Estimating the contribution of Greenland Halibut (Reinhardtius hippoglossoides) stocks to nurseries by means of genotyping-by-sequencing: Sex and time matter.

Identification of stocks and quantification of their relative contribution to recruitment are major objectives toward improving the management and conservation of marine exploited species. Next-generation sequencing allows for thousands of genomic markers to be analyzed, which provides the resolution needed to address these questions in marine species with weakly differentiated populations. Greenland Halibut (Reinhardtius hippoglossoides) is one of the most important exploited demersal species throughout the North Atlantic, in particular in the Gulf of St. Lawrence, Canada. There, two nurseries are known, the St. Lawrence Estuary and the northern Anticosti Island, but their contribution to the renewal of stocks remains unknown. The goals of this study were (a) to document the genetic structure and (b) to estimate the contribution of the different identified breeding stocks to nurseries. We sampled 100 juveniles per nursery and 50 adults from seven sites ranging from Saguenay Fjord to offshore Newfoundland, with some sites sampled over two consecutive years in order to evaluate the temporal stability of the contribution. Our results show that after removing sex-linked markers, the Estuary/Gulf of St. Lawrence represents a single stock which is genetically distinct from the Atlantic around Newfoundland (F ST = 0.00146, p-value = .001). Population assignment showed that recruitment in both nurseries is predominantly associated with the St. Lawrence stock. However, we found that the relative contribution of both stocks to the nurseries is temporally variable with 1% contribution of the Newfoundland stock one year but up to 33% for the second year, which may be caused by year-to-year variation in larval transport into the Gulf of St. Lawrence. This study serves as a model for the identification of stocks for fisheries resources in a context where few barriers to dispersal occur, in addition to demonstrating the importance of considering sex-linked markers and temporal replicates in studies of population genomics.

Nonselective ETA/ETB-receptor blockade increases systemic blood pressure of Bio 14.6 cardiomyopathic hamsters.

To examine the role of endothelin ETA and ETB receptors in congestive heart failure due to cardiomyopathy, the effect of chronic treatment with selective ETA- and ETB-receptor antagonists (atrasentan and A-192621, respectively), alone and in combination, was assessed on functional and biochemical parameters of 52-week-old Bio 14.6 cardiomyopathic hamsters. Compared with control animals, cardiomyopathic hamsters treated for 9 weeks with atrasentan showed no variation in MAP; however, selective ETB- and combined nonselective ETA- and ETB-receptor antagonists increased systemic blood pressure. After selective ETB-receptor blockade, plasma endothelin levels were augmented. Importantly, this increase was highly enhanced (more than 8-fold) by concomitant ETA-receptor antagonism. Furthermore, the left ventricle:body weight ratio of cardiomyopathic hamsters treated with A-192621, alone or in combination with atrasentan, was significantly increased. On the other hand, decreased left ventricular end-diastolic pressure was observed in cardiomyopathic hamsters after selective ETA- or combined nonselective ETA/ETB-receptor antagonism, while only selective ETA-receptor blockade reduced left ventricular endothelin levels. Our results suggest that, in congestive heart failure, ETB receptors are essential to limit circulating endothelin levels, which may argue for improved cardiac benefits after long-term treatment with highly selective ETA-receptor antagonists.

The inducible nitric-oxide synthase modulates endothelin-1-dependent release of prostacyclin and inhibition of platelet aggregation ex vivo in the mouse.

Nitric oxide and other reactive oxygen species generated by nitric-oxide synthases (NOS) modulate, among several other cellular responses, the production of eicosanoids and platelet aggregation. The roles of specific NOS in these two phenomena remain to be determined. Thus, the present study assessed whether inducible NOS (iNOS) and endothelial NOS (eNOS) modulate in a similar manner the production of eicosanoids and platelet aggregation. Mice knocked out for eNOS (eNOS-/-) or iNOS (iNOS-/-) and their wild-type (WT) congeners were used to analyze agonist-induced increases in plasma levels of eicosanoids as well as inhibition of platelet aggregation ex vivo. Systemically administered endothelin-1 (ET-1) triggered an increase in plasma levels of 6-keto prostaglandin F(1alpha) (6-keto PGF(1alpha)) in WT and eNOS-/- but not in iNOS-/- mice. ET-1 (0.01-1 nmol/kg) also induced a dose-dependent inhibition of platelet aggregation in WT and eNOS-/- but not in iNOS-/- mice. Another agonist, bradykinin (10 nmol/kg), triggered the release of 6-keto PGF(1alpha) and inhibited platelet aggregation in all strains of mice studied. In addition, ADP-induced platelet aggregation in vitro was similarly reduced by iloprost (100 nM) in iNOS-/- mice and WT congeners. In another series of experiments, ET-1 (0.1 nmol/kg) significantly increased 8-isoprostane plasma levels in WT but not in iNOS-/- mice. Finally, a 3-week treatment with anti-oxidants inhibited the capacity of ET-1 to significantly increase plasma 6-keto PGF(1alpha) in WT mice. We show for the first time that iNOS is involved in the control of ET-1-induced prostacyclin release and related inhibition of platelet aggregation in the murine model.

Cardiovascular diseases: new insights from knockout mice.

Knockout (KO) mice models have generated a wealth of new information on the developmental and physiopathological roles of several hormones and their receptors. In these mice, KO of a specific gene can be lethal at embryonic stages or during early adulthood. Furthermore, in conditions of non-lethality, KO mice may compensate for the repression of a particular protein expression. As a result of these two aspects, various phenotypic expressions occur in KO mice models for several peptides and their respective receptors, as well as for the enzymes involved in their processing.

Influence of 24-hour sleep deprivation on respiration in lambs.

The aim of this study was first to examine the effects of 24-h sleep deprivation on apnea index and duration in lambs. The effects on sleep architecture and sigh and swallowing indices were also studied. The impact of postnatal maturation on all measured variables was assessed by studying two different age groups. Twelve lambs (six aged 1-2 d and six aged 23-24 d on the day of surgery) were chronically instrumented for polysomnographic recordings including sleep state assessment, nasal flow, diaphragm electromyogram, and glottal constrictor muscle electromyogram. Two recordings, one control and one after 24-h sleep deprivation, were performed in all lambs. Results show that the effects of sleep deprivation predominate in rapid eye movement sleep in the younger group, with increased rapid eye movement sleep proportion and apnea, sigh, and swallowing index. Our results in lambs suggest that the consequences of sleep deprivation upon respiration are predominant early after birth. Although the potential relationship of these observations to neonatal apneas and sudden infant death syndrome has yet to be defined, awareness of the effects of sleep deprivation is important for neonatal care.