Anti-OLR1 polyclonal antibody [Biotin]

China produces over 200 tonnes of rice straw (RS) a year. This is an underutilized energy source that is often burned in the fields causing pollution and health problems for populations near and far. Anaerobic digestion (AD) can produce methane (CH4) rich biogas (45-55%) from waste RS as an alternative to burning whilst being affordable. Five 2L reactors were used to test the effect of feeding frequency (FF) and organic loading rates (OLR) on the anaerobic digestion of rice straw with input rates of between 5 feeds per week and one feed every 3 weeks. Two OLRs were used: 1gVS/L/d (OLR1) for 56 days and 2gVS/L/d (OLR2) for 83 days. At the lower OLR1, the best average biogas yield was 300ml/L of reactor/d at 50% CH4 and at OLR2 the best reactor achieved a mean biogas yield of 447ml/L/d at 52% CH4. The best performing FF at OLR1 was 1/21 day whilst at OLR2 the 5/7 day FF produced the highest volume and quality of biogas. Results confirm that biogas from rice straw anaerobic digestion could be used with combined heat and power (CHP) technology to potentially produce 0.5-0.8MWh of electricity per day per tonne of rice straw. (C) 2017 The Authors. Published by Elsevier Ltd.

Atherogenesis is the narrowing of arteries due to plaque build-up that results in cardiovascular disease that can lead to death. The macrophage lectin-like oxidized LDL receptor-1 (LOX-1), also called the oxidized low-density lipoprotein receptor 1 (OLR1), is currently thought to aid in atherosclerotic disease progression; therefore metabolic studies have potential to both provide mechanistic validation for the role of LOX-1 in disease progression and provide valuable information regarding biomarker strategies and clinical imaging. One such mechanistic study is the upregulation of LOX-1 by methylated bacterial DNA and deoxycytidylate-phosphate-deoxy-guanylate-DNA (CpG)-DNA exposure. CpG-DNA is known to promote oxidative burst responses in macrophages, due to its direct binding to toll-like receptor 9 (TLR9) leading to the initiation of an NF-kappa B mediated immune response. In addition to the upregulation of macrophage LOX-1 expression, these studies have also examined the macrophage metabolic response to murine LOX-1/OLR1 antibody exposure. Our data suggests the antibody exposure effectively blocks LOX1 dependent oxLDL metabolic activation of the macrophage, which was quantified using the multianalyte microphysiometer (MAMP). Using the MAMP to examine metabolic fluctuations during various types of oxLDL exposure, LOX-1 upregulation and inhibition provide valuable information regarding the role of LOX-1 in macrophage activation of oxidative burst.