RESUMEN
Background: Number of markers of inflammation has been associated with coronary artery disease and various studies have shown increased levels during chronic stable angina, acute myocardial infarction, and percutaneous coronary intervention. However, co-relation to final outcomes of percutaneous coronary intervention with these markers has not been studied. Aim of this study was to try and find a correlation between markers of inflammation released during percutaneous coronary intervention and incidence of restenosis on follow up at 06 moths on patients undergoing percutaneous coronary intervention with Bare Metal Stent (BMS).Methods: 36 consecutive only Bare Metal Stent (BMS) angioplasties done at our centre between July 2015 and June 2016 were analysed for markers of inflammation from peripheral venous sample before the procedure and coronary sinus sample after the procedure. Pts were kept on follow up for 6 months and assessed as per their clinical symptoms and Coronary Angiogram was done where indicated and results tabulated.Results: There was increase in the studied markers of inflammation post percutaneous coronary intervention but they did not correlate with or predict possible restenosis.Conclusions: This study showed that markers of inflammation are elevated during percutaneous coronary intervention but none of these markers correlates with subsequent restenosis.
RESUMEN
The interferon (IFN)-inducible, 2′,5′-oligoadenylate (2-5A)-dependent ribonuclease L (RNase L) plays key role in antiviral defense of mammalian cells. Induction by IFN and activation by double-stranded RNA lead to 2-5A cofactor synthesis, which activates RNase L by causing its dimerization. Active RNase L degrades single-stranded viral as well as cellular RNAs causing apoptosis of virus-infected cells. Earlier, we had reported that expression of recombinant human RNase L caused RNA-degradation and cell-growth inhibition in E. coli without the need for exogenous 2-5A. Expression of human RNase L in E. coli usually leads to problems of leaky expression, low yield and degradation of the recombinant protein, which demands number of chromatographic steps for its subsequent purification thereby, compromising its biochemical activity. Here, we report a convenient protocol for expression of full-length, soluble and biochemically active recombinant human RNase L as GST-RNase L fusion protein from E. coli utilizing a single-step affinity purification with an appreciable yield of the highly purified protein. Recombinant RNase L was characterized by SDS-PAGE, immunoblotting and MALDI-TOF analysis. A semi-quantitative agarose-gel-based ribonuclease assay was developed for measuring its 2-5A-dependent RNase L activity against cellular large rRNAs as substrates. The optimized expression conditions minimized degradation of the protein, making it a convenient method for purification of RNase L, which can be utilized to study effects of various agents on the RNase L activity and its protein– protein interactions.
RESUMEN
Fibrinogen is an independent risk factor for coronary events in population-based studies and inpatients with coronary heart disease, but there is an uncertainty about its prediction for stroke, particularly in secondary prevention. In view of this uncertainty, study was conducted to establish the role of serum fibrinogen in ischemic stroke. Fifty six patients with acute ischemic stroke of less than 7 days duration were recruited for the study. Fourty two age and sex matched candidates served as control. Baseline characteristics and blood pressure were recorded at admission to hospital. Computer tomography head was done in all patients as per protocol. Sampling took place in the early morning (7-9 AM) using all necessary precaution and serum fibrinogen was measured by method of Clauss. Statiscal analysis was performed using student t test and fisher exact test. In present study, mean plasma fibrinogen in patients group was 326.45 mg/dl, which was significantly higher than control group (202.23 mg/dl) (p<0.001). Mean plasma fibrinogen level in lacunar infarct and non-lacunar infarct did not differ significantly (307.47 mg/dl Vs. 333.19 mg/dl). Smoking was found to be a significant predictor of fibrinogen with 36.7% predictability whereas other parameters (risk factors for ischemic stroke) had little or no predictable value regarding serum fibrinogen. After adjustment for other possible ischemic stroke risk factors; plasma fibrinogen levels was found to be still significantly high in patients as compared to controls (p<0.001). Mean plasma fibrinogen level between patients who survived and who expired does not differ significantly. Present study concluded that fibrinogen is a powerful predictor of ischemic stroke though it does not predict the type and prognosis of stroke.