No abstract

No abstract

In the present study, chronic behavioural stress resulting from low social status affected the physiological responses of rainbow trout (Oncorhynchus mykiss) to a subsequent acute stressor, exposure to hypoxia. Rainbow trout were confined in fork-length matched pairs for 48-72 h, and social rank was assigned based on behaviour. Dominant and subordinate fish were then exposed individually to graded hypoxia (final water PO(2), PwO(2) = 40 Torr). Catecholamine mobilization profiles differed between dominant and subordinate fish. Whereas dominant fish exhibited generally low circulating catecholamine levels until a distinct threshold for release was reached (PwO(2) = 51.5 Torr corresponding to arterial PO(2), PaO(2) = 24.1 Torr), plasma catecholamine concentrations in subordinate fish were more variable and identification of a distinct threshold for release was problematic. Among fish that mobilized catecholamines (i.e. circulating catecholamines rose above the 95% confidence interval around the baseline value), however, the circulating levels achieved in subordinate fish were significantly higher (459.9 ± 142.2 nmol L(-1), mean ± SEM, N = 12) than those in dominant fish (130.9 ± 37.9 nmol L(-1), N = 12). The differences in catecholamine mobilization occurred despite similar P(50) values in dominant (22.0 ± 1.5 Torr, N = 6) and subordinate (22.1 ± 2.2 Torr, N = 8) fish, and higher PaO(2) values in subordinate fish under severely hypoxic conditions (i.e. PwO(2) < 60 Torr). The higher PaO(2) values of subordinate fish likely reflected the greater ventilatory rates and amplitudes exhibited by these fish during severe hypoxia. At the most severe level of hypoxia, subordinate fish were unable to defend arterial blood O(2) content, which fell to approximately half (0.60 ± 0.13 mL O(2) g(-1) haemoglobin, N = 9) that of dominant fish (1.08 ± 0.09 mL O(2) g(-1) haemoglobin, N = 9). Collectively, these data indicate that chronic social stress impacts the ability of trout to respond to the additional, acute stress of hypoxia.

Therapy for cystic fibrosis (CF) has progressed during the past several decades. Much of this progress is because of advances in genetic testing to precisely identify the underlying cause of CF transmembrane regulator (CFTR) dysfunction. However, with more than 1900 mutations that can produce a faulty CFTR, the management of CF can remain a challenge. Several innovative drugs recently approved by the Food and Drug Administration, termed genetic modulators, target the underlying disease by modulating the CFTR defect. This review provides physicians with an established simple classification scheme to guide their use of these drugs. The treatment challenge of 1900 CFTR mutations has been simplified into 6 physiologic classes, each paired with an available therapy to offer patients the most functional improvement. Drug therapy monitoring, adverse effects, and indications for discontinuation must also be considered.

This longitudinal study elucidates the response of marrow adipose tissue adipocytes in weight-bearing joints to changes in different mechanical environments, and we provide insight on the malleability of the changes over time. In a rat animal model, knee immobilization induced hyperplasia and accelerated the age-dependent hypertrophy of adipocytes. Changes in adipocyte number and size were sustained despite unassisted remobilization. Multimodal distributions of cell size were characteristic of bone marrow adipocytes.