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This comprehensive review offers a chemical analysis of cutting fluids, delving into both their formulation and deformulation processes. The study covers a wide spectrum of cutting fluid formulations, ranging from simple compositions predominantly comprising oils, whether mineral or vegetable, to emulsions. The latter involves the integration of surfactants, encompassing both nonionic and anionic types, along with a diverse array of additives. Concerning oils, the current trend leans towards the use of vegetable oils instead of mineral oils for environmental reasons. As vegetable oils are more prone to oxidation, chemical alterations, the addition of antioxidant may be necessary. The chemical aspects of the different compounds are scrutinized, in order to understand the role of each component and its impact on the fluid's lubricating, cooling, anti-wear, and anti-corrosion properties. Furthermore, the review explores the deformulation methodologies employed to dissect cutting fluids. This process involves a two-step approach: separating the aqueous and organic phases of the emulsions by physical or chemical treatments, and subsequently conducting a detailed analysis of each to identify the compounds. Several analytical techniques, including spectrometric or chromatographic, can be employed simultaneously to reveal the chemical structures of samples. This review aims to contribute to the improvement of waste treatment stemming from cutting fluids. By gathering extensive information about the formulation, deformulation, and chemistry of the ingredients, there is a potential to enhance the waste management and disposal effectively.

The direct incorporation of low viscosity organic liquids (OL) such as dodecane and tributylphosphate (TBP) into fresh geopolymers (GP) is difficult and generally leads to variable amounts of un-incorporated OL remaining outside the hardened geopolymer. Experimentally, it is observed that a regular torque increase during OL incorporation corresponds to a suitable dispersion of the OL in the form of fine micrometric droplets. This can be obtained for TBP and dodecane by adding a small quantity of quaternary ammoniums salts (QAs) such as cetyltrimethylammonium bromide (CTAB). Shorter alkyl chains QAs, such as hexamethyltrimethylammonium (HMTA) can also be used but with a reduced efficiency. The positive impact of CTAB is then confirmed by the Washburn capillary rise method, showing that the interactions between TBP and CTAB-modified metakaolin are weaker compared to untreated powder. Finally, it is observed that the incorporation of TBP into geopolymer slurries is much easier than the incorporation of dodecane. The low interfacial tension measured between TBP and the activating solution (around 8 mN·m -1 ), contrasting with dodecane (29 mN·m -1 ), explains that the dispersion of TBP droplets in fresh metakaolin suspensions is more efficient.

Purpose: Germline loss-of-function variants in CTNNB1 cause neurodevelopmental disorder with spastic diplegia and visual defects (NEDSDV; OMIM 615075) and are the most frequent, recurrent monogenic cause of cerebral palsy (CP). We investigated the range of clinical phenotypes owing to disruptions of CTNNB1 to determine the association between NEDSDV and CP., Methods: Genetic information from 404 individuals with collectively 392 pathogenic CTNNB1 variants were ascertained for the study. From these, detailed phenotypes for 52 previously unpublished individuals were collected and combined with 68 previously published individuals with comparable clinical information. The functional effects of selected CTNNB1 missense variants were assessed using TOPFlash assay., Results: The phenotypes associated with pathogenic CTNNB1 variants were similar. A diagnosis of CP was not significantly associated with any set of traits that defined a specific phenotypic subgroup, indicating that CP is not additional to NEDSDV. Two CTNNB1 missense variants were dominant negative regulators of WNT signaling, highlighting the utility of the TOPFlash assay to functionally assess variants., Conclusion: NEDSDV is a clinically homogeneous disorder irrespective of initial clinical diagnoses, including CP, or entry points for genetic testing., Competing Interests: Conflict of Interest F.M. and M.M.M. are employees of GeneDX, Inc. All other authors declare no conflict of interest., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Purpose: CTR9 is a subunit of the PAF1 complex (PAF1C) that plays a crucial role in transcription regulation by binding CTR9 to RNA polymerase II. It is involved in transcription-coupled histone modification through promoting H3K4 and H3K36 methylation. We describe the clinical and molecular studies in 13 probands, harboring likely pathogenic CTR9 missense variants, collected through GeneMatcher., Methods: Exome sequencing was performed in all individuals. CTR9 variants were assessed through 3-dimensional modeling of the activated human transcription complex Pol II-DSIF-PAF-SPT6 and the PAF1/CTR9 complex. H3K4/H3K36 methylation analysis, mitophagy assessment based on tetramethylrhodamine ethyl ester perchlorate immunofluorescence, and RNA-sequencing in skin fibroblasts from 4 patients was performed., Results: Common clinical findings were variable degrees of intellectual disability, hypotonia, joint hyperlaxity, speech delay, coordination problems, tremor, and autism spectrum disorder. Mild dysmorphism and cardiac anomalies were less frequent. For 11 CTR9 variants, de novo occurrence was shown. Three-dimensional modeling predicted a likely disruptive effect of the variants on local CTR9 structure and protein interaction. Additional studies in fibroblasts did not unveil the downstream functional consequences of the identified variants., Conclusion: We describe a neurodevelopmental disorder caused by (mainly) de novo variants in CTR9, likely affecting PAF1C function., Competing Interests: Conflict of Interest Amber Begtrup is an employee of GeneDx, Inc. Stylianos E. Antonarakis and Emmanuelle Ranza are cofounders of MediGenome. All other authors declare no conflicts of interest., (Copyright © 2022 American College of Medical Genetics and Genomics. Published by Elsevier Inc. All rights reserved.)