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Background Published information regarding survival and long-term cardiac remodeling after patent ductus arteriosus ( PDA) closure in dogs is limited. Objectives To report outcome and identify prognostic variables in dogs with PDA, and to identify risk factors for persistent remodeling in dogs with a minimum of 12 months of follow-up after closure. Animals Five hundred and twenty client-owned dogs. Methods Retrospective review of medical records of 520 dogs with PDA. Outcome was determined by contacting owners and veterinarians. Dogs with PDA closure and ≥ 12 months of follow-up were asked to return for a re-evaluation. Results In multivariable analysis of 506 dogs not euthanized at the time of diagnosis, not having a PDA closure procedure negatively affected survival (HzR = 16.9, P < .001). In 444 dogs undergoing successful PDA closure, clinical signs at presentation (HzR = 17, P = .02), concurrent congenital heart disease ( HD) (HzR = 4.8, P = .038), and severe mitral regurgitation ( MR) documented within 24 hours of closure (HzR = 4.5, P = .028) negatively affected survival. Seventy-one dogs with ≥ 12 months follow-up demonstrated a significant reduction in radiographic and echocardiographic measures of heart size ( P = 0) and increased incidence of acquired HD ( P = .001) at re-evaluation. Dogs with increased left ventricular size and low fractional shortening at baseline were more likely to have persistent remodeling at re-evaluation. Conclusions and Clinical Importance Patent ductus arteriosus closure confers important survival benefits and results in long-term reverse remodeling in most dogs. Clinical signs at presentation, concurrent congenital HD, and severe MR negatively affect survival. Increased left ventricular systolic dimensions and systolic dysfunction at baseline correlated significantly with persistent remodeling. [ABSTRACT FROM AUTHOR]

Background Chagas disease ( Trypanosomiasis) is a cause of myocarditis in the southern United States causing cardiac conduction abnormalities, arrhythmias, and heart failure. Objectives To report clinical findings and outcome in Chagas positive ( CP) dogs requiring pacemaker implantation for bradyarrhythmias. Animals One hundred and forty-four client-owned dogs requiring pacemaker implantation. Methods Retrospective case series. Information regarding history, physical exam, laboratory and diagnostic imaging findings, treatment, and survival were obtained from medical records, with additional follow-up information obtained by contacting referring veterinarians and owners. Results Of the 144 dogs requiring pacemaker implantation from January 2001 to May 2010, 83 (57.6%) had a Chagas titer performed and 9 (10%) were CP. Concurrent ventricular arrhythmias (odds ratio 1.61, P = .005) or atrioventricular ( AV) block (odds ratio 4.18, P < .001) increased the likelihood that a Chagas titer was submitted. Median age for CP dogs was 6.2 years (range, 0.3-10); 7 were male. Bradyarrhythmias included high-grade 2nd or 3rd degree AV block (n = 8) and sinus bradycardia with 1st degree AV block (n = 1); 5 had concurrent ventricular arrhythmias. A positive Chagas titer had a negative impact on survival (hazard ratio 4.04; 95% CI 1.36-12.1, P = .012) with a reported median survival time of 365 days (interquartile range, 84-973 days). Conclusions and Clinical Importance Bradyarrhythmias can result in clinical signs requiring pacemaker implantation in CP dogs, and although the diagnosis negatively impacts survival, pacemaker therapy is a viable treatment option. [ABSTRACT FROM AUTHOR]

The article presents information on a study which determined whether polymerase chain reaction (PCR) can identify circulating bacteria in dogs with suspected bacterial endocarditis better than standard blood culture techniques. Information on infectious endocarditis is provided along with findings on 16s ribosomal primer based sequencing. Dogs subjected to the study are presented together with the process of evaluating blood samples with single-sample PCR and standard 3-sample blood culture techniques. Results suggest the use of both techniques.

Compares two measures of macroalgal abundance, percent cover estimated from video transects and biomass estimated from harvested quadrats, to assess the effects of no-take marine reserves in the Florida Keys National Marine Sanctuary. Greater species-specific resolution of assemblage in the biomass sampling; Advocacy of the inclusion and standardization of the estimation and reporting of reef macroalgal abundance.

Analyzes the changes in the abundance and distribution of acroporid corals at Looe Key National Marine Sanctuary in Florida. Identification of the habitat of reef fish species; Structural instability of the reefs; Factors to consider in coral management.

The developing central nervous system is a primary target of ethanol toxicity. The teratogenic effect of ethanol may result from its action on prostaglandins. Prostaglandins are generated through the release of arachidonic acid (AA) by the action of cytosolic phospholipase A[sub 2] (cPLA[sub 2]) on membrane-bound phospholipids and the catalytic conversion of AA to prostaglandin E[sub 2] (PGE[sub 2]) by cyclo-oxygenase (COX). COX is expressed in two isoforms, constitutive COX1 and inducible COX2. Cultured astrocytes and neurons from immature cerebral cortex were used as in vitro models to investigate the effect of ethanol on PGE[sub 2] synthesis. In both cell types, neither the activity nor the expression of cPLA[sub 2] was affected by ethanol. PGE[sub 2] was synthesized by astrocytes and neurons. Ethanol (200–400 mg/dL for 24 h) significantly increased PGE[sub 2] production in both cell types and the ethanol-induced increase in PGE[sub 2] accumulation in astrocytes was significantly greater than in neurons. These increases resulted from the effects of ethanol on COX. Overall COX activity was up-regulated by ethanol in astrocytes and neurons, and indomethacin, a nonselective blocker for COX, eliminated the ethanol-induced increases of COX activity in both cell types. Increased COX activity in astrocytes resulted from an increase in COX2 expression. NS-398, a selective COX2 blocker, completely inhibited ethanol-induced alterations in COX activity. In neurons, however, ethanol had a direct effect on COX activity in the absence of a change in COX expression. NS-398 only partially blocked ethanol-induced increases in neuronal COX activity. Thus, astrocytes are a primary target of ethanol and ethanol-induced increases in glial PGE[sub 2] synthesis are mediated by COX, principally COX2. Ethanol toxicity may be mediated through PGE[sub 2] in immature cortical cells. [ABSTRACT FROM AUTHOR]

Investigates the pattern of recruitment and juvenile mortality as structuring factors for reef benthic communities in Biscayne National Park in Florida. Measurement of juvenile and adult coral densities; Size-frequency distributions of smaller coral size classes.

A procedure was developed to remove trophectoderm cells from day-8 blastocysts of the marmoset monkey. Using micro-manipulative techniques, a tear was made in the zona pellucida opposite the inner cell mass which facilitated the controlled herniation of trophectoderm cells as the blastocysts developed . After 24 h (day-9 blastocysts) and 48 h (day-10 blastocysts) of culture ˜20% and ˜50% respectively of the blastocyst had herniated. The herniated trophectoderm was cut off by freehand and the biopsied blastocysts transferred to recipients. Normal offspring were born but pregnancies could be established from day-10 blastocysts only if the recipients were treated with human chorionic gonadotrophin during early pregnancy. One pregnancy was established after the transfer of three frozen biopsied day-10 blastocysts. Biopsies of 30–50 cells from day-10 blastocysts could be readily grown as trophoblast vesides to in excess of 1000 cells but biopsies of <20 cells from day-9 blastocysts formed a monolayer of binucleated and multinucleated cells with limited cell replication. Assuming human trophectoderm cells have a similar capacity to the marmoset to grow , the application of this technique to human blastocysts would provide sufficient cells on which the pre implantation diagnosis of a genetic disorder could be made. [ABSTRACT FROM PUBLISHER]

Navassa Island is a small uninhabited island, approximately 60 km west of the south-west tip of Haiti (18°242N, 75°002W). Haiti laid claim to the island in 1804, however the USA claimed it under the Guano Act of 1856 and recently placed it under jurisdiction of the US Fish and Wildlife Service (USFWS). Remoteness from USFWS administration in Puerto Rico and disputed sovereignty by Haiti make enforcement of management impractical. Artisanal fishers from Haiti have frequented Navassa over the past several decades. Given the lack of current land-based development and limited transient land-based activity (for example salting fish and gear construction), Navassa provides a case study where fishing is largely isolated as the dominant human impact on coastal resources. [ABSTRACT FROM PUBLISHER]