44 research outputs found

    Sustainable agriculture systems

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    viii, 305 hal; 21 c

    Production of soma and gonad in maturing female Illex argentinus (Mollusca: Cephalopoda)

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    Samples of female lllex argentinus were taken from the catch of a Japanese squid jigging vessel on the Patagonian Shelf during March 1986. Morphometrics of the somatic and reproductive organ systems and the histological structure of the mantle in relation to maturation were examined. The data suggest that growth and maturation occur simultaneously during most of the time that lllex argentinus females are on the feeding grounds. In a squid of a ‘standard’ mantle length the whole body mass increases relative to mantle length during maturation and growth of the reproductive organs. This is accompanied by a small but significant decrease in the relative mass of the mantle, head and viscera whilst the mass of the digestive gland remains constant. Although mantle mass of a ‘standard’ female squid decreases relative to mantle length with maturity this is not associated with degeneration of the mantle muscles. Energy and nutrient resources for maturation are apparently derived from the squid's food, not from reserves, and during the course of maturation there is an increasing shift of emphasis from somatic growth to production of gonad and accessory reproductive organs

    Cerebellar hypoplasia in mice lacking selenoprotein biosynthesis in neurons.

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    Selenium exerts many, if not most, of its physiological functions as a selenocysteine moiety in proteins. Selenoproteins are involved in many biochemical processes including regulation of cellular redox state, calcium homeostasis, protein biosynthesis, and degradation. A neurodevelopmental syndrome called progressive cerebello-cortical atrophy (PCCA) is caused by mutations in the selenocysteine synthase gene, SEPSECS, demonstrating that selenoproteins are essential for human brain development. While we have shown that selenoproteins are required for correct hippocampal and cortical interneuron development, little is known about the functions of selenoproteins in the cerebellum. Therefore, we have abrogated neuronal selenoprotein biosynthesis by conditional deletion of the gene encoding selenocysteyl tRNA([Ser]Sec) (gene symbol Trsp). Enzymatic activity of cellular glutathione peroxidase and cytosolic thioredoxin reductase is reduced in cerebellar extracts from Trsp-mutant mice. These mice grow slowly and fail to gain postural control or to coordinate their movements. Histological analysis reveals marked cerebellar hypoplasia, associated with Purkinje cell death and decreased granule cell proliferation. Purkinje cell death occurs along parasagittal stripes as observed in other models of Purkinje cell loss. Neuron-specific inactivation of glutathione peroxidase 4 (Gpx4) used the same Cre driver phenocopies tRNA([Ser]Sec) mutants in several aspects: cerebellar hypoplasia, stripe-like Purkinje cell loss, and reduced granule cell proliferation. Parvalbumin-expressing GABAergic interneurons (stellate and/or basket cells) are virtually absent in tRNA([Ser]Sec)-mutant mice, while some remained in Gpx4-mutant mice. Our data show that selenoproteins are specifically required in postmitotic neurons of the developing cerebellum, thus providing a rational explanation for cerebellar hypoplasia as occurring in PCCA patients

    Disruption of thioredoxin reductase 1 protects mice from acute acetaminophen-induced hepatotoxicity through enhanced NRF2 activity.

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    The critical importance of glutathione in mitigating the deleterious effects of electrophile generating drugs such as acetaminophen (APAP) is well established. However, the role of other antioxidant systems, such as that provided by thioredoxin, has not been extensively studied. Selenoprotein thioredoxin reductase 1 (Txnrd1) is important for attenuating activation of the apoptosis signaling-regulating kinase 1 (ASK1) and the c-Jun N-terminal kinase (JNK) pathway caused by high doses of APAP. Therefore, a detailed investigation of the role of Txnrd1 in APAP-induced hepatotoxicity was conducted. Liver-specific Txnrd1 knockout mice (Txnrd1(ΔLiv)) were generated and treated with a hepatotoxic dose (400 mg/kg) of APAP for 1 or 6 h. Liver toxicity was assessed by measuring the activities of liver enzymes aspartate aminotransferase and alanine aminotransferase in serum, in addition to histopathological analysis of liver sections and analysis of glutathione levels. At 1 h post-APAP treatment, total and mitochondrial glutathione levels in control and Txnrd1(ΔLiv) mice were similarly depleted. However, at 6 h post-APAP treatment, Txnrd1(ΔLiv) mice were resistant to APAP toxicity as liver enzymes and histology were not significantly different from the corresponding untreated mice. Analyses revealed the compensatory up-regulation of many of the nuclear factor erythroid 2-related factor 2 (NRF2) target genes and proteins in Txnrd1(ΔLiv) mice with and without APAP treatment. Yet, JNK was phosphorylated to a similar extent in APAP-treated control mice. The results suggest that Txnrd1(ΔLiv) mice are primed for xenobiotic detoxication primarily through NRF2 activation

    Targeted disruption of glutathione peroxidase 4 in mouse skin epithelial cells impairs postnatal hair follicle morphogenesis that is partially rescued through inhibition of COX-2.

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    Selenoproteins are essential molecules for the mammalian antioxidant network. We previously demonstrated that targeted loss of all selenoproteins in mouse epidermis disrupted skin and hair development, and caused premature death. In the current study, we targeted specific selenoproteins for epidermal deletion to determine whether similar phenotypes developed. Keratinocyte-specific knockout mice lacking either the glutathione peroxidase 4 (GPx4) or thioredoxin reductase 1 (TR1) gene were generated by cre-lox technology using K14-cre. TR1 knockout mice had a normal phenotype in resting skin, whereas GPx4 loss in the epidermis caused epidermal hyperplasia, dermal inflammatory infiltrate, dysmorphic hair follicles, and alopecia in perinatal mice. Unlike epidermal ablation of all selenoproteins, mice ablated for GPx4 recovered after 5 weeks and had a normal life span. GPx1 and TR1 were upregulated in the skin and keratinocytes of GPx4-knockout mice. GPx4 deletion reduces keratinocyte adhesion in culture and increases lipid peroxidation and cyclooxygenase-2 (COX-2) levels in cultured keratinocytes and whole skin. Feeding a COX-2 inhibitor to nursing mothers partially prevents development of the abnormal skin phenotype in knockout pups. These data link the activity of cutaneous GPx4 to the regulation of COX-2 and hair follicle morphogenesis, and provide insight into the function of individual selenoprotein activity in maintaining cutaneous homeostasis

    Body size and composition of National Football League players

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    The purpose of this study was to present a profile of body size and composition of National Football League (NFL) players prior to the start of the regular season. Fifty-three members of the Indianapolis Colts professional football team were measured for height, body mass, and percentage body fat using the BOD POD air-displacement plethysmography system during summer camp of the 2003 football season. These data were categorized by position for comparison with previous studies of NFL football players. The relationships observed were as follows (= represents nonsignificant; > represents p ≤ 0.05): Height: Offensive Line = Defensive Line = Quarterbacks/Kickers/Punters = Tight Ends > Linebackers > Running Backs = Wide Receivers = Defensive Backs. Body Mass: Offensive Line = Defensive Line > Tight Ends = Linebackers > Running Backs = Quarterbacks/ Kickers/Punters > Wide Receivers = Defensive Backs. Percentage Body Fat: Offensive Line > Defensive Line > Quarterbacks/ Kickers/Punters = Linebackers = Tight Ends > Running Backs = Wide Receivers = Defensive Backs. Comparisons to teams in the 1970s indicate that body mass has increased only for offensive and defensive linemen; however, height and body fat among player positions have not dramatically changed. Furthermore, the body mass index is not an accurate measure or representation of body fat or obesity in NFL players. These data provide a basic template for size profiles and differences among various positions and allow comparisons with other studies for changes in the NFL over the past 3 decades

    The selenocysteine tRNA STAF-binding region is essential for adequate selenocysteine tRNA status, selenoprotein expression and early age survival of mice.

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    STAF [Sec (selenocysteine) tRNA gene transcription activating factor] is a transcription activating factor for a number of RNA Pol III- and RNA Pol II-dependent genes including the Trsp [Sec tRNA gene], which in turn controls the expression of all selenoproteins. Here, the role of STAF in regulating expression of Sec tRNA and selenoproteins was examined. We generated transgenic mice expressing the Trsp transgene lacking the STAF-binding site and made these mice dependent on the transgene for survival by removing the wild-type Trsp. The level of Sec tRNA was unaffected or slightly elevated in heart and testis, but reduced similar to 60% in liver and kidney, similar to 70% in lung and spleen and similar to 80% in brain and muscle compared with the corresponding organs in control mice. Moreover, the ratio of the two isoforms of Sec tRNA that differ by methylation at position 34 (Um34) was altered significantly, and the Um34-containing form was substantially reduced in all tissues examined. Selenoprotein expression in these animals was most affected in tissues in which the Sec tRNA levels were most severely reduced. Importantly, mice had a neurological phenotype strikingly similar to that of mice in which the selenoprotein P gene had been removed and their life span was substantially reduced. The results indicate that STAF influences selenoprotein expression by enhancing Trsp synthesis in an organ-specific manner and by controlling Sec tRNA modification in each tissue examined

    Corn stover harvest N and energy budgets in central Iowa.

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    Harvesting corn stover removes N from the fields, but its effect on subsurface drainage and other N losses is uncertain. We used the Root Zone Water Quality Model (RZWQM) to examine N losses with 0 (NRR) or 50% (RR) corn residue removal within a corn and soybean rotation over a 10-yr period. In general, all simulations used the same pre-plant or post-emergence N fertilizer rate (200 kg ha−1 yr−1). Simulated annual corn yields averaged 10.7 Mg ha−1 for the post emergence applications (NRRpost and RRpost), and 9.5 and 9.4 Mg ha−1 yr−1 for NRRpre and RRpre. Average total N input during corn years was 19.3 kg N ha−1 greater for NRRpre compared to RRpre due to additional N in surface residues, but drainage N loss was only 1.1 kg N ha−1 yr−1 greater for NRRpre. Post-emergence N application with no residue removal (NRRpost) reduced average drainage N loss by 16.5 kg ha−1 yr−1 compared to pre-plant N fertilization (NRRpre). The farm-gate net energy ratio was greatest for RRpost and lowest for NRRpre (14.1 and 10.4 MJ output per MJ input) while greenhouse gas intensity was lowest for RRpost and highest for NRRpre (11.7 and 17.3 g CO2-eq. MJ−1 output). Similar to published studies, the simulations showed little difference in N2O emissions between scenarios, decreased microbial immobilization for RR compared to NRR, and small soil carbon changes over the 10-yr simulation. In contrast to several previous modeling studies, the crop yield and N lost to drain flow were nearly the same between NRR and RR without supplemental N applied to replace N removed with corn stover. These results are important to optimizing the energy and nitrogen budgets associated with corn stover harvest and for developing a sustainable bioenergy industry.This article is published as Malone, R. W., S. Herbstritt, L. Ma, T. L. Richard, R. Cibin, P. W. Gassman, H. H. Zhang et al. "Corn stover harvest N and energy budgets in central Iowa." Science of the Total Environment 663 (2019): 776-792. DOI: 0.1016/j.scitotenv.2019.01.328. Works produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. The content of this document is not copyrighted
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