Age- and sex-adjusted SNP two-point VC analyses for quantitative trait ttth1 on chromosome 7

<p><b>Copyright information:</b></p><p>Taken from "Comparison of the power between microsatellite and single-nucleotide polymorphism markers for linkage and linkage disequilibrium mapping of an electrophysiological phenotype"</p><p></p><p>BMC Genetics 2005;6(Suppl 1):S7-S7.</p><p>Published online 30 Dec 2005</p><p>PMCID:PMC1866712.</p><p></p

Microsatellite marker multipoint VC analyses for quantitative trait ttth1 on chromosome 7

<p><b>Copyright information:</b></p><p>Taken from "Comparison of the power between microsatellite and single-nucleotide polymorphism markers for linkage and linkage disequilibrium mapping of an electrophysiological phenotype"</p><p></p><p>BMC Genetics 2005;6(Suppl 1):S7-S7.</p><p>Published online 30 Dec 2005</p><p>PMCID:PMC1866712.</p><p></p

Multipoint variance-component linkage analysis results with outliers for time points 1970, 1978, 1986, and mean BMI of the three exams

<p><b>Copyright information:</b></p><p>Taken from "Comparison of the linkage results of two phenotypic constructs from longitudinal data in the Framingham Heart Study: analyses on data measured at three time points and on the average of three measurements"</p><p>http://www.biomedcentral.com/1471-2156/4/s1/S20</p><p>BMC Genetics 2003;4(Suppl 1):S20-S20.</p><p>Published online 31 Dec 2003</p><p>PMCID:PMC1866455.</p><p></p> LOD scores on chromosomes 3, 6, 9, and 16 were calculated by the SOLAR version 1.7.4 software package

Table1_25-hydroxyvitamin D levels in children of different ages and with varying degrees of Helicobacter pylori infection and immunological features.docx

BackgroundHelicobacter pylori (HP) is a major cause of upper digestive tract diseases. However, the relationship between HP infection and 25-hydroxyvitamin D [25(OH)D] levels in children has not been fully elucidated. This study investigated the levels of 25(OH)D in children of different ages and with varying degrees of HP infection and immunological features as well as the correlations between 25(OH)D levels in children infected with HP and their ages and degrees of infection.Materials and methodsNinety-four children who underwent upper digestive endoscopy were divided into an HP-positive group without peptic ulcers (Group A), an HP-positive group with peptic ulcers (Group B) and an HP-negative control group (Group C). The serum levels of 25(OH)D and immunoglobulin and the percentages of lymphocyte subsets were determined. HP colonization, the degree of inflammation, and the degree of activity were further evaluated by HE staining and immunohistochemical staining in gastric mucosal biopsy.ResultsThe 25(OH)D level of the HP-positive groups (50.93 ± 16.51 nmol/L) was significantly lower than that of the HP-negative group (62.89 ± 19.18 nmol/L). The 25(OH)D level of Group B (47.79 ± 14.79 nmol/L) was lower than that of Group A (51.53 ± 17.05 nmol/L) and was significantly lower than that of Group C (62.89 ± 19.18 nmol/L). The 25(OH)D level decreased with increasing age, and there was a significant difference between Group C subjects who were ≤5 years old and those who were aged 6–9 years and ≥10 years. The 25(OH)D level was negatively correlated with HP colonization (r = −0.411, P ConclusionsThe 25(OH)D level was negatively correlated with HP colonization and the degree of inflammation. As the age of the children increased, the level of 25(OH)D decreased, and the susceptibility to HP infection increased.</p

brain_231sample.ped

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brain_231_sample_ageatdeath_covariate

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brain_231sample_genotype_data_with_key

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Comparative lipid profile of post-mortem brain tissue obtained from patients diagnosed with various neurological conditions.

<p>Comparative lipid profile of post-mortem brain tissue obtained from patients diagnosed with various neurological conditions. The individual lipid subclasses of each group of patients was expressed as relative to control group levels for 2 separate sets of experiments (<i>i</i>.<i>e</i>. AD and LBD GBA mutation carrier relative to Control S1, LBD non carrier (wildtype) relative to Control S2). Statistical analysis for the AD and LBD Mutation samples was based on the one way analysis of variance followed by post hoc Fisher’s least significant difference test while the LBD non carrier (wildtype) samples was based on Student’s T-test. A false discovery rate control was used to correct for multiple comparisons. * <i>q</i><0.05, ** <i>q</i><0.01, *** <i>q</i><0.001. PC, phosphatidylcholine; ePC, ether phosphatidylcholine; PE, phosphatidylethanolamine; pPE, plasmalogen phosphatidylethanolamine; PS, phosphatidylserine; PI, phosphatidylinositol; PA, phosphatidic acid; PG, phosphatidylglycerol; LBPA, lysobisphosphatidic acid; Cer, ceramide; SM, sphingomyelin; dhSM, dihydrosphingomyelin; GalCer, galactosylceramide; GluCer, glucosylceramide; Sulf, sulfatide; Sulf-h, hydroxylated sulfatide; GM3, monosialodihexosylganglioside</p

GCase and HexA activity in autopsy brain tissue.

<p>A) GCase activity was significantly reduced in LBD cases carrying <i>GBA</i> mutations (n = 16) compared to LBD non-<i>GBA</i> carriers (n = 18) and controls (n = 30). Differences in activity for <i>HEXA</i> were not significant in any group. B) GCase was significantly reduced in LBD cases with mutations classified as ‘severe’ type (L444P, 84insGG etc.) compared to controls, and to LBD cases with ‘mild’ mutations (N370S) or variants of unknown phenotypic effect (E326K, T369M). Differences in activity for <i>HEXA</i> were not significant. * <i>p</i><0.05, ** <i>p</i><0.01, *** <i>p</i><0.001.</p

Heat Maps showing significant changes in lipid classes.

<p>A) Heat map showing statistically significant changes in major lipid subclasses in LBD <i>GBA</i> mutation carriers compared to LBD wildtype, AD cases and controls and <b>B)</b> Heat map showing statistically significant changes in lipid classes in LBD <i>GBA</i> mutation carriers compared to LBD wildtype, AD cases and controls. The heat map columns reflect all significant lipid changes (<i>q</i><0.05) in a diseased compared to control patients. The color bar represents the log2 value of the ratio of each lipid species. Statistical analysis for the AD and LBD Mutation samples was based on the one way analysis of variance followed by post hoc Fisher’s least significant difference test while the LBD (wildtype) samples was based on Student’s T-test. A false discovery rate control was used to correct for multiple comparisons.</p