2 research outputs found
A novel criticality analysis method for assessing obesity treatment efficacy
Human gait is a significant indicator of overall health and well-being due to its dependence on metabolic requirements. Abnormalities in gait can indicate the presence of metabolic dysfunction, such as diabetes or obesity. However, detecting these can be challenging using classical methods, which often involve subjective clinical assessments or invasive procedures. In this work, a novel methodology known as Criticality Analysis (CA) was applied to the monitoring of the gait of teenagers with varying amounts of metabolic stress who are taking part in an clinical intervention to increase their activity and reduce overall weight. The CA approach analysed gait using inertial measurement units (IMU) by mapping the dynamic gait pattern into a nonlinear representation space. The resulting dynamic paths were then classified using a Support Vector Machine (SVM) algorithm, which is well-suited for this task due to its ability to handle nonlinear and dynamic data. The combination of the CA approach and the SVM algorithm demonstrated high accuracy and non-invasive detection of metabolic stress. It resulted in an average accuracy within the range of 78.2% to 90%. Additionally, at the group level, it was observed to improve fitness and health during the period of the intervention. Therefore, this methodology showed a great potential to be a valuable tool for healthcare professionals in detecting and monitoring metabolic stress, as well as other associated disorders
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Congenital chloride-losing diarrhea in a Mexican child with the novel homozygous SLC26A3 mutation G393W
Congenital chloride diarrhea is an autosomal recessive disease caused by mutations in the intestinal lumenal membrane Cl−/HCO−3 exchanger, SLC26A3. We report here the novel SLC26A3 mutation G393W in a Mexican child, the first such report in a patient from Central America. SLC26A3 G393W expression in Xenopus oocytes exhibits a mild hypomorphic phenotype, with normal surface expression and moderately reduced anion transport function. However, expression of HA-SLC26A3 in HEK-293 cells reveals intracellular retention and greatly decreased steady-state levels of the mutant polypeptide, in contrast to peripheral membrane expression of the wildtype protein. Whereas wildtype HA-SLC26A3 is apically localized in polarized monolayers of filter-grown MDCK cells and Caco2 cells, mutant HA-SLC26A3 G393W exhibits decreased total polypeptide abundance, with reduced or absent surface expression and sparse punctate (or absent) intracellular distribution. The WT protein is similarly localized in LLC-PK1 cells, but the mutant fails to accumulate to detectable levels. We conclude that the chloride-losing diarrhea phenotype associated with homozygous expression of SLC26A3 G393W likely reflects lack of apical surface expression in enterocytes, secondary to combined abnormalities in polypeptide trafficking and stability. Future progress in development of general or target-specific folding chaperonins and correctors may hold promise for pharmacological rescue of this and similar genetic defects in membrane protein targeting