Fishery catch records support machine learning-based prediction of illegal fishing off US West Coast.

Illegal, unreported, and unregulated (IUU) fishing is a major problem worldwide, often made more challenging by a lack of at-sea and shoreside monitoring of commercial fishery catches. Off the US West Coast, as in many places, a primary concern for enforcement and management is whether vessels are illegally fishing in locations where they are not permitted to fish. We explored the use of supervised machine learning analysis in a partially observed fishery to identify potentially illicit behaviors when vessels did not have observers on board.

UPRLIMET: UPstream Regional LiDAR Model for Extent of Trout in stream networks.

Predicting the edges of species distributions is fundamental for species conservation, ecosystem services, and management decisions. In North America, the location of the upstream limit of fish in forested streams receives special attention, because fish-bearing portions of streams have more protections during forest management activities than fishless portions. We present a novel model development and evaluation framework, wherein we compare 26 models to predict upper distribution limits of trout in streams.

Insights into estuary habitat loss in the western United States using a new method for mapping maximum extent of tidal wetlands.

Effective conservation and restoration of estuarine wetlands require accurate maps of their historical and current extent, as well as estimated losses of these valued habitats. Existing coast-wide tidal wetland mapping does not explicitly map historical tidal wetlands that are now disconnected from the tides, which represent restoration opportunities; nor does it use water level models or high-resolution elevation data (e.g.

Impact of multiple stressors on juvenile fish in estuaries of the northeast Pacific.

A key step in identifying global change impacts on species and ecosystems is to quantify effects of multiple stressors. To date, the science of global change has been dominated by regional field studies, experimental manipulation, meta-analyses, conceptual models, reviews, and studies focusing on a single stressor or species over broad spatial and temporal scales. Here, we provide one of the first studies for coastal systems examining multiple stressor effects across broad scales, focused on the nursery function of 20 estuaries spanning 1,600 km of coastline, 25 years of monitoring, and seven fish and invertebrate species along the northeast Pacific coast.

Crosstalk between leptin and interleukin-1β abrogates negative inotropic effects in a model of chronic hyperleptinemia.

Interleukin 1 beta (IL-1β) is a proinflammatory cytokine with potent cardiosuppressive effects. Previous studies have shown that leptin blunts the negative inotropic effects of IL-1β in isolated adult rat cardiac myocytes. However, the interactions between leptin and IL-1β in the heart have not been examined on a background of chronic hyperleptinemia.

Endurance exercise training reduces cardiac sodium/calcium exchanger expression in animals susceptible to ventricular fibrillation.

Aim: Increased sodium/calcium exchanger activity (NCX1, an important regulator of cardiomyocyte cystolic calcium) may provoke arrhythmias. Exercise training can decrease NCX1 expression in animals with heart failure improving cytosolic calcium regulation, and could thereby reduce the risk for ventricular fibrillation (VF).

Methods: To test this hypothesis, a 2-min coronary occlusion was made during the last minute of exercise in dogs with healed myocardial infarctions; 23 had VF (S, susceptible) and 13 did not (R, resistant).

Adipokines: a review of biological and analytical principles and an update in dogs, cats, and horses.

In addition to its role as an energy storage depot, adipose tissue is now recognized as a complex endocrine organ. Adipose tissue releases a variety of factors, termed adipokines, that regulate energy metabolism, cardiovascular function, reproductive status, and immune function. Some of the better-studied adipokines include leptin, adiponectin, and components of the renin-angiotensin system such as angiotensinogen.

Salt-induced cardiac hypertrophy is independent of blood pressure and endothelin in obese, heart failure-prone SHHF rats.

The interaction of salt sensitivity and obesity in development of cardiac hypertrophy is incompletely understood. The SHHF/Mcc-fa(cp) (SHHF) rat model was used to examine the effect of high salt on cardiac hypertrophy and expression of endothelin (ET) and nitric oxide synthase (NOS) isoforms. Homozygous lean (+/+) and obese (fa(cp)/fa(cp)) SHHF were fed a low-salt diet (0.

Leptin modulates the negative inotropic effect of interleukin-1beta in cardiac myocytes.

Interleukin-1beta (IL-1beta) is a potent negative inotrope implicated in the functional abnormalities of heart failure. Because the adipokine, leptin, protects against some of the cardiovascular effects of endotoxin, we hypothesized that leptin may modulate the cardiosuppressive effects of IL-1beta in isolated cardiomyocytes. Ventricular cardiac myocytes isolated from adult male Sprague Dawley rats were analyzed simultaneously for electrically stimulated contractility and calcium transients following 30 min exposure to IL-1beta (10 ng/ml) with or without 60 min pretreatment with leptin (25 ng/ml).

Exercise training normalizes beta-adrenoceptor expression in dogs susceptible to ventricular fibrillation.

Previous studies demonstrated an enhanced beta(2)-adrenoceptor (AR) responsiveness in animals susceptible to ventricular fibrillation (VF) that was eliminated by exercise training. The present study investigated the effects of endurance exercise training on beta(1)-AR and beta(2)-AR expression in dogs susceptible to VF. Myocardial ischemia was induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise in dogs with healed infarctions: 20 had VF [susceptible (S)] and 13 did not [resistant (R)].

Combined effects of low-dose oral spironolactone and captopril therapy in a rat model of spontaneous hypertension and heart failure.

The effects of low-dose oral spironolactone (SPIRO) in a rat model of hypertensive heart failure (spontaneously hypertensive heart failure rat) were compared with its effects when combined with captopril (CAP). Twenty-six spontaneously rats with hypertensive heart failure were treated with either placebo (CON), SPIRO (20 mg/kg/d by mouth), CAP (100 mg/kg/d by mouth), or both SPIRO and CAP for 12 weeks. This dose of oral SPIRO did not affect blood pressure, left ventricular end-diastolic diameter, left ventricular ejection fraction, plasma atrial natriuretic peptide concentration, or cardiac fibrosis; however, in combination with CAP, it exerted a significant depressor effect after 12 weeks of treatment that was accompanied by increased urine output and decreased urinary protein excretion.

Increased salt sensitivity secondary to leptin resistance in SHHF rats is mediated by endothelin.

A link between leptin resistance, obesity, and salt sensitivity has been suggested. SHHF/Mcc-fa(cp) rats (SHHF) were used to study the effect of gene dosage of a null mutation of the leptin receptor (cp) on salt sensitivity and response to a combined endothelin A and B receptor antagonist (bosentan). Obese (cp/cp), heterozygous (+/cp), and homozygous lean (+/+) male SHHF were fed a low salt diet (0.

Gender modulates activation of renin-angiotensin and endothelin systems in hypertension and heart failure.

Sexual dimorphism may occur during the development of hypertension and congestive heart failure (CHF). Male and female spontaneous hypertension heart failure (SHHF) rats with established hypertension, but before CHF (age 5-8 mo) and during cardiac decompensation leading to CHF (age 18-20 mo in male rats and 22-24 mo in female rats), were studied. At 5-8 mo, male SHHF rats showed early activation of the renin-angiotensin system (RAS), as indicated by increased plasma renin activity (PRA) and higher serum angiotensin-converting enzyme activity compared with female rats.

Obese female SHHF/Mcc-fa(cp) rats resist antihypertensive effects of renin-angiotensin system inhibition.

Gender and obesity may influence response to pharmacological modulation of the renin-angiotensin system. We used SHHF/Mcc-fa(cp) rats to study effect of obesity and gender on the ability of an AT1 receptor antagonist to decrease blood pressure. After 2 weeks treatment with irbesartan (50 mg/kg), only lean and obese males showed significant decreases in blood pressure, while obese females were completely resistant.

Microsphere-adenoviral complexes target and transduce the glomerulus in vivo.

Background: Developing new treatments for glomerulonephritis makes the glomerulus a logical target for gene therapy. Microspheres may lodge in the glomerulus, and replication-deficient recombinant adenoviruses are potent mediators of gene transfer. We postulated that adenoviral-microsphere complexes could result in DNA transfer (transduction) into glomerular cells in vivo.

Endothelial dysfunction and peroxynitrite formation are early events in angiotensin-induced cardiovascular disorders.

Angiotensin II (ANG II) is a well-established participant in many cardiovascular disorders, but the mechanisms involved are not clear. Vascular cell experiments suggest that ANG II is a potent stimulator of free radicals such as superoxide anion, an agent known to inactivate nitric oxide and promote the formation of peroxynitrite. Here we hypothesized that ANG II reduces the efficacy of NO-mediated vascular relaxation and promotes vascular peroxynitrite formation in vivo.

Myocardial tumor necrosis factor-alpha secretion in hypertensive and heart failure-prone rats.

Acute increases in blood pressure (BP) increase myocardial tumor necrosis factor (TNF)-alpha production, but it is not known whether chronic hypertensive stress elevates myocardial TNF-alpha production, possibly contributing to cardiac remodeling, decreased cardiac function, and faster progression to heart failure. BP, cardiac function, and size were evaluated in normotensive [Sprague-Dawley (SD)], spontaneously hypertensive (SHR), and spontaneously hypertensive heart failure-prone (SHHF) rats at 6, 12, 15, and 18 mo of age and in failing SHHF. Left ventricular tissues were evaluated for secretion of bioactive TNF-alpha and inhibition of TNF-alpha secretion by phosphodiesterase inhibitors.

Effect of ovariectomy and estrogen replacement on cardiovascular disease in heart failure-prone SHHF/Mcc- fa cp rats.

The importance of endogenous and exogenous estrogen levels to the development of cardiovascular disease in women in controversial. The purpose of our study was to examine the effect of estrogen on the development of hypertension, cardiac hypertrophy, ventricular function, and gene expression for atrial natriuretic peptide (ANP) and components of the renin angiotensin system in spontaneously hypertensive heart failure rats (SHHF/Mcc- facp). Development of hypertension was prevented in 3-month-old ovariectomized rats receiving subcutaneous 17 beta -estradiol implants (EST) compared to ovariectomized (OVX) and controls (CON).

Comparison of irbesartan with captopril effects on cardiac hypertrophy and gene expression in heart failure-prone male SHHF/Mcc-fa(cp) rats.

Angiotensin-converting enzyme (ACE) inhibitors have proven an effective means to control hypertension and manage cardiac hypertrophy. It is presently unknown if newer specific angiotensin II subtype 1 receptor (AT1R) antagonists are as effective or more effective in treating these conditions compared with ACE inhibitors. There is evidence that these classes of drugs may affect cardiac hypertrophy by different mechanisms.

Effect of ovariectomy in heart failure-prone SHHF/Mcc-facp rats.

The importance of the loss of ovarian function to the progression of hypertension and heart disease in women is controversial. We investigated whether ovariectomy would accelerate development of hypertension, congestive heart failure, and neurohumoral activation in adult spontaneous hypertension heart failure (SHHF) rats, a genetic model of heart failure. Six months after ovariectomy, no significant differences between control and ovariectomized rats were seen in systolic or diastolic blood pressure, left ventricular fractional shortening by echocardiography, or heart weight.

Age-dependent augmentation of cardiac endothelial NOS in a genetic rat model of heart failure.

Alterations in nitric oxide (NO) biosynthesis in the heart have been implicated in the pathophysiology of heart failure. We compared changes in cardiac nitric oxide synthase (NOS) activity and expression in genetically heart failure-prone (SHHF) rats at 6, 12, and 18 mo of age with those in age-matched spontaneously hypertensive (SHR) and Sprague-Dawley (SD) rats. Systolic blood pressure was significantly higher in SHHF and SHR rats compared with SD rats; however, it declined with age in SHHF rats only.

Plasma renin activity in heart failure-prone SHHF/Mcc-facp rats.

Plasma renin activity (PRA) increases during heart failure; however, PRA is altered by drug therapy, and it is difficult to study the natural progression of elevated PRA in humans and the possible factors that contribute to its rise. This study evaluated PRA in a drug-naive hypertensive rat model (SHHF/Mcc-facp) that has a genetic program resulting in heart failure (HF). Mean arterial blood pressure and PRA were determined and correlated to heart weight index in conscious normotensive, spontaneously hypertensive rats and HF rats of various ages.

Pharmacological modulation of myocardial tumor necrosis factor alpha production by phosphodiesterase inhibitors.

Phosphodiesterase (PDE) inhibitors are used as therapeutic agents for management of congestive heart failure. PDE inhibitors are potent inotropic and vasodilator drugs, which have also been shown to inhibit tumor necrosis factor alpha (TNF-alpha) production. TNF-alpha is a pleiotropic cytokine that has the ability to produce cardiac depressant and other cardiovascular effects in many disease conditions.