Publications by authors named "Kenji Watabe"

A 43-year-old woman experienced acute nausea, diarrhea, and abdominal pain, leading her to our hospital. No relevant medical history or physical abnormalities were noted. Symptoms persisted for a month, causing weight loss and abdominal bloating.

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Article Synopsis
  • The tumor microenvironment is crucial for tumor progression, with cancer-associated fibroblasts being key players, especially when TP53-deficient cancer cells are involved.
  • Research focused on exosomes from TP53-deficient colon cancer cells showed they can enhance fibroblast proliferation and tumor growth, indicating an oncogenic role.
  • Analysis revealed specific microRNAs in these exosomes that suppress TP53 expression in fibroblasts, suggesting that targeting these exosomes could be a promising new approach in colon cancer treatment.
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Background And Aim: Colorectal laterally spreading tumors (LSTs) are morphologically subdivided into granular (LST-G) and nongranular (LST-NG) categories. We aimed to elucidate the differences in oncogenic characteristics between the two types.

Methods: Laterally spreading tumors resected by endoscopic submucosal dissection and surgery from March 2009 to May 2017 were examined for p53 positivity, Ki-67 labeling index (LI), microvessel density, degree of fibrosis, intensities of inducible nitric oxide synthase (iNOS) and nitrotyrosine (NT), and expression of acid mucins.

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Background: Many reports indicate that a high-serum trough level of anti-tumor necrosis factor (TNF) agents is required for sustained remission in patients with Crohn's disease The pharmacokinetics of anti-TNF agents in inflamed intestinal tissue, however, is not well investigated. We investigated the association between the tissue concentration of anti-TNF agents and long-term disease outcome.

Methods: This was a prospective single-center study that enrolled 25 patients with Crohn's disease who were administered infliximab or adalimumab.

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Cancer-associated fibroblasts (CAFs) create a microenvironment that contributes to tumor growth; however, the mechanism by which fibroblasts are phenotypically altered to CAFs remains unclear. Loss or mutation of the tumor suppressor p53 plays a crucial role in cancer progression. Herein, we analyzed how the p53 status of cancer cells affects fibroblasts by investigating the in vivo and in vitro effects of loss of p53 function in cancer cells on phenotypic changes in fibroblasts and subsequent tumor progression in human colon cancer cell lines containing wild-type p53 and in cells with a p53 functional deficiency.

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A 23-year-old man presented tonic-clonic seizure a week after an episode of antecedent infection. Although several anticonvulsants were used, convulsive attacks were not resolved and intravenous anesthetics were used to stop status epileptics. After combination of immunotherapies (high-dose intravenous methylprednisolone, immune absorbance and intravenous immunoglobulin (IVIg) therapies), frequency of convulsive attacks decreased, however, disturbance of consciousness was not recovered.

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Background: Although conventional endoscopy (CE) and EUS are considered useful for predicting the invasion depth (T-staging) in early gastric cancer (EGC), no effective diagnostic strategy has been established.

Objective: To produce simple CE criteria and to elucidate an efficient diagnostic method by combining CE and EUS for accurate T-staging.

Design: Single-center retrospective analysis.

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Recent studies have demonstrated that cancer stem cells (CSCs) can initiate and sustain tumor growth and exhibit resistance to clinical cytotoxic therapies. Therefore, CSCs represent the main target of anticancer therapy. Interleukin-6 (IL-6) promotes cellular proliferation and drug resistance in colorectal cancer, and its serum levels correlate with patient survival.

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The emergence of chemoresistance is a major limitation of current cancer therapies, and checkpoint kinase (Chk1) 1 positively correlates with resistance to chemo‑ or radio‑therapy. Cancer cells lacking p53 pathways are completely dependent on the S and G2/M checkpoints via Chk1; therefore, Chk1 inhibition enhances the cytotoxicity of DNA‑damaging agents only in p53‑deficient cells. However, little is known about the synergistic effect of Chk1 inhibition with 5‑FU, the most frequently used antimetabolite, in chemoresistant colorectal cells.

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Background: Adiponectin is an adipose tissue-derived secretory hormone whose plasma concentrations are lower in obese individuals. Obesity is a risk factor for the development and growth of pancreatic cancer, and hypoadiponectinemia was suggested to be involved in the growth of Pan02 murine pancreatic cancer cells that were inoculated into the flanks of congenitally obese mice.

Aim: The aim of this study was to clarify the role of adiponectin in the growth of pancreatic cancer cells.

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This paper presents a gastric contraction imaging system for assessment of gastric motility using a 3-D endoscope. Gastrointestinal diseases are mainly based on morphological abnormalities. However, gastrointestinal symptoms are sometimes apparent without visible abnormalities.

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Choroidal or cutaneous metastasis of gastric cancer is rare. Gastrointestinal cancer was found in only 4% in patients with uveal metastasis. Choroidal metastasis from gastric cancer was reported in two cases in earlier literature.

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Article Synopsis
  • The study investigates the link between serum adiponectin levels, central obesity, insulin resistance, and liver dysfunction in relation to alcohol consumption among 5,588 healthy Japanese males.
  • Results show that mild drinkers had lower liver enzyme levels and higher adiponectin levels compared to non-light and moderate drinkers, while central obesity decreased in importance as alcohol consumption increased.
  • The conclusion highlights that low adiponectin levels are a crucial factor in liver dysfunction associated with fatty liver, regardless of how much alcohol is consumed, whereas central obesity does not significantly impact liver function in this context.
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Adiponectin is an anti-inflammatory molecule released from adipocytes, and serum adiponectin concentrations are reduced in obesity. We previously reported that gastric erosion occurs in association with obesity and low serum adiponectin levels. In the present study, we examined adiponectin-knockout (APN-KO) mice to elucidate the role of adiponectin in gastric mucosal injury.

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Obesity has become a major concern among gastroenterologists due to its large influence on gastrointestinal and hepatic diseases: reflux esophagitis, pancreatitis, gallstone disease, liver fibrosis, and neoplastic tumors of the esophagus, pancreas, and colon. Studies of morbid obese subjects undergoing bariatric surgery have revealed that obesity is related with an increased prevalence of endoscopic and histologic gastritis. A recent study of health check-up subjects demonstrated an association of obesity with endoscopic gastritis and gastric ulcers.

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Background: Obesity is a risk factor for gastro-esophageal reflux disease (GERD). It is generally considered that intra-abdominal pressure in obese subjects is involved in the pathogenesis of GERD through acid exposure to the esophagus. Recently, visceral fat has been recognized as an endocrine organ that secretes various adipocytokines including adiponectin.

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A man in his thirties with epigastric pain was referred to our hospital for detailed examinations. Abdominal computed tomography showed an abdominal cystic lesion with a longest dimension of 7 cm, located behind the stomach. Endoscopic ultrasonography through the stomach showed a cystic lesion and the wall of the lesion revealed continuity to the proper muscle layer of the gastric wall.

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Background: Obesity is recently known as a risk factor for endoscopic gastritis. Adiponectin is an anti-inflammatory cytokine secreted from fat tissue, and its serum concentrations are reduced in obesity. The relation between adiponectin and gastritis remains unclear.

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Plasma adiponectin levels are reduced in obese people, and hypoadiponectinemia is recently reported to associate with cholesterol gallstone formation in human. The aim of this study was to examine the role of adiponectin in gallstone formation using adiponectin knockout mice. We analyzed male knockout and C57BL6J mice fed normal or lithogenic diet for 6 weeks.

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Background: Adiponectin is recognized as an antiinflammatory and antifibrotic protein derived from adipocytes, and low serum adiponectin levels are present in obesity. Recent studies have highlighted the relationship between obesity and pancreatic diseases. However, the role of adiponectin in chronic pancreatitis remains uncertain.

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Background: CD9 is a member of the tetraspanins, and has been shown to be involved in a variety of cellular activities such as motility, cell signaling, proliferation, adhesion, and metastasis. However, very little is known about the involvement of CD9 in the process of development of primary tumors. In the present study, we investigated whether anti-CD9 monoclonal antibody (ALB6) has antitumor effects in human gastric cancer cell xenografts.

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Purpose: Interstitial cells of Cajal (ICC) play important roles in autonomic gut motility as electrical pacemakers and mediators of neural regulation of smooth muscle functions. Insufficiency of ICC has been reported in a wide range of gut dysmotilities. Thus, restoration of ICC may be a therapeutic modality in these diseases.

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A 40's-year-old woman who had abdominal pain with fever was referred to our hospital for further examinations. Abdominal computed tomography showed no focal lesion, and no causative lesion was found after a gynecological examination, upper gastrointestinal endoscopy and colonoscopy. Tuberculin test and QuantiFERON-TB were positive, and thus tuberculous peritonitis was suspected.

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Background And Aim: Diabetes mellitus (DM) often causes gastrointestinal dysmotility. Interstitial cells of Cajal (ICC), which express c-kit receptor tyrosine kinase (KIT), are considered the pacemaker cells for gastrointestinal movement. The present study was designed to determine the role of ICC in the pathogenesis of gastroenteropathy in type 2 DM.

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Background: Promoter hypermethylation of E-cadherin plays an important role on gastric carcinogenesis. We have previously reported that the odds ratio for gastric carcinoma and the prevalence of diffuse-type early gastric carcinoma in Helicobacter pylori-induced enlarged fold gastritis increased with increasing fold width. Thus, we examined E-cadherin methylation in gastric mucosa from H.

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