Live and carcass production traits for progeny of an F1 USDA Prime-Yield Grade 1 carcass clone sire compared to progeny of popular beef terminal sires.

The cloning of beef carcasses that grade United States Department of Agriculture (USDA) Prime-yield grade (YG) 1 (P1) has produced a sire that ranked well against high-performing bulls from multiple breeds. An F1 (P1 × P1 - first generation offspring) sire would ideally outperform its high-performing parents. A terminal sire study was conducted comparing progeny of an F1 (P1 × P1) sire (AxG1) against progeny (heifers and steers) of four high-performing sires of varying breeds {P1 (ALPHA); Angus; Simmental; Angus × Simmental}.

Live and carcass production traits for progeny of purebred sires in comparison with the clone of a USDA prime yield grade one carcass.

Cloning is a technology by which an animal's tissue can be salvaged and replicated. Carcasses that grade USDA prime-yield grade 1 (P1) represent a rare and antagonistic outcome and are a goal for terminal sire selection in the United States. A terminal sire progeny test generated offspring for a crossbred bull (14% Zebu, 86% Angus; ALPHA), born in 2012 via somatic cell nuclear transfer (SCNT) from a carcass that graded P1.

A new model of oxidative stress in rat pups.

Background: With current evidence, no specific oxygen concentration can yet be recommended in the resuscitation of the depressed term neonate.

Objectives: To design a neonatal rat model of resuscitation that mimics birth hypoxia and allows the study of the effects of resuscitation on outcome.

Methods: Several key determinants were established utilizing P12 Sprague-Dawley rat pups.

Neuroprotection in diet-induced ketotic rat brain after focal ischemia.

Neuroprotective properties of ketosis may be related to the upregulation of hypoxia inducible factor (HIF)-1alpha, a primary constituent associated with hypoxic angiogenesis and a regulator of neuroprotective responses. The rationale that the utilization of ketones by the brain results in elevation of intracellular succinate, a known inhibitor of prolyl hydroxylase (the enzyme responsible for the degradation of HIF-1alpha) was deemed as a potential mechanism of ketosis on the upregulation of HIF-1alpha. The neuroprotective effect of diet-induced ketosis (3 weeks of feeding a ketogenic diet), as pretreatment, on infarct volume, after reversible middle cerebral artery occlusion (MCAO), and the upregulation of HIF-1alpha were investigated.

Biochemical methods to assess the coupling of brain energy metabolism in control and disease states.

Mitochondrial dysfunction has been increasingly shown as a critical process that makes certain areas of the brain more susceptible not only to neurological disease but also to aging. Quantitative histochemistry is a series of procedures for measuring select metabolites in discrete regions of the brain, as they exist in vivo. The development of this method has been useful in establishing energy imbalance following ischemia but more recently has become useful in studying those processes related to the mitochondria which make the brain more susceptible to a variety of neurological insults.

Regional metabolic status of the E-18 rat fetal brain following transient hypoxia/ischemia.

Increasing evidence indicates that fetal metabolic stress may result in a variety of post-natal perturbations during brain development. The goal of the study was to determine the duration of hypoxia/ischemia that would elicit a demonstrable regional depression of metabolism in the fetal brain and further to examine several end-points to determine if the metabolic stress affects the developing brain. The uterine artery and uterine branch of the ovarian artery were occluded with aneurysm clamps for a period of 45 min, the clips removed and the metabolites in five regions of the perinatal brain were measured at 0, 2 and 6 h of reflow.

Adaptation to chronic hypoxia during diet-induced ketosis.

It is recognized that brain oxygen deprivation results in increased glycolysis and lactate accumulation. Moreover, glucose metabolism is altered during starvation or diet, resulting in increased plasma ketones (acetoacetate + beta-hydroxybutyrate; BHB). We investigated glucose and lactate adaptation to hypoxia in concurrence with diet-induced ketosis.

Adenosine treatment delays postischemic hippocampal CA1 loss after cardiac arrest and resuscitation in rats.

Resuscitation from cardiac arrest results in reperfusion injury that leads to increased postresuscitation mortality and delayed neuronal death. One of the many consequences of resuscitation from cardiac arrest is a derangement of energy metabolism and the loss of adenylates, impairing the tissue's ability to regain proper energy balance. In this study, we investigated the effects of adenosine (ADO) on the recovery of the brain from 12 min of ischemia using a rat model of cardiac arrest and resuscitation.

Neuronal migration is transiently delayed by prenatal exposure to intermittent hypoxia.

Background: Neonatal neurodevelopment is influenced by a variety of external factors, although the mechanisms responsible are poorly understood. Prenatal hypoxia, from physiological or chemical sources, can have no discernible effect, or can result in a broad spectrum of abnormalities.

Methods: To mimic some of the maternal effects of smoking, we developed a model that investigates the effects of intermittent hypoxia (IH), with or without concurrent nicotine in timed pregnant Sprague-Dawley rats.

Pc 4 photodynamic therapy of U87-derived human glioma in the nude rat.

Background And Objectives: As a potential therapy for malignant glioma, we tested the phthalocyanine photosensitizer Pc 4 for: (1) rapid clearance from the vasculature, (2) specificity for glioma, and (3) tumoricidal photosensitizing capability.

Study Design/materials And Methods: Parenchymal injection of U87 cells into athymic rat brains (N = 100) was followed after 12 days by tail vein injection of 0.5 mg/kg Pc 4.

Developmental changes induced by graded prenatal systemic hypoxic-ischemic insults in rats.

In infants, a common consequence of systemic perinatal insults is disruption of neonatal brain development. Such insults can cause cerebral palsy, cognitive delay, epilepsy and other chronic neurologic deficits in children. The mechanisms underlying disruption of brain development after perinatal insults are poorly defined.

Comparison of glucose influx and blood flow in retina and brain of diabetic rats.

Diabetes is associated with extensive microvascular pathology and decreased expression of the glucose transporter (GLUT-1) in retina, but not brain. To explore the basis of these differences, the authors simultaneously measured glucose influx (micromol x g(-1) x min(-1)) and blood flow (mL x g(-1) x min(-1)) in retina and brain cortex of nondiabetic control rats (normoglycemic and acute-hyperglycemic) and in rats with streptozotocin-induced diabetes (with or without aminoguanidine (AMG) treatment) using a single-pass, dual-label indicator method. In addition, tissue glucose and adenosine triphosphate (nmol/mg dry weight) levels were measured.

Compromised metabolic recovery following spontaneous spreading depression in the penumbra.

Spreading depression (SD) has been demonstrated following focal ischemia, and the additional workload imposed by SD on a tissue already compromised by a marked reduction in blood flow may contribute to the evolution of irreversible damage in the ischemic penumbra. SD was elicited in one group of rats by injecting KCl directly into a frontal craniectomy and the wave of depolarization was recorded in two craniectomies 3 and 6 mm posterior to the first one. In a second group, the middle cerebral artery was occluded using the monofilament technique and a recording electrode was placed 5 mm lateral to the midline and 0.

Changing metabolic and energy profiles in fetal, neonatal, and adult rat brain.

The regional energy status and the availability of metabolic substrates during brain development are important, since a variety of fetal metabolic insults have been increasingly implicated in the evolution of neonatal brain disorders. The response of the brain to a metabolic insult is determined, in large part, by the ability to utilize the various substrates for intermediary metabolism in order to maintain energy stores within the tissue. To ascertain if metabolic conditions of the fetal brain make it more or less vulnerable to a stress, the high-energy phosphates and glucose-related compounds were examined in five regions of the embryonic day 18 (E-18) fetal brain.

Activation of caspase-12, an endoplasmic reticulum resident caspase, after permanent focal ischemia in rat.

The endoplasmic reticulum (ER) is emerging as a contributory component of cell death after ischemia. Since caspase-12 has been localized to the ER and is a novel signal for apoptosis, we examined the message levels and protein expression of caspase-12 after cerebral ischemia in vivo. Animals underwent permanent middle cerebral artery occlusion (MCAO) and were sacrificed 24 h after ischemia.

Delayed changes in regional brain energy metabolism following cerebral concussion in rats.

Traumatic brain injury (TBI) results in an acute altered metabolic profile of brain tissue which resolves within hours of initial insult and yet some of the functional deficits and cellular perturbations persist for days. It is hypothesized that a delayed change in energy status does occur and is a factor in the neural tissue's ability to survive and regain function. Regional metabolic profile and glucose consumption were determined at either 1 or 3 days following two different intensities of parasagittal fluid-percussion (F-P).

Caspase-9 inhibition after focal cerebral ischemia improves outcome following reversible focal ischemia.

Cerebral ischemia initiates a program of cell death known as apoptosis. Early steps in these death promoting events are the release of cytochrome c from the mitochondria and activation of caspase-9. The purpose of this report is to determine if the administration of a specific caspase-9 inhibitor, Z-Leu-Glu(Ome)-His-Asp(Ome)-FMK x TFA (Z-LEHD-FMK) would attenuate apoptosis and the resultant brain injury after ischemia.

Alterations in matrix metalloproteinase-9 levels and tissue inhibitor of matrix metalloproteinases-1 expression in a transforming growth factor-beta transgenic model of hydrocephalus.

The development of spontaneous hydrocephalus in mouse models resulting from the overexpression of transforming growth factor-beta (TGFbeta-1) has been previously described, although the mechanism by which this occurs remains obscure. It has been previously demonstrated that increased expression of TGFbeta has consequences for the levels of matrix metalloproteinases (MMPs) and their specific inhibitors (tissue inhibitors of MMPs, or TIMPs). These remodeling proteins play an important role in extracellular matrix (ECM) maintenance through degradation and deposition of ECM components.

Ischemic cell death: dynamics of delayed secondary energy failure during reperfusion following focal ischemia.

Reperfusion injury is believed to contribute to the pathophysiology of ischemic cell death, but the precipitating factors have yet to be completely elucidated. The goal of this study was to examine if reflow-induced secondary energy failure is a component in the events that lead to cell death following increasing periods of middle cerebral artery (MCA) occlusion in Wistar rats. Discrete sections within the MCA distribution were dissected and analyzed for high-energy phosphates and glucose.