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  1. Article: Effusion into the Brain.

    Davey, James George

    Western journal of medicine and surgery

    2024  Volume 8, Issue 1, Page(s) 70–71

    Language English
    Publishing date 2024-01-11
    Publishing country United States
    Document type Journal Article
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The Delusions of the Insane.

    Davey, James George

    Journal of psychological medicine and mental pathology (London, England : 1875)

    2017  Volume 1, Issue 1, Page(s) 88–97

    Language English
    Publishing date 2017-09-14
    Publishing country England
    Document type Journal Article
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Pathology of Insanity: To the Editor of the Psychological Journal.

    Davey, James George

    Journal of psychological medicine and mental pathology (London, England : 1848)

    2017  Volume 7, Issue 26, Page(s) 291–296

    Language English
    Publishing date 2017-09-14
    Publishing country England
    Document type Journal Article
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: The Localisation of the Functions of the Brain.

    Davey, James George

    Journal of psychological medicine and mental pathology (London, England : 1875)

    2017  Volume 2, Issue Pt 2, Page(s) 252–262

    Language English
    Publishing date 2017-09-14
    Publishing country England
    Document type Journal Article
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Reminiscences of Lunacy Practice.

    Davey, James George

    Journal of psychological medicine and mental pathology (London, England : 1875)

    2017  Volume 1, Issue 2, Page(s) 200–221

    Language English
    Publishing date 2017-09-14
    Publishing country England
    Document type Journal Article
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Suicide in Its Social Relations.

    Davey, James George

    Journal of psychological medicine and mental pathology (London, England : 1875)

    2017  Volume 4, Issue Pt 2, Page(s) 230–255

    Language English
    Publishing date 2017-09-14
    Publishing country England
    Document type Journal Article
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: RE: Exploring the cross-cancer effect of circulating proteins and discovering potential intervention targets for 13 site-specific cancers.

    Yarmolinsky, James / Tzoulaki, Ioanna / Gunter, Marc J / Travis, Ruth C / Davey Smith, George / Smith-Byrne, Karl

    Journal of the National Cancer Institute

    2024  Volume 116, Issue 5, Page(s) 764–765

    MeSH term(s) Humans ; Neoplasms/drug therapy ; Biomarkers, Tumor/blood ; Biomarkers, Tumor/metabolism ; Blood Proteins/metabolism
    Chemical Substances Biomarkers, Tumor ; Blood Proteins
    Language English
    Publishing date 2024-03-15
    Publishing country United States
    Document type Letter ; Journal Article
    ZDB-ID 2992-0
    ISSN 1460-2105 ; 0027-8874 ; 0198-0157
    ISSN (online) 1460-2105
    ISSN 0027-8874 ; 0198-0157
    DOI 10.1093/jnci/djae064
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Prevalence, risk factors, and clinical implications of preserved ratio impaired spirometry: a UK Biobank cohort analysis.

    Higbee, Daniel H / Granell, Raquel / Davey Smith, George / Dodd, James W

    The Lancet. Respiratory medicine

    2021  Volume 10, Issue 2, Page(s) 149–157

    Abstract: Background: Preserved ratio impaired spirometry (PRISm) is defined as a FEV: Methods: For this cohort analysis, we used data from the UKBiobank to assess PRISm prevalence, risk factors and associated symptoms, and associated comorbidities in a large ... ...

    Abstract Background: Preserved ratio impaired spirometry (PRISm) is defined as a FEV
    Methods: For this cohort analysis, we used data from the UKBiobank to assess PRISm prevalence, risk factors and associated symptoms, and associated comorbidities in a large adult population. Participants with spirometry deemed acceptable by an investigator (best measure FEV
    Findings: Participants were recruited by UK Biobank between Dec 19, 2006, and Oct 10, 2010. We included 351 874 UK Biobank participants (189 247 women and 162 627 men) in our study, with a median follow-up of 9·0 years (IQR 8·0-10·0). 38 639 (11·0%) of 351 874 participants had PRISm at baseline. After adjustment, PRISm was strongly associated with obesity (odds ratio [OR] 2·40 [2·26-2·55], p<0·0001), current smoking (1·48 [1·36-1·62], p<0·0001), and patient reported doctor-diagnosed asthma (1·76 [1·66-1·88], p<0·0001). Other risk factors identified included female sex, being overweight, trunk fat mass, and trunk fat percentage. PRISm was strongly associated with symptoms and comorbidity including increased risk of breathlessness (adjusted OR 2·0 [95% CI 1·91-2·14], p<0·0001) and cardiovascular disease (adjusted OR 1·71 [1·64-1·83], p<0·0001 for heart attack). Longitudinal analysis showed that 241 (12·2%) of 1973 participants who had PRISm at baseline had transitioned to airflow obstruction consistent with COPD. PRISm was associated with increased all-cause mortality (adjusted hazard ratio 1·61 [95% CI 1·53-1·69], p<0·0001) versus control participants.
    Interpretation: PRISm was associated with breathlessness, multimorbidity, and increased risk of death, which does not seem to be explained by smoking, obesity, or existing lung disease. Although for many patients PRISm is transient, it is important to understand which individuals are at risk of progressive lung function abnormalities. Further research into the genetic, structural and functional pathophysiology of PRISm is warranted.
    Funding: UK Medical Research Council and University of Bristol.
    MeSH term(s) Adult ; Biological Specimen Banks ; Cohort Studies ; Female ; Forced Expiratory Volume ; Humans ; Lung ; Male ; Prevalence ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/epidemiology ; Risk Factors ; Spirometry ; United Kingdom/epidemiology ; Vital Capacity
    Language English
    Publishing date 2021-11-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2686754-0
    ISSN 2213-2619 ; 2213-2600
    ISSN (online) 2213-2619
    ISSN 2213-2600
    DOI 10.1016/S2213-2600(21)00369-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Association between genetically proxied PCSK9 inhibition and prostate cancer risk: A Mendelian randomisation study.

    Fang, Si / Yarmolinsky, James / Gill, Dipender / Bull, Caroline J / Perks, Claire M / Davey Smith, George / Gaunt, Tom R / Richardson, Tom G

    PLoS medicine

    2023  Volume 20, Issue 1, Page(s) e1003988

    Abstract: Background: Prostate cancer (PrCa) is the second most prevalent malignancy in men worldwide. Observational studies have linked the use of low-density lipoprotein cholesterol (LDL-c) lowering therapies with reduced risk of PrCa, which may potentially be ... ...

    Abstract Background: Prostate cancer (PrCa) is the second most prevalent malignancy in men worldwide. Observational studies have linked the use of low-density lipoprotein cholesterol (LDL-c) lowering therapies with reduced risk of PrCa, which may potentially be attributable to confounding factors. In this study, we performed a drug target Mendelian randomisation (MR) analysis to evaluate the association of genetically proxied inhibition of LDL-c-lowering drug targets on risk of PrCa.
    Methods and findings: Single-nucleotide polymorphisms (SNPs) associated with LDL-c (P < 5 × 10-8) from the Global Lipids Genetics Consortium genome-wide association study (GWAS) (N = 1,320,016) and located in and around the HMGCR, NPC1L1, and PCSK9 genes were used to proxy the therapeutic inhibition of these targets. Summary-level data regarding the risk of total, advanced, and early-onset PrCa were obtained from the PRACTICAL consortium. Validation analyses were performed using genetic instruments from an LDL-c GWAS conducted on male UK Biobank participants of European ancestry (N = 201,678), as well as instruments selected based on liver-derived gene expression and circulation plasma levels of targets. We also investigated whether putative mediators may play a role in findings for traits previously implicated in PrCa risk (i.e., lipoprotein a (Lp(a)), body mass index (BMI), and testosterone). Applying two-sample MR using the inverse-variance weighted approach provided strong evidence supporting an effect of genetically proxied inhibition of PCSK9 (equivalent to a standard deviation (SD) reduction in LDL-c) on lower risk of total PrCa (odds ratio (OR) = 0.85, 95% confidence interval (CI) = 0.76 to 0.96, P = 9.15 × 10-3) and early-onset PrCa (OR = 0.70, 95% CI = 0.52 to 0.95, P = 0.023). Genetically proxied HMGCR inhibition provided a similar central effect estimate on PrCa risk, although with a wider 95% CI (OR = 0.83, 95% CI = 0.62 to 1.13, P = 0.244), whereas genetically proxied NPC1L1 inhibition had an effect on higher PrCa risk with a 95% CI that likewise included the null (OR = 1.34, 95% CI = 0.87 to 2.04, P = 0.180). Analyses using male-stratified instruments provided consistent results. Secondary MR analyses supported a genetically proxied effect of liver-specific PCSK9 expression (OR = 0.90 per SD reduction in PCSK9 expression, 95% CI = 0.86 to 0.95, P = 5.50 × 10-5) and circulating plasma levels of PCSK9 (OR = 0.93 per SD reduction in PCSK9 protein levels, 95% CI = 0.87 to 0.997, P = 0.04) on PrCa risk. Colocalization analyses identified strong evidence (posterior probability (PPA) = 81.3%) of a shared genetic variant (rs553741) between liver-derived PCSK9 expression and PrCa risk, whereas weak evidence was found for HMGCR (PPA = 0.33%) and NPC1L1 expression (PPA = 0.38%). Moreover, genetically proxied PCSK9 inhibition was strongly associated with Lp(a) levels (Beta = -0.08, 95% CI = -0.12 to -0.05, P = 1.00 × 10-5), but not BMI or testosterone, indicating a possible role for Lp(a) in the biological mechanism underlying the association between PCSK9 and PrCa. Notably, we emphasise that our estimates are based on a lifelong exposure that makes direct comparisons with trial results challenging.
    Conclusions: Our study supports a strong association between genetically proxied inhibition of PCSK9 and a lower risk of total and early-onset PrCa, potentially through an alternative mechanism other than the on-target effect on LDL-c. Further evidence from clinical studies is needed to confirm this finding as well as the putative mediatory role of Lp(a).
    MeSH term(s) Humans ; Male ; Proprotein Convertase 9/genetics ; Genome-Wide Association Study ; Cholesterol, LDL ; Polymorphism, Single Nucleotide ; Prostatic Neoplasms/genetics ; Testosterone ; Mendelian Randomization Analysis
    Chemical Substances PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; Cholesterol, LDL ; Testosterone (3XMK78S47O)
    Language English
    Publishing date 2023-01-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2185925-5
    ISSN 1549-1676 ; 1549-1277
    ISSN (online) 1549-1676
    ISSN 1549-1277
    DOI 10.1371/journal.pmed.1003988
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Genetically proxied impaired GIPR signaling and risk of 6 cancers.

    Rogers, Miranda / Gill, Dipender / Ahlqvist, Emma / Robinson, Tim / Mariosa, Daniela / Johansson, Mattias / Cortez Cardoso Penha, Ricardo / Dossus, Laure / Gunter, Marc J / Moreno, Victor / Davey Smith, George / Martin, Richard M / Yarmolinsky, James

    iScience

    2023  Volume 26, Issue 6, Page(s) 106848

    Abstract: Preclinical and genetic studies suggest that impaired glucose-dependent insulinotropic polypeptide receptor (GIPR) signaling worsens glycemic control. The relationship between GIPR signaling and the risk of cancers influenced by impaired glucose ... ...

    Abstract Preclinical and genetic studies suggest that impaired glucose-dependent insulinotropic polypeptide receptor (GIPR) signaling worsens glycemic control. The relationship between GIPR signaling and the risk of cancers influenced by impaired glucose homeostasis is unclear. We examined the association of a variant in
    Language English
    Publishing date 2023-05-09
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.106848
    Database MEDical Literature Analysis and Retrieval System OnLINE

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