| Records |
Author  |
Branchi, I.; Bichler, Z.; Berger-Sweeney, J.; Ricceri, L. |
| Title |
Animal models of mental retardation: from gene to cognitive function |
Type |
Journal Article |
| Year |
2003 |
Publication |
Neuroscience and Biobehavioral Reviews |
Abbreviated Journal |
Neurosci Biobehav Rev |
| Volume |
27 |
Issue |
1-2 |
Pages |
141-153 |
| Keywords |
Animals; Animals, Genetically Modified/growth & development; Behavior/physiology; Behavior, Animal; Brain/*growth & development; Cognition/*physiology; *Disease Models, Animal; Environment; Genes; Genetic Diseases, Inborn/physiopathology; Humans; Mental Retardation/classification/*genetics/*physiopathology |
| Abstract |
About 2-3% of all children are affected by mental retardation, and genetic conditions rank among the leading causes of mental retardation. Alterations in the information encoded by genes that regulate critical steps of brain development can disrupt the normal course of development, and have profound consequences on mental processes. Genetically modified mouse models have helped to elucidate the contribution of specific gene alterations and gene-environment interactions to the phenotype of several forms of mental retardation. Mouse models of several neurodevelopmental pathologies, such as Down and Rett syndromes and X-linked forms of mental retardation, have been developed. Because behavior is the ultimate output of brain, behavioral phenotyping of these models provides functional information that may not be detectable using molecular, cellular or histological evaluations. In particular, the study of ontogeny of behavior is recommended in mouse models of disorders having a developmental onset. Identifying the role of specific genes in neuropathologies provides a framework in which to understand key stages of human brain development, and provides a target for potential therapeutic intervention. |
| Address |
Section of Behavioural Pathophysiology, Laboratorio di Fisiopatologia di Organo e di Sistema, Istituto Superiore di Sanita, Viale Regina Elena 299, 00161 Roma, Italy. branchi@iss.it |
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| Language |
English |
Summary Language |
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Original Title |
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Series Issue |
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Edition |
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| ISSN |
0149-7634 |
ISBN |
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| Notes |
PMID:12732230 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2805 |
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| Author |
Cowell, P.E.; Fitch, R.H.; Denenberg, V.H. |
| Title |
Laterality in animals: relevance to schizophrenia |
Type |
Journal Article |
| Year |
1999 |
Publication |
Schizophrenia Bulletin |
Abbreviated Journal |
Schizophr Bull |
| Volume |
25 |
Issue |
1 |
Pages |
41-62 |
| Keywords |
Adult; Animals; Cognition; *Disease Models, Animal; Functional Laterality/*physiology; Humans; Language; Motor Activity/physiology; Schizophrenia/*physiopathology |
| Abstract |
Anomalies in the laterality of numerous neurocognitive dimensions associated with schizophrenia have been documented, but their role in the etiology and early development of the disorder remain unclear. In the study of normative neurobehavioral organization, animal models have shed much light on the mechanisms underlying and the factors affecting adult patterns of both functional and structural asymmetry. Nonhuman species have more recently been used to investigate the environmental, genetic, and neuroendocrine factors associated with developmental language disorders in humans. We propose that the animal models used to study the basis of lateralization in normative development and language disorders such as dyslexia could be modified to investigate lateralized phenomena in schizophrenia. |
| Address |
Dept. of Human Communication Sciences, University of Sheffield, United Kingdom |
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English |
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Series Issue |
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Edition |
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| ISSN |
0586-7614 |
ISBN |
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Medium |
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Conference |
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| Notes |
PMID:10098913 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2827 |
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| Author |
Harman, F.S.; Nicol, C.J.; Marin, H.E.; Ward, J.M.; Gonzalez, F.J.; Peters, J.M. |
| Title |
Peroxisome proliferator-activated receptor-delta attenuates colon carcinogenesis |
Type |
Journal Article |
| Year |
2004 |
Publication |
Nature medicine |
Abbreviated Journal |
Nat Med |
| Volume |
10 |
Issue |
5 |
Pages |
481-483 |
| Keywords |
Animals; Azoxymethane/toxicity; Colonic Neoplasms/etiology/genetics/*prevention & control; Colonic Polyps/etiology/genetics/pathology/prevention & control; Disease Models, Animal; Mice; Mice, Knockout; Mice, Mutant Strains; Phenotype; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*physiology; Transcription Factors/deficiency/genetics/*physiology |
| Abstract |
Peroxisome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-delta. In contrast to previous reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis. |
| Address |
Department of Veterinary Science and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. jmp21@psu.edu |
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English |
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Series Issue |
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Edition |
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| ISSN |
1078-8956 |
ISBN |
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Medium |
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| Notes |
PMID:15048110 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
77 |
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| Author |
Milinovich, G.J.; Trott, D.J.; Burrell, P.C.; van Eps, A.W.; Thoefner, M.B.; Blackall, L.L.; Al Jassim, R.A.M.; Morton, J.M.; Pollitt, C.C. |
| Title |
Changes in equine hindgut bacterial populations during oligofructose-induced laminitis |
Type |
Journal Article |
| Year |
2006 |
Publication |
Environmental Microbiology |
Abbreviated Journal |
Environ Microbiol |
| Volume |
8 |
Issue |
5 |
Pages |
885-898 |
| Keywords |
Animal Feed; Animals; Bacteria/classification/*isolation & purification; DNA, Bacterial/analysis; Disease Models, Animal; Feces/microbiology; Foot Diseases/etiology/microbiology/*veterinary; Horse Diseases/*etiology/metabolism/microbiology; Horses; In Situ Hybridization, Fluorescence; Intestines/*microbiology; Oligosaccharides/*administration & dosage/*metabolism; Phylogeny; Polymerase Chain Reaction; RNA, Bacterial/analysis; RNA, Ribosomal, 16S/analysis |
| Abstract |
In the horse, carbohydrate overload is thought to play an integral role in the onset of laminitis by drastically altering the profile of bacterial populations in the hindgut. The objectives of this study were to develop and validate microbial ecology methods to monitor changes in bacterial populations throughout the course of experimentally induced laminitis and to identify the predominant oligofructose-utilizing organisms. Laminitis was induced in five horses by administration of oligofructose. Faecal specimens were collected at 8 h intervals from 72 h before to 72 h after the administration of oligofructose. Hindgut microbiota able to utilize oligofructose were enumerated throughout the course of the experiment using habitat-simulating medium. Isolates were collected and representatives identified by 16S rRNA gene sequencing. The majority of these isolates collected belonged to the genus Streptococcus, 91% of which were identified as being most closely related to Streptococcus infantarius ssp. coli. Furthermore, S. infantarius ssp. coli was the predominant oligofructose-utilizing organism isolated before the onset of lameness. Fluorescence in situ hybridization probes developed to specifically target the isolated Streptococcus spp. demonstrated marked population increases between 8 and 16 h post oligofructose administration. This was followed by a rapid population decline which corresponded with a sharp decline in faecal pH and subsequently lameness at 24-32 h post oligofructose administration. This research suggests that streptococci within the Streptococcus bovis/equinus complex may be involved in the series of events which precede the onset of laminitis in the horse. |
| Address |
Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Queensland, Australia. g.milinovich@uq.edu.au |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
1462-2912 |
ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
PMID:16623745 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2625 |
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| Author |
Pennisi, E. |
| Title |
Schizophrenia clues from monkeys |
Type |
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| Year |
1997 |
Publication |
Science (New York, N.Y.) |
Abbreviated Journal |
Science |
| Volume |
277 |
Issue |
5328 |
Pages |
900 |
| Keywords |
Animals; Antipsychotic Agents/pharmacology; Behavior, Animal/drug effects; *Cercopithecus aethiops; Clozapine/pharmacology; Cognition/drug effects; *Disease Models, Animal; Dopamine/*metabolism; Excitatory Amino Acid Antagonists/pharmacology; Memory/drug effects; Phencyclidine/*pharmacology; Prefrontal Cortex/*metabolism; Schizophrenia/chemically induced/drug therapy/*metabolism; Schizophrenic Psychology |
| Abstract |
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Thesis |
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Place of Publication |
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Editor |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
0036-8075 |
ISBN |
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Medium |
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Conference |
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| Notes |
PMID:9281070 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2844 |
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| Author |
Williams, D.O.; Boatwright, R.B.; Rugh, K.S.; Garner, H.E.; Griggs, D.M.J. |
| Title |
Myocardial blood flow, metabolism, and function with repeated brief coronary occlusions in conscious ponies |
Type |
Journal Article |
| Year |
1991 |
Publication |
The American journal of physiology |
Abbreviated Journal |
Am J Physiol |
| Volume |
260 |
Issue |
1 Pt 2 |
Pages |
H100-9 |
| Keywords |
Animals; Consciousness/*physiology; Coronary Circulation/*physiology; Coronary Disease/pathology/*physiopathology; Disease Models, Animal; Hemodynamic Processes/physiology; Horses/*physiology; Hydrogen/metabolism; Lactates/metabolism; Myocardium/*metabolism/pathology; Norepinephrine/metabolism; Potassium/metabolism; Regional Blood Flow |
| Abstract |
Studies were performed in the conscious pony instrumented with a Doppler flow probe and hydraulic occluder on the left anterior descending coronary artery (LAD), sonomicrometry crystals and intraventricular micromanometer in the left ventricle, and catheters in the left atrium and anterior interventricular vein. Two-minute LAD occlusions were performed every 30 min continuously or during working hours. Data on release of catabolites (potassium, hydrogen ions, and lactate) and norepinephrine from the initially dysfunctional region were obtained periodically during a regimen of 445 +/- 56 occlusions in six animals. Regional myocardial blood flow was measured (microsphere method) before and after an occlusion regimen in four animals. Marked release of catabolites and norepinephrine from the initially dysfunctional region was noted in association with early occlusions when myocardial segment function was severely reduced. With further occlusions, release of these substances decreased while segment function improved. Blood flow was markedly decreased in the initially dysfunctional region during an early occlusion but was at the control level during a later occlusion. Although the metabolic findings are consistent with protection due to “ischemic preconditioning” and no increase in collateral perfusion, the inverse relationship noted between catabolite release and segment function is best explained by flow-dependent mechanisms. These results, together with the myocardial blood flow data, serve to validate a previous assumption that protection against regional myocardial dysfunction under these conditions is due to increased collateral perfusion. |
| Address |
Department of Physiology, University of Missouri, Columbia 65212 |
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Thesis |
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Place of Publication |
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Editor |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
0002-9513 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:1992786 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
98 |
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