Comparative genome mapping of the deer mouse (Peromyscus maniculatus) reveals greater similarity to rat (Rattus norvegicus) than to the lab mouse (Mus musculus)

<p>Abstract</p> <p>Background</p> <p>Deer mice (<it>Peromyscus maniculatus</it>) and congeneric species are the most common North American mammals. They represent an emerging system for the genetic analyses of the physiological and behavioral bases of habitat adaptation. Phylogenetic evidence suggests a much more ancient divergence of <it>Peromyscus </it>from laboratory mice (<it>Mus</it>) and rats (<it>Rattus</it>) than that separating latter two. Nevertheless, early karyotypic analyses of the three groups suggest <it>Peromyscus </it>to be exhibit greater similarities with <it>Rattus </it>than with <it>Mus</it>.</p> <p>Results</p> <p>Comparative linkage mapping of an estimated 35% of the deer mouse genome was done with respect to the Rattus and Mus genomes. We particularly focused on regions that span synteny breakpoint regions between the rat and mouse genomes. The linkage analysis revealed the Peromyscus genome to have a higher degree of synteny and gene order conservation with the Rattus genome.</p> <p>Conclusion</p> <p>These data suggest that: 1. the <it>Rattus </it>and <it>Peromyscus </it>genomes more closely represent ancestral Muroid and rodent genomes than that of <it>Mus</it>. 2. the high level of genome rearrangement observed in Muroid rodents is especially pronounced in <it>Mus</it>. 3. evolution of genome organization can operate independently of more commonly assayed measures of genetic change (e.g. SNP frequency).</p

Depression is a risk factor for incident coronary heart disease in women: an 18-year longitudinal study

BACKGROUND: According to a recent position paper by the American Heart Association, it remains unclear whether depression is a risk factor for incident Coronary Heart Disease (CHD). We assessed whether a depressive disorder independently predicts 18-year incident CHD in women. METHOD: A prospective longitudinal study of 860 women enrolled in the Geelong Osteoporosis Study (1993-2011) was conducted. Participants were derived from an age-stratified, representative sample of women (20-94 years) randomly selected from electoral rolls in South-Eastern Australia. The exposure was a diagnosis of a depressive disorder using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Outcomes data were collected from hospital medical records: (1) Primary outcome: a composite measure of cardiac death, non-fatal Myocardial Infarction or coronary intervention. (2) Secondary outcome: any cardiac event (un/stable angina, cardiac event not otherwise defined) occurring over the study period. RESULTS: Seven participants were excluded based on CHD history. Eighty-three participants (9.6%) recorded &ge;1 cardiac event over the study period; 47 had a diagnosis that met criteria for inclusion in the primary analysis. Baseline depression predicted 18-year incidence, adjusting for (1) anxiety (adj. OR:2.39; 95% CIs:1.19-4.82), plus (2) typical risk factors (adj. OR:3.22; 95% CIs:1.45-6.93), plus (3) atypical risk factors (adj. OR:3.28; 95% CIs:1.36-7.90). This relationship held when including all cardiac events. No relationship was observed between depression and recurrent cardiac events. CONCLUSION: The results of this study support the contention that depression is an independent risk factor for CHD incidence in women. Moreover, the strength of association between depression and CHD incidence was of a greater magnitude than any typical and atypical risk factor

Comparison of the organization of genes on Chrs 1, 6, 9, and 10, and Chr 17 with the linkage of their orthologous genes in

The break in the continuity of the linkage groups indicates a lack of detectable linkage between the groups.<p><b>Copyright information:</b></p><p>Taken from "Comparative genome mapping of the deer mouse () reveals greater similarity to rat () than to the lab mouse ()"</p><p>http://www.biomedcentral.com/1471-2148/8/65</p><p>BMC Evolutionary Biology 2008;8():65-65.</p><p>Published online 26 Feb 2008</p><p>PMCID:PMC2266908.</p><p></p

Comparison of the organization of genes on Chr 6, and Chrs 5, 12, and 17, with the linkage of their orthologous genes in

The break in the continuity of the linkage groups indicates a lack of detectable linkage between the groups.<p><b>Copyright information:</b></p><p>Taken from "Comparative genome mapping of the deer mouse () reveals greater similarity to rat () than to the lab mouse ()"</p><p>http://www.biomedcentral.com/1471-2148/8/65</p><p>BMC Evolutionary Biology 2008;8():65-65.</p><p>Published online 26 Feb 2008</p><p>PMCID:PMC2266908.</p><p></p

Comparison of the organization of genes on Chrs 5, 9, and 13, and Chrs 1 and 4 with the linkage of their orthologous genes in

The break in the continuity of the linkage groups indicates a lack of detectable linkage between the groups.<p><b>Copyright information:</b></p><p>Taken from "Comparative genome mapping of the deer mouse () reveals greater similarity to rat () than to the lab mouse ()"</p><p>http://www.biomedcentral.com/1471-2148/8/65</p><p>BMC Evolutionary Biology 2008;8():65-65.</p><p>Published online 26 Feb 2008</p><p>PMCID:PMC2266908.</p><p></p

Comparison of the organization of genes on Chr 1, and Chrs 7, 10, 17, and 19, with the linkage of their orthologous genes in

The break in the continuity of the linkage groups indicates a lack of detectable linkage between the groups.<p><b>Copyright information:</b></p><p>Taken from "Comparative genome mapping of the deer mouse () reveals greater similarity to rat () than to the lab mouse ()"</p><p>http://www.biomedcentral.com/1471-2148/8/65</p><p>BMC Evolutionary Biology 2008;8():65-65.</p><p>Published online 26 Feb 2008</p><p>PMCID:PMC2266908.</p><p></p

Comparison of the organization of genes on Chrs 1 and 2, and Chr 13, with the linkage of their orthologous genes in

The break in the continuity of the linkage groups indicates a lack of detectable linkage between the groups.<p><b>Copyright information:</b></p><p>Taken from "Comparative genome mapping of the deer mouse () reveals greater similarity to rat () than to the lab mouse ()"</p><p>http://www.biomedcentral.com/1471-2148/8/65</p><p>BMC Evolutionary Biology 2008;8():65-65.</p><p>Published online 26 Feb 2008</p><p>PMCID:PMC2266908.</p><p></p

Comparison of the organization of genes on Chrs 16, 17, and 19, and Chrs 2 and 8, with the linkage of their orthologous genes in

The break in the continuity of the linkage groups indicates a lack of detectable linkage between the groups.<p><b>Copyright information:</b></p><p>Taken from "Comparative genome mapping of the deer mouse () reveals greater similarity to rat () than to the lab mouse ()"</p><p>http://www.biomedcentral.com/1471-2148/8/65</p><p>BMC Evolutionary Biology 2008;8():65-65.</p><p>Published online 26 Feb 2008</p><p>PMCID:PMC2266908.</p><p></p

Comparison of the organization of genes on Chrs 4, 6, 12, 14, and 19, and Chr 5 with the linkage of their orthologous genes in

The break in the continuity of the linkage groups indicates a lack of detectable linkage between the groups.<p><b>Copyright information:</b></p><p>Taken from "Comparative genome mapping of the deer mouse () reveals greater similarity to rat () than to the lab mouse ()"</p><p>http://www.biomedcentral.com/1471-2148/8/65</p><p>BMC Evolutionary Biology 2008;8():65-65.</p><p>Published online 26 Feb 2008</p><p>PMCID:PMC2266908.</p><p></p

The addition of depression to the Framingham Risk Equation model for predicting coronary heart disease risk in women

BACKGROUND: Depression is widely considered to be an independent and robust predictor of Coronary Heart Disease (CHD), however is seldom considered in the context of formal risk assessment. We assessed whether the addition of depression to the Framingham Risk Equation (FRE) improved accuracy for predicting 10-year CHD in a sample of women. DESIGN: A prospective, longitudinal design comprising an age-stratified, population-based sample of Australian women collected between 1993 and 2011 (n=862). METHODS: Clinical depressive disorder was assessed using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders (SCID-I/NP), using retrospective age-of-onset data. A composite measure of CHD included non-fatal myocardial infarction, unstable angina coronary intervention or cardiac death. Cox proportional-hazards regression models were conducted and overall accuracy assessed using area under receiver operating characteristic (ROC) curve analysis. RESULTS: ROC curve analyses revealed that the addition of baseline depression status to the FRE model improved its overall accuracy (AUC:0.77, Specificity:0.70, Sensitivity:0.75) when compared to the original FRE model (AUC:0.75, Specificity:0.73, Sensitivity:0.67). However, when calibrated against the original model, the predicted number of events generated by the augmented version marginally over-estimated the true number observed. CONCLUSIONS: The addition of a depression variable to the FRE equation improves the overall accuracy of the model for predicting 10-year CHD events in women, however may over-estimate the number of events that actually occur. This model now requires validation in larger samples as it could form a new CHD risk equation for women