specimens,which indicated the presence of significantly more Kupffer cells in NAFLD after PD than in NAFLD associated with metabolic syndrome.Similarly,more CD14+ cells,namely,LPS-sensitized Kupffer cells,were observed in NAFLD after PD than in NAFLD associated with metabolic syndrome.Regarding NASH,more CD68+ cells and CD14+ cells were observed in NASH after PD specimens than in NASH associated with metabolic syndrome.This showed that more Kupffer cells and more LPS-sensitized Kupffer cells were present in NASH after PD than in NASH associated with metabolic syndrome.These observations suggest that after PD,Kupffer cells and LPS-sensitized Kupffer cells were significantly upregulated,not only in NASH,but also in simple fatty liver.CONCLUSION:NAFLD after PD is characterized by both malnutrition and the up-regulation of CD14 on Kupffer cells.Gut-derived endotoxin appears central to the development of NAFLD after PD. | Daisuke Satoh Takahito Yagi Takeshi Nagasaka Susumu Shinoura Yuzo Umeda Ryuichi Yoshida Masashi Utsumi Takehiro Tanaka Hiroshi Sadamori Toshiyoshi Fujiwara | 2013 | World Journal of Hepatology2013，5，4： | 3 |
| 5 | Electrostatic micro torsion mirrors for an optical switch matrix 显示文摘 | H Toshiyoshi H Fujita | 1996 | J Microelectromech Syst1996，5，： | 2 |
| 6 | Oral administration of FAK inhibitor TAE226 inhibits the progression of peritoneal dissemination of colorectal cancer显示文摘 | Hui-fang Hao Munenori Takaoka Xiao-hong Bao Zhi-gang Wang Yasuko Tomono Kazufumi Sakurama Toshiaki Ohara Takuya Fukazawa Tomoki Yamatsuji Toshiyoshi Fujiwara Yoshio Naomoto | 2012 | Biochemical and Biophysical Research Communications2012，，： | 1 |
| 7 | Electrostatic micro-torsion mirrors for an optical switch matrix 显示文摘 | Toshiyoshi H Fujita H | 1996 | J Microelectromech Syst1996，，5： | 1 |
| 8 | Electrostatic micro torsion mirrots for an optical switch matrix显示文摘 | Hiroyuki Fujita | 1996 | Journal for Microelectromechanical Systems1996，5，4： | 1 |
| 9 | A retroviral wild-type p53 expression vector penetractes human lung cancer spheroids and inhibits growth by inducing apoptosis显示文摘 | Toshiyoshi F Griman EA Makhopadhyay T | 1993 | Cancer Res1993，53，18： | 1 |
| 10 | Electrostatic micro torsion mirrors for an optical switch matrix显示文摘 | Hiroshi Toshiyoshi Hiroyuki Fujita | 1996 | Journal of Microelectromechanical Systems1996，5，4： | 1 |
| 11 | An out - of- plane polysilicon actuator with a smooth vertical mirror for optical fibers switch application 显示文摘 | M Mita D Miyauchi H Toshiyoshi | 1998 | Proc of IEEE MEMS1998，，： | 1 |
| 12 | Light actuation of liquid by optoelectrowetting显示文摘 | Chioua P Y Moon H Toshiyoshi H | 2003 | Sensors and Actuators2003，104，3： | 1 |
| 13 | Electrostatic Micro Torsion Mirrors for an Optical Switch Matrix显示文摘 | TOSHIYOSHI H FUJITA H | 1998 | Microelectromechanical System1998，5，4： | 1 |
| 14 | Electromagnetic torsion mirrors for self-aligned fiber-optic crossconnectors by silicon micromachining显示文摘 | Miyauchi D Fujita H | 1999 | IEEE Joural of selected topics in quantum electronics1999，5，1： | 1 |
| 15 | Electrostatic micro torsion mirrors for an optical switch matrix显示文摘 | Toshiyoshi H Fujita | 1998 | Microelectromechanical System1998，5，4： | 1 |
| 16 | 显示文摘 | Toshiyoshi T Ken-ichi H Masakazu G | 2005 | Animal Science Journal2005，76，： | 1 |
| 17 | Fabric-ation of single-crystal Si cantilever array显示文摘 | SAYA D FUKUSHIMA K TOSHIYOSHI H | 2002 | Sensor and Actuator A2002，95，23： | 1 |
| 18 | Electrostatica micro torsion mirrors for an optical switch matrix显示文摘 | Toshiyoshi H Fujita H | 1996 | Journal of Micro-Electro-Mechanical Systems1996，5，4： | 1 |
| 19 | Light actuation of liquid by optoelectrowetting显示文摘 | Pei Yu Chioua Hyejin Moon Hiroshi Toshiyoshi | 2003 | Sensors and Actuators2003，104，3： | 1 |
| 20 | Prevention of acute liver failure in rats with reversibly immortalized human hepatocytes显示文摘 | NAOYA K TOSHIYOSHI F | 2000 | Science2000，287，18： | 1 |
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