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The Effect of Different Fructose Diets on the Lifespan of C. elegans

Chen et al. | May 10, 2020

The Effect of Different Fructose Diets on the Lifespan of <em>C. elegans</em>

High-fructose diets consumed widely in modern societies predisposes to metabolic diseases such as diabetes. Using the worm C. elegans, the authors of this study investigated the effect of fructose on the worm's survival rates. They found that worms fed 15% fructose had a lower life expectancy than those on a fructose-free diet. These results suggest that, like in humans, fructose has a negative effect on worm survival, which makes them an easy, attractive model to study the effects of fructose on health.

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Synergistic Effects of Metformin and Captopril on C. elegans

Kadıoğlu et al. | Jul 10, 2018

Synergistic Effects of Metformin and Captopril on <em>C. elegans</em>

Kadıoğlu and Oğuzalp study the synergistic effects of Metformin and Captopril, two commonly prescribed drugs for type 2 diabetes and hypertension, respectively. Using C. elegans nematodes as a model system, the authors find that the nematodes decreased in average body length when exposed to Metformin or Captopril individually, but grew 11% in body length when both drugs were used together. Because C. elegans body size is regulated in part by the TGF-β signaling pathway, the authors suggest that synergistic effects of these two drugs may be modulating TGF-β activity, a previously uncharacterized phenomenon.

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Astragalus membranaceus Root Concentration and Exposure Time: Role in Heat Stress Diminution in C. elegans

Chen et al. | Oct 17, 2018

Astragalus membranaceus Root Concentration and Exposure Time: Role in Heat Stress Diminution in <em>C. elegans</em>

In this study, the authors investigated the biological mechanism underlying the actions of a traditional medicinal plant, Astragalus membranaceus. Using C. elegans as an experimental model, they tested the effects of AM root on heat stress responses. Their results suggest that AM root extract may enhance the activity of endogenous pathways that mediate cellular responses to heat stress.

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The Effects of Altered Microbiome on Caenorhabditis elegans Egg Laying Behavior

Gohari et al. | Aug 12, 2019

The Effects of Altered Microbiome on <em>Caenorhabditis elegans</em> Egg Laying Behavior

Since the discovery that thousands of different bacteria colonize our gut, many of which are important for human wellbeing, understanding the significance of balancing the different species on the human body has been intensely researched. Untangling the complexity of the gut microbiome and establishing the effect of the various strains on human health is a challenge in many circumstances, and the need for simpler systems to improve our basic understanding of microbe-host interactions seems necessary. C. elegans are a well-established laboratory animal that feed on bacteria and can thus serve as a less complex system for studying microbe-host interactions. Here the authors investigate how the choice of bacterial diet affects worm fertility. The same approach could be applied to many different outcomes, and facilitate our understanding of how the microbes colonizing our guts affect various bodily functions.

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Expression of Anti-Neurodegeneration Genes in Mutant Caenorhabditis elegans Using CRISPR-Cas9 Improves Behavior Associated With Alzheimer’s Disease

Mishra et al. | Sep 14, 2019

Expression of Anti-Neurodegeneration Genes in Mutant <em>Caenorhabditis elegans</em> Using CRISPR-Cas9 Improves Behavior Associated With Alzheimer’s Disease

Alzheimer's disease is one of the leading causes of death in the United States and is characterized by neurodegeneration. Mishra et al. wanted to understand the role of two transport proteins, LRP1 and AQP4, in the neurodegeneration of Alzheimer's disease. They used a model organism for Alzheimer's disease, the nematode C. elegans, and genetic engineering to look at whether they would see a decrease in neurodegeneration if they increased the amount of these two transport proteins. They found that the best improvements were caused by increased expression of both transport proteins, with smaller improvements when just one of the proteins is overly expressed. Their work has important implications for how we understand neurodegeneration in Alzheimer's disease and what we can do to slow or prevent the progression of the disease.

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