scholarly journals Genetic vulnerability of exposures to antenatal maternal treatments in 1– to 2‐month‐old infants

Infancy ◽  
2021 ◽  
Vol 26 (3) ◽  
pp. 515-532
Author(s):  
Kristina Denisova
Keyword(s):  
Genetic Vulnerability

Genetic Vulnerability and Germplasm Resources of the True Clovers 1

Crop Science ◽  
1977 ◽  
Vol 17 (4) ◽  
pp. 632-634 ◽  
Author(s):  
N. L. Taylor ◽  
P. B. Gibson ◽  
W. E. Knight
Keyword(s):  
Germplasm Resources ◽  
Genetic Vulnerability

scholarly journals Genetic Vulnerability and the Relationship of Commercial Germplasms of Maize in Brazil with the Nested Association Mapping Parents

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0163739 ◽  
Author(s):  
Luciano Rogério Braatz de Andrade ◽  
Roberto Fritsche Neto ◽  
Ítalo Stefanine Correia Granato ◽  
Gustavo César Sant’Ana ◽  
Pedro Patric Pinho Morais ◽  
...  
Keyword(s):  
Association Mapping ◽  
Nested Association Mapping ◽  
Genetic Vulnerability ◽  
Relationship Of ◽  
The Relationship

scholarly journals PL8 * GENETIC VULNERABILITY OF DRUG ADDICTION

2014 ◽  
Vol 49 (suppl 1) ◽  
pp. i2-i2
Author(s):  
I. Sora
Keyword(s):  
Drug Addiction ◽  
Genetic Vulnerability

Variation in the PRNP gene of Pere David’s deer (Elaphurus davidianus) may impact genetic vulnerability to chronic wasting disease

2021 ◽  
Author(s):  
Tolulope I. N. Perrin-Stowe ◽  
Yasuko Ishida ◽  
Emily E. Terrill ◽  
Dan Beetem ◽  
Oliver A. Ryder ◽  
...  
Keyword(s):  
Chronic Wasting Disease ◽  
Prnp Gene ◽  
Wasting Disease ◽  
Genetic Vulnerability ◽  
Père David’S Deer ◽  
Elaphurus Davidianus

scholarly journals When Distress Becomes Somatic: Dementia Family Caregivers’ Distress and Genetic Vulnerability to Pain and Sleep Problems

2018 ◽  
Author(s):  
Stephanie J Wilson ◽  
Avelina C Padin ◽  
Daniel J Birmingham ◽  
William B Malarkey ◽  
Janice K Kiecolt-Glaser
Keyword(s):  
Family Caregivers ◽  
Sleep Problems ◽  
Genetic Vulnerability

Panic Disorder: Evidence for Genetic Vulnerability

1987 ◽  
Vol 21 (2) ◽  
pp. 197-208 ◽  
Author(s):  
Fiona K. Judd ◽  
Graham D. Burrows ◽  
David A. Hay
Keyword(s):  
At Risk ◽  
Panic Disorder ◽  
Genetic Predisposition ◽  
Single Gene ◽  
Twin Data ◽  
Gene Association ◽  
Genetic Vulnerability ◽  
Preventative Intervention ◽  
Mode Of Transmission

Many studies have suggested that a genetic predisposition to the development of panic disorder exists. These studies are examined and their limitations discussed. It is suggested that only by the analysis of comprehensive family and twin data, coupled with other measures such as the search for possible single gene association or linkage and study of the children of panic disorder patients, will the mechanism for the ‘familiality’ noted in panic disorder patients be elucidated. Delineation of the mode of transmission of panic disorder may allow preventative intervention with those at risk before they develop panic.

Major depression and phobias: the genetic and environmental sources of comorbidity

1993 ◽  
Vol 23 (2) ◽  
pp. 361-371 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Michael C. Neale ◽  
Ronald C. Kessler ◽  
Andrew C. Heath ◽  
Lindon J. Eaves
Keyword(s):  
Risk Factors ◽  
Major Depression ◽  
Social Phobia ◽  
Environmental Risk ◽  
Population Based ◽  
Environmental Risk Factors ◽  
The Other ◽  
Genetic Vulnerability ◽  
Animal Phobias ◽  
Shared Genetic

SynopsisIn a population based sample of 2163 personally interviewed female twins, substantial comorbidity was observed between DSM-III-R defined major depression (MD) and 4 subtypes of phobia: agoraphobia, social phobia, animal phobia and situational phobia. However, the level of comorbidity of MD with agoraphobia was much greater than that found with the other phobic subtypes. We conducted bivariate twin analyses to decompose the genetic and environmental sources of comorbidity between MD and the phobias. Our results suggest that a modest proportion of the genetic vulnerability to MD also influences the risk for all phobic subtypes, with the possible exception of situational phobias. Furthermore, the magnitude of comorbidity resulting from this shared genetic vulnerability is similar across the phobic subtypes. By contrast, the non-familial environmental experiences which predispose to depression substantially increase the vulnerability to agoraphobia, have a modest impact on the risk for social and situational phobias and no effect on the risk for animal phobias. The increased comorbidity between MD and agoraphobia results, nearly entirely, from individual-specific environmental risk factors for MD which also increase the risk for agoraphobia but not for other phobias.

No evidence of associations between genetic liability for schizophrenia and development of cannabis use disorder

2019 ◽  
pp. 1-6 ◽  
Author(s):  
Carsten Hjorthøj ◽  
Md Jamal Uddin ◽  
Theresa Wimberley ◽  
Søren Dalsgaard ◽  
David M. Hougaard ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Psychiatric Disorders ◽  
Strong Predictor ◽  
Autism Spectrum ◽  
Cannabis Use ◽  
Risk Scores ◽  
Cannabis Use Disorder ◽  
Standard Deviation Increase ◽  
Genetic Vulnerability ◽  
Shared Genetic

Abstract Background Cannabis use and cannabis use disorder (CUD) is increased in patients with schizophrenia. It is important to establish if this is explained by non-causal factors, such as shared genetic vulnerability. We aimed to investigate whether the polygenic risk scores (PRS) for schizophrenia and other psychiatric disorders would predict CUD in controls, patients with schizophrenia, and patients with other psychiatric disorders. Methods We linked nationwide Danish registers and genetic information obtained from dried neonatal bloodspots in an observational analysis. We included people with schizophrenia, other psychiatric disorders, and controls. The exposures of interest were the PRS for schizophrenia, attention-deficit hyperactivity disorder (ADHD) autism spectrum disorder, and anorexia nervosa. The main outcome of interest was the diagnosis of CUD. Results The study included 88 637 individuals. PRS for schizophrenia did not predict CUD in controls [hazard ratio (HR) = 1.16, 95% CI 0.95–1.43 per standard-deviation increase in PRS, or HR = 1.47, 95% CI 0.72–3.00 comparing highest v. remaining decile], but PRS for ADHD did (HR = 1.27, 95% CI 1.08–1.50 per standard-deviation increase, or HR = 2.02, 95% CI 1.27–3.22 for the highest decile of PRS). Among cases with schizophrenia, the PRS for schizophrenia was associated with CUD. While CUD was a strong predictor of schizophrenia (HR = 4.91, 95% CI 4.36–5.53), the inclusion of various PRS did not appreciably alter this association. Conclusion The PRS for schizophrenia was not associated with CUD in controls or patients with other psychiatric disorders than schizophrenia. This speaks against the hypothesis that shared genetic vulnerability would explain the association between cannabis and schizophrenia.

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