ABSTRACT
Thickener, also known as a gelling agent, is a critical component of lubricating greases. The most critical property of thickener, temperature resistance, is determined by the molecular structure of the compounds. Currently, all high-temperature-resistant thickeners are based on 12-hydroxystearic acid, which is exclusively produced from castor oil. Since castor oil is also an important reagent for other processes, finding a sustainable alternative to 12-hydroxystearic acid has significant economic implications. This study synthesises an alternative thickener from abundant agricultural waste, cashew nut shell liquor (CNSL). The synthesis and separation procedure contains three steps: (i) forming and separating calcium anacardate by precipitation, (ii) forming and separating anacardic acid (iii) forming lithium anacardate. The obtained lithium anacardate can be used as a thickener for lubricating grease. It was found that the recovery of anacardic acid was around 80%. The optimal reaction temperature and time conditions for lithium anacardate were 100 °C and 1 h, respectively. The method provides an economical alternative to castor and other vegetable oils. The procedure presents a simple pathway to produce the precursor for the lubricating grease from agricultural waste. The first reaction step can be combined with the existing distillation of cashew nut shell processing. An effective application can promote CNSL to a sustainable feedstock for green chemistry. The process can also be combined with recycled lithium from the spent batteries to improve the sustainability of the battery industry.
ABSTRACT
OBJECTIVE: Activating mutations in the GUCY2C gene, which encodes the epithelial receptor guanylate cyclase C, cause diarrhea due to increased loss of sodium chloride to the intestinal lumen. Patients with familial GUCY2C diarrhea syndrome (FGDS) are predisposed to inflammatory bowel disease (IBD). We investigated whether genes in the guanylate cyclase C pathway are enriched for association with IBD and reversely whether genetic or transcriptional changes associated with IBD are found in FGDS patients. METHODS: (1) A set of 27 genes from the guanylate cyclase C pathway was tested for enrichment of association with IBD by Gene Set Enrichment Analysis, using genome-wide association summary statistics from 12,882 IBD patients and 21,770 controls. (2) We genotyped 163 known IBD risk loci and sequenced NOD2 in 22 patients with FGDS. Eight of them had concomitant Crohn's disease. (3) Global gene expression analysis was performed in ileal tissue from patients with FGDS, Crohn's disease and healthy individuals. RESULTS: The guanylate cyclase C gene set showed a significant enrichment of association in IBD genome-wide association data. Risk variants in NOD2 were found in 7/8 FGDS patients with concomitant Crohn's disease and in 2/14 FDGS patients without Crohn's disease. In ileal tissue, downregulation of metallothioneins characterized FGDS patients compared to healthy controls. CONCLUSIONS: Our results support a role of guanylate cyclase C signaling and disturbed electrolyte homeostasis in development of IBD. Furthermore, downregulation of metallothioneins in the ileal mucosa of FGDS patients may contribute to IBD development, possibly alongside effects from NOD2 risk variants.