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Biomedical subjects

Kentaro Sugano

Publications and source records attributed to Kentaro Sugano.

At least 55 records · Page 3Linked to original sources
PubMed2004

Angiotensin II stimulates DNA synthesis of rat pancreatic stellate cells by activating ERK through EGF receptor transactivation.

Although angiotensin II (Ang II) is known to participate in pancreatic fibrosis, little is known as to the mechanism by which Ang II promotes pancreatic fibrosis. To elucidate the mechanism, we examined the action of Ang II on the proliferation of rat pancreatic stellate cells (PSCs) that play central roles in pancreatic fibrosis. Immunocytochemistry and Western blotting demonstrated that both Ang II type 1 and type 2 receptors were expressed in PSCs. [3H]Thymidine incorporation assay revealed that Ang II enhanced DNA synthesis in PSCs, which was blocked by Ang II type 1 receptor antagonist losartan. Western blotting using anti-phospho-epidermal growth factor (EGF) receptor and anti-phospho-extracellular signal regulated kinase (ERK) antibodies showed that Ang II-activated EGF receptor and ERK. Both EGF receptor kinase inhibitor AG1478 and MEK1 inhibitor PD98059 attenuated ERK activation and DNA synthesis enhanced by Ang II. These results indicate that Ang II stimulates PSC proliferation through EGF receptor transactivation-ERK activation pathway.

Angiotensin II↗
PubMed2004

Gastrointestinal stromal tumor in the jejunum: diagnosis and control of bleeding with electrocoagulation by using double-balloon enteroscopy.

A 43-year-old man presented with gastrointestinal bleeding. A tumor with central ulceration was observed in the jejunum, with the use of a new enteroscopy system called "double-balloon enteroscopy". Bleeding after biopsy sampling of the tumor was controlled endoscopically by using electrocoagulation. Histological findings of the biopsy specimens were consistent with gastrointestinal stromal tumor, and this was surgically resected. Double-balloon enteroscopy was useful for the diagnosis as well as the control of bleeding in this patient.

Adult↗
PubMed2004

Laparoscopic radiofrequency ablation of hepatocellular carcinoma in the caudate lobe by using a new laparoscopic US probe with a forward-viewing convex-array transducer.

BACKGROUND: The use of a new end-fire type laparoscopic US probe with a forward-viewing convex-array transducer allows the caudate lobe of the liver to be accessed. This study evaluated the preliminary results of treatment of hepatocellular carcinoma in the caudate lobe by using this new instrument. METHODS: Three patients with hepatocellular carcinoma in the caudate lobe were selected. A laparoscopic US probe, with a forward-viewing convex-array transducer at the tip and a guide groove for puncture on the back, was used to monitor the position of the radiofrequency ablation needle during the treatment. RESULTS: Ablation was performed without complication in all cases. Complete necrosis of the tumor was confirmed by postoperative CT. At a mean follow-up of 30.3 months, no local recurrence was observed in any patient. CONCLUSIONS: Radiofrequency ablation of hepatocellular carcinoma in the caudate lobe of the liver by using a new laparoscopic US probe with a forward-viewing convex-array transducer at the tip was safe and effective.

Aged↗
PubMed2004

Clinical outcomes of double-balloon endoscopy for the diagnosis and treatment of small-intestinal diseases.

BACKGROUND & AIMS: A specialized system for a new method for enteroscopy, the double-balloon method, was developed. The aim of this study was to evaluate the usefulness of this endoscopic system for small-intestinal disorders. METHODS: The double-balloon endoscopy system was used to perform 178 enteroscopies (89 by the anterograde approach and 89 by the retrograde approach) in 123 patients. The system was assessed on the basis of the rates of success in jejunal and ileal insertion and the entire examination of the small intestine, diagnostic yields, ability to perform treatment, and complications. RESULTS: Insertion of the endoscope beyond the ligament of Treitz or ileocecal valve was possible in all 178 procedures. It was possible to observe approximately one half to two thirds of the entire small intestine by each approach, and observation of the entire small intestine was possible in 24 (86%) of 28 trials. The source of bleeding was identified in 50 (76%) of 66 patients with GI bleeding, scrutiny of strictures was possible in 23 patients, and a tumor was examined endoscopically in 17 patients. Two complications (1.1%) occurred. Endoscopic therapies in the small intestine including hemostasis (12 cases), polypectomy (1 case), endoscopic mucosal resection (1 case), balloon dilation (6 cases), and stent placement (2 cases) were performed successfully. CONCLUSIONS: Double-balloon endoscopy permits the exploration of the small intestine with a high success rate of total enteroscopy. The procedure is safe and useful, and it provides high diagnostic yields and therapeutic capabilities.

Adolescent↗
PubMed2004

Direct observation with double-balloon enteroscopy of an intestinal intramural hematoma resulting in anticoagulant ileus.

In the case presented here, we have succeeded in describing the endoscopic findings of anticoagulant ileus and evaluated the degree of bleeding as well as ischemia through endoscopic observation. We have demonstrated that enteroscopy using the double-balloon method is a useful diagnostic tool in the evaluation of a patient suspected to have anticoagulant ileus.

Anticoagulants↗
PubMed2004

Recurrent peptic ulcers in patients following successful Helicobacter pylori eradication: a multicenter study of 4940 patients.

OBJECTIVE: Although curative treatment of Helicobacter pylori infection markedly reduces the relapse of peptic ulcers, the details of the ulcers that do recur is not well characterized. The aim of this study is to describe the recurrence rate and specific features of peptic ulcers after cure of H. pylori infection. METHODS: This was a multicenter study involving 4940 peptic ulcer patients who were H. pylori negative after successful eradication treatment and were followed for up to 48 months. The annual incidence of ulcer relapse in H. pylori-cured patients, background of patients with relapsed ulcers, time to relapse, ulcer size, and site of relapsed ulcers were investigated. RESULTS: Crude peptic ulcer recurrence rate was 3.02% (149/4940). The annual recurrence rates of gastric, duodenal and gastroduodenal ulcer were 2.3%, 1.6%, and 1.6%, respectively. Exclusion of patients who took NSAIDs led annual recurrence rates to 1.9%, 1.5% and 1.3%, respectively. The recurrence rate was significantly higher in gastric ulcer. Recurrence rates of patients who smoked, consumed alcohol, and used NSAIDs were significantly higher in those with gastric ulcer recurrence compared to duodenal ulcer recurrence (e.g. 125 of 149 [83.9%] relapsed ulcers recurred at the same or adjacent sites as the previous ulcers). CONCLUSIONS: Curative treatment of H. pylori infection is useful in preventing ulcer recurrence. Gastric ulcer is more likely to relapse than duodenal ulcer. Recurrent ulcer tended to recur at the site of the original ulcers.

Alcohol Drinking↗
PubMed2004

Gastrointestinal angiodysplasia in a patient with type 2 von Willebrand's disease and analysis of exon 28 of the von Willebrand factor gene.

Although the association between gastrointestinal angiodysplasia and von Willebrand's disease has been suggested, molecular mechanisms involved in the formation of angiodysplasia in patients with von Willebrand's disease remained undetermined. We examined exon 28 of the von Willebrand factor gene in a patient with both von Willebrand's disease and recurrent bleeding from angiodysplasia in the duodenum as well as his father's, and found a point mutation, C 3916-->T (amino acid substitution; Arg 543-->Trp), in the A1 domain of the von Willebrand factor gene. This mutation was identical with a previously reported mutation in a patient with von Willebrand's disease complicated with gastrointestinal angiodysplasia.

Adult↗
PubMed2004

New diagnostic approaches for early detection of gastric cancer.

Detection of gastric cancer in early stages is vitally important for ascertaining better prognosis and quality of life for the patients. Therefore, every endoscopist should be trained to master enough diagnostic skills to identify early gastric cancer that often shows minimal alteration from the surrounding mucosa, easily evading detection. For the first step, it is essential that endoscopists understand the normal gastric mucosa as well as the mucosal changes caused by chronic H. pylori infection, a high-risk condition for the development of gastric cancer. Once a suspicious lesion is identified, use of a dye-spraying method may be useful to clarify structural alteration caused by neoplastic changes and facilitate the biopsy sampling. Development of zoom (magnifying) endoscopy enabling 80x magnification with a one-touch switch from conventional endoscopic observation helps to identify the detailed surface structure as well as the vascular architecture of the mucosa without tissue biopsy. Combined with chromoendoscopy, this powerful endoscopic method can be used to identify small cancer foci or delineate the margin of early gastric cancer that can be treatable by mucosal dissection. Other new modalities using a variety of optical devices have been developed but the real value of their utility still remains to be proven in the actual clinical settings.

Diagnosis, Differential↗
PubMed2004

[Strategy for peptic ulcer therapy in the era of H. pylori eradication therapy].

The Japanese guideline for gastric ulcer therapy published 2003 has adopted a policy that eradication therapy for H. pylori as the first line therapy on ulcer patients with positive H. pylori status. For NSAID-induced gastric ulcer patients, cessation should be considered. In patients who cannot stop NSAIDs, proton-pump inhibitors or prostaglandin drugs is recommended. Similar strategy can be applied for duodenal ulcer patients. Implementation of this basic strategy in daily clinical practice, however, require further efforts to wider recognition of the new guideline for gastric ulcer therapy as well as to solve several barriers caused by discrepant health reimbursement policy.

Duodenal Ulcer↗
PubMed2004

[Japanese guideline for the management of gastric ulcer].

Japanese guideline for the management of gastric ulcer prepared by a research group supported by government funding was published in 2003 as a concise book for use in general practice. Overall management strategy classified based on etiology of ulcer was shown as a flow chart. Recommendation of treatment strategy for NSAID ulcer with PPI, and for H. pylori-positive gastric ulcer with eradication therapy are in line with internationally acknowledged consensus. A number of so-called mucoprotective drugs most of which are available in Japanese market alone, however, were given low priority when choosing single regimen, and their use in combination with acid suppressant, the most popular ulcer regimens in Japan, was not recommended due to lack of reliable evidence. Though it will take some time for general physicians to widely adopt this guideline, it undoubtedly will serve for reasonable gastric ulcer management in Japan.

Evidence-Based Medicine↗
PubMed2003

Distinct roles of Smad2-, Smad3-, and ERK-dependent pathways in transforming growth factor-beta1 regulation of pancreatic stellate cellular functions.

Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor-beta(1) (TGF-beta(1)) regulates PSC activation and proliferation in an autocrine manner. The intracellular signaling pathways of the regulation were examined in this study. Immunoprecipitation and immunocytochemistry revealed that Smad2, Smad3, and Smad4 were functionally expressed in PSCs. Adenovirus-mediated expression of Smad2, Smad3, or dominant-negative Smad2/3 did not alter TGF-beta(1) mRNA expression level or the amount of autocrine TGF-beta(1) peptide. However, expression of dominant-negative Smad2/3 inhibited PSC activation and enhanced their proliferation. Co-expression of Smad2 with dominant-negative Smad2/3 restored PSC activation inhibited by dominant-negative Smad2/3 expression without changing their proliferation. By contrast, co-expression of Smad3 with dominant-negative Smad2/3 attenuated PSC proliferation enhanced by dominant-negative Smad2/3 expression without altering their activation. Exogenous TGF-beta(1) increased TGFbeta(1) mRNA expression in PSCs. However, PD98059, a specific inhibitor of mitogen-activated protein kinase kinase (MEK1), inhibited ERK activation by TGF-beta(1), and consequently attenuated TGF-beta(1) enhancement of its own mRNA expression in PSCs. We propose that TGF-beta(1) differentially regulates PSC activation, proliferation, and TGF-beta(1) mRNA expression through Smad2-, Smad3-, and ERK-dependent pathways, respectively.

Animals↗
PubMed2003

Aberrant expression of CDX2 in Barrett's epithelium and inflammatory esophageal mucosa.

BACKGROUND: There have been no detailed reports directly comparing the expression of CDX1 with that of CDX2 in the inflammatory esophageal mucosa and Barrett's epithelium. The present study was designed to examine the expression of CDX 1/2 in inflammatory esophageal mucosa with or without Barrett's epithelium. METHODS: The expression of CDX1/2 genes was analyzed using the reverse transcriptase-polymerase chain reaction (RT-PCR) in 34 human esophageal biopsy specimens, and CDX2 expression was also evaluated immunohistochemically, using anti-human CDX2 monoclonal antibody. The biopsy specimens for RNA extraction were taken endoscopically from esophageal mucosa with mucosal break due to gastroesophageal reflux disease (GERD), Barrett's epithelium, and normal epithelium. The expressions of mucin markers (MUC2) and intestine-specific genes (sucrase-isomal-tase, human defensin-5, alkaline phosphatase) were also comparatively analyzed. RESULTS: CDX1/2 expression was not found in the normal esophageal mucosa. The prevalence of CDX1/2 mRNA expression was significantly higher in the mucosa with Barrett's epithelium than in the mucosa without Barrett's epithelium. It is noteworthy, however, that the CDX2 mRNA expression was initiated at the stage of esophagitis, when neither CDX1 nor intestine-specific genes had emerged yet. In contrast to CDX2, CDX1 was expressed only in Barrett's epithelium. Immunohistochemical study demonstrated strong and extensive nuclear immunoreactivity for CDX2 in Barrett's epithelium. Furthermore, fine granular cytoplasmic staining was also observed in the cytoplasm in Barrett's epithelium, as well as in inflammatory esophageal mucosa. CONCLUSIONS: We report here, for the first time, that CDX2 is expressed in patients with Barrett's epithelium and inflammatory esophageal mucosa. These findings imply that the expression of CDX2 may be an early event leading to the development of Barrett's esophagus.

Adult↗