16 research outputs found

    Anatomy and Histology of the Male Reproductive Complex of the Onion Maggot Fly, \u3ci\u3eDelia Antiqua\u3c/i\u3e, (Diptera: Anthomyiidae) Including Some Comparisons With \u3ci\u3eD. Platura\u3c/i\u3e and \u3ci\u3eD. Radicum\u3c/i\u3e

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    In Delia antiqua (Meigen) (Diptera: Anthomyiidae), the male reproductive complex is composed of a pair of testes, paired vas deferens connecting the testes to the anterior ejaculatory duct, and a pair of paragonial (accessory) glands. Each D. antiqua paragonial gland consists of a single layer of secretory epithelial cells surrounded by a thin sheath of muscle tissue. The paragonial cells appear to be largely homogeneous in form, however a minor number of cells exhibit unique staining characteristics distinct from the main cells of the gland. This is preliminary evidence for a secondary cell type as has been found for Drosophila and Aedes paragonial glands. In contrast to the testis and vas deferens, where most of the growth occurs during the pupal stage, the D. antiqua paragonial glands expanded markedly due to secretory accumulation during the first days of adult life. Based on histochemical analyses, the paragonial secretion contained abundant protein, with evidence of glycoprotein. The reproductive complex in all three Delia species (D. antiqua, D. radicum (Bouche) and D. platura (Meigen)) appears similar, with the exception of size differences and timing of paragonial secretory accumulation and sperm maturation. Paragonial glands of D. radicum were the largest in both length and width, and only this species possessed abundant sperm upon eclosion. Of the three species, D. radicum appears most capable of mating immediately after eclosion based on the histology of its reproductive complex, which is consistent with biochemical and behavioral observations made earlier in this laboratory

    An Allometric Study of the Boxelder Bug, \u3ci\u3eBoisea Trivittata\u3c/i\u3e (Heteroptera: Rhopalidae)

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    An allometric study was conducted on the boxelder bug, Boisea trivittata, to confirm the number ofinstars and to identify characteristics most useful for rapid instar identification of field samples. Analysis of field populations collected throughout the 1990-92 seasons indicated that there were five instars, clearly defined on the basis of size and the presence of wing pads. This finding is in contrast with the only other published study on stages of the boxelder bug, which claims there are six nymphal instars. Size data gathered from field populations were substantiated by laboratory growth studies. Head width and/or second antennal segment length were identified as the most useful parameters for instar identification

    Egg Production in the Boxelder Bug \u3ci\u3eBoisea Trivittata\u3c/i\u3e (Hemiptera: Rhopalidae)

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    Boxelder bug females emerged from overwintering sites in the spring and rapidly provisioned eggs with yolk materials. Five discrete egg stages were identified based on egg size, protein content, and degree of chorion sclerotization. Females did not accumulate yolk materials into the egg until after melanization was completed, as unmelanized animals rarely possessed even stage 2 eggs. All adult females entering overwintering sites possessed only immature stage eggs (stage 1 and 2). The rate of egg vitellogenesis in the spring was rapid; a major change in numbers of more mature stage eggs (stage 3 and above) in the ovary occurred within approximately 6 days. Most mating pairs recovered in the field (92%, 12/13) possessed ovaries full of eggs in stages 3, 4 or 5. The remaining female contained only immature eggs of stage 1 and 2. This finding indicates that fully provisioned ovaries are not an absolute requirement for mating to occur. The signals that initiate vitellogenesis and control the movement of materials from fat body into eggs are unknown for the boxelder bug

    Egg Production in the Boxelder Bug \u3ci\u3eBoisea Trivittata\u3c/i\u3e (Hemiptera: Rhopalidae)

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    Boxelder bug females emerged from overwintering sites in the spring and rapidly provisioned eggs with yolk materials. Five discrete egg stages were identified based on egg size, protein content, and degree of chorion sclerotization. Females did not accumulate yolk materials into the egg until after melanization was completed, as unmelanized animals rarely possessed even stage 2 eggs. All adult females entering overwintering sites possessed only immature stage eggs (stage 1 and 2). The rate of egg vitellogenesis in the spring was rapid; a major change in numbers of more mature stage eggs (stage 3 and above) in the ovary occurred within approximately 6 days. Most mating pairs recovered in the field (92%, 12/13) possessed ovaries full of eggs in stages 3, 4 or 5. The remaining female contained only immature eggs of stage 1 and 2. This finding indicates that fully provisioned ovaries are not an absolute requirement for mating to occur. The signals that initiate vitellogenesis and control the movement of materials from fat body into eggs are unknown for the boxelder bug

    Effect of genetically low 25-hydroxyvitamin D on mortality risk: Mendelian randomization analysis in 3 large European cohorts

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    Source at https://doi.org/10.3390/nu11010074.The aim of this study was to determine if increased mortality associated with low levels of serum 25-hydroxyvitamin D (25(OH)D) reflects a causal relationship by using a Mendelian randomisation (MR) approach with genetic variants in the vitamin D synthesis pathway. Individual participant data from three European cohorts were harmonized with standardization of 25(OH)D according to the Vitamin D Standardization Program. Most relevant single nucleotide polymorphisms of the genes CYP2R1 (rs12794714, rs10741657) and DHCR7/NADSYN1 (rs12785878, rs11234027), were combined in two allelic scores. Cox proportional hazards regression models were used with the ratio estimator and the delta method for calculating the hazards ratio (HR) and standard error of genetically determined 25(OH)D effect on all-cause mortality. We included 10,501 participants (50.1% females, 67.1±10.1 years) of whom 4003 died during a median follow-up of 10.4 years. The observed adjusted HR for all-cause mortality per decrease in 25(OH)D by 20 nmol/L was 1.20 (95% CI: 1.15–1.25). The HR per 20 nmol/L decrease in genetically determined 25(OH)D was 1.32 (95% CI: 0.80–2.24) and 1.35 (95% CI of 0.81 to 2.37) based on the two scores. In conclusion, the results of this MR study in a combined sample from three European cohort studies provide further support for a causal relationship between vitamin D deficiency and increased all-cause mortality. However, as the current study, even with ~10,000 participants, was underpowered for the study of the effect of the allele score on mortality, larger studies on genetics and mortality are needed to improve the precision

    Vitamin D and mortality: Individual participant data meta-analysis of standardized 25-hydroxyvitamin D in 26916 individuals from a European consortium

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    Source at http://doi.org/10.1371/journal.pone.0170791Background:Vitamin D deficiency may be a risk factor for mortality but previous meta-analyses lacked standardization of laboratory methods for 25-hydroxyvitamin D (25[OH]D) concentrations and used aggregate data instead of individual participant data (IPD). We therefore performed an IPD meta-analysis on the association between standardized serum 25(OH)D and mortality.Methods:In a European consortium of eight prospective studies, including seven general population cohorts, we used the Vitamin D Standardization Program (VDSP) protocols to standardize 25(OH)D data. Meta-analyses using a one step procedure on IPD were performed to study associations of 25(OH)D with all-cause mortality as the primary outcome, and with cardiovascular and cancer mortality as secondary outcomes. This meta-analysis is registered at ClinicalTrials.gov, number NCT02438488.Findings:We analysed 26916 study participants (median age 61.6 years, 58% females) with a median 25(OH)D concentration of 53.8 nmol/L. During a median follow-up time of 10.5 years, 6802 persons died. Compared to participants with 25(OH)D concentrations of 75 to 99.99 nmol/L, the adjusted hazard ratios (with 95% confidence interval) for mortality in the 25(OH)D groups with 40 to 49.99, 30 to 39.99, and Interpretation:In the first IPD meta-analysis using standardized measurements of 25(OH)D we observed an association between low 25(OH)D and increased risk of all-cause mortality. It is of public health interest to evaluate whether treatment of vitamin D deficiency prevents premature deaths

    Effects of Vitamin D supplementation on markers for cardiovascular disease and type 2 diabetes:An individual participant data meta-analysis of randomized controlled trials

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    Background Evidence from randomized controlled trials (RCTs) for the causal role of vitamin D on noncommunicable disease outcomes is inconclusive. Objective The aim of this study was to investigate whether there are beneficial or harmful effects of cholecalciferol (vitamin D 3) supplementation according to subgroups of remeasured serum 25-hydroxyvitamin D [25(OH)D] on cardiovascular and glucometabolic surrogate markers with the use of individual participant data (IPD) meta-analysis of RCTs. Design Twelve RCTs (16 wk to 1 y of follow-up) were included. For standardization, 25(OH)D concentrations for all participants (n = 2994) at baseline and postintervention were re-measured in bio-banked serum samples with the use of a certified liquid chromatography-tandem mass spectrometry method traceable to a reference measurement procedure. IPD meta-analyses were performed according to subgroups of remeasured 25(OH)D. Main outcomes were blood pressure and glycated hemoglobin (HbA1c). Secondary outcomes were LDL, HDL, and total cholesterol and triglycerides; parathyroid hormone (PTH); fasting glucose, insulin, and C-peptide; and 2-h glucose. In secondary analyses, other potential effect modifiers were studied. Results Remeasurement of 25(OH)D resulted in a lower mean 25(OH)D concentration in 10 of 12 RCTs. Vitamin D supplementation had no effect on the main outcomes of blood pressure and HbA1c. Supplementation resulted in 10-20% lower PTH concentrations, irrespective of the 25(OH)D subgroups. The subgroup analyses according to achieved 25(OH)D concentrations showed a significant decrease in LDL-cholesterol concentrations after vitamin D supplementation in 25(OH)D subgroups with <75, <100, and <125 nmol of -0.10 mmol/L (95% CI: -0.20, -0.00 mmol/L), -0.10 mmol/L (95% CI: -0.18, -0.02 mmol/L), and -0.07 mmol/L (95% CI: -0.14, -0.00 mmol/L), respectively. Patient features that modified the treatment effect could not be identified. Conclusions For the main outcomes of blood pressure and HbA1c, the data support no benefit for vitamin D supplementation. For the secondary outcomes, in addition to its effect on PTH, we observed indications for a beneficial effect of vitamin D supplementation only on LDL cholesterol, which warrants further investigation
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