Effects of air transportation cause physiological and biochemical changes indicative of stress leading to regulation of chaperone expression levels and corticosterone concentration.

Laboratory animals generally experience numerous unfamiliar environmental and psychological influences such as noises, temperatures, handling, shaking, and smells during the process of air transportation. To investigate whether stress induced by air transportation affects stress-related factors in animals, the levels of hormone and chaperone protein were measured in several tissues of F344 rats transported for 13 h and not transported. Herein, we conclude that the levels of corticosterone, HSP70, and GRP78 were significantly increased in the transported group compare to not transported group, but they were rapidly restored to the not transported group level after a recovery period of one week.

Exercise training acts as a therapeutic strategy for reduction of the pathogenic phenotypes for Alzheimer's disease in an NSE/APPsw-transgenic model.

Alzheimer's disease (AD) is a progressive neurodegenerative disease for which there are few therapeutic regimens that influence the underlying pathogenic phenotypes. However, of the currently available therapies, exercise training is considered to be one of the best candidates for amelioration of the pathological phenotypes of AD. Therefore, we directly investigated exercise training to determine whether it was able to ameliorate the molecular pathogenic phenotypes in the brain using a neuron-specific enolase (NSE)/Swedish mutation of amyloid precursor protein (APPsw) transgenic (Tg) mice as a novel AD model.

Reduced anxiety in the mice expressing mutant (N141I) presenilin 2.

Alzheimer's disease (AD) is characterized by progressive cognitive impairment. The effect of presenilin 1 (PS1) and PS2 mutation on cognition has been well characterized in a variety of transgenic mice. However, noncognitive behaviors have not been considered in these mice.

Role of protein kinase Cdelta in paraquat-induced glial cell death.

Paraquat (1,1'-dimethyl-4,4'-bipyridinium) is structurally similar to the neurotoxin 1-methyl-4-phenyl-4-phenylpyridium ion (MPP+), the active metabolite of the parkinsonism-inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which can induce the parkinsonism property in rodents, nonhuman primates, and human. In contrast to the neurotoxic effects of paraquat, little is known about its effects on glial cells. Here, we examined the mechanisms of paraquat toxicity in glial cells in culture.

The effects of long-duration, low-temperature ground transportation on physiological and biochemical indicators of stress in mice.

Transportation can cause stress to laboratory animals and alter physiological characteristics that may confound experimental results. The authors investigated stress-related effects of 3-4 h of transportation by truck in two strains of mice (C57BL/6, which are known to be aggressive, and ICR, which are less aggressive). Transported mice had sufficient space and access to water, though temperature in the truck was lower than what is usually recommended.

Overexpression of human selenoprotein M differentially regulates the concentrations of antioxidants and H2O2, the activity of antioxidant enzymes, and the composition of white blood cells in a transgenic rat.

Selenoprotein is associated with a variety of serious diseases, including infectious diseases, neurodegenerative disorders, cancer and cardiovascular disease. The aim of this study was to produce a new transgenic (Tg) rat expressing human selenoprotein M (SelM) in order to examine the protective function of the antioxidant status in vivo. To achieve this, a new lineage of Tg rats was produced by the microinjection of pCMV/GFP-hSelM constructs into a fertilized rat egg.

Mutant presenilin 2 increased oxidative stress and p53 expression in neuronal cells.

The learning and memory impairment of presenilin 2 transgenic mice was mentioned previously. In this study, exposing the presenilin 2 transfected PC12 cells to the 50 microM Abeta(25-35), 30 mM l-glutamate and 50 microM H(2)O(2) resulted in significant increase 8-oxodG and p53 levels of the cells expressing the mutant gene. The increase was also found in the mutant presenilin 2 transgenic mice brains age-dependently in comparison to that in the wild-type presenilin 2-transgenic mice and non-transgenic ones.

Significant change in insulin production, glucose tolerance and ER stress signaling in transgenic mice coexpressing insulin-siRNA and human IDE.

The dual expression system for the suppression and clearance of insulin has not been previously used to produce transgenic mice for diabetes-related disease. The aim of this study was to produce new transgenic mice coexpressing specific insulin small interfering RNA (siRNA) sequences and the human insulin degrading enzyme (hIDE) gene in order to examine the diabetes-like phenotype. To achieve this, a new lineage of transgenic mice was produced by the microinjection of the dual expression constructs (pH1/siRNAinsulin-CMV/hIDE) into mouse fertilized eggs.

Mutant presenilin 2 causes abnormality in the brain lipid profile in the development of Alzheimer's disease.

Mutation in the presenilin 2 (PS2mt) is known to be one of factors involved in the development of Alzheimer's disease (AD). It was recently revealed that an abnormality of lipid metabolism is a phenomenon occurring in AD. Therefore, the aim of this study was to investigate the potential relationship between the mutation of PS2 and alterations of the lipid profile within the brain.

Microbiological monitoring of guinea pigs reared conventionally at two breeding facilities in Korea.

In this study, microbiological monitoring of guinea pigs reared conventionally in two facilities was performed twice in 2004, with a three-month-interval between surveys. This study was based on the recommendations of the FELASA Working Group, with some modifications. In serological tests in the first survey, some animals from facility A showed positive results for Encephalitozoon cuniculi, Sendai virus, pneumonia virus of mice (PVM), and Reovirus-3 (Reo-3); facility B showed a positive result only for E.

Ryanodine receptor-mediated interference of neuronal cell differentiation by presenilin 2 mutation.

Neuronal cell differentiation alterations induced by mutant presenilin 2 (PS2) were investigated in transgenic mice expressing wild-type or mutant-type PS2. Progressive increases in differentiation and marker protein expression were found in neuronal cells expressing wild-type PS2, whereas these processes were much perturbed in mutant-type PS2 with elevated ryanodine-receptor (RyR) expression and intracellular calcium levels. Moreover, dantrolene, a blocker of RyR reduced the PS2 mutation-induced interference of cell differentiation and calcium release, but caffeine, an activator of RyR, exacerbated PS2 mutation-induced interference with cell differentiation.

Mutant presenilin 2 increases acetylcholinesterase activity in neuronal cells.

A presenilin 2 mutation is believed to be involved in the development of Alzheimer's disease. In addition, transgenic mice with a presenilin 2 mutation have been reported to have learning and memory impairments. In this study, exposing PC12 cells expressing mutant presenilin 2 to 50 microM AP25-35, 30 mM L-glutamate and 50 microM H2O2 caused a significant increase in acetylcholine esterase activity.

Decrease in NF-kappaB, AP-1 and SP-1 activities in neuronal cells expressing presenilin 2.

Decreases in activities of the NF-kappaB, AP-1 and SP-1 transcription factors, which could act as antiapoptotic factors, in the presenilin 2 transfected PC12 cells, either in nontreatment conditions or under apoptotic stimulation, were found in this study. Similar results were also found in mice brain cells carrying presenilin 2, especially in the mutant gene expressed ones. These findings suggested that presenilin 2 may be implicated in neuronal cell death by altering the antiapoptotic activity of the transcription factors.