Background: Platelets and their activity have a crucial role in acute coronary events. Larger platelets are enzymatically and metabolically more active and have a higher potential thrombotic ability as compared with smaller platelets.

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Introduction: Correct cell enumeration and differential analysis of body fluids are important in the diagnosis and management of several diseases. Currently, microscopic analysis is still considered the "gold standard". The introduction of automated analysis has reduced interoperator variability, improved turnaround time and precision. The present study was designed to determine the shelf life and appropriate anticoagulant for automated cell counter and to compare manual and automated cell count in ascitic fluid. Methods: We examined total 250 ascitic fluid samples. Total and differential cell counting of each sample has been conducted with the Sysmex XT-4000i and the manual method (Neubauer chamber). Linearity, carryover, precision and correlation were also assessed. Results:The precision analysis of random sample with high cell count indicated that the Sysmex XT-4000i demonstrated good precision for RBC, WBC, MN#, PMN# at 0 and 6 hour in all vials resulted in CVs <0.012%. Carryover effect was negligible for both WBC and RBC count in ascitic fluid. It never exceeded 0.180%. Sysmex XT-4000i showed significant positive correlation for WBC count in plain vial (r=0.984, p<0.001s), EDTA vial (r= 0.998, p<0.001s), PT vial (r=0.958,

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Aplastic anaemia (AA) is a rare hypocellular bone marrow disease which can be acquired or constitutional. Nearly 10-30% patients with apparently acquired AA have mutations in telomerase reverse transcriptase gene (TERT) leading to bone marrow failure. The TERT plays a crucial role in regulating the telomerase ribonucleoprotein complex which otherwise causes short telomeres leading to AA. We used our benchmarked whole exome sequencing (WES) pipeline and systems bioinformatics approaches to identify sequence variants underlying AA in adult Indian subjects with apparently acquired AA. For 36 affected individuals, we sequenced coding regions to a mean coverage of 100× and a sufficient depth was achieved. The downstream validation and filtering was done to call the variants wherein we identified a host of candidate genes associated with AA who were treated with Cyclosporine A (CsA). Across all samples, six genes were shown to be associated with the AA phenotype with one non-coding SNP underlying intronic region as an exceptional case from interferon gamma (IFNG). While these variants (across the genes, viz. TERT (G/X), IFNG ( T/C), PIGA (T/X) or (T/A), NBS1/NBN(T/X), MPL (G/C) and CYP3A5) spanned across the subjects, a majority of control samples do not have these variants. We demonstrate the application of WES to discover the variants associated with CsA responders and non-responders in the Indian cohort.