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Structural factors influencing the biodegradation of imides.

Comparative studies on the biodegradability of amides and imides are presented. Low-molecular-weight imides of varying chain lengths (4, 6, 7, 8, 18, and 20 carbons) were biodegrable. N-alkyl substitution of amides and imides resulted in non-biodegrable derivatives when the amide portion was greater than two carbons in length. N-alkyl-substituted derivatives of acetamide or diacetamide, however, were biodegrable. Several soil isolates, including Aspergillus niger and species of Flavobacterium and Alcaligenes, were capable of growth with imides as sole N or C sources.

Alcaligenes

Dihydropyrimidinase. Metabolism of some cyclic imides of different ring size.

The ability of dihydropyrimidinase (EC 3.5.2.2) to hydrolyze cyclic imides of different ring size was investigated. Succinimide, glutarimide, and adipimide are five-, six-, and seven-membered cyclic imides, respectively. The ring-opened compounds that correspond to these cyclic imides are, respectively, succinamic, glutaramic, and adipamic acid. In incubations of cyclic imides (pH 8, 1 hr) with a rat liver dihydropyrimidinase preparation from which omega-amidase had been removed, adipimide was classed as a good substrate and succinimide and glutarimide were classed as very poor but definite substrates. alpha-Phenylsuccinimide, the N-demethylated metabolite of phensuximide, was a much better substrate than succinimide. alpha-Phenylglutarimide was not a substrate. The in vitro studies of the present investigation were in agreement with observations made in previous in vivo studies.

Amidohydrolases

Effects of dicyclohexylcarbodi-imide on proton translocation coupled to fumarate reduction in anaerobically grown cells of Escherichia coli K-12.

The addition of dicyclohexylcarbodi-imide to anaerobic cells of Escherichia coli K12 decreases both the observed extent of proton translocation coupled to fumarate reduction by endogenous substrates and the t 1/2 of proton re-entry after such translocation, but does not affect fumarate uptake. Dicyclohexylcarbodi-imide also inhibits fumarate reductase activity in cell extracts.

Anaerobiosis

Circular dichroism studies of imide derivatives of amines.

Circular dichroism curves have been measured for phthaloyl-, maleyl- and itaconyl-derivatives of a number of amines having a general formula R--CH(NH2)--R' (in which R and R' are alkyl-, aryl- or cyclohexyl-groups) and of 1,2,3,4-tetrahydro-1-naphthylamine and 1,2,3,4-tetrahydro-2-naphthylamine. We conclude that the determination of absolute configuration of amines examined can be made on the basis of C.D. curves of their phthaloyl-, maleyl- and itaconyl-derivatives, referring to that portion of the curve relating to the imide chromophore absorption.

1-Naphthylamine

Purification of the chloroplast-membrane dicyclohexylcarbodi-imide-binding proteolipid by ion-exchange chromatography.

An efficient, mild and rapid procedure is reported for the separation of the dicyclohexyl-carbodi-imide-binding protein of chloroplast membranes from endogenous lipid components. By the use of ion-exchange chromatography the chloroplast proteolipid can be successfully separated from the major part of chlorophyll and other membrane lipids while being retained in a butan-1-ol milieu.

Carbodiimides

Shared genetic architecture and therapeutic targets across paediatric immune-mediated diseases.

OBJECTIVES: Paediatric-onset immune-mediated inflammatory diseases (IMIDs), including juvenile idiopathic arthritis and related rheumatic diseases, remain genetically undercharacterised. We aimed to define shared and category-specific genetic architecture across paediatric IMIDs, compare signals with adult IMIDs, and identify therapeutic opportunities. METHODS: We analysed 24 paediatric IMIDs classified as autoimmune, polygenic-autoinflammatory, mixed-pattern, or allergic. Genome-wide association analyses included 18,086 cases and 131,019 controls of European ancestry. We estimated single nucleotide polymorphism (SNP)-based heritability, genetic correlations, and polygenic overlap; performed subset-based meta-analysis; and conducted functional annotation, gene prioritisation, pathway and protein network analyses, adult-IMID comparison, and drug-target prioritisation. RESULTS: SNP-based heritability ranged from 28.9% for allergic IMIDs to 61.9% for autoimmune IMIDs. Genetic correlation and polygenic modelling supported partial sharing across categories with category-specific components. Meta-analysis identified 39 genome-wide significant loci outside the Major Histocompatibility Complex (MHC) region, including 15 previously unreported loci; 19 loci were shared between categories. Gene-prioritisation and protein interaction analyses identified a core MHC-centred antigen-presentation network, with category-enriched modules involving complement, innate/barrier pathways, epithelial biology, and type 2 immunity. Enriched pathways included nuclear factor κB signalling, T helper 17 related pathways, Janus kinase-signal transducer and activator of transcription signalling, programmed cell death protein 1/programmed death‑ligand 1, cytotoxic T‑lymphocyte associated protein 4 regulation, and osteoclast differentiation, several of which are relevant to rheumatic diseases. Paediatric IMIDs shared broad polygenic architecture with adult IMIDs, whereas top-ranked genes converged strongly with adult rheumatic diseases. Priority Index analysis identified 178 high-scoring genes, including 43 approved or investigational IMID drug targets. CONCLUSIONS: Paediatric-onset IMIDs share core pathways with adult forms but exhibit distinct genetic architecture shaped by age-specific immune and neurodevelopmental biology. These findings provide a genomic framework for paediatric precision medicine, guiding classification, risk prediction, and therapeutic development.

Humans