Cellular and organismic copper (Cu) homeostasis is regulated by Cu transporters and Cu chaperones to ensure the controlled uptake, distribution and export of Cu ions. Many of these processes have been extensively investigated in mammalian cell culture, as well as in humans and in mammalian model organisms. Most of the human genes encoding proteins involved in Cu homeostasis have orthologs in the model organism, Caenorhabditis elegans (C. elegans). Starting with a compilation of human Cu proteins and their orthologs, this review presents an overview of Cu homeostasis in C. elegans, comparing it to the human system, thereby establishing the basis for an assessment of the suitability of C. elegans as a model to answer mechanistic questions relating to human Cu homeostasis.

Selenium (Se) is an essential trace element for humans and animals, but high-dose supplementation with Se compounds, most notably selenite, may exert cytotoxic and other adverse effects. On the other hand, bacteria, including Escherichia coli (E. coli), are capable of reducing selenite to red elemental Se that may serve as a safer Se source. Here, we examined how a diet of Se-enriched E. coli bacteria affected vital parameters and age-associated neurodegeneration in the model organism Caenorhabditis elegans (C. elegans). The growth of E. coli OP50 for 48 h in medium supplemented with 1 mM sodium selenite resulted in reddening of the bacterial culture, accompanied by Se accumulation in the bacteria. Compared to nematodes supplied with the standard E. coli OP50 diet, the worms fed on Se-enriched bacteria were smaller and slimmer, even though their food intake was not diminished. Nevertheless, given the choice, the nematodes preferred the standard diet. The fecundity of the worms was not affected by the Se-enriched bacteria, even though the production of progeny was somewhat delayed. The levels of the Se-binding protein SEMO-1, which serves as a Se buffer in C. elegans, were elevated in the group fed on Se-enriched bacteria. The occurrence of knots and ruptures within the axons of cholinergic neurons was lowered in aged nematodes provided with Se-enriched bacteria. In conclusion, C. elegans fed on Se-enriched E. coli showed less age-associated neurodegeneration, as compared to nematodes supplied with the standard diet.

Background/Objectives: Although discrepancies between bioelectrical impedance analysis (BIA) devices are well documented, their clinical relevance in vulnerable populations remains unclear. This study aims to assess the impact of device choice on muscle mass classification criteria in patients with cancer or obesity and to identify modifiers of device variability. Methods: BIA data from 224 adults (85 with cancer, 139 with obesity) measured with two segmental multi-frequency devices (seca mBCA 515 and InBody 970) were analyzed. Device differences were assessed using the Wilcoxon signed-rank test and agreement analyses. Differences in classification of body composition cut-offs cited in the GLIM criteria for malnutrition and the ESPEN and EASO criteria for sarcopenic obesity were evaluated using McNemar’s test. The impact of disease type, sex, and age on device differences was examined through multivariable models. Results: Significant device differences were found for all parameters (all p ≤ 0.005). Discrepancies were largest for skeletal muscle mass (kg and %), with effect sizes r > 0.8 and poor agreement (Lin’s CCC < 0.90). A significant impact of device choice on muscle mass classification was observed for both cancer and obesity patients (p < 0.001), with seca classifying more patients as having low fat-free mass (50% vs. 20%) and as having a body composition consistent with sarcopenic obesity (90% vs. 50%) than InBody. Discrepancies were more pronounced in cancer patients and females. Conclusions: Muscle mass assessment by BIA is highly dependent on device choice, potentially leading to clinically relevant discrepancies in classification when rigid cut-offs are applied. An individualized interpretation of BIA data and further validation of prediction equations in disease-specific subpopulations is warranted.

Aging is accompanied by progressive functional decline and morphological defects of cholinergic neurons. Some probiotic bacteria with proficiency for biofilm formation in the gut are being discussed as potentially neuroprotective. Here, we screened Bacillus subtilis (B. subtilis) strains for biofilm production, using an in vitro assay. Thereafter, a transgenic Caenorhabditis elegans (C. elegans) strain with its cholinergic neurons expressing green fluorescent protein (GFP) was fed for up to 15 days on either the identified biofilm-producing B. subtilis strain B4U 50 or the control B. subtilis strain 168, with or without addition of a standardized Ginkgo biloba preparation. The morphology of the cholinergic neurons was monitored at several consecutive days by fluorescence microscopy. The occurrence of morphological defects such as knots and ruptures within the axons of cholinergic neurons, as observed with increasing age, was significantly lower in nematodes provided with the B4U 50 strain. Even worms whose diet was switched to B4U 50 later in life showed less damage of their neurons, as compared to worms fed on the control strain. Supplementation with the Ginkgo biloba preparation was neuroprotective in worms fed on either B. subtilis strain, while a stronger beneficial effect was observed upon combined administration of B. subtilis B4U 50 and the Ginkgo biloba preparation. In conclusion, feeding a B. subtilis strain proficient for biofilm formation, B4U 50, was neuroprotective when compared to a diet consisting of control B. subtilis, delaying the onset of aging-associated morphological defects in cholinergic neurons of C. elegans. Graphical Abstract