Yasuo Kato

Compression artifact reduction based on total variation regularization method for MPEG-2

In accordance with the recent improvement in the quality of image displays for consumer electronics, digital image compression artifacts are visible than ever. Noise removable methods are key issues not only in research areas such as image sensing and satellite imaging but also in consumer electronics such as television signal conversion, DVD and Blu-ray encodings. Among various compression artifact removable methods, the Total Variation (TV) regularization method is one of the most promising solutions. However, there are two problems: one is loss of image minuteness in the texture components, and the other is insufficient compression artifact removal in low bit rates. In this paper, we propose a new noise removable method utilizing the TV regularization method for moving pictures compressed by MPEG-2. We obtain fine experimental results in image quality improvement, and our method is possible to be applied to the other DCT based-image compression standards such as MPEG-4 and H.264.

Gastropleural fistula derived from malignant lymphoma

An 88-year-old man developed pneumothorax and pleural effusion. After the finding of ingesta in the pleural effusion, a gastropleural fistula was diagnosed. A biopsy specimen of the stomach revealed non-Hodgkin lymphoma, diffuse large-cell, B-cell type. Autopsy examination demonstrated that the malignant lymphoma had originated from high-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Gastropleural fistula is an uncommon condition, as the diaphragm forms a thick barrier between the stomach and the thoracic cavity. We review 25 reported cases of gastropleural fistula found in a MEDLINE search from 1966 to 2000. In only 3 of the 25 patients was malignant lymphoma reported to have caused the gastropleural fistula.

Aging of phrenic nerve conduction in the elderly

OBJECTIVEnWe elucidated the possible relationship between age and conduction parameters of phrenic nerve in subjects above the sixth decade, comparing with the data from middle-age controls.nnnMETHODSnDiaphragmatic action potentials (DAPs) were recorded on bilateral hemithoraces of 41 volunteers aged 60-101 years (old group) and 25 volunteers aged 35-55 years (middle-age group). Statistical analyses were performed to assess the effects of aging on latency, latency corrected by size (Lat/Dist), amplitude, and the right-left difference of these DAP parameters.nnnRESULTSnIn all 61 subjects, age showed a significant quadratic correlation with latency and with Lat/Dist, and a linear correlation with amplitude. The right-left differences ranged from 0.0 to 14.5% for latency and from 6.5 to 112.4% for amplitude in the elderly.nnnCONCLUSIONSnThe normal ranges of DAP parameters should be determined according to age. The left-right difference may be a useful reference in diagnosing unilateral phrenic nerve lesion.nnnSIGNIFICANCEnThe precise normal ranges of phrenic nerve conduction parameters presented will encourage investigations of neuropathies in subjects aged above 60.

Phenotypic alteration of interstitial cells of Cajal in idiopathic sigmoid megacolon

BackgroundInterstitial cells of Cajal (ICCs) are detected as a pacemaker of gastrointestinal movement and express c-kit and CD34. Recently, ICCs have implicated pathogenesis in several human diseases presenting gastrointestinal motor dysfunction. This study was performed to clarify the role of ICCs in idiopathic sigmoid megacolon using histological and immunohistochemical examinations.MethodsFour adult patients with idiopathic sigmoid megacolon and 11 controls were studied. Histology and immunocytochemistry using NSE, S100, c-kit, and CD34 were performed in conjunction with quantitative analysis using the public domain NIH image program.ResultsLittle histological change in neuromuscular structures in megacolon was observed. Immunohistochemistry demonstrated remarkable decrease of c-kit expressing ICCs without reduction of CD34 expression in the similar interstitial cell population. This observation was further supported by quantitative assessment using public domain NIH image program.ConclusionsA specific downregulation of c-kit in ICCs may be a cause of idiopathic sigmoid megacolon in adults.

Oncocytic Type Intraductal Papillary Mucinous Neoplasm of the Pancreas with Unusually Low Mucin Production Mimicking Intraductal Tubulopapillary Neoplasm: A Report of a Case Diagnosed by a Preoperative Endoscopic Biopsy

We herein report the case of a 78-year-old woman with an intraductal tumor with scant mucin production in a moderately dilated main pancreatic duct that resembled an intraductal tubulopapillary neoplasm (ITPN) on imaging. An endoscopic transpapillary forceps biopsy enabled an accurate preoperative diagnosis of the tumor as an oncocytic type intraductal papillary mucinous neoplasm (IPMN) of the pancreas microscopically showing papillary growth consisting of oncocytic cells with a typical mucin expression profile, although with few intraepithelial lumina containing mucin. This is the first case of an oncocytic type IPMN mimicking an ITPN that was able to be diagnosed preoperatively.

Abstract 3474: The effect of forced expression of k-ras mutation on gastrointestinal cancer cells and IGF-IR targeting therapy

Background & Aims: Mutation in k-ras plays important roles in both the progression and the resistance for anti-EGFR therapy in gastrointestinal tumors. Insulin-like growth factor-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of many tumors. We have previously shown successful therapy for gastrointestinal cancer cell lines with k-ras mutation using recombinant adenoviruses expressing dominant negative IGF-IR (IGF-IR/dn) and an anti-IGF-IR monoclonal antibody. In this study, we sought to evaluate the effect of k-ras mutation on gastrointestinal cancer cell lines and IGF-IR targeting therapies for those cells. Methods: We made stable transfectants of mutated k-ras in gastrointestinal cancer cell lines. We assessed the effect of forced expression of mutated k-ras on proliferartion, apoptosis induction, migration, and invasion in gastrointestinal cancer cell lines. Then we assessed the anti-tumor effect of IGF-IR/dn on mutated k-ras transfctomas. Results: Overexpression of mutated k-ras let gastrointestinal cancer cell lines be more agrressive phenotypes, such as more proliferative, more anti-apoptotic, more movable, and more invasive. IGF-IR/dn inhibited cell growth, colony formation, migration, and invasion, but induceed apoptosis of gastrointestinal cancer cells with or without mutated k-ras expression. Conclusions: K-ras mutation might be inportant for progressive phonotype in gastrointestinal cancers. IGF-IR might be a good molecular therapeutic target for gastrointestinal cancers even if k-ras is mutated. Citation Format: Yasushi Adachi, Yasutaka Matsunaga, Yasushi Sasaki, Katsuhiko Nosho, Hiroyuki Yamamoto, Yoshiaki Arimura, Takao Endo, Yasuo Kato, Takashi Tokino, David P. Carbone, Yasuhisa Shinomura. The effect of forced expression of k-ras mutation on gastrointestinal cancer cells and IGF-IR targeting therapy. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3474. doi:10.1158/1538-7445.AM2015-3474

Abstract 609: Targeting IGF-I receptor for hepatocellular carcinoma

Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CAnnAims; Hepatocellular carcinoma (HCC) is one of worse prognostic diseases. Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and tumor development of many malignancies and is thought to be a next molecular target. We have previously shown successful therapy for gastrointestinal carcinomas, including colon, stomach, esophageal, pancreatic, and biliary tract cancers, using recombinant adenoviruses expressing dominant negative IGF-IR (IGF-IR/dn). In this study, we want to assess the roles of IGF axis on HCC and to develop potential targeted therapeutics for HCC.nnMethods; We assessed mRNA expressions of IGFs and those receptors in HCC cell lines. We assessed the effect of IGF-IR blockade on signal-transduction, growth, apoptosis-induction, and migration. To block IGF signals, we used IGF-IR/dn, short hairpin RNA, monoclonal antibody, and tyrosin kinase inhibitor for IGF-IR.nnResults; IGF-I messages expressed in 63%, IGF-II mRNA in 44%, and IGF-IR in 89% of HCC cell lines. All IGF-IR blockades suppressed significantly both in vitro cell growth and colony formation. Each anti-IGF-IR up-regulated both stressor- and chemotherapy-induced apoptosis. IGF-IR inhibitor down-regulated cell migration. IGF-IR targeting strategies effectively blocked ligands induced receptor activation and the downstream signals.nnConclusions; IGF axis might play a key role in tumor progression of human HCC. Every strategy to block IGF-IR shows a useful anticancer therapeutic for HCC, indicating that IGF-IR may be a candidate molecular target for HCC.nnCitation Format: Yasushi Adachi, Yasutaka Matsunaga, Hiroyuki Yamamoto, Katsuhiko Nosho, Hiromu Suzuki, Yoshiaki Arimura, Takao Endo, Yasuo Kato, David P. Carbone, Yasuhisa Shinomura. Targeting IGF-I receptor for hepatocellular carcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 609. doi:10.1158/1538-7445.AM2014-609

Abstract 867: IGF-I receptor targeting therapy for esophageal carcinomas.

Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DCnnInsulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for tumorigenicity and cancer development of many malignancies, however this pathway has not been well studied in human esophageal carcinomas. Esophageal cancer is one of worst prognostic disease, main types of which are squamous cell carcinomas (ESCC) and adenocarcinoma (EAC). Previously we have reported that the IGF axis may play a key role in tumor progression of ESCC and its detection may be useful for the prediction of recurrence and poor prognosis and possibly for selecting patients for targeting therapy for IGF-IR. We have previously shown successful therapy for several gastrointestinal cancers using recombinant adenoviruses expressing dominant negative forms of IGF-IR (Ad-IGF-IR/dn). In this study, we wanted to develop potential targeted therapeutics to IGF-1R; therefore, we assessed the effect of IGF-IR blockade in both types of esophageal cancer. We analyzed immunohistochemical expression of IGF-IR in a tissue array. A tyrosine kinase inhibitor, BMS-536924, and Ad-IGF-IR/dn were used to treat several ESCC lines, such as TE1, TE8, TT, TTn, and EAC lines, including OE19 and OE33. We assessed the effect of both IGF-IR blockade on signal transduction, growth, and apoptosis. IGF-IR is expressed frequently in esophageal tumors, but not in normal mucosa. IGF-IR was produced in ESCC more than EAC, and is detected in metastasized similar to the primary site. IGF-IR inhibition suppressed proliferation and colony formation in both types of cancer. Blockade of IGF-IR up-regulated both stress- and chemotherapy-induced apoptosis in both esophageal tumor type. Although IGF-IR/dn blocked ligand-induced activation of Akt-1 mainly, BMS-536924 effectively blocked both activation of Akt and MAPK. Thus, the IGF axis may play a key role in tumor progression of human esophageal carcinomas. The IGF-IR targeting strategies might be useful anticancer therapeutics which can be used widely for human esophageal malignancies.nnCitation Format: Yasushi Adachi, Hiroyuki Yamamoto, Hirokazu Ohashi, Yasutaka Matsunaga, Katsuhiko Nosho, Hiromu Suzuki, Hiroaki Taniguchi, Yoshiaki Arimura, Takao Endo, Yasuo Kato, Kohzoh Imai, David P. Carbone, Yasushisa Shinomura. IGF-I receptor targeting therapy for esophageal carcinomas. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 867. doi:10.1158/1538-7445.AM2013-867

Abstract 3476: Combined blockade of IGF-I receptor and VEGF for gastric cancer

Background Insulin-like growth factor-I receptor (IGF-IR) signaling is required for tumorigenicity and tumor progression of gastrointestinal (GI) cancers. We have shown successful therapy for GI cancers using adenoviruses expressing dominant negative IGF-IR (IGF-IR/dn). On the other hand, IGF-IR signaling affects on vascular endotherial growh factor (VEGF) expression in some tumors. Here, we sought to evaluate the roles of IGF-IR on tumor angiogenesis and lymphangiogenesis and to develop targeting therapy for gastric cancer. Methods The impact of IGF signals on VEGF-A/C expression in gastric cancer cell was assessed. The effects of IGF-IR/dn alone and with bevacizumab on angiogenesis / lymphangiogenesis in mouse xenogfarts were assessed. Results IGFs induced expressions of VEGFs and up-regulated in vitro vascular vessel formation. IGF-IR/dn reduced those expressions and vascular formation. IGF-IR/dn down-regulated tumor size on mice via inhibiting both angiogenesis and lymphangiogenesis. The combination of IGF-IR/dn and bevacizumab was highly effective against tumors on mice. This combination reduced the expression of VEGF and induced apoptosis in the murine tumors most of all. Conclusions IGF-IR is involved in angiogenesis and lymphangiogenesis in gastric cancer. Targeting IGF-IR alone and with blocking VEGF may have therapeutic utility of prevention for gastric cancer progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3476.