Critical Evaluation of Animal Models of Gastrointestinal Disorders

Author(s):  
Anthony C. Johnson ◽  
Beverley Greenwood-Van Meerveld

Physiology ◽  
2019 ◽  
Vol 34 (3) ◽  
pp. 216-229 ◽  
Author(s):  
Joline E. Brandenburg ◽  
Matthew J. Fogarty ◽  
Gary C. Sieck

Spastic cerebral palsy (CP), despite the name, is not consistently identifiable by specific brain lesions. CP animal models focus on risk factors for development of CP, yet few reproduce the diagnostic symptoms. Animal models of CP must advance beyond risk factors to etiologies, including both the brain and spinal cord.



2019 ◽  
Vol 32 (4) ◽  
Author(s):  
Anthony C. Johnson ◽  
Adam D. Farmer ◽  
Timothy J. Ness ◽  
Beverley Greenwood‐Van Meerveld


2000 ◽  
Vol 6 (1) ◽  
pp. 21-31 ◽  
Author(s):  
Philip Noel Newsome ◽  
John Nicholas Plevris ◽  
Leonard Joseph Nelson ◽  
Peter Clive Hayes


2000 ◽  
Vol 6 (1) ◽  
pp. 21-31
Author(s):  
P NEWSOME ◽  
J PLEVRIS ◽  
L NELSON ◽  
P HAYES


2010 ◽  
Vol 7 (1) ◽  
pp. 8 ◽  
Author(s):  
Ilpo Huhtaniemi ◽  
Maria Alevizaki ◽  
◽  

The concept of the direct involvement of gonadotrophins in tumorigenesis has been around for a long time. First, because the gonads are direct targets of gonadotrophin action, their tumours have been proposed to be gonadotrophin-dependent. Second, the recent findings of gonadotrophin receptors in extragonadal tissues has prompted the hypothesis that some extragonadal tumours (e.g. breast, uterus, prostate, pituitary and adrenal) could also be under the direct regulatory action of gonadotrophins. However, although supported by numerousin vitroexperiments and experimental animal models, the clinical evidence for a direct tumorigenic role of gonadotrophins remains weak. The purpose of this brief review is to present a critical evaluation of current information, both clinical and experimental, about the involvement of gonadotrophins in the induction and growth of gonadal and extragonadal tumours.



Author(s):  
Mr. Katkure Pawan Mahadev

Abstract: The use of current research into schizophrenia has remained highly fragmented, much like the clinical presentation of the disease itself. Differing theories as to the cause and progression of schizophrenia, as well as the heterogeneity of clinical symptoms, have made it difficult to develop a coherent framework suitable for animal modeling. However, a number of limited animal models have been developed to explore various causative theories and to test specific mechanistic hypotheses. Historically, these models have been based on the manipulation of neurotransmitter systems believed to be involved in schizophrenia. In recent years, the emphasis has shifted to targeting relevant brain regions in an attempt to explore potential etiologic hypotheses. The specific animal models developed within these frameworks are described in this review. Emphasis is placed on the critical evaluation of currently available models because these models help to shape the direction of future research.







1995 ◽  
Vol 7 (2) ◽  
pp. 27-29 ◽  
Author(s):  
J.M. Koolhaas ◽  
P. Meerlo ◽  
S.F. de Boer ◽  
J.H. Strubbe ◽  
B. Bohus

Our current understanding of the physiological mechanisms underlying depressive disorders is not only based on behavioral, neuroendocrine and pharmacological studies in depressed humans, but also on experimental studies in a wide variety of animal models of depression. Ideally, the two approaches should operate in close interaction, each providing additional information to the other approach. However, in practice the animal model approach seems to be rather independent from the human studies. In a critical evaluation of the available animal models of depression, Willner concluded that none of the models fulfilled the criteria of a sufficient face, construct and predictive validity. Although this evaluation was made ten years ago, we feel that the situation has improved very little since that time. Most animal models fail to sufficiently mimic both the etiology and the symptomatology of human depressive disorders. With respect to the etiology, stress and major life events are generally considered to be an important factor in the development of depression. Most of the animal models however use stressors which bear little or no relationship to the biology of the species, i.e. to the situations an animal may meet in its everyday life in a natural habitat. Moreover, these models do not pay attention to the temporal dynamics of the disease. In humans, the disease is characterized by its gradual onset, which is often preceded by symptoms of anxiety. Moreover, a relatively large number of patients suffers from recurrent episodes of depression, which tend to occur with decreasing intervals and increasing duration and severity. If we want to improve our knowledge of the causal mechanisms of depression, animal models which allow an experimental analysis of the temporal dynamics of the disease are essential.



Sign in / Sign up

Export Citation Format

Share Document