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Naoshi Nakamura

Publications and source records attributed to Naoshi Nakamura.

11 recordsLinked to original sources

Induction of peripheral lymph node addressin in human gastric mucosa infected by Helicobacter pylori.

Helicobacter pylori infects over half the world's population and is a leading cause of peptic ulcer and gastric cancer. H. pylori infection results in chronic inflammation of the gastric mucosa, and progression of chronic inflammation leads to glandular atrophy and intestinal metaplasia. However, how this chronic inflammation is induced or maintained is not well known. Here, we show that chronic inflammation caused by H. pylori infection is highly correlated with de novo synthesis of peripheral lymph node addressin (PNAd) presented on high-endothelial venule (HEV)-like vessels. The number of HEV-like vessels dramatically increases as chronic inflammation progresses. We found that the PNAd is bound by L-selectin.IgM chimeric protein, and decorated by NCC-ST-439 antibody, which is suggested to recognize both nonsulfated and 6-sulfated sialyl Lewis X on core 2 branched O-glycans, and MECA-79 antibody, which reacts with 6-sulfo N-acetyllactosamine on extended core 1 O-glycans. These results indicate that PNAd on HEV-like vessels present in the gastric mucosa subsequent to H. pylori infection is similar to those on HEVs present in the secondary lymphoid organs, which are essential for lymphocyte circulation. Moreover, eradication of H. pylori is associated with the disappearance of HEV-like vessels in the gastric mucosa. By contrast, very few PNAd were found in the gastric mucosa of patients with chemical gastritis caused by nonsteroidal antiinflammatory drugs. These results strongly suggest that PNAd in HEV-like vessels plays a critical role in lymphocyte recruitment during chronic inflammation induced by H. pylori infection.

Animals↗

Autoimmune pancreatitis is closely associated with gastric ulcer presenting with abundant IgG4-bearing plasma cell infiltration.

BACKGROUND: Autoimmune pancreatitis is characterized by high serum IgG4 concentrations and lymphoplasmacytic infiltration. Because of the diversity of extrapancreatic involvement in this disease, the present study sought to identify other associated GI-tract lesions. METHODS: EGD findings were compared between a group of 23 patients with autoimmune pancreatitis undergoing ERCP for obstructive jaundice and 230 age- and gender-matched control patients. To clarify the histopathologic differences found between these two groups, the histopathologic findings (Updated Sydney System) and the immunohistochemistry of each IgG subclass were compared between 8 patients with autoimmune pancreatitis and gastric ulcer, and 23 control patients with gastric ulcer from which biopsy specimens had been obtained. RESULTS: Gastric ulcer was found significantly more frequently in patients with autoimmune pancreatitis compared with control patients (34.8% vs. 13.5%; p=0.007). There was no significant difference between the groups with respect to the frequency of other GI lesions. Four of 8 gastric ulcers in patients with autoimmune pancreatitis were linear, with the long axis perpendicular to the incisura on the lesser curvature of the stomach. The activity score for the gastric lesions was significantly lower in patients with autoimmune pancreatitis compared with control patients (mean score 0.38 vs. 1.08; p=0.012). There were no significant differences in histopathologic findings with respect to inflammation, atrophy, metaplasia, or Helicobacter pylori scores between the two groups. IgG4-bearing plasma cells were significantly more abundant in gastric lesions in patients with autoimmune pancreatitis compared with those in control patients (mean score 1.75 vs. 0.39; p=0.0008). CONCLUSIONS: Autoimmune pancreatitis is closely associated with gastric ulcer with abundant IgG4-bearing plasma cell infiltration.

Aged↗

Possible relationship between Helicobacter pylori infection and cap polyposis of the colon.

BACKGROUND: Cap polyposis is a rarely encountered disease characterized by multiple distinctive inflammatory colonic polyps located from the rectum to the distal colon. The etiology of this disease is still unknown, and no specific treatment has been established. AIM: We report three cases of cap polyposis that were cured following eradication therapy for Helicobacter pylori infection. METHODS AND RESULTS: Three women were referred to Shinshu University Hospital because of mucoid and/or bloody diarrhea. Laboratory data showed hypoproteinemia in all cases; markers of inflammation such as C-reactive protein were negative. Colonoscopy revealed multiple sessile polyps with mucus adherent on the apices of the mucosal folds in the rectum and/or the sigmoid colon. The intervening mucosa was normal. Microscopic examinations of biopsy specimens taken from sessile polyps revealed inflamed mucosa with elongated tortuous crypts attenuated towards the mucosal surface. A granulation tissue 'cap' was observed on the surface of the mucosa. Various treatments were unsuccessful, including administration of metronidazole or prednisolone, avoidance of straining at defecation, and surgical or endoscopic resection. All were diagnosed with H. pylori infection in the stomach. Helicobacter pylori was not detected in the biopsy specimens from the colonic inflammatory polyps by immunohistochemical study using polyclonal anti-H. pylori antibody. After successful eradication therapy the clinical symptoms improved. Disappearance of cap polyposis was confirmed by colonoscopy in all three cases. CONCLUSION: We speculate that H. pylori infection might play a role in the pathogenesis of cap polyposis.

Adult↗

Phenol Congo red staining enhances the diagnostic value of abdominal fat aspiration biopsy in reactive AA amyloidosis secondary to rheumatoid arthritis.

OBJECTIVE: Systemic reactive AA amyloidosis is an intractable complication in patients with a long history of rheumatoid arthritis (RA). To help to more easily and reliably detect the presence of this form of amyloidosis in patients with RA and start intensive treatment as early as possible, we examined the sensitivity and usefulness of abdominal fat aspiration biopsy with phenol Congo red staining in the diagnosis of AA amyloidosis. PATIENTS AND METHODS: Ten patients were diagnosed with systemic reactive AA amyloidosis secondary to RA (all women; mean age, 70.2 +/- 6.4 years; mean disease duration of RA, 20.3 +/- 11.2 years) based on histopathological examinations of biopsied specimens mainly from the gastroduodenal mucosa. Abdominal fat aspiration biopsy was performed in these patients, and the specimens were treated with both classical alkaline and phenol Congo red staining. RESULTS: Phenol Congo red staining revealed amyloid deposits in all 10 patients, while conventional alkaline Congo red staining showed a positive result in 7 patients. In the patients with a positive result with alkaline Congo red staining, reactivity of one grade or two higher was demonstrated by the phenol Congo red method. CONCLUSION: Phenol Congo red staining is superior to the classical alkaline Congo red staining with respect to the detection of AA-amyloid deposits in biopsied abdominal fat tissue specimens. In addition to easy access and procedural safety, abdominal fat aspiration biopsy might contribute reliably to the diagnosis of systemic reactive AA amyloidosis secondary to RA when phenol Congo red staining is employed.

Abdomen↗

Abdominal fat aspiration biopsy and genotyping of serum amyloid A contribute to early diagnosis of reactive AA amyloidosis secondary to rheumatoid arthritis.

OBJECTIVE: To detect amyloid deposits in the early phase of illness, we investigated the usefulness of abdominal fat aspiration biopsy along with genotyping of serum amyloid A (SAA) in patients with rheumatoid arthritis (RA). PATIENTS AND METHODS: We performed abdominal fat aspiration biopsy with phenol Congo red staining and determined inflammatory markers, including CRP and SAA, in 217 patients with an RA history longer than 5 years (mean age, 64.1 +/- 10.6 years). Genotypes of SAA1 and 2 were investigated in 127 patients with RA by a polymerase chain reaction-restriction fragment length polymorphism analysis. RESULTS: In the abdominal fat aspiration biopsy 17 patients (7.8%) demonstrated amyloid deposits, which were confirmed as AA type by immunostaining on biopsied tissues from other organs, and nine of them showed no clinical symptoms ascribable to amyloidosis. RA patients with amyloidosis showed significantly higher serum levels of CRP (p < 0.05) and SAA (p < 0.0001) than those without amyloidosis. In the genotyping, amyloid deposition was significantly correlated with the frequency of SAA1.3 (p < 0.005 vs. 1.1, p < 0.05 vs. 1.5). Comparison of inflammatory markers between the number of SAA1.3 alleles showed that the SAA/CRP ratio and SAA concentration were higher in the 1.3 homozygote than in the others (p < 0.05). Two patients demonstrated amyloid deposits at the second abdominal fat biopsy one year after the first, and their SAA1 genotypes were 1.3/1.5 and 1.3/1.3. CONCLUSION: In RA patients confirmed as having SAA1.3, serial examinations with abdominal fat aspiration biopsy might contribute greatly to the early detection of amyloidosis during the long-term follow-up.

Abdomen↗

Detection of genetic alterations in the p53 suppressor gene and the K-ras oncogene among different grades of dysplasia in patients with colorectal adenomas.

BACKGROUND: Although it is believed that p53 suppressor gene mutations, compared with mutations in the K-ras oncogene, occur at a later stage of colorectal tumorigenesis, the distribution of these genetic alterations at an early stage remains poorly characterized. METHODS: The authors analyzed the immunoreactivity for p53 protein (p53 protein expression), which reflects the functionally altered p53 gene, and K-ras mutations at codons 12 in 68 colorectal adenomas with both low-grade and high-grade dysplasia obtained from 62 patients. RESULTS: The prevalence of p53 positive immunostaining was significantly greater compared with the prevalence of K-ras mutations both in low-grade dysplasia and in high-grade dysplasia. Twenty-two adenomas (32.3%) showed positive immunostaining for p53 protein in high-grade dysplasia and also were positive for p53 in surrounding low-grade dysplastic tissues; 20 adenomas (29.4%) showed positive immunostaining for p53 protein in high-grade dysplasia and were negative for p53 in surrounding low-grade dysplastic tissues; 8 adenomas (11.7%) showed negative immunostaining for p53 protein in high-grade dysplasia and were positive for p53 in surrounding low-grade dysplastic tissues; and 18 adenomas (26.4%) showed negative immunostaining for p53 protein in both high-grade dysplasia and in surrounding low-grade dysplastic tissues. On the whole, a significant difference (P < 0.05) was seen in the frequency of p53 positive immunostaining between low-grade dysplasia and high-grade dysplasia (44.1% and 61.8%, respectively) but not in that of K-ras mutations (20.3% and 23.4%, respectively). CONCLUSIONS: The results of this study suggest that mutation of the p53 suppressor gene occurs earlier in the adenoma-carcinoma sequence than K-ras mutation, providing a clue for further understanding of the role of the p53 gene in the early stage of colorectal tumorigenesis.

Adenoma↗

Local gastric and serum concentrations of rebamipide following oral ingestion in healthy volunteers.

The purpose of this study was to investigate whether sufficient concentrations of rebamipide (COR) are actually present in the stomach after its oral ingestion at an ordinary clinical dose. Twenty healthy volunteers (total 42 man-days) participated in the study. After ingestion of 100, 200, or 300 mg of rebamipide, endoscopy was performed at 1, 2, 4, and 6 hr, and gastric mucosa or gastric mucus was taken from the antrum. Venous blood samples were taken simultaneously. Samples were analyzed by high-performance liquid chromatography. The COR in the gastric mucosa and gastric mucus did not depend on the original amount ingested. After ingestion of rebamipide, each COR was higher than 10(-4) M (37 microg/g tissue) at 1 or 2 hr. On the other hand, the COR in serum did depend on the amount ingested and was lower than 10(-6) M (0.37 microg/ml) at every time tested. These results suggest that the COR in the stomach exceeds the levels that are needed for various antiulcer actions and that the rebamipide levels present in the gastric mucosa and gastric mucus result from local penetration.

Administration, Oral↗

Gastric volvulus in living, related liver transplantation donors and usefulness of endoscopic correction.

BACKGROUND: For cultural reasons, liver transplantation from living, related donors is common in Japan. This is the first description of gastric volvulus as a complication in living, related liver donors and of the usefulness of endoscopic correction. METHODS: One hundred fifteen donors from whom liver grafts were harvested for living, related liver transplantation between June 1990 and December 1999 were studied. Left lobectomy of the liver was performed in 47 cases, left lateral segmentectomy in 41, expanded lateral segmentectomy in 20, and expanded left lobectomy in 7 to provide liver grafts for recipients. If donors complained of symptoms of upper GI obstruction, EGD was performed. The diagnosis of gastric volvulus was based on characteristic endoscopic findings, and endoscopic correction was attempted. RESULTS: Gastric mesenteroaxial volvulus was recognized in 13 of 115 donors (11.3%) after grafts of the liver were harvested. No significant correlation was found among gender, age, portion of the liver harvested, and the occurrence of gastric volvulus. After endoscopic correction, all donors except 1 became asymptomatic; after correction, recurrence of the volvulus was not observed. In the single donor who continued to have symptoms, insertion of a nasogastric tube for 14 days resulted in correction of the volvulus. CONCLUSIONS: The frequency of gastric volvulus among donors involved in living, related liver transplantation is high. Endoscopic correction of the volvulus is useful in dealing with this complication.

Adult↗

Pseudosigmoidea: A new genus for a hyphomycete (ATCC 16660) formerly identified as Sigmoidea prolifera.

A new hyphomycetous genus, Pseudosigmoidea, is established with a single species, P. cranei, based on ATCC 16660 previously identified as Sigmoidea prolifera. The conidial ontogeny of Pseudosigmoidea is enteroblastic, and its conidiogenesis is phialidic. On the other hand, Sigmoidea is redescribed with holoblastic conidial ontogeny and with conidiogenous cells proliferating sympodially.

Journal Article↗