Eyes of the world on a warmer, less frozen, and greener Arctic.

Rapid atmospheric warming and sea-ice retreat are driving widespread changes in Arctic ecosystems, among the most pervasive of which is the "greening of the Arctic"-an increase in the cover and biomass of vegetation observed by satellites across much of the Arctic tundra biome. Determining the drivers, impacts, and feedbacks of Arctic greening requires continued investment in robust field, remote-sensing, and model-based capabilities, and improved integration of the knowledge base of Arctic peoples. These tools and approaches support the triangulation of complex problems and the development of improved projections for the warmer Arctic tundra biome of the future.

Ancient plant DNA reveals High Arctic greening during the Last Interglacial.

Summer warming is driving a greening trend across the Arctic, with the potential for large-scale amplification of climate change due to vegetation-related feedbacks [Pearson et al., (3), 673-677 (2013)]. Because observational records are sparse and temporally limited, past episodes of Arctic warming can help elucidate the magnitude of vegetation response to temperature change.

Landscape impacts of 3D-seismic surveys in the Arctic National Wildlife Refuge, Alaska.

Although three-dimensional (3D) seismic surveys have improved the success rate of exploratory drilling for oil and gas, the impacts have received little scientific scrutiny, despite affecting more area than any other oil and gas activity. To aid policy-makers and scientists, we reviewed studies of the landscape impacts of 3D-seismic surveys in the Arctic. We analyzed a proposed 3D-seismic program in northeast Alaska, in the northern Arctic National Wildlife Refuge, which includes a grid 63,000 km of seismic trails and additional camp-move trails.

Vegetation on mesic loamy and sandy soils along a 1700-km maritime Eurasia Arctic Transect.

Questions: How do plant communities on zonal loamy vs. sandy soils vary across the full maritime Arctic bioclimate gradient? How are plant communities of these areas related to existing vegetation units of the European Vegetation Classification? What are the main environmental factors controlling transitions of vegetation along the bioclimate gradient?

Location: 1700-km Eurasia Arctic Transect (EAT), Yamal Peninsula and Franz Josef Land (FJL), Russia.

Methods: The Braun-Blanquet approach was used to sample mesic loamy and sandy plots on 14 total study sites at six locations, one in each of the five Arctic bioclimate subzones and the forest-tundra transition.

Cumulative geoecological effects of 62 years of infrastructure and climate change in ice-rich permafrost landscapes, Prudhoe Bay Oilfield, Alaska.

Many areas of the Arctic are simultaneously affected by rapid climate change and rapid industrial development. These areas are likely to increase in number and size as sea ice melts and abundant Arctic natural resources become more accessible. Documenting the changes that have already occurred is essential to inform management approaches to minimize the impacts of future activities.

Evaluation of the built environment: staff and family satisfaction pre- and post-occupancy of the Children's Hospital.

Objective: To evaluate and compare the impact of an existing and newly built hospital environment on family and staff satisfaction related to light, noise, temperature, aesthetics, and amenities, as well as safety, security, and privacy.

Background: The United States is engaged in an unprecedented healthcare building boom driven by the need to replace aging facilities, understand the impact of the built environment on quality and safety, incorporate rapidly emerging technologies, and enhance patient- and family-centered care. More importantly, there is heightened attention to creating optimal physical environments to achieve the best possible outcomes for patients, families, and staff.

No effect of angiotensin-converting enzyme gene polymorphism on disease progression and left ventricular hypertrophy in autosomal dominant polycystic kidney disease.

Background: Autosomal dominant polycystic kidney disease (ADPKD) shows a variable clinical course suggesting that genetic modifiers might play a role. There are conflicting results about the effect of angiotensin-converting enzyme (ACE) gene polymorphism on the progression of renal failure in ADPKD. Also, the association between ACE gene polymorphism and the occurrence of left ventricular hypertrophy (LVH) has not been investigated in patients with ADPKD.

Characterization of rat parotid and submandibular acinar cell apoptosis in primary culture.

Apoptosis is a highly organized cellular process that is critical for maintaining glandular homeostasis. We have used primary rat salivary acinar cells from the parotid and submandibular glands to investigate the critical regulatory events involved in apoptosis. Caspase-3 activity, cleavage of caspase substrates, and deoxyribonucleic acid (DNA) fragmentation were assayed in cells treated with etoposide, a DNA-damaging agent, or brefeldin A (BFA), a Golgi toxin.

Angiotensin-converting enzyme DD genotype in patients with primary pulmonary hypertension: increased frequency and association with preserved haemodynamics.

Unlabelled: HYPOTHESIS/INTRODUCTION: A polymorphic marker within the angiotensin- converting enzyme (ACE) gene has been associated with circulating and tissue ACE activity and with a variety of forms of cardiovascular disease. Since angiotensin II (Ang II) causes pulmonary vasoconstriction and vascular and myocardial remodelling, we postulated a role for the renin-angiotensin system and the ACE DD genotype in the pathophysiology of primary pulmonary hypertension (PPH) and in the right ventricular response to pressure overload in these patients.

Methods And Results: The incidence of the ACE DD genotype was evaluated in 60 patients with severe PPH compared with two normal control populations, a group of healthy population-based controls (n=158) and subjects found suitable for cardiac organ donation (n=79).

Myocardial-directed overexpression of the human beta(1)-adrenergic receptor in transgenic mice.

The beta(1)-adrenergic receptor (AR) is the dominant subtype in non-failing and failing myocardium. beta(1)-AR signaling, by the endogenous neurotransmitter norepinephrine, is central to the regulation of myocardial contractility. In heart failure, the beta(1)-AR undergoes subtype-selective downregulation which may protect against the increased cardiac adrenergic drive associated with this pathophysiological state.

Deletion polymorphism of the angiotensin converting enzyme gene is associated with an increase in left ventricular mass in men with type 2 diabetes mellitus.

Previous studies evaluating the angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism have revealed that expression of the DD genotype is associated with an increase in myocardial infarction, cardiomyopathy, and left ventricular (LV) mass in nondiabetic patients. In the present study, a cross-sectional analysis was performed to evaluate the potential relationship between the ACE I/D genotypes and the LV mass index in 289 non-insulin-dependent diabetes mellitus (NIDDM) subjects without known coronary artery disease. Two dimensional directed M-mode echocardiograms along with selected patient characteristics were obtained from the study population.

Angiotensin-1 converting enzyme polymorphisms in chronic beryllium disease.

To test the hypothesis that the angiotensin converting enzyme (ACE) genotype is associated with chronic beryllium disease (CBD) and disease severity, we studied 50 cases of CBD and compared their ACE genotype to that of two different control groups, consisting of: (1) 50 participants from a beryllium machining facility; and (2) 50 participants from a non-beryllium-associated workplace. We found no statistically significant difference in the frequency of the I or D allele or of the DD genotype among cases of CBD and either control group. The odds ratio (OR) for the CBD DD genotype as compared with the non-DD genotype was 1.

Angiotensin-converting enzyme gene polymorphism in non-insulin dependent diabetes mellitus and its relationship with diabetic nephropathy.

Previous studies have shown that the angiotensin-converting enzyme (ACE) gene polymorphism is associated with an increased risk of vascular disease in non-diabetic patients. The present study was conducted on 509 NIDDM patients who underwent a screening test to determine their ACE genotype for the Appropriate Blood Pressure Control in Diabetes (ABCD) Trial. Various baseline indices were correlated with the three ACE polymorphisms.

Selective downregulation of the angiotensin II AT1-receptor subtype in failing human ventricular myocardium.

Background: The regulation of angiotensin II receptors and the two major subtypes (AT1 and AT2) in chronically failing human ventricular myocardium has not been previously examined.

Methods And Results: Angiotensin II receptors were measured by saturation binding of 125I-[Sar1,Ile8]angiotensin II in crude membranes from nonfailing (n = 19) and failing human left ventricles with idiopathic dilated cardiomyopathy (IDC; n = 31) or ischemic cardiomyopathy (ISC; n = 21) and membranes from a limited number of right ventricles in each category. The AT1 and AT2 fractions were determined by use of an AT1-selective antagonist, losartan.

The role of genetic variants in angiotensin I converting enzyme, angiotensinogen and the angiotensin II type-1 receptor in the pathophysiology of heart muscle disease.

The cardiac vasculature and myocardium contain components of the renin-angiotensin system (RAS), which may regulate local growth and cellular function. Alterations in the expression or action of these components, which include angiotensin converting enzyme (ACE), angiotensinogen, and angiotensin II type-1 receptors, may contribute to the development of disease, such as hypertension, left ventricular hypertrophy, myocardial infarction, and end-stage heart failure. ACE is one RAS component found to have genetic variants associated with cardiovascular disease.

Angiotensin II formation in the intact human heart. Predominance of the angiotensin-converting enzyme pathway.

It has been proposed that the contribution of myocardial tissue angiotensin converting enzyme (ACE) to angiotensin II (Ang II) formation in the human heart is low compared with non-ACE pathways. However, little is known about the actual in vivo contribution of these pathways to Ang II formation in the human heart. To examine angiotensin II formation in the intact human heart, we administered intracoronary 123I-labeled angiotensin I (Ang I) with and without intracoronary enalaprilat to orthotopic heart transplant recipients.

Expression and preferential inhibition of inducible nitric oxide synthase in aortas of endotoxemic rats.

Septic shock is associated with high mortality. There is in vitro evidence that the induction of nitric oxide synthase (iNOS) in vascular smooth muscle cells may be an important mediator of the systemic vasodilation and hypotension associated with sepsis. In this study, an in vivo murine model of sepsis was used to further examine this important question.

Importance of angiotensin-converting enzyme in pulmonary hypertension.

Angiotensin II causes pulmonary vasoconstriction in man and in animals, and angiotensin-converting enzyme (ACE) inhibitors have prevented the development of chronic pulmonary hypertension in animals models. Angiotensin II may contribute to lung vascular remodeling in pulmonary hypertensive disease, since cilazapril, an inhibitor of ACE, reduces pulmonary vascular medical thickening in chronically hypoxic rats with established pulmonary hypertension. Furthermore, the ACE DD genotype, which has been associated with increased circulating and tissue ACE activity, has been associated with left ventricular hypertrophy in human hypertensive disorders.

Reduced beta 1 receptor messenger RNA abundance in the failing human heart.

Heart failure in humans is characterized by alterations in myocardial adrenergic signal transduction, the most prominent of which is down-regulation of beta 1-adrenergic receptors. We tested the hypothesis that down-regulation of beta 1-adrenergic receptors in the failing human heart is related to decreased steady-state levels of beta 1 receptor mRNA. Due to the extremely low abundance of beta 1 receptor mRNA, measurements were possible only by quantitative polymerase chain reaction (QPCR) or by RNase protection methods.

Angiotensin-converting enzyme DD genotype in patients with ischaemic or idiopathic dilated cardiomyopathy.

Polymorphism in the angiotensin-converting enzyme (ACE) gene has been shown to correlate with circulating ACE concentrations, and also to be an independent risk factor for the development of myocardial infarction, particularly in men thought to be at low risk by standard criteria. We determined the genotypes of individuals with end-stage heart failure due to either ischaemic dilated cardiomyopathy (102) or idiopathic dilated cardiomyopathy (112) and compared these to organ donors with normally functioning hearts (79). Genotypes were determined by the polymerase chain reaction with oligonucleotide primers flanking the polymorphic region in intron 16 of the ACE gene to amplify template DNA isolated from patients.

Structure of the rat gonadotropin releasing hormone (rGnRH) gene promoter and functional analysis in hypothalamic cells.

The gonadotropin releasing hormone (GnRH) gene encodes a protein which plays a critical role in mammalian reproductive physiology. Its expression is predominantly restricted to the hypothalamus although it has also been described in the placenta. To begin to determine the promoter elements important for tissue specific expression and to examine the mechanisms of developmental and hormonal regulation of the rat GnRH (rGnRH) gene, we cloned the rGnRH gene from a rat liver genomic DNA library.

Lipoprotein lipase gene expression in rat adipocytes is regulated by isoproterenol and insulin through different mechanisms.

Lipoprotein lipase (LPL) is highly regulated by catecholamines and insulin in adipocytes. Isoproterenol, a beta-adrenergic agonist, decreases LPL enzyme activity, whereas insulin increases LPL activity. We have isolated an 868-basepair rat LPL cDNA clone to assess hormone-mediated changes in LPL steady state mRNA levels and LPL gene transcription rates in adipocytes.

Comparison of immunoreactive gonadotropin-releasing hormone and human chorionic gonadotropin in term placentas from normal women and those with insulin-dependent and gestational diabetes.

We measured prohormone gonadotropin-releasing hormone (high-molecular-weight gonadotropin-releasing hormone), gonadotropin-releasing hormone and human chorionic gonadotropin concentrations in term placentas from normal women and those with insulin-dependent and gestational diabetes. The placental immunoreactive gonadotropin-releasing hormone levels were significantly higher in normal tissues than in tissues from insulin-dependent and gestational diabetes (p less than 0.01).