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The present study was conducted to determine the effects of formulated feed (IRG: Italian ryegrass, WCC: whole crop corn, and fermented feed) on growth performance, carcass characteristics, and meat quality of Hanwoo steers during early and late fattening periods. Twelve Hanwoo steers were randomly assigned into two groups: control and treatment (n = 6/group). The control group received rice straw with concentrate; the Treatment group received formulated feed for 13 months. Results revealed that formulated feed supplementation significantly (p < 0.05) increased effects on dry matter (DM) intake, body weight, average daily gain, and carcass yield than control feed. Hanwoo steers fed formulated feed showed higher meat quality, carcass yield, and ribeye area than steers fed control feed. However, meat quality characteristics (such as cooking loss, fat thickness, marbling score, meat color, and crude fat), sensory characteristics, and pH values were similar between the two groups (all p > 0.05). There was no significant difference in FA compositions of steers between the two groups (p > 0.05). Overall, these results indicate that feeding Hanwoo steers with formulated feed can improve their growth efficacy, carcass yield, and meat quality characteristics during early and late fattening periods. Regarding an economic strategy, our research findings suggest that formulated feed is effective and profitable for feeding Hanwoo steers during early and late fattening periods without causing adverse effects. [ABSTRACT FROM AUTHOR]

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Abstract Background Type I interferons are major players against viral infections and mediate their function by the induction of Interferon regulated genes (IRGs). Recently, it became obvious that these cytokines have a multitude of additional functions. Due to the unique features of the chickens’ immune system, available data from mouse models are not easily transferable; hence we performed an extensive analysis of chicken IRGs. Results A broad database search for homologues to described mammalian IRGs (common IRGs, cIRGs) was combined with a transcriptome analysis of spleen and lung at different time points after application of IFNα. To apply physiological amounts of IFN, half-life of IFN in the chicken was determined. Interestingly, the calculated 36 min are considerably shorter than the ones obtained for human and mouse. Microarray analysis revealed many additional IRGs (newly identified IRGs; nIRGs) and network analysis for selected IRGs showed a broad interaction of nIRGs among each other and with cIRGs. We found that IRGs exhibit a highly tissue and time specific expression pattern as expression quality and quantity differed strongly between spleen and lung and over time. While in the spleen for many affected genes changes in RNA abundance peaked already after 3 h, an increasing or plateau-like regulation after 3, 6 and 9 h was observed in the lung. Conclusions The induction or suppression of IRGs in chickens is both tissue and time specific and beside known antiviral mechanisms type I IFN induces many additional cellular functions. We confirmed many known IRGs and established a multitude of so far undescribed ones, thus providing a large database for future research on antiviral mechanisms and additional IFN functions in non-mammalian species.

The present study was conducted to determine the effects of formulated feed (IRG: Italian ryegrass, WCC: whole crop corn, and fermented feed) on growth performance, carcass characteristics, and meat quality of Hanwoo steers during early and late fattening periods. Twelve Hanwoo steers were randomly assigned into two groups: control and treatment (n = 6/group). The control group received rice straw with concentrate; the Treatment group received formulated feed for 13 months. Results revealed that formulated feed supplementation significantly (p < 0.05) increased effects on dry matter (DM) intake, body weight, average daily gain, and carcass yield than control feed. Hanwoo steers fed formulated feed showed higher meat quality, carcass yield, and ribeye area than steers fed control feed. However, meat quality characteristics (such as cooking loss, fat thickness, marbling score, meat color, and crude fat), sensory characteristics, and pH values were similar between the two groups (all p > 0.05). There was no significant difference in FA compositions of steers between the two groups (p > 0.05). Overall, these results indicate that feeding Hanwoo steers with formulated feed can improve their growth efficacy, carcass yield, and meat quality characteristics during early and late fattening periods. Regarding an economic strategy, our research findings suggest that formulated feed is effective and profitable for feeding Hanwoo steers during early and late fattening periods without causing adverse effects.

Copyright of Al Bashaer Economic Journal is the property of Al Bashaer Economic Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Finance & Business Economies Review is the property of Finance & Business Economies Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Al Bashaer Economic Journal is the property of Al Bashaer Economic Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Many intracellular pathogens survive and replicate within vacuole-like structures in the cytoplasm. It has been unclear how the host immune system controls such pathogen-containing vacuoles. Interferon-inducible GTPases are dynamin-like GTPases that target the membranes of pathogen-containing vacuoles. Upon their oligomerization on the membrane, the vacuole structure disintegrates and the pathogen gets exposed to the hostile cytoplasm. What has been obscure is how the immune system detects and directs the GTPases to these pathogen shelters. Using a common protist parasite of mice,Toxoplasma gondii, we found that the LC3 conjugation system of autophagy is necessary and sufficient for targeting the interferon-inducible GTPases to membranes. We dubbed this process Targeting by AutophaGy proteins (TAG). In canonical autophagy, the LC3 conjugation system is required to form membrane-bound autophagosomes, which encircle and deliver cytosolic materials to lysosomes for degradation. In TAG, however, the conjugation system is required to mark the membranes of pathogen-containing vacuoles with ubiquitin-like LC3 homologs, which function as molecular beacons to recruit the GTPases to their target membranes. Our data suggest that the LC3 conjugation system of autophagy plays an essential role in detecting and marking pathogen-containing vacuoles for immune effector targeting by the host immune system. [ABSTRACT FROM AUTHOR]

Recent excitement regarding immune clearance of intracellular microorganisms has focused on two systems that maintain cellular homeostasis. One system includes cellular autophagy components that mediate degradation of pathogens in membrane-bound compartments, in a process termed xenophagy. The second system is driven by interferon-regulated GTPases that promote rupture of pathogen-containing vacuoles and microbial degradation. In the case of xenophagy, pathogen sequestration and compartmentalization suppress inflammation. In contrast, interferon-driven events can lead to exposure of pathogen-associated molecular patterns to the host cytosol with consequent inflammasome activation. Paradoxically, signals and factors involved in xenophagy also mobilize interferon-regulated GTPases, which drive the inflammatory response, indicating considerable cross-talk between these pathways. How these responses are prioritized remains to be understood. In this review, we describe mechanisms of intracellular pathogen clearance that rely on the autophagy machinery and interferon-regulated GTPases, and speculate how these pathways engage each other to balance pathogen elimination with inflammation. [ABSTRACT FROM AUTHOR]

Background: Type I interferons are major players against viral infections and mediate their function by the induction of Interferon regulated genes (IRGs). Recently, it became obvious that these cytokines have a multitude of additional functions. Due to the unique features of the chickens’ immune system, available data from mouse models are not easily transferable; hence we performed an extensive analysis of chicken IRGs. Results: A broad database search for homologues to described mammalian IRGs (common IRGs, cIRGs) was combined with a transcriptome analysis of spleen and lung at different time points after application of IFNα. To apply physiological amounts of IFN, half-life of IFN in the chicken was determined. Interestingly, the calculated 36 min are considerably shorter than the ones obtained for human and mouse. Microarray analysis revealed many additional IRGs (newly identified IRGs; nIRGs) and network analysis for selected IRGs showed a broad interaction of nIRGs among each other and with cIRGs. We found that IRGs exhibit a highly tissue and time specific expression pattern as expression quality and quantity differed strongly between spleen and lung and over time. While in the spleen for many affected genes changes in RNA abundance peaked already after 3 h, an increasing or plateau-like regulation after 3, 6 and 9 h was observed in the lung. Conclusions: The induction or suppression of IRGs in chickens is both tissue and time specific and beside known antiviral mechanisms type I IFN induces many additional cellular functions. We confirmed many known IRGs and established a multitude of so far undescribed ones, thus providing a large database for future research on antiviral mechanisms and additional IFN functions in non-mammalian species. [ABSTRACT FROM AUTHOR]

Cell-autonomous immunity is essential for host organisms to defend themselves against invasive microbes. In vertebrates, both the adaptive and the innate branches of the immune system operate cell-autonomous defenses as key effector mechanisms that are induced by pro-inflammatory interferons (IFNs). IFNs can activate cell-intrinsic host defenses in virtually any cell type ranging from professional phagocytes to mucosal epithelial cells. Much of this IFN-induced host resistance program is dependent on four families of IFN-inducible GTPases: the myxovirus resistance proteins, the immunity-related GTPases, the guanylate-binding proteins (GBPs), and the very large IFN-inducible GTPases. These GTPase families provide host resistance to a variety of viral, bacterial, and protozoan pathogens through the sequestration of microbial proteins, manipulation of vesicle trafficking, regulation of antimicrobial autophagy (xenophagy), execution of intracellular membranolytic pathways, and the activation of inflammasomes. This review discusses our current knowledge of the molecular function of IFN-inducible GTPases in providing host resistance, as well as their role in the pathogenesis of autoinflammatory Crohn's disease. While substantial advances were made in the recent past, few of the known functions of IFN-inducible GTPases have been explored in any depth, and new functions await discovery. This review will therefore highlight key areas of future exploration that promise to advance our understanding of the role of IFN-inducible GTPases in human diseases. [ABSTRACT FROM AUTHOR]

Determination of luminal diameter is critical to the function of small single-celled tubes. A series of EXC proteins, including EXC-1, prevent swelling of the tubular excretory canals in Caenorhabditis elegans. In this study, cloning of exc-1 reveals it to encode a homolog of mammalian IRG proteins, which play roles in immune response and autophagy and are associated with Crohn's disease. Mutants in exc-1 accumulate early endosomes, lack recycling endosomes, and exhibit abnormal apical cytoskeletal structure in regions of enlarged tubules. EXC-1 interacts genetically with two other EXC proteins that also affect endosomal trafficking. In yeast two-hybrid assays, wild-type and putative constitutively active EXC-1 binds to the LIM-domain protein EXC-9, whose homolog, cysteine-rich intestinal protein, is enriched in mammalian intestine. These results suggest a model for IRG function in forming and maintaining apical tubule structure via regulation of endosomal recycling. [ABSTRACT FROM AUTHOR]

Toxoplasmosis is the clinical and pathological consequence of acute infection with the obligate intracellular apicomplexan parasite Toxoplasma gondii. Symptoms result from tissue destruction that accompanies lytic parasite growth. This review updates current understanding of the host cell invasion, parasite replication, and eventual egress that constitute the lytic cycle, as well as the ways T. gondii manipulates host cells to ensure its survival. Since the publication of a previous iteration of this review 15 years ago, important advances have been made in our molecular understanding of parasite growth and mechanisms of host cell egress, and knowledge of the parasite's manipulation of the host has rapidly progressed. Here we cover molecular advances and current conceptual frameworks that include each of these topics, with an eye to what may be known 15 years from now. [ABSTRACT FROM AUTHOR]

Mammalian cells respond to interferons (IFNs) secreted during infection by the transcriptional upregulation of as many as a thousand genes. This remarkable transition prepares cells and organisms for resistance to infection, and many IFN-regulated gene products are players in well-understood resistance programs. Oddly, however, many of the most abundantly induced proteins are GTPases whose functions are not well understood. Here we review the progress that has been made toward understanding the roles of individual GTPase families in disease resistance and the hints of common mechanisms that are now available. [ABSTRACT FROM AUTHOR]

A study was made of alterations in exocrine and endocrine function of the pancreas following infusion of a 10% fat emulsion preparation (Intralipid) into 5 patients after pancreaticoduodenectomy and in 5 dogs with a chronic pancreatic fistula. Pancreatic exocrine secretion was significantly increased by 18.3% in the volume, 27.5% in the output of bicarbonate in humans and 8.9% in the volume, 26.1% in the output of amylase, 7.6% in the output of bicarbonate in dogs, by intravenous administration of the fat emulsion. The administration of the fat emulsion was followed by slight to minimal changes in blood sugar, amylase and IRI. The blood IRG level was significantly elevated but showed small fluctuations. The increase in pancreatic exocrine secretion induced by the fat emulsion was considered not to be mediated by intrinsic hormones but rather to be due to other humoral mechanisms. [ABSTRACT FROM AUTHOR]

Summary All viruses with positive-sense RNA genomes replicate on membranous structures in the cytoplasm called replication complexes (RCs). RCs provide an advantageous microenvironment for viral replication, but it is unknown how the host immune system counteracts these structures. Here we show that interferon-gamma (IFNG) disrupts the RC of murine norovirus (MNV) via evolutionarily conserved autophagy proteins and the induction of IFN-inducible GTPases, which are known to destroy the membrane of vacuoles containing bacteria, protists, or fungi. The MNV RC was marked by the microtubule-associated-protein-1-light-chain-3 (LC3) conjugation system of autophagy and then targeted by immunity-related GTPases (IRGs) and guanylate-binding proteins (GBPs) upon their induction by IFNG. Further, the LC3 conjugation system and the IFN-inducible GTPases were necessary to inhibit MNV replication in mice and human cells. These data suggest that viral RCs can be marked and antagonized by a universal immune defense mechanism targeting diverse pathogens replicating in cytosolic membrane structures. [ABSTRACT FROM AUTHOR]

Several studies in the last decade have highlighted the role of the type I interferon (IFN-I) pathway, and particularly interferon alpha (IFNα) in SLE pathogenesis. As a result, a multitude of potential treatments targeting IFNα have emerged in the last few years, a few of which have already completed phase II clinical trials. Some of the treatment strategies have focused on blocking IFNα or its receptor and others the plasmacytoid dendritic cell (pDC), which is the principal IFNα producing cell. In this review, we will discuss the evidence supporting a pathogenic role of IFNα and pDC in SLE, provide an update on the current status of these therapeutic strategies, and discuss the potential advantages and disadvantages of each therapeutic approach., (Copyright © 2013 Elsevier Inc. All rights reserved.)