Non-genetic factors that influence methamphetamine intake in a genetic model of differential methamphetamine consumption

AbstractSeveral nonparametric bootstrap methods are tested to obtain better confidence intervals for the quantitative trait loci (QTL) positions, i.e., with minimal width and unbiased coverage probability. Two selective resampling schemes are proposed as a means of conditioning the bootstrap on the number of genetic factors in our model inferred from the original data. The selection is based on criteria related to the estimated number of genetic factors, and only the retained bootstrapped samples will contribute a value to the empirically estimated distribution of the QTL position estimate. These schemes are compared with a nonselective scheme across a range of simple configurations of one QTL on a one-chromosome genome. In particular, the effect of the chromosome length and the relative position of the QTL are examined for a given experimental power, which determines the confidence interval size. With the test protocol used, it appears that the selective resampling schemes are either unbiased or least biased when the QTL is situated near the middle of the chromosome. When the QTL is closer to one end, the likelihood curve of its position along the chromosome becomes truncated, and the nonselective scheme then performs better inasmuch as the percentage of estimated confidence intervals that actually contain the real QTL's position is closer to expectation. The nonselective method, however, produces larger confidence intervals. Hence, we advocate use of the selective methods, regardless of the QTL position along the chromosome (to reduce confidence interval sizes), but we leave the problem open as to how the method should be altered to take into account the bias of the original estimate of the QTL's position.

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MMP2 Polymorphism Affects Plasma Matrix Metalloproteinase (MMP)-2 Levels, and Correlates with the Decline in Lung Function in Hypersensitivity Pneumonitis Positive to Autoantibodies Patients.

Biomolecules ◽

10.3390/biom9100574 ◽

2019 ◽

Vol 9 (10) ◽

pp. 574 ◽

Cited By ~ 1

Author(s):

Santiago-Ruiz ◽

Buendía-Roldán ◽

Pérez-Rubio ◽

Ambrocio-Ortiz ◽

Mejía ◽

...

Keyword(s):

Hypersensitivity Pneumonitis ◽

Vital Capacity ◽

Genetic Factors ◽

Genetic Model ◽

Linear Regression Analysis ◽

Clinical Manifestations ◽

Nucleotide Polymorphisms ◽

Single Nucleotide ◽

Dominant Genetic Model ◽

Pulmonary Remodeling

Among hypersensitivity pneumonitis (HP) patients have been identified who develop autoantibodies with and without clinical manifestations of autoimmune disease. Genetic factors involved in this process and the effect of these autoantibodies on the clinical phenotype are unknown. Matrix metalloproteinases (MMPs) have an important role in architecture and pulmonary remodeling. The aim of our study was to identify polymorphisms in the MMP1, MMP2, MMP9 and MMP12 genes associated with susceptibility to HP with the presence of autoantibodies (HPAbs+). Using the dominant model of genetic association, comparisons were made between three groups. For rs7125062 in MMP1 (CC vs. CT+TT), we found an association when comparing groups of patients with healthy controls: HPAbs+ vs. HC (p < 0.001, OR = 10.62, CI 95% = 4.34 − 25.96); HP vs. HC (p < 0.001, OR = 7.85, 95% CI 95% = 4.54 − 13.57). This rs11646643 in MMP2 shows a difference in the HPAbs+ group by the dominant genetic model GG vs. GA+AA, (p = 0.001, OR = 8.11, CI 95% = 1.83 − 35.84). In the linear regression analysis, rs11646643 was associated with a difference in basal forced vital capacity (FVC)/12 months (p = 0.013, = 0.228, 95% CI95% = 1.97 − 16.72). We identified single-nucleotide polymorphisms (SNPs) associated with the risk of developing HP, and with the evolution towards the phenotype with the presence of autoantibodies. Also, to the decrease in plasma MMP-2 levels.

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Inheritance of Flowering Habit in Russian Dandelion

Journal of the American Society for Horticultural Science ◽

10.21273/jashs.140.6.614 ◽

2015 ◽

Vol 140 (6) ◽

pp. 614-619 ◽

Cited By ~ 1

Author(s):

Katrina J.M. Hodgson-Kratky ◽

David J. Wolyn

Keyword(s):

North America ◽

Natural Rubber ◽

Genetic Factors ◽

Genetic Model ◽

Cold Period ◽

Vernalization Requirement ◽

Dominant Allele ◽

Winter Type ◽

Segregation Ratios ◽

Spring Type

Russian dandelion [Taraxacum kok-saghyz (TKS)] is a latex-producing, temperate species that has the potential to be grown as a source of natural rubber in North America. Flowering habit varies within the species; winter-type plants require a cold period or vernalization to flower, whereas spring-type plants flower without this treatment. Because flowering habit is correlated with rubber yield, understanding the genetic factors governing the trait would be useful for breeding. The objective of this research was to determine the inheritance of vernalization requirement in TKS. Winter-type and spring-type plants were intercrossed to create the F1, F2, and backcross generations and progeny segregation ratios were analyzed. A genetic model with three major genes is proposed, where a dominant allele at locus A, in combination with homozygous recessive alleles at either or both of two loci, B and C, confers winter type, whereas spring type is conferred by homozygous recessive alleles at A, regardless of genotype at B or C, or dominant alleles at A, B, and C.

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Enhanced accumulation of reduced glutathione by Scopoletin improves survivability of dopaminergic neurons in Parkinson’s model

Cell Death and Disease ◽

10.1038/s41419-020-02942-8 ◽

2020 ◽

Vol 11 (9) ◽

Author(s):

Priyadarshika Pradhan ◽

Olivia Majhi ◽

Abhijit Biswas ◽

Vinod Kumar Joshi ◽

Devanjan Sinha

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Dopaminergic Neurons ◽

Genetic Factors ◽

Genetic Model ◽

Reduced Glutathione ◽

Redox Balance ◽

Oxidative Markers ◽

Cellular Inclusions ◽

Antioxidant Machinery

Abstract Parkinson’s disease (PD) is a neuromotor disorder, primarily manifested by motor anomalies due to progressive loss of dopaminergic neurons. Although alterations in genetic factors have been linked with its etiology, exponential accumulation of environmental entities such as reactive oxygen species (ROS) initiate a cyclic chain reaction resulting in accumulation of cellular inclusions, dysfunctional mitochondria, and overwhelming of antioxidant machinery, thus accelerating disease pathogenesis. Involvement of oxidative stress in PD is further substantiated through ROS induced Parkinsonian models and elevated oxidative markers in clinical PD samples; thereby, making modulation of neuronal oxidative load as one of the major approaches in management of PD. Here we have found a potent antioxidant moiety Scopoletin (Sp), a common derivative in most of the nootropic herbs, with robust neuroprotective ability. Sp increased cellular resistance to ROS through efficient recycling of GSH to prevent oxidative damage. The Sp treated cells showed higher loads of reduced glutathione making them resistant to perturbation of antioxidant machinery or neurotoxin MPP+. Sp could restore the redox balance, mitochondrial function, and prevented oxidative damage, leading to recovery of dopaminergic neural networks and motion abilities in Drosophila genetic model of PD. Our data also suggest that Sp, in combination increases the therapeutic potency of L-DOPA by mitigating its chronic toxicity. Together, we highlight the possible ability of Sp in preventing oxidative stress mediated loss of dopaminergic neurons and at the same time enhance the efficacy of dopamine recharging regimens.

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Predicting of fentanyl-associated neurotoxicity in pancreatic cancer with clical, genetic model

Experimental and Clinical Gastroenterology ◽

10.31146/1682-8658-ecg-187-3-136-145 ◽

2021 ◽

pp. 136-145

Author(s):

O. P. Bobrova ◽

N. A. Shnayder ◽

M. M. Petrova ◽

S. N. Zobova ◽

Yu. A. Dykhno ◽

...

Keyword(s):

Pancreatic Cancer ◽

Personalized Medicine ◽

Genetic Factors ◽

Genetic Model ◽

Clinical Genetic ◽

Relationship Of ◽

The Relationship

Aim. To develop a model for the implementation of opioid - associated neurotoxicity in patients with pancreatic cancer based on an analysis of the relationship of clinical and genetic factors. Materials and methods. In 45 patients with pancreatic cancer, 54 clinical and genetic factors were studied for predicting the implementation of opioid-associated neurotoxicity, receiving a transdermal form of fentanyl. Results. A clinical genetic model of the implementation of opioid - associated neurotoxicity in patients with pancreatic cancer was developed using the example of a transdermal form of fentanyl Conclusion. The clinical genetic model for predicting the risk of opioid-associated neurotoxicity in patients with pancreatic cancer is important from the perspective of personalized medicine.

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A Genetic Model Compatible with a Dimensional View of Schizophrenia

The British Journal of Psychiatry ◽

10.1192/bjp.158.4.451 ◽

1991 ◽

Vol 158 (4) ◽

pp. 451-456 ◽

Cited By ~ 5

Author(s):

David Roberts ◽

Gordon Claridge

Keyword(s):

Biological Sciences ◽

Genetic Factors ◽

Genetic Model ◽

Reasonable Doubt ◽

The Social ◽

Wide Range ◽

History Of ◽

The 1960S ◽

Almost All ◽

Genetic Hypothesis

Throughout the history of schizophrenia as a psychiatric concept, opinions have differed sharply over its essential nature and its causes, giving rise to a wide range of explanations that have drawn upon ideas from almost all of the social and biological sciences. Only one fact has truly survived the vicissitudes of argument about the condition: that genetic factors contribute to its aetiology. Even that conclusion, first reached in the very early days of schizophrenia research, sank temporarily out of sight during the radical psychiatry challenges of the 1960s. However, the continuing collection of family, twin, adoption and other data over that period put the genetic hypothesis beyond reasonable doubt (McGuffin, 1988).

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Genetic and Environmental Contributions to Humor Styles: A Replication Study

Twin Research and Human Genetics ◽

10.1375/twin.11.1.44 ◽

2008 ◽

Vol 11 (1) ◽

pp. 44-47 ◽

Cited By ~ 21

Author(s):

Philip A. Vernon ◽

Rod A. Martin ◽

Julie Aitken Schermer ◽

Lynn F. Cherkas ◽

Tim D. Spector

Keyword(s):

Individual Differences ◽

North America ◽

Environmental Factors ◽

Genetic Factors ◽

Genetic Model ◽

Model Fitting ◽

Humor Styles ◽

Same Sex ◽

The United Kingdom ◽

Mz Twins

AbstractOne thousand and seventy three pairs of adult monozygotic (MZ) twins and 895 pairs of same sex adult dizygotic (DZ) twins from the United Kingdom (UK) completed the Humor Styles Questionnaire: a 32-item measure which assesses two positive and two negative styles of humor. MZ correlations were approximately twice as large as DZ correlations for all four humor styles, and univariate behavioral genetic model fitting indicated that individual differences in all of them can be accounted for entirely by genetic and nonshared environmental factors, with heritabilities ranging from .34 to .49. These results, while perhaps not surprising, are somewhat at odds with a previous study that we conducted in North America (Vernon et al., in press) in which genetic factors contributed significantly to individual differences in the two positive humor styles, but contributed far less to the two negative styles, variance in which was instead largely due to shared and nonshared environmental factors. We suggest that differences between North American and UK citizens in their appreciation of different kinds of humor may be responsible for the different results obtained in these two studies.

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The association between emotional eating and depressive symptoms: a population-based twin study in Sri Lanka

Global Health Epidemiology and Genomics ◽

10.1017/gheg.2019.3 ◽

2019 ◽

Vol 4 ◽

Cited By ~ 1

Author(s):

Moritz P. Herle ◽

Carol Kan ◽

Kaushalya Jayaweera ◽

Anushka Adikari ◽

Sisira Siribaddana ◽

...

Keyword(s):

Depressive Symptoms ◽

Environmental Factors ◽

Emotional Eating ◽

Genetic Factors ◽

Genetic Model ◽

Genetic Research ◽

Model Fitting ◽

Population Based ◽

Study Phase ◽

Sri Lankan

AbstractThis study investigated the genetic and environmental contributions to emotional overeating (EOE) and depressive symptoms, and their covariation, in a Sri-Lankan population, using genetic model-fitting analysis. In total, 3957 twins and singletons in the Colombo Twin and Singleton Study-Phase 2 rated their EOE behaviour and depressive symptoms, which were significantly associated (men: r = 0.11, 95% confidence interval (CI) 0.06–0.16, women: r = 0.12, 95% CI 0.07–0.16). Non-shared environmental factors explained the majority of variance in men (EOE e2 = 87%, 95% CI 78–95%; depressive symptoms e2 = 72%, 95% CI 61–83%) and women (EOE e2 = 76%, 95% CI 68–83%; depressive symptoms e2 = 64%, 95% CI 55–74%). Genetic factors were more important for EOE in women (h2 = 21%, 95% CI 4–32%) than men (h2 = 9%, 95% CI 0–20%). Shared-environmental factors were more important for depressive symptoms in men (c2 = 25%, 95% CI 10–36%) than women (c2 = 9%, 95% CI 0–35%). Non-shared environmental factors explained the overlap between depressive symptoms and EOE in women but not in men. Results differed from high-income populations, highlighting the need for behavioural genetic research in global populations.

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Next-Generation Computational Genetic Analysis: Multiple Complement Alleles Control Survival after Candida albicans Infection

Infection and Immunity ◽

10.1128/iai.05666-11 ◽

2011 ◽

Vol 79 (11) ◽

pp. 4472-4479 ◽

Cited By ~ 18

Author(s):

Gary Peltz ◽

Aimee K. Zaas ◽

Ming Zheng ◽

Norma V. Solis ◽

Mason X. Zhang ◽

...

Keyword(s):

Candida Albicans ◽

Survival Data ◽

Genetic Factors ◽

Genetic Model ◽

Inbred Mouse ◽

Host Susceptibility ◽

Mouse Strains ◽

Next Generation ◽

Content Type ◽

Factors Affecting

ABSTRACTCandida albicansis a fungal pathogen that causes severe disseminated infections that can be lethal in immunocompromised patients. Genetic factors are known to alter the initial susceptibility to and severity ofC. albicansinfection. We developed a next-generation computational genetic mapping program with advanced features to identify genetic factors affecting survival in a murine genetic model of hematogenousC. albicansinfection. This computational tool was used to analyze the median survival data after inbred mouse strains were infected withC. albicans, which provides a useful experimental model for identification of host susceptibility factors. The computational analysis indicated that genetic variation within early classical complement pathway components (C1q,C1r, andC1s) could affect survival. Consistent with the computational results, serum C1 binding to this pathogen was strongly affected byC1rsalleles, as was survival of chromosome substitution strains. These results led to a combinatorial, conditional genetic model, involving an interaction betweenC5andC1r/salleles, which accurately predicted survival after infection. Beyond applicability to infectious disease, this information could increase our understanding of the genetic factors affecting susceptibility to autoimmune and neurodegenerative diseases.

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Genetic Factors Account for Half of the Phenotypic Variance in Liability to Sleep-Related Bruxism in Young Adults: A Nationwide Finnish Twin Cohort Study

Twin Research and Human Genetics ◽

10.1017/thg.2012.54 ◽

2012 ◽

Vol 15 (6) ◽

pp. 714-719 ◽

Cited By ~ 18

Author(s):

Katariina Rintakoski ◽

Christer Hublin ◽

Frank Lobbezoo ◽

Richard J. Rose ◽

Jaakko Kaprio

Keyword(s):

Cohort Study ◽

Gender Difference ◽

Genetic Factors ◽

Genetic Model ◽

Large Population ◽

Population Based ◽

Genetic Effects ◽

Phenotypic Variance ◽

Birth Cohorts ◽

Additive Genetic Effects

Objectives: The aim of the present study was to examine the role of genetic and environmental factors in the phenotypic variance of bruxism in a large population-based cohort of young adult twins in Finland.Methods: The material of the present study derives from the FinnTwin16 cohort study consisting of five birth cohorts of twin pairs born in 1975–1979 who completed a questionnaire (at mean age 24, range 23–27 years) with data on frequency of sleep-related bruxism in 2000–2002. We used quantitative genetic modeling, based on the genetic similarity of monozygotic and dizygotic twins, to estimate the most probable genetic model for bruxism, based on decomposition of phenotypic variance into components: additive genetic effects (A), dominant genetic effects (D), and non-shared environmental effects (E).Results: On average, 8.7% experienced bruxism weekly, 23.4% rarely, and 67.9% never, with no significant gender difference (p = .052). The best fitting genetic model for bruxism was the AE-model. Additive genetic effects accounted for 52% (95% CI 0.41–0.62) of the total phenotypic variance. Sex-limitation model revealed no gender differences.Conclusions: Genetic factors account for a substantial proportion of the phenotypic variation of the liability to sleep-related bruxism, with no gender difference in its genetic architecture.

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