Anti-CNO (aa 114-143) polyclonal antibody

Thiocyanate (SCN -) can be naturally produced by some plant species during assimilation of endogenous cyanide at very low levels, but higher concentration is detected in the environment from various industrial activities, which poses a potential threat to living organisms. In this study, uptake, transport, subcellular distribution and assimilation of SCN - were investigated using rice seedlings exposed to C-13 and N-15-labbled potassium thiocyanate. Our results showed that rice seedlings had a higher potential for SCN (-) uptake, and more was recovered in roots than shoots. Analysis of subcellular partition revealed that SCN- were mainly deposited in cell wall, and followed by cytosol and organelle fractions. Analysis of stable isotopes in rice tissues showed that the molar ratios of C-13 to N-15 content were inconsistent in roots (0.66) and shoots (0.98). PCR analysis revealed different expression arrangements to 20 selected genes in rice tissues, suggesting that involvements of genes encoding with different enzymes in SCN (-) assimilation are tissue specific. These unique genes should regulate and determine degradation pathway of SCN-. Data from stable isotopes and PCR analysis suggests that "TMT (thiol methylation) pathway", "COS (carbonyl sulfide) pathway" and "CNO (cyanate) pathway" are involved in detoxification of SCN- in rice tissues concurrently at the first-degradation phase; Rice seedlings are also able to degrade both CNO and COS in roots effectively, while innate pools of enzymes cyanase (CYN) and carbonyl sulfide hydrolase (COSase) are non-sufficient for further degrade both intermediates in shoots. Our results presented here provide convincing evidence to clarify transport and detoxification pathways of SCN - in rice seedlings.

The pathophysiology of chronic nonbacterial osteomyelitis (CNO) remains incompletely understood. Increased NLRP3 inflammasome activation and IL-1 beta release in monocytes from CNO patients was suggested to contribute to bone inflammation. Here, we dissect immune cell infiltrates and demonstrate the involvement of monocytes across disease stages. Differences in cell density and immune cell composition may help to discriminate between BOM and CNO. However, differences are subtle and infiltrates vary in CNO. In contrast to other cells involved, monocytes are a stable element during all stages of CNO, which makes them a promising candidate in the search for "drivers" of inflammation. Furthermore, we link increased expression of inflammasome components NLRP3 and ASC in monocytes with site-specific DNA hypomethylation around the corresponding genes NLRP3 and PYCARD. Our observations deliver further evidence for the involvement of pro-inflammatory monocytes in the pathophysiology of CNO. Cellular and molecular alterations may serve as disease biomarkers and/or therapeutic targets.