PubMed · 9892319
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S M Razali, A M Hamzah. 1999. Case vignette in a community-based study.. https://doi.org/10.1176/ajp.156.1.158
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The association between Human Pegivirus 1 (HPgV-1, Pegivirus hominis, family Hepaciviridae) with disease etiology remains unclear, yet this virus is widely distributed among people exposed to contaminated blood. This study aimed to identify the prevalence and characterize HPgV-1 genomes obtained from acute febrile patients (n = 92 from 2019) and from blood donors (n = 633 from 2022) sampled in Mato Grosso, Brazil. The serum samples were tested by RT-qPCR for a conserved 5' UTR region of HPgV-1. Nucleic acid of 28 positive samples was converted to ds-cDNA, purified and sequenced with an Illumina NextSeq platform. The prevalence of HPgV-1 among acute febrile patients was 4.35% (4/92), who were mostly female (3/4; 75.00%) mean 28.86 (12-67) years-old; whereas among blood donors it was 3.79% (24/633), which were predominantly male (16/24; 66.67%), aged 30-45 years-old (13/24; 54.17%). Eight HPgV-1 genomic sequences (7,708-9,248) were recovered; two belong to subgenotype 2a and clustered with strains from United States, Brazil, France and Japan, while the remaining six genomes from subgenotype 2b grouped with strains from Pará, Brazil and abroad. HPgV-1 detection in acute febrile patients and in healthy blood donors highlights the necessity to investigate the epidemiological aspects of this infection, as well as the possible impact to public health in Midwestern Brazil.
BACKGROUND: Asthma is a heterogeneous disease influenced by genetic and environmental factors. Fine particulate matter (PM2.5) exacerbates asthma, likely through oxidative stress pathways, but whether genetic variation modifies this effect remains unclear. METHODS: We analysed data on 948 adults with asthma from the Severe Asthma Research Program (SARP), linking ZIP-code-level PM2.5 exposure with whole-genome sequencing data. We tested 4337 single nucleotide polymorphisms (SNPs) in 120 oxidative stress pathway genes for gene-environment (GxE) interactions with PM2.5 on lung function (forced expiratory volume in 1 s [FEV1] % predicted) using weighted linear regression. Gene expression data from bronchial epithelial cells (n = 170) were used to assess cis-expression quantitative trait loci (eQTLs). FINDINGS: Higher PM2.5 exposure was associated with lower FEV1% predicted (β per μg/m3 = -0.7, p = 0.01). We identified 20 SNPs across seven genes (OXSR1, PXDN, TPO, LRRK2, APP, MSRA, MSRB2) with significant GxE interactions after multiple-testing correction. Five SNPs were also eQTLs, linking PM2.5-modified gene expression to lung function. Minor alleles in OXSR1 and PXDN were associated with reduced gene expression and worsened FEV1% under high PM2.5 exposure. Conversely, TPO variants were associated with higher baseline expression and lower lung function, but under increasing PM2.5 exposure, minor allele carriers showed suppressed TPO expression and improved FEV1%. INTERPRETATION: This study identified 20 SNPs in oxidative stress pathway genes that modify the effect of PM2.5 on lung function in asthma. These findings highlight the importance of integrating environmental context in genetic studies and suggest potential therapeutic targets for pollution-sensitive asthma phenotypes. FUNDING: Supported by NIH grants.
The contribution of evoked potential (EP) latency jitter, a measure of CNS temporal variability, on startle and EP gating defects in schizophrenic subjects has not been characterized. The amplitude of the N100/P200 EP complex (peak to trough) derived using a time-locked averaging procedure, N100 EP latency jitter derived from single trial analysis, acoustic startle response and clinical symptoms were measured in 51 schizophrenic subjects. N100 latency jitter was inversely correlated with N100/P200 EP amplitude in both cross-sectional and longitudinal analysis. Subjects with elevated EP gating ratios (>0.5) had similar latency jitter values for initial (S1) and test (S2) stimuli, while subjects with a low gating ratio (0-0.5) had a lower level of S1 latency jitter. Temporal variability thus plays a significant and complex role in previously reported sensory gating deficits in schizophrenic subjects.