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Previous studies have established a relationship between bacterial proteins and autoimmune diseases through several mechanisms. Infective endocarditis is known for its immunological phenomena, and the presence of antineutrophil cytoplasmic antibodies (ANCA) antibodies has been previously demonstrated in several infectious diseases. This retrospective, comparative, and descriptive study examined the relationship between infective endocarditis and the presence of ANCA antibodies. Ninety infective endocarditis cases were included in the study and tested for ANCA antibodies. The prevalence of ANCA positivity was determined, along with the differences in characteristics and prognosis between infective endocarditis patients with positive and negative serology for ANCA antibodies. The results showed that the characteristics of endocarditis patients who underwent ANCA serology testing were similar to those who did not, except for a higher prevalence of central line and chronic kidney disease in patients with ANCA serology (6.7% compared to 1.1% and 25.6% compared to 12.9%, respectively). Of the 90 endocarditis patients tested for ANCA serology, 18% were ANCA-positive, consistent with other prospective studies. There were no statistically significant differences in the primary outcome, six-month and one-year mortality, between patients with positive and negative ANCA serology. Similarly, in the secondary outcomes of acute kidney injury, heart surgery, and days of hospitalization, there were no statistically significant differences between patients with positive and negative ANCA serology. However, there were statistically significant differences in certain characteristics between the two groups. Patients with positive ANCA serology were found to have a higher prevalence of Enterococcus involvement (29.4% compared to 9.6% with P-value 0.046) and Q fever (23.5% compared to 4.1% P-value 0.02%). In contrast, patients with negative ANCA serology had a higher prevalence of fever (73% compared to 41% P-value 0.033).
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Aim: The aim of this study was to test the reliability of the University of California, Los Angeles Scleroderma Clinical Trial Consortium Gastrointestinal Tract (UCLA SCTC GIT) 2.0 questionnaire in Hebrew. Methods: UCLA SCTC GIT 2.0 was translated into Hebrew using the translation-retranslation method. The Hebrew version of the UCLA SCTC GIT 2.0 and the Hebrew version of the Short Form 36 (SF-36) were administered to 19 Hebrew-speaking patients with systemic sclerosis. Internal reliability was assessed using Cronbach's alpha. The Hebrew questionnaire was then tested for external validity using Spearman's correlation coefficient. Correlations (rho) ⩽ 0.29 were considered small, 0.30 to 0.49 were moderate, and those ⩾0.50 were considered large. Differences were considered statistically significant at p < 0.05. Results: A group of 19 patients treated at Sheba Medical Center meeting the ACR/EULAR classification system for systemic sclerosis were included in the study. The mean age of the participants was 60.4 ± 12 years with a female predominance (84%). Diffuse cutaneous scleroderma accounted for 10 of the participants (54%), 7 had limited cutaneous scleroderma (36%) with 2 having an overlap syndrome (10%). The Cronbach's alpha value for the UCLA SCTC GIT 2.0 scale was 0.908 showing reliability. In addition, the UCLA SCTC GIT 2.0 showed correlation to the SF-36. Conclusion: The translation of the Hebrew UCLA SCTC GIT 2.0 scale was reliable and valid with a total Cronbach's alpha score among the participants of 0.908. Cronbach's alpha was particularly reliable in reflux, bloating, social function, and emotional well-being. Our results suggest that our Hebrew version of the UCLA SCTC GIT 2.0 scale can be used as a tool in future studies with Hebrew-speaking patients. In the abstract conclusion, it states that "Cronbach's alpha was particularly reliable in reflux, bloating, social function, and emotional well-being." The related data should be listed in the results section and then an interpretation of the results should be listed in the conclusions section. Please revise.
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Biofilms are differentiated microbial communities held together by an extracellular matrix. µCT X-ray revealed structured mineralized areas within biofilms of lung pathogens belonging to two distant phyla - the proteobacteria Pseudomonas aeruginosa and the actinobacteria Mycobacterium abscessus. Furthermore, calcium chelation inhibited the assembly of complex bacterial structures for both organisms with little to no effect on cell growth. The molecular mechanisms promoting calcite scaffold formation were surprisingly conserved between the two pathogens as biofilm development was similarly impaired by genetic and biochemical inhibition of calcium uptake and carbonate accumulation. Moreover, chemical inhibition and mutations targeting mineralization significantly reduced the attachment of P. aeruginosa to the lung, as well as the subsequent damage inflicted by biofilms to lung tissues, and restored their sensitivity to antibiotics. This work offers underexplored druggable targets for antibiotics to combat otherwise untreatable biofilm infections.
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The insulin-like growth factor 1 receptor (IGF1R) is a tyrosine kinase, transmembrane receptor expressed in most body tissues and required for normal growth of cells. In cell culture, overexpression of the receptor has been shown to promote transformation and enhance cell survival in response to selected cytotoxic agents. As tumors develop, abnormalities in vascularization lead to a heterogeneous environment that includes areas of hypoxia, low pH and low glucose. Here we report that the overexpression of the IGF1R promotes increased survival in cells exposed to hypoxia, low pH and low glucose. Furthermore, cells lacking the receptor due to targeted disruption of the IGF1R gene do not survive as well as normal cells in such conditions. In addition, we find that cells can activate the IGF1R gene promoter in response to these conditions, and immunoblot analyses show increased receptor protein levels in cell exposed to hypoxia. Our results suggest a pathway of cancer cell adaptation to the tumor microenvironment in which conditions of the environment may induce expression of IGF1R, and this subsequent overexpression of the receptor may increase cell survival in such conditions.