Screening and activity of potential gastrointestinal probiotic lactic acid bacteria against Yersinia ruckeri O1b.

Yersiniosis of cultured Atlantic salmon is a recurrent fish health management challenge in many continents. The causative organism, Yersinia ruckeri, can reside latently in the gut and lead to acute infection and disease during hatchery and sea-transfer stages. One potential prevention approach is the administration of probiotic bacteria to suppress gut colonization of Y.

Size-dependent resistance to amoebic gill disease in naïve Atlantic salmon (Salmo salar).

Amoebic gill disease, caused by the protozoan ectoparasite Neoparamoeba perurans, remains a significant threat to commercial Atlantic salmon aquaculture operations worldwide, despite partial control afforded by selective breeding and therapeutic intervention. Anecdotal reports from commercial producers suggest that historically, smaller Atlantic salmon smolts are more susceptible to AGD than larger smolts. Here, large (>350 g) and small (<200 g) commercially sourced, AGD-naïve Atlantic salmon cohorts were experimentally exposed to 50 N.

The Effect of Antimicrobial Treatment upon the Gill Bacteriome of Atlantic Salmon ( L.) and Progression of Amoebic Gill Disease (AGD) In Vivo.

Branchial surfaces of finfish species contain a microbial layer rich in commensal bacteria which can provide protection through competitive colonization and production of antimicrobial products. Upon disturbance or compromise, pathogenic microbiota may opportunistically infiltrate this protective barrier and initiate disease. Amoebic gill disease (AGD) is a globally significant health condition affecting salmonid mariculture.

Immersion challenge of naïve Atlantic salmon with cultured Nolandella sp. and Pseudoparamoeba sp. did not increase the severity of Neoparamoeba perurans-induced amoebic gill disease (AGD).

Amoebic gill disease (AGD) is one of the main health issues impacting farmed Atlantic salmon. Neoparamoeba perurans causes AGD; however, a diversity of other amoeba species colonizes the gills and there is little understanding of whether they are commensal or potentially involved in different stages of gill disease development. Here, we conduct in vivo challenges of naïve Atlantic salmon with cultured Nolandella sp.

Bacteriomic Profiling of Branchial Lesions Induced by Challenge Reveals Commensal Dysbiosis and an Association with in AGD-Affected Atlantic Salmon ( L.).

Amoebic gill disease is a parasitic condition that commonly affects marine farmed Atlantic salmon. The causative agent, , induces a marked proliferation of the gill mucosa and focal superficial necrosis upon branchial lesions. The effect that amoebic branchialitis has upon gill associated commensal bacteria is unknown.

Pigment-depletion in Atlantic salmon (Salmo salar) post-smolt starved at elevated temperature is not influenced by dietary carotenoid type and increasing α-tocopherol level.

Pigment-depletion in the fillets of farmed Atlantic salmon (Salmo salar) arises after periods of elevated water temperatures with voluntary starving. This study tested the effects of dietary pre-loading with different pigment carotenoids (astaxanthin and/or canthaxanthin) combined with two α-tocopherol levels (normal and high: 500 and 1000 mg/kg, respectively) on pigment-depletion in vivo in Atlantic salmon after four weeks of challenge. We also tested whether oxidative stress manifested as an underlying depletion mechanism.

Branchial Pathomorphology of Southern Bluefin Tuna (Castelnau, 1872) Infected by Helminth and Copepodan Parasites.

Three metazoan parasites, a monogenean and two species of copepods and are known to parasitize the gills of ranched southern bluefin tuna (SBT) and other tuna species. However, there is no detailed information describing the pathological response to infection by these parasites in this species. Wild southern bluefin tuna (approximately 3 years of age), captured and towed to a grow-out site in the waters immediately south of Port Lincoln, South Australia were subsequently sampled ( = 10) monthly from March until August 2004 during commercial harvest operations.

Multigenic Delineation of Lower Jaw Deformity in Triploid Atlantic Salmon (Salmo salar L.).

Lower jaw deformity (LJD) is a skeletal anomaly affecting farmed triploid Atlantic salmon (Salmo salar L.) which leads to considerable economic losses for industry and has animal welfare implications. The present study employed transcriptome analysis in parallel with real-time qPCR techniques to characterise for the first time the LJD condition in triploid Atlantic salmon juveniles using two independent sample sets: experimentally-sourced salmon (60 g) and commercially produced salmon (100 g).

Transcriptome profiling the gills of amoebic gill disease (AGD)-affected Atlantic salmon (Salmo salar L.): a role for tumor suppressor p53 in AGD pathogenesis?

Neoparamoeba spp. are amphizoic amoebae with the capacity to colonize the gills of some marine fish, causing AGD. Here, the gill tissue transcriptome response of Atlantic salmon (Salmo salar L.

A murine model of invasive aspergillosis: variable benefit of interferon-gamma administration under in vitro and in vivo conditions.

Background: Interferon-gamma modulates host defense in a number of infectious diseases. Previous studies have shown that systemic administration of interferon-gamma (IFN-gamma) can enhance survival in experimental invasive aspergillosis (IA).

Methods: Using a novel model of murine IA that is characterized by primary pulmonary infection, we investigated the role of IFN-gamma in the phagocytosis and killing of Aspergillus fumigatus by murine neutrophils and pulmonary alveolar macrophages in vitro and the impact of systemic and regional administration of IFN-gamma on the course of IA in glucocorticoid-treated mice.

Post-translational modification of manganese superoxide dismutase in acutely rejecting cardiac transplants: role of inducible nitric oxide synthase.

Background: Nitration of a critical tyrosine residue in the active site of manganese superoxide dismutase (MnSOD) can lead to enzyme inactivation. In this study, we examined the effect of inducible nitric oxide synthase (iNOS) on MnSOD expression, activity and nitration in acutely rejecting cardiac transplants.

Methods: Lewis (isograft) or Wistar-Furth (allograft) donor hearts were transplanted into Lewis recipient rats.

Hierarchical change in antioxidant enzyme gene expression and activity in acute cardiac rejection: role of inducible nitric oxide synthase.

Reactive oxygen and nitrogen may mediate inflammation injury, but the status of the antioxidant defense system that might influence this process is unknown. In the present study, we examined the expression profile of the antioxidant enzymes, manganese superoxide dismutase (MnSOD), catalase and glutathione peroxidase (GPX) in acutely rejecting cardiac allografts and the potential role of inducible nitric oxide synthase (iNOS) in modulating antioxidant gene expression and activity. Donor hearts from Lewis (isograft) or Wistar-Furth (allograft) rats were transplanted into Lewis recipient rats.

Human heredity and politics: A comparative institutional study of the Eugenics Record Office at Cold Spring Harbor (United States), the Kaiser Wilhelm Institute for Anthropology, Human Heredity, and Eugenics (Germany), and the Maxim Gorky Medical Genetics Institute (USSR).

Despite the fact that much has been written in recent years about the science of heredity under the Third Reich, there is as yet no satisfying analysis of two central questions: What, if anything, was peculiarly "Nazi" about human genetics under National Socialism? How, under whatever set of causes, did at least some of Germany's most well-known and leading biomedical practioners become engaged in entgrenzte Wissenschaft (science without moral boundaries)? This paper attempts to provide some answers to these two questions comparing three institutes that studied eugenics and human heredity in the 1920s and 1930s: the Eugenics Record Office at Cold Spring Harbor, New York, directed by Charles B. Davenport; the Kaiser Wilhelm Institute for Anthropology, Human Heredity and Eugenics, in Berlin, directed by Eugen Fischer; and the Maxim Gorky Medical Genetics Institute in Moscow, directed by Solomon G. Levit.

Treatment with {alpha}-phenyl-N-tert-butylnitrone, a free radical-trapping agent, abrogates inflammatory cytokine gene expression during alloimmune activation in rat cardiac allografts.

Spin-trapping nitrones such as alpha-phenyl-N-tert-butylnitrone (PBN) have traditionally been used to trap and stabilize free radicals for detection by electron paramagnetic resonance (EPR) spectroscopy. Unlike classical antioxidants, these agents have never been evaluated therapeutically in allograft transplantation. In the present study, we examined potential mechanisms of action of treatment with PBN in a rat model of acute cardiac allograft transplantation.

Inhibition of nitrosylation, nitration, lymphocyte proliferation, and gene expression in acute and delayed cardiac allograft rejection by an orally active dithiocarbamate.

Dithiocarbamate derivatives sequester metals such as iron and may have benefits in inflammatory diseases. We examined the actions of a new dithiocarbamate-based oral formulation, NOX-700, on protein modification by nitric oxide (NO), gene expression, and lymphocyte proliferation in a model of acute and delayed cardiac rejection. Chronic treatment with NOX-700 prolonged graft survival.

Variable efficacy of N6-(1-iminoethyl)-L-lysine in acute cardiac transplant rejection.

We examined the efficacy and mechanism of action of N(6)-(1-iminoethyl)-L-lysine (L-NIL), a highly selective inhibitor of inducible nitric oxide (NO) synthase (iNOS), on acute cardiac transplant rejection. L-NIL produced a concentration-dependent attenuation of plasma NO by-products and a decrease in nitrosylation of heme protein without altering protein levels of iNOS. At postoperative day 4, L-NIL did not alter the increased binding activities for transcription factors nuclear factor-kappaB and activator protein-1.

Beta tryptase levels are not elevated in patients undergoing liver transplantation.

Reperfusion syndrome during liver transplantation and anaphylaxis are clinical syndromes that share similarities in physiological responses. The liver and intestine contain a variety of immunologically active cells, including mast cells. The purpose of this study is to investigate the possibility that mast-cell degranulation occurs routinely during transplantation and thereby contributes to hemodynamic instability and coagulopathy.

Mechanisms of the protective action of diethyldithiocarbamate-iron complex on acute cardiac allograft rejection.

In this study, we examined the actions of diethyldithiocarbamate-iron (DETC-Fe) complex in acute graft rejection heterotopically transplanted rat hearts. Chronic treatment with DETC-Fe inhibited the increase in plasma nitric oxide (NO) metabolites and nitrosylation of myocardial heme protein as determined by electron paramagnetic resonance (EPR) spectroscopy. Pulse injection with DETC-Fe normalized NO metabolites.

Non-heme iron protein: a potential target of nitric oxide in acute cardiac allograft rejection.

We examined iron nitrosylation of non-heme protein and enzymatic activity of the Fe-S cluster protein, aconitase, in acute cardiac allograft rejection. Heterotopic transplantation of donor hearts was performed in histocompatibility matched (isografts: Lewis --> Lewis) and mismatched (allografts: Wistar-Furth --> Lewis) rats. On postoperative days (POD) 4-6, Western blot analysis and immunohistochemistry revealed inducible nitric-oxide synthase (iNOS) protein in allografts but not isografts.

Cholinergic and nitrergic regulation of in vivo giant migrating contractions in rat colon.

The aim of this study was to characterize in vivo rat colonic motor activity in normal and inflamed states and determine its neural regulation. Circular muscle contractions were recorded by surgically implanted strain-gauge transducers. The rat colon exhibited predominantly giant migrating contractions (GMCs) whose frequency decreased distally.

A ruthenium (III) polyaminocarboxylate complex, a novel nitric oxide scavenger, enhances graft survival and decreases nitrosylated heme protein in models of acute and delayed cardiac transplant rejection.

Nitric oxide (NO) derived from the up-regulation of inducible NO synthase (iNOS) is believed to play an important role in organ rejection. In experimental models of acute cardiac transplant rejection (i.e.