Population dynamics of silverbelly Leiognathus jonesi in Palk bay

Based on catoh, effort and length-distribution data on Leiognathus jonesi collected at Mandapam over a period of sk seasons, age and growth, selection factor, coefficient of total mortality (Z) and coefficient of natural mortality (M) were derived1. For the estimated' natural mortality rclte (2.1) and for the mesh size (25 mm codend) now in operation, the optimum effort has been found to bs 50,000 standard night effort, (= 5,000 std. day effort), the yield per hundred recruits being 310 g. The isopleth diagram indicates that there was overfishing of silverbellies in 1973-74 and 1974-75 when the effort far exceeded the optimum level. The isopleth diagram also shows that the present mesh size yields the best catch and an increase in mesh size to 35 mm or decrease to 15 mm leads only to a decrease in yield. For a scientific rwanagetnemt of the fishery, it is suggested that the effort be maintained at 50,0000 night standard effort with the present mesh size at 25 mm so as to obtain sustained yield of this fish in the coming years

Not Available

Not AvailableBased on catoh, effort and length-distribution data on Leiognathus jonesi collected at Mandapam over a period of sk seasons, age and growth, selection factor, coefficient of total mortality (Z) and coefficient of natural mortality (M) were derived1. For the estimated' natural mortality rclte (2.1) and for the mesh size (25 mm codend) now in operation, the optimum effort has been found to bs 50,000 standard night effort, (= 5,000 std. day effort), the yield per hundred recruits being 310 g. The isopleth diagram indicates that there was overfishing of silverbellies in 1973-74 and 1974-75 when the effort far exceeded the optimum level. The isopleth diagram also shows that the present mesh size yields the best catch and an increase in mesh size to 35 mm or decrease to 15 mm leads only to a decrease in yield. For a scientific rwanagetnemt of the fishery, it is suggested that the effort be maintained at 50,0000 night standard effort with the present mesh size at 25 mm so as to obtain sustained yield of this fish in the coming years.Not Availabl

PCR-Based Cloning and Differential Screening of RNAs from Xenopus Primordial Germ Cells - 4

Primordial germ cells (PGCs) are a small population of unique cells from which all germ cells arise in an organism. In this sense, PGCs can be considered the stem cells of the species. An important characteristic of PGCs is their ability to remain developmentally totipotent,whereas somatic cells become restricted in their fates. Understanding the genetic program that underlies the retention of totipotency is a major goal in the stem cell field. To accomplish this goal, methods must be considered for both the isolation of these cells and the purification of the RNAs they express. The isolation of PGCs from any organism presents certain challenges. Because PGCs arise outside the gonad during early embryogenesis, their exact location within a germ layer is unknown. In addition, PGCs are relatively rare in number compared to somatic cells (on the order of 0.05% or less). This chapter presents detailed procedures for isolating live PGCs from Xenopus laevis embryos and for cloning their expressed genes, should be applicable to other organisms that have PGCs rich in mitochondria

Overactive Epidermal Growth Factor Receptor Signaling Leads to Increased Fibrosis after Severe Acute Respiratory Syndrome Coronavirus Infection

© 2017 American Society for Microbiology. All Rights Reserved. Severe acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic respiratory virus that causes morbidity and mortality in humans. After infection with SARS-CoV, the acute lung injury caused by the virus must be repaired to regain lung function. A dysregulation in this wound healing process leads to fibrosis. Many survivors of SARS-CoV infection develop pulmonary fibrosis (PF), with higher prevalence in older patients. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth factor receptor (EGFR), is critical to recovery from SARS-CoV-induced tissue damage. In mice with constitutively active EGFR [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection, the EGFR ligands amphiregulin and heparin-binding EGF-like growth factor (HB-EGF) are upregulated, and exogenous addition of these ligands during infection leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses

Fas-Associated Death Domain-Containing Protein-Mediated Antiviral Innate Immune Signaling Involves the Regulation of Irf7

The induction of type I (alphabeta) IFN following virus infection is necessary for the stimulation of effective antiviral host defense. In fibroblasts, a subset of primary genes (including those encoding IFN-beta and IFN-alpha4) are induced directly by intracellular dsRNA generated by the virus during its replication. These primary type I IFNs induce expression of IFN regulatory factor (IRF)-7, required for production of a second cascade of IFN-alpha subtypes and the further establishment of a complete antiviral state. Previously, we had reported on a role for Fas-associated death domain-containing protein (FADD) in the control of TLR-independent innate immune responses to virus infection. Our data in this study demonstrate that FADD is not only required for efficient primary gene induction, but is also essential for induction of Irf7 and effective expression of secondary IFN-alphas and other antiviral genes. Ectopic overexpression of IRF-7 partially rescued dsRNA responsiveness and IFN-alpha production, and a constitutively active variant of IRF-7 displayed normal activity in Fadd(-/-) murine embryonic fibroblasts. MC159, a FADD-interacting viral protein encoded by the molluscum contagiosum poxvirus was found to inhibit dsRNA-activated signaling events upstream of IRF-7. These data indicate that FADD's antiviral activity involves regulation of IRF-7-dependent production of IFN-alpha subtypes and consequent induction of secondary antiviral genes

Loss of DExD/H Box RNA Helicase LGP2 Manifests Disparate Antiviral Responses

The DExD/H box RNA helicase retinoic acid-inducible gene I (RIG-I) and the melanoma differentiation-associated gene 5 (MDA5) are key intracellular receptors that recognize virus infection to produce type I IFN. A third helicase gene, Lgp2, is homologous to Rig-I and Mda5 but lacks a caspase activation and recruitment domain. We generated Lgp2-deficient mice and report that the loss of this gene greatly sensitizes cells to cytosolic polyinosinic/polycytidylic acid-mediated induction of type I IFN. However, negative feedback inhibition of IFN-beta transcription was found to be normal in the absence of LGP2, indicating that LGP2 is not the primary negative regulator of type I IFN production. Our data further indicate that Lgp2-/- mice exhibited resistance to lethal vesicular stomatitis virus infection, a virus whose replicative RNA intermediates are recognized specifically by RIG-I rather than by MDA5 to trigger the production of type I IFN. However, mice lacking LGP2 were observed to exhibit a defect in type I IFN production in response to infection by the encephalomyocarditis virus, the replication of which activates MDA5-dependent innate immune responses. Collectively, our data indicate a disparate regulatory role for LGP2 in the triggering of innate immune signaling pathways following RNA virus infection

PhIP-Seq Reveals Autoantibodies for Ubiquitously Expressed Antigens in Viral Myocarditis

Enteroviruses such as group B coxsackieviruses (CVB) are commonly suspected as causes of myocarditis that can lead to dilated cardiomyopathy (DCM), and the mouse model of CVB3 myocarditis is routinely used to understand DCM pathogenesis. Mechanistically, autoimmunity is suspected due to the presence of autoantibodies for select antigens. However, their role continues to be enigmatic, which also raises the question of whether the breadth of autoantibodies is sufficiently characterized. Here, we attempted to comprehensively analyze the autoantibody repertoire using Phage ImmunoPrecipitation Sequencing (PhIP-Seq), a versatile and high-throughput platform, in the mouse model of CVB3 myocarditis. First, PhIP-Seq analysis using the VirScan library revealed antibody reactivity only to CVB3 in the infected group but not in controls, thus validating the technique in this model. Second, using the mouse peptide library, we detected autoantibodies to 32 peptides from 25 proteins in infected animals that are ubiquitously expressed and have not been previously reported. Third, by using ELISA as a secondary assay, we confirmed antibody reactivity in sera from CVB3-infected animals to cytochrome c oxidase assembly factor 4 homolog (COA4) and phosphoinositide-3-kinase adaptor protein 1 (PIK3AP1), indicating the specificity of antibody detection by PhIP-Seq technology. Fourth, we noted similar antibody reactivity patterns in CVB3 and CVB4 infections, suggesting that the COA4- and PIK3AP1-reactive antibodies could be common to multiple CVB infections. The specificity of the autoantibodies was affirmed with influenza-infected animals that showed no reactivity to any of the antigens tested. Taken together, our data suggest that the autoantibodies identified by PhIP-Seq may have relevance to CVB pathogenesis, with a possibility that similar reactivity could be expected in human DCM patients