Erm outcome after surgical intervention and interventional procedures for the management of takayasu's arteritis in children. J Thorac Cardiovasc Surg 2006, 132(3):656?64.doi:10.1186/1546-0096-12-21 Cite this article as: Szugye et al.: Takayasu Arteritis in the pediatric population: a contemporary United States-Based Single Center Cohort. Pediatric Rheumatology 2014 12:21.Submit your next manuscript to BioMed Central and take full advantage of:?Convenient online submission ?Thorough peer review ?No space constraints or color figure charges ?Immediate publication on acceptance ?Inclusion in PubMed, CAS, Scopus and Google Scholar ?Research which is freely available for redistributionSubmit your manuscript at www.biomedcentral.com/submit

Mukherjee et al. Clinical Proteomics 2-Bromo-1,3-difluoro-4-nitrobenzene 2014, 11:35 http://www.clinicalproteomicsjournal.com/content/11/1/CLINICAL PROTEOMICSRESEARCHOpen AccessProteomic analysis of human plasma in chronic rheumatic mitral stenosis reveals proteins involved in the complement and coagulation cascadeSomaditya Mukherjee1, Mashanipalya G Jagadeeshaprasad2, Tanima Banerjee1, Sudip PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/11834444 K Ghosh3, Monodeep Biswas4, Santanu Dutta5, Mahesh J Kulkarni2, Sanjib Pattari6 and Arun Bandyopadhyay1*AbstractBackground: Rheumatic fever in childhood is the most common cause of Mitral Stenosis in developing countries. The disease is characterized by damaged and deformed mitral valves predisposing them to scarring and narrowing (stenosis) that results in left atrial hypertrophy followed by heart failure. Presently, echocardiography is the main imaging technique used to diagnose Mitral Stenosis. Despite the high prevalence and increased morbidity, no biochemical indicators are available for prediction, diagnosis and management of the tert-Butyl (2-bromothiazol-5-yl)carbamate disease. Adopting a proteomic approach to study Rheumatic Mitral Stenosis may therefore throw some light in this direction. In our study, we undertook plasma proteomics of human subjects suffering from Rheumatic Mitral Stenosis (n = 6) and Control subjects (n = 6). Six plasma samples, three each from the control and patient groups were pooled and subjected to low abundance protein enrichment. Pooled plasma samples (crude and equalized) were then subjected to in-solution trypsin digestion separately. Digests were analyzed using nano LC-MSE. Data was acquired with the Protein Lynx Global Server v2.5.2 software and searches made against reviewed Homo sapiens database (UniProtKB) for protein identification. Label-free protein quantification was performed in crude plasma only. Results: A total of 130 proteins spanning 9?92 kDa were identified. Of these 83 proteins were common to both groups and 34 were differentially regulated. Functional annotation of overlapping and differential proteins revealed that more than 50 proteins are involved in inflammation and immune response. This was corroborated by findings from pathway analysis and histopathological studies on excised tissue sections of stenotic mitral valves. Verification of selected protein candidates by immunotechniques in crude plasma corroborated our findings from label-free protein quantification. Conclusions: We propose that this protein profile of blood plasma, or any of the individual proteins, could serve as a focal point for future mechanistic PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/8833965 studies on Mitral Stenosis. In addition, some of the proteins associated with this disorder may be candidate biomarkers for disease diagnosis and prognosis. Our findings might help to enrich existing knowledge on the molecula.