Gastric Autoantigenic Proteins in Helicobacter Pylori Infection

Purpose

This study tried to identify novel gastric autoimmune antigens that might be involved in aggravating the atrophic gastritis among patients with Helicobacter pylori infection using two-dimensional immunoblotting analysis.

Materials and Methods

Proteins from gastric mucosal antrectomy specimens and AGS cells (gastric adenocarcinoma cell lines derived from a Caucasian patient who had received no prior therapy) were 2-dimensionally immunoblotted separately with a pool of 300 sera from H. pylroi-infected patients at Gyeongsang National University Hospital.

Results

Thirty-eight autoantigenic proteins including alcohol dehydrogenase [NADP+], alpha enolase, gastrokine-1, gastric triacylglycerol lipase, heat shock 70 kDa protein 1, and peroxiredoxin-2 were identified in the gastric mucosal tissue. Fourteen autoantigenic proteins including programmed cell death 6-interacting protein, serum albumin and T-complex protein 1 subunit gamma were identified in the AGS cells. Albumin, alpha-enolase, annexin A3, cytoplasmic actin 1, heat shock cognate 71 kDa protein and leukocyte elastase inhibitor were commonly observed autoantigenic proteins in both gastric mucosal tissue and AGS cells. Alpha-enolase, glutathione S-transferase P, heat shock cognate 71 kDa protein, heat shock 70 kDa protein 1, human mitochondrial adenosine triphosphate synthase (ATP) subunit beta, mitochondrial 60 kDa heat shock protein, peroxiredoxin-2, 78 kDa glucose-regulated protein precursor, tyrosine-protein phosphatase non-receptor type 11 and Tryptophan-Aspartic acid (WD) repeat-containing protein 1 showed 60% or higher amino acid positivity.

Conclusion

These newly identified gastric autoimmune antigens might be useful in the control and prevention of gastroduodenal disorders, and might be valuable in breaking the vicious circle that exists in gastroduodenal disorders if their pathophysiological roles could be understood in the progress of chronic atrophic gastritis, gastroduodenal ulcers, intestinal metaplasia, and gastric carcinogenesis.     

The Quality of Health Information on Allergic Rhinitis,Rhinitis, and Sinusitis Available on the Internet

PurposeThe internet has become one of the most important media outlets used to obtain health information. Therefore, the quality of health information available on the internet is very important. We evaluated the quality of internet-derived health information on allergic rhinitis, rhinitis and sinusitis and compared these results to those of previous studies performed five years ago.MethodsThe terms "allergic rhinitis (AR)", "rhinitis" and "sinusitis" were searched among the four most commonly used search engines in South Korea. These websites were evaluated according to the author, the Journal of the American Medical Association (JAMA) benchmarks, the DISCERN questionnaire and the Allergic rhinitis and its Impact on Asthma (ARIA) 2008 Update.ResultsA total of 120 websites were obtained and analyzed. For all diseases, "Oriental physician" had the largest portion (almost half of all websites), followed by "Western physician". Based on analyses using the JAMA benchmark, "Attribution" and "Disclosure" were ignored in almost all surveyed websites. According to the scores of the DISCERN question, the majority of websites did not supply appropriate references for their health information, and information on the negative aspects of treatment such as risks and uncertainty was not provided in several websites. In an analysis based on the ARIA 2008 Update concepts, 65% of websites pertaining to health information on AR contained unreliable information.ConclusionsThe quality of health information on the internet was not acceptable. Thus, governmental regulation or control to improve the quality of health information is required.     

Fulminant onset of acute leukemia from normal hematopoiesis within 3 months of follow up for multiple myeloma treated with total therapy protocols

Assiduous surveillance for genetic aberrations is necessary in patients on cytotoxic therapies to detect therapy‐related myeloid neoplasms (t‐MN). Current modalities include metaphase cytogenetics and FISH. Since t‐MN may develop abruptly in cytogenetically normal patients, a discussion exploring additional methods such as SNP‐array and targeted‐deep‐sequencing to detect subchromosomal abnormalities is needed.