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The nematode Caenorhabditis elegans is a useful model to study aging due to its short lifespan, ease of manipulation, and available genetic tools. Several molecules and extracts derived from plants and fungi extend the lifespan of C. elegans by modulating aging-related pathways that are conserved in more complex organisms. Modulation of aging pathways leads to activation of autophagy, mitochondrial biogenesis and expression of antioxidant and detoxifying enzymes in a manner similar to caloric restriction. Low and moderate concentrations of plant and fungal molecules usually extend lifespan, while high concentrations are detrimental, consistent with a lifespan-modulating mechanism involving hormesis. We review here molecules and extracts derived from plants and fungi that extend the lifespan of C. elegans, and explore the possibility that these natural substances may produce health benefits in humans.

Microbes constitute the most prevalent life form on Earth, yet their remarkable diversity remains mostly unrecognized. Microbial diversity in vertebrate models presents a significant challenge for investigating host–microbiome interactions. The model organism Caenorhabditis elegans has many advantages for delineating the effects of host genetics on microbial composition. In the wild, the C. elegans gut contains various microbial species, while in the laboratory it is usually a host for a single bacterial species. There is a potential host–microbe interaction between microbial metabolites, drugs, and C. elegans phenotypes. This mini-review aims to summarize the current understanding regarding the microbiome in C. elegans. Examples using C. elegans to study host–microbe–metabolite interactions are discussed. [ABSTRACT FROM AUTHOR]

We report a novel pathway for arsenic detoxification in the legume symbiont Sinorhizobium meliloti. Although a majority of ars operons consist of three genes, arsR (transcriptional regulator), arsB [As[(OH).sub.3]/[H.sup.+] antiporter], and arsC (arsenate reductase), the S. meliloti ars operon includes an aquaglyceroporin (aqpS) in place of arsB. The presence of AqpS in an arsenic resistance operon is interesting, since aquaglyceroporin channels have previously been shown to adventitiously facilitate uptake of arsenite into cells, rendering them sensitive to arsenite. To understand the role of aqpS in arsenic resistance, S. meliloti aqpS and arsC were disrupted individually. Disruption of aqpS resulted in increased tolerance to arsenite but not arsenate, while cells with an arsC disruption showed selective sensitivity to arsenate. The results of transport experiments in intact cells suggest that AqpS is the only protein of the S. meliloti ars operon that facilitates transport of arsenite. Coexpression of S. meliloti aqpS and arsC in a strain of E. coli lacking the ars operon complemented arsenate but not arsenite sensitivity. These results imply that, when S. meliloti is exposed to environmental arsenate, arsenate enters the cell through phosphate transport systems and is reduced to arsenite by ArsC. Internally generated arsenite flows out of the cell by downhill movement through AqpS. Thus, AqpS confers arsenate resistance together with ArsC-catalyzed reduction. This is the first report of an aquaglyceroporin with a physiological function in arsenic resistance.

Many ferromagnetic metals have, either by design or by happenstance, a very thin surface layer of reduced magnetic permeability. Such a layer might occur intrinsically or it might be induced by surface treatments such as case hardening, shot peening, or surface alloying. We studied the frequency-dependent impedance of a small air-cored coil of wire placed flat upon ferromagnetic metal plates. The impedance changes for nickel and iron could not be fitted to the half-space model for any values of conductivity and permeability. It is likely that the permeability varies continuously with depth in the near-surface region. Hence, it is possible that a multiple-layer model would yield a better representation of the data with a layer depth closer to that observed. In this paper, we illustrate that the multiple-layer model improves the agreement between the measured data and the approximate analytic solution. The results show that the permeability of pure nickel and pure iron decay exponentially from the base to surface. Index Terms--Eddy currents, ferromagnetic metal, surface condition.

Background and Aims: Scarce data exist on the effect of nucleos(t)ide analogue (NA) discontinuation on hepatocellular carcinoma (HCC) risk in HBeAg‐negative chronic hepatitis B (CHBe−). Therefore, we assessed whether HCC risk is increased in non‐cirrhotic CHBe− patients who discontinue compared to those remaining on NAs. Methods: This cohort study included 650 consecutive non‐cirrhotic Caucasian or Asian patients with CHBe− without a history of HCC who discontinued NAs after a median of 5 or 3 years (cases, n = 325; Caucasians: 143, Asians: 182) or remained on NA therapy beyond 5 or 3 years respectively (controls, n = 325; Caucasians: 223, Asians: 102). Propensity score (PS) 1:1 matching was applied to adjust for patients' origin, age and sex. Results: During a median follow‐up of 44 months, HCC developed in 7/325 cases and 9/325 controls or 7/245 PS‐matched cases and 7/245 PS‐matched controls with 5‐year cumulative HCC incidence of 5.1% and 4.9% respectively (log‐rank, P =.836). No difference in 5‐year HCC risk was observed between cases and controls of Caucasian (3.0% vs 4.8%; log‐rank, P =.510) or Asian origin (1.3% vs 2.2%; log‐rank, P =.873). In both cases and controls, HCC incidence was independently associated with age and PAGE‐B score. In cases alone, HCC development after NA discontinuation was associated only with pretreatment platelet counts and PAGE‐B score, but not with any type of relapse or HBsAg loss. Conclusions: Our findings suggest that discontinuation of effective long‐term NA therapy in non‐cirrhotic CHBe− patients are not associated with increased HCC risk, which is not affected by post‐NA relapses and/or HBsAg loss. [ABSTRACT FROM AUTHOR]