A Novel Machine Learning Model and a Web Portal for Predicting the Human Skin Sensitization Effects of Chemical Agents.

Skin sensitization is a significant concern for chemical safety assessments. Traditional animal assays often fail to predict human responses accurately, and ethical constraints limit the collection of human data, necessitating a need for reliable in silico models of skin sensitization prediction. This study introduces HuSSPred, an in silico tool based on the Human Predictive Patch Test (HPPT).

DEP-1 is a brain insulin receptor phosphatase that prevents the simultaneous activation of counteracting metabolic pathways.

A healthy metabolism relies on precise regulation of anabolic and catabolic pathways. While insulin deficiency impairs anabolism, insulin resistance in obesity causes metabolic dysfunction, especially via altered brain insulin receptor (IR) activity. Density-enhanced phosphatase 1 (DEP-1) negatively modulates the IR in peripheral tissues.

Biocatalytic sulfation of aromatic and aliphatic alcohols catalyzed by arylsulfate sulfotransferases.

Many relevant metabolites, as well as chemical commodities, contain at least one sulfate ester group. Consequently, biocatalytic strategies to attach sulfate to a molecule under mild conditions are of high interest. In order to expand the enzymatic toolbox available, five new arylsulfate sulfotransferases (ASSTs) were identified in this study.

Novel postzygotic mutation in a patient with Parkes Weber syndrome: A case report and literature review.

Key Clinical Message: Not only germline but also postzygotic mutations in the or genes can lead to capillary malformation-arteriovenous malformation (CM-AVM) syndrome. As it is not always possible to clinically distinguish between constitutional variants and postzygotic mosaicism, a sufficiently high sequencing depth must be used in genetic diagnostics to detect both.

Abstract: Capillary malformation-arteriovenous malformation (CM-AVM) syndrome, with or without Parkes Weber syndrome, is a rare autosomal dominant disease caused by pathogenic or variants.