Increased Mortality in a Colony of Zebra Finches Exposed to Continuous Light

Over a 1-mo period, increased morbidity and mortality occurred in a flock of zebra finches (Taeniopygia guttata). Complete postmortem examination was performed on 6 of the affected birds, 4 of which subsequently were diagnosed with the avian gastric yeast previously known as megabacteriosis (Macrorhabdus ornithogaster). The remaining 2 birds were diagnosed with a cloacal abscess and with large bowel perforation and peritonitis. All the birds had been prophylactically treated with amphotericin B for megabacteria 2 mo previously. An environmental assessment revealed that the light cycle had been altered, and the birds were being exposed to constant light. With correction of the light cycle, the health of the birds improved dramatically. The remaining birds were treated again with amphotericin B, and baseline mortality returned to normal. The birds in this report show several similarities to previous reports of sleep deprivation syndrome in mammals.Over a 1-mo period (from late April to late May 2011), a marked increase in morbidity and mortality was noted in a flock of zebra finches (Taeniopygia guttata) at our facility (University of Washington). These birds were involved in a project studying the neural mechanisms of vocal learning. The finches were obtained from Magnolia Bird Farm (Anaheim, CA). In March 2011, a shipment of 50 male birds arrived and was moved into a new space with 2 rooms. One room housed breeding birds in cages containing breeding pairs and offspring; the other room, into which these new arrivals were placed, housed adult male birds in cages of 4 to 9 birds.Birds in the room containing the adult nonbreeders were affected exclusively. Clinical signs consisted of puffed and ruffled feathers, lethargy, increased respiratory effort, and feather loss. These signs were noted in birds that had not undergone experimental manipulation. Several of the birds that died or were euthanized after becoming sick and lethargic were necropsied. Findings on postmortem examination for the majority of cases included emaciated body condition, necrotizing enteritis and colitis and, in individual cases, included bowel perforation and peritonitis and severe pyogranulomatous abscessation. Megabacteriosis (avian gastric yeast; Macrorhabdus ornithogaster) was diagnosed histologically in 4 of the 6 birds evaluated. A light meter was placed in the housing room; results showed that the dark period of the light cycle was absent. The light cycle was corrected, and morbidity and mortality decreased dramatically.     

Interleukin-1β and interleukin-1α stimulate the N-acetyl-β-glucosaminidase activity of human synovial cells

Summary The properties of synovial cells are altered in vitro by monocyte-macrophage polypeptides (monokines), and these changes could explain some of the properties of the inflamed synovium in rheumatoid disease. Purified monokines have become available only recently for testing on the target synovial cells. We report here that purified human interleukin (IL)-1 and recombinant human Il-1 stimulate the extracellular activity of the lysosomal hydrolase, N-acetyl--glucosaminidase (NAG), of human synovial fibroblast-like cells. In contrast, another monokine, synovial activator, does not increase the NAG activity. Thus NAG is another cellular activity which can be modulated by interleukin-1.     

Stimulation of the hyaluronic acid levels of human synovial fibroblasts by recombinant human tumor necrosis factor alpha, tumor necrosis factor beta (lymphotoxin), interleukin-1 alpha, and interleukin-1 beta

Monocyte/macrophage polypeptides (monokines) alter the properties of synovial cells. This interaction could explain some of the properties of the inflamed synovium in rheumatic disease. Only recently has it been possible to test the action of purified monokines on the target synovial cells. We report here that recombinant human tumor necrosis factor alpha, tumor necrosis factor beta (lymphotoxin), interleukin-1 alpha, and interleukin-1 beta stimulate the hyaluronic acid (HA) levels of human synovial fibroblast-like cells. The effect of monokines was generally inhibited by indomethacin, suggesting the involvement of an endogenous cyclooxygenase product in the stimulation, and by the glucocorticoid, dexamethasone. In contrast, all-trans-retinoic acid stimulated synovial cell plasminogen activator activity but did not increase the HA levels. These findings could help to explain the raised HA levels found in the joint fluids and in the circulation of patients with rheumatic disease.     

Transforming growth factor beta stimulates urokinase-type plasminogen activator and DNA synthesis, but not prostaglandin E2 production, in human synovial fibroblasts.

Transforming growth factor beta (TGF-beta) is usually associated with matrix formation and tissue repair; in contrast, cellular expression of the serine proteinase, urokinase-type plasminogen activator (u-PA) is often correlated with tissue remodeling, as well as with cell migration and transformation. We report here that purified recombinant human TGF-beta (greater than or equal to 300 pg/ml) can stimulate rapidly (within 2 h) the u-PA activity of nonrheumatoid synovial fibroblast-like cells. As for interleukin 1 (IL-1), u-PA mRNA levels are raised in response to TGF-beta, but unlike IL-1, no increase in prostaglandin E2 levels occurs. In contrast to a number of other examples in the literature, in which these two cytokines have opposing actions, TGF-beta can potentiate the action of optimal concentrations of IL-1 in enhancing u-PA expression. These effects of TGF-beta are similar to those of all-trans-retinoic acid. In addition, synovial fibroblast DNA synthesis was stimulated by TGF-beta. Because TGF-beta has been detected in the synovia of patients with rheumatoid arthritis and has been shown to reduce the collagenase levels and proliferation of synovial fibroblast-like cells, it has been proposed by others to be involved beneficially in the reparative processes occurring in arthritic lesions. However, on the basis of our findings, we propose alternative functions for this cytokine--namely, roles in the destructive events as well as in the synovial hyperplasia observed in rheumatoid joints.     

Clinical application of radionuclide quantitation of left to right cardiac shunts in children

The results of 341 radionuclide studies, using the method of Maltz and Treves to quantify left to right shunts, were reviewed to evaluate Its clinical usefulness in routine practice. In 245 children in whom a shunt was suspected, 140 were shown to have shunts at cardiac catheterlzatlon, the pulmonary to systemic blood flow ratio ($\text{Q}\text{?}\text{p}\text{Q}\text{?}\text{s}$) being greater than 1.15 in 121. In 92 of 105 normal children, the ratio was less than 1.05. Nineteen children with a shunt had a ratio in the borderline range of 1.05 to 1.15 as did 13 normal children. Only one normal child had a $\text{Q}\text{?}\text{p}\text{Q}\text{?}\text{s}$ ratio greater than 1.10 whereas seven children with a shunt had a ratio of less than 1.10, including one with a ratio of less than 1.05. A highly significant correlation (r = 0.71) existed between the shunt sizes estimated with the radionuclide method and with oximetry. However, in 10 of these patients a small shunt shown with the radionuclide method was not detected with oximetry but observed on indocyanine green dye curves. In 41 children, therefore, shunt size measured with the radionuclide method, oximetry and indocyanine green dye curves was compared. The correlation of shunt size was comparable with the three techniques. The radionuclide estimation is therefore considered to be more sensitive than oximetry in the detection of small shunts. The procedure was also valuable in 96 children studied after cardiac surgery; a $\text{Q}\text{?}\text{p}\text{Q}\text{?}\text{s}$ value greater than 1.15 was present in 17 children, 12 of whom have to date been shown to have a residual shunt.