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Model Rats (model + rat)
Selected AbstractsOpen-field Behaviors and Water-maze Learning in the F Substrain of Ihara Epileptic RatsEPILEPSIA, Issue 1 2006Yoko Okaichi Summary:,Purpose: Genetically epileptic model rats, Ihara epileptic rat (IER/F substrain), have neuropathologic abnormalities and develop generalized convulsive seizures when they reach the age of ,5 months. Because the neuromorphologic abnormalities are centered in the hippocampus, we expected to observe spatial cognitive deficits. The present study aimed to evaluate emotionality and learning ability of the F substrain of IER. Methods: To determine whether deficits are caused by inborn neuropathologic abnormalities or by repeated generalized convulsions, we tested nine 6- to 12-week-old IER/F rats that had not yet experienced seizures (experiment 1) and nine 7- to 9-month-old IER/F rats that had repeatedly experienced seizures (experiment 2) with identical tasks: an open-field test and the Morris water-maze place and cue tasks. Results: Both groups of IER/Fs showed behaviors that were different from those of control rats in the open-field test, and extensive learning impairments were seen in both the place task, which requires spatial cognition, and the cue task, which does not require spatial cognition but requires simple association learning. Their impaired performance of the cue task indicates that their deficiency was not limited to spatial cognition. Conclusions: Because young IER/F rats without seizure experiences also showed severe learning impairments, genetically programmed microdysgenesis in the hippocampus was suspected as a cause of the severe learning deficits of IER/Fs. [source] Efficacy and limitation of bone marrow transplantation in the treatment of acute and subacute liver failure in ratsHEPATOLOGY RESEARCH, Issue 11 2009Hirotaka Tokai Aim:, Recent reports have shown that bone marrow cells (BMC) retain the potential to differentiate into hepatocytes. Thus, the BMC have been recognized as an attractive source for liver regenerative medicine. However, it has not been clarified whether BMC transplantation can be used to treat liver damage in vivo. In the present study, we explored whether BMC possess therapeutic potential to treat acute and/or subacute liver failure. Methods:, Fulminant hepatic failure (FHF) was induced by 70% hepatectomy with ligation of the right lobe pedicle (24% liver mass), followed by transplantation of BMC into the spleen. Dipeptidyl peptidase IV-positive (DPPIV+) BMC were then transplanted into DPPIV-negative (DPPIV - ) recipients following hepatic irradiation (HIR) in which 70% of the liver was resected and the remnant liver irradiated. Results:, There was no benefit of BMC transplantation towards survival in the FHF model. DPPIV+ hepatocytes appeared in the liver tissues of the DPPIV - HIR model rats, but DPPIV+ hepatocytes replaced less than 13% of the recipient liver. Conclusion:, BMC transplantation may have limitations in the treatment of fulminant or acute liver failure because they do not have sufficient time to develop into functional hepatocytes. Preparative HIR may be beneficial in help to convert the transplanted BMC into host hepatocytes, and provide a survival benefit. Although, However, the precise mechanism warrants further studies. [source] Influence for testicular development and histological peculiarity in the testes of flutamide-induced cryptorchid rat modelINTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2007Kentaro Mizuno Objectives: To investigate influence for the testicular development and to assess the usefulness as an animal model, cryptorchid rats were induced by exposure to flutamide during the fetal period and their testes examined histologically. Methods: Flutamide was injected into the abdomen of pregnant rats for 7 days from the 14th to 20th day of gestation. The male offspring in which cryptorchidism was observed at 28 days after birth were defined as the model rats. They were divided into four groups by dosage of flutamide (2.5 mg, 5 mg, 7.5 mg, 15 mg per day), and their testicular weight, spermatogenesis (modified Johnsen score), and germ cell apoptosis were examined histochemically at 10 weeks after birth. Results: The incidence of cryptorchidism including both unilateral and bilateral in the 2.5, 5, 7.5 and 15-mg flutamide groups was 58.3%, 81.9%, 93.6% and 91.0%, respectively. In the model rats, the undescended testes were located at the caudal end of the abdominal cavity, and these testes weighed less than the contra-descended testes in each group. Histologically, apoptotic cells were markedly increased, the seminiferous tubules were degenerated and disturbance of spermatid differentiation was observed in the undescended testes compared with the normal or contra-lateral descended testes. Conclusions: We found out that the incidence of undescended testes increased in a flutamide dose-dependent manner. The findings of histological examination were independent of the administrated dose of flutamide and it is suggested that exposure of the testes to abdominal temperature causes spermatogenic arrest with germ cell apoptosis. The present animal model indicates high incidence of above 90%, has no surgical stress and dose not require special techniques. We believe that the present model is a useful tool for the understanding of pathogenesis and treatment of cryptorchidism and further biological research into spermatogenesis. [source] Disease progression of human SOD1 (G93A) transgenic ALS model ratsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2006Arifumi Matsumoto Abstract The recent development of a rat model of amyotrophic lateral sclerosis (ALS) in which the rats harbor a mutated human SOD1 (G93A) gene has greatly expanded the range of potential experiments, because the rats' large size permits biochemical analyses and therapeutic trials, such as the intrathecal injection of new drugs and stem cell transplantation. The precise nature of this disease model remains unclear. We described three disease phenotypes: the forelimb-, hindlimb-, and general-types. We also established a simple, non-invasive, and objective evaluation system using the body weight, inclined plane test, cage activity, automated motion analysis system (SCANET), and righting reflex. Moreover, we created a novel scale, the Motor score, which can be used with any phenotype and does not require special apparatuses. With these methods, we uniformly and quantitatively assessed the onset, progression, and disease duration, and clearly presented the variable clinical course of this model; disease progression after the onset was more aggressive in the forelimb-type than in the hindlimb-type. More importantly, the disease stages defined by our evaluation system correlated well with the loss of spinal motor neurons. In particular, the onset of muscle weakness coincided with the loss of approximately 50% of spinal motor neurons. This study should provide a valuable tool for future experiments to test potential ALS therapies. © 2005 Wiley-Liss, Inc. [source] Human neural stem cells genetically modified for brain repair in neurological disordersNEUROPATHOLOGY, Issue 3 2004Seung U. Kim Existence of multipotent neural stem cells (NSC) has been known in developing or adult mammalian CNS, including humans. NSC have the capacity to grow indefinitely and have multipotent potential to differentiate into three major cell types of CNS, neurons, astrocytes and oligodendrocytes. Stable clonal lines of human NSC have recently been generated from the human fetal telencephalon using a retroviral vector encoding v-myc. One of the NSC lines, HB1.F3, carries normal human karyotype of 46XX and has the ability to self-renew, differentiate into cells of neuronal and glial lineages, and integrate into the damaged CNS loci upon transplantation into the brain of animal models of Parkinson disease, HD, stroke and mucopolysaccharidosis. F3 human NSC were genetically engineered to produce L-dihydroxyphenylalanine (L-DOPA) by double transfection with cDNA for tyrosine hydroxylase and guanosine triphosphate cylohydrolase-1, and transplantation of these cells in the brain of Parkinson disease model rats led to L-DOPA production and functional recovery. Proactively transplanted F3 human NSC in rat striatum, supported the survival of host striatal neurons against neuronal injury caused by 3-nitropro-pionic acid in rat model of HD. Intravenously introduced through the tail vein, F3 human NSC were found to migrate into ischemic lesion sites, differentiate into neurons and glial cells, and improve functional deficits in rat stroke models. These results indicate that human NSC should be an ideal vehicle for cell replacement and gene transfer therapy for patients with neurological diseases. In addition to immortalized human NSC, immortalized human bone marrow mesenchymal stem cell lines have been generated from human embryonic bone marrow tissues with retroviral vectors encording v-myc or teromerase gene. These immortalized cell lines of human bone marrow mesenchymal stem cells differentiated into neurons/glial cells, bone, cartilage and adipose tissue when they were grown in selective inducing media. There is further need for investigation into the neurogenic potential of the human bone marrow stem cell lines and their utility in animal models of neurological diseases. [source] STUDIES ON THE EXPRESSION LEVELS OF STEROL-METABOLIZING ENZYMES IN THE OBESE MODEL SHR/NDmcr- cp RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2004Makiko Kudo SUMMARY 1.,Expression levels of four key enzymes of cholesterol metabolism, namely 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, lanosterol 14-demethylase (CYP51), cholesterol 7,-hydroxylase (CYP7A1) and sterol 12,-hydroxylase (CYP8B1), in metabolic syndrome model rats (SHR/NDmcr-cp) were examined. 2.,Decreased expression of CYP51, which may be linked to the development of obesity, was found in the rats. 3.,Expression of CYP8B1 was significantly higher in young rats. 4.,No substantial change was observed in the mRNA levels of the dominant rate-limiting enzymes of sterol metabolism, namely HMG-CoA reductase and CYP7A1, in the rats. 5.,These findings suggest that the expression levels of two key enzymes managing the downstream parts of the cholesterol-metabolizing pathways are altered in the rats, although little change was observed in the expression levels of the dominant rate-limiting enzymes of cholesterol metabolism. 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