A chronic mouse model of Parkinson's disease has a reduced gait pattern certainty

The purpose of this investigation was to determine if a chronic Parkinson's disease mouse model will display less certainty in its gait pattern due to basal ganglia dysfunction. A chronic Parkinson's disease mouse model was induced by injecting male C57/BL mice with 10 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg) (MPTP) and probenecid (250 mg/kg) (P) over 5 weeks. This chronic model produces a severe and persistent loss of nigrostriatal neurons resulting in dopamine depletion and locomotor impairment. The control mice were treated with probenecid alone. Fifteen weeks after the last MPTP/P treatment, the mice were videotaped in the sagittal plane with a digital camera (60 Hz) as they ran on a motorized treadmill at a speed of 10 m/min. The indices of gait and gait variability were calculated. Stride length was significantly (p = 0.016) more variable in the chronic MPTP/P mice. Additionally, the chronic MPTP/P mice had a statistically less certain gait pattern when compared to the control mice (p = 0.02). These results suggest that variability in the gait pattern can be used to evaluate changes in neural function. Additionally, our results imply that disorder of the basal ganglia results in less certainty in modulating the descending motor command that controls the gait pattern.     

Isolation and characterisation of microsatellite loci in the tire track eel,Mastacembelus favus and cross-species amplification

Nine microsatellite loci were isolated and characterized in the tire track eel, Mastacembelus favus by using library enriched for microsatellite region. Among 47 specimens collected from Mekong River, the number of alleles ranged from 2 to 17 while levels of observed and expected heterozygosities ranged from 0.021 to 0.873 and from 0.021 to 0.893, respectively. The primers were successfully tested in six closely related species, hence valuable for investigating population genetics and other related aspects of M. favus and its congener species.     

Pathogenicity,sequence and phylogenetic analysis of <Emphasis Type="Italic">Malaysian Chicken anaemia virus</Emphasis> obtained after low and high passages in MSB-1 cells

Summary. Specific-pathogen-free (SPF) chickens inoculated with low passage Chicken anaemia virus (CAV), SMSC-1 and 3-1 isolates produced lesions suggestive of CAV infection. Repeated passages of the isolates in cell culture until passage 60 (P60) and passage 123 produced viruses that showed a significantly reduced level of pathogenicity in SPF chickens compared to the low passage isolates. Sequence comparison indicated that nucleotide changes in only the coding region of the P60 passage isolates were thought to contribute to virus attenuation. Phylogenetic analysis indicated that SMSC-1 and 3-1 were highly divergent, but their P60 passage derivatives shared significant homology to a Japanese isolate A2.     

Aldrin-induced stimulation of locomotor activity and brain regional glutamate.

Single administration of aldrin (2-10 mg/kg) to adult male albino rats (120-130 g) enhanced locomotor activity (LA), with the maximum effect reached 2 h after treatment. The measurement of steady state levels of glutamate, glutamine and the activities of their metabolizing enzymes in different regions of the brains of rats treated with aldrin under its nontolerant condition showed that aldrin enhanced the activity of the neuronal glutamate system in the cerebral cortex, cerebellum and hypothalamus. Moreover, treatment with the glutamatergic NMDA receptor antagonist D,L-2-amino-7-phosphonoheptanoic acid, in the absence and presence of aldrin, reduced the LA of control rats and attenuated the aldrin-induced increase in LA of treated rats. These results suggest that aldrin-induced activation of the central glutamate system may be a cause of stimulation of LA with aldrin under its nontolerant condition.     

Alpha lipoic acid posses dual antioxidant and lipid lowering properties in atherosclerotic-induced New Zealand White rabbit

There is accumulating data demonstrated hypercholesterolemia and oxidative stress play an important role in the development of atherosclerosis. In the present study, a protective activity of alpha-lipoic acid; a metabolic antioxidant in hypercholesterolemic-induced animals was investigated. Eighteen adult male New Zealand White (NZW) rabbit were segregated into three groups labelled as group K, AT and ALA (n = 6). While group K was fed with normal chow and acted as a control, the rest fed with 100 g/head/day with 1% high cholesterol diet to induce hypercholesterolemia. 4.2 mg/body weight of alpha lipoic acid was supplemented daily to the ALA group. Drinking water was given ad-libitum. The study was designed for 10 weeks. Blood sampling was taken from the ear lobe vein at the beginning of the study, week 5 and week 10 and plasma was prepared for lipid profile estimation and microsomal lipid peroxidation index indicated with malondialdehyde (MDA) formation. Animals were sacrificed at the end of the study and the aortas were excised for intimal lesion analysis. The results showed a significant reduction of lipid peroxidation index indicated with low MDA level (p < 0.05) in ALA group compared to that of the AT group. The blood total cholesterol (TCHOL) and low density lipoprotein (LDL) levels were found to be significantly low in ALA group compared to that of the AT group (p < 0.05). Histomorphometric intimal lesion analysis of the aorta showing less of atheromatous plaque formation in alpha lipoic acid supplemented group (p < 0.05) compared to that of AT group. These findings suggested that apart from its antioxidant activity, alpha lipoic acid may also posses a lipid lowering effect indicated with low plasma TCHOL and LDL levels and reduced the athero-lesion formation in rabbits fed a high cholesterol diet.     

Evaluation of acute coronary syndromes by cardiac magnetic resonance imaging

The use of cardiovascular magnetic resonance (CMR) imaging for the evaluation of patients with acute chest pain and acute coronary syndromes has great potential. The strength of CMR relies on its ability to provide information on anatomy, physiology, and function in a single scanning session in a noninvasive manner without the need for iodinated contrast, radiation, or the need to undergo invasive procedures. Specifically, with regard to imaging patients with acute chest pain and/or myocardial infarction (MI), CMR has the ability to qualitatively and quantitatively evaluate global and regional right and left ventricular systolic functions, myocardial edema, myocardial perfusion, and myocardial infarct size and transmurality/viability. This review will focus on CMR imaging for the following applications: (1) imaging for the evaluation of ventricular function and infarct size in patients with acute chest pain and/or acute MI, (2) for triage and prognosis of patients presenting to the emergency department with acute chest pain, (3) for evaluating patients after sustaining an acute MI, and (4) for stem cell research.     

Postischemic myocardial "stunning". Identification of major differences between the open-chest and the conscious dog and evaluation of the oxygen radical hypothesis in the conscious dog

Recent studies suggest that oxygen-derived free radicals contribute to the pathogenesis of postischemic myocardial dysfunction (myocardial "stunning"). This concept, however, is predicated exclusively on results obtained in open-chest preparations, which are subject to the confounding influence of many unphysiological conditions. The lack of supporting evidence in more physiological animal models represents a major persisting limitation of the oxy-radical hypothesis of myocardial stunning. The goal of this study was to address two fundamental (and related) questions: 1) Does the open-chest animal model alter the phenomenon of myocardial stunning? 2) If so, how valid are the concepts, derived from such a model, regarding the pathogenetic role of oxy-radicals? In part 1 of the study, myocardial stunning after a 15-minute coronary occlusion was compared in 30 pentobarbital-anesthetized open-chest dogs and in 19 conscious dogs. For any given level of collateral flow during occlusion, the recovery of systolic wall thickening after reperfusion was markedly less in open-chest animals. In an additional group of five open-chest dogs, a close inverse relation was noted between body temperature and postischemic wall thickening, indicating that the recovery of the stunned myocardium in acute experiments may vary markedly depending on how temperature is controlled. Because of these major differences between open-chest and conscious dogs, the oxy-radical hypothesis needs to be tested in the latter model. Thus, in part 2 of the study, conscious unsedated dogs undergoing a 15-minute coronary occlusion were randomized to an intravenous infusion of either saline (19 coronary occlusions) or superoxide dismutase (SOD) plus catalase (CAT) (21 coronary occlusions). Despite the fact that the plasma levels of SOD and CAT declined rapidly after reperfusion, postischemic wall thickening was significantly greater in treated compared with control dogs throughout the first 6 hours of reflow. Thus, a brief (60-minute) infusion of SOD and CAT produced a sustained improvement of recovery of contractility. The magnitude of this beneficial effect was a function of the severity of ischemia: the lower the collateral perfusion, the greater the improvement effected by the enzymes. The accelerated recovery produced by SOD and CAT was not followed by any deterioration of contractility, suggesting that postischemic dysfunction is not a teleologically "protective" phenomenon. In conclusion, the severity of myocardial stunning is greatly exaggerated by the unphysiological conditions present in the barbiturate-anesthetized open-chest dog.(ABSTRACT TRUNCATED AT 400 WORDS)