AI Article Synopsis
- Global changes in amino acid levels were studied in Ugandan children with severe malaria (SM) to assess their long-term health outcomes, particularly kidney function and cognition.
- The study found deficiencies in certain sulfur-containing amino acids and identified specific amino acid increases related to mortality and chronic kidney disease (CKD).
- Unique amino acid profiles in children with SM were linked to negative health consequences, including higher risks of mortality and cognitive issues, especially attention problems in younger children.
Article Abstract
Background: Global changes in amino acid levels have been described in severe malaria (SM), but the relationship between amino acids and long-term outcomes in SM has not been evaluated.
Methods: We measured enrollment plasma concentrations of 20 amino acids using high-performance liquid chromatography in 500 Ugandan children aged 18 months to 12 years, including 122 community children and 378 children with SM. The Kidney Disease: Improving Global Outcomes criteria were used to define acute kidney injury (AKI) at enrollment and chronic kidney disease (CKD) at 1-year follow-up. Cognition was assessed over 2 years of follow-up.
Results: Compared to laboratory-defined, age-specific reference ranges, there were deficiencies in sulfur-containing amino acids (methionine, cysteine) in both community children and children with SM. Among children with SM, global changes in amino acid concentrations were observed in the context of metabolic complications including acidosis and AKI. Increases in threonine, leucine, and valine were associated with in-hospital mortality, while increases in methionine, tyrosine, lysine, and phenylalanine were associated with postdischarge mortality and CKD. Increases in glycine and asparagine were associated with worse attention in children <5 years of age.
Conclusions: Among children with SM, unique amino acid profiles are associated with mortality, CKD, and worse attention.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10205609 | PMC |
| http://dx.doi.org/10.1093/infdis/jiac392 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Network analysis combined with genome-wide association study helps identification of genes related to amino acid contents in soybean.
BMC Genomics
January 2025
Department of Horticulture and Crop Science, The Ohio State University, Columbus, OH, 43210, USA.
Background: Additional to total protein content, the amino acid (AA) profile is important to the nutritional value of soybean seed. The AA profile in soybean seed is a complex quantitative trait controlled by multiple interconnected genes and pathways controlling the accumulation of each AA. With a total of 621 soybean germplasm, we used three genome-wide association study (GWAS)-based approaches to investigate the genomic regions controlling the AA content and profile in soybean.
View Article and Find Full Text PDFβ-C-H bond functionalization of ketones and esters by cationic Pd complexes.
Nature
January 2025
Department of Chemistry, The Scripps Research Institute, La Jolla, CA, USA.
C-H activation is the most direct way of functionalizing organic molecules. Many advances in this field still require specific directing groups to achieve the necessary activity and selectivity. Developing C-H activation reactions directed by native functional groups is essential for their broad application in synthesis.
View Article and Find Full Text PDFSite-saturation mutagenesis of 500 human protein domains.
Nature
January 2025
Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Missense variants that change the amino acid sequences of proteins cause one-third of human genetic diseases. Tens of millions of missense variants exist in the current human population, and the vast majority of these have unknown functional consequences. Here we present a large-scale experimental analysis of human missense variants across many different proteins.
View Article and Find Full Text PDFRegulation of mutant huntingtin mitochondrial toxicity by phosphomimetic mutations within its N-terminal region.
J Neurosci
January 2025
Neuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213;
Huntington's disease (HD), a neurodegenerative disease, affects approximately 30,000 people in the United States, with 200,000 more at risk. Mitochondrial dysfunction caused by mutant huntingtin (mHTT) drives early HD pathophysiology. mHTT binds the translocase of mitochondrial inner membrane (TIM23) complex, inhibiting mitochondrial protein import and altering the mitochondrial proteome.
View Article and Find Full Text PDF[Genetic analysis of a Chinese pedigree affected with Charcot-Marie-Tooth type 2A2A due to a missense variant of MFN2 gene].
Zhonghua Yi Xue Yi Chuan Xue Za Zhi
January 2025
Prenatal Diagnosis Center, Xuzhou Central Hospital, Xuzhou Clinical College of Xuzhou Medical University, Xuzhou, Jiangsu 221009, China.
Objective: To explore the genotype-phenotype correlation in a Charcot-Marie-Tooth type 2A2A (CMT2A2A) pedigree and to provide genetic counseling for its subsequent pregnancies.
Methods: A Chinese pedigree presenting with "lower limb muscle atrophy and movement disorders" at the Prenatal Diagnosis Center of Xuzhou Central Hospital between January and August 2024 was selected as the study subject. Relevant clinical data were collected from the pedigree members.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!