[Transgenic animals].

K Urasawa; A Kitabatake

Home/Archive/PubMed

PubMed · 9796313

[Transgenic animals].

K Urasawa·A Kitabatake

View original source ↗Export metadata ↓

Abstract

Molecular biological technique has enabled us to create numerous transgenic animals characterized by enhanced or reduced expression of target gene products. These animal models are very useful not only to study the physiological roles of target gene products but also to evaluate the clinical usefulness of newly developed drugs and other therapeutic measures. Unfortunately, we still do not have a genetically engineered animal model that spontaneously develops acute coronary syndrome. However, there are several transgenic mice showing abnormal lipid metabolism and developing premature atherosclerosis. In this chapter, recent advance in the field of atherosclerotic animal models will be summarized.

Explore related subjects

Acute Disease Animals Animals, Genetically Modified Coronary Artery Disease Coronary Disease Disease Models, Animal Fibroblast Growth Factor 5 Fibroblast Growth Factors Humans Hyperlipidemias Lipid Metabolism Mice Mice, Transgenic Neovascularization, Physiologic Rabbits Syndrome English Abstract Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

K Urasawa, A Kitabatake. 1998. [Transgenic animals].. https://pubmed.ncbi.nlm.nih.gov/9796313/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Loss of noradrenaline transporter sites in frontal cortex of rats with acute (ischemic) liver failure.

There is increasing evidence that central noradrenaline (NA) transport mechanisms are implicated in the central nervous system complications of acute liver failure. In order to assess this possibility, binding sites for the high affinity NA transporter ligand [3H]-nisoxetine were measured by quantitative receptor autoradiography in the brains of rats with acute liver failure resulting from hepatic devascularization and in appropriate controls. In vivo microdialysis was used to measure extracellular brain concentrations of NA. Severe encephalopathy resulted in a significant loss of [3H]-nisoxetine sites in frontal cortex and a concomitant increase in extracellular brain concentrations of NA in rats with acute liver failure. A loss of transporter sites was also observed in thalamus of rats with acute liver failure. This loss of NA transporter sites could result from depletion of central NA stores due to a reserpine-like effect of ammonia which is known to accumulate to millimolar concentrations in brain in ischemic liver failure. Impaired NA transport and the consequent increase in synaptic concentrations and increased stimulation of neuronal and astrocytic noradrenergic receptors could be implicated in the pathogenesis of the encephalopathy and brain edema characteristic of acute liver failure.

Acute Disease↗

PubMed2000

Modeling axonal injury in vitro: injury and regeneration following acute neuritic trauma.

Traumatic injury to axons was modeled in vitro using sympathetic principal neurons from the rat superior cervical ganglion. Neurons were grown as a pure culture on collagen in parallel tracks, with cell somata confined to the center, and neurites occupying the periphery of the culture dish. Growing as fascicles on tracks, the neurites demonstrated periodic varicosities. Neuritic transection was reliably and reproducibly achieved with a motor driven rubber impactor injury device. During a period lasting at least 1 h, dieback involving the proximal neurites averaged 105 +/- 10 microm. This was followed by neurite regeneration, with the injured segment being traversed within 36 h at an average rate of regeneration of 595 +/- 15 microm/day. The distal neurite segments showed degenerative changes within 1 h following transection, with initial receding of neurites progressing to vacuolation, beading, blebbing, and eventual detachment from the underlying matrix. This in vitro model of axonal injury allows neuritic injury to be studied at the cellular and molecular levels, and also provides a unique opportunity to test potential neuromodulatory and neuroprotective strategies.

Acute Disease↗

PubMed2000

Expression of interferon regulatory factor 4 in chronic myeloid leukemia: correlation with response to interferon alfa therapy.

PURPOSE: Mice experiments have established an important role for interferon regulatory factor (IRF) family members in hematopoiesis. We wanted to study the expression of interferon regulatory factor 4 (IRF4) in various hematologic disorders, especially chronic myeloid leukemia (CML), and its association with response to interferon alfa (IFN-alpha) treatment in CML. MATERIALS AND METHODS: Blood samples from various hematopoietic cell lines, different leukemia patients (70 CML, 29 acute myeloid leukemia [AML], 10 chronic myelomonocytic leukemia [CMMoL], 10 acute lymphoblastic leukemia, and 10 chronic lymphoid leukemia patients), and 33 healthy volunteers were monitored for IRF4 expression by reverse transcriptase polymerase chain reaction. Then, with a focus on CML, the IRF4 level was determined in sorted cell subpopulations from CML patients and healthy volunteers and in in vitro-stimulated CML cells. Furthermore, IRF4 expression was compared in the CML samples taken before IFN-alpha therapy and in 47 additional CML samples taken during IFN-alpha therapy. IRF4 expression was then correlated with cytogenetic response to IFN-alpha. RESULTS: IRF4 expression was significantly impaired in CML, AML, and CMMoL samples. The downregulation of IRF4 in CML samples was predominantly found in T cells. In CML patients during IFN-alpha therapy, a significant increase in IRF4 levels was detected, and this was also observed in sorted T cells from CML patients. The increase seen during IFN-alpha therapy was not due to different blood counts. In regard to the cytogenetic response with IFN-alpha, a good response was associated with high IRF4 expression. CONCLUSION: IRF4 expression is downregulated in T cells of CML patients, and its increase is associated with a good response to IFN-alpha therapy. These data suggest IRF4 expression as a useful marker to monitor, if not predict, response to IFN-alpha in CML.

Acute Disease↗