Biomedical subjects

Yoshio Araki

Publications and source records attributed to Yoshio Araki.

At least 19 recordsLinked to original sources

PubMed2007

Germinated barley foodstuff suppresses dextran sulfate experimental colitis in rats: the role of mast cells.

Recent studies have suggested that dietary fiber exerts a therapeutic effect on inflammatory bowel disease patients. The aim of this study was to evaluate the effects of a dietary fiber, germinated barley foodstuff (GBF), derived from the aleurone and scutellum fraction of germinated barley against dextran sulfate sodium (DSS)-induced experimental colitis in rats. Sprague-Dawley rats were fed a 3% DSS diet containing GBF or alpha-cellulose for 8 days. The mucosal damage (macroscopic and microscopic inflammation) was then quantified. In addition, we evaluated the alterations in the mucosal mast cells and connective tissues. GBF effectively prevented mucosal damage. In addition, GBF suppressed the infiltration of the mucosal mast cells, and prevented the distraction of both collagen and elastic fibers. These effects may be closely associated with its inhibitory effects on mucosal mast cells, and the destruction of the mucosal connective tissues.

Animals↗

PubMed2006

Global gene expression analysis of yeast cells during sake brewing.

During the brewing of Japanese sake, Saccharomyces cerevisiae cells produce a high concentration of ethanol compared with other ethanol fermentation methods. We analyzed the gene expression profiles of yeast cells during sake brewing using DNA microarray analysis. This analysis revealed some characteristics of yeast gene expression during sake brewing and provided a scaffold for a molecular level understanding of the sake brewing process.

DNA, Fungal↗

PubMed2006

The free radical scavengers edaravone and tempol suppress experimental dextran sulfate sodium-induced colitis in mice.

Recent studies have suggested that the enhanced release of reactive oxygen species (ROS) plays an important role in the pathogenesis of clinical inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn's disease. In the present study, we investigated the effects of the free radical scavengers edaravone and tempol in the development of experimental dextran sulfate sodium (DSS)-induced colitis in mice. Male BALB/cA mice were fed 4% (w/w of diet) DSS in standard powder chow for 8 days. Edaravone, tempol, or vehicle saline were then injected subcutaneously twice per day. After the experimental period, the colonic length, histological damage score, and mucosal myeloperoxidase (MPO) and serum interleukin-6 (IL-6) levels were measured. Edaravone (15 mg/kg/day) and tempol (5-15 mg/kg/day) suppressed the colonic shortening and the damage score. In particular, tempol at 15 mg/kg/day significantly attenuated the colonic shortening and damage score. Edaravone and tempol suppressed the serum IL-6 levels, and significantly suppressed the increased colonic MPO levels. These results strongly support the involvement of ROS in the pathogenesis of DSS-induced colitis. A clinical effect for edaravone and tempol in IBD patients is strongly expected.

Animals↗

PubMed2006

In vitro effects of dextran sulfate sodium on a Caco-2 cell line and plausible mechanisms for dextran sulfate sodium-induced colitis.

Pathogenic mechanisms responsible for inflammatory bowel disease (IBD) are poorly understood. In an IBD animal model, the oral administration of polysaccharides such as dextran sulfate sodium (DSS) induces colitis, which exhibit several clinical and histological features for IBD. However, pathogenic factors in the development of colitis remain unclear. Therefore, we investigated possible mechanisms for DSS-induced colitis, and mainly focused on biological responses from an intestinal epithelial cell line, Caco-2. Cytotoxicity and cytokine release were measured using MTS assays and ELISA, respectively. The effect of DSS on the transepithelial electrical resistance (TEER) of Caco-2 cell monolayers was also evaluated. Cell cycle progression was estimated using antibodies directed against p53 and cdc-2 proteins. The generation of reactive oxygen species (ROS) was measured using a DCFH-DA method. Pyridylamino-DSS (PA-DSS) was used as a fluorometric label in order to investigate fluorescence-microscopically the location of DSS in Caco-2 cells. DSS induced cytotoxicity on Caco-2 cells at 5%. DSS also induced strong TEER decrease at 3%. DSS induced the weak release of IL-8, IL-6, and TGF-beta1. Remarkably DSS arrested Caco-2 cell cycle and reduced the intracellular generation of ROS. Under fluorescence microscopy, PA-DSS entered cells and bound to the nucleus, indicating this binding of DSS may be involved in the cell cycle arrest of Caco-2 cells. The cell cycle arrest and reduced intracellular generation of ROS may be involved during initiation or throughout the early stages of DSS-induced colitis.

Caco-2 Cells↗

PubMed2005

Bile acid modulates transepithelial permeability via the generation of reactive oxygen species in the Caco-2 cell line.

The barrier functions in epithelial and endothelial cells seem to be very important for maintaining normal biological homeostasis. However, it is unclear whether or how bile acids affect the epithelial barrier. We examined the bile acid-induced disruption of the epithelial barrier. We measured the transepithelial electrical resistance (TEER) of Caco-2 cells as a marker of disruption of the epithelial barrier. Reactive oxygen species (ROS) generation was also measured. Cholic acid (CA) decreased the TEER and increased intracellular ROS generation. PLA2 (phospholipase A2), COX (cyclooxygenase), PKC (protein kinase), ERK 1/2 (extracellular signal-regulated kinase 1/2), PI 3 K (phosphatidylinositol 3-kinase), p38 MAPK (p38 mitogen-activated protein kinase), MLCK (myosin light-chain kinase), NADH dehydrogenase, and XO (xanthine oxidase) inhibitors or ROS scavengers prevented the CA-induced TEER decrease. PLA2, COX, PKC, NADH dehydrogenase, and XO inhibitors prevented the CA-induced ROS generation but not ERK 1/2, PI 3 K, p38 MAPK, and MLCK inhibitors. If the cells were treated with ROS generators such as superoxide dismutase, the TEER decreased. ERK 1/2, PI 3 K, p38 MAPK, and MLCK inhibitors prevent these ROS generators from inducing the TEER decrease. These results suggest that ROS play an important role. In addition, PLA2, COX, PKC, NADH dehydrogenase, and XO are located upstream of the ROS generation, but ERK 1/2, PI 3 K, p38 MAPK, and MLCK are downstream during the signaling of CA-induced TEER alterations.

Bile Acids and Salts↗

PubMed2005

Single molecular multianalyte sensor: jewel pendant ligand.

[structure: see text] The jewel pendant ligand has multiple chromogenic units combined in a single molecule with the dyes linked to a semiselective binding site by three heteroatoms (O, N, S) having different HSAB characteristics, to indicate diverse response to individual transition metal ions. Using a single-molecular multianalyte sensor, multiple analytes could be determined with a minimal sensing system.

Journal Article↗

PubMed2005

Budd-Chiari syndrome: a case with a combination of hepatic vein and superior vena cava occlusion.

We here report a recent, rare case of Budd-Chiari syndrome, associated with a combination of hepatic vein and superior vena cava occlusion. A young female, who had been in good health, was admitted to our hospital because of massive ascites. The patient had used no oral contraceptives. Tests for coagulation disorders, hematological disorders, and antiphospholipid syndrome were all negative. Budd-Chiari syndrome was diagnosed by radiographic examination. The patient was suffering from a combination of hepatic vein and superior vena cava occlusion. In particular, the venous flow returned from the liver mainly through a right accessory hepatic vein, and stenosis was recognized at the orifice of this collateral vein into the vena cava. Subsequently, the patient underwent percutaneous balloon dilatation therapy for this stenosis. After this treatment, the massive ascites was gradually reduced, and she was discharged from our hospital. It has now been one year since discharge, and the patient has been doing well. If deteriorating liver function or intractable ascites occur again, a liver transplantation may be anticipated. This is the first case report of Budd-Chiari syndrome associated with a superior vena cava occlusion.

Adult↗

PubMed2005

Phosphorylation of Ser-446 determines stability of MKP-7.

MAPK cascades can be negatively regulated by members of the MAPK phosphatase (MKP) family. However, how MKP activity is regulated is not well characterized. MKP-7, a JNK-specific phosphatase, possesses a unique COOH-terminal stretch (CTS) in addition to domains conserved among MKP family members. The CTS contains several motifs such as a nuclear localization signal, a nuclear export signal, PEST sequences, and a serine residue (Ser-446) that can be phosphorylated by activated ERK, suggesting an important regulatory role(s).(35)S-pulse labeling experiments indicate that the half-life of MKP-7 is 1.5 h, a period significantly elongated by deleting the CTS. We also show that overexpressed MKP-7 is polyubiquitinated when co-expressed with ubiquitin and that proteasome inhibitors markedly inhibit MKP-7 degradation. We also determined that MKP-7 phosphorylated at Ser-446 has a longer half-life than unphosphorylated form of the wild type protein, as does a phospho-mimic mutant of MKP-7. These results indicate that activation of the ERK pathway strongly blocks JNK activation through stabilization of MKP-7 mediated by phosphorylation.

Amino Acid Motifs↗

PubMed2005

Interleukin-17 augments tumor necrosis factor-alpha-induced granulocyte and granulocyte/macrophage colony-stimulating factor release from human colonic myofibroblasts.

BACKGROUND: Interleukin (IL)-17 is a newly identified T-cell-specific cytokine. In this study, we investigated the effects of IL-17 on colony-stimulating factor (CSF) release in human colonic subepithelial myofibroblasts (SEMFs). METHODS: CSF release and mRNA expression were determined by enzyme-linked immunosorbent assay (ELISA) and Northern blotting, respectively. Nuclear factor (NF)-kappaB- and activating protein (AP-1)-DNA binding activities were evaluated by electrophoretic gel mobility shift assays (EMSAs). RESULTS: Unstimulated cells secreted a small amount of granulocyte G- and granulocyte/macrophage (GM)-CSF, and a considerable amount of M-CSF. IL-17 weakly enhanced G-CSF release, but did not affect GM- and M-CSF release. IL-17 selectively enhanced tumor necrosis factor (TNF)-alpha-induced G- and GM-CSF release. The combination of IL-17 plus TNF-alpha induced a marked increase in NF-kappaB- and AP-1-DNA binding activities. The adenovirus-mediated transfer of a stable form of IkappaBalpha and/or a dominant negative mutant of c-Jun markedly inhibited the IL-17 plus TNF-alpha-induced G- and GM-CSF mRNA expression. Furthermore, a stability study showed that IL-17 plus TNF-alpha markedly enhanced the stability of G- and GM-CSF mRNA. CONCLUSIONS: IL-17 augments TNF-alpha-induced G- and GM-CSF release via transcriptional and posttranscriptional mechanisms.

Blotting, Northern↗

PubMed2005

Interleukin-22, a member of the IL-10 subfamily, induces inflammatory responses in colonic subepithelial myofibroblasts.

BACKGROUND & AIMS: Interleukin (IL)-22, a member of the IL-10 subfamily, is a recently identified T-cell-derived cytokine. We investigated IL-22 expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and analyzed its biologic activities in human colonic subepithelial myofibroblasts (SEMFs). METHODS: Mucosal IL-22 expression was evaluated by immunohistochemical procedures. The effects of IL-22 on colonic SEMFs were investigated by cDNA microarrays, Northern blots, enzyme-linked immunosorbent assay, and electrophoretic gel mobility shift assays (EMSAs). RESULTS: IL-22 was not detectable in normal colonic mucosa. In IBD mucosa, IL-22 expression was detectable in CD4-positive T cells. IL-22-positive cells were increased in ulcerative colitis and even more so in Crohn's disease. IL-22 receptor expression colocalized with a marker of SEMFs. IL-22 did not modulate SEMF proliferation and collagen synthesis. cDNA microarray analyses demonstrated that, in colonic SEMFs, IL-22 increased the messenger RNA (mRNA) expression of inflammatory cytokines (IL-6, IL-8, IL-11, and leukemia inhibitory factor [LIF]), chemokines, and matrix metalloproteinases. IL-22 induced an activation of nuclear factor (NF)-kappaB and activating protein (AP)-1 within 1 hour, and a blockade of NF-kappaB and AP-1 activation markedly reduced IL-22 induction of IL-6, IL-8, IL-11, and LIF mRNA. MAP-kinase inhibitors (PD98059, U0216, and SB202190) significantly reduced IL-22 induction of cytokine secretion. The combination of either IL-17 plus IL-22 or IL-19 plus IL-22 additively up-regulated cytokine secretion. CONCLUSIONS: IL-22 derived from activated T cells acts on SEMFs to elicit expression of proinflammatory cytokines and matrix-degrading molecules indicating proinflammatory/remodeling roles in IBD.

Colon↗

PubMed2005

Elevated circulating platelet-derived microparticles in patients with active inflammatory bowel disease.

OBJECTIVES: Platelet-derived microparticles (PDMPs) are active molecules involved in the hemostatic and inflammatory responses. To evaluate the changes in the platelet function in patients with inflammatory bowel disease (IBD), we measured circulating PDMP levels. METHODS: Twenty-five healthy controls, 44 patients with ulcerative colitis (UC), and 43 patients with Crohn's Disease (CD) were studied. The PDMP and soluble P-selectin (sP-selectin) levels were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: In the healthy controls, the PDMP levels were 17.2 +/- 6.2 U/mL. Significant differences were not observed between the healthy controls and inactive UC patients (20.8 +/- 9.5 U/mL, n = 25) or between the healthy controls and inactive CD patients (17.6 +/- 7.8 U/mL, n = 24). In contrast, the PDMP levels were significantly higher in both active UC (49.2 +/- 33.6 U/mL, n = 19) and active CD (48.6 +/- 42.8 U/mL, n = 19) patients than in the healthy controls. A significant correlation was found between the PDMP levels and the clinical activity indexes (CAI) of UC patients (r = 0.65, p < 0.01, n = 44), and between the PDMP levels and Crohn's disease activity indexes (CDAI) (r = 0.72, p < 0.01, n = 43). Elevated PDMP levels in active patients were significantly reduced after remission. A significant correlation was observed between the PDMP levels and the sP-selectin levels (r = 0.60, p < 0.01, n = 122). CONCLUSION: Elevated circulating PDMPs in active IBD patients suggest a role for platelets in the pathogenesis of IBD.

Acute Disease↗

PubMed2005

An anomalous case of the left gastric artery, the splenic artery and hepato-mesenteric trunk independently arising from the abdominal aorta.

This report describes a rare case of an arterial anomaly in the celiaco-mesenteric region, encountered in a Japanese female cadaver for dissection at the gross anatomy laboratory of Kurume University School of Medicine in 2003. The usual celiac trunk was not identified, and the left gastric artery, the splenic artery and the hepato-mesenteric trunk independently arose from the abdominal aorta. Moreover, the hepatic artery arising from the hepato-mesenteric trunk ran behind the portal vein. The classification for this type of arterial anomaly is a Type II' of Morita's classification and Type II of Higashi and Hirai's classification, not belong to the Adachi's.

Aged↗

PubMed2005

Development of dextran sulfate sodium-induced colitis is aggravated in mice genetically deficient for complement C5.

The complement system is a potent effector of innate immunity. To elucidate the pathophysiological role of the complement system in inflammatory bowel disease (IBD), we evaluated the development of dextran sulfate sodium (DSS)-induced colitis in genetically complement C5-deficient mice. We used DBA2/J mice, which are genetically deficient in complement C5. DBA1/J mice have a normal complement system, and were used as controls. Experimental colitis was induced by the oral administration of 3.5% (w/v) DSS in their drinking water for 10 days. On day 10, all mice were sacrificed and their colons were collected. The development of colitis was assessed by the histological score, disease activity index, myeloperoxidase (MPO) activity, and macroscopic changes of the colon. Body weight loss was more apparent in the DBA2/J mice than in control DBA1/J mice. The colon length was shorter in the DBA2/J mice than in DBA1/J mice. The disease activity index, histological colitis score, and MPO activity were all significantly higher in the DBA2/J mice than in DBA1/J mice. Microscopically, mucosal edema, cellular infiltration and disruption of the epithelium were much more severe in the DBA2/J mice than in DBA1/J mice. The development of DSS colitis was aggravated in genetically C5-deficient DBA2/J mice. These findings suggest that the complement system might play a protective role in the development of DSS-induced experimental colitis.

Animals↗

PubMed2004

Inflixmab as a possible treatment for the hemorrhagic type of Crohn's disease.

Acute lower gastrointestinal bleeding is a rare complication of Crohn's disease (CD). Although anti-tumor necrosis factor-alpha (TNF-alpha, infliximab) therapy has been established for patients with inflammatory and fistulous CD, there has been little evidence on whether infliximab is effective for the hemorrhagic type of CD. We report a case of a 31-year-old man with CD who had recurrent sudden-onset bloody stool. After a second surgery, he visited our hospital because of bloody stool. Infusion of infliximab stopped the bleeding and promoted the healing of ulcers in the ileum and ileocolon anastomosis. We suggest that infliximab therapy should be tried to stop acute gastrointestinal bleeding in CD before there is a surgical emergency.

Adult↗

PubMed2004

Neutralization of interleukin-17 aggravates dextran sulfate sodium-induced colitis in mice.

We evaluated the effects of rat anti-mouse IL-17 neutralizing monoclonal antibody (mAb) on the development of dextran sulfate sodium (DSS)-induced colitis. Tissue samples were evaluated by standard immunohistochemical procedure. The mucosal mRNA expression of cytokines was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). In the mice treated with the anti-IL-17 mAb, the body weight was significantly lower, and anal prolapse and colon shortening were apparent. A histological analysis indicated that the anti-IL-17 mAb markedly enhanced the severity of colitis. The mucosal infiltration of CD4-positive helper T cells and CD11b-positive granulocytes-monocytes was increased in the anti-IL-17 mAb-treated mice. Treatment with the anti-IL-17 mAb increased the mucosal expression of mRNAs of tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, IL-6, RANTES, and IP-10. Blocking of IL-17 activity in vivo using the anti-IL-17 mAb enhanced the development of DSS-colitis in mice. This suggests an inhibitory role for IL-17 in the development of DSS-colitis.

Animals↗

PubMed2004

Complex formation of CD23/surface immunoglobulin and CD23/CD81/MHC class II on an EBV-transformed human B cell line and inferable role of tetraspanin.

CD23, a low-affinity IgE receptor, is a type II transmembrane protein having a C-type lectin domain and it associates noncovalently with MHC class II on B cells. The results of our immunoprecipitation analysis suggest that CD23 co-exists with at least two additional molecules, surface immunoglobulin (sIg) and CD81 (and/or CD9), on the cell surface of L-KT9 cells (an Epstein-Barr virus (EBV)-transformed human B cell line). When both CD23 and sIg molecules were stimulated simultaneously by the corresponding antibodies, a large increase in CD81 in the immunoprecipitation was observed as compared with the case of stimulation by only one antibody. Simultaneous stimulation by anti-CD23 and anti-Ig may mimic the situation of B cells stimulated by an antigen/IgE complex. In addition, a large increase in MHC class II in the immunoprecipitation was also observed by cross-linking of CD23 with anti-CD23 and its second antibody as compared with the case of stimulation by anti-CD23 alone. The cross-linking of CD23 with anti-CD23 and its antibody may mimic the situation of B cells stimulated by an IgE/antigen/IgE complex. Therefore, the complex formation among CD23, sIg, MHC class II, and CD81 on the cell surface of L-KT9 cells by the antigen/IgE or IgE/antigen/IgE complex is most likely to be closely related to B cell regulatory events by signaling through sIg or MHC class II. Tetraspanins such as CD81 and CD9 are thought to be involved in the formation and the preservation of various different membrane complexes consisting of several functional proteins.

Antigen-Antibody Complex↗

PubMed2004

Clostridium butyricum, a probiotic derivative, suppresses dextran sulfate sodium-induced experimental colitis in rats.

Recent studies have suggested that probiotics or short chain fatty acids (SCFAs) exert a therapeutic effect on inflammatory bowel disease (IBD) patients. In a previous study, we demonstrated that Clostridium butyricum produces high levels of SCFAs in culture. In addition, a yogurt-based additive effectively masked, completely eliminating the unpleasant odor derived from the SCFAs. We recently reported that the oral administration of both high and low dose diets (50% w/w for 17 days and 5% w/w for 16 months, respectively) of the Clostridium butyricum derivative did not cause pathological abnormalities in rats. In the present study, we evaluated the effects of this product against dextran sulfate sodium (DSS)-induced experimental colitis in rats. Five-week-old male Wistar Hannover GALAS rats were given a mixture of a standard diet containing 3% (w/w) of DSS for 8 days. In the derivative-fed group, Clostridium butyricum derivative (20% w/w) with 0.1% (w/w) additive was also added to their diet. The control-fed group was given tap water (20% w/w) with 0.1% (w/w) additive. After 8 days, a laparotomy was performed, and macroscopic and microscopic inflammation scoring was determined. The Clostridium butyricum derivative effectively prevented bloody diarrhea. In addition, mucosal damage to the derivative-fed group was significantly reduced macroscopically compared to that of the control-fed group. The potential clinical efficacy of the Clostridium butyricum derivative in IBD patients is also discussed.

Administration, Oral↗

PubMed2004

Germinated barley foodstuff prolongs remission in patients with ulcerative colitis.

Germinated barley foodstuff (GBF) is a prebiotic which increases luminal butyrate production by modulating the microfloral distribution. GBF has been shown to reduce both clinical activity and mucosal damage in active ulcerative colitis (UC) with mild to moderate activity. However, the efficacy of GBF in patients with UC during the remission stage is unknown. The aim of this study was to investigate the efficacy of GBF as a maintenance therapy in patients with UC while in remission. Fifty-nine patients with UC in remission according to Rachmilewitz's clinical activity index (CAI) score of </=4 were enrolled and divided into two groups, control (n=37) and GBF (n=22). Patients in the control group were given conventional treatment alone for 12 months, while patients in the GBF group received conventional therapy plus 20 g of GBF daily. The response to treatments was assessed by monitoring the CAI and endoscopic score according to Matts. Significantly better CAI values were seen in the GBF group at 3, 6, and 12 months compared with the values in the control group. The cumulative recurrence rate in the GBF group with steroid tapering treatment was significantly lower compared with the value in the control group. No side effects related to GBF were observed. GBF appeared to be effective and safe as a maintenance therapy to taper steroid dose and prolong remission in patients with UC.

Adult↗