PubMed Health⌕ Search
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 DiseaseAnimalsAnimals, Genetically ModifiedCoronary Artery DiseaseCoronary DiseaseDisease Models, AnimalFibroblast Growth Factor 5Fibroblast Growth FactorsHumansHyperlipidemiasLipid MetabolismMiceMice, TransgenicNeovascularization, PhysiologicRabbitsSyndromeEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

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

PubMed1999

Hallucinations in the acute schizophrenic-type psychosis: effects of gender and age of illness onset.

Our objective was to test the hypothesis that gender, the age of illness onset, or the interaction between these two variables, would distinguish acutely ill schizophrenic and schizoaffective patients who hallucinated from those who did not. Hallucinatory experiences were measured by the hallucination item of the Brief Psychiatric Rating Scale in a sample of 160 drug-free inpatients admitted for the treatment of an acute episode. Patients were categorized as either non-hallucinators or hallucinators. An additional analysis included only those who had 'severe' hallucinations (i.e., score > or = 5). Female gender, but not age of onset, predicted a higher frequency of hallucinations (irrespective of degree of severity) in the total sample, but specifically in the schizophrenic patients. These results indicate that there may be gender differences in the propensity to experience hallucinations during the acute schizophrenic episode.

Acute Disease↗
PubMed1999

Prognostic implication of FLT3 and N-RAS gene mutations in acute myeloid leukemia.

Internal tandem duplication of the FLT3 gene and point mutations of the N-RAS gene are the most frequent somatic mutations causing aberrant signal-transduction in acute myeloid leukemia (AML). However, their prognostic importance is unclear. In this study, their prognostic significance was analyzed in 201 newly diagnosed patients with de novo AML except acute promyelocytic leukemia. Three patients had mutations in both genes, 43 had only the FLT3 gene mutation, 25 had only the N-RAS gene mutation, and 130 had neither. These mutations seemed to occur independently. Both mutations were related to high peripheral white blood cell counts, and the FLT3 gene mutation was infrequently observed in the French-American-British (FAB)-M2 type. AML cases with wild FLT3/mutant N-RAS had a lower complete remission (CR) rate than those with wild FLT3/wild N-RAS, whereas the presence of mutant FLT3 did not affect the CR rate. Univariate analysis showed that unfavorable prognostic factors for overall survival were age 60 years or older (P =.0002), cytogenetic data (P =.002), FAB types other than M2 (P =.002), leukocytosis over 100 +/- 10(9)/L (P =.003), and the FLT3 gene mutation (P =.004). However, the N-RAS gene mutation was only a marginal prognostic factor (P =.06). For the subjects under 60 years old, multivariate analysis showed that the FLT3 gene mutation was the strongest prognostic factor (P =.008) for overall survival. The FLT3 gene mutation, whose presence is detectable only by genomic polymerase chain reaction amplification and gel electrophoresis, might serve as an important molecular marker to predict the prognosis of patients with AML.

Acute Disease↗