This
PKC412 molecular weight effect should be further investigated for DC stunning. Very few birds stunned with AC resumed breathing following stunning, indicating stun to kill. Pulsed DC stunning showed a lower effect on the induction of death. The level of wing flapping, indicating convulsions and possible meat quality defects, was higher for the AC treatments.”
“Increase of sympathetic nervous activity and tachycardia at rest or during physical exertions are associated with increase of morbimortality, even in the absence of clinical signs of cardiac disease. Considering the importance of the alpha(2A)/alpha(2C)-adrenergic receptors in the modulation of the nervous activity and heart rate (HR), the present study uses a genetic model of cardiomyopathy AL3818 induced by excess of circulating catecholamine in the gene inactivation of the alpha(2A)/alpha(2)-adrenergic receptors in mice (alpha(2A)/alpha(2C)KO) to verify the HR response to physical exercise (PE), as well as the sympathetic-vagal control of the HR to
PE. The hypothesis is that there would be exacerbated tachycardic response during PE in alpha(2A)/alpha(2C)KO mice even when the cardiac function was still preserved at rest, being the alpha(2A)-adrenergic receptor the main reason for this response. Male mice of the C57Bl6J lineage, control (CO) and with gene inactivation for the a(2A) (alpha(2A)KO), alpha(2C) alpha(2C)KO) and alpha(2A)/alpha(2C)KO receptors were submitted to tolerance to a physical exercise test. Two other groups of mice, CO and alpha(2A)/alpha(2C)KO, were submitted to pharmacological blocking of the muscarinic and beta-adrenergic receptors as well as to progressive PE to assess the sympathetic-vagal contribution to PE tachycardia. Intolerance to physical exercise (1.220 +/- 18 and 1.460 +/- 34 vs. 2.630 +/- 42m, respectively) and higher tachycardia to check details PE (765 +/- 16 e 792 +/- 13 vs. 603 +/- 18 bpm, respectively) in the alpha(2C)KO and alpha(2A)/alpha(2C)KO vs. CO mice was observed. Moreover, the autonomic balance was altered in
the alpha(2A)/alpha(2C)KO mice by the sympathetic hyperactivity and lower cardiac vagal effect. These outcomes demonstrated the importance of the alpha(2A)/alpha(2C)-adrenergic receptors in autonomic control not only at rest, but also during PE, being the alpha(2A)-adrenergic receptor responsible for the sympathetic hyperactivity and lower vagal effect observed. This exacerbated tachycardic response in alpha(2A)/alpha(2C)KO mice is present even when cardiac dysfunction is not observed.”
“Body fluids of mammals, including semen, are increasingly recognized to harbour anti-microbial proteins which play a role in host defence against a myriad of pathogens. Human seminal plasma inhibin (hSPI) is reported to be a multifunctional protein, well-studied primarily for its fertility-related effects and recently for its anti-fungal activity.