Project description:Cross-generational and cross-dialectal variation in vowels among speakers of American English was examined in terms of vowel identification by listeners and vowel classification using pattern recognition. Listeners from Western North Carolina and Southeastern Wisconsin identified 12 vowel categories produced by 120 speakers stratified by age (old adults, young adults, and children), gender, and dialect. The vowels /ɝ, o, ʊ, u/ were well identified by both groups of listeners. The majority of confusions were for the front /i, ɪ, e, ɛ, æ/, the low back /ɑ, ɔ/ and the monophthongal North Carolina /aɪ/. For selected vowels, generational differences in acoustic vowel characteristics were perceptually salient, suggesting listeners' responsiveness to sound change. Female exemplars and native-dialect variants produced higher identification rates. Linear discriminant analyses which examined dialect and generational classification accuracy showed that sampling the formant pattern at vowel midpoint only is insufficient to separate the vowels. Two sample points near onset and offset provided enough information for successful classification. The models trained on one dialect classified the vowels from the other dialect with much lower accuracy. The results strongly support the importance of dynamic information in accurate classification of cross-generational and cross-dialectal variations.
Project description:Attention-deficit/hyperactivity disorder (ADHD) predisposes to drug abuse (DA) and twin studies suggest shared genetic effects. We here seek to determine, using adoption and adoption-like samples, the magnitude of the cross-generational transmission from DA in parents to ADHD in their children and clarify the degree to which this arises from genetic v. rearing effects.We ascertained ADHD and DA from multiple Swedish registries. Statistical analysis was performed by Cox and path models.Risk for ADHD was significantly and similarly increased in the offspring of biological mothers and fathers with DA who did v. did not rear their offspring. Risk for ADHD was not elevated in the offspring of adoptive or step-parents with DA.Cross-generational transmission was observed from DA in parents to ADHD in their children. An analysis of adoptive and adoptive-like parent-offspring relationships suggested that this transmission results from genetic and not from rearing effects.
Project description:The importance of trans-generational effects in shaping an individuals' phenotype and fitness, and consequently even impacting population dynamics is increasingly apparent. Most of the research on trans-generational effects still focuses on plants, mammals, and birds. In the past few years, however, increasing number of studies, especially on maternal effects, have highlighted their importance also in many insect systems. Lepidoptera, specifically butterflies, have been used as model systems for studying the role of phenotypic plasticity within generations. As ectotherms, they are highly sensitive to environmental variation, and indeed many butterflies show adaptive phenotypic plasticity in response to environmental conditions. Here, we synthesize what is known about trans-generational effects in Lepidoptera, compile evidence for different environmental cues that are important drivers of trans-generational effects, and point out which offspring traits are mainly impacted. Finally, we emphasize directions for future research that are needed for better understanding of the adaptive nature of trans-generational effects in Lepidoptera in particular, but potentially also in other organisms.
Project description:Vietnamese Living Standard Surveys showed that the rate of overweight and obese in Vietnamese adults doubled between 1992 and 2002, from 2% to 5.5%, respectively with no significant difference in the proportions of overweight/obesity between men and women.Considering the increasing public health concern over the double burden of malnutrition in Vietnam, we investigated micronutrient deficiencies among women of reproductive age according to their Body Mass Index.A transversal study was conducted in 2010 among 1530 women of reproductive age from 19 provinces. Participating women were asked to give a non-fasting blood sample for plasma iron, vitamin A, folate, vitamin B12 and zinc assessment.Although % body fat was associated with haemoglobin, ferritin, retinol and zinc concentrations, BMI category was only associated with marginal vitamin A status (19% among underweight vs 7% among overweight/obese; p<0.0001) and not with iron deficiency anemia, zinc deficiency, vitamin B12 deficiency or folate status. The prevalence of iron, and vitamin B12 deficiencies was respectively 11.4% and 15% among the 20% overweight/obese women; prevalence of zinc deficiency and marginal/deficient folate status was much higher, affecting respectively 61.1% and 25.8%. Intra-individual double burden of malnutrition (overweight/obesity (OW) and micronutrient deficiency) was observed among 2.0% for OW-anemia, 2.3% OW-iron deficient, 3.0% for OW-Vitamin B12 deficiency, 12.2% for OW-Zinc deficiency and 5.2% for OW-marginal/deficient folate status.This large, cross-sectional survey demonstrated that micronutrient deficiencies are an issue across the weight spectrum among women in Vietnam, with only vitamin A status being better among overweight than underweight women. It is therefore essential for Vietnam to actively prevent women of reproductive age from overweight/obesity and at same time to control micronutrient deficiencies in this population to limit their economic and health consequences.
Project description:Extensive research shows that dietary variation and toxicant exposure impact the gut microbiome, yielding effects on host physiology. However, prior work has mostly considered such exposure-microbiome interactions through the lens of single-factor exposures. In practice, humans exposed to toxicants vary in their dietary nutritional status, and this variation may impact subsequent exposure of the gut microbiome. For example, chronic arsenic exposure affects 200 million people globally and is often comorbid with zinc deficiency. Zinc deficiency can enhance arsenic toxicity, but it remains unknown how zinc status impacts the gut microbiome's response to arsenic exposure and whether this response links to host toxicity. Using 16S amplicon sequencing, we examined the combinatorial effects of exposure to environmentally relevant concentrations of arsenic on the composition of the microbiome in C57BL/6 mice fed diets varying in zinc concentration. Arsenic exposure and marginal zinc deficiency independently altered microbiome diversity. When combined, their effects on microbiome community structure were amplified. Generalized linear models identified microbial taxa whose relative abundance in the gut was perturbed by zinc deficiency, arsenic, or their interaction. Further, we correlated taxonomic abundances with host DNA damage, adiponectin expression, and plasma zinc concentration to identify taxa that may mediate host physiological responses to arsenic exposure or zinc deficiency. Arsenic exposure and zinc restriction also result in increased DNA damage and decreased plasma zinc. These physiological changes are associated with the relative abundance of several gut taxa. These data indicate that marginal zinc deficiency sensitizes the microbiome to arsenic exposure and that the microbiome associates with some toxicological effects of arsenic.IMPORTANCE Xenobiotic compounds, such as arsenic, have the potential to alter the composition and functioning of the gut microbiome. The gut microbiome may also interact with these compounds to mediate their impact on the host. However, little is known about how dietary variation may reshape how the microbiome responds to xenobiotic exposures or how these modified responses may in turn impact host physiology. Here, we investigated the combinatorial effects of marginal zinc deficiency and physiologically relevant concentrations of arsenic on the microbiome. Both zinc deficiency and arsenic exposure were individually associated with altered microbial diversity and when combined elicited synergistic effects. Microbial abundance also covaried with host physiological changes, indicating that the microbiome may contribute to or be influenced by these pathologies. Collectively, this work demonstrates that dietary zinc intake influences the sensitivity of the microbiome to subsequent arsenic exposure.
Project description:Trans-generational maternal effects have been shown to influence a broad range of offspring phenotypes. However, very little is known about paternal trans-generational effects. Here, we tested the trans-generational effects of maternal and paternal age, and their interaction, on daughter and son reproductive fitness in Drosophila melanogaster. We found significant effects of parent ages on offspring reproductive fitness during a 10 day postfertilization period. In daughters, older (45 days old) mothers conferred lower reproductive fitness compared with younger mothers (3 days old). In sons, father's age significantly affected reproductive fitness. The effects of 2 old parents were additive in both sexes and reproductive fitness was lowest when the focal individual had 2 old parents. Interestingly, daughter fertility was sensitive to father's age but son fertility was insensitive to mother's age, suggesting a sexual asymmetry in trans-generational effects. We found the egg-laying dynamics in daughters dramatically shaped this relationship. Daughters with 2 old parents demonstrated an extreme egg dumping behavior on day 1 and laid >2.35× the number of eggs than the other 3 age class treatments. Our study reveals significant trans-generational maternal and paternal age effects on fertility and an association with a novel egg laying behavioral phenotype in Drosophila.
Project description:Marginal deficiency of vitamin B-6 is common among segments of the population worldwide. Because pyridoxal 5'-phosphate (PLP) serves as a coenzyme in the metabolism of amino acids, carbohydrates, organic acids, and neurotransmitters, as well as in aspects of one-carbon metabolism, vitamin B-6 deficiency could have many effects. Healthy men and women (age: 20-40 y; n?=?23) were fed a 2-day controlled, nutritionally adequate diet followed by a 28-day low-vitamin B-6 diet (<0.5 mg/d) to induce marginal deficiency, as reflected by a decline of plasma PLP from 52.6±14.1 (mean ± SD) to 21.5±4.6 nmol/L (P<0.0001) and increased cystathionine from 131±65 to 199±56 nmol/L (P<0.001). Fasting plasma samples obtained before and after vitamin B6 restriction were analyzed by (1)H-NMR with and without filtration and by targeted quantitative analysis by mass spectrometry (MS). Multilevel partial least squares-discriminant analysis and S-plots of NMR spectra showed that NMR is effective in classifying samples according to vitamin B-6 status and identified discriminating features. NMR spectral features of selected metabolites indicated that vitamin B-6 restriction significantly increased the ratios of glutamine/glutamate and 2-oxoglutarate/glutamate (P<0.001) and tended to increase concentrations of acetate, pyruvate, and trimethylamine-N-oxide (adjusted P<0.05). Tandem MS showed significantly greater plasma proline after vitamin B-6 restriction (adjusted P<0.05), but there were no effects on the profile of 14 other amino acids and 45 acylcarnitines. These findings demonstrate that marginal vitamin B-6 deficiency has widespread metabolic perturbations and illustrate the utility of metabolomics in evaluating complex effects of altered vitamin B-6 intake.
Project description:BACKGROUND: The etiology of myelodysplastic syndromes (MDS) is largely unknown. Exposure to cigarette smoke (CS) is reported to be associated with MDS risk. There is inconsistent evidence that deficiency of NAD(P)H-quinone: oxidoreductase 1 (NQO1) increases the risk of MDS. Earlier we had shown that CS induces toxicity only in marginal vitamin C-deficient guinea pigs but not in vitamin C-sufficient ones. We therefore considered that NQO1 deficiency along with marginal vitamin C deficiency might produce MDS in CS-exposed guinea pigs. METHODOLOGY AND PRINCIPAL FINDINGS: Here we show that CS exposure for 21 days produces MDS in guinea pigs having deficiency of NQO1 (fed 3 mg dicoumarol/day) conjoint with marginal vitamin C deficiency (fed 0.5 mg vitamin C/day). As evidenced by morphology, histology and cytogenetics, MDS produced in the guinea pigs falls in the category of refractory cytopenia with unilineage dysplasia (RCUD): refractory anemia; refractory thrombocytopenia that is associated with ring sideroblasts, micromegakaryocytes, myeloid hyperplasia and aneuploidy. MDS is accompanied by increased CD34(+) cells and oxidative stress as shown by the formation of protein carbonyls and 8-oxodeoxyguanosine. Apoptosis precedes MDS but disappears later with marked decrease in the p53 protein. MDS produced in the guinea pigs are irreversible. MDS and all the aforesaid pathophysiological events do not occur in vitamin C-sufficient guinea pigs. However, after the onset of MDS vitamin C becomes ineffective. CONCLUSIONS AND SIGNIFICANCE: CS exposure causes MDS in guinea pigs having deficiency of NQO1 conjoint with marginal vitamin C deficiency. The syndromes are not produced in singular deficiency of NQO1 or marginal vitamin C deficiency. Our results suggest that human smokers having NQO1 deficiency combined with marginal vitamin C deficiency are likely to be at high risk for developing MDS and that intake of a moderately large dose of vitamin C would prevent MDS.
Project description:Human-assisted, trans-generational exposure to ocean warming and acidification has been proposed as a conservation and/or restoration tool to produce resilient offspring. To improve our understanding of the need for and the efficacy of this approach, we characterized life-history and physiological responses in offspring of the marine polychaete Ophryotrocha labronica exposed to predicted ocean warming (OW: + 3°C), ocean acidification (OA: pH -0.5) and their combination (OWA: + 3°C, pH -0.5), following the exposure of their parents to either control conditions (within-generational exposure) or the same conditions (trans-generational exposure). Trans-generational exposure to OW fully alleviated the negative effects of within-generational exposure to OW on fecundity and egg volume and was accompanied by increased metabolic activity. While within-generational exposure to OA reduced juvenile growth rates and egg volume, trans-generational exposure alleviated the former but could not restore the latter. Surprisingly, exposure to OWA had no negative impacts within- or trans-generationally. Our results highlight the potential for trans-generational laboratory experiments in producing offspring that are resilient to OW and OA. However, trans-generational exposure does not always appear to improve traits and therefore may not be a universally useful tool for all species in the face of global change.
Project description:Recent clinical studies have provided evidence that marginal biotin deficiency is more common than previously thought. The validity of that conclusion rests on two indicators of biotin status that depend on renal function. Our goal was to develop and assess the usefulness of two additional indicators in detecting marginal biotin status in a rat model, i.e., 1) activity of the biotin-dependent enzyme propionyl-CoA carboxylase in lymphocytes; and 2) urinary excretion of 3-hydroxypropionic acid, an organic acid that reflects decreased activity of propionyl-CoA carboxylase. Marginal-to-moderate biotin deficiency was induced experimentally by an egg-white diet (deficient rats); the biotin-supplemented rats were fed the egg-white diet plus supplemental biotin. Propionyl-CoA carboxylase activity was determined by an optimized H(14)CO(3)(-) incorporation assay. Urinary organic acids were determined by gas chromatography/mass spectrometry. Lymphocyte propionyl-CoA carboxylase activity decreased dramatically and in parallel with hepatic propionyl-CoA carboxylase activity. By d 7, lymphocyte propionyl-CoA carboxylase activity in each rat in the deficient group had decreased to less than the lowest value of any rat on d 0. By two-way ANOVA, the effects of diet (P < 0.0001), time (P < 0.005) and their interaction (P < 0.0001) were all significant. The urinary excretion of 3-hydroxypropionic acid did not differ between the two groups. Lymphocyte propionyl-CoA carboxylase activity is an early and sensitive indicator of marginal biotin deficiency, whereas the urinary excretion of 3-hydroxypropionic acid is not.