Novel endoscopic hemostasis technique for use during endoscopic submucosal dissection.
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Biomedical subjects
Publications and source records attributed to M Iguchi.
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BACKGROUND AND STUDY AIM: We have previously reported that gastric ulcers artificially created by endoscopic submucosal dissection (ESD) would heal within 8 weeks regardless of size and location. The details of the healing process remain unclear, and we aimed to clarify the mechanism by histopathological investigation. PATIENTS AND METHODS: 21 post-ESD ulcers were examined histopathologically, using surgically resected specimens from patients who had subsequently undergone gastrectomy due to submucosal invasion and/or lymphovascular infiltration by the tumor. The grade of ulcer, appearance of regenerative mucosa, scar formation, and extent of fibrosis were evaluated. RESULTS: Fibrosis and wall thickening were observed from 2 weeks after ESD, but regenerative mucosa was not observed until 5 weeks. Among 12 patients who underwent gastrectomy later than 8 weeks after ESD, a mucosal defect was still observed in two patients. In these two patients the lesion was associated with severe fibrosis due to previous peptic ulcer or submucosal invasion by the lesion. CONCLUSION: Size reduction in these ulcers occurs by contraction in the early phase, then regenerative mucosa covers the remaining mucosal defect within 8 weeks. If there is fibrosis under the lesion before ESD, there is a possibility that the artificially created ulcer will not heal within 8 weeks.
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BACKGROUND AND STUDY AIMS: One of the major complications of endoscopic mucosal resection (EMR) for gastrointestinal tumors is perforation, and the most effective way of preventing perforation is to elevate the lesion sufficiently by endoscopic injection of fluid into the submucosa. MATERIALS AND METHODS: In order to compare the lesion-lifting properties of several different solutions, 1 ml of each of the following solutions was injected into the submucosa of the resected porcine stomach: normal saline, 3.75 % NaCl, 20 % dextrose water, 10 % glycerin with 0.9 % NaCl plus 5 % fructose, and two sodium hyaluronate (SH) solutions. RESULTS: Significantly higher initial elevation was produced by both SH solutions, and it remained higher than that achieved by the other solutions at all times. Hypertonic solutions, especially 10 % glycerin with 0.9 % NaCl plus 5 % fructose, tended to produce and maintain greater mucosal elevation than normal saline, but the difference was not significant. CONCLUSIONS: SH solutions were the most suitable ones for producing and maintaining long-term mucosal elevation, while the superiority of hypertonic solutions over normal saline was not clearly demonstrated.
BACKGROUND AND STUDY AIMS: Sodium hyaluronate (SH) is a promising submucosal injection solution during endoscopic mucosal resection, but its high cost is an obstacle to more widespread use. The aim of this study was to identify an appropriate low-cost SH solution by varying the molecular weight of SH and mixing various solutions with it. MATERIALS AND METHODS: The viscoelasticity of various SH solutions was first measured. The concentrations of two 1 % SH preparations with different molecular weights (800 kDa and 1900 kDa) were adjusted to 0.5 %, 0.25 %, and 0.125 %, using 0.9 %/3.75 % normal saline (NS), 5 %/20 % dextrose water (DW), and a glycerin solution (Glyceol): 10 % glycerin with 0.9 % normal saline plus 5 % fructose. The ability of these SH solutions to create submucosal fluid cushions (SFCs) was then investigated in the stomachs of two live minipigs. RESULTS: The 0.25 % 1900 kDa SH/NS solution and the 0.125 % 1900 kDa SH/20 % DW solution created a similar viscoelasticity to that of the 0.5 % 800 kDa SH/NS solution. The ability of these solutions to create SFCs was also similar. In addition, the 0.125 % 1900 kDa SH/Glyceol solution created similar SFCs, with a synergistic effect of increased viscoelasticity and the hypertonic nature of glycerin. CONCLUSIONS: A mixture of higher molecular weight sodium hyaluronate with a sugar solution (particularly 20 % dextrose), with or without glycerin, should be regarded as a cost-effective option for creating SFCs instead of the conventional SH solution made with the same amount of a 1 % 800 kDa SH preparation and normal saline.
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BACKGROUND: We have previously shown that the intraluminal concentration of NO in H. pylori-positive patients is significantly reduced compared to that in H. pylori-negative patients. AIM: The aim of this study was to evaluate the effect of H. pylori infection on gastric motor activity in relation to the level of NO and nitrite in the stomach in humans. METHODS: Thirty-two H. pylori-negative and 32 H. pylori-positive patients with dyspepsia were studied. Gastric myoelectrical activity was recorded for 24 h using surface electrogastrography. Intraluminal gas and juice were endoscopically collected from the stomach to determine NO and nitrite and nitrate (NOx) levels using a chemiluminescence system. RESULTS: The percentage of tachygastria in the morning preprandial state was significantly higher (P = 0.005) in H. pylori-positive than -negative patients. In H. pylori-negative patients, there was a significant positive correlation between NO levels and the percentage of bradygastria (r = 0.56, P = 0.001) and a significant negative correlation between NOx levels and the percentage of normal electrical activity (r = - 0.57, P=0.001) in the preprandial state. CONCLUSIONS: Gastric motor activity is associated with NO and NOx levels in the gastric lumen. H. pylori infection may play a role in the pathogenesis of abnormal gastric myoelectrical activity.
Using seed crystal method, whole-urine method, and scanning electron microscopy, the inhibitory effects of sialic acid and osteopontin (OPN) on aggregation/growth of CaOx crystals were investigated. Using the seed crystal method, sialic acid showed an inhibitory effect on CaOx crystal aggregation/growth in a concentration-dependent manner, but almost no effect was observed using the whole-urine method. OPN showed an inhibitory effect on aggregation/growth in both experimental systems. The inhibitory effect of asialo-OPN on aggregation/growth was approximately 20% lower than that of OPN in the experiment using the seed crystal method and approximately 15% lower in the experiment using the whole-urine method. Scanning electron microscopy showed that OPN and sialic acid inhibit the aggregation of CaOx crystals. The above findings show that sialic acid accounts for about 15-20% of the involvement of OPN in CaOx crystallization.
We report two cases of atretic cephalocele, a diverse form of cranium bifidum. The patients were 15-year-old and 3-month-old girls, who each had a hard, nonpulsatile, nonreducible lump covered by alopecic scalp in the parieto-occipital area. They were surgically treated. In case 2, microscopical examination of the operative specimen revealed a meninges under the mass, which was devoid of nervous tissue. Such lesions have rarely been reported, and their essential nature is still the subject of controversy. Pathological and embryological aspects of atretic cephalocele are discussed on the basis of the findings; the neural crest remnant was assumed to be the developmental origin of the lesion in each of these cases.
Osteopontin (OPN) is a urinary protein which inhibits calcium oxalate (CaOx) crystal growth in the seed crystal system. The aim of this study was to evaluate the effects of OPN immobilized on collagen granules (CG) for CaOx crystal growth and aggregation in this system. OPN-immobilized CG showed a 30% decrease in inhibitory activity compared with non-OPN-immobilized CG. Scanning electron microscopy revealed that 1) OPN-immobilized CG showed more marked aggregation and adhesion of seed crystals (smaller than 0.5 microm in diameter) than non-OPN-immobilized CG, 2) the amount of adherent large type crystals (2-3 microm in diameter) did not differ between OPN immobilized and non-OPN-immobilized CG. In conclusion, immobilized OPN promotes aggregation and adhesion of CaOx crystals smaller than 0.5 microm on CG. These observations suggest that crystal adhesion to immobilized OPN plays a role in the retention of crystals in the kidney.
The Rab small G protein family participates in intracellular vesicle transport, including exocytosis and endocytosis. The cDNA encoding a novel Rab-related small G protein (Rab38) has been cloned from rat lung cDNA library and recorded in GenBank (accession no. M94043). However, the expression and localization of the protein in the lung remains primarily unknown. We produced polyhistidine-tagged recombinant Rab38 and a polyclonal antibody with a synthetic peptide. Immunohistochemistry demonstrated that the protein is specifically localized in alveolar type II cells and in bronchial epithelial cells. In situ hybridization using a digoxygenin-labeled RNA riboprobe clearly showed that the mRNA of the protein is localized in alveolar type II cells and bronchial epithelial cells, especially terminal airway epithelial cells. Western blot and reverse transcriptase-polymerase chain reaction showed distinct expression of the protein and mRNA in isolated alveolar type II cells, but not in alveolar macrophages. The native protein was predominantly hydrophobic and was enriched in a high-density vesicle fraction but was barely detectable in nuclear and lamellar body fractions in alveolar type II cells. Immunofluorescence cytochemistry performed on cultured alveolar type II cells showed that Rab38 distributed extensively in the cytoplasm with a distribution pattern similar to endoplasmic reticulum rather than other subcellular organelles. These results suggest that this novel rab small G protein (Rab38) mediates vesicular transport in terminal airway epithelium.
Leptin, a satiety-regulating cytokine, is predominantly expressed by adipocytes, although recently the nonadipose tissue production of leptin has been reported. To investigate the possibility of leptin production by human scalp hair follicles, we examined leptin production and its mRNA expression by cultured human follicular papilla cells. We isolated 12 human follicular papilla cell lines from different individuals. They were identified by their morphology, their high alpha-smooth-muscle actin expression, their inability to differentiate into adipocytes, and by the lack of mRNA for adipose-specific fatty acid binding protein. All the human follicular papilla cell lines, but not neonatal human dermal fibroblasts, produced significant amounts of leptin demonstrable by enzyme-linked immunosorbent assay. We demonstrated leptin mRNA expression by human follicular papilla cell lines, but not by neonatal human dermal fibroblasts, by reverse transcription polymerase chain reaction. By immunohistochemistry and in situ hybridization, we detected both leptin protein and mRNA at the lower portion of the hair follicle, i.e., hair matrix, inner root sheath of the hair bulb, and human follicular papilla cells. In contrast, the leptin receptor with intracytoplasmic signal sequence was detected in the follicular papilla cells immunohistochemically, and the long isoform of the leptin receptor mRNA was demonstrated in the human follicular papilla cell lines by reverse transcription polymerase chain reaction. Finally, by using these human follicular papilla cell lines, we showed that cytokines such as interleukin-1 beta, tumor necrosis factor alpha, interferon-gamma, and interleukin-4, and growth factors such as epidermal growth factor, basic fibroblast growth factor, and transforming growth factor beta1, but not vascular endothelial growth factor, hepatocyte growth factor, keratinocyte growth factor, and insulin-like growth factor 1, significantly downregulated the production of leptin. These data demonstrated that human follicular papilla cells produce leptin and express the functional leptin receptor in vivo and in vitro, suggesting its autocrine function. Moreover, the regulation pattern of its production by various factors suggests a pivotal role of leptin in hair biology.
BACKGROUND: There is interest in the development of GERD after Helicobacter pylori eradication. In contrast, the development of duodenal erosions after therapy has received scant attention. Patients were examined after eradication of H pylori infection to determine the frequency of post-therapy duodenal erosions (primary outcome) and whether there was a relation between development of duodenal and esophageal erosions. Additionally, factors were searched for that would identify patients at increased risk for duodenal erosions. METHODS: A single-center, endoscopist-blinded, observational study was conducted of 196 patients in whom H pylori was eradicated. The presence of esophageal or duodenal erosions was evaluated 4 weeks and 6 months after eradication. Serum gastrin and pepsinogen I (PG I) and II (PG II) levels were also determined for 83 patients entering the study during its final year. RESULTS: Multiple small duodenal erosions developed in 8.6% of patients after H pylori eradication and were more common in patients with pre-eradication duodenal ulcer (27.8%) compared with those with gastric ulcer (6.7%) or atrophic gastritis (1.4%) (p < 0.05). Duodenal erosions were associated with high levels of PG I before and after eradication. The frequency of duodenal erosions decreased over time (3.1% by 6 months). CONCLUSION: Duodenal erosions occur after H pylori eradication and appear to be related to duodenal ulcer and increased PG I levels, both of which are associated with increased acid secretion. Measurement of PG I may help to identify patients who have duodenal erosions develop after H pylori therapy for studies of the pathogenesis of these lesions.
OBJECTIVES: The low incidence of atherosclerosis and other degenerative disease, including urolithiasis, in the Greenland Eskimo has been attributed to their high consumption of oily fish with its high concentration of eicosapentaenoic acid (EPA). With a westernized diet, the oxygenated products of renal prostaglandin synthesis are metabolites of the n-6 series and these are known to play important roles in several pathophysiological processes involved in calcium stone formation. Buck's group presented a hypothesis that the initiating factor for lithiasis triggers prostaglandin synthesis, and showed that this influenced by EPA treatment. METHOD: In order to ascertain the effects of EPA on plasma lipids and urinary parameters, we undertook a clinical study whereby a highly purified preparation was administrated (1,800 mg/day) to 88 patients with urinary stones for 3 months (short term) and 18 months (long term). RESULTS: Hyperlipemia improved the affected individuals and urinary calcium was significantly reduced in the hypercalciuric but not in the normocalciuric group. CONCLUSION: The results suggest that EPA by reducing urinary calcium might favorably affect urine composition in a way that possibly reduces the risk of calcium stone formation.
The expression of cytokeratins and involucrin was analyzed to identify the skin cells which compose the epidermis of dogs. The distribution of cytokeratins and involucrin in normal dog skin was immunohistochemically examined with 27 commercial monoclonal antibodies for human use. Antibodies, No.4. OV-TL12/13, 35betaH11, 4.1.18, CAM5.2, NCL5D3, Ks.13.1, Ks.18.04, Ks.19.1, 170.2.]4 and Ks.20.8 stained hair follicles and/or the sweat gland duct, but not the epidermis. Antibodies, 34betaB4, AE3, 34betaE12. LP34, RCK102, MNF116, AE1, KLI, DE-K10 and DE-K13 reacted with every layer of the epidermis, hair follicles and the sweat gland duct. These results were similar to those reported in the human skin. No positive staining, however, could be detected in the epidermis, hair follicles and the sweat gland duct with commercial antibodies, 6B10, Ks.7.18, Mu146-uc, E3, RCK108 and involucrin. Therefore, immunohistochemical investigation with these commercial antibodies developed for human skin examination might be available for investigating the origin of skin tumors in dogs.
We experienced a rare case of tumor-forming type of chronic pyelonephritis that could hardly be differentiated from renal cell carcinoma. A 62-year-old man was admitted to our department with right renal tumor which was discovered when he underwent examination for gastric cancer. Abdominal ultrasound sonography and computed tomography revealed a mass in the middle portion of the right kidney, measuring 3.8 x 3.5 cm in diameter, with irregular surface and isoechoic and isodense inner mass. Renal angiography demonstrated a hypervascular area in the middle portion. Radical nephrectomy and subtotal gastrectomy were performed under a tentative diagnosis of right renal cell carcinoma and early gastric cancer. The excised specimen macroscopically demonstrated a yellowish mass in the middle portion and microscopically revealed many lymphocytes and few neutrophils, macrophages or foam cells. The patient was diagnosed as tumor-forming type of chronic pyelonephritis. Such obvious inflammatory findings very rarely exist in the tumor-forming type of chronic pyelonephritis. Therefore, caution should be exercised in the differential diagnosis between this disease and renal cell carcinoma.
A 34-year-old man visited our hospital with the complaint of right scrotal swelling. Right high orchiectomy was performed under the diagnosis of testicular tumor. Pathological examination was seminoma, pT2pN0pM0 and 3 courses of chemotherapy (cisplatin, vinblastine, bleomycin) were performed. The patient had undergone testicular biopsy for infertility at another hospital 6 years before this visit. Re-examination of the biopsy specimen revealed a intratubular germ cell tumor. No evidence of recurrence or metastasis was found 2 years after surgery.
A 36-year-old woman admitted to our hospital because of numbness in the left limbs and weakness in the right arm, and was subsequently given a diagnosis of intramedullary spinal cord metastases from lung cancer. The patient had lung adenocarcinoma with metastases to the brain, spine and lymph nodes. Occipital craniotomy, radiation therapy and chemotherapy were performed on the lesions in the year following June 1994. In June 1995, however, she complained of numbness in the left limbs and weakness in the right arm. Compatible with her neurological manifestation, MRI demonstrated tumors in the right side of the cord at the spinal level of C3-4 and C7-Th1, both of which were of high density in T2-enhanced conditions with enhancement by gadolinium-diethylenetriamine pentaacetic acid. No invasion from spinal metastasis was detected by CT, scintigraphy or MRI. We therefore diagnosed her manifestation as Brown-Séquard syndrome caused by intramedullary spinal cord metastatic tumors of lung adenocarcinoma. In order to avoid paraplegia and dysfunction of the bladder and bowel, radiation therapy of the cord lesions with total dose of 44 Gy was performed. Her neurologic manifestation was improved, restoring her quality of life, as the tumor size estimated by MRI decreased. Four months later, however, she died of lung adenocarcinoma that developed accompanied with severe peritonitis carcinomatosa and multiple metastases.