Body Condition of Endangered Humpback Chub in Relation to Temperature and Discharge in the Lower Colorado River

Determining the population status of endangered Humpback Chub Gila cypha is a major component of the adaptive management program designed to inform operation of Glen Canyon Dam upstream from Grand Canyon, Arizona. In recent decades, resource managers have identified a portfolio of management actions (with intermittent implementation) to promote population recovery of Humpback Chub, including nonnative fish removal, changes in water release volumes and discharge ramping schedules, and reductions in hydropower peaking operations. The Humpback Chub population in Grand Canyon has increased over this same period, causal factors for which are unclear. We took advantage of unusual hydrology in the Colorado River basin in 2011 to assess trends in juvenile Humpback Chub length–weight relationships and condition in the Colorado River below Glen Canyon Dam as well as in the unregulated Little Colorado River. Within each river, we observed higher length–weight b-parameter estimates (exponent of the standard power equation) at higher water temperatures. We also found higher slope estimates for the length–weight relationship at higher temperatures in the Little Colorado River. Slope estimates were more variable in the Colorado River, where mean water temperatures were more uniform. The next step is to examine whether Humpback Chub length–weight relationships influence population metrics such as abundance or survival. If these relationships exist, then monitoring condition in juvenile Humpback Chub would provide a quick and low-cost technique for assessing population response to planned management experiments or changing environmental conditions

Cognitive dysfunction in naturally occurring canine idiopathic epilepsy

Globally, epilepsy is a common serious brain disorder. In addition to seizure activity, epilepsy is associated with cognitive impairments including static cognitive impairments present at onset, progressive seizure-induced impairments and co-morbid dementia. Epilepsy occurs naturally in domestic dogs but its impact on canine cognition has yet to be studied, despite canine cognitive dysfunction (CCD) recognised as a spontaneous model of dementia. Here we use data from a psychometrically validated tool, the canine cognitive dysfunction rating (CCDR) scale, to compare cognitive dysfunction in dogs diagnosed with idiopathic epilepsy (IE) with controls while accounting for age. An online cross-sectional study resulted in a sample of 4051 dogs, of which n = 286 had been diagnosed with IE. Four factors were significantly associated with a diagnosis of CCD (above the diagnostic cut-off of CCDR ≥50): (i) epilepsy diagnosis: dogs with epilepsy were at higher risk; (ii) age: older dogs were at higher risk; (iii) weight: lighter dogs (kg) were at higher risk; (iv) training history: dogs with more exposure to training activities were at lower risk. Impairments in memory were most common in dogs with IE, but progression of impairments was not observed compared to controls. A significant interaction between epilepsy and age was identified, with IE dogs exhibiting a higher risk of CCD at a young age, while control dogs followed the expected pattern of low-risk throughout middle age, with risk increasing exponentially in geriatric years. Within the IE sub-population, dogs with a history of cluster seizures and high seizure frequency had higher CCDR scores. The age of onset, nature and progression of cognitive impairment in the current IE dogs appear divergent from those classically seen in CCD. Longitudinal monitoring of cognitive function from seizure onset is required to further characterise these impairments

Attenuation of Na/K-ATPase Mediated Oxidant Amplification with pNaKtide Ameliorates Experimental Uremic Cardiomyopathy

We have previously reported that the sodium potassium adenosine triphosphatase (Na/K-ATPase) can effect the amplification of reactive oxygen species. In this study, we examined whether attenuation of oxidant stress by antagonism of Na/K-ATPase oxidant amplification might ameliorate experimental uremic cardiomyopathy induced by partial nephrectomy (PNx). PNx induced the development of cardiac morphological and biochemical changes consistent with human uremic cardiomyopathy. Both inhibition of Na/K-ATPase oxidant amplification with pNaKtide and induction of heme oxygenase-1 (HO-1) with cobalt protoporphyrin (CoPP) markedly attenuated the development of phenotypical features of uremic cardiomyopathy. In a reversal study, administration of pNaKtide after the induction of uremic cardiomyopathy reversed many of the phenotypical features. Attenuation of Na/K-ATPase oxidant amplification may be a potential strategy for clinical therapy of this disorder