Satellite Formation Control Using Atmospheric Drag

This study investigates the use of a linear quadratic terminal controller to reconfigure satellite formations using atmospheric drag actuated control while minimizing the loss of energy of the formation. The linearized Clohessy-Wiltshire equations of motion are used to describe the motion of the two-satellite formation about an empty reference position maintained at the formation center. Reconfigurations to final in-plane and elliptical formations are simulated at orbital radii of 6800 km and 7000 km, and the altitude loss and a ?v budget were recorded as performance measures for each reconfiguration. The final states of the spacecraft upon reconfiguration were propagated forward in time over 20 orbital periods to ensure the final conditions were achieved. Simulations proved that minimizing the loss of orbital energy effectively minimizes the loss in altitude, and drag actuated control is fully capable of controlling the radial and in-track motion of satellite formations, although the cross-track motion is uncontrollable

The Socialization of Adolescent Risk Behavior: Parent and Peer Influences in a Large, Longitudinal Sample

Previous research has not been explicitly clear about which relational influences, parents or peers, affect individual risk behavior, and vice versa. This may be attributed to the use of various methodological designs. This study examined the reciprocal influences of parents and peers on individual risk behavior by explicitly testing two different sociological theories: the group socialization theory (Harris, 1995) and the stage-environment fit theory (Eccles et al., 1993). Longitudinal data were used from the National Institute of Child Health and Human Development (NICHD) to investigate peer risk behavior, individual risk behavior, and child-parent relationship quality influences in the early to middle adolescent stages of development. Longitudinal cross-lagged latent variable panel models were used to investigate the interrelatedness of these relationships using a general construct of risk behavior. Results supported full strong longitudinal measurement invariance for individual risk behavior and child-parent relationship quality, but only weak invariance for peer risk behavior. The latent parameters (factor variances, latent means) were mostly non-invariant across the stages of development, with increases in individual risk behavior with concomitant decreases in child-parent relationship quality over time. After controlling for previous levels of peer risk behavior, individual risk behavior explained changes in subsequent peer risk behavior and in the same magnitude (β = .33 to .61) across the stages of development. Peer risk behavior did not explain changes in subsequent individual risk behavior. Child-parent relationship quality did not explain changes beyond itself. Individual risk behavior and child-parent relationship quality were stable across the stages of development, whereas peer risk behavior was less stable. Those structural relations that were tested in multi-group longitudinal panel models showed that the latent regression pathways were invariant across gender groups. These findings provide limited support for the stage-environment fit theory (Eccles et al., 1993) and the group socialization theory (Harris, 1995)

Phylogenetic Origins and Age-Based Proportions of Malacho (Elops smithi) Relative to Ladyfish (Elops saurus): Species on the Move in the Western Gulf of Mexico

Two species of ladyfish occur in the Gulf of Mexico (GOM), Elops saurus and Elops smithi, that are morphologically indistinguishable except for vertebral counts but can also be identified by mitochondrial DNA haplotypes. Here we expand on previous work, most of which has occurred in Florida, and examine the demography, phylogenetics, geographic distribution, and age—structure of ladyfishes in Texas estuaries. Fishery—independent gill net data demonstrated that ladyfishes increase in abundance from north to south along the Texas coast. The abundance of ladyfishes also increased in Texas waters from 1982–2021, which coincides with recent trends of warmer winters. Genetic data confirmed that both E. saurus and E. smithi occur in Texas waters; however, E. smithi was far less common. Contrary to previous research, we observed higher levels of genetic diversity in E. saurus due to larger sample size and thorough sampling of the western portion of its geographic range. Phylogenetic analysis supported the existence of E. saurus as a distinct species but indicated that E. smithi may be paraphyletic with other species of Elops. Otolith analysis showed that the ages of E. saurus and E. smithi ranged from 0–3 years. The lack of individuals \u3e age—3 suggests that ladyfishes migrate to the offshore GOM at age 3 and do not return to coastal areas. This study enhances knowledge of the biology of ladyfishes in inshore waters of the northwestern GOM. Future management would benefit from expanding this research to the entire geographic range of the genus Elops

Protein Targets of Thioacetamide Metabolites in Rat Hepatocytes

This document is the Accepted Manuscript version of a Published Work that appeared in final form in Chemical Research in Toxicology, copyright © American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see http://pubs.acs.org/doi/abs/10.1021/tx400001xThioacetamide (TA) has long been known as a hepatotoxicant whose bioactivation requires S-oxidation to thioacetamide S-oxide (TASO) and then to the very reactive S,S-dioxide (TASO2). The latter can tautomerize to form acylating species capable of covalently modifying cellular nucleophiles including phosphatidylethanolamine (PE) lipids and protein lysine side chains. Isolated hepatocytes efficiently oxidize TA to TASO but experience little covalent binding or cytotoxicity because TA is a very potent inhibitor of the oxidation of TASO to TASO2. On the other hand hepatocytes treated with TASO show extensive covalent binding to both lipids and proteins accompanied by extensive cytotoxicity. In this work, we treated rat hepatocytes with [14C]-TASO and submitted the mitochondrial, microsomal and cytosolic fractions to 2DGE which revealed a total of 321 radioactive protein spots. To facilitate the identification of target proteins and adducted peptides we also treated cells with a mixture of TASO/[13C2D3]-TASO. Using a combination of 1DGE- and 2DGE-based proteomic approaches, we identified 187 modified peptides (174 acetylated, 50 acetimidoylated and 37 in both forms) from a total of 88 non-redundant target proteins. Among the latter, 57 are also known targets of at least one other hepatotoxin. The formation of both amide- and amidine-type adducts to protein lysine side chains is in contrast to the exclusive formation of amidine-type adducts with PE phospholipids. Thiobenzamide (TB) undergoes the same two-step oxidative bioactivation as TA, and it also gives rise to both amide and amidine adducts on protein lysine side chains but only amidine adducts to PE lipids. Despite their similarity in functional group chemical reactivity, only 38 of 62 known TB target proteins are found among the 88 known targets of TASO. The potential roles of protein modification by TASO in triggering cytotoxicity are discussed in terms of enzyme inhibition, protein folding and chaperone function, and the emerging role of protein acetylation in intracellular signaling and the regulation of biochemical pathways

Metabolism and Toxicity of Thioacetamide and Thioacetamide SOxide in Rat Hepatocytes

“This document is the Accepted Manuscript version of a Published Work that appeared in final form in Chemical Research in Toxicology, copyright © American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see http://pubs.acs.org/doi/abs/10.1021/tx3002719The hepatotoxicity of thioacetamide (TA) has been known since 1948. In rats, single doses cause centrilobular necrosis accompanied by increases in plasma transaminases and bilirubin. To elicit these effects TA requires oxidative bioactivation leading first to its S-oxide (TASO) and then to its chemically reactive S,S-dioxide (TASO2) which ultimately modifies amine-lipids and proteins. To generate a suite of liver proteins adducted by TA metabolites for proteomic analysis, and to reduce the need for both animals and labeled compounds, we treated isolated hepatocytes directly with TA. Surprisingly, TA was not toxic at concentrations up to 50 mM for 40 hr. On the other hand, TASO was highly toxic to isolated hepatocytes as indicated by LDH release, cellular morphology and vital staining with Hoechst 33342/propidium iodide. TASO toxicity was partially blocked by the CYP2E1 inhibitors diallyl sulfide and 4-methylpyrazole, and was strongly inhibited by TA. Significantly, we found that hepatocytes produce TA from TASO relatively efficiently by back-reduction. The covalent binding of [14C]-TASO is inhibited by unlabeled TA which acts as a “cold-trap” for [14C]-TA and prevents its re-oxidation to [14C]-TASO. This in turn increases the net consumption of [14C]-TASO despite the fact that its oxidation to TASO2 is inhibited. The potent inhibition of TASO oxidation by TA, coupled with the back-reduction of TASO and its futile redox cycling with TA may help explain phenomena previously interpreted as “saturation toxicokinetics” in the in vivo metabolism and toxicity of TA and TASO. The improved understanding of the metabolism and covalent binding of TA and TASO facilitates the use of hepatocytes to prepare protein adducts for target protein identification

Covalent Modification of Lipids and Proteins in Rat Hepatocytes, and In Vitro, by Thioacetamide Metabolites

This document is the Accepted Manuscript version of a Published Work that appeared in final form in Chemical Research in Toxicology, copyright © American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see http://pubs.acs.org/doi/abs/10.1021/tx3001658Thioacetamide (TA) is a well-known hepatotoxin in rats. Acute doses cause centrilobular necrosis and hyperbilirubinemia while chronic administration leads to biliary hyperplasia and cholangiocarcinoma. Its acute toxicity requires its oxidation to a stable S-oxide (TASO) that is oxidized further to a highly reactive S,S-dioxide (TASO2). To explore possible parallels between the metabolism, covalent binding and toxicity of TA and thiobenzamide (TB) we exposed freshly isolated rat hepatocytes to [14C]-TASO or [13C2D3]-TASO. TLC analysis of the cellular lipids showed a single major spot of radioactivity that mass spectral analysis showed to consist of N-acetimidoyl PE lipids having the same side chain composition as the PE fraction from untreated cells; no carbons or hydrogens from TASO were incorporated into the fatty acyl chains. Many cellular proteins contained N-acetyl- or N-acetimidoyl lysine residues in a 3:1 ratio (details to be reported separately). We also oxidized TASO with hydrogen peroxide in the presence of dipalmitoyl phosphatidylenthanolamine (DPPE) or lysozyme. Lysozyme was covalently modified at five of its six lysine side chains; only acetamide-type adducts were formed. DPPE in liposomes also gave only amide-type adducts, even when the reaction was carried out in tetrahydrofuran with only 10% water added. The exclusive formation of N-acetimidoyl PE in hepatocytes means that the concentration or activity of water must be extremely low in the region where TASO2 is formed, whereas at least some of the TASO2 can hydrolyze to acetylsulfinic acid before it reacts with cellular proteins. The requirement for two sequential oxidations to produce a reactive metabolite is unusual, but it is even more unusual that a reactive metabolite would react with water to form a new compound that retains a high degree of chemical reactivity toward biological nucleophiles. The possible contribution of lipid modification to the hepatotoxicity of TA/TASO remains to be determined

Microplastic ingestion of juvenile fish in Corpus Christi bay and upper Laguna Madre, Texas

Microplastic pollution and the negative effects of microplastics entering the marine food web has come into the focus of research in recent years. For early life stages of fish this is of particular concern due to their high energy demand, since sufficient food availability is necessary for fast growth and survival. However, not much is currently known about the extent of microplastic pollution in Corpus Christi Bay and the Upper Laguna Madre, and whether it presents a possible risk to juvenile fishes who may ingest microplastic together with similarly sized prey items. This study presents the first baseline information on microplastic pollution in Corpus Christi Bay and the Upper Laguna Madre, which are important nursery areas for fish species such as, Red Drum (Sciaenops ocellatus), Atlantic Croaker (Micropogonias undulatus) and Mullet (Mugil spp). Juvenile fish from Corpus Christi Bay and Upper Laguna Madre showed several unique differences and spatial patterns. Over 81% of the juveniles had one or more ingested pieces of suspected microplastics. Several species (Leiostomus xanthurus, Brevoortia spp. and Menidia spp.) had higher mean amounts of suspected microplastics in their digestive tracts, likely due to a difference in feeding guilds or prey preferences. In addition, juveniles collected from highly urbanized areas (Ingleside and Oso Bay) had larger or higher amounts of suspected microplastic in them. This thesis showed that microplastic fibers are regularly found in the digestive tracts of early juveniles of eight species of fish in the Corpus Christi Bay and Upper Laguna Madre area. Further studies are needed to evaluate potential health and survival concerns caused by the documented microplastic ingestion of early juvenile fish.Life SciencesCollege of Science and Engineerin