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Biomedical subjects

Yuji Naito

Publications and source records attributed to Yuji Naito.

At least 91 records · Page 5Linked to original sources
PubMed2004

[Pro-inflammatory chemokine IL-8 in gastroesophageal reflux disease].

Recent reports have demonstrated significantly higher expression levels of interleukin-8 (IL-8) in patients with gastroesophageal reflux disease (GERD) including non-erosive reflux disease (NERD). The levels of IL-8 mRNA expression were significantly decreased after proton pump inhibitor. The esophageal expression of CINCs, rat IL-8-like chemokines, was markedly enhanced in the models of acute or chronic esophagitis in rats. The production of IL-8 from esophageal mucosal cells was enhanced by the exposure to bile acid. These results suggest that IL-8 chemokine may play a major role in the pathogenesis of esophageal inflammation in GERD.

Animals↗
PubMed2003

Hyperthermia enhances tumor necrosis factor alpha-induced apoptosis of a human gastric cancer cell line.

We have investigated the effects of hyperthermia on the apoptosis induced by tumor necrosis factor alpha (TNF-alpha). Confluent monolayers of human gastric cancer cell line MKN45 were either treated or untreated with hyperthermia for 1 h. The cells were subsequently stimulated with TNF-alpha. A 24-h incubation with TNF-alpha did not affect cell viabilities; however, pretreatment with hyperthermia significantly enhanced the level of apoptosis induced by TNF-alpha. Pretreating MKN45 cells with hyperthermia (42.0 degrees C) significantly inhibited the TNF-alpha-induced increase in the binding activity of NF-kappaB to DNA. This study suggests that hyperthermia can inhibit the TNF-alpha-induced NF-kappaB activation and that hyperthermia renders human gastric cancer cells susceptible to the TNF-alpha-induced apoptosis, possibly via inhibition of the NF-kappaB pathway.

Apoptosis↗
PubMed2003

Cancer chemopreventive effects of oral feeding alpha-tocopherol on ultraviolet light B induced photocarcinogenesis of hairless mouse.

Ultraviolet light is the most common cause of skin cancers in humans and several effects of ultraviolet light B (UVB: 290-320 nm) are thought to contribute to skin photocarcinogenesis. The generation of free radicals and related oxidants produced by UVB exposure, result in photocarcinogenesis by directly damaging DNA. On the other side, activating of transcription factor, activator protein 1 (AP-1) induced by UVB exposure causes tumor promotion. alpha-tocopherol has two principal physiological activities and one is an antioxidant activity through which alpha-tocopherol protects unsaturated fatty acids, protein and DNA from oxidation. The other activity is to stabilize the structure of the biomembrane. In addition to these two activities, it has been recently established that alpha-tocopherol plays important roles in cell signal transduction. In course of these studies, we examined such effects of alpha-tocopherol on UVB induced skin photocarcinogenesis in hairless mice. These results indicate that oral feeding of alpha-tocopherol including diet exhibited a marked inhibitory effects on both tumor incidence and multiplicity in UVB induced mouse skin photocarcinogenesis.

Administration, Oral↗
PubMed2003

Blocking of NF-kappaB activation enhances the tumor necrosis factor alpha-induced apoptosis of a human gastric cancer cell line.

The transcription factor NF-kappaB is constitutively activated in many human cancers and induces the expression of multiple genes, including those of anti-apoptotic proteins. This study investigated the mechanism by which human gastric cancer cells (MKN45) are resistant to apoptosis induced by tumor necrosis factor alpha (TNF-alpha). Confluent monolayers of MKN45 cells were either pretreated or not for 60 min with PSI, a peptide aldehyde known to specifically inhibit the chymotrypsin-like activity of 26S proteasome. Cells were subsequently stimulated with recombinant human TNF-alpha, and cell viabilities were determined by the WST-1 assay. Apoptosis was confirmed by fluorescence microscopy after staining with Hoechst 33342, and DNA fragmentation was determined by a DNA fragmentation detection kit. A 24-h incubation with either TNF-alpha or PSI alone did not affect cell viabilities; however, pretreatment with PSI significantly enhanced the level of apoptosis induced by TNF-alpha. Therefore, this study suggests the possibility that blocking of NF-kappaB activity renders gastric cancer cells susceptible to the apoptosis induced by TNF-alpha.

Apoptosis↗
PubMed2003

Tumor initiating activity of Helicobacter pylori water extract on mouse skin carcinogenesis.

Helicobacter pylori (H. pylori) infection has been associated with gastric carcinogenesis, but responsible and detail mechanisms are insufficient by the absence of adequate data. To obtain direct evidence regarding the carcinogenicity of H. pylori, we investigated the initiating and promoting activity of H. pylori water extract (HPE) in two-stage mouse skin carcinogenesis model. HPE treatment, as an initiation, significantly enhanced tumor formation compared with control group. Moreover, HPE treatment increased production of 8-hydroxydeoxyguanosine in epidermal cells and HPE-initiated/TPA-promoted papillomas demonstrated a point mutation of the Ha-ras gene. These results suggest an initiating activity of HPE on two-stage mouse skin carcinogenesis.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2003

Reoperation in mitral valve repair for regurgitant mitral valve disease.

OBJECTIVES: Reviewing reoperative mitral valve repair, we evaluated a predictor for future reoperation by comparing degenerative and rheumatic mitral regurgitation. METHODS: From June 1988 to September 2002, 159 patients with mitral valve regurgitation underwent a variety of surgical reconstruction. Our 9 subjects--2 men and 7 women with a mean age of 55.3 years--including 1 undergoing initial repair at an other hospital, underwent reoperation for mitral valve lesions. Four patients had rheumatic (Group R) and 5 degenerative (Group D) mitral valve disease. We studied reoperative outcomes and initial procedures were retrospectively. RESULTS: The mean interval from initial repair was 111 months. Mitral valve lesions at reoperation in Group D were annular dilation in 3, leaflet prolapse in 1, and suture disruption in 1, while that in Group R involved severe thickening of both leafle. Rerepair was possible in 3 patients of Group D, but all others, (including Group R patients) required valve replacement. All survived reoperation. CONCLUSIONS: Rerepair in rheumatic mitral regurgitation, rerepair was difficult. In degenerative mitral valve regurgitation, however, rerepair was possible because procedure-related origin was a major cause of reoperation. Reoperation can be prevented by proper technical improvement at initial repair.

Adult↗
PubMed2003

Unexpected durability of Smeloff-Cutter aortic ball valve prosthesis.

We report a case in which replacement of a Smeloff-Cutter aortic ball prosthesis was required 28 years after initial implantation. A 57-year-old woman underwent aortic valve replacement with a 21-mm Smeloff-Cutter ball prosthesis and open mitral commissurotomy for aortic stenosis, aortic regurgitation, and mitral stenosis in 1973. Severe aortic regurgitation occurred in April 2001, and aortic valve reoperation combined with mitral valve replacement was successfully performed. The patient's aortic ball valve was nearly intact with perivalvular leakage probably causing the aortic regurgitation. Our experience documents longer durability for the Smeloff-Cutter prosthesis than has been reported to date.

Aortic Valve↗
PubMed2003

Subdural hemorrhagic injury after open heart surgery.

We report two cases of acute subdural hematoma after cardiac surgery using cardiopulmonary bypass. In both patients, emergency removal and drainage of a subdural hematoma was performed by neurosurgeons, and complete recovery followed. Subdural hemorrhagic brain injury after cardiac surgery is rare and devastating; however, we consider early diagnosis and proper treatment to be effective because organic brain damage did not occur.

Aged↗
PubMed2003

A novel vitamin E derivative (TMG) protects against gastric mucosal damage induced by ischemia and reperfusion in rats.

The aim of the present study was to investigate the antioxidative effects of water-soluble vitamin E derivative, 2-(alpha-D-glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol (TMG), on ischemia-reperfusion (I/R) -induced gastric mucosal injury in rats. Gastric ischemia was induced by applying a small clamp to the celiac artery and reoxygenation was produced by removal of the clamp. The area of gastric mucosal erosion, the concentration of thiobarbituric acid-reactive substances, and the myeloperoxidase activity in gastric mucosa significantly increased in I/R groups compared with those of sham-operated groups. These increases were significantly inhibited by pretreatment with TMG. The contents of both mucosal TNF-alpha and CINC-2beta in I/R groups were also increased compared with the levels of those in sham-operated groups. These increases of the inflammatory cytokines were significantly inhibited by the treatment with TMG. It is concluded that TMG inhibited lipid peroxidation and reduced development of the gastric mucosal inflammation induced by I/R in rats.

Animals↗
PubMed2003

Different effects of constitutive nitric oxide synthase and heme oxygenase on pulmonary or liver metastasis of colon cancer in mice.

It has recently been reported that not only endogenous nitric oxide (NO) but also carbon monoxide (CO) produced by heme oxygenase (HO) have many physiological functions. The objective of the present study was to determine whether endogenous NO or CO is involved in the experimental pulmonary or liver metastasis of colon cancer in mice. Intravenous or intrasplenic injection of colon 26 cells from a mouse colon adenocarcinoma cell line resulted in multiple pulmonary or liver metastases. NG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NO synthase (NOS), or zinc deuteroporphyrin 2, 4-bis glycol (ZnDPBG), a competitive inhibitor of HO, was administered to the mice only on the day of tumor inoculation. We assessed the number of tumor cells 24 h later and the outcome of metastases of the target organ. In the pulmonary metastasis model, L-NAME increased both the number of tumor cells 24 h later and outcome of metastases 18 days later, but did not have a significant effect on liver metastasis. On the other hand, metastasis to the liver, but not that to the lung, increased following administration of ZnDPBG. These results suggest that the activities of NOS and HO could influence experimental metastasis in an organ-specific manner.

Animals↗
PubMed2003

Enhanced intestinal inflammation induced by dextran sulfate sodium in tumor necrosis factor-alpha deficient mice.

BACKGROUND AND AIMS: Tumor necrosis factor-alpha (TNF-alpha) is a potent pro-inflammatory cytokine thought to be involved in the pathogenesis of inflammatory bowel disease. To further define the role of TNF-alpha in intestinal inflammation, we studied the effects of dextran sulfate sodium (DSS) administration in mice with targeted deletions of TNF-alpha gene. METHODS: Acute colitis was induced in female TNF-alpha-/- and TNF-alpha+/+ mice by administering 4.5% DSS orally in drinking water for seven days. The colonic mucosal injury and inflammation was evaluated based on body weight changes, total colon length, luminal hemoglobin, and histological findings. Colonic mRNA expression for inducible nitric oxide synthase (iNOS), TNF-alpha, interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) were measured by reverse transcription polymerase chain reaction (RT-PCR), and nuclear factor kappaB (NF-kappaB) activation was evaluated by electrophoretic mobility shift assay. RESULTS: In each assessment, colonic injury was significantly aggravated in DSS-treated TNF-alpha-/- mice compared with DSS-treated TNF-alpha+/+ mice. The survival rate of TNF-alpha-/- mice on day seven was 40%; in contrast, all TNF-alpha+/+ mice were alive. Histological study also showed an enhanced infiltration of inflammatory cells, especially neutrophils, and mucosal cell disruption in DSS-treated TNF-alpha-/- mice compared with DSS-treated TNF-alpha+/+ mice. On day seven, mRNA levels of IFN-gamma and IL-4 in the colons of TNF-alpha-/- mice were faint or not detected; in contrast, those of TNF-alpha+/+ mice were detected. Although the expression of iNOS mRNA and luminal nitrite levels were similarly increased in both mice on day seven, this induction was delayed in TNF-alpha-/- mice during the early phase. The degree of NF-kappaB binding activity seemed to be similar between the two types of mice on day seven. CONCLUSION: DSS-induced inflammation is significantly enhanced in TNF-alpha-/- mice compared to TNF-alpha+/+ mice. These data suggest that persistent and marked blockage of TNF-alpha bioactivity may provide a detrimental effect on acute intestinal inflammation.

Acute Disease↗
PubMed2003

Astaxanthin limits exercise-induced skeletal and cardiac muscle damage in mice.

Dietary antioxidants may attenuate oxidative damage from strenuous exercise in various tissues. Beneficial effects of the antioxidant astaxanthin have been demonstrated in vitro, but not yet in vivo. We investigated the effect of dietary supplementation with astaxanthin on oxidative damage induced by strenuous exercise in mouse gastrocnemius and heart. C57BL/6 mice (7 weeks old) were divided into groups: rested control, intense exercise, and exercise with astaxanthin supplementation. After 3 weeks of exercise acclimation, both exercise groups ran on a treadmill at 28 m/min until exhaustion. Exercise-increased 4-hydroxy-2-nonenal-modified protein and 8-hydroxy-2'-deoxyguanosine in gastrocnemius and heart were blunted in the astaxanthin group. Increases in plasma creatine kinase activity, and in myeloperoxidase activity in gastrocnemius and heart, also were lessened by astaxanthin. Astaxanthin showed accumulation in gastrocnemius and heart from the 3 week supplementation. Astaxanthin can attenuate exercise-induced damage in mouse skeletal muscle and heart, including an associated neutrophil infiltration that induces further damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2003

An AT1-receptor antagonist and an angiotensin-converting enzyme inhibitor protect against hypoxia-induced apoptosis in human aortic endothelial cells through upregulation of endothelial cell nitric oxide synthase activity.

The protective effects and roles of AT1-receptor antagonists (AT1-RA) or angiotensin-converting enzyme inhibitors (ACEI) on vascular endothelial cell (EC) injury during hypoxia are not entirely known. Therefore, we investigated these effects and mechanisms in human aortic (HA) EC. DNA fragmentation, Lactate dehydrogenase (LDH) release, and caspase-3 activity were measured in cultured HAEC after exposure to hypoxia in the presence or absence of an AT1-RA (candesartan, CS) and/or an ACEI (temocaprilat, TC). Next, we investigated endothelial cell nitric oxide synthase (ecNOS) and inducible (i) NOS to determine the role of the bradykinin(BK)-NO pathway in the protective effect on ACEI and AT1-RA in the setting of hypoxia-induced apoptosis. Exposure to hypoxia increased DNA fragmentation in HAEC associated with the activation of caspase-3, but did not affect LDH release. In addition, hypoxia induced ecNOS mRNA but not mRNA iNOS. CS and/or TC reduced apoptosis induced by hypoxia in a dose-dependent manner, and significantly increased BK and ecNOS expression. This effect was attenuated by the kinin B2 receptor antagonist, HOE 140, and the NOS inhibitor, N-nitro-L-arginine methylester (L-NMMA). Hypoxia activates the pathway leading to apoptosis by enhancing caspase-3 activity. Both CS and TC can ameliorate hypoxia-induced apoptosis in HAEC through inhibiting caspase-3 activation by enhancing ecNOS activity, via the accumulation of BK.

Angiotensin II Type 1 Receptor Blockers↗