Genetics and juveniles

There is general agreement that behavior, including antisocial and delinquent behavior, is the result of a complex interplay of individual biological and genetic factors and environmental factors, starting during fetal development and continuing throughout life Bock and Goode, Clearly, genes affect biological development, but there is no biological development without environmental input.

This article has been cited by other articles in PMC. Abstract Juvenile idiopathic arthritis JIA is the most common chronic arthropathy of childhood which is believed to be influenced by both genetic and environmental factors.

The progress in identifying genes underlying JIA susceptibility using candidate gene association studies has been slow. Several associations between JIA and variants in the genes encoding the human leukocyte antigens HLA have been confirmed and replicated in independent cohorts.

While a large number of non-HLA candidate genes have been tested for associations, only a handful of reported associations such as PTPN22 have been validated.

In this review we discuss the principles behind genetic studies of complex traits like JIA, and comprehensively catalogue non-HLA candidate-gene association studies performed in JIA to date and review several validated associations.

Most candidate gene studies are underpowered and do not detect associations, and those that do are often not replicated. We also discuss the principles behind genome-wide association studies and discuss possible implications for identifying genes underlying JIA. Finally we discuss several genetic variants underlying multiple clinically distinct autoimmune phenotypes.

Juvenile idiopathic arthritis rers to a group of chronic arthropathies of childhood[ 1 ]. The relatively homogeneous subtypes of JIA share clinical features with other chronic autoimmune disorders Genetics and juveniles as rheumatoid arthritis RApsoriasis or spondyloarthropathies [ 3 ].

While clinical and laboratory features distinguish many of these autoimmune disorders, there is accumulating evidence to support the hypothesis that clinically distinct autoimmune phenotypes share common genetic susceptibility factors.

In this review, we will examine the genetic factors that underlie JIA susceptibility, and discuss some of the genetic factors that underlie multiple autoimmune phenotypes. JIA is an autoimmune disorder All subtypes of JIA are characterized by persistent joint swelling caused by an accumulation of synovial fluid and thickening of the synovial lining.

There is evidence to support the involvement of different components of the immune system in the etiopathogenesis of JIA. The synovial tissue contains various inflammatory cells including neutrophils, plasma cells, dendritic cells and a high proportion of activated T-cells [ 4 - 6 ].

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The recruitment of pro-inflammatory cells into the synovium of a child with JIA is believed to be mediated by chemokines that selectively attract Th1 T-cells [ 7 - 9 ]. Many other autoimmune disorders including RA, inflammatory bowel disease IBDpsoriasis, and type 1 diabetes mellitus T1DM are also associated with Th1-dominant responses[ 1011 ].

Several studies have demonstrated that Th1 cytokines also predominate in the synovial tissue and synovial fluid samples from children with JIA [ 12 - 15 ]. Pro-inflammatory cytokines including sCD are significantly elevated in sera of children with JIA as well [ 16 ].

Thus, there is compelling evidence that activated T-lymphocytes play a role in the pathogenesis of JIA. Involvement of the other components of the immune system is also evident in JIA.

For instance a significant proportion of children with JIA have antinuclear antibodies, and some children have rheumatoid factors, suggesting a role of the humoral component of the immune system.

The predominance of neutrophils in the synovial fluid of children with JIA, elevated levels of monocyte derived inflammatory cytokines, and complement activation have led to investigations of the involvement of innate immune system in JIA.

Using gene expression analysis, Jarvis et al have found that neutrophils in children with polyarticular JIA show differences in levels of expression of over genes compared to healthy controls [ 17 ].

These differences persisted despite clinical responses to pharmacological therapy, suggesting that neutrophils might be intrinsically involved in the pathogenesis of polyarticular subtypes of JIA.

Evidence that genetic factors underlie JIA susceptibility Twin and family studies have provided evidence for genetic contributions to susceptibility of JIA. Similarly examination of affected sibling pairs with JIA reveals concordance for disease onset, and disease course[ 2021 ]. Furthermore siblings were more likely to develop JIA at the same age of onset, rather than the same calendar year.

The prevalence of JIA among siblings of probands is about 15—30 times that of the general population prevalence[ 2223 ]. Finally a computerized probabilistic record-linking analysis identified several clusters of children with JIA sharing common ancestors [ 23 ].

Together these studies provide compelling evidence for a substantial genetic component underlying JIA susceptibility. JIA is a complex genetic trait Complex genetic traits are those phenotypes that do not exhibit classic Mendelian inheritance patterns which could be attributed to variants in a single gene locus[ 2425 ].

Complex traits are often believed to be determined by a number of genetic and environmental factors.

Relatives of JIA probands have increased prevalence of other autoimmune disorders [ 2627 ]. The best characterized genetic factors, i. These factors support the notion that JIA is a complex phenotype[ 22 ].

Exploring the genetic basis of disease Linkage and association studies are analytical approaches used to dissect the genetic basis of common diseases. Both studies rely on the same principles and assumptions, namely the co-inheritance of polymorphisms linked to a disease allele [ 2930 ].

Linkage studies test whether a phenotype and a marker allele show correlated transmission within a pedigree[ 24 ].Blog Post December 07, The genetics of violent behavior Dolores Garcia-Arocena, Ph.D.

JIA is an autoimmune disorder

The prevalence of violence in our society has motivated biomedical researchers, sociologists and psychologists to look for genetic markers, predictors and causes for this destructive human behavior.

The Relationship Between Race and Juvenile Delinquency Words | 8 Pages. The Relationship Between Race and Juvenile Delinquency Four years now researcher in the fields of psychology sociology, genetics, and the juvenile justice system have contemplated the reason why some youth turn to delinquency and violence.

Juvenile primary osteoporosis is a skeletal disorder characterized by thinning of the bones (osteoporosis) that begins in yunusemremert.comorosis is caused by a shortage of calcium and other minerals in bones (decreased bone mineral density), which makes the bones brittle and prone to fracture.

The juvenile justice system is a network of agencies that deal with juveniles whose conduct has come in conflict with the law. These agencies include police, prosecutor, detention, court, probation, and the Department of Juvenile Corrections.

Jul 21,  · A comprehensive review of the genetics of juvenile idiopathic arthritis Sampath Prahalad 1 and David N Glass 2 1 Assistant Professor of Pediatrics, Division of Immunology and Rheumatology, Department of Pediatrics, University of Utah School of Medicine, P.O Box Salt Lake City, UT , USA.

Juvenile myoclonic epilepsy is a condition characterized by recurrent seizures (epilepsy). This condition begins in childhood or adolescence, usually between ages 12 and 18, and lasts into adulthood. The most common type of seizure in people with this condition is myoclonic seizures, which cause rapid, uncontrolled muscle jerks. Nov 03,  · Juvenile Paget disease is a very rare condition that affects bone growth. This condition causes bones to be abnormally large, misshapen, and easily broken (fractured). This condition causes bones to be abnormally large, misshapen, and easily broken (fractured). Juvenile idiopathic arthritis (JIA) is a complex heterogeneous phenotype with different clinical features, and genetic associations. Several variants underlying .

Juvenile idiopathic arthritis (JIA) is a complex heterogeneous phenotype with different clinical features, and genetic associations. Several variants underlying .