Publications by authors named "Premont J"

Purpose: To evaluate bacterial contamination of conjunctiva and aqueous humor in dogs undergoing phacoemulsification following asepsis with 0.5% povidone iodine and determine the influence of intravenous antibiotics on outcome of contamination.

Methods: Client-owned dogs were prospectively enrolled and randomly assigned to a control group, receiving 22 mg/kg intravenous cefazolin at induction prior to sampling, or experimental group receiving no antibiotic prior to sampling, masked to the surgeon.

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Objective: To describe the effects of gabapentin on ocular and behavioral parameters following oral administration in healthy cats.

Materials And Methods: Masked, placebo-controlled, randomized crossover-design study. Ten young, healthy cats were scheduled for two veterinary visits 7 days apart and randomly assigned to receive a compounded capsule containing 100 mg of gabapentin or placebo (100 mg lactose powder) at the first visit and the opposite treatment at the second visit.

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Objective: To characterize the clinical presentation, advanced imaging features, and outcome of orbital disease in a referral population of dogs and cats that underwent computed tomography (CT) or magnetic resonance imaging (MRI).

Animals Studied: Client-owned animals.

Procedures: Animals referred for orbital disease undergoing ophthalmic examination and either head MRI or CT were included.

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Objective: To report outcomes and follow-up of Baerveldt implant surgery in dogs with primary closed-angle glaucoma (PCAG).

Materials And Methods: Record review of client-owned dogs with PCAG that underwent Baerveldt implant surgery during a 6-year period. Postoperative intraocular pressure (IOP), vision and daily number of anti-glaucoma drops at fixed time points (3, 12, and 24 months) were compared with preoperative values; complications were recorded.

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Objective: To describe the phenotype of canine macular corneal dystrophy (MCD) including the clinical presentation, multimodal ocular imaging, histopathology, and ultrastructural analysis in ten Labrador Retrievers.

Procedure: Multicentered data collection.

Results: Labrador Retrievers affected by MCD were presented between the age of 4.

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A 6-year-old neutered female Jack Russell terrier was investigated for sudden onset prechiasmatic bilateral blindness, left circling, reduced proprioception in the right pelvic limb and right facial allodynia. Electroretinography was normal. Magnetic resonance imaging (MRI) examination revealed that the right optic nerve and the optic chiasm were hyperintense on diffusion weighted imaging and hypointense on apparent diffusion coefficient map consistent with ischemic optic neuropathy.

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Background: Nematodes of the genus Angiostrongylus are important causes of potentially life-threatening diseases in several animal species and humans. Angiostrongylus vasorum affects the right ventricle of the heart and the pulmonary arteries in dogs, red foxes and other carnivores. The diagnosis of canine angiostrongylosis may be challenging due to the wide spectrum of clinical signs.

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Nematode worms were retrieved from the left eyes of two dogs presented for unilateral ocular discharge in Belgium. Morphological and molecular identification were performed and the parasites were identified as Thelazia callipaeda. The history suggested that the infection had been acquired in south-western France and southern Italy where the disease has been observed regularly for the last 6 and 12 years, respectively.

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The objective of this prospective study was to investigate the success rate, practicality and complications of a new perilimbal pocket technique for the replacement of prolapsed nictitans gland in 30 dogs (44 eyes). A first incision was made in the bulbar conjunctiva, 2-3 mm from and parallel to the infero-nasal limbus, a second incision on the bulbar aspect of the nictitating membrane (NM), 2-3 mm parallel to the free edge. The gland was returned to its normal position by suturing the subconjunctival tissues of the NM to the episcleral tissues, using four to six interrupted horizontal mattress sutures.

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The neurotrophin brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) have emerged as key mediators in the pathophysiology of several mood disorders, including anxiety and depression. However, therapeutic compounds that interact with TrkB receptors have been difficult to develop. Using a combination of structure-based in silico screening and high-capacity functional assays in recombinant and neuronal cells, we identified a low-molecular weight TrkB ligand (ANA-12) that prevented activation of the receptor by BDNF with a high potency.

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Background And Purpose: By interacting with trkB receptors, brain-derived neurotrophic factor (BDNF) triggers various signalling pathways responsible for neurone survival, differentiation and modulation of synaptic transmission. Numerous reports have implicated BDNF and trkB in the pathogenesis of various central nervous system affections and in cancer, thus representing trkB as a promising therapeutic target. In this study, we used an antibody-based approach to search for trkB-selective functional reagents.

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In the last decades, few mechanistically novel therapeutic agents have been developed to treat mental and neurodegenerative disorders. Numerous studies suggest that targeting BDNF and its TrkB receptor could be a promising therapeutic strategy for the treatment of brain disorders. However, the development of potent small ligands for the TrkB receptor has proven to be difficult.

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Despite the tremendous importance of D1 and NMDA receptors to cognition (working memory, executive functions) and synaptic plasticity in the prefrontal cortex (PFC), little is known about the molecular mechanisms underlying D1-NMDA receptors interactions in this brain area. Here, we show that D1 receptors and the NMDA receptor co-localize in single pyramidal neurons and interneurons in adult rat PFC. NR1 and NR2A expression are found in different neuronal types.

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The brain is particularly vulnerable to ischaemia; however, neurons can become tolerant to ischaemic insult. This tolerance has been shown to involve activation of NMDA receptors, but its mechanisms have not yet been fully elucidated. Using a preconditioning protocol, we show that neurons surviving to a transient NMDA exposure become resistant to the glutamatergic agonist.

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Cerebral ischaemia is associated with brain damage and inhibition of neuronal protein synthesis. A deficit in neuronal metabolism and altered excitatory amino acid release may both contribute to those phenomena. In the present study, we demonstrate that both NMDA and metabolic impairment by 2-deoxyglucose or inhibitors of mitochondrial respiration inhibit protein synthesis in cortical neurons through the phosphorylation of eukaryotic elongation factor (eEF-2), without any change in phosphorylation of initiation factor eIF-2alpha.

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CRMP1, CRMP2, and CRMP5 have been identified as cytosolic proteins relaying semaphorin 3A signalling, one of the molecular cues conducting axon and dendrite growth and guidance. They are highly expressed during brain ontogenesis, but, because of their lower levels in the adult, their distribution in the mature brain is poorly documented. By using specific antibodies, we investigated the cellular distribution of these CRMPs in different adult brain structures and in neural cell cultures with a special focus on the splice variants CRMP2A and CRMP2B.

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Zinc released from a subpopulation of glutamatergic synapses, mainly localized in the cerebral cortex and the hippocampus, facilitates or reduces glutamatergic transmission by acting on neuronal AMPA and NMDA receptors, respectively. However, neurons are not the only targets of zinc. In the present study, we provide evidence that zinc inhibits protein synthesis in cultured astrocytes from the cerebral cortex of embryonic mice.

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Transient cerebral ischemia, which is accompanied by a sustained release of glutamate, strongly depresses protein synthesis. We have previously demonstrated in cortical neurons that a glutamate-induced increase in intracellular Ca(2+) is likely responsible for the blockade of the elongation step of protein synthesis. In this study, we provide evidence indicating that NMDA mobilizes a thapsigargin-sensitive pool of intracellular Ca(2+).

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In the present study, GABA was shown to induce a necrotic neuronal death in cultured striatal neurones from mouse embryos. This effect did not depend on the activation of GABA(A), GABA(B) or GABA(C) receptors as it was neither antagonized by bicuculline, saclofen or picrotoxin, respectively, nor reproduced by the GABA receptor agonists, muscimol and baclofen. Excluding the participation of glutamate, GABA neurotoxicity persisted in the presence of either the antagonists of ionotropic and metabotropic glutamate receptors or glutamate pyruvate transaminase, which induces an immediate catabolism of glutamate.

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Edg-2 is a member of the G-protein-coupled seven-transmembrane receptor family recently identified in oligodendrocytes. Here we show that both in vitro and in vivo, Edg-2 transcripts are not detected during early stages of oligodendroglial development, but are expressed only in mature oligodendrocytes, shortly before the onset of myelination. Lysophosphatidic acid (LPA) has been reported to be a ligand of Edg-2 receptor in different cell types.

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Glutamatergic transmission is mediated by ionotropic receptors that directly gate cationic channels and metabotropic receptors that are coupled to second messenger generating systems and to ionic channels via heterotrimeric guanine-nucleotide binding- (G) proteins. This distinction cannot be made for the ionotropic receptor subclass activated by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), which has been shown to be physically associated with the alpha-subunit of Gi1 protein and activates this G-protein. Here, we report that, in addition to a Ca2+ influx, AMPA induces the mobilization of Ca2+ from the mitochondrial pool by reversing the mitochondrial Na+/Ca2+ exchanger in mouse neurons in primary culture.

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Sphingosine-1-phosphate (S1P) is a potent lysophospholipid mediator mostly released by activated platelets. It is involved in several functions in peripheral tissues, but its effects in the central nervous system are poorly documented. Therefore, we have examined the effects of S1P on the proliferation of striatal astrocytes from the mouse embryo.

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Sphingosine-1-phosphate (S1P) is a potent lysophospholipid mediator mostly released by activated platelets. It is involved in several functions in peripheral tissues, but its effects in the central nervous system are poorly documented. Therefore, we have examined the effects of S1P on the proliferation of striatal astrocytes from the mouse embryo.

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Transient cerebral ischemia, which is accompanied by a sustained release of glutamate and zinc, as well as H(2)O(2) formation during the reperfusion period, strongly depresses protein synthesis. We have previously demonstrated that the glutamate-induced increase in cytosolic Ca(2+) is likely responsible for blockade of the elongation step of protein synthesis, whereas Zn(2+) preferentially inhibits the initiation step. In this study, we provide evidence indicating that H(2)O(2) and thapsigargin mobilized a common intracellular Ca(2+) pool.

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Exposure of central neurons to Zn2+ triggers neuronal death. The routes of Zn2+ entry were investigated in living cortical neurons from the mouse using the specific Zn2+ fluorescent dye N-(6-methoxy-8-quinolyl)-p-toluene sulphonamide (TSQ), which preferentially detects membrane-bound Zn2+. Exposure of cortical neurons to increasing concentrations of Zn2+ (1-100 microM) induced a progressive increase in the fluorescence of TSQ.

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