6,208 research outputs found
Father Andrew Mullen 1790-1818: a study in early nineteenth century spirituality
Full text linkThis thesis is laid out in three parts: Part I. The life and death of Andrew Mullen. The life is based, to a large extent, on a long letter to his mother, Catherine Mullen, dated 7 January 1810. The letter gives a definite insight into his spirituality based on his membership of the Archconfraternity of the Blessed Sacrament. There is a hint that he had a premonition of an early death. Part II. The burial of Andrew Mullen and the immediate cult to him This is based on documentary evidence. Part III. Most of this part is a catalogue of testimonies taken from 1993 onwards. Then there is the conclusion on the popular devotion to Andrew Mullen stressing the theological aspect of the subject. In the course of writing the thesis it was decided to separate the documentary evidence from the oral tradition. This was advantageous in developing the thesis, and the documents provided a secure basis for the oral tradition. Two pieces of information were found in March 1997. They are death notices: 2 January 1819, The Leinster Journal and 7 January 1819, The Car low Morning Post. There is a slight discrepancy between the two on the date of his death. Also this discrepancy shows a slight difference from the date of the tombstone
Identification of polymorphic and off-target probe binding sites on the Illumina Infinium MethylationEPIC BeadChip
Full text linkGenome-wide analysis of DNA methylation has now become a relatively inexpensive technique thanks to array-based methylation profiling technologies. The recently developed Illumina Infinium MethylationEPIC BeadChip interrogates methylation at over 850,000 sites across the human genome, covering 99% of RefSeq genes. This array supersedes the widely used Infinium HumanMethylation450 BeadChip, which has permitted insights into the relationship between DNA methylation and a wide range of conditions and traits. Previous research has identified issues with certain probes on both the HumanMethylation450 BeadChip and its predecessor, the Infinium HumanMethylation27 BeadChip, which were predicted to affect array performance. These issues concerned probe-binding specificity and the presence of polymorphisms at target sites. Using in silico methods, we have identified probes on the Infinium MethylationEPIC BeadChip that are predicted to (i) measure methylation at polymorphic sites and (ii) hybridise to multiple genomic regions. We intend these resources to be used for quality control procedures when analysing data derived from this platform
Dispelling the Myths Behind First-author Citation Counts
Full text linkWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
WeissOpenPracticesDisclosure – Supplemental material for Conditioning on a Collider May or May Not Explain the Relationship Between Lower Neuroticism and Premature Mortality in the Study by Gale et al. (2017): A Reply to Richardson, Davey Smith, and Munafó (2019)
No full textSupplemental material, WeissOpenPracticesDisclosure for Conditioning on a Collider May or May Not Explain the Relationship Between Lower Neuroticism and Premature Mortality in the Study by Gale et al. (2017): A Reply to Richardson, Davey Smith, and Munafó (2019) by Alexander Weiss, Catharine R. Gale, Iva Čukić, G. David Batty, Andrew M. McIntosh and Ian J. Deary in Psychological Science</p
WeissSupplementalMaterial – Supplemental material for Conditioning on a Collider May or May Not Explain the Relationship Between Lower Neuroticism and Premature Mortality in the Study by Gale et al. (2017): A Reply to Richardson, Davey Smith, and Munafó (2019)
No full textSupplemental material, WeissSupplementalMaterial for Conditioning on a Collider May or May Not Explain the Relationship Between Lower Neuroticism and Premature Mortality in the Study by Gale et al. (2017): A Reply to Richardson, Davey Smith, and Munafó (2019) by Alexander Weiss, Catharine R. Gale, Iva Čukić, G. David Batty, Andrew M. McIntosh and Ian J. Deary in Psychological Science</p
Conditioning on a collider may or may not explain the relationship between lower neuroticism and premature mortality in Gale et al. (2017):A reply to Richardson, Davey Smith, and Munafó (2018)
Full text linkIn their Commentary, Richardson, Davey Smith, and Munafó (2018) note that our findings of a health-protective effect of neuroticism could be due to our conditioning on a collider (self-rated health). They conducted exploratory analyses on 18 covariates and found evidence in support of this interpretation. However, in our paper and this Reply, we carried out analyses that suggested that the health-protective effects of neuroticism were attributable to a neuroticism facet related to worry and vulnerability These analyses did not condition upon self-rated health or other possible colliders. As such, our results suggest that self-rated health may have been a suppressor variable. This interpretation is consistent with previous findings. Future studies will reveal whether self-rated health is a collider, a suppressor, or both. Until then, however, these results and those of our earlier study recommend an in-depth study of the mortality and neuroticism at the level of facets
Pharmacoepidemiology_of_Antidepressant_Exposure_in_a_UK_Cohort_Record_SUPPLEMENTARY_revised – Supplemental material for Pharmaco-epidemiology of antidepressant exposure in a UK cohort record-linkage study
No full textSupplemental material, Pharmacoepidemiology_of_Antidepressant_Exposure_in_a_UK_Cohort_Record_SUPPLEMENTARY_revised for Pharmaco-epidemiology of antidepressant exposure in a UK cohort record-linkage study by Jonathan D Hafferty, Eleanor M Wigmore, David M Howard, Mark J Adams, Toni-Kim Clarke, Archie I Campbell, Donald J MacIntyre, Kristin K Nicodemus, Stephen M Lawrie, David J Porteous and Andrew M McIntosh in Journal of Psychopharmacology</p
Large-scale neuroimaging studies of major depressive disorder, associated traits and polygenic risk
Full text linkMajor depressive disorder (MDD) is a highly prevalent and disabling condition with a
heritability of around 37%. Key symptoms of MDD include low mood and
psychological distress, but the mechanisms underlying MDD and its symptoms are
unclear. Genetic and neuroimaging techniques are important methods with which to
better understand the aetiology and mechanisms of depression. Recently, through
the availability of the UK Biobank and ENIGMA datasets, it has been possible to
conduct well-powered imaging studies of heterogeneous traits like MDD, with
genome-wide genetic data. These genetic data can act as causal instruments and
can be utilised to identify differences in neurobiological mechanisms.
The current thesis presents neurobiological associations with depressive symptoms
and genetic risk for MDD using data from the UK Biobank imaging project (N range
from 5,000 to 12,000). My overall aims were to investigate the neurobiological basis
of MDD status, depressive symptoms and MDD polygenic risk.
First, MDD case-control differences in subcortical volumes and white matter
microstructure indexed by fractional anisotropy and mean diffusivity, are presented
using the largest structural neuroimaging samples to date. MDD was associated
with worse white matter microstructure in the thalamic-radiation subset and forceps
major (posterior corpus callosum). No group difference was found for the volume of
any subcortical structure.
Next, associations between depressive symptom severity (including longitudinal and
cross-sectional measures) with white matter microstructure were tested. Over 8,000
participants had repeated measure of depressive symptoms assessed on 2-4
occasions across 5.89 to 10.69 years. I found several novel associations between
measures of depressive symptom severity (at the time of imaging, their variance
within individuals over time, and with longitudinal increasing depression severity) all
associated with lower white matter microstructure in the thalamic radiations. This
was the first study of this size looking at imaging associations with longitudinal
symptom measures and demonstrates consistent findings implicating
thalamocortical connections.
The third study presents results of phenotype wide association (‘PheWAS’) analysis
of polygenic risk for MDD, including imaging and other available phenotypes. In
total, 1,744 phenotypes were tested, covering sociodemographic, physical health,
mental health, subcortical volumes, white matter microstructure assessed with FA
and MD (mean diffusivity) and resting-state connectivity. I found that MDD polygenic
risk was associated with MDD-related phenotypes including severity of depression
and neuroticism, sleep, smoking, subjective well-being as well as neurobiological
phenotypes including white matter microstructure and resting-state connectivity.
In my final data chapter, neurobiological associations with cognition, as an important
risk factor of major depressive disorder, were also reported. I found that higher
connectivity related to the default mode network was associated with better
cognitive performance.
These studies suggest two features of neurobiology related to MDD traits and
genetic risk. First, they implicate microstructure of thalamic white matter connections
as an important biomarker for MDD risk, psychological distress and genetic risk, as
reflected by its consistent associations with depressive status, depressive
symptoms, within-subject variability of depression and MDD polygenic risk.
Secondly, the aberrant connections within the default mode network were related to
MDD phenotypes and polygenic risk. These findings, therefore, provide evidence
that these features may play a key role in MDD-related neuroarchitecture
When is higher Neuroticism protective against premature death? Findings from the UK Biobank
No full text- …
