- Last 7 days
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manuscripts.jamanetworkopen.com manuscripts.jamanetworkopen.com
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Within Black populations, the frequencies of certain known genetic risk variants for prostate and breast156cancer incidence are higher among those who are genetically similar to native West African157populations
I am sure there are also some that are higher in other genetic similarity groups
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polygenic disease risk scores
Saying that PRS for disease can be used to estimate genetic admixture?
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scaled to county-specific quintiles,
treats bottom quantile for each county the same?
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- Nov 2024
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manuscripts.jamanetworkopen.com manuscripts.jamanetworkopen.com
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genetic similarity measures that are developed373without reference to existing sociopolitical groupings29, and rely purely on genetics for stratification (Box374
mention continuum
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We did not accoun
Did not have access to this data
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polygenic risk scores
PRS are mentioned in the intro and here but aren't really an aspect of this study. May be distracting
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Some high-risk genetic variants for disease cluster within SIRE groups, but359these examples are rare
Even in those cases, looking at the genetic variant is going to be a lot more robust then proxy with GA
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behavioral factors
I would be careful here.
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residential racial
Still using race as a tag here. Not a super fan but if carefully explained how this is being used as a measure for systemic and structural racism and show how it correlates with income and thus likely other unmeasured determinants.
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SDH measures capture current and historical social processes that344explain SIRE-based variation in environmental, behavioral, and access-related risk factors which345influence health outcomes. %AGA, as a genetic construct, should not substitute or replace social346constructs like SIRE or SSDH when explaining health disparitie
I would like to see data that supports that this is actually a much better predictor. Compare R^2 of the models using one vs the other
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ehavioral factors, component census tract measures of nSES, and Income324ICE as covariates had a 48% relative increase compared to the model with just demographic and325behavioral factors alone (5.64%, 95% CI: 4.67%-6.60%).
I think the point is to show how related these things are. - correlated. I do not think predicting African percent ancestry from these factors is good. I worry it is potentially stimitizing to say lower income (etc) predicts how much African ancestry someone has.
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(P>0.05; eFigure 2
Messy and hard to read figure, a lot going on, hard to understand what the take home message is supposed to be
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Quintile 5 to Quintile 1, income ICE (aHR: 1.32, 95% CI: 1.18-1.48, Ptrend <.0001) and nSES (aHR: 1.40,30595% CI: 1.23-1.60, Ptrend <.0001
Why this versus a continuous measure?
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%AGA as the outcome, including baseline demographic and behavioral predictors and separately adding280SSDH measures
I don't like this - seems problematic. I think I understand what they are trying to show but I don't like predicting genetics from behavioral predictors
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Model 3 included all factors in Model 2 plus %AGA
Why not also have Model 1 + %AGA if part of the point is that doing this does tag mortality - I would like to see that here
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ace ICE measure based on the228concentration of non-Hispanic Black to White residents in each census trac
This will probably tag a lot of other things
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acialized income ICE measure, which classified census tracts based on226concentration of non-Hispanic Black residents in the lowest quintile of income, vs non-Hispanic White227residents in the highest quintile of income
Unsure how I feel about baking race into the SSDH measure
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ategorical age group: 45-51.7 years; 51.7-58.4 years, 58.4-65.2 years, 65.2-69.8259years, 69.8-78.0 year
Why not keep continous?
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- Jul 2022
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academic.oup.com academic.oup.com
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Repetitive reads also present a challenge to genome assemblers (Treangen and Salzberg 2011).
see more beta chromatin in the genomics
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- Jun 2022
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adminliveunc-my.sharepoint.com adminliveunc-my.sharepoint.com
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pericentric heterochromatin.
area we are interested in
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260-bpandRespondersatellites
was mentioned in other article
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genome stability and chromosome segregation.
function
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adminliveunc-my.sharepoint.com adminliveunc-my.sharepoint.com
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10 kb by Lohe et al. (1993)were not detected with our method, whereas all satellite repeats thatwere estimated above 140 kb by Lohe et al. (1993) were detectablewith our method (Table 4).
?
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morphologically indistinguishable in all specie
how do we overcome this? does it even matter for what we are doing?
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ybrid incompatibility caused by satellite DNAamong closely related species
explination for divergence
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(Waringand Pollack 1987; Bonaccorsi and Lohe 1991; Abad et al. 1992; Loheet al. 1993; Dernburg et al. 1996)
Read these to find repeats
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remain obscure
May play a role in heterochromatin formation
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criticalimportance of the regulation
Indicates they are not actually "junk"
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kinetochore/centromere function, meiotic chromosome segregation,and X chromosome recognition
I wonder how the divergent sequences would play a role in this
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- May 2022
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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how perturbing chromatin structure affects replication initiation.
main research question
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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the latest replicating regions are not replicated each endocycle, resulting in under-replicated domains
effect of this? done on purpose? Highly repetative DNA likely lately replicated because doesn't matter if under replicated
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associated with human disease
always important to relate to human disease
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leading to DNA copy gain in pericentric heterochromatin.
does this actually have a phenotypic effect? Are there any other effects of H3K9-R9 mutation?
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latest replicating regions of polyploid salivary gland genomes, composed primarily of pericentric heterochromatic enriched in H3K9 methylation, are not replicated each endocycle, resulting in under-replicated domains with reduced ploidy.
interesting, I wonder why that is
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polyploidization
the multiplication of a complete chromosome set of a certain species to give birth to a new species
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