Ocular Effects of Prenatal Carotenoid Supplementation in the Mother and Her Child: The Lutein and Zeaxanthin in Pregnancy (L-ZIP) Randomized Trial - Report Number 2.

Purpose: Lutein (L) and zeaxanthin (Z) are xanthophyll carotenoids that have been promoted to enhance maternal health and infant visual and neurodevelopment. In this study, we determined the effects of prenatal L and Z supplementation on systemic and ocular carotenoid status in the mother and her newborn infant (NCT03750968). This report focuses on the ocular effects of prenatal carotenoid supplementation.

Systemic Effects of Prenatal Carotenoid Supplementation in the Mother and her Child: The Lutein and Zeaxanthin in Pregnancy (L-ZIP) Randomized Trial -Report Number 1.

Background: Adding carotenoids, particularly lutein (L) and zeaxanthin (Z), to prenatal micronutrient formulations has been promoted to enhance infant visual and neural development and to maintain maternal health. Although these claims are biologically plausible, they are not yet supported by a compelling prospective trial.

Objective: We investigated the effect of prenatal carotenoid supplementation on biomarkers of maternal and infant systemic carotenoid status.

Patient-Derived Mutant Forms of NFE2L2/NRF2 Drive Aggressive Murine Hepatoblastomas.

Background & Aims: Hepatoblastoma (HB), the most common pediatric liver cancer, often bears β-catenin mutations and deregulates the Hippo tumor suppressor pathway. Murine HBs can be generated by co-expressing β-catenin mutants and the constitutively active Hippo effector YAP. Some HBs and other cancers also express mutants of NFE2L2/NRF2 (NFE2L2), a transcription factor that tempers oxidative and electrophilic stress.

Acquired deficiency of peroxisomal dicarboxylic acid catabolism is a metabolic vulnerability in hepatoblastoma.

Metabolic reprogramming provides transformed cells with proliferative and/or survival advantages. Capitalizing on this therapeutically, however, has been only moderately successful because of the relatively small magnitude of these differences and because cancers may further adapt their metabolism to evade metabolic pathway inhibition. Mice lacking the peroxisomal bifunctional enzyme enoyl-CoA hydratase/3-hydroxyacyl CoA dehydrogenase (Ehhadh) and supplemented with the 12-carbon fatty acid lauric acid (C12) accumulate the toxic metabolite dodecanedioic acid (DDDA), which causes acute hepatocyte necrosis and liver failure.

β-Catenin mutations as determinants of hepatoblastoma phenotypes in mice.

Hepatoblastoma (HB) is the most common pediatric liver cancer. Although long-term survival of HB is generally favorable, it depends on clinical stage, tumor histology, and a variety of biochemical and molecular features. HB appears almost exclusively before the age of 3 years, is represented by seven histological subtypes, and is usually associated with highly heterogeneous somatic mutations in the catenin β1 () gene, which encodes β-catenin, a Wnt ligand-responsive transcriptional co-factor.

Inhibition of hepatocellular carcinoma by metabolic normalization.

In two different mouse liver cancer models, we recently showed that a switch from oxidative phosphorylation (Oxphos) to glycolysis (the Warburg effect) is invariably accompanied by a marked decline in fatty acid oxidation (FAO) and a reciprocal increase in the activity of pyruvate dehydrogenase (PDH), which links glycolysis to the TCA cycle. We now show that short-term implementation of either medium-chain (MC) or long-chain (LC) high fat diets (HFDs) nearly doubled the survival of mice with c-Myc oncoprotein-driven hepatocellular carcinoma (HCC). Mechanistically, HFDs forced tumors to become more reliant on fatty acids as an energy source, thus normalizing both FAO and PDH activities.

Metabolic and oncogenic adaptations to pyruvate dehydrogenase inactivation in fibroblasts.

Eukaryotic cell metabolism consists of processes that generate available energy, such as glycolysis, the tricarboxylic acid (TCA) cycle, and oxidative phosphorylation (Oxphos), and those that consume it, including macromolecular synthesis, the maintenance of ionic gradients, and cellular detoxification. By converting pyruvate to acetyl-CoA (AcCoA), the pyruvate dehydrogenase (PDH) complex (PDC) links glycolysis and the TCA cycle. Surprisingly, disrupting the connection between glycolysis and the TCA cycle by inactivation of PDC has only minor effects on cell replication.

Predictions of particle size and lattice diffusion pathway requirements for sodium-ion anodes using η-Cu6Sn5 thin films as a model system.

Geometrically well-defined Cu6Sn5 thin films were used as a model system to estimate the diffusion depth and diffusion pathway requirements of Na ions in alloy anodes. Cu6Sn5 anodes have an initial reversible capacity towards Li of 545 mA h g(-1) (Li3.96Sn or 19.

Ordered mesoporous carbon/α-alumina nanosheet composites.

Novel α-alumina crystalline nanosheets are used for the preparation of alumina-carbon composites, in which the latter component is phenolic resin-based ordered mesoporous carbon. A unique feature of these composites is perpendicular orientation of ordered mesopores of the carbon to the (001) facets of nonporous α-alumina nanosheets accompanied by significant enlargement of these mesopores in comparison to those present in the bulk carbon.

Mesoporous metal organic framework-boehmite and silica composites.

Mesoporous composites of metal organic frameworks (MOFs) with boehmite and silica were prepared by one-pot microwave hydrothermal synthesis in the presence of Pluronic-type triblock-copolymer.

[Fluorescence of age in serum in detecting liver cirrhosis and hepatocellular carcinoma among patients with anti-HCV antibodies].

Objective: To evaluate usefulness of total fluorescence of advanced glycation end products (AGE) and haptoglobin (Hp) measurement in human serum as parameters in liver cirrhosis and hepatocellular carcinoma development among patients with anti-HCV antibodies.

Materials And Methods: 43 patients (20 women and 23 men) with chronic hepatitis HCV were examined (14 individuals with liver cirrhosis and 9 with primary liver cancer). The control group numbers 20.