PubMed Health⌕ Search

PubMed · 16184164

Study design I.

Abstract

This is the first of a series of articles that will describe the different types of study design; considerations when choosing a study design; and the advantages and disadvantages of each type of study. This first article explains the importance of choosing an appropriate design and the decisions to be made when doing so.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Kate Ann Levin. 2005. Study design I.. https://doi.org/10.1038/sj.ebd.6400355

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Human pegivirus 1 in healthy blood donors and in acute febrile patients from Mato Grosso, Midwestern Brazil.

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.

Cross-Sectional Studies↗

A cross-sectional study of oxidative stress pathway genotypes and their interactions with environmental pollutant levels identifies associations with gene expression and lung function.

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.

Cross-Sectional Studies↗

Socioeconomic inequalities in health: a comparative longitudinal analysis using the European Community Household Panel.

This study measures socioeconomic inequalities in health across European Union Member States between 1994 and 2001. The analysis is based on the European Community Household Panel Users' Database (ECHP-UDB) and uses two binary indicators of health limitations for the full 8 waves of available data. Short- and long-run concentration indices together with mobility and health achievement indices are derived for indicators of severe health limitation and any health limitation. Results demonstrate the existence of socioeconomic inequality in health across Member States in both the short-term (1 year) and the long-term (up to 8 years), with health limitations concentrated among those with lower incomes. For all countries, the long-run indices show that income-related inequalities in health widen over time, in the sense that the longer the period over which an individual's health and income are measured the greater the measure of income-related health inequality. The ranking of countries according to their prevalence of illness differs from ranking by overall health achievement, which takes account of inequalities. This means that an equity-efficiency trade-off has to be faced in evaluating the performance of different countries and in comparing countries with diverse health and social welfare systems.

Cross-Sectional Studies↗