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A series of Mesozoic sedimentary basins extends across the broad continental shelf of Newfoundland. So far it has been demonstrated that only the Jeanne d'Arc Basin and environs contain potentially commercial quantities of oil and gas. The development in this area of hydrocarbon source rocks, reservoir rocks, source rock maturity, and hydrocarbon migration and trapping mechanisms was controlled by the cyclic development of extensional forces related to the opening of the North Atlantic Ocean. Geophysical exploration of the Grand Banks region began in the early 1950s. The first industry seismic program for the Jeanne d'Arc Basin was undertaken by Amoco in 1965. Drilling in the Jeanne d'Arc Basin and environs began in 1971 and, after a hiatus from 1975 to 1978, drilling activity peaked in 1984. A total of 67 wells have been drilled, and over 150 000 km of seismic data have been recorded in the study area to the end of 1989. In Part I of the report, 15 hydrocarbon exploration plays are defined by area and type of trap and by the lithostratigraphic horizon providing the reservoir facies. In Part II, seismic and well data for each play are used as input data in statistical estimations of the total and remaining hydrocarbon potential of the Jeanne d'Arc Basin and environs.

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A unique occurrence of Mesozoic breccia cut by lamprophyric-carbonatite dikelets, near Makkovik, Labrador is interpreted to relate to the opening of the Labrador Sea. The breccia has been dated by nannofossils; vitrinite reflectance studies show that some time during or after deposition the rock was heated to at least 170 °C. It is suggested that shallow seas extended westward beyond the present Labrador Marginal Trough during early Jurassic time and that the period of late alkaline igneous activity is related to the rifting between Greenland and Labrador that commenced about the middle of the Mesozoic Era.

Adropin is a peptide largely secreted by the liver and known to regulate energy homeostasis; however, it also exerts cardiovascular effects. Herein, we tested the hypothesis that low circulating levels of adropin in obesity and type 2 diabetes (T2D) contribute to arterial stiffening. In support of this hypothesis, we report that obesity and T2D is associated with reduced levels of adropin (in liver and plasma) and increased arterial stiffness in mice and humans. Establishing causation, we show that mesenteric arteries from adropin knockout mice are also stiffer, relative to arteries from wild-type counterparts, thus recapitulating the stiffening phenotype observed in T2D db/db mice. Given the above, we performed a set of follow-up experiments, in which we found that: 1) exposure of endothelial cells or isolated mesenteric arteries from db/db mice to adropin reduces filamentous actin (F-actin) stress fibers and stiffness; 2) adropin-induced reduction of F-actin and stiffness in endothelial cells and db/db mesenteric arteries is abrogated by inhibition of nitric oxide (NO) synthase; and 3) stimulation of smooth muscle cells or db/db mesenteric arteries with a NO mimetic reduces stiffness. Last, we demonstrated that in vivo treatment of db/db mice with adropin for four weeks reduces stiffness in mesenteric arteries. Collectively, these findings indicate that adropin can regulate arterial stiffness, likely via endothelial-derived NO, and thus support the notion that "hypoadropinemia" should be considered as a putative target for the prevention and treatment of arterial stiffening in obesity and T2D.

Vascular insulin resistance is a feature of obesity and type 2 diabetes that contributes to the genesis of vascular disease and glycemic dysregulation. Data from preclinical models indicate that vascular insulin resistance is an early event in the disease course preceding the development of insulin resistance in metabolically-active tissues. Whether this is translatable to humans requires further investigation. To this end, we examined if vascular insulin resistance develops when young healthy individuals (n = 18 men, n = 18 women) transition to an obesogenic lifestyle that would ultimately cause whole-body insulin resistance. Specifically, we hypothesized that short-term (10 days) exposure to reduced ambulatory activity (from >10,000 to <5,000 steps/day) and increased consumption of sugar-sweetened beverages (six cans/day) would be sufficient to prompt vascular insulin resistance. Furthermore, given that incidence of insulin resistance and cardiovascular disease is lower in premenopausal women compared to men, we postulated that young females would be protected against vascular insulin resistance. Consistent with this hypothesis, we report that after reduced ambulation and increased ingestion of carbonated beverages high in sugar, young healthy men, but not women, exhibited a blunted leg blood flow response to insulin, as well as suppressed skeletal muscle microvascular perfusion. These findings were associated with a decrease in plasma adropin and nitrite concentrations. This is the first evidence in humans that vascular insulin resistance can be provoked by short-term adverse lifestyle changes. It is also the first documentation of a sexual dimorphism in the development of vascular insulin resistance in association with changes in adropin levels.

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