bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suspected drug‐induced infiltrative lung disease culminating in acute respiratory failure in a dog treated with cytarabine and prednisone
Authors: Hart Samantha K. , Waddell, Lori 
Published: April 2016

AbstractObjectiveTo describe a case of suspected drug‐induced infiltrative lung disease (ILD) and acute respiratory failure associated with the administration of cytarabine and prednisone in a dog requiring mechanical ventilation.Case SummaryA 4.5‐year‐old, female spayed Yorkshire Terrier presented to the ICU with acute onset of respiratory distress following a 24‐hour cytarabine infusion. The patient was previously diagnosed with meningoencephalitis of unknown etiology (MUO), caudal occipital malformation, and syringohydromyelia, and was being treated with oral prednisone and levetiracetam, and cytarabine infusions. The patient developed tachypnea and dyspnea, and had diffuse crackles on auscultation of all lung fields, and hypoxemia 6 hours following completion of the fourth cytarabine infusion (300 mg/m2). Thoracic radiographs revealed diffuse, bilateral infiltrates consistent with noncardiogenic pulmonary edema or acute respiratory distress syndrome. Respiratory distress and hypoxemia persisted despite oxygen supplementation and furosemide therapy and led to initiation of mechanical ventilation. Approximately 12 hours later, the dog became progressively hypoxemic with worsening pulmonary edema. The owners elected euthanasia. Postmortem examination revealed pulmonary edema and diffuse interstitial pneumonia. Histopathologic evaluation revealed pulmonary edema, severe acute neutrophilic and histiocytic pneumonia, and multifocal interstitial fibrosis. Bacterial culture yielded no growth.New or Unique Information ProvidedDrug‐induced ILD is rarely reported in the veterinary literature, and has not previously been reported in dogs receiving cytarabine. As with administration of any medication, adverse events may occur. While ILD is unlikely to be commonly recognized, it may be considered in veterinary patients receiving chemotherapy that acutely become dyspneic.
Impact of fungal species cultured on outcome in horses with fungal keratitis
Authors: Sherman Amanda B. , Clode Alison B. , Gilger Brian C. 
Published: April 2016

AbstractPurposeTo determine the significance ofAspergillusandFusariumspp., as identified by culture, on clinical outcome in equine keratomycosis.MethodsRetrospective analysis of 66 horses (66 eyes) evaluated at the NCSU‐VH diagnosed with keratomycosis from whichAspergillusorFusariumspp. were cultured. Horses were classified into those who improved with medical management alone or those who required surgical intervention to improve. Horses who underwent surgery were divided into globe‐sparing procedures or enucleation. Effects of bacterial co‐infection, previous topical steroid or antifungal use, and time of year on fungal genus and outcome were evaluated.ResultsAspergillusspp. was cultured from 41 eyes (63%), while 24 eyes (37%) culturedFusariumspp. One horse cultured both species and was not included in further evaluation. From the horses that culturedAspergillusspp., 28 eyes (68%) required surgical intervention to control the infection: 21 (75%) of these eyes maintained globe integrity, while 7 eyes (25%) were enucleated. Of those horses withFusariumspp., 14 eyes (58%) required surgical intervention: 11 (79%) of these eyes maintained globe integrity, while 3 eyes (21%) were enucleated. Genus of fungus cultured was not significantly associated with the need for surgical intervention nor was it significantly associated with the necessity of globe‐sparing surgery versus enucleation. Additionally, bacterial co‐infection, previous steroidal or antifungal use, and time of year did not affect outcome or type of fungal species cultured.ConclusionEquine keratomycosis fromFusariumspp. compared to keratomycosis fromAspergillusspp. is not associated with a different clinical outcome.
Combined Campylobacter jejuni and Campylobacter coli Rapid Testing and Molecular Epidemiology in Conventional Broiler Flocks
Authors: Schallegger G. , Muri‐Klinger S. , Brugger K. , Lindhardt C. , John L. , Glatzl M. , Wagner M. , Stessl B. 
Published: April 2016

SummaryCampylobacter spp. are important causes of bacterial zoonosis, most often transmitted by contaminated poultry meat. From an epidemiological and risk assessment perspective, further knowledge should be obtained on Campylobacter prevalence and genotype distribution in primary production. Consequently, 15 Austrian broiler flocks were surveyed in summer for their thermophilic Campylobacter spp. contamination status. Chicken droppings, dust and drinking water samples were collected from each flock at three separate sampling periods. Isolates were confirmed by PCR and subtyped. We also compared three alternative methods (culture‐based enrichment in Bolton broth, culture‐independent real‐time PCR and a lateral‐flow test) for their applicability in chicken droppings. Twelve flocks were found to be positive for thermophilic Campylobacter spp. during the entire sampling period. Seven flocks (46.6%) were contaminated with both, C. jejuni and C. coli, five flocks harboured solely one species. We observed to a majority flock‐specific C. jejuni and C. coli genotypes, which dominated the respective flock. Flocks within a distance <2 km shared the same C. jejuni genotypes indicating a cross‐contamination event via the environment or personnel vectors. Multilocus sequence typing (MLST) of C. jejuni revealed that the majority of isolates were assigned to globally distributed clonal complexes or had a strong link to the human interface (CC ST‐446 and ST4373). The combination of techniques poses an advantage over risk assessment studies based on cultures alone, as, in the case of Campylobacter, occurrence of a high variety of genotypes might be present among a broiler flock. We suggest applying the lateral‐flow test under field conditions to identify ‘high‐shedding’ broiler flocks at the farm level. Consequently, poultry farmers and veterinarians could improve hygiene measurements and direct sanitation activities, especially during the thinning period. Ultimately, real‐time PCR could be applied to quantify Campylobacter spp. directly from chicken droppings and avoid non‐interpretable results achieved by culture‐dependent methods.
Lessons from the laboratory; integrated regulation of cerebral blood flow during hypoxia
Authors: Ainslie Philip N. , Hoiland Ryan L. , Bailey Damian M. 
Published: April 2016

New Findings

What is the topic of this review?
What is the mechanism underlying the control of human cerebral blood flow in hypoxia and what are the consequences?

What advances does it highlight?
Although appropriate elevations in cerebral blood flow occur in acute and chronic hypoxia, neuronal processes are more sensitive to even small hypoxic insults; hence, they can result in maladaptive consequences despite maintenance of global oxygen delivery.

Exposure to acute or chronic hypoxaemia in otherwise healthy humans results in compensatory increases in cerebral blood flow (CBF) at rest and during exercise, referred to as hypoxic cerebral vasodilatation. These elevations in CBF offset the reduction in arterial oxygen content and maintain cerebral O2 delivery, conforming to the conservation of mass principle. In this review, we discuss the fundamental principles that contribute to the defence of cerebral O2 delivery and the corresponding implications for metabolism. We critically address to what extent the increase in CBF reflects an adaptive or indeed maladaptive physiological response. The molecular mechanisms of CBF regulation in hypoxia are also briefly discussed and future directions proposed.
Mitochondria in the middle: exercise preconditioning protection of striated muscle
Authors: Lawler John M. , Rodriguez Dinah A. , Hord Jeffrey M. 
Published: April 2016

AbstractCellular and physiological adaptations to an atmosphere which became enriched in molecular oxygen spurred the development of a layered system of stress protection, including antioxidant and stress response proteins. At physiological levels reactive oxygen and nitrogen species regulate cell signalling as well as intracellular and intercellular communication. Exercise and physical activity confer a variety of stressors on skeletal muscle and the cardiovascular system: mechanical, metabolic, oxidative. Transient increases of stressors during acute bouts of exercise or exercise training stimulate enhancement of cellular stress protection against future insults of oxidative, metabolic and mechanical stressors that could induce injury or disease. This phenomenon has been termed both hormesis and exercise preconditioning (EPC). EPC stimulates transcription factors such as Nrf‐1 and heat shock factor‐1 and up‐regulates gene expression of a cadre of cytosolic (e.g. glutathione peroxidase and heat shock proteins) and mitochondrial adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome proliferator activated receptor γ coactivator‐1 (PGC‐1)). Stress response and antioxidant enzyme inducibility with exercise lead to protection against striated muscle damage, oxidative stress and injury. EPC may indeed provide significant clinical protection against ischaemia–reperfusion injury, Type II diabetes and ageing. New molecular mechanisms of protection, such as δ‐opioid receptor regulation and mitophagy, reinforce the notion that mitochondrial adaptations (e.g. heat shock proteins, antioxidant enzymes and sirtuin‐1/PGC‐1 signalling) are central to the protective effects of exercise preconditioning.
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Anti‐inflammatory properties of the vagus nerve: potential therapeutic implications of vagus nerve stimulation
Authors: Bonaz Bruno , Sinniger Valérie , Pellissier Sonia 
Published: April 2016

AbstractBrain and viscera interplay within the autonomic nervous system where the vagus nerve (VN), containing approximately 80% afferent and 20% efferent fibres, plays multiple key roles in the homeostatic regulations of visceral functions. Recent data have suggested the anti‐inflammatory role of the VN. This vagal function is mediated through several pathways, some of them still debated. The first one is the anti‐inflammatory hypothalamic–pituitary–adrenal axis which is stimulated by vagal afferent fibres and leads to the release of cortisol by the adrenal glands. The second one, called the cholinergic anti‐inflammatory pathway, is mediated through vagal efferent fibres that synapse onto enteric neurons which release acetylcholine (ACh) at the synaptic junction with macrophages. ACh binds to α‐7‐nicotinic ACh receptors of those macrophages to inhibit the release of tumour necrosis (TNF)α, a pro‐inflammatory cytokine. The last pathway is the splenic sympathetic anti‐inflammatory pathway, where the VN stimulates the splenic sympathetic nerve. Norepinephrine (noradrenaline) released at the distal end of the splenic nerve links to the β2 adrenergic receptor of splenic lymphocytes that release ACh. Finally, ACh inhibits the release of TNFα by spleen macrophages through α‐7‐nicotinic ACh receptors. Understanding of these pathways is interesting from a therapeutic point of view, since they could be targeted in various ways to stimulate anti‐inflammatory regulation in TNFα‐related diseases such as inflammatory bowel disease and rheumatoid arthritis. Among others, VN stimulation, either as an invasive or non‐invasive procedure, is becoming increasingly frequent and several clinical trials are ongoing to evaluate the potential effectiveness of this therapy to alleviate chronic inflammation.
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Emerging roles of the myocardin family of proteins in lipid and glucose metabolism
Authors: Swärd Karl , Stenkula Karin G , Rippe Catarina , Alajbegovic Azra , Gomez Maria F. , Albinsson Sebastian 
Published: April 2016

AbstractMembers of the myocardin family bind to the transcription factor serum response factor (SRF) and act as coactivators controlling genes of relevance for myogenic differentiation and motile function. Binding of SRF to DNA is mediated by genetic elements called CArG boxes, found often but not exclusively in muscle and growth controlling genes. Studies aimed at defining the full spectrum of these CArG elements in the genome (i.e. the CArGome) have in recent years, unveiled unexpected roles of the myocardin family proteins in lipid and glucose homeostasis. This coactivator family includes the protein myocardin (MYOCD), the myocardin‐related transcription factors A and B (MRTF‐A/MKL1 and MRTF‐B/MKL2) and MASTR (MAMSTR). Here we discuss growing evidence that SRF‐driven transcription is controlled by extracellular glucose through activation of the Rho‐kinase pathway and actin polymerization. We also describe data showing that adipogenesis is influenced by MLK activity through actions upstream of peroxisome proliferator‐activated receptor γ with consequences for whole body fat mass and insulin sensitivity. The recently demonstrated involvement of myocardin coactivators in the biogenesis of caveolae, Ω‐shaped membrane invaginations of importance for lipid and glucose metabolism, is finally discussed. These novel roles of myocardin proteins may open the way for new unexplored strategies to combat metabolic diseases such as diabetes, which, at the current incidence, is expected to reach 333 million people worldwide by 2025.This review highlights newly discovered roles of myocardin‐related transcription factors in lipid and glucose metabolism as well as novel insights into their well‐established role as mediators of stretch‐dependent effects in smooth muscle. As co‐factors for serum response factor (SRF), MKLs regulates transcription of genes involved in the contractile function of smooth muscle cells. In addition to mechanical stimuli, this regulation has now been found to be promoted by extracellular glucose levels in smooth muscle. Recent reports also suggest that MKLs can regulate a subset of genes involved in the formation of lipid‐rich invaginations in the cell membrane called caveolae. Finally, a potential role of MKLs in non‐muscle cells has been discovered as they negatively influence adipocyte differentiation.
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Hepatic mitochondrial oxidative phosphorylation is normal in obese patients with and without type 2 diabetes
Authors: Lund Michael Taulo , Kristensen Marianne , Hansen Merethe , Tveskov Louise , Floyd Andrea Karen , Støckel Mikael , Vainer Ben , Poulsen Steen Seier , Helge Jørn Wulff , Prats Clara , Dela Flemming 
Published: April 2016

Key points
Hepatic insulin resistance in patients with obesity or type 2 diabetes has been suggested to result from hepatic mitochondrial dysfunction.
High‐resolution respirometry (HRR) can be used to assess oxidative phosphorylation by measuring the mitochondrial oxygen consumption rate in the individual complexes of the mitochondria.
By using HRR, the present study demonstrates no difference in hepatic mitochondrial oxidative phosphorylation among subjects with obesity with or without type 2 diabetes and non‐obese controls.
Furthermore, the amount of mitochondria, assessed by the citrate synthase activity, is not different between the three groups.
Together the present findings indicate that hepatic mitochondrial oxidative phosphorylation capacity is not impaired in patients with obesity or type 2 diabetes.
AbstractObese patients with type 2 diabetes (T2DM) and without type 2 diabetes (OB) are characterized by high hepatic lipid content and hepatic insulin resistance. This may be linked to impaired hepatic mitochondrial oxidative phosphorylation (OXPHOS) capacity. The aim of the present study was to investigate and compare hepatic mitochondrial OXPHOS capacity in T2DM, OB and non‐obese controls (CON). Seventeen obese patients (nine OB and eight T2DM) and six CON patients had perioperative liver biopsies taken. Samples were divided into three parts to measure (1) complex I, II and IV linked respiration, (2) citrate synthase (CS) activity and (3) lipid droplet (LD) size and area (% of total tissue area filled by LDs). State 3 respiration of complex I, II and IV and the CS activity did not differ in OB, T2DM and CON. LD size was significantly higher in T2DM compared with CON, and LD area tended (P = 0.10) to be higher in T2DM and OB compared with CON. The present findings indicate that hepatic OXPHOS capacity is not different in patients with markedly different weight and glycaemic control. Furthermore, the results do not support impaired hepatic mitochondrial respiratory capacity playing a major role in the development of obesity‐induced type 2 diabetes.
Immature endothelial cells initiate endothelin‐mediated constriction of newborn arteries
Authors: Chang Fumin , Flavahan Sheila , Flavahan Nicholas A. 
Published: April 2016

Key points
Endothelial expression and the release of endothelin‐1 (ET‐1) in levels sufficient to initiate vasoconstriction is considered to be a hallmark feature of pathological endothelial dysfunction.
During the immediate postnatal period, arterial endothelial cells undergo remarkable structural and functional changes as they transition to a mature protective cell layer, which includes a marked increase in NO dilator activity.
The present study demonstrates that endothelial cells lining newborn central arteries express high levels of ET‐1 peptides and, in response to endothelial stimulation, rapidly release ET‐1 and initiate powerful ET‐1‐mediated constriction. This activity is lost as the endothelium matures in the postnatal period.
Heightened activity of ET‐1 in the neonatal endothelium might contribute to inappropriate responses of immature arteries to stress or injury. Indeed, the immature endothelium resembles dysfunctional endothelial cells, and retention or re‐emergence of this phenotype may contribute to the development of vascular disease.
AbstractEndothelial cells lining fetal and newborn arteries have an unusual phenotype, including reduced NO activity, prominent actin stress fibres and poorly developed cellular junctions. Experiments were performed to determine whether the immature endothelium of newborn arteries also expresses and releases endothelin‐1 (ET‐1) and initiates endothelium‐dependent constriction. Carotid arteries were isolated from newborn (postnatal day 1; P1), postnatal day 7 (P7) and postnatal day 21 (P21) mice and assessed in a pressure myograph system. Endothelial stimulation with A23187 or thrombin caused constriction in P1 arteries, no significant change in diameter of P7 arteries, and dilatation in P21 arteries. In P1 arteries, constriction to thrombin or A23187 was inhibited by endothelial‐denudation, by ET‐1 receptor antagonists (BQ123 plus BQ788) or by inhibition of endothelin‐converting enzyme (phosphoramidon or SM19712). ET‐1 receptor antagonism did not affect responses to thrombin or A23187 in more mature arteries. Exogenous ET‐1 caused similar concentration‐dependent constrictions of P1, P7 and P21 arteries. Endothelial stimulation with thrombin rapidly increased the endothelial release of ET‐1 from P1 but not P21 aortas. Endothelial expression of ET‐1 peptides, as assessed by immunofluorescence analysis, was increased in P1 compared to P21 arteries. Therefore, newborn endothelial cells express high levels of ET‐1 peptides, rapidly release ET‐1 in response to endothelial stimulation, and initiate ET‐1‐mediated endothelium‐dependent constriction. This activity is diminished as the endothelium matures in the immediate postnatal period. Heightened activity of ET‐1 in neonatal endothelium probably reflects an early developmental role of the peptide, although this might contribute to inappropriate responses of immature arteries to stress or injury.
An augmented CO2 chemoreflex and overactive orexin system are linked with hypertension in young and adult spontaneously hypertensive rats
Authors: Li Aihua , Roy Sarah H. , Nattie Eugene E. 
Published: April 2016

Key points
Activation of central chemoreceptors by CO2 increases sympathetic nerve activity (SNA), arterial blood pressure (ABP) and breathing. These effects are exaggerated in spontaneously hypertensive rats (SHRs), resulting in an augmented CO2 chemoreflex that affects both breathing and ABP.
The augmented CO2 chemoreflex and the high ABP are measureable in young SHRs (postnatal day 30–58) and become greater in adult SHRs.
Blockade of orexin receptors can normalize the augmented CO2 chemoreflex and the high ABP in young SHRs and normalize the augmented CO2 chemoreflex and significantly lower the high ABP in adult SHRs.
In the hypothalamus, SHRs have more orexin neurons, and a greater proportion of them increase their activity with CO2.
The orexin system is overactive in SHRs and contributes to the augmented CO2 chemoreflex and hypertension. Modulation of the orexin system may be beneficial in the treatment of neurogenic hypertension.
AbstractActivation of central chemoreceptors by CO2 increases arterial blood pressure (ABP), sympathetic nerve activity and breathing. In spontaneously hypertensive rats (SHRs), high ABP is associated with enhanced sympathetic nerve activity and peripheral chemoreflexes. We hypothesized that an augmented CO2 chemoreflex and overactive orexin system are linked with high ABP in both young (postnatal day 30–58) and adult SHRs (4–6 months). Our main findings are as follows. (i) An augmented CO2 chemoreflex and higher ABP in SHRs are measureable at a young age and increase in adulthood. In wakefulness, the ventilatory response to normoxic hypercapnia is higher in young SHRs (mean ± SEM: 179 ± 11% increase) than in age‐matched normotensive Wistar–Kyoto rats (114 ± 9% increase), but lower than in adult SHRs (226 ± 10% increase; P < 0.05). The resting ABP is higher in young SHRs (122 ± 5 mmHg) than in age‐matched Wistar–Kyoto rats (99 ± 5 mmHg), but lower than in adult SHRs (152 ± 4 mmHg; P < 0.05). (ii) Spontaneously hypertensive rats have more orexin neurons and more CO2‐activated orexin neurons in the hypothalamus. (iii) Antagonism of orexin receptors with a dual orexin receptor antagonist, almorexant, normalizes the augmented CO2 chemoreflex in young and adult SHRs and the high ABP in young SHRs and significantly lowers ABP in adult SHRs. (iv) Attenuation of peripheral chemoreflexes by hyperoxia does not abolish the augmented CO2 chemoreflex (breathing and ABP) in SHRs, which indicates an important role for the central chemoreflex. We suggest that an overactive orexin system may play an important role in the augmented central CO2 chemoreflex and in the development of hypertension in SHRs.
Effects of tensor couplings of ω and ρ mesons on 1S0 nucleon superfluidity in neutron star matter
Authors: Huang Xiu-Lin , Xu Yan , Liu Cheng-Zhi , Liu Guang-Zhou 
Published: April 2016

The [Formula: see text] nucleon superfluidity in neutron star matter was investigated in the framework of relativistic [Formula: see text] model with the tensor couplings of [Formula: see text] and [Formula: see text] mesons using the relativistic Hartree–Fock (RHF) approximation. It was found that the tensor couplings of [Formula: see text] and [Formula: see text] mesons lead to a clear growth of the [Formula: see text] neutron pairing gap in the density range where there exists [Formula: see text] neutron superfluidity. The [Formula: see text] pairing gap of proton with the tensor couplings of [Formula: see text] and [Formula: see text] mesons in the density range of [Formula: see text]–[Formula: see text][Formula: see text]fm[Formula: see text] is lower and then in the density range of [Formula: see text]–[Formula: see text][Formula: see text]fm[Formula: see text] higher than the corresponding value without the tensor couplings of [Formula: see text] and [Formula: see text] mesons. Our results provide a basic to understand the influence of the tensor couplings of [Formula: see text] and [Formula: see text] mesons on the cooling properties of neutron star.