The relationship between population genetic structure and pelagic larval duration in coral reef fishes on the Great Barrier Reef

Pelagic larval duration (PLD) is a commonly used proxy for dispersal potential in coral reef fishes. Here we examine the relationship between PLD, genetic structure and genetic variability in geographically widespread and ecological generalist species from one coral reef fish family (Pomacentridae) that differs in mean larval duration by more than a month. The genetic structure was estimated in eight species using a mitochondrial molecular marker (D-loop) and in a sub-set of five species using nuclear molecular markers (ISSRs). Estimates of genetic differentiation were similar among species with pelagic larvae, but differed between molecular markers. The mtDNA indicated no structure in all species except one, while the ISSR indicated some structure between the sampling locations in all species. We detected a relationship between PLD and genetic structure using both markers. These relationships, however, were caused by a single species, Acanthochromis polyacanthus, which differs from all the other species examined here in lacking a larval phase. With this species excluded, there was no relationship between PLD and genetic structure using either marker despite a range of PLDs of more than 20 days. Genetic diversities were generally high in all species and did not differ significantly among species and locations. Nucleotide diversity and total heterozygosity were negatively related to maximum PLD but again these relationships were caused by A. polyacanthus and disappeared when this species was excluded. These genetic patterns are consistent with moderate gene flow among well-connected locations and indicate that at this phylogenetic level (i.e., within family) the duration of the pelagic larval phase is unrelated to the patterns of genetic differentiation

Propafenone for the prevention of atrial tachyarrhythmias after cardiac surgery: a randomized, double-blind placebo-controlled trial

We studied the efficacy of propafenone in preventing atrial tachyarrhythmias after cardiac surgery, and the possible relationships between CYP2D6 polymorphism and the efficacy, pharmacokinetics, and tolerability of propafenone. One hundred and sixty patients were randomized (double blind) to receive propafenone (n= 78) or placebo (n= 82) for 1 week after cardiac surgery. The patients who were assigned to the propafenone group received 1 mg/kg infused in 1 h, followed by a continuous infusion at a rate of 4 mg/kg/24 h until the following morning, and subsequently 450 mg/day orally until the sixth postoperative day. Thirty-seven patients completed the trial in the propafenone group and 45 in the placebo group. The frequency of occurrence of atrial tachyarrhythmia was lower in the propafenone group than in the placebo group (29.7% vs. 53.3% , P< 0.05; relative risk, 0.56). Plasma propafenone concentrations were markedly influenced by CYP2D6 genotype-derived phenotype.K Mörike...M Eichelbaum...et al

Hearing Loss After Cisplatin: Oxidative Stress Pathways and Potential for Protection

Cisplatin is an old drug but remains a cornerstone of treatment for many solid malignant tumors. One important side-effect of cisplatin treatment is toxic injury to the cochlea, leading to hearing loss and/or tinnitus in a large portion of patients receiving high-dose treatment. Cisplatin and its hydrated complex MHC produce DNA-dependent and non-DNA-dependent cytotoxic effects. In experimental hearing research, a number of oxidative stress pathways have been shown to be disrupted by cisplatin treatment, including the glutaredoxin system. The oxidative stress may be a consequence of toxic platinum-DNA adducts formed by cisplatin and/or MHC. However, it can likely be generated independently of platinum-DNA adducts due to the avidity of cisplatin and/or MHC to react with nucleophiles involved in the cellular antioxidant defense, e.g., GSH. The sequence and cellular specificity of the reactions leading to ototoxicity remain to be better characterized. Furthermore, more data supporting the role of oxidative stress in humans are needed. The principle finding of oxidative stress in cisplatin ototoxicity provides the background for search of a new therapeutic approach for otoprotection in patients undergoing cisplatin treatment