Polyphenol-Retaining Decaffeinated Cocoa Powder Obtained by Supercritical Carbon Dioxide Extraction and Its Antioxidant Activity

Cocoa beans contain many functional ingredients such as theobromine and polyphenols, but also contain a relatively high amount of caffeine, which can negatively impact human health. It is therefore desirable to reduce caffeine levels in cocoa powder used to make chocolate or cocoa beverages while retaining functional ingredients. We have established conditions for supercritical carbon dioxide (SCCO2) extraction that remove 80.1% of the caffeine from cocoa powder while retaining theobromine (94.1%) and polyphenols (84.7%). The antioxidant activity of the decaffeinated cocoa powder (DCP) made with this optimized SCCO2 extraction method was 85.3% that of non-processed cocoa powder. The total procyanidin and total polyphenol concentrations of the DCPs resulting from various SCCO2 extractions showed a significant positive correlation with oxygen radical absorbance capacity (ORAC). The correlation coefficient between total polyphenols and ORAC was higher than that between total procyanidins and ORAC; thus, the concentration of total polyphenols might be a greater factor in the antioxidant activity of DCP. These results indicate that we could remove large quantities of caffeine from conventional high-cocoa products while retaining the functional benefits of high polyphenol content. This SCCO2 extraction method is expected to be applicable high-cocoa products, such as dark chocolate

Immunodeficiency with susceptibility to lymphoma with complex genotype affecting energy metabolism (FBP1, ACAD9) and vesicle trafficking (RAB27A).

Peer reviewed: TrueINTRODUCTION: Inborn errors of immunity (IEI) are characterized by a dysfunction of the immune system leading to increased susceptibility to infections, impaired immune regulation and cancer. We present a unique consanguineous family with a history of Hodgkin lymphoma, impaired EBV control and a late onset hemophagocytic lymphohistiocytosis (HLH). METHODS AND RESULTS: Overall, family members presented with variable impairment of NK cell and cytotoxic T cell degranulation and cytotoxicity. Exome sequencing identified homozygous variants in RAB27A, FBP1 (Fructose-1,6-bisphosphatase 1) and ACAD9 (Acyl-CoA dehydrogenase family member 9). Variants in RAB27A lead to Griscelli syndrome type 2, hypopigmentation and HLH predisposition. DISCUSSION: Lymphoma is frequently seen in patients with hypomorphic mutations of genes predisposing to HLH. We hypothesize that the variants in FBP1 and ACAD9 might aggravate the clinical and immune phenotype, influence serial killing and lytic granule polarization by CD8 T cells. Understanding of the interplay between the multiple variants identified by whole exome sequencing (WES) is essential for correct interpretation of the immune phenotype and important for critical treatment decisions

Compositional dependence of structures and hydrogen evolution reaction activity of platinum-group-metal quinary RuRhPdIrPt alloy nanoparticles

Platinum-group-metal quinary RuRhPdIrPt alloy nanoparticles were synthesised with compositions slightly away from equimolar, and their crystal and electronic structures were investigated. Their lattice constant changed linearly with composition, while the d-band centre changed nonlinearly. Their catalytic activities for the hydrogen evolution reaction were not correlated with their d-band centre

Immunodeficiency with susceptibility to lymphoma with complex genotype affecting energy metabolism (FBP1, ACAD9) and vesicle trafficking (RAB27A)

Inborn errors of immunity (IEI) are characterized by a dysfunction of the immune system leading to increased susceptibility to infections, impaired immune regulation and cancer. We present a unique consanguineous family with a history of Hodgkin lymphoma, impaired EBV control and a late onset hemophagocytic lymphohistiocytosis (HLH). Overall, family members presented with variable impairment of NK cell and cytotoxic T cell degranulation and cytotoxicity. Exome sequencing identified homozygous variants in RAB27A, FBP1 (Fructose-1,6-bisphosphatase 1) and ACAD9 (Acyl-CoA dehydrogenase family member 9). Variants in RAB27A lead to Griscelli syndrome type 2, hypopigmentation and HLH predisposition. Lymphoma is frequently seen in patients with hypomorphic mutations of genes predisposing to HLH. We hypothesize that the variants in FBP1 and ACAD9 might aggravate the clinical and immune phenotype, influence serial killing and lytic granule polarization by CD8 T cells. Understanding of the interplay between the multiple variants identified by whole exome sequencing (WES) is essential for correct interpretation of the immune phenotype and important for critical treatment decisions

Varp Is a Novel Rab32/38-binding Protein That Regulates Tyrp1 Trafficking in Melanocytes

Two small GTPase Rabs, Rab32 and Rab38, have recently been proposed to regulate trafficking of melanogenic enzymes to melanosomes in mammalian epidermal melanocytes; however, the exact molecular mechanism of Rab32/38-mediated transport of melanogenic enzymes has never been clarified, because no Rab32/38-specific effector has ever been identified. In this study, we screened for a Rab32/38-specific effector by a yeast two-hybrid assay using a guanosine triphosphate (GTP)-locked Rab32/38 as bait and found that VPS9-ankyrin-repeat protein (Varp)/Ankrd27, characterized previously as a guanine nucleotide exchange factor (GEF) for Rab21, functions as a specific Rab32/38-binding protein in mouse melanocyte cell line melan-a. Deletion analysis showed that the first ankyrin-repeat (ANKR1) domain functions as a GTP-dependent Rab32/38-binding domain, but that the N-terminal VPS9 domain (i.e., Rab21-GEF domain) does not. Small interfering RNA-mediated knockdown of endogenous Varp in melan-a cells caused a dramatic reduction in Tyrp1 (tyrosinase-related protein 1) signals from melanosomes but did not cause any reduction in Pmel17 signals. Furthermore, expression of the ANKR1 domain in melan-a cells also caused a dramatic reduction of Tyrp1 signals, whereas the VPS9 domain had no effect. Based on these findings, we propose that Varp functions as the Rab32/38 effector that controls trafficking of Tyrp1 in melanocytes