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Corrigendum to "A validated clinical risk prediction model for lung cancer in smokers of all ages and exposure types: A HUNT study" [EBioMedicine 31 (2018) 36-46].

ABSTRACT:

SUBMITTER: Markaki M

PROVIDER: S-EPMC9309413 | biostudies-literature |

REPOSITORIES: biostudies-literature

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A Validated Clinical Risk Prediction Model for Lung Cancer in Smokers of All Ages and Exposure Types: A HUNT Study.

Project description:Lung cancer causes >1·6 million deaths annually, with early diagnosis being paramount to effective treatment. Here we present a validated risk assessment model for lung cancer screening. The prospective HUNT2 population study in Norway examined 65,237 people aged >20years in 1995-97. After a median of 15·2years, 583 lung cancer cases had been diagnosed; 552 (94·7%) ever-smokers and 31 (5·3%) never-smokers. We performed multivariable analyses of 36 candidate risk predictors, using multiple imputation of missing data and backwards feature selection with Cox regression. The resulting model was validated in an independent Norwegian prospective dataset of 45,341 ever-smokers, in which 675 lung cancers had been diagnosed after a median follow-up of 11·6years. Our final HUNT Lung Cancer Model included age, pack-years, smoking intensity, years since smoking cessation, body mass index, daily cough, and hours of daily indoors exposure to smoke. External validation showed a 0·879 concordance index (95% CI [0·866-0·891]) with an area under the curve of 0·87 (95% CI [0·85-0·89]) within 6years. Only 22% of ever-smokers would need screening to identify 81·85% of all lung cancers within 6years. Our model of seven variables is simple, accurate, and useful for screening selection.

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HIV Glasgow 2018, 28-31 October 2018, Glasgow, UK.

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Corrigendum to "Deficiency in AK9 causes asthenozoospermia and male infertility by destabilising sperm nucleotide homeostasis" [EBioMedicine 96(2023) 104798].

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Project description:Two CMY-2 derivatives, CMY-31 (Gln(215)-->Arg) from Salmonella enterica serotype Newport and CMY-36 (Ala(77)-->Cys and Gln(193)-->Glu) from Klebsiella pneumoniae, were characterized. Both cephalosporinases functionally resembled CMY-2. bla(CMY) alleles occurred as parts of a putative transposon comprising ISEcp1B and a Citrobacter freundii-derived sequence carried by ColE1-like plasmids similar to CMY-5-encoding pTKH11 from Klebsiella oxytoca.

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Corrigendum to "Modulation of mitochondrial complex I activity averts cognitive decline in multiple animal models of familial Alzheimer's disease" [EBioMedicine 2 (2015) 294-305].

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IL-36 Cytokines Promote Inflammation in the Lungs of Long-Term Smokers.

Project description:Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory lung disease with high morbidity and mortality. The IL-36 family are proinflammatory cytokines that are known to shape innate immune responses, including those critical to bacterial pneumonia. The objective of this study was to determine whether IL-36 cytokines promote a proinflammatory milieu in the lungs of long-term smokers with and without COPD. Concentrations of IL-36 cytokines were measured in plasma and BAL fluid from subjects in a pilot study (n = 23) of long-term smokers with and without COPD in vivo and from a variety of lung cells (from 3-5 donors) stimulated with bacteria or cigarette smoke components in vitro. Pulmonary macrophages were stimulated with IL-36 cytokines in vitro, and chemokine and cytokine production was assessed. IL-36α and IL-36γ are produced to varying degrees in murine and human lung cells in response to bacterial stimuli and cigarette smoke components in vitro. Moreover, whereas IL-36γ production is upregulated early after cigarette smoke stimulation and wanes over time, IL-36α production requires a longer duration of exposure. IL-36α and IL-36γ are enhanced systemically and locally in long-term smokers with and without COPD, and local IL-36α concentrations display a positive correlation with declining ventilatory lung function and increasing proinflammatory cytokine concentrations. In vitro, IL-36α and IL-36γ induce proinflammatory chemokines and cytokines in a concentration-dependent fashion that requires IL-36R and MyD88. IL-36 cytokine production is altered in long-term smokers with and without COPD and contributes to shaping a proinflammatory milieu in the lungs.

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Project description:MicroRNAs (miRNAs) are small non-coding RNAs of ? 22 nucleotides that are involved in negative regulation of mRNA at the post-transcriptional level. Previously, we developed miRTarBase which provides information about experimentally validated miRNA-target interactions (MTIs). Here, we describe an updated database containing 422 517 curated MTIs from 4076 miRNAs and 23 054 target genes collected from over 8500 articles. The number of MTIs curated by strong evidence has increased ?1.4-fold since the last update in 2016. In this updated version, target sites validated by reporter assay that are available in the literature can be downloaded. The target site sequence can extract new features for analysis via a machine learning approach which can help to evaluate the performance of miRNA-target prediction tools. Furthermore, different ways of browsing enhance user browsing specific MTIs. With these improvements, miRTarBase serves as more comprehensively annotated, experimentally validated miRNA-target interactions databases in the field of miRNA related research. miRTarBase is available at http://miRTarBase.mbc.nctu.edu.tw/.

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Corrigendum: Emergence of Getah Virus Infection in Horse With Fever in China, 2018.

Project description:[This corrects the article DOI: 10.3389/fmicb.2019.01416.].

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Corrigendum to "Anti-α-synuclein ASO delivered to monoamine neurons prevents α-synuclein accumulation in a Parkinson's disease-like mouse model and in monkeys" [EBioMedicine 2020; 59:102944].

Project description: Not available

| S-EPMC8639415 | biostudies-literature

Socio-economic distribution of e-cigarette use among recent former regular smokers and current smokers at ages 25-26 in England.

Project description:Background and aimsE-cigarettes may potentially help young adult smokers to quit smoking, yet little is known about differences among socio-economic groups. We examined associations between key socio-economic characteristics and e-cigarette use among recent former smokers and current smokers in a sample of young adults in England.Design, setting, participants and measurementsWe used data on 346 recent former regular (daily for 12+ months) smokers and 1913 current smokers from the ages 25-26 wave of the Next Steps cohort study (2015-2016). In multinomial logistic regression, we estimated relative risk ratios (RRR) of e-cigarette use (never, former, non-daily, daily) by educational attainment, social class [using the National Statistics Socio-economic classification (NS-SEC)] and employment status [full-time, part-time, unemployed and other 'inactivity' (e.g. stay-at-home parents and permanantly disabled)], adjusting for sex.FindingsAmong recent former regular smokers, there were no patterns of association between socio-economic characteristics and e-cigarette use. Among current smokers: (1) compared with higher occupation (NS-SEC I/II), intermediate occupation (NS-SEC III/IV) was positively associated with non-daily e-cigarette use [RRR = 1.77, 95% confidence interval (CI) = 1.03-3.03]; (2) compared with full-time employment, unemployment was negatively associated with non-daily and daily e-cigarette use (RRR = 0.38, 95% CI = 0.18-0.81; RRR = 0.12, 95% CI = 0.02-0.56) and other economic inactivity was negatively associated with daily e-cigarette use (RRR = 0.39, 95% CI = 0.16-0.93).ConclusionsAmong young adult smokers in England, lower-status occupational groups were more likely to use e-cigarettes on a non-daily basis than to have never used compared with higher status occupational groups. Compared with people in full-time employment, those without employment were less likely to use e-cigarettes daily than to have never used.

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