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Goldblatt D Hussain M Andrews N Ashton L Virta C Melegaro A Pebody R George R Soininen A Edmunds J Gay N Kayhty H Miller E 《The Journal of infectious diseases》2005,192(3):387-393
BACKGROUND: Natural immunity to Streptococcus pneumoniae is thought to be induced by exposure to S. pneumoniae or cross-reactive antigens. No longitudinal studies of carriage of and immune responses to S. pneumoniae have been conducted using sophisticated immunological laboratory techniques. METHODS: We enrolled 121 families with young children into this study. Nasopharyngeal (NP) swabs were collected monthly for 10 months from all family members and were cultured in a standard fashion. Cultured S. pneumoniae isolates were serotyped. At the beginning (month 0) and end (month 10) of the study, venous blood was collected from family members >18 years old. Serotype-specific antipolysaccharide immunoglobulin G (IgG) and functional antibody and antibodies to pneumolysin, pneumococcal surface protein A (PspA), and pneumococcal surface antigen A (PsaA) were measured in paired serum samples. RESULTS: Levels of anticapsular IgG increased significantly after carriage of serotypes 9V, 14, 18C, 19F, and 23F by an individual or family member. For serotype 14, a higher level of anticapsular IgG at the beginning of the study was associated with reduced odds of carriage (P = .006). There was a small (approximately 20%) but significant increase in titers of antibodies to PsaA and pneumolysin but no change in titers of antibody to PspA. CONCLUSIONS: Adults respond to NP carriage by mounting anticapsular and weak antiprotein antibody responses, and naturally induced anticapsular IgG can prevent carriage. 相似文献
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Matthew D. Edwards Anna Symbor-Nagrabska Lindsey Dollard David K. Gifford Gerald R. Fink 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(21):7719-7722
The measurement of any nonchromosomal genetic contribution to the heritability of a trait is often confounded by the inability to control both the chromosomal and nonchromosomal information in a population. We have designed a unique system in yeast where we can control both sources of information so that the phenotype of a single chromosomal polymorphism can be measured in the presence of different cytoplasmic elements. With this system, we have shown that both the source of the mitochondrial genome and the presence or absence of a dsRNA virus influence the phenotype of chromosomal variants that affect the growth of yeast. Moreover, by considering this nonchromosomal information that is passed from parent to offspring and by allowing chromosomal and nonchromosomal information to exhibit nonadditive interactions, we are able to account for much of the heritability of growth traits. Taken together, our results highlight the importance of including all sources of heritable information in genetic studies and suggest a possible avenue of attack for finding additional missing heritability.A fundamental problem in genetics is unraveling the link between genotype and phenotype. Ascertaining the heritability of a trait is a key step toward harnessing the predictive capacity of genetic information for human disease risk assessment and therapy (1). Knowledge of all of the elements contributing to heritability would facilitate the establishment of a causal relationship between the information that is passed down from generation to generation and the resulting phenotype. Genome-wide association studies (GWASs) have successfully identified many human polymorphisms that are associated with traits such as height, eye color, or susceptibility to common diseases, but these variants typically explain only a small proportion of the observed heritability of a trait (2, 3).A number of explanations for missing heritability have been suggested (2), including the existence of many weak variants with effects too small to achieve statistical significance (4), interactions between variants that cannot be identified with current studies (5), rare variants that were not identified by GWAS, and epigenetic effects (6–8). The contribution of nonchromosomal information to the missing heritability is rarely considered, despite the fact that there is a long history documenting the effect in many organisms of diverse cytoplasmic elements on phenotype. Recent work on a mouse model of Crohn disease supports a combinatorial model of complex disease traits in which the pathology requires the interaction between a specific mutation in the mouse and a specific strain of virus (9). Another recent study showed strong effects on the plant metabolome stemming from variation in mitochondrial and chloroplast genomes (10). In humans, the importance of nonchromosomal information has been supported by targeted analyses, but these studies have not analyzed its impact on heritability in a well-controlled context (11–13). Such nonchromosomal interactions might help explain why shared mutations in humans do not always produce the same phenotype, thus reducing the apparent heritability of a trait (14, 15).We sought to characterize explicitly how nonchromosomal modifiers collectively influence the heritability of a trait, colony size, in a system unique to yeast where we use a defined chromosomal genotype and vary the cytoplasmic genetic information. Yeast has at least four well-studied sources of inherited, nonchromosomal information: mitochondrial DNA, an endogenous dsRNA virus (16, 17), prions (18, 19), and a 2µ plasmid (20, 21).Our results show that the nonchromosomal contribution to heritability can be large, adding another dimension to the estimation of heritability in wild populations. Nonchromosomal information is not under the usual constraints of the nuclear genome. These nonchromosomal elements are extremely unstable: they mutate at higher frequencies than the DNA of the chromosomal genome, may be lost at high frequencies without loss of viability, and can vary in copy number from cell to cell. Thus, careful controls and measurements are necessary to characterize the effects of nonchromosomal modifiers. 相似文献
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Lindsey A. Greene Siqi Chen Caroline Seery Allison M. Imahiyerobo James B. Bussel 《British journal of haematology》2014,166(4):592-600
Platelet counts (PC) estimate bleeding risk in Immune Thrombocytopenia (ITP). We investigated whether measures of thromboelastometry and absolute immature platelet fraction (A‐IPF) would correlate better with acute bleeding score (ABS) than PC or mean platelet volume (MPV). Simultaneous determination of ABS, complete blood count and thromboelastometry was performed in 141 ITP patients; 112 underwent A‐IPF testing. Subgroup analyses were performed for paediatric subjects, PC <60 × 109/l and <30 × 109/l. PC significantly inversely correlated with ABS in all subjects, PC <30 × 109/l and total paediatric cohort. MPV did not correlate with ABS in any subgroup. Thromboelastometry measures of clot firmness, but not PC, significantly correlated with ABS in all subjects with PC <60 × 109/l, and children with PC <60 × 109/l and <30 × 109/l. A‐IPF demonstrated stronger correlation with ABS than did PC among all subjects, those with PC <60 × 109/l, all children and children with PC <30 × 109/l (r = ?0·37; r = ?0·34; r = ?0·44; r = ?0·60) versus ABS with PC (r = ?0·36; ns; r = ?0·32; ns). Stronger correlations of both thromboelastometry measures of clot firmness and A‐IPF than PC with ABS suggest factors beyond PC, i.e. related to platelet function, contribute to ITP bleeding pathophysiology. Thromboelastometry, A‐IPF and ABS can be incorporated into routine or acute visits. 相似文献
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Vivek Pillai Lindsey A. Steenburg Jeffrey A. Ciesla Thomas Roth Christopher L. Drake 《Journal of psychosomatic research》2014
Objectives
Trait ruminators exhibit significantly higher levels of sleep disturbance than those without this cognitive vulnerability. However, support for the sleep disruptive effects of state rumination, especially in the pre-sleep period, is rare, and hindered by methodological drawbacks such as self-report and single night assays of sleep. Finally, despite the pervasiveness of the ruminative response style among individuals with depression, the association between rumination and sleep disturbance has not been explored in this population. The present study employed a week-long daily sampling approach to examine the effects of naturally occurring pre-sleep rumination on self-reported and actigraphy-based sleep among individuals with high depressive symptomatology.Methods
Forty-two university students (19.6 ± 3.2 yo;73.8% female), all of whom reported at least moderate levels of depressive symptoms, completed a short questionnaire after waking each morning for seven days. On this questionnaire, they self-reported sleep indices from the previous night and levels of engagement in pre-sleep rumination. Sleep was also monitored throughout this period via wrist actigraphy. Hierarchical-linear-modeling was used to examine the association between nightly rumination and sleep.Results
Nightly variations in pre-sleep rumination were predictive of significantly longer actigraphy- and diary-based sleep onset latency (SOL). Notably, a 1 SD increase on the pre-sleep rumination scale was associated with an approximately 7 minute increase in actigraphy-based SOL, even after controlling for baseline sleep disturbance and depressive symptoms.Conclusions
These data offer compelling evidence for the impact of pre-sleep rumination on sleep onset, providing insight into one potential mechanism that triggers sleep disturbance among individuals with depressive symptoms. 相似文献70.
KA Pennington JL Harper AN Sigafoos LM Beffa SM Carleton CL Phillips LC Schulz 《Endocrinology》2012,153(9):4556-4567
Metabolic disease is a significant global health and economic problem. In a phenomenon referred to as fetal programming, offspring of underweight or overweight mothers have an increased incidence of adulthood obesity and metabolic disease. Undernourished individuals have decreased levels of leptin, a regulator of energy balance, whereas obese people develop hyperleptinemia and leptin resistance. We hypothesize that alterations in circulating leptin during pregnancy contribute to programming events caused by maternal nutritional status. To test this hypothesis, pregnant mice were randomly placed in one of three treatment groups: ad libitum feed plus saline injection (control, n = 5), 50% food restriction plus saline injection (restricted, n = 4), or 50% food restriction plus 1 mg/kg·d leptin injection (restricted, leptin treated, n = 4). Mice were treated from 1.5 to 11.5 d after conception and then returned to ad libitum feeding until weaning. At 19 wk after weaning, offspring were placed on a 45% fat diet and then followed up until 26 wk after weaning, at which time they were killed, and samples were collected for further analysis. Our results demonstrate that males are more negatively impacted by high-fat diet than females, regardless of maternal treatment. We provide evidence that differential response to leptin may mediate the sexual dimorphism observed in fetal programming in which male offspring are more affected by maternal undernutrition and female offspring by maternal overnutrition. We show that female offspring born to food-restricted, leptin-supplemented mothers are obese and insulin resistant. This may mimic fetal programming events seen in offspring of overweight women. 相似文献