Publications by authors named "Masaaki Kuroda"

Aims: Cardiovascular events are the leading cause of death among patients with non-alcoholic fatty liver disease (NAFLD), but their relationship remains unclear. This study examined the association between coronary atherosclerosis and liver fibrosis, represented by the coronary artery calcification (CAC) score and non-invasive fibrosis markers, respectively.

Methods: Among 698 patients with chest pain or electrocardiographic abnormalities who underwent coronary computed tomography (CT) between April 2006 and March 2010, those with known liver disorders or history of emergency coronary angioplasty were excluded, leaving 366 patients for this study.

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Helicobacter pylori infection, which is a common cause of atrophic gastritis, has been reported to represent a causal factor increasing the vascular damage and consequent albuminuria. On the other hand, decreased serum pepsinogen (PG) I/II ratio can be used to assess gastric mucosal atrophy. To the best of our knowledge, there are no studies investigating the correlation between PG I/II ratio and diabetic nephropathy.

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Background And Aims: Esophageal visceral hypersensitivity has been proposed to be a pathogenesis of heartburn in nonerosive reflux disease (NERD), but its further mechanisms are unclear. Recently, it has been suggested that nociceptors and neuropeptides control sensory and pain mechanisms. Therefore, the objective of the present study was to estimate expression of acid-sensitive nociceptors such as transient receptor potential vanilloid 1 (TRPV1) and acid-sensing ion channel 3, protease-activated receptor 2 (PAR2), neuropeptides such as substance P and calcitonin-gene-related peptide, and their receptors such as neurokinin 1 receptor (NK1R) and receptor activity-modifying protein 1 in the esophageal mucosa of NERD patients.

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Atrophic gastritis is characterized by chronic inflammation of gastric mucosa by Helicobacter pylori infection and other factors. Helicobacter pylori infection has been linked to coronary artery disease. To our knowledge, however, no reports are available on the relationship between atrophic gastritis and coronary artery disease.

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Objective: Under- and overnutrition are associated with a worse prognosis and constitute independent risk factors for morbidity and mortality. It is increasingly important to understand the factors that affect nutritional and metabolic statuses. The purpose of this study was to assess the relation between the pepsinogen I/II ratio and several biochemical markers.

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We have investigated the flow birefringence property and assembly process of desmin, a muscle specific intermediate protein. Solution of non-polar desmin filaments showed birefringence when aligned in the sheared flow. The amount of birefringence of desmin filaments was considerably lower when compared with that of F-actin solution.

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Larval-to-adult myogenic conversion occurs in the dorsal muscle but not in the tail muscle during Xenopus laevis metamorphosis. To know the mechanism for tail-specific suppression of adult myogenesis, response character was compared between adult myogenic cells (Ad-cells) and larval tail myogenic cells (La-cells) to a Sonic hedgehog (Shh) inhibitor, notochord (Nc) cells, and spinal cord (SC) cells in vitro. Cyclopamine, an Shh inhibitor, suppressed the differentiation of cultured Ad (but not La) cells, suggesting the significance of Shh signaling in promoting adult myogenesis.

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N-terminal actin-binding domain of α-actinin is connected to central rod domain through flexible neck region that is susceptible to proteolysis. It is suggested that the neck region assumes variable orientations by actin binding. In order to examine the effect of actin binding to α-actinin, we carried out limited digestion of α-actinin by chymotrypsin in the presence and absence of F-actin.

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Isoforms of myosin heavy chain and tropomyosin convert during metamorphosis of Xenopus laevis with larval-to-adult remodeling of dorsal muscle (Nishikawa and Hayashi, 1994 , Dev. Biol. 165: 86-94).

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Background And Aim: Induction of inducible nitric oxide synthase (iNOS) may be involved in carcinogenesis of the stomach, because nitric oxide (NO) derived from iNOS can exert DNA damage and post-transcriptional modification of target proteins. In the present study, we investigated the correlation between endoscopic findings and iNOS mRNA expression/NO-modified proteins in the gastric mucosa.

Methods: Fifty patients were prospectively selected from subjects who underwent upper gastrointestinal chromoendoscopy screening for abdominal complaints.

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We have reported that rebamipide, a gastroprotective drug, suppresses indomethacin-induced gastric mucosal injury in humans and rats. However, the mechanisms of the cytoprotective actions of rebamipide have not been fully addressed. In the present study, we determined mRNA expression profile of the gastric mucosa treated with indomethacin in rats, and investigated the cytoprotective effects of rebamipide against indomethacin-induced injury with a high-density oligonucleotide array (Rat Toxicology U34 GeneChip array).

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Recent studies have shown that esophageal mucosal inflammatory response is involved in the pathophysiology of gastro-esophageal reflux disease. The aim of the present study was to identify specific gene expression profiles of the esophageal mucosa in a rat model of combined-type chronic reflux esophagitis. Esophagogastroduodenal anastomosis was carried out in male Wistar rats by anastomosing the jejunum to the gastroesophageal junction under diethyl-ether inhalation anesthesia.

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We have demonstrated that astaxanthin reduces glomerular oxidative stress as well as inhibits the increase in urinary albumin in diabetic db/db mice. The aim of the present study was to determine the gene expression patterns in the glomerular cells of the diabetic mouse kidney, and to investigate the effects of astaxanthin on the expression of these genes using a high-density DNA microarray. The diet administered to the astaxanthin-supplementation group was prepared by mixing a control powder with astaxanthin at a concentration of 0.

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Objective: Mast cell tryptase has been proposed to be involved in the pathogenesis of human inflammatory bowel disease (IBD). Recently, it was reported that a low dose of nafamostat mesilate (NM), a serine protease inhibitor that is widely used to treat disseminated intravascular coagulation (DIC) and acute pancreatitis, can selectively inhibit human tryptase activity. The aim of this study was to investigate the anti-inflammatory effects of NM on experimental colitis in rats.

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Background: Reflux of the duodenal contents with gastric acid has been reported to contribute to the development of esophageal mucosal damage and inflammation. Recent studies show that pancreatic trypsin can stimulate the production of inflammatory mediators, including chemokines and prostaglandins from human esophageal epithelial cells in vitro. The aim of the present study was to investigate the role of pancreatic trypsin in the pathogenesis of chronic esophageal inflammation induced by gastroduodenal reflux in rats.

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Aim: To investigate the protective effect of rosuvastatin on ischemia-reperfusion (I-R)-induced small intestinal injury and inflammation in rats, and to determine the effect of this agent on the expression of endothelial nitric oxide synthase (eNOS) protein.

Methods: Intestinal damage was induced in male Sprague-Dawley rats by clamping both the superior mesenteric artery and the celiac trunk for 30 min, followed by reperfusion for 60 min. Rosuvastatin dissolved in physiological saline was administered intraperitoneally 60 min before ischemia.

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Lipid peroxidation mediated by oxygen free radicals plays an important role in the pathogenesis of inflammatory bowel disease (IBD). Vitamin E is a lipid-soluble antioxidant and is generally considered to protect against lipid peroxidation of the cell membrane and to scavenge singlet oxygen and superoxide anion radical. Therefore, vitamin E or its derivatives are expected to have particular application for patients suffering from IBD.

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The spread of capsule endoscopy has led to a focus on small intestinal injury induced by non-steroidal anti-inflammatory drugs (NSAIDs). However, it has been proposed that proton pump inhibitors (PPI), a strong anti-secretary agent, have anti-inflammatory action beyond acid suppression. Therefore, we evaluated the biological effects of lansoprazole, a PPI used in the clinical area, in the setting of experimental rat non-steroidal anti-inflammatory drug-induced enteritis.

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Oxygen radical-mediated lipid peroxidation and neutrophil activation may be involved in the development of gastric mucosal injury induced by non-steroidal anti-inflammatory drugs (NSAIDs). Vitamin E is one of the lipid-soluble antioxidants and is generally considered to protect against lipid peroxidation of the cell membrane and to scavenge singlet oxygen and superoxide anion radicals. Our object was to investigate the antioxidative effects of water-soluble vitamin E derivative, 2-(alpha-D-glucopyranosyl)methyl-2,5,7,8-tetra-methylchroman-6-ol (TMG), on aspirin-induced gastric mucosal injury in rats.

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Partially hydrolyzed guar gum (PHGG), a water-soluble dietary fiber produced by a controlled partial enzymatic hydrolysis of guar gum beans, has various physiological actions. The aim of the present study was to elucidate the beneficial effects of PHGG on colonic mucosal damage and on the inflammatory response in a dextran sulfate sodium (DSS) colitis model. After 2 weeks of prefeeding of PHGG, acute colitis was induced with 8% DSS in female BALB/c mice.

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Rebamipide, a gastromucosal protective drug, suppresses indomethacin-induced gastropathy in humans and rodents. Effects of rebamipide on gene expression in indomethacin-treated gastric mucosal cells (RGM1) were investigated using high-density oligonucleotide arrays. Indomethacin induced apoptosis in RGM1 cells in a dose-dependent manner.

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The migration of circulating monocytes into the subendothelial space occurs through the expressing of some adhesion molecules on endothelial cells. In the present study, using human aortic endothelial cells (HAECs), we investigated whether a model compound for oxysterols, 25-hydroxycholesterol, can enhance the monocyte adherence to HAECs exposed to 25-hydroxycholesterol via increasing expression of vascular cell adhesion molecule-1 (VCAM-1). We also aimed to determine the in vitro effects of tocotrienols on the enhanced interaction between monocytes and endothelial cells.

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Introduction: Recent studies have demonstrated the anti-inflammatory action of 15-deoxy-Delta12,14-prostaglandin J(2) (15d-PGJ(2)), a derivative of the PGD(2) metabolic pathway. Acute inflammation, including neutrophil activation, plays a critical role in the pathogenesis of ischemia-reperfusion (I/R). The aim of the present study was to determine the effect of 15d-PGJ(2) on I/R-induced gastric mucosal injury in rats.

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The aim of the present study was to assess the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), monocytic adhesion of human aortic endothelial cells (HAECs), and the production of intracellular reactive oxygen species (ROS), when HAECs were stimulated by 7-ketocholesterol. 7-ketocholesterol enhances surface expression of ICAM-1 and VCAM-1 as determined by EIA, induces their mRNA expression by RT-PCR, and stimulates adhesiveness of HAECs to U937 monocytic cells. We confirmed up-regulation of ROS production of HAECs treated with 7-ketocholesterol.

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The objectives were to determine the effects of alacepril, an angiotensin-converting enzyme inhibitor, on the expression of adhesion molecules and monocyte adherence to endothelial cells induced by 7-ketocholesterol (7-KC) and tumor necrosis factor (TNF)-alpha. We used human aortic endothelial cells (HAECs) and U937 monocytic cells. Surface expression and mRNA levels of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) were determined by EIA and RT-PCR.

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