8 research outputs found
LC–MS-Based Urinary Metabolite Signatures in Idiopathic Parkinson’s Disease
Increasing
evidence has shown that abnormal metabolic phenotypes
in body fluids reflect the pathogenesis and pathophysiology of Parkinson’s
disease (PD). These body fluids include urine; however, the relationship
between, specifically, urinary metabolic phenotypes and PD is not
fully understood. In this study, urinary metabolites from a total
of 401 clinical urine samples collected from 106 idiopathic PD patients
and 104 normal control subjects were profiled by using high-performance
liquid chromatography coupled to high-resolution mass spectrometry.
Our study revealed significant correlation between clinical phenotype
and urinary metabolite profile. Metabolic profiles of idiopathic PD
patients differed significantly and consistently from normal controls,
with related metabolic pathway variations observed in steroidogenesis,
fatty acid beta-oxidation, histidine metabolism, phenylalanine metabolism,
tryptophan metabolism, nucleotide metabolism, and tyrosine metabolism.
In the fruit fly <i>Drosophila melanogaster</i>, the alteration
of the kynurenine pathway in tryptophan metabolism corresponded with
pathogenic changes in the alpha-synuclein overexpressed <i>Drosophila</i> model of PD. The results suggest that LC–MS-based urinary
metabolomic profiling can reveal the metabolite signatures and related
variations in metabolic pathways that characterize PD. Consistent
PD-related changes across species may provide the basis for understanding
metabolic regulation of PD at the molecular level
Pregnancy-Induced Metabolic Phenotype Variations in Maternal Plasma
Metabolic
variations occur during normal pregnancy to provide the growing fetus
with a supply of nutrients required for its development and to ensure
the health of the woman during gestation. Mass spectrometry-based
metabolomics was employed to study the metabolic phenotype variations
in the maternal plasma that are induced by pregnancy in each of its
three trimesters. Nontargeted metabolomics analysis showed that pregnancy
significantly altered the profile of metabolites in maternal plasma.
The levels of six metabolites were found to change significantly throughout
pregnancy, with related metabolic pathway variations observed in biopterin
metabolism, phospholipid metabolism, amino acid derivatives, and fatty
acid oxidation. In particular, there was a pronounced elevation of
dihydrobiopterin (BH<sub>2</sub>), a compound produced in the synthesis
of dopa, dopamine, norepinephrine, and epinephrine, in the second
trimester, whereas it was markedly decreased in the third trimester.
The turnover of BH<sub>2</sub> and tryptophan catabolites indicated
that the fluctuations of neurotransmitters throughout pregnancy might
reveal the metabolic adaption in the maternal body for the growth
of the fetus. Furthermore, 11 lipid classes and 41 carnitine species
were also determined and this showed variations in the presence of
long-chain acylcarnitines and lysophospholipids in later pregnancy,
suggesting changes of acylcarnitines and lysophospholipids to meet
the energy demands in pregnant women. To our knowledge, this work
is the first report of dynamic metabolic signatures and proposed related
metabolic pathways in the maternal plasma for normal pregnancies and
provided the basis for time-dependent metabolic trajectory against
which disease-related disorders may be contrasted
Principal component analysis of transcriptome profiling in <i>D. radiodurans</i> R1.
<p>A, the plot of the principal component 1 (PC1) versus principal component 2 (PC2) was presented. B, Loadings plot of PC1. C, Hierarchical clustering analyses of the selected genes that have a high correlation with PC1. D, Loadings plot of PC2. E, Hierarchical clustering analyses of the selected genes that have a high correlation with PC2.</p
Expression patterns of selected genes for DNA repair pathway system (* <i>padj</i><0.1).
<p>A, base excision repair. B, nucleotide excision repair. C, homologous recombination. D. mismatch repair.</p
Strand-Specific RNA-seq analysis of the genes from <i>D. radiodurans</i> R1.
<p>Strand-specific coverage plot is shown. (Orange indicates the chromosome 1; violet, chromosome 2; green, plasmid 1; red, plasmid 2).</p
The differentially expressed TCA cycle genes during <i>D. radiodurans</i> R1 irradiation and recovery.
<p>The significant level (<i>padj</i>-value <0.1) of genes are indicated by the asterisks.</p
Overview of network components including genes and antioxidants in <i>D. radiodurans</i> that prevent cell damage from extreme irradiation.
<p>Red arrows and green arrows indicate the up-regulation and down-regulation, respectively. The representative <i>D.radiodurans</i> gene name is shown. The response of the DNA repair system activated in different stages of irradiation is listed. DC: wild type before radiation. D1: wild type with 1000 Gy radiation; D3: wild type with 3000 Gy radiation. DR: wild type one hour after 3000 Gy radiation.</p
Gene expression patterns in stages of <i>D. radiodurans</i> R1 irradiation and recovery.
<p>A, The differentially expressed genes in stages of <i>D. radiodurans</i> R1 irradiation and recovery. B, The expression pattern of annotated CDS and ncRNA reads. DC: wild type before radiation. D1: wild type with 1000 Gy radiation; D3: wild type with 3000 Gy radiation. DR: wild type one hour after 3000 Gy radiation.</p