scholarly journals HLA Polymorphisms and Food Allergy Predisposition

2020 ◽  
Vol 09 (02) ◽  
pp. 077-086
Author(s):  
Maria Kostara ◽  
Vasiliki Chondrou ◽  
Argyro Sgourou ◽  
Konstantinos Douros ◽  
Sophia Tsabouri
Keyword(s):  
Food Allergy ◽  
Human Leucocyte Antigen ◽  
Genetic Factors ◽  
Immune Disorders ◽  
Biological Mechanisms ◽  
Immune Disorder ◽  
Complex Disorder ◽  
Leading Role ◽  
Gene Functions ◽  
Genetic Mechanisms

AbstractFood allergy (FA) is a growing health problem that affects ∼8% of the children worldwide. Although the prevalence of FA is increasing, the underlying genetic mechanisms responsible for the onset of this immune disorder are not yet clarified. Genetic factors seem to play a leading role in the development of FA, though interaction with environmental factors cannot be excluded. The broader network of genetic loci mediating the risk of this complex disorder remains to be identified. The human leucocyte antigen (HLA) has been associated with various immune disorders, including FA. This review aims to unravel the potential associations between HLA gene functions and the manifestation and outcome of FA disorders. Exploring new aspects of FA development with the perspective to improve our understanding of the multifaceted etiology and the complex biological mechanisms involved in FA is essential.

Identification of Potential Pleiotropic Genes for Immune and Skeletal Diseases Using Multivariate MetaCCA Analysis

2021 ◽  
Vol 23 ◽  
Author(s):  
Pei He ◽  
Rong- Rong Cao ◽  
Fei- Yan Deng ◽  
Shu- Feng Lei
Keyword(s):  
Association Study ◽  
Canonical Correlation ◽  
Genetic Factors ◽  
Genome Wide Association Study ◽  
Summary Statistics ◽  
Immune Disease ◽  
Histocompatibility Complex ◽  
Genome Wide ◽  
Genetic Mechanisms ◽  
Shared Genetic

Background: Immune and skeletal systems physiologically and pathologically interact with each other. The immune and skeletal diseases may share potential pleiotropic genetics factors, but the shared specific genes are largely unknown Objective: This study aimed to investigate the overlapping genetic factors between multiple diseases (including rheumatoid arthritis (RA), psoriasis, osteoporosis, osteoarthritis, sarcopenia and fracture) Methods: The canonical correlation analysis (metaCCA) approach was used to identify the shared genes for six diseases by integrating genome-wide association study (GWAS)-derived summary statistics. Versatile Gene-based Association Study (VEGAS2) method was further applied to refine and validate the putative pleiotropic genes identified by metaCCA. Results: About 157 (p<8.19E-6), 319 (p<3.90E-6) and 77 (p<9.72E-6) potential pleiotropic genes were identified shared by two immune disease, four skeletal diseases, and all of the six diseases, respectively. The top three significant putative pleiotropic genes shared by both immune and skeletal diseases, including HLA-B, TSBP1 and TSBP1-AS1 (p<E-300) were located in the major histocompatibility complex (MHC) region. Nineteen of 77 putative pleiotropic genes identified by metaCCA analysis were associated with at least one disease in the VEGAS2 analysis. Specifically, majority (18) of these 19 putative validated pleiotropic genes were associated with RA. Conclusion: The metaCCA method identified some pleiotropic genes shared by the immune and skeletal diseases. These findings help to improve our understanding of the shared genetic mechanisms and signaling pathways underlying immune and skeletal diseases.

Food allergies are associated with increased disease activity in multiple sclerosis

2018 ◽  
Vol 90 (6) ◽  
pp. 629-635 ◽  
Author(s):  
Rami Fakih ◽  
Camilo Diaz-Cruz ◽  
Alicia S Chua ◽  
Cindy Gonzalez ◽  
Brian C Healy ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Food Allergy ◽  
Disease Activity ◽  
Food Allergies ◽  
Cumulative Number ◽  
Biological Mechanisms ◽  
Longitudinal Investigation ◽  
Disability Status ◽  
History Of ◽  
Self Administered Questionnaire

ObjectiveThe association between allergy and multiple sclerosis (MS) is still unclear. In our study, we assessed the association between a self-reported history of allergic conditions with MS clinical and MRI disease activity.MethodsA subset of 1349 patients enrolled in the Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women’s Hospital (CLIMB) study completed a self-administered questionnaire on environmental, food and drug allergies. Patients were distributed among four allergy groups: (1) environmental, (2) food, (3) drug, (4) no known allergies (NKA). Clinical (number of attacks, expanded disability status scale (EDSS), MS severity score (MSSS)) and radiological variables (presence of gadolinium-enhancing lesions and lesion count), and their associations with the different allergy groups or those with NKA, were assessed.ResultsThe food allergy group had a 1.38 times higher rate for cumulative number of attacks compared with the NKA group (P=0.0062); this difference remained significant in the adjusted analysis (relapse rate ratio 1.27, P=0.0305). The food allergy group showed more than twice the likelihood (OR 2.53, P=0.0096) of having gadolinium-enhancing lesions on MRI. The environmental and drug allergy groups did not show significant differences when compared with the NKA group. The EDSS and MSSS were not affected by any type of allergy.ConclusionsMS patients with food allergy had more relapses and a higher likelihood of gadolinium-enhancing lesions compared with patients with no known allergy. Future prospective studies are needed to confirm our findings and investigate underlying biological mechanisms, which may unveil new therapeutic and preventative strategies for MS.

On the processes of sympatric speciation in the group of «yellow» wagtails in the Middle Volga region

2021 ◽  
pp. 105-111
Author(s):  
Elena Artemieva
Keyword(s):  
Genetic Divergence ◽  
Sympatric Speciation ◽  
Genetic Distances ◽  
Middle Volga Region ◽  
Intraspecific Hybridization ◽  
Yellow Wagtail ◽  
Leading Role ◽  
European Part Of Russia ◽  
Genetic Mechanisms ◽  
Spatio Temporal

This article discusses the mechanisms of sympatric speciation in the group of species of «yellow» wagtails based on hybridization. Interspecific and intraspecific hybridization can be attributed to the genetic mechanisms of divergence of populations of «yellow» wagtails. The existence of hybridization between the subspecies of the white-eared yellow wagtail M. flava beema and the yellow-fronted wagtail M. lutea leads to the emergence and further accumulation in the population of individuals with a light-colored head to varying degrees, the so-called «gray-headed» individuals. Intraspecific hybridization of subspecies forms of the yellow wagtail M. flava — nominative M. f. flava and white-eared M. f. beema leads to constantly occurring genotypic splits, which support intraspecific polymorphism of populations and provide the basis for further genetic divergence of these subspecies and species. The form of "gray-headed" hybrids is characterized by maximum genetic distances (1306.67–1375.67), which may correspond to the species rank. The modern polytypic complex of M. flava (in the narrow sense, a series of species and subspecies of only M. flava) probably formed in historical time on the basis of fan hybridization between the original forms of M. f. flava and M. lutea. Thus, the factors of genetic differentiation and divergence, along with ecological and geographical isolation, play a leading role in the formation of the spatio-temporal and genetic structure of the genus Motacilla. Currently, there is an active process of genetic divergence and separation of subspecies and species forms of «yellow» wagtails under conditions of wide sympatry within a single polytypic complex based on intraspecific and interspecific hybridization in the European part of Russia.

Transgressive segregation and maternal genetic effects of non–target site fluazifop-P-butyl tolerance in Zoysia spp.

Weed Science ◽  
2019 ◽  
Vol 67 (05) ◽  
pp. 504-509
Author(s):  
Wenwen Liu ◽  
Kevin E. Kenworthy ◽  
Gregory E. MacDonald ◽  
J. Bryan Unruh ◽  
Laurie E. Trenholm ◽  
...  
Keyword(s):  
Genetic Factors ◽  
Breeding Population ◽  
Transgressive Segregation ◽  
Target Site ◽  
Multiple Traits ◽  
Intermediate Phenotypes ◽  
Wide Range ◽  
Genetic Mechanisms ◽  
Tolerant Line ◽  
Biomass Reduction

AbstractZoysia germplasm exhibit different levels of sensitivity to fluazifop-P-butyl, but the genetic factors responsible for such differences are unknown. Segregation patterns of the fluazifop-P-butyl tolerance trait were studied under greenhouse conditions. In total, 244 F1 lines were generated from multiple crosses between the tolerant line 5337-2 (non–target site tolerance) and three more-sensitive lines (123, 252, and 5330-23). Progeny segregation showed that fluazifop-P-butyl tolerance within zoysiagrass (Zoysia spp.) is expressed as a quantitative trait with a wide range of intermediate phenotypes between parental phenotypes. Transgressive segregation was extensive and largely favored susceptibility in most families, but was especially evident for 5337-2 × 123 and 5337-2 × 5330-23. The segregation patterns for biomass reduction and percent injury were different within reciprocal crosses and among three different family crosses. Reciprocal effects were observed in growth reduction for 5337-2 × 5330-23, in percent injury at 3 wk after the treatment (WAT), and for 5337-2 × 252 at 6 WAT. This indicated that fluazifop-P-butyl tolerance was not completely controlled by nuclear genetic factors in 5337-2 and maternal/cytoplasmic inheritance was also partially responsible. These results suggested that fluazifop-P-butyl tolerance may be attributed to multiple genetic mechanisms, which could present a challenge for future breeding efforts because of the difficulty of fixing multiple traits within a breeding population.

Genetic factors in anorexia nervosa

1999 ◽  
Vol 14 (4) ◽  
pp. 189-198 ◽  
Author(s):  
A. Kipman ◽  
P. Gorwood ◽  
M.C. Mouren-Siméoni ◽  
J. Adès
Keyword(s):  
Anorexia Nervosa ◽  
Genetic Factors ◽  
Monozygotic Twins ◽  
Twin Studies ◽  
Vulnerability Factors ◽  
Adoption Studies ◽  
Complex Disorder ◽  
Dizygotic Twins ◽  
The One ◽  
Familial Environment

SummaryAnorexia nervosa is a severe and complex disorder with incompletely known vulnerability factors. It is generally recognized that anorexia nervosa is a familial disorder, but the majority of twin studies have shown that the concordance rate for monozygotic twins is higher (on average 44%) than for dizygotic twins (on average 12.5%). This difference in concordance rates shows that genetic factors, more than common familial environment, may explain why the `anorexia nervosa' phenotype runs in families. In order to estimate the heritability in the broad sense of anorexia nervosa according to published familial and twin studies, we first assessed the intrapair correlation between monozygotic and dizygotic twins, and secondly calculated the deviation threshold of relatives of affected probands from the relative mean. In this review, we obtained an estimation of the heritability at 0.72 according to all published controlled familial studies (six references quoted in MEDLINE®), and 0.71 for all published twin studies (59 references quoted in MEDLINE®). This estimation is close to the ones previously proposed, between 0.5 and 0.8.Familial and twin studies may also help to define the boundaries of the phenotype, shedding light on the complex relationship between anorexia nervosa on the one hand, and bulimia nervosa, mood disorders, and alcoholism on the other. Demonstrating the importance of genetic factors in anorexia nervosa, and more specifically for anorexia of the restrictive type, requires not only prospective and adoption studies (which are still lacking), but also genetic polymorphisms analyses, which began very recently.

scholarly journals The Differential Role of Human Cationic Trypsinogen (PRSS1) p.R122H Mutation in Hereditary and Nonhereditary Chronic Pancreatitis: A Systematic Review and Meta-Analysis

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Cheng Hu ◽  
Li Wen ◽  
Lihui Deng ◽  
Chenlong Zhang ◽  
Aurelia Lugea ◽  
...  
Keyword(s):  
Systematic Review ◽  
Chronic Pancreatitis ◽  
Environmental Factors ◽  
Genetic Factors ◽  
Meta Analysis ◽  
Case Control Studies ◽  
Complex Disorder ◽  
Increased Risk ◽  
Cationic Trypsinogen

Background. Environmental factors and genetic mutations have been increasingly recognized as risk factors for chronic pancreatitis (CP). ThePRSS1p.R122H mutation was the first discovered to affect hereditary CP, with 80% penetrance. We performed here a systematic review and meta-analysis to evaluate the associations ofPRSS1p.R122H mutation with CP of diverse etiology.Methods. The PubMed, EMBASE, and MEDLINE database were reviewed. The pooled odds ratio (OR) with 95% confidence intervals was used to evaluate the association of p.R122H mutation with CP. Initial analysis was conducted with all etiologies of CP, followed by a subgroup analysis for hereditary and nonhereditary CP, including alcoholic or idiopathic CP.Results. A total of eight case-control studies (1733 cases and 2415 controls) were identified and included. Overall,PRSS1p.R122H mutation was significantly associated with an increased risk of CP (OR = 4.78[1.13–20.20]). Further analysis showed p.R122H mutation strongly associated with the increased risk of hereditary CP (OR = 65.52[9.09–472.48]) but not with nonhereditary CP, both alcoholic and idiopathic CP.Conclusions. Our study showing the differential role of p.R122H mutation in various etiologies of CP indicates that this complex disorder is likely influenced by multiple genetic factors as well as environmental factors.

scholarly journals Which genetic mechanisms underlie the relationship between preschool vocabulary and later literacy skills?

2021 ◽  
Keyword(s):  
Vocabulary Acquisition ◽  
Genetic Factors ◽  
Literacy Skills ◽  
Language And Literacy ◽  
Genetic Mechanisms ◽  
The Relationship ◽  
Genetic Amplification

Preschool vocabulary acquisition is associated with later language and literacy skills. Genetic factors might partially explain this link, but the precise mechanisms are unclear. Thus far, twin-based studies have implicated mechanisms involving genetic amplification or genetic innovation.

scholarly journals Response to Therapeutic Sleep Deprivation: A Naturalistic Study of Clinical and Genetic Factors and Post-Treatment Depressive Symptom Trajectory

2018 ◽  
Author(s):  
Nina Trautmann ◽  
Jerome C. Foo ◽  
Josef Frank ◽  
Stephanie H. Witt ◽  
Fabian Streit ◽  
...  
Keyword(s):  
Depressive Symptom ◽  
Sleep Deprivation ◽  
Genetic Factors ◽  
Disease Onset ◽  
Depression Symptom ◽  
Healthy Controls ◽  
Biological Mechanisms ◽  
Global Improvement ◽  
Genetic Burden ◽  
The Impact

AbstractResearch has shown that therapeutic sleep deprivation (SD) has rapid antidepressant effects in the majority of depressed patients. Investigation of factors preceding and accompanying these effects may facilitate the identification of the underlying biological mechanisms. This exploratory study aimed to examine clinical and genetic factors predicting response to SD and determine the impact of SD on illness course. Mood and tiredness during SD were also assessed via visual analogue scales (VAS). Depressed inpatients (n = 78) and healthy controls (n = 15) underwent ~36hrs of SD. Response to SD was defined as a score of ≤2 on the Clinical Global Impression Scale for Global Improvement. Depressive symptom trajectories were evaluated for up to a month using self/expert ratings. Impact of genetic burden was calculated using polygenic risk scores for major depressive disorder. 72% of patients responded to SD. Responders and nonresponders did not differ in baseline self/expert depression symptom ratings, but mood subjectively measured by VAS scale differed. Response was associated with lower age (p = 0.007) and later age at life-time disease onset (p = 0.003). Higher genetic burden of depression was observed in non-responders than healthy controls. Up to a month post-SD, depressive symptoms decreased in both patients groups, but more in responders, in whom effects were sustained. The present findings suggest that re-examining SD with a greater focus on biological mechanisms will lead to better understanding of mechanisms of depression.

scholarly journals Increased Risk of Kawasaki Disease in Infants Born of Mothers With Immune Disorders

2021 ◽  
Vol 9 ◽  
Author(s):  
Hsiao-Wen Chu ◽  
Chien-Heng Lin ◽  
Ming-Chih Lin ◽  
Ya-Chi Hsu
Keyword(s):  
Kawasaki Disease ◽  
Autoimmune Disorder ◽  
Allergic Diseases ◽  
Population Based ◽  
Control Group ◽  
Research Database ◽  
Immune Disorders ◽  
Immune Disorder ◽  
Inherited Susceptibility ◽  
Increased Risk

Introduction: Genetic susceptibility and immune dysregulation play important roles in the pathogenesis of Kawasaki disease (KD). However, it is still unclear whether KD causes immune disorder later in life or whether inherited susceptibility to immune disorders causes KD. The aim of this study was to elucidate whether inherited immune disease properties from mothers increase the risk of KD from a population-based perspective.Method: Taiwan's National Health Insurance Research Database was the main data source in this study. Parents and children were linked using the Taiwan Maternal and Child Health Database. Patients diagnosed with KD and younger than 18 years from 2004 to 2015 were enrolled as the study population. The control group was randomly selected from individuals without the diagnosis of KD matched by age, index year, sex, and urbanization level at a ratio of 1 to 10. The prevalence of maternal autoimmune and allergic diseases was compared between groups.Results: In total, 7,178 children were found to have been diagnosed with Kawasaki disease. Then 71,780 children matched by index year, gender, and urbanization were randomly selected to serve as the control group. Children born from mothers with asthma and allergic rhinitis had a higher risk of developing KD. Children of mothers with an autoimmune disorder had a significantly increased tendency to develop KD. Maternal numbers of autoimmune disorders showed a dose-dependent relationship with KD incidence.Conclusion: This is the first population-based study to investigate maternal immune diseases and the risk of KD in their children. Children of mothers with immune disorders tend to have a higher risk of KD.

scholarly journals Genetic factors and cancer: diagnosis, prognosis and future perspectives

2021 ◽  
Vol 11 (3) ◽  
pp. 1-2
Author(s):  
Fernando Russo Costa do Bomfim
Keyword(s):  
Genetic Factors ◽  
Environmental Changes ◽  
Genetic Diseases ◽  
Genetic Modifications ◽  
Increased Risk ◽  
Wide Range ◽  
Different Types ◽  
Genetic Mechanisms ◽  
External Causes ◽  
And Behavior

Genetics is specifically responsible for several pathologies or, at the least, it is associated with a wide range of them, either as a primary causal agent (congenital genetic diseases) or secondary, being a factor within several possible for a given disease. One of the most critical genetic concepts is developed from the phenotype, equivalent to the genotype associated with the environment. In other words, for a condition to manifest itself, cancer, for example, we need a genetic alteration within the environment, which somehow influences carcinogenesis from stochastic or induced interactions. Cancer cases are approximately 80% and 90% associated with external causes, and environmental changes are mainly motivated by human actions, habits, and behavior, leading to an increased risk of different types of cancer. These changes lead to the formation of a cycle since man promotes environmental changes, leading to genetic modifications responsible for 10-20% of cancer formation. Although the percentage seems not to be significant, we have, in fact, several genetic mechanisms that will lead to the emergence of the most diverse types of cancer, including polymorphisms, mutations, oxidative stress, oncogenes, and genes that regulate the cell cycle, including apoptosis.

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