Fish stress and mortality can be predicted using reflex impairment

Fish stress and mortality can be significant problems in both capture and culture operations. In addition to inexpensive and real-time metrics, ones that are simple to use are also desirable for measuring fish stress and predicting mortality. Current methods to define stress rely on expensive, laboratory-based measurements of changes in fish pathology such as disease, necropsy and histology, in physiology such as plasma cortisol, lactate, glucose and ions and in complex behaviour determined from swimming, feeding and predator evasion. All of these methods are often not rigorously linked to fitness outcomes. An alternative is to observe reflex impairment as a direct sign of stress which can be easily and rapidly measured in free swimming or restrained fish responding to peripheral stimuli such as gravity, light, sound and touch. Reflex impairment is correlated with stress and mortality outcomes, eliminating the need for prolonged holding or monitoring of fish. A few examples of reflexes that may be impaired include orientation, startle responses, fin erection, body flex upon restraint, operculum and mouth clamping or gaping, gag response and vestibular–ocular response. Reflex impairment combines the effects of stressors and their interactions and is not dependent on fish size, motivation states and acclimation which make it a consistent sign of stress across a wide range of stressor types and fish ages. Use of reflex impairment to measure stress and predict mortality would significantly improve monitoring of fish health and welfare in many types of field operations such as commercial and recreational fishing, aquaculture, live transport, stock enhancement and tagging.     

Phosphorylation by p38 MAPK as an alternative pathway for GSK3beta inactivation

Glycogen synthase kinase 3beta (GSK3beta) is involved in metabolism, neurodegeneration, and cancer. Inhibition of GSK3beta activity is the primary mechanism that regulates this widely expressed active kinase. Although the protein kinase Akt inhibits GSK3beta by phosphorylation at the N terminus, preventing Akt-mediated phosphorylation does not affect the cell-survival pathway activated through the GSK3beta substrate beta-catenin. Here, we show that p38 mitogen-activated protein kinase (MAPK) also inactivates GSK3beta by direct phosphorylation at its C terminus, and this inactivation can lead to an accumulation of beta-catenin. p38 MAPK-mediated phosphorylation of GSK3beta occurs primarily in the brain and thymocytes. Activation of beta-catenin-mediated signaling through GSK3beta inhibition provides a potential mechanism for p38 MAPK-mediated survival in specific tissues.     

Multifocal idiopathic pyogranulomatous bone disease in a dog

Disseminated, multifocal idiopathic pyogranulomatous bone disease in a five-year-old neutered female crossbred cattle dog is described. The dog was presented for neck pain and reluctance to exercise. Radiography demonstrated polyostotic bone disease, the predominant change consisting of a mottled pattern of osteosclerosis interspersed with punctate foci of osteolysis. Numerous bones of the axial and appendicular skeleton were affected including cervical vertebrae, ribs, scapulae and humeri. Biopsy revealed sterile pyogranulomatous osteomyelitis. This was confirmed at necropsy which showed that lesions were restricted to bone. Idiopathic granulomatous or pyogranulomatous conditions have been described in the dog in relation to skin but not bone. In people, idiopathic granulomatous bone disease is one of a group of conditions collectively called histiocytosis X, which are thought to be immunoregulatory disorders related to Tlymphocyte suppressor cell deficiency and Langerhans' cell proliferation.