Publications by authors named "Shabnam Eslamfam"

Gastrointestinal homeostasis is a dynamic balance under the interaction between the host, GI tract, nutrition and energy metabolism. Glucose is the main energy source in living cells. Thus, glucose metabolic disorders can impair normal cellular function and endanger organisms' health.

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Glucose and lipid are the major energy sources, and pivotal components of organic metabolism in mammals. Inappropriate diet directly influences the metabolic rate, and can alter the body's homeostasis. The underlying changes in energy storage and utilization would manifest as metabolic syndrome including obesity and high blood pressure, and high blood glucose, which are predisposing factors that significantly increase the risk for cardiovascular diseases and Type 2 Diabetes (T2D).

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Dietary protein is a vital nutrient for humans and animals, which is primarily digested into peptides and free amino acids (FAAs) in the upper gastrointestine with the help of proteases. The products are absorbed by the enterocytes and are metabolized in different organs of body. Dietary protein, peptides and FAAs that escape digestion and absorption of the small intestine will enter the large intestine for further fermentation by the vast gut microbiota.

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Background: Phenotypic data are routinely used to elucidate gene function in organisms amenable to genetic manipulation. However, previous to this work, there was no generalizable system in place for the structured storage and retrieval of phenotypic information for bacteria.

Results: The Ontology of Microbial Phenotypes (OMP) has been created to standardize the capture of such phenotypic information from microbes.

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Article Synopsis
  • Screening chemical libraries to find compounds affecting cell proliferation is common, but it’s often unclear how those compounds impact specific cell cycle transitions.
  • Researchers tested an FDA-approved drug library on yeast to see how different pharmaceuticals influence cell cycle progression, finding significant effects from drugs like gemfibrozil and fluoxetine.
  • The study highlights a unique interaction between gemfibrozil, which delays DNA replication, and fluoxetine, which stalls mitosis, suggesting that exploring drug combinations could help in identifying effective treatments that alter cell proliferation.
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