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Figure 1 depicts a body cell showing the cytoplasm, nucleus and chromosomes (23 pairs per nucleated cells), with an enlargement of one of the pairs of chromosomes to show the gene loci (the positions of the genes on the chromosomes). This results in an exchange of genes between the chromosomes, that is, a new assortment of genes on each chromosome, but no new genes. From DNA to blood groups Chromosomal locations of genes encoding blood group systems The specific positioning, i.e. assignment and sub-localisation to a specific human chromosome, of the genes encoding for blood group system expression are known and illustrated in Fig. Parts of the RHCE gene can join the RHD gene and parts of RHD gene can join the RHCE gene, generating new hybrid genes. [Extracted from the article]

Figure 1 depicts a body cell showing the cytoplasm, nucleus and chromosomes (23 pairs per nucleated cells), with an enlargement of one of the pairs of chromosomes to show the gene loci (the positions of the genes on the chromosomes). This results in an exchange of genes between the chromosomes, that is, a new assortment of genes on each chromosome, but no new genes. GLO:8W7P/01dec20:voxs12592-fig-0010.jpg PHOTO (COLOR): 10 Chromosomal locations of genes encoding blood group systems. gl Encoding of genes or gene families that have been ratified to particular blood group systems, by the International Society of Blood Transfusion, have been localized to single cytogenetic bands on 16 of the 22 autosomes (genes for 38 systems) or on the X chromosome (genes for 2 systems). Parts of the I RHCE i gene can join the I RHD i gene and parts of I RHD i gene can join the I RHCE i gene, generating new hybrid genes. [Extracted from the article]

Summary: Objective: Low inhibitory control is linked with weight gain among youth. Inhibitory problems are associated with disruption to the hypothalamic–pituitary–adrenal axis cortisol response. Increased cortisol predicts appetite and weight gain (though may be gender specific). This study hypothesized that cortisol reactivity explains the association between inhibition and weight gain while considering the moderating factors of early stressors to the hypothalamic–pituitary–adrenal axis (e.g. prenatal‐drug exposure) and gender. Methods: Adolescents with prenatal‐drug exposure (n = 76) and non‐exposed comparison adolescents (NE; n = 61) completed the Conner's Continuous Performance Test and provided salivary cortisol samples. BMI z‐score were measured at the initial and 12‐month follow‐up evaluations. A bootstrapped moderated mediation analysis was conducted to test for conditional indirect effects of cortisol reactivity. Results: Lower inhibition was associated with increased cortisol reactivity among youth who were NE, and increased cortisol reactivity was associated with weight gain among girls. Cortisol reactivity mediated the relation between inhibition and BMI z‐score change for the girls in the group who was NE. Conclusion: Increased cortisol reactivity may play a mechanistic role in predicting weight gain among non‐prenatally drug‐exposed girls. Cortisol reactivity may be a biomarker for targeted interventions to improve biological regulation and ultimately health risk among girls. [ABSTRACT FROM AUTHOR]