Publications by authors named "Resibois A"

Three cases of feline cerebellar hypoplasia are presented. At the time of examination, the ages of the cats ranged from 2 months to 1 year. Necropsy revealed cerebellar and pons hypoplasia.

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Three 4-month-old kittens from the same litter were presented, two of which were exhibiting cerebellar signs. Euthanasia was requested. No cerebellum atrophy was disclosed on necropsy.

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Biosynthesis of the tetrahydrobiopterin (BH(4)) cofactor, essential for catecholamines and serotonin production and nitric oxide synthase (NOS) activity, requires the enzymes GTP cyclohydrolase I (GTPCH), 6-pyruvoyl-tetrahydropterin synthase (PTPS), and sepiapterin reductase (SR). Upon studying the distribution of GTPCH and PTPS with polyclonal immune sera in cross sections of rat brain, prominent nuclear staining in many neurons was observed besides strong staining in peri-ventricular structures. Furthermore, localization studies in transgenic mice expressing a Pts-LacZ gene fusion containing the N-terminal 35 amino acids of PTPS revealed beta-galactosidase in the nucleus of neurons.

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Two otherwise healthy adult cats were presented with progressive cerebellar signs of different severity. Owners requested euthanasia. Necropsy disclosed whole cerebellum and pontine atrophy, with a severity paralleling the neurologic dysfunction.

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A European case of laminin alpha2 deficiency-associated muscular dystrophy in a 12-month-old, female Maine coon pedigree cat is reported. The history and eventual clinical presentation of this cat differed from those of two cats reported in the USA. In this case, the myopathy was characterised by progressively worsening weakness, muscle atrophy and joint contracture.

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We used human umbilical vein endothelial cells (HUVEC) cultures to investigate in vitro the antiproliferative effects of suramin and of its analogue, Eriochrome Black T. The cell cycle phases of interest were characterised with specific immune sera raised against cyclin D(1), cyclin E and proliferating nuclear cell antigen (PCNA). Simultaneous detection of two cell cycle markers was ensured by double colour immunofluorescence.

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The calbindin (CB) and the calretinin (CR) immunoreactivities were studied in the dog cochlea during its postnatal maturation from birth to the 33rd postnatal day. At birth, CB was expressed in the Kölliker's organ, in the immature inner (IHC) and outer hair cells (OHC), in neurons of the spiral ganglion, and in nerve fibers running in the basilar membrane of the apical turn. During the cochlear maturation, non-sensorineuronal structures, such as the Kölliker's organ, the rods of Corti, and the inner sulcus cells, displayed a transient CB-staining.

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Two puppies, a 4-month-old female Maltese terrier and a 6-week-old male Great Pyrenean, were presented for confirmation of bilateral deafness by electrophysiological testing. In both puppies, brainstem auditory potentials were not evoked by 90 dB NHL click stimulation of each ear. Examination of the inner ear revealed a bilateral cochleo-saccular degeneration in both animals.

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The bifunctional protein, PCD/DCoH, is both a pterin-4alpha-carbinolamine dehydratase (PCD) and a dimerization cofactor of the hepatic nuclear factor 1alpha (DCoH). In association with brain tyrosine hydroxylase (TH), which is required for dopamine synthesis, PCD catalyses dehydration and thus recycling of the cofactor tetrahydrobiopterin (BH(4)). PCD immunoreactivity in the catecholaminergic system of the rat brain was studied using a rabbit polyclonal antibody.

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Pterin-4a-carbinolamine dehydratase (PCD) is a bifunctional protein also known as DCoH (dimerization co-factor of hepatocyte nuclear factor 1 (HNF1)). PCD/DCoH modulates the DNA binding specificity of HNF1, thus acting on its transcriptional activity. In addition, it participates in the recycling of tetrahydrobiopterin (BH(4)), an essential cofactor of several metabolic reactions.

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The bifunctional protein PCD/DCoH is both a pterin-4alpha-carbinolamine dehydratase (PCD) involved in the recycling of tetrahydrobiopterin (BH4) and a dimerisation cofactor (DCoH) of the hepatic nuclear factor 1alpha (HNF-1alpha). An antiserum raised against rat PCD/DCoH was used to localise the protein in peripheral organs. In liver, all the hepatocytes but not the other cell types are immunoreactive.

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Background & Aims: An absence or a presence of mutated transforming growth factor (TGF)-beta receptors is a possible hypothesis explaining the resistance of cancer cells to the growth-inhibitory effect of TGF-beta. Mutations involving microsatellite-like regions of the type II TGF-beta receptor have been described in subgroups of colorectal cancers. The aim of this study was to investigate the expression and distribution of TGF-beta receptors in sporadic colorectal cancers and normal tissues.

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GTPCH-I immunoreactive structures in the rat brain were studied using a polyclonal antibody raised in the chick. General mapping was made using the avidin-biotin-peroxidase technique and compared with the distribution of tyrosine hydroxylase and serotonin immunoreactivities. Double immunofluorescence was performed in order to establish real intracellular colocalization.

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The lurcher mutation induces Purkinje cell degeneration in heterozygous mice, and neonatal death in homozygous animals. Using the D6Mit16 Simple Sequence Length Polymorphic marker in F2 hybrids between AKR +/+ mice and B6+/Lc mice, homozygous lurcher fetuses and newborns as well as heterozygous and normal littermates were identified, and their brain morphology was analysed. In homozygous lurcher embryos at embryonic day 18 and neonates the cerebellum was hypotrophic, particularly in the posterior half.

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Pancreatic neoplasms harbor different prognoses according to their histological type: a benign course for serous cystadenoma, a low malignant potential for intraductal papillary mucinous neoplasms (IPMN), and high aggressiveness for ductal adenocarcinoma (ADC). Transforming growth factor beta 1 (TGF beta 1) may regulate tumor growth. The present study analyzes and compares the expression of its precursor beta 1-latency-associated peptide (beta 1-LAP), its latent binding protein (LTBP), and its mRNA in ductal adenocarcinoma (n = 10), in IPMN (n = 8), in serous cystadenoma (n = 2), and in normal tissues (n = 5).

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Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional cytokine and is thought to be involved in colorectal tumorigenesis as a regulator of cell growth and differentiation. This role is mainly supported by in vitro studies while its role in vivo remains unclear. The aim of the present study was to investigate whether the TGF-beta 1 precursor (beta 1-LAP) and the latent TGF-beta 1 binding protein (LTBP) are expressed in colorectal adenomas, the presumed precursors of most of colorectal adenocarcinomas.

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Background & Aims: Transforming growth factor beta (TGF-beta) is a putative mediator of fibrosis in several chronic diseases. Recently, chronic pancreatitis was suggested to be related to acute pancreatitis in the so-called necrosis-fibrosis sequence hypothesis. The present study investigated whether TGF-beta is able to promote chronic fibrosis after repeated courses of necrotizing acute pancreatitis induced by cerulein in mice.

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Background/aims: Transforming growth factor beta 1 (TGF-beta 1) is thought to be the mediator of fibrosis in liver, glomerular, and pulmonary fibrosis. This study investigated the expression of TGF-beta 1 precursor (beta 1 latency-associated peptide), latent TGF-beta 1-binding protein (LTBP), and TGF-beta 1 messenger RNA (mRNA) in chronic pancreatitis.

Methods: Beta 1 latency-associated peptide and LTBP expression were studied by immunohistochemistry, and TGF-beta 1 mRNA expression was studied by reverse-transcription polymerase chain reaction analysis in normal pancreatic parenchyma and in tissues from patients with chronic pancreatitis of different etiologies.

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The distribution of the calcium-binding protein calretinin was investigated by immunohistochemistry in the hippocampus, the subicular areas, and the entorhinal cortex in patients with Alzheimer's disease and in control subjects. By double immunolabelling, the calretinin immunoreactivity was compared to the immunoreactivity for beta/A4 amyloid or for tau proteins. Calretinin-positive neurons were mainly observed in the molecular layer of the gyrus dentatus, the stratum radiatum of the Ammon's horn, and in layers II and III of the entorhinal cortex.

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Calretinin and calbindin-D28k are homologous calcium-binding proteins, each present in a variety of neurons in the brain. Their distributions in the rat brain have been compared at the cellular level to determine whether they tend to occur in the same or in different cells, and to determine whether calbindin-positive cells show any common features once crossreaction with calretinin has been eliminated. The results show great heterogeneity.

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Calretinin is a calcium-binding protein related to calbindin-D28k; both are present in different though overlapping sets of neurons in brains of birds and mammals. We describe in detail the pattern of calretinin immunoreactivity in the rat brain. As in chick brain, calretinin immunoreactivity is abundant in various sensory pathways (particularly certain cells and fibres of the cochlear nuclei and olfactory bulb), in the heterogeneous parts of the brainstem and in parts of the hypothalamus.

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Calbindin D28k and D9k are two cytosolic calcium-binding proteins abundant in intestinal absorptive cells which appear to play a role in calcium translocation. Until today, calbindin D28k was found in avian and reptilian absorptive cells but not in mammalian ones. We have described the presence of calbindin D28k-immunoreactivity in intestinal absorptive cells of pig and jerboa (Jaculus jaculus).

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1. We have devised a radioimmunoassay for atrial natriueretic factor (ANF). Its application to rat brain extract led to the discovery of ANF in the brain.

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Calbindin 28K and calretinin are very similar calcium binding proteins which are both present in the central nervous system (CNS). They respectively bind 4 and 5 Ca++ ions. We have compared by immunohistochemistry and in situ hybridization their localisation in the brain and the retina.

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