Inter-Judge Agreement: An Analysis of the 1990 NFA and AFA-NIET National Individual Events Tournaments

Given the increasing concern about the judge\u27s role in individual events tournaments, and given the paucity of literature specifically pertaining to inter-judge agreement, we sought to analyze the degree of inter-judge agreement at two national level tournaments which employ multiple judge panels in preliminary rounds. The results of the 1990 National Forensics Association Tournament and the 1990 American Forensic Association - National Individual Events Tournament serve as a basis for the analysis

769-2 Progression and Regression of Coronary Atherosclerosis Occur within the Same Patient During Placebo Treatment and During Lipid-Lowering Therapy with Pravastatin

REGRESS (Regression Growth Evaluation Statin Study) is a placebo controlled multicenter study to asses the effect of 2-yr treatment with Pravastatin (PRAV) on progression and regression of angiographically documented coronary atherosclerosis (CA) in patients with a serum cholesterol between 4–8mmol/l (155-310mg/dl). Analyses of the coronary arteriograms were performed by quantitative computer analysis. The primary endpoints of the study, change in Mean Segment Diameter and Minimum Obstruction Diameter (MOD) averaged per patient, showed significant retardation of mean progression of CA in the PRAY-group as compared to the placebo (PLAC)-group. However, these mean changes per treatment group are hardly informative about individual CA-behavior. Therefore we determined for all 641 patients included in the primary MOD-analysis: 1. a mean progression score (MPS)-cumulative value of all >0.4mm progressing obstructions divided by the number of contributing obstructions-, and 2. a mean regression score (MRS)-cumulative value of all>0.4mm regressing obstructions divided by the number of contributing obstructions. Obstructions changing ≤0.4mm were considered stable and do not contribute to the scores. Thus, each patient is characterized by a MPS and a MRS. An overview of the patient MPS and MRS is presented in the figure below.Conclusionsignificant progression and regression of CA within the same patient occurred in 41 (13%) PRAY-patients and in 27 (9%) PLAC-patients. Thus, although pravastatin slows mean progression of CA, progression and regression of CA within the same patient still occurs in a considerable number of patients during lipid lowering therapy

Lipoprotein lipase activity is decreased in a large cohort of patients with coronary artery disease and is associated with changes in lipids and lipoproteins

Lipoprotein lipase (LPL) is crucial in the hydrolysis of triglycerides (TG) in TG-rich lipoproteins in the formation of HDL particles. As both these lipoproteins play an important role in the pathogenesis of atherosclerotic vascular disease, we sought to assess the relationship between post-heparin LPL (PH-LPL) activity and lipids and lipoproteins in a large, well-defined cohort of Dutch males with coronary artery disease (CAD). These subjects were drawn from the REGRESS study, totaled 730 in number and were evaluated against 75 healthy, normolipidemic male controls. Fasting mean PH-LPL activity in the CAD subjects was 108 46 mU/ml, compared to 138 44 mU/ml in controls (P < 0.0001). When these patients were divided into activity quartiles, those in the lowest versus the highest quartile had higher levels of TG (P < 0.001), VLDLc and VLDL-TG (P = 0.001). Conversely, levels of TC, LDL, and HDLc were lower in these patients (P = 0.001, P = 0.02, and P = 0.001, respectively). Also, in this cohort PH-LPL relationships with lipids and lipoproteins were not altered by apoE genotypes. The frequency of common mutations in the LPL gene associated with partial LPL deficiency (N291S and D9N carriers) in the lowest quartile for LPL activity was more than double the frequency in the highest quartile (12.0% vs. 5.0%; P = 0.006). By contrast, the frequency of the S447X LPL variant rose from 11.5% in the lowest to 18.3% (P = 0.006) in the highest quartile. This study, in a large cohort of CAD patients, has shown that PH-LPL activity is decreased (22%; P = 0.001) when compared to controls; that the D9N and N291S, and S447X LPL variants are genetic determinants, respectively, in CAD patients of low and high LPL PH-LPL activities; and that PH-LPL activity is strongly associated with changes in lipids and lipoproteins

Q fever: the Dutch policy

Between 2007 and 2010, the Netherlands experienced an unprecedented outbreak of Q fever of more than 4000 human cases. Q fever infections of dairy goats, leading to abortion waves, were considered to be the cause of this outbreak. Measures to combat the outbreak had to be taken based on limited scientific knowledge and were aimed at the interruption of the infection cycle. Next to a notification obligation, hygienic and manure measures were made obligatory. A voluntary vaccination programme started in 2008 in the risk region and was made compulsory and extended to the whole country in the years thereafter. Unexpectedly, the implemented measures did not lead to the desired result and the number of patients increased instead of decreased in the second year of the epidemic. The measures were not effective, and the scientific knowledge was still limited and did not provide the necessary answers in 2008. To curb the epidemic, the control had to change from a risk-based approach to the precautionary principle which finally, during the lambing season of 2009/2010, led to the culling of more than 50,000 pregnant goats from infected herds. After taking this drastic measure, on top of the hygiene measures and compulsory vaccination of all dairy goats in the country, the number of patients decreased to the pre-outbreak level and in 2012 the epidemic could be declared ended

Presence of European bat lyssavirus RNas in apparently healthy Rousettus aegyptiacus bats

Apparently healthy Rousettus aegyptiacus bats were randomly chosen from a Dutch colony naturally infected with European bat lyssavirus subgenotype 1a (EBL1a). These bats were euthanised three months after the first evidence of an EBL1a infection in the colony. EBL1a genomic and antigenomic RNAs of the nucleoprotein gene were detected by nested reverse transcriptase PCR in 75% of the examined Rousettus aegyptiacus bats. The EBL1a RNAs of the nucleoprotein gene were detected mainly in brain tissues, but also in other organs. EBL1a messenger RNAs of the nucleoprotein gene and the glycoprotein gene were detected in brain tissues. The standard fluorescent antibody test revealed the presence of lyssavirus antigens in brain tissues from 7 (17.5%) Rousettus aegyptiacus bats. Furthermore, EBL1a could not be detected by virus isolation on murine neuroblastoma cells or by intracerebral inoculation of suckling mice. Neutralising antibodies directed against EBL1 were detected in 11% of the examined bats. This study shows that at least 85% of the apparently healthy Rousettus aegyptiacus bats must have been infected with EBL1a, and that these bats may survive from an EBL1a infection. Furthermore, the study supports the possibility of a long-term maintenance of EBL1a genome in Rousettus aegyptiacus bats

455G/A polymorphism of the beta-fibrinogen gene is associated with the progression of coronary atherosclerosis in symptomatic men: Proposed role for an acute-phase reaction pattern of fibrinogen

Increased plasma fibrinogen levels have been identified as a risk indicator for myocardial infarction, stroke, and thrombosis. Both environmental and genetic factors make an important contribution to plasma fibrinogen levels in humans. In the present study we evaluated, in patients with serum cholesterol levels between 4 and 8 mmol/L, the relation of plasma levels and polymorphisms of fibrinogen with coronary artery disease (CAD), cross-sectionally at baseline and after a 2-year follow-up period in which they received either a placebo or pravastatin. Higher plasma fibrinogen levels (3.9 g/L) were observed at baseline in patients with the -455AA genotype than in patients with the -455GA (3.2 g/L) and -455GG (3.1 g/L) genotypes of the -455G/A fibrinogen β gene polymorphism (P < .05). Plasma levels of fibrinogen were not related to the baseline angiographic variables (mean segment diameter [MSD] and minimum obstruction diameter [MOD]), nor to the quantitative changes in these angiographic variables. However, in the placebo group, patients with the - 455AA genotype had more progression of CAD, expressed by a significantly greater decrease of the MSD and MOD, after the 2-year follow-up period than patients with the other genotypes. The - 455G/A polymorphism was related to the progression of CAD, and pravastatin therapy seemed to offset this deleterious effect. We hypothesized that the - 455A allele may promote a stronger acute-phase response in fibrinogen and that the resulting higher fibrinogen levels may form the pathogenetic basis for the stronger progression of coronary atherosclerosis. Experiments to verify this hypothesis are being proposed and advocated, in view of the possibility of identifying a genetic marker that can recognize a subgroup of patients with an increased risk who may benefit from early treatment with lipid-lowering or anticoagulant drugs

Improvement of serum oxidation by pravastatin might be one of the mechanisms by which endothelial function in dilated coronary artery segments is ameliorated

BACKGROUND: Oxidation susceptibility of lipids in vitro is considered to reflect the exposure of lipids to oxidation stress in vivo which is related to cardiovascular morbidity. This study examined the effect of pravastatin therapy on serum oxidation susceptibility, particularly in relation to endothelial function of coronary arteries. METHODS: The participants were recruited from the Pravastatin-Related Effects Following Angioplasty on Coronary Endothelium trial, a double-blinded, placebo-controlled, randomized, multi-center study designed to analyze the effect of pravastatin treatment on endothelial function in previously dilated and normal coronary arteries. Serial, graded, intra-coronary acetylcholine infusions were used to assess endothelial function. In vitro, copper-induced, serum oxidation parameters were determined at randomization and at time of coronary endothelial function assessment. RESULTS: Oxidation parameters were determined in 45 patients (pravastatin 23, placebo 22). Pravastatin therapy significantly improved serum oxidation lag time (+8%, P <0.05), maximal diene formation rate (-22%, P <0.01) and total amount of dienes formed after 5 h (-16%, P <0.01). These parameters remained essentially unchanged in the placebo group. Acetylcholine-evoked responses were positively correlated to therapy-induced change in serum oxidation susceptibility in the dilated segment group (r2=0.56, P=0.006). CONCLUSION: Pravastatin's beneficial effect on endothelial dysfunction of dilated coronary segments may be secondary to pravastatin's improvement of oxidation susceptibilit