Given the importance of monocytes in pathogenesis of infectious and other inflammatory disorders, delineating functional and phenotypic characterization of monocyte subsets has emerged as a critical requirement. Although human monocytes have been subdivided into three different populations based on surface expression of CD14 and CD16, published reports suffer from contradictions with respect to subset phenotypes and function. This has been attributed to discrepancies in reliable gating strategies for flow cytometric characterization and purification protocols contributing to significant changes in receptor expression. By using a combination of multicolour flow cytometry and a high-dimensional automated clustering algorithm to confirm robustness of gating strategy and analysis of ex-vivo activation of whole blood with LPS we demonstrate the following: a. ‘Classical’ monocytes are phagocytic with no inflammatory attributes, b. ‘Non-classical’ subtype display ‘inflammatory’ characteristics on activation and display properties for antigen presentation and c. ‘Intermediate’ subtype that constitutes a very small percentage in circulation (under physiological conditions) appear to be transitional monocytes that display both phagocytic and inflammatory function. Analysis of blood from patients with Sepsis, a pathogen driven acute inflammatory disease and Systemic Lupus Erythmatosus (SLE), a chronic inflammatory disorder validated the broad conclusions drawn in the study.

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Septic shock is a major medical problem with high morbidity and mortality and incompletely understood biology. Integration of multiple data sets into a single analysis framework empowers discovery of new knowledge about the condition that may have been missed by individual analysis of each of these datasets. Electronic search was performed on medical literature and gene expression databases for selection of transcriptomic studies done in circulating leukocytes from human subjects suffering from septic shock. Gene-level meta-analysis was conducted on the six selected studies to identify the genes consistently differentially expressed in septic shock. This was followed by pathway-level analysis using three different algorithms (ORA, GSEA, SPIA). The identified up-regulated pathway, Osteoclast differentiation pathway (hsa04380) was validated in two independent cohorts. Of the pathway, 25 key genes were selected that serve as an expression signature of Septic Shock.

There are very few and conflicting Indian data regarding the bacteriological etiology of community acquired pneumonia (CAP). Adding to this agony, there is no credible data from the eastern part of India. This is a cross-sectional study and descriptive in nature over a period of 1-year. Of the 464 cases of the study population, we could isolate aerobic bacteria in 149 patients (32.1%). Streptococcus pneumoniae has been identified as the most common organism causing CAP (68/149). Gram-negative bacilli (GNB) as a group exceeded marginally over S. pneumoniae (69/149). Among GNB, Pseudomonas aeruginosa was the most common organism (31/69), followed by Klebsiella pneumoniae (29/69). Staphylococcus aureus was identified in (12/149) cases. Co-amoxyclav is still the most sensitive drug for S. pneumoniae. P. aeruginosa was most sensitive to imipenam followed by piperacillin-tazobactam.

BACKGROUND Portal hypertension is one of the serious complications of cirrhosis of liver leading to unwanted life-threatening variceal bleeding. Loss of liver architecture and fibrosis lead to increased resistance to blood flow through portal vein causing portal hypertension and ultimately leading to ascites, oesophageal varices and splenomegaly. The aim of the study is to find out correlation of portal vein diameter and splenic size with oesophageal varices in cirrhosis of liver. MATERIALS AND METHODS A descriptive study was conducted in Department of Medicine of SCB Medical College, Cuttack and consecutively 50 adult patients of cirrhosis of liver were included in the study. Ultrasonography was done in all patients to measure splenic size and portal vein diameter. Upper GI endoscopy was done in all to record oesophageal varices. RESULTS Out of 50 patients, 34 (68%) had oesophageal varices of various grades and 16 (32%) had no varices. Average portal vein diameter of patients with oesophageal varices was 13.46 ± 0.98 mm and that of patients without varices was 10.91 ± 0.65 mm (p=0.03). Average splenic size in patients with oesophageal varices was 14.7± 0.82 cm and that of patients without varices was 12.2 ± 1.01 cm (p=0.007). Portal vein diameter and splenic size were increased in patients with oesophageal varices than patients without varices.