Genetics Clause Samples
The Genetics clause governs the collection, use, and disclosure of genetic information within the context of an agreement. It typically outlines the circumstances under which genetic data may be obtained, how it will be stored or shared, and the rights of individuals regarding their genetic information. For example, it may specify that genetic testing results cannot be used for discriminatory purposes or require explicit consent before any genetic data is accessed. The core function of this clause is to protect individuals' privacy and prevent misuse of sensitive genetic information, thereby ensuring compliance with applicable laws and ethical standards.
Genetics. Seals are primarily rehabilitated for animal welfare reasons. No negative effects of rehabilitation on the populations have yet been documented. It is, however, sometimes argued that release of rehabilitated animals may eventually have negative consequences for the population where there are individuals with genetic weaknesses among the admitted seals. Orphanage (both seals species) and parasitic pneumonia (common seals only) are the main causes of seals being admitted to rehabilitation (Chapter 1). For orphans, disturbance and extreme weather conditions are considered to be the most probable causes of separations between mothers and their pups. These two factors are expected to affect the seals in a random manner. A number of marine mammal studies postulate a relationship between disease and heterozygosity, which is the level of genetic variation within an individual animal selected at random from the population (▇▇▇▇▇▇▇- ▇▇▇▇▇▇▇▇▇▇ et al. 2003; ▇▇▇▇▇▇▇▇▇ et al. 2004; ▇▇▇▇▇ et al. 2008). Disease can also be related to a specific locus rather than overall genetic variability (▇▇▇▇▇ et al. 2005; ▇▇▇▇▇▇▇- ▇▇▇▇▇▇▇▇▇▇ et al. 2009).
Genetics. In terms of genetic features, populations speaking Chibchan languages show a rather homogeneous picture and have peculiarities that set them apart from other indigenous groups in the Americas (e.g., ▇▇▇▇▇▇▇▇▇ 1990; ▇▇▇▇▇ et al. 2013). It has repeatedly been observed, for instance, that the diversity of mitochondrial DNA (mtDNA) is relatively low among populations speaking Chibchan languages (▇▇▇▇▇▇ et al. 2007). Four main mtDNA haplogroups occur in the Americas (A, B, C, and D), indicating four founding mother lineages of Amerind people (▇▇▇▇▇▇ & ▇▇▇▇▇▇ 2004; ▇▇▇▇▇▇▇▇▇▇▇ et al. 1995), and a clear pattern emerges for peoples speaking Chibchan languages, namely a high proportion of haplogroup A, and a near absence of haplogroup D (Torroni et al. 1994; ▇▇▇▇▇▇▇ et al. 1995; ▇▇▇▇▇▇ et al. 2002; ▇▇▇▇▇▇ et al. 1994; ▇▇▇▇▇▇ et al. 2007; ▇▇▇▇▇▇ 2008). A possible interpretation of this relatively uniform picture is genetic drift, due to a small founding population (cf. ▇▇▇▇ 1942) with little subsequent gene flow, that is, little subsequent admixture of women with different mtDNA. The investigation of autosomes, which include information from both parents, likewise produces a homogeneous picture: A slightly lower level of heterozygosity among Chibchan- speaking groups (compared with neighboring populations) was observed by ▇▇▇▇ et al. (2007: 2060), who investigated genome-wide patterns of variation among Amerindian peoples, namely 678 autosomal microsatellite markers. These reduced levels of heterozygosity among Chibchan-speaking groups may likewise reflect genetic drift, that is, a rather small Proto-Chibchan founding population, which may have spread relatively recently or not over the Intermediate Area. 4 The only gold artifact from the Intermediate Area that arguably reached eastern South America is a double-headed eagle or vulture made of guanín, which was dredged from the bottom of the mid-Mazaruni river in Guyana (▇▇▇▇▇▇▇▇▇ 1990), and which is “pure Colombian in style” (▇▇▇▇ 1997: 47). Genetic data suggest a relatively close link between Chibchan-speaking groups and peoples from eastern South America. In terms of external relations as reflected in autosomal markers, ▇▇▇▇ et al. (2007) find strong support (97%) for clustering together the Cabécar, Guaymí (Ngäbe), Ika, Kogi, with the geographically adjacent Wayuu (Maipuran), Zenú (unknown linguistic affiliation), Emberá and Waunana (both Chocoan). Additionally, the authors propose “a reasonably well-supported cl...
Genetics. RA is a complex disease and is often heterogeneous in its clinical presentation. This heterogeneity can continue throughout the course of disease with variable disease progression, severity and response to treatment. This variability between individuals is likely secondary to genetic factors. The role of HLA DRB1 genes has been known for many years. The first clue that T cells may be an important driver of inflammation in RA came with the discovery of the link between RA and HLA-DR4/DR1 [Winchester 1981]. The only known function of DR molecules is to present antigen to T cells. Several different HLA DRB1 alleles have been shown to be associated with RA and some alleles have much stronger associations than others; HLA DRB1*0404 is a much stronger susceptibility factor than HLA DRB1*0401. [▇▇▇▇▇▇ et al. 1992] In contrast some HLA DRB1 alleles may actually be protective. Recent thinking suggests that the association between HLA DRB1 and RA is related to severity of disease rather than risk of development of disease. [▇▇▇▇ et al. 1994] Twin studies have shown that RA has a heritability of approximately 60%. [▇▇▇▇▇▇▇▇▇ et al. 2000]
Genetics. There is considerable evidence that genetic susceptibility plays a role in the pro- gression from substance use to dependence and ultimately addiction. Like for most diseases, the genetic contribution to addiction is highly complex, as heredity reflects both the variance attributable to genetic factors themselves and the variance result- ing from interactions between genes and environment 132. Thus, genetic factors not only determine individual differences in drug pharmacokinetics and vulnerability to the reinforcing properties of drugs, but also susceptibility to the effects of life events thereupon 710. Twin studies have indicated that addictions are among the most heritable of psy- chiatric disorders 254. Although most research has focused on alcohol and tobacco abuse, which have much higher prevalences that illicit drug use, several studies have indicated that there is a substantial genetic component in vulnerability to the reinforcing properties of cocaine 348,670, which is more pronounced for cocaine abuse than use 348. Interestingly, it has been proposed that the genetic component in drug addiction is not substance-specific but rather extends to all classes of abused drugs 349. In addition, there may be genes that are specific to a certain type of drug and its neurobiological and pharmacological profile. Studies in humans have identified several genes that are associated with cocaine dependence, of which the D2 receptor gene has gained most attention. There is a strong association between cocaine dependence and certain alleles of the D2 receptor gene (A1 and B1) 475 and the A1 allele has also been associated with the occurrence of severe alcoholism 121, nicotine and opioid dependence, polysub- stance abuse and obesity (for a review see: 473,476). Conflicting data have, however, also been reported 231. Carriers of the A1 allele have lower numbers of D2 receptors in the striatal complex and several additional metabolic and neurophysiological differences within dopamine rich brain regions (reviewed in: 474). Interestingly, this allele has also been associated with the occurrence of post-traumatic stress disorder (PTSD) 123, which is intriguing in view of the high co-morbidity between PTSD and drug abuse (see section 5.5). This finding suggests that the D2 receptor gene might engage in gene-environment interactions, which has been supported by studies showing that cigarette craving 198 and cognitive function 41 were differentially af- fected by stress i...
Genetics. Any treatment, device, drug, or supply to alter the body’s genes, genetic make-up, or the expression of the body’s genes except for the correction of congenital birth defects.
Genetics. It might be considered as the ultimate proof of causality when subjects who are exposed to high CRP their whole life due to genetic predisposition have increased risk of CVD. No environmental factors that determine risk are expected to contribute in this analysis. Very recently, it has become firmly established that a genetic component exists for basal levels of CRP. Baseline levels of CRP show a clear heritability of 40% 55 and 39% 56 in family studies. In twin studies, ▇▇▇▇▇▇▇▇▇ and colleagues57 observed 26% heritability in middle-aged twins; ▇▇ ▇▇▇▇ et al (unpublished data, 2004) observed heritability of 20% in elderly twins. ▇▇▇▇▇ et al58 reported the involvement of genetics to CRP, not only with respect to baseline CRP levels, but in particular to the response to stimuli. Genetic research on CRP can add to knowledge about the mechanisms of involvement of CRP in disease processes that may affect the use of CRP as a marker. Important lessons can be learned from the genetic approach and the consequences of the results. ▇▇▇▇▇▇ et al59 reported on a GT repeat polymorphism in intron 1 of the CRP gene. Alleles that are associated with low CRP levels differ in length by exactly 10 bp, which is sufficient for one complete turn of helical double-stranded DNA. This polymorphism disrupts a consensus sequence for the hormone response element HRE-3, suggesting that this polymorphism directly affects the regulation of CRP expression. ▇▇▇ and colleagues reported no association between CRP haplotype, consisting of the exonic 1059G/C (dbSNP rs1800947) and the intronic T/A (dbSNP rs1417938) polymorphisms, and venous thromboembolism in a nested case-control sample of the Physicians Health Study60. They had reported previously that the CRP concentrations were significantly reduced among carriers of the 1059C-allele, but the polymorphism was not associated with risk of arterial thrombosis61. A more extensive haplotype analysis in 586 UK simplex systemic lupus erythematosus (SLE) families, including –286C/T/A (dbSNP rs 3091244), 188L/L (1059G/C, dbSNP rs1800947), 988C/T (dbSNP rs1130864), 1846G/A (dbSNP rs1205) and CRP(GT)n, showed that there was a strong linkage disequilibrium within the CRP gene. The rare allele of the 1846G/A polymorphism was associated with the development of SLE. The 188L/L and the 1846G/A polymorphisms made independent contributions to the basal CRP level in these subjects. For the 3’ polymorphism (dbSNP rs1205) this association may be explained by an...