Prostate apoptosis response factor‐4 (Par‐4) is an ubiquitously expressed pro‐apoptotic and tumour suppressive protein that can both activate cell‐death mechanisms and inhibit pro‐survival factors. Par‐4 contains a highly conserved coiled‐coil region that serves as the primary recognition domain for a large number of binding partners. Par‐4 is also tightly regulated by the aforementioned binding partners and by post‐translational modifications. Biophysical data obtained in the present study indicate that Par‐4 primarily comprises an intrinsically disordered protein. Bioinformatic analysis of the highly conserved Par‐4 reveals low sequence complexity and enrichment in polar and charged amino acids. The high proteolytic susceptibility and an increased hydrodynamic radius are consistent with a largely extended structure in solution. Spectroscopic measurements using CD and NMR also reveal characteristic features of intrinsic disorder. Under physiological conditions, the data obtained show that Par‐4 self‐associates via the C‐terminal domain, forming a coiled‐coil. Interruption of self‐association by urea also resulted in loss of secondary structure. These results are consistent with the stabilization of the coiled‐coil motif through an intramolecular association.
Introduction: Pleural effusion is the abnormal accumulation of fluid in the pleural space. TB is the most common cause of pleural effusion worldwide (30-60%). The pleural fluid activity of adenosine deaminase (ADA) is one of the best, providing reliable basis for a treatment decision, particularly in excluding the diagnosis of tuberculosis, due to its high sensitivity1. Aims and Objectives: To assess the importance of adenosine deaminase(ADA) level in the diagnosis of pleural effusion. To assess Adenosine Deaminase Activity (ADA) in tuberculosis pleural effusion and assess the sensitivity and specificity of ADA levels. Materials and Methods: This study was performed at the Department of Pulmonary Medicine at tertiary care centre. The study comprised of 75 patients of pleural effusion having Age > 14 years, Clinical and Radiological evidence of Pleural Effusions & Patients willing for ADA examination. Patients having Age > 65 years, minimal nontappable effusion, not giving consent for ADA examination patient were excluded from the study. Detailed history, thorough physical examination, radiological findings, haematological and biochemical findings were recorded in the proforma. Pleural aspiration was performed on all patients. Macroscopic findings, cytological, microbiological and biochemical analysis of pleural fluid were performed in all patients including ADA level. PCR for Mycobacterium tuberculosis was also assessed in pleural fluid. Pleural fluid Adenosine deaminase level was measured by Giusti and Galanti method. Result: In our study out of 45 patients with tuberculosis pleural effusion ADA was more than 40IU/L in 42 (93.33%) and less than40IU/L in 3 (6.66 %) . Our study showed a mean ADA of 107.7 IU/L Using a cut off of greater 40IU/L we got a sensitivity and specificity of 93.3% and 90% respectively and Positive predictive value 93.3% and Negative predictive value 90%. Conclusion: Pleural fluid ADA activity has been shown to be a valuable biochemical marker that has a high sensitivity and specificity for TB diagnosis.
Introduction: Pleural effusion is the abnormal accumulation of fluid in the pleural space. TB is the most common cause of pleural effusion worldwide (30-60%). The pleural fluid activity of adenosine deaminase (ADA) is one of the best, providing reliable basis for a treatment decision, particularly in excluding the diagnosis of tuberculosis, due to its high sensitivity1. Aims and Objectives: To assess the importance of adenosine deaminase(ADA) level in the diagnosis of pleural effusion. To assess Adenosine Deaminase Activity (ADA) in tuberculosis pleural effusion and assess the sensitivity and specificity of ADA levels. Materials and Methods: This study was performed at the Department of Pulmonary Medicine at tertiary care centre. The study comprised of 75 patients of pleural effusion having Age > 14 years, Clinical and Radiological evidence of Pleural Effusions & Patients willing for ADA examination. Patients having Age > 65 years, minimal nontappable effusion, not giving consent for ADA examination patient were excluded from the study. Detailed history, thorough physical examination, radiological findings, haematological and biochemical findings were recorded in the proforma. Pleural aspiration was performed on all patients. Macroscopic findings, cytological, microbiological and biochemical analysis of pleural fluid were performed in all patients including ADA level. PCR for Mycobacterium tuberculosis was also assessed in pleural fluid. Pleural fluid Adenosine deaminase level was measured by Giusti and Galanti method. Result: In our study out of 45 patients with tuberculosis pleural effusion ADA was more than 40IU/L in 42 (93.33%) and less than40IU/L in 3 (6.66 %). Our study showed a mean ADA of 107.7 IU/L Using a cut off of greater 40IU/L we got a sensitivity and specificity of 93.3% and 90% respectively and Positive predictive value 93.3% and Negative predictive value 90%. Conclusion: Pleural fluid ADA activity has been shown to be a valuable biochemical marker that has a high sensitivity and specificity for TB diagnosis.
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