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CON Group (con + group)
Selected AbstractsLaminar xanthine oxidase, superoxide dismutase and catalase activities in the prodromal stage of black-walnut induced equine laminitisEQUINE VETERINARY JOURNAL, Issue 1 2007J. P. LOFTUS Summary Reasons for study: Xanthine oxidase (XO)-dependent production of superoxide anion and hydrogen peroxide, a characteristic of ischaemia-reperfusion injury, may contribute to the development of equine laminitis. Objective: To determine the levels of XO and antioxidant enzymes (catalase, superoxide dismutase [SOD]) in the digital laminae of normal horses (CON) and horses in the developmental stage of laminitis using the black walnut extract (BWE) model. Methods: Healthy horses (n = 12) were administered BWE (BWE group, n = 6), or water (CON group, n = 6) through a nasogastric tube. At the onset of leucopenia in the BWE-treated animals, all horses were anaesthetised, digital laminae and other samples collected rapidly and flash frozen, and the animals subjected to euthanasia. Extracts of the frozen tissues were assayed for the 2 conformational forms of xanthine: oxygen oxidoreductase (XOR), namely, xanthine dehydrogenase (XDH) and xanthine oxidase (XO), as well as the antioxidant enzymes, SOD and catalase. Results: Extracts of liver, lungs and skin, but not digital laminae, from either CON or BWE-treated horses had endogenous SOD, whereas all had endogenous XO and catalase. The levels of XDH, XO and catalase were similar in extracts of laminae from CON and BWE-treated horses as was the ratio of XDH to XO in extracts. Conclusions and potential relevance: The absence of increased XO activity suggest against the involvement of this reactive oxygen intermediate-generating system in the development of laminar pathology in BWE-treated horses. Conversely, the absence of SOD from extracts of equine digital laminae, but not other tissues, suggests that the equine digital laminae are highly susceptible to damage by superoxide anion, produced, for example, by emigrant inflammatory leucocytes. [source] Inter-hemispheric inhibition is impaired in mirror dystoniaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2009S. Beck Abstract Surround inhibition, a neural mechanism relevant for skilled motor behavior, has been shown to be deficient in the affected primary motor cortex (M1) in patients with focal hand dystonia (FHD). Even in unilateral FHD, however, electrophysiological and neuroimaging studies have provided evidence for bilateral M1 abnormalities. Clinically, the presence of mirror dystonia, dystonic posturing when the opposite hand is moved, also suggests abnormal interhemispheric interaction. To assess whether a loss of inter-hemispheric inhibition (IHI) may contribute to the reduced surround inhibition, IHI towards the affected or dominant M1 was examined in 13 patients with FHD (seven patients with and six patients without mirror dystonia, all affected on the right hand) and 12 right-handed, age-matched healthy controls (CON group). IHI was tested at rest and during three different phases of a right index finger movement in a synergistic, as well as in a neighboring, relaxed muscle. There was a trend for a selective loss of IHI between the homologous surrounding muscles in the phase 50 ms before electromyogram onset in patients with FHD. Post hoc analysis revealed that this effect was due to a loss of IHI in the patients with FHD with mirror dystonia, while patients without mirror dystonia did not show any difference in IHI modulation compared with healthy controls. We conclude that mirror dystonia may be due to impaired IHI towards neighboring muscles before movement onset. However, IHI does not seem to play a major role in the general pathophysiology of FHD. [source] Trimetazidine Reduces Basal Cytosolic Ca2+ Concentration During Hypoxia in Single Xenopus Skeletal MyocytesEXPERIMENTAL PHYSIOLOGY, Issue 3 2003C. M. Stary We tested the hypotheses that: (1) Ca2+ handling and force production would be irreversibly altered in skeletal muscle during steady-state contractions when subjected to severe, prolonged hypoxia and subsequent reoxygenation; and (2) application of the cardio-protective drug trimetazidine would attenuate these alterations. Single, living skeletal muscle fibres from Xenopus laevis were injected with the Ca2+ indicator fura 2, and incubated for 1 h prior to stimulation in 100 ,M TMZ-Ringer solution (TMZ; n = 6) or standard Ringer solution (CON; n = 6). Force and relative free cytosolic Ca2+ concentration ([Ca2+]c) were measured during continuous tetanic contractions produced every 5 s as fibres were sequentially perfused in the following manner: 3 min high extracellular PO2 (159 mmHg), 15 min hypoxic perfusion (3-5 mmHg) then 3 min high PO2. Hypoxia caused a decrease in force and peak [Ca2+]c in both the TMZ and CON fibres, with no significant (P < 0.05) difference between groups. However, basal [Ca2+]c was significantly lower during hypoxia in the TMZ group vs. the CON group. While reoxygenation generated only modest recovery of relative force and peak [Ca2+]c in both groups, basal [Ca2+]c remained significantly less in the TMZ group. These results demonstrated that in contracting, single skeletal muscle fibres, TMZ prevented increases in basal [Ca2+]c generated during a severe hypoxic insult and subsequent reoxygenation, yet failed to protect the cell from the deleterious effects of prolonged hypoxia followed by reoxygenation. [source] A Rodent Model of Alcoholic Heart Muscle Disease and Its Evaluation by EchocardiographyALCOHOLISM, Issue 3 2001Shann D. Kim Background: Transthoracic echocardiography was used in a rodent animal model to determine whether long-term alcohol consumption (8 and 12 months) was associated with the development of a dilated cardiomyopathy. We also investigated whether alcohol-induced changes in cardiac structure corresponded to activation of the renin-angiotensin system and the natriuretic peptide (NP) system. Methods: Male rats received either the Lieber-DeCarli liquid alcohol diet (EtOH) (9%v/v) (n= 8) or control diet (CON) (n= 8). Echocardiography (echo) was used to determine left-ventricular (LV) dimensions, and isolated heart studies (Langendorff and atrium) were used to assess ex vivo contractility. Plasma and tissue angiotensin-I converting enzyme (ACE) activity was measured. Gene expression, plasma, and tissue levels of the NPs were determined by northern blot analysis and radioimmunoassay, respectively. Results: After 8 months of alcohol consumption, there was a trend for the end diastolic dimension, end systolic dimension, and LV mass to be greater in the 8 month EtOH group compared with the CON group. However, after 12 months of alcohol consumption, significant increases were found between the groups in several echo parameters. Tissue ACE activity (nmoles/min/mg protein) was greater in the 12 month EtOH group compared with the 12 month CON and 8 month EtOH group (p < 0.05). We found no differences between groups in gene expression (messenger RNA), plasma, and tissue levels of the NPs. Conclusions: Echocardiography revealed that 8 to 12 months of alcohol consumption was associated with the development of a dilated cardiomyopathy. However, this was not preceded by an increase in tissue ACE activity, and these changes occurred in the absence of increased plasma and LV tissue levels of the NPs. [source] Prophylactic Bisphosphonate Treatment Prevents Bone Fractures After Liver TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2007M. Bodingbauer A randomized controlled prospective open-label single center trial was performed. At the time of transplantation patients were randomly assigned to one of two treatment arms: The study group of 47 patients received zoledronic acid (ZOL, 8 infusions at 4 mg during the first 12 months after LT), calcium (1000 mg/d) and vitamin D (800 IE/d). The control group consisted of 49 patients who received calcium and vitamin D at same doses (CON). The incidence of bone fractures or death was predefined as the primary endpoint. Secondary endpoints included bone mineral density (BMD), serum biochemical markers of bone metabolism, parameters of trabecular bone histomorphometry and mineralization density distribution (BMDD). Patients were followed up for 24 months. Analysis was performed on an intention-to-treat basis. The primary endpoint fracture or death was reached in 26% of patients in the ZOL group and 46% in the CON group (p = 0.047, log rank test). Densitometry results were different between the groups at the femoral neck at 6 months after LT (mean+/-SD BMD ZOL: 0.80 ± 0.19 g/cm2 vs. CON: 0.73 ± 0.14 g/cm2, p = 0.036). Mixed linear models of biochemical bone markers showed less increase of osteocalcin in the ZOL group and histomorphometry and BMDD indicated a reduction in bone turnover. Prophylactic treatment with the bisphosphonate zoledronic acid reduces bone turnover and fractures after liver transplantation. [source] Prefrontal cortex oxygenation during incremental exercise in chronic fatigue syndromeCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2008J. Patrick Neary Summary This study examined the effects of maximal incremental exercise on cerebral oxygenation in chronic fatigue syndrome (CFS) subjects. Furthermore, we tested the hypothesis that CFS subjects have a reduced oxygen delivery to the brain during exercise. Six female CFS and eight control (CON) subjects (similar in height, weight, body mass index and physical activity level) performed an incremental cycle ergometer test to exhaustion, while changes in cerebral oxy-haemoglobin (HbO2), deoxy-haemoglobin (HHb), total blood volume (tHb = HbO2 + HHb) and O2 saturation [tissue oxygenation index (TOI), %)] was monitored in the left prefrontal lobe using a near-infrared spectrophotometer. Heart rate (HR) and rating of perceived exertion (RPE) were recorded at each workload throughout the test. Predicted VO2peak in CFS (1331 ± 377 ml) subjects was significantly (P , 0·05) lower than the CON group (1990 ± 332 ml), and CFS subjects achieved volitional exhaustion significantly faster (CFS: 351 ± 224 s; CON: 715 ± 176 s) at a lower power output (CFS: 100 ± 39 W; CON: 163 ± 34 W). CFS subjects also exhibited a significantly lower maximum HR (CFS: 154 ± 13 bpm; CON: 186 ± 11 bpm) and consistently reported a higher RPE at the same absolute workload when compared with CON subjects. Prefrontal cortex HbO2, HHb and tHb were significantly lower at maximal exercise in CFS versus CON, as was TOI during exercise and recovery. The CFS subjects exhibited significant exercise intolerance and reduced prefrontal oxygenation and tHb response when compared with CON subjects. These data suggest that the altered cerebral oxygenation and blood volume may contribute to the reduced exercise load in CFS, and supports the contention that CFS, in part, is mediated centrally. [source] Post-conditioning with cyclosporine A fails to reduce the infarct size in an in vivo porcine modelACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2010R. H. LIE Background: Cyclosporine A has generated intense interest in the field of cardioprotection due to its ability to protect the mitochondria at reperfusion by blocking the opening of the mitochondrial permeability transition pore. The aim of our study was to examine the cardioprotective effect of Sandimmun®, a clinically available formulation of cyclosporine A, in an in vivo large mammal model. Methods: Forty-eight pigs were randomly allocated to one of three groups: (i) Control group (Con, n=19), (ii) Cyclosporine group, (Cyclo, n=19) Sandimmun® 10 mg/kg i.v. bolus 5 min before reperfusion and (iii) Pre-conditioning group (Precon, n=10) two cycles of 10 min ischemia interspersed with 30-min reperfusion. The study was further sub-divided into a metabolic protocol, evaluating myocardial metabolism by measuring changes in the interstitial lactate concentration, and a coronary flow protocol. All animals were subjected to 40 min of left anterior descending coronary artery occlusion, followed by 180 min of reperfusion before histochemical staining and assessment of infarct size by planimetry. Results: Infarct sizes were measured as: Con 51.4 ± 16.5%, Cyclo 47.3 ± 15.7% and Precon 2.4 ± 3.6%, with no significant difference between the Con and Cyclo groups but a highly significant difference between the Precon and Cyclo and Con groups (P<0.0001 for both comparisons). In the Cyclo group, the interstitial lactate concentration was significantly increased compared with the Con group at 6-min reperfusion, although significantly lower at 14 min presumably due to accelerated washout. Conclusion: In this large animal model, a 10 mg/kg bolus administration of Sandimmun® 5 min before reperfusion did not reduce the infarct size. [source] | |||||||||||||