953 resultados para 13200-030


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Regrouping female rabbits in group-housing systems is common management practice in rabbit breeding, which may, however, induce agonistic interactions resulting in social stress and severe injuries. Here we compared two methods of regrouping female rabbits with respect to their effects on behaviour, stress and injuries. Thus, we introduced two unfamiliar rabbits into a group of rabbits either in the group's familiar pen (HOME) or in a novel disinfected pen (NOVEL), and assessed the effects of these treatments on general activity, number and duration of agonistic interactions, number and severity of injuries and body temperature as a measure of stress. General activities were not affected by the method of regrouping. Also, treatment had no effect on the number and duration of agonistic interactions. However, the numbers of injuries (P=0.030) as well as body temperature on the first clay after regrouping (p=0.0036) were increased in rabbits regrouped in a novel clean pen. These findings question the recommendation to introduce unfamiliar does into established groups in a neutral environment and indicate that regrouping in the group's home pen may decrease the risk of severe injuries and social stress. (C) 2011 Elsevier B.V. All rights reserved.

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The association between the contagious Staphylococcus aureus genotype B (GTB) and the presence of coagulase-negative staphylococci (CNS) and Streptococcus spp. (non-agalactiae streptococci), was investigated, and the identification of problem herds without genotyping was evaluated. Milk samples from 10 herds with Staph. aureus GTB herd problems (PH cases) were compared with samples from 19 herds with at least one Staph. aureus isolate of non-B genotype (CH cases). All samples were bacteriologically analysed and Staph. aureus genotyping carried out using a ribosomal spacer-PCR. Cow and quarter prevalences of Staph. aureus, CNS and Streptococcus spp. differed significantly between PH and CH groups. PH cases were highly associated with decreased cow prevalences of CNS and Streptococcus spp. These altered prevalences also contributed significantly to the identification of problem herds without resorting to genotyping. Common herd-level risk factors did not explain the difference between the prevalences in PH and CH cases.

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The aim of this study was to test the hypothesis that ear oximetry immediately after the release of a sustained Valsalva maneuver accurately detects patent foramen ovale (PFO). One hundred sixty-five scuba divers underwent transesophageal echocardiography (TEE; reference method) for PFO assessment. Ear oximetry of the right earlobe was performed in a different room within a time frame of 2 hours before or after TEE. The subject and the oximetry operator were unaware of the results of TEE. Oxygen saturation (SO(2)) measurements were obtained at baseline and during the release phase of 4 Valsalva maneuvers within 10 minutes, and the average SO(2) change (SO(2) at baseline minus SO(2) at Valsalva release) was determined as the primary study end point. One hundred seventeen divers had no PFO, and 48 (29%) had PFO by TEE (mean age 39 ± 8 years). The average SO(2) change was 0.79 ± 1.13% (i.e., a slight absolute SO(2) decrease in response to the Valsalva maneuver) in the group without PFO and 1.67 ± 1.19% in the PFO group (p <0.0001). Using receiver-operating characteristic curve analysis, a PFO as defined by TEE could be detected at a threshold of a Valsalva-induced decrease in SO(2) of ≥0.825 percentage points in comparison to baseline (sensitivity 0.756, specificity 0.706, area under the receiver-operating characteristic curve 0.763, p <0.0001, negative predictive value 0.882). In conclusion, the entirely noninvasive method of ear oximetry in response to repetitive Valsalva maneuvers is accurate and useful as a screening method for the detection of a PFO, as shown in this study of divers.

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We evaluated the feasibility of a modified embolization technique of pulmonary arteriovenous malformations (PAVM) using venous sac embolization with detachable coils combined with the feeding artery embolization with the Amplatzer vascular plug (AVP).

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OBJECTIVE: Brugada syndrome (BS) is an inherited electrical cardiac disorder characterized by right bundle branch block pattern and ST segment elevation in leads V1 to V3 on surface electrocardiogram that can potentially lead to malignant ventricular tachycardia and sudden cardiac death. About 20% of patients have mutations in the only so far identified gene, SCN5A, which encodes the alpha-subunit of the human cardiac voltage-dependent sodium channel (hNa(v)1.5). Fever has been shown to unmask or trigger the BS phenotype, but the associated molecular and the biophysical mechanisms are still poorly understood. We report on the identification and biophysical characterization of a novel heterozygous missense mutation in SCN5A, F1344S, in a 42-year-old male patient showing the BS phenotype leading to ventricular fibrillation during fever. METHODS: The mutation was reproduced in vitro using site-directed mutagenesis and characterized using the patch clamp technique in the whole-cell configuration. RESULTS: The biophysical characterization of the channels carrying the F1344S mutation revealed a 10 mV mid-point shift of the G/V curve toward more positive voltages during activation. Raising the temperature to 40.5 degrees C further shifted the mid-point activation by 18 mV and significantly changed the slope factor in Na(v)1.5/F1344S mutant channels from -6.49 to -10.27 mV. CONCLUSIONS: Our findings indicate for the first time that the shift in activation and change in the slope factor at a higher temperature mimicking fever could reduce sodium currents' amplitude and trigger the manifestation of the BS phenotype.

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BACKGROUND/AIMS: Mammalian target of rapamycin (mTOR) signalling is central in the activation of hepatic stellate cells (HSCs), the key source of extracellular matrix (ECM) in fibrotic liver. We tested the therapeutic potential of the mTOR inhibitor rapamycin in advanced cirrhosis. METHODS: Cirrhosis was induced by bile duct-ligation (BDL) or thioacetamide injections (TAA). Rats received oral rapamycin (0.5 mg/kg/day) for either 14 or 28 days. Untreated BDL and TAA-rats served as controls. Liver function was quantified by aminopyrine breath test. ECM and ECM-producing cells were quantified by morphometry. MMP-2 activity was measured by zymography. mRNA expression of procollagen-alpha1, transforming growth factor-beta1 (TGF-beta1) and beta2 was quantified by RT-PCR. RESULTS: Fourteen days of rapamycin improved liver function. Accumulation of ECM was decreased together with numbers of activated HSCs and MMP-2 activity in both animal models. TGF-beta1 mRNA was downregulated in TAA, TGF-beta2 mRNA was downregulated in BDL. 28 days of rapamycin treatment entailed a survival advantage of long-term treated BDL-rats. CONCLUSIONS: Low-dose rapamycin treatment is effectively antifibrotic and attenuates disease progression in advanced fibrosis. Our results warrant the clinical evaluation of rapamycin as an antifibrotic drug.