Complement C3c and C4c as predictors of death in heart failure

Abstract

A Slurry Bubble Column Reactor (SBCR) is a gas-liquid-solid reactor in which the finely divided solid catalyst is suspended in the liquid by the rising gas bubbles. SBCR offers many advantages over fixed-bed type reactors such as: 1) improved heat transfer and mass transfer; 2) isothermal temperature profile is maintained; and 3) relatively low capital and operating cost. Fischer-Tropsch Synthesis (FTS) takes place in a SBCR where the synthesis gas is converted on catalysts suspended as fine particles in a liquid. The synthesis gas flows in a bubble phase through the catalyst/wax suspension. The volatile products are removed with unconverted gases, and the liquid products are separated from the suspension. A gas distributor located in the bottom of the reactor produces the bubbles in the reactor.A considerable interest has been expressed in using the SBCR to carry out FTS particularly for the conversion of stranded natural gas into liquids. Currently, the Center for Applied Energy Research (CAER) is utilizing a Prototype Integrated Process Unit (PIPU) system for scale-up research of the FTS. The purpose of this study was to compare the performance and activity decline of a precipitated Fe/K Fischer Tropsch Synthesis (FTS) catalyst in a revamped slurry bubble column reactor (SBCR) to that of previous CSTR and SBCR runs using the same catalyst and operating conditions. The activity decline measured in the revamped SBCR system was shown to be similar to that of the CSTR experiments. The apparent activity decline in a previous SBCR run was due a transient startup effect from the slurry filtration system.

Evaluation of Innate Immunity Biomarkers on Admission and at Discharge From an Acute Heart Failure Episode

“…Although our data lack the potential to be external validated, we are strongly convicted that it is an essential starting point for larger, multicenter studies to be appropriately planned and powered. Furthermore, our results are in agreement with our previous study, where we document the prognostic value of C3 and C4, at discharge, as predictors of death patients suffering from an acute episode of HF . Therefore, it is consistent with the hypothesis that these proteins are involved in the progression of HF.…”

“…Knowing that the activation of innate immunity is not limited to TLRs and that inflammation is known to be a downstream effector of the innate immune system, it is most likely that other innate immunity markers may be activated in HF. In previous studies of our group, we already demonstrated that lower levels of the complement protein C3, at the time of discharge, are a strong and independent predictor of unfavorable outcome in patients following an acute episode of HF . In this context, we aimed to evaluate the variation in this and other innate immunity markers in patients suffering from an episode of acute HF, upon hospitalization and at discharge.…”

Complement activation products in acute heart failure: Potential role in pathophysiology, responses to treatment and impacts on long-term survival

“…In a multivariate analysis, low C3c levels at discharge were independently associated with 6-month mortality. 27 However, while we also observed some association between CAPs and BNP levels in our study, we could not find any association between CAPs and mortality. These differences might be due to the different parameters being measured (C3c and C4c versus C4d and C3a), different methods used for their quantification (nephelometry versus enzyme immunoassays) and differences in time and character of storage of samples prior to analysis.…”

Serum Proteomic Changes in Dogs with Different Stages of Chronic Heart Failure

“…In stage C dogs, C3, a member of the complement system, was up-regulated, whereas other complement proteins (i.e., C4a, C7, and C8) were down-regulated, indicating a pathophysiological involvement of the complement system. The increases in C3 in human patients with CHF is related to chronic immune-inflammatory activation, leading to adverse left ventricular remodeling and aggravation of heart failure [ 31 , 32 ], and poorer outcome [ 31 , 33 ]. The role of complement proteins, as potent therapeutic and prophylactic targets to slow the progression of CHF, should be explored in the future.…”