SUMMARY Helicobacter suis hosted by hogs is the most prevalent gastric non- Helicobacter pylori Helicobacter species found in humans. Recent studies suggest that the H. suis infection has already induced many cases of gastric disease. However, the infection period and route of H. suis from hogs remain unclear. Because diagnostic methods based on the urease activity of H. suis often yield negative judgments, there is no reliable method for diagnosing H. suis infection in clinical practice without gastric biopsy specimens. We developed the world’s first ELISA to simultaneously diagnose H. suis and H. pylori infection in a single test. The area under the ROC curve was 0.9648 or 0.9200 for identifying H. suis or H. pylori infection, respectively. The sensitivity, specificity, and positive and negative predictive values for identifying H. suis infection were 100%, 92.6%, 76.9%, and 100%, and those for identifying H. pylori infection were 88.2%, 87.5%, 65.2%, and 96.6%, respectively. (150 words)
Deuterium ion irradiation has been carried out with incident energies of 100 eV and flux of 1 /spl times/ 10/sup 22/ D/sup +/m/sup -2/s/sup -1/ at a temperature in range between 333 K and 1130 K up to a dose of 1 /spl times/ 10/sup 26/ D/sup +/m/sup -2/. Three kinds of tungsten used are pure tungsten made by powder metallurgy tungsten (PM-W), vacuum plasma spray tungsten (VPS-W) and single crystal tungsten (SC-W). Surface morphology before and after the irradiation is observed with a SEM. Retention property of deuterium after the irradiation is also examined with a TDS. Blisters with a diameter of about 0.2-2.0 /spl mu/m are formed on PM-W by deuterium irradiation at 333 K and 673 K but size and shape of those blisters change depending on the irradiation temperatures. However, no blisters are found on PM-W at elevated temperatures between 723 and 1130 K. On the other hand, blisters with a diameter of about 2 /spl mu/m are formed on SCW irradiated at 343 K but no blisters are observed on SCW irradiated at 383, 623 and 1123 K. In the case of VPS-W irradiated at 333, 723 and 1123 K, modification like blister with a diameter of about 0.2 /spl mu/m occurs. TDS measurement also shows that deuterium is not retained in sample, which the blisters are not formed.
Approximately 90% of patients with gastric mucosa-associated lymphoid tissue (MALT) lymphoma are infected with H. pylori. The eradication of H. pylori leads to complete remission (CR) of the disease in 70-80% of the gastric MALT lymphoma with H. pylori infection. We reported three cases of H. pylori negative gastric MALT lymphoma that were confirmed as CR treating by radiation therapy (RT) . All cases confirmed H. pylori negative by 4 or 5 H. pylori tests. In addition, H. heilmannii was negative in all cases. CR was confirmed at the time of 1 or 2 years after RT. In conclusion, RT is useful for treating H. pylori negative gastric MALT lymphoma.
Helicobacter pylori (H. pylori) gastritis has been approved by Ministry of Health, Labour and Welfare as an additional indication for H. pylori eradication in Japan on Feburary 21, 2013. Diagnostic methods of H. pylori infection have been divided into direct (invasive) and indirect (non-invasive). Invasive tests requiring endoscopic biopsy include culture, histology and rapid urease test (RUT). Non-invasive tests not requiring endoscopic biopsy include measurement of H. pylori antibody(serum, urine), urea breath test(UBT) and stool antigen test. Assessment of the efficacy of H. pylori eradication therapy should be performed at least 4 weeks after the completion of treatment. UBT and monoclonal stool antigen test are both recommended for the assessment of H. pylori eradication. When the results obtained is doubtful for assessment of H. pylori eradication, it is preferable to perform another test or follow-up.
Infection with Helicobacter suis, which causes many cases of gastric disease, is not reliably diagnosed. Here, we present a protocol for detecting H. suis infection. We describe steps for collecting gastric biopsies and sera from patients, preparing DNA for PCR, and targeting the H. suis-specific gene. We then define procedures for inoculating biopsies onto primary agar plates and transferring colonies to secondary agar plates. Finally, we detail whole-genome sequencing of bacteria and assess H. suis infection in sera with ELISA. For complete details on the use and execution of these protocols, please refer to Matsui et al.
Purpose: Cowden's disease (CD) is a non-adenomatous gastrointestinal polyposis syndrome. To date, there is a little information on the association of Heliobacter pylori (H. pylori) infection with gastric manifestations of CD. And there are several reports that hyperplastic gastric polyps disappear in 40–70% patients after eradication of H. pylori. Methods: We describe a 53-year-old woman with H. pylori positive CD with hyperplastic gastric polyposis treated with H. pylori eradication. Abnormalities involving thyroid, skin and ovary were found in this patient. Gastroduodenal endoscopy revealed multiple hyperplastic polyposis in the antrum. There were also esophageal glycogenic acanthosis. Colonoscopy also revealed multiple hyperplastic polyps in the rectum and left-side colon. H. pylori infection was detected urea breath test and culture. The patient was treated H. pylori infection with a 1 week course of triple therapy consisting of lansoplazole, amoxicillin and clarithromycin. Results: Three month later, repeat gastroscopy showed substantial decrease in size and number of the polyposis, and urea breath test, culture and Giemsa staining were negative. 1-year follow up gastroscopy revealed almost complete regression of the lesion. Patient is underwent endoscopy every 1 year after H. pylori eradication, and 10 years after eradication, H. pylori infection is still negative by the urea breath test, and gastroscopy revealed almost complete regression of the lesion. Conclusion: It was concluded that H. pylori infection might affect the growth of gastric hyperplastic polyposis with CD.
Recently, the frequency of nonrheumatic aortic regurgitation (AR) has apparently increased, accompanied by a decrease in frequency of rheumatic fever. The purpose of the present study was to ascertain the echocardiographic features of nonrheumatic AR. We had 24 surgically- or autopsy-proven cases of nonrheumatic AR admitted during a two year period. These were 10 cases of infective endocarditis (IE), five with ventricular septal defect of type I, three with syphilis, and two with prosthetic valve malfunctions, and the remainder five were difficult to diagnose clinically. These five were three men and two women, whose ages ranged from 40 to 67 years and averaged 50 years, and their final diagnoses were annulo-aortic ectasia (AAE), Behcet's disease, and the aortitis syndrome (Takayasu's arteritis), and two other cases were of unknown etiology. The echocardiographic manifestations were compared with the operative, autopsy, and pathological findings. Echocardiographically, there were few or no increased intensities of aortic valvular echoes, and aortic roots had a tendency to dilate, leading to the failure of coaptation of valve leaflets, for a relative lack of valvular surface area to cross-sectional area of the aortic ring. Three of the five had flail aortic valves and three had associated MVP. Three were diagnosed as floppy aortic valves at the time of surgery. Excised valves revealed little hyperplasia or sclerosis grossly. Fibrinoid necrosis or mucoid degeneration were noted by light microscopy. Some specimens of aortic walls also revealed cystic medial necrosis or disruption of elastic fibers. All these findings were based on degenerative processes of connective tissue, and not on inflammatory processes. These pathological findings and the coexistence of mitral valve prolapse (MVP), which were not regarded as coincidental, suggest that connective tissue fragility--congenital or acquired--may play an important role in the genesis of nonrheumatic AR.
