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Vivo Animal Models (vivo + animal_models)
Selected AbstractsDual-mode reflectance and fluorescence near-video-rate confocal microscope for architectural, morphological and molecular imaging of tissueJOURNAL OF MICROSCOPY, Issue 1 2007ALICIA L. CARLSON Summary We have developed a near-video-rate dual-mode reflectance and fluorescence confocal microscope for the purpose of imaging ex vivo human specimens and in vivo animal models. The dual-mode confocal microscope (DCM) has light sources at 488, 664 and 784 nm, a frame rate of 15 frames per second, a maximum field of view of 300 × 250 ,m and a resolution limit of 0.31 ,m laterally and 1.37 ,m axially. The DCM can image tissue architecture and cellular morphology, as well as molecular properties of tissue, using reflective and fluorescent molecular-specific optical contrast agents. Images acquired with the DCM demonstrate that the system has the sub-cellular resolution needed to visualize the morphological and molecular changes associated with cancer progression and has the capability to image animal models of disease in vivo. In the hamster cheek pouch model of oral carcinogenesis, the DCM was used to image the epithelium and stroma of the cheek pouch; blood flow was visible and areas of dysplasia could be distinguished from normal epithelium using 6% acetic acid contrast. In human oral cavity tissue slices, DCM reflectance images showed an increase in the nuclear-to-cytoplasmic ratio and density of nuclei in neoplastic tissues as compared to normal tissue. After labelling tissue slices with fluorescent contrast agents targeting the epidermal growth factor receptor, an increase in epidermal growth factor receptor expression was detected in cancerous tissue as compared to normal tissue. The combination of reflectance and fluorescence imaging in a single system allowed imaging of two different parameters involved in neoplastic progression, providing information about both the morphological and molecular expression changes that occur with cancer progression. The dual-mode imaging capabilities of the DCM allow investigation of both morphological changes as well as molecular changes that occur in disease processes. Analyzing both factors simultaneously may be advantageous when trying to detect and diagnose disease. The DCM's high resolution and near-video-rate image acquisition and the growing inventory of molecular-specific contrast agents and disease-specific molecular markers holds significant promise for in vivo studies of disease processes such as carcinogenesis. [source] Sensory nerve conduction deficit in experimental monoclonal gammopathy of undetermined significance (MGUS) neuropathyMUSCLE AND NERVE, Issue 6 2001Michael W. Lawlor BS Abstract An emerging body of evidence from in vitro studies and in vivo animal models supports a pathogenic role of antibodies in the development of peripheral neuropathy associated with monoclonal gammopathy of undetermined significance (MGUS). Although the assessment of motor and sensory nerve fiber function is of clinical importance, it is seldom applied experimentally. We describe the application of an electrophysiologic method for the evaluation of motor and sensory nerve fiber function using an experimental model of MGUS neuropathy. Supramaximal stimulation of the tibial nerve elicited an early motor response (M-wave, 1.7 ± 0.1 ms, n = 10) and a late sensory (H-reflex, 7.8 ± 0.1 ms, n = 10) response that was recorded from the hind foot of anesthetized rats. Intraneural injection of serum antibodies from a MGUS patient with sensorimotor polyneuropathy, but not from an age-matched control subject, produced a marked attenuation of the H-reflex (P < 0.01, n = 10) without affecting the M-wave. Light and electron microscopy of affected nerve showed myelinoaxonal degeneration with sparing of the smaller unmyelinated nerve fibers. The combined electrophysiologic and morphologic findings presented in this study are consistent with a selective sensory conduction deficit in MGUS neuropathy. Selective injury of afferent nerve fibers by this patient's serum antibodies may result from reactivity to neural antigens uniquely expressed by sensory neurons. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 809,816, 2001 [source] Recent Insights into PDGF-Induced GliomagenesisBRAIN PATHOLOGY, Issue 3 2010Filippo Calzolari Abstract Gliomas are aggressive and almost incurable glial brain tumors which frequently display abnormal platelet-derived growth factor (PDGF) signaling. Evidence gained from studies on several in vivo animal models has firmly established a causal connection between aberrant PDGF signaling and the formation of some gliomas. However, only recently has significant knowledge been gained regarding crucial issues such as the glioma cell of origin and the relationship between the transforming stimulus and the cellular characteristics of the resulting tumor. Based on recent evidence, we propose that PDGF can bias cell-fate decisions, driving the acquisition of cell type-specific features by the progeny of multipotent neural progenitors, thus determining the shape and direction of the transformation path. Furthermore, recent data about the cellular mechanisms of PDGF-driven glioma progression and maintenance indicate that PDGF may be required, unexpectedly, to override cell contact inhibition and promote glioma cell infiltration rather than to stimulate cell proliferation. [source] 4245: Non-surgical strategies for PCO preventionACTA OPHTHALMOLOGICA, Issue 2010IM WORMSTONE Purpose Surgical approaches and IOL design have gone some way to reduce the rate of PCO progression. Despite these efforts PCO remains a common and important problem which diminishes the visual quality of patients and is a major financial burden on healthcare providers. If we are to effectively respond to the problem of PCO then a biological solution has to be adopted to reduce/prevent formation of light scattering changes. Methods Methods have been employed to investigate PCO development, which include in vitro cell culture and capsular bag models; in vivo animal models and post-mortem analysis. These have greatly aided our understanding of PCO. Results A number of basic approaches have been identified to prevent PCO. 1) To kill the entire lens epithelial population. This will require a pharmacological agent, therefore delivery of this drug needs to be localised to the target cells, but have limited access to non-target cells; closed capsular bag systems such as perfect capsule provides opportunity to achieve this aim. 2) Maintenance of a cell monolayer on the posterior capsule. In particular the role of TGF, has been investigated, which is known to cause matrix deformation. Disruption of TGF, signalling pathways can suppress matrix deformation and thus reduce light scatter. 3) Recreation of a lens is the ultimate solution. While it has been shown that lens fibre differentiation can be promoted in animal systems, perfect formation of the lens is not achieved and the protein density is typically low relative to the native lens. Conclusion Strategies to prevent PCO are being actively developed, which will are greatly aided by improved drug delivery systems. The development of biological/pharmacological approaches in concert with improved surgical methods and IOL designs should yield benefit to patients. Commercial interest [source] G,q -PROTEIN CARBOXYL TERMINUS IMITATION POLYPEPTIDE GCIP-27 ATTENUATES CARDIAC HYPERTROPHY IN VITRO AND IN VIVOCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2007Hai-Gang Zhang SUMMARY 1Various Gq -protein-coupled receptors, such as ,1 -adrenoceptors, angiotension AT1 receptors, endothelin ETA receptors, neuropeptide Y1 receptors etc., contribute to cardiac hypertrophy. In G-protein signalling pathways, the carboxyl terminus of the G, subunit plays a vital role within G-protein,receptor interaction. The present study was designed to explore the effects of the synthetic G,q carboxyl terminal imitation peptide GCIP-27 on cardiac hypertrophy. 2Hypertrophy of rat cultured cardiomyocytes was induced by noradrenaline (NA) or angiotensin (Ang) II in vitro. Protein content, [3H] incorporation and [Ca2+]i were determined in cardiomyocytes cultured with GCIP-27. Three in vivo animal models of cardiac hypertrophy were prepared using intraperitoneal injections of NA in mice and rats and suprarenal abdominal aortic stenosis in rats. After treatment with GCIP-27 (10,100 µg/L) for 15 or 20 days, indices of cardiac hypertrophy were measured. The effect of GCIP-27 on the mRNA expression of c-fos and c-jun was detected using reverse transcription,polymerase chain reaction. 3At 10,100 µg/L, GCIP-27 significantly decreased protein content and [3H]-leucine incorporation in cultured cardiomyocytes compared with 1 µmol/L NA- and 1 µmol/L AngII-treated groups. After treatment with GCIP-27 (10, 30 or 100 µg/kg) for 15 days, the heart index (HI) and left ventricular index (LVI) in mice decreased significantly compared with the NA control group. In rats, GCIP-27 significantly reduced HI and LVI compared with the NA and aortic stenosis groups. Moreover, [Ca2+]i in cardiomyocytes in the GCIP-27 (3, 10, 30 µg/L)-treated groups was lower than that in the control groups. Expression of c-fos and c-jun mRNA decreased significantly in the myocardium from 5,45 µg/L GCIP-27-treated rats compared with NA controls. 4The results indicate that GCIP-27 can attenuate cardiac hypertrophy effectively in various models in vitro and in vivo. [source] | ||||||||||