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The study presented here investigated the effect of common and uncommon elements on class merger as predicted by Sidman in his reconceptualization of stimulus equivalence suggesting that common elements among contingencies can facilitate emergent performances (1994, 1997, 2000). Eight adult participants were exposed to a procedure that arranged for stimulus-reinforcer correlations in Phase 1 and response-reinforcer correlations in Phase 2 of a 3-phase study. In the common element group, the visual images serving as reinforcers were the same in Phase 1 and Phase 2. In the uncommon elements group, the images serving as reinforcers were different in Phases 1 and 2. In Phase 3, participants were given an opportunity to respond but no feedback was programmed. The results showed that participants' responding was well differentiated in the common element group and undifferentiated in the uncommon elements group. These results are predicted by Sidman's revised formulation of the provenance and scope of equivalence relations. Specifically, these data support Sidman's (1994, 1997, 2000) suggestion that elements of a contingency enter into an equivalence class and common elements among contingencies are sufficient to produce class mergers. The findings highlight an emergent simple discrimination and raise some interesting considerations about the definition of equivalence under the new formulation.Climate plays a key role in shaping population trends and determining the geographic distribution of species because of limits in species' thermal tolerance. An evaluation of species tolerance to temperature change can therefore help predict their potential spatial shifts and population trends triggered by ongoing global warming. We assessed inter- and intraspecific variations in heat resistance in relation to body mass, local mean temperatures, and evolutionary relationships in 39 bumblebee species, a major group of pollinators in temperate and cold ecosystems, across 3 continents, 6 biomes, and 20 regions (2386 male specimens). Based on experimental bioassays, we measured the time before heat stupor of bumblebee males at a heatwave temperature of 40 °C. Interspecific variability was significant, in contrast to interpopulational variability, which was consistent with heat resistance being a species-specific trait. Moreover, cold-adapted species are much more sensitive to heat stress than temperate and Mediterranean species. Relative to their sensitivity to extreme temperatures, our results help explain recent population declines and range shifts in bumblebees following climate change.Scavenger receptor CD36 contributes significantly to lipid homeostasis, inflammation, and amyloid deposition, while CD36 deficiency is associated with restored cerebrovascular function in an Alzheimer's disease (AD) mouse model. Yet the distribution of CD36 has not been examined in the brain. Cyclopamine Here, we characterized CD36 gene and protein expression in the brains of young, middle aged, aged, and elderly male and female C57BL/6J mice. Age-related increases in CD36 mRNA expression were observed in the male hippocampus and female midbrain. Additionally, male mice had greater CD36 mRNA expression than females in the striatum, hippocampus, and midbrain. CD36 protein was primarily expressed intravascularly, and this expression differed by region, age, and sex in the mouse brain. Although male mice brains demonstrated an increase in CD36 protein with age in several cortices, basal ganglia, hippocampus, and midbrain, a decrease with age was observed in female mice in the same regions. These data suggest that distinctive age, region, and sex expression of CD36 in the brain may contribute to Aβ deposition and neuroinflammation in AD.Furan, a significant food contaminant, was found in many cooked foods. In most cooked foods, furan has been found to be coexisted with some alkylated derivatives such as 2-methylfuran. 2-methylfuran was found to be potent hepatotoxins. Little toxicological data is available for 2-methylfuran. The objective of this study was to investigate metabolite changes in the liver samples from mice fed with 2-methylfuran by untargeted metabolomic approach. Metabolomic analysis was conducted by using gas chromatography coupled with mass spectrometry (GC-MS). Twenty-four metabolites were identified as differential metabolites. The important metabolic pathway was linoleic acid metabolism, glycine, serine, and threonine metabolism, methane metabolism, ascorbate, and aldarate metabolism, valine, leucine, and isoleucine biosynthesis, arachidonic acid metabolism, alanine, aspartate, and glutamate metabolism, aminoacyl-tRNA biosynthesis, cysteine, and methionine metabolism, inositol phosphate metabolism, and pyruvate metabolism. These newly identified pathways provide evidence for investigating toxic mechanism of 2-methylfuran. PRACTICAL APPLICATION Furan in foods has caused public health concern for its hepatotoxicity and hepatic carcinogenicity in rodents. The metabolomics method was constructed to find more biomarkers to study underlying hepatotoxic mechanisms of 2-methylfuran. It will offer important information for official limits of 2-methylfuran in foods.The mechanisms responsible for dysregulation of iron metabolism in response to ethanol ingestion are poorly understood. Relatively brief ethanol exposures in rodents are associated with reduced hepatic hepcidin expression without increases in hepatic iron content. This study evaluated the effects of long-term ethanol treatment on hepatic iron metabolism in two mouse strains. Ethanol was administered in the drinking water to C57BL/6 and BALB/c mice for up to 11 months. Hepatic histology and iron concentrations (HIC) were assessed, along with expression of relevant genes and proteins by real-time RT-PCR and western blot, respectively. The livers of ethanol-consuming mice of both strains showed mild steatosis without inflammation or fibrosis. Stainable hepatocyte iron was modestly increased in both strains ingesting ethanol, although hepatic iron concentrations were significantly higher only in C57BL/6 mice. Long-term ethanol did not affect hepcidin mRNA (Hamp1 or Hamp2) in either strain, nor was the expression of several oxidative stress-responsive genes (glutamate cysteine ligase, gamma-glutamyl transpeptidase, heme oxygenase-1 and growth differentiation factor 15) altered in response to ethanol, suggesting that oxidative stress and suppression of hepcidin expression in short-term ethanol feeding models may be transient phenomena that resolve as mice adapt to ethanol exposure.