186,632 research outputs found

    The human SLC25A42 protein, ortholog of mitochondrial carrier Leu5p of S. cerevisiae, transports Coenzyme A and Adenosine 3’, 5’- diphosphate

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    The human SLC25A42 protein, ortholog of mitochondrial carrier Leu5p of S. cerevisiae, transports Coenzyme A and Adenosine 3’,5’-diphosphate G. Fiermonte, E. Paradies, S. Todisco, C.M.T. Marobbio, M.A Di Noia, and F. Palmieri Department of Pharmaco-Biology, Laboratory and Molecular Biology, University of Bari, Bari, Italy The essential cofactor Coenzyme A (CoA) is required in many intra-mitochondrial metabolic pathways. The CoA is synthesized outside the mitochondrial matrix, therefore must be transported into mitochondria. In S. cerevisiae, the mitochondrial carrier Leu5p is involved in the accumulation of CoA in the mitochondrial matrix. In fact, deletion of LEU5 (leu5) causes a reduction of mitochondrial coenzyme A (CoA) levels and growth defect on YP supplemented with glycerol or other non fermentative carbon sources. The closest relatives of Leu5p in human are SLC25A16 (37% identity) and SLC25A42 (31% identity). In this study we provide direct evidence that SLC25A42 is a novel transporter of CoA. SLC25A42 is localized in the mitochondrial inner membrane and is highly expressed in virtually all tissues. This protein was overexpressed in Escherichia coli, purified, reconstituted in phospholipid vesicles, and shown to transport CoA, dephospho-CoA, Adenosine 3’,5’-diphosphate (PAP), and (deoxy)adenine nucleotides with high specificity and by a counter-exchange mechanism. The expression of SLC25A42 protein in LEU5 cells fully restores the phenotype of the LEU5 strain, indicating that the main function of both proteins is probably to catalyze the entry of CoA into mitochondria in exchange for adenine nucleotides and PAP

    Jejunal hemorrhage sindrome in dairy cattle associated with Clostridia infection”

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    JEJUNAL HEMORRHAGE SYNDROME IN DAIRY CATTLE ASSOCIATED WITH CLOSTRIDIA INFECTION. Ceci L., Paradies P., Greco G., Buonavoglia D., Capucchio M.T.*, Guarda F.*, Carelli G. Department of Animal Health Welfare, Faculty of Veterinary Medicine, University of Bari. Department Animal Pathology*, University of Torino, Italy A survey based on clinical, anatomohystophatological observations and microbiological investigations was performed on 11 italian brown breed dairy cattle affected with depression, anorexia, agalaxia, ruminal hypomotility, abdominal pain and melaena. Macroscopic lesions of 8 animals consisted of hemorrhagic enteritis in the small intestine. Clostridium perfringens type A was isolated from the tissues of 7 animals and the beta2-toxin gene was detected in 4 out of 7 type A isolates. Based on these observations 8 animals were considered affected with Jejunal Hemorrhage Syndrome

    Cardiovascular effects of continuous positive airway pressure (CPAP) in dogs under anesthesiaassessed by Doppler echocardiography

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    General anesthesia impairs respiratory functionby the development of atelectasis in association with alteredventilation at pulmonary bases1. Applying Continuous Positive Airways Pressure (CPAP) in spontaneously breathing patients reduce the work of breathing, increases functional residualcapacity and is often recommended to prevent orreduce alveolar collapse1. In human medicine it has been widely recognized that an increase in intra-thoracic pressure is associated with a decrease in cardiac outputbecause of the reduction of venous return2. Nevertheless, conflictingresults (increases, decreases, or no change) in CO have beenreported and it was studied that the effects of CPAP on cardiac function were influenced by increasing CPAP levels. Doppler echocardiography represents a way to investigate how cardiac parameters can be affected and can change during CPAP application. What about CPAP application and its cardiovascular consequences in dogs? Aim of the study The aim of this study is to investigate by Doppler echocardiographythe cardiovascular effects of a low level of CPAP(5 cm H2O) in dogs under anesthesia. Materials and Methods 20 dogs have been enrolled in the study and divided into two groups. Both groups underwent anesthesia with a standard protocol and in Group A (10 dogs) CPAP was administered (5 cmH2O). Group B (10 dogs) served as control group and did not receive CPAP. Cardiovascular parameters (heart rate, mean arterial pressure and echocardiographic indices) were registered before (T0) and 15 minutes after anesthesia induction (T1), during anesthesia with or without CPAP(T2) and during recovery (T3).All patients were anesthetizedwith acepromazine (20 μg/kg), morphine (0.3 mg/kg), propofol (4 mg/kg) and isoflurane (end-tidal concentration 1.3 %)in spontaneous ventilation. Standard echocardiography (Esaote ultrasound system MyLab30) was performed usinga 2.5 MHz transducer. The following parameters were calculated as indicators of cardiovascular function: ejection fraction (EF%), left and right cardiac index (CI), left ventricle end diastolic volume index (LV-EDVI ml/m2), ratio of isovolumetric contraction time to ejection time (IVCT/ET), ratio of early rapid filling peak to atrial peak filling of transatrioventricular inflow (E/A), time velocity integral of atrioventricular inflow (TVI), aortic max velocity (AoVmax) and pulmonary max velocity (P Vmax). Results and Conclusions On the whole no statistical differences have been revealed in cardiovascular parameters at T2 compared to T1 in both groups.Interestingly a significant difference was revealed in EF between CPAP group and control group at T2. Myocardial diastolic properties remained unchanged. The right cardiac index do not change.Results of this study suggest not only that application of low levels of CPAP during anesthesia of healthy dogs does not negatively affect cardiac function and hemodynamic parameters, but also that it could positivelyinfluence the global left ventricular systolic function. In conclusion the application of this level of CPAP during anesthesia in healthy dogs could be considered safe. References 1Russo et al, 2013. J. CLIN. ANESTH. 25, 314-320.2Huemer et al, 1994. CHEST 106, 67-7
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