Publications by authors named "C Deval"

Objective: Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia/reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis.

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Activating transcription factor 4 (ATF4) is involved in muscle atrophy through the overexpression of some atrogenes. However, it also controls the transcription of genes involved in muscle homeostasis maintenance. Here, we explored the effect of ATF4 activation by the pharmacological molecule halofuginone during hindlimb suspension (HS)-induced muscle atrophy.

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The WEPPcloud interface is a new online decision-support tool for the Water Erosion Prediction Project (WEPP) model that facilitates data preparation and model runs, and summarizes model outputs into tables and maps that are easily interpretable by users. The interface can be used by land and water managers in United States, Europe, and Australia interested in simulating streamflow, sediment and pollutant loads from both undisturbed and disturbed (e.g.

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Article Synopsis
  • The ubiquitin proteasome system (UPS) plays a crucial role in muscle wasting associated with various diseases, with the E3 ligase MuRF1/TRIM63 targeting important contractile proteins for degradation.
  • This study highlights UBE2L3's significant impact on the degradation of alpha-actin and myosin heavy chain (MHC) in muscle cells, showing that knockdown of UBE2L3 can promote muscle growth, while its overexpression exacerbates muscle loss in stressed mice.
  • The research also reveals that MuRF1 shows a stronger binding affinity for filamentous F-actin compared to G-actin and that binding interactions differ for MHC, indicating complex regulatory mechanisms in muscle protein degradation.
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Muscle atrophy arises from a multiplicity of physio-pathological situations and has very detrimental consequences for the whole body. Although knowledge of muscle atrophy mechanisms keeps growing, there is still no proven treatment to date. This study aimed at identifying new drivers for muscle atrophy resistance.

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