The role of cholecystokinin in radiographic opacification of the gallbladder

Studies of the effect of cholecystokinin (CCK) on hepatic elimination of intravenously administered iopanoate and on gallbladder opacification were performed using nonoperated dogs with intact enterohepatic circulation and normal endogenous bile salt pool. Intravenous administration of CCK (3 units/kg) resulted in a 32% increase in apparent transport maximum (maximum rate of elimination) of iopanoate and earlier and enhanced gallbladder opacification. This increase in apparent transport maximum was abolished by cholecystectomy, indicating that the increase was a result of the release of bile salts from the gallbladder rather than a direct effect of the hormone on the hepatic elimination of iopanoate. The early gallbladder opacification and increased density of contrast material in the gallbladder were related to CCK-induced emptying of the gallbladder and subsequent filling with opacified bile.     

Interfacing digitiezed Disa anemometer output to an Apple II computer

For measuring the velocities in a fluctuating fluid flow, the new Disa 56C00 multichannel constant-temperature anemometer system can be used with the 56N00 signal analysis equipment to provide a digital output of mean, root mean square or correlation values. A simple interface arrangement and appropriate software control for reading data directly into an Apple II computer are described. With these the subsequent calculation of derived parameters, such as displacement and momentum thickness of boundary layers and turbulence intensity, can be quickly and easily completed.     

Interleukin-12 is required for control of the growth of attenuated aromatic-compound-dependent salmonellae in BALB/c mice: role of gamma interferon and macrophage activation

The attenuated S. typhimurium SL3261 (aroA) strain causes mild infections in BALB/c mice. We were able to exacerbate the disease by administering anti-interleukin-12 (IL-12) antibodies, resulting in bacterial counts in the spleens and livers of anti-IL-12-treated mice that were 10- to 100-fold higher than the ones normally observed in premortem mice; yet the animals showed only mild signs of illness. Nevertheless, they eventually died of a slow, progressive disease. Mice infected with salmonellae become hypersusceptible to endotoxin. We found that IL-12 neutralization prevented the death of infected mice following subcutaneous injection of lipopolysaccharide. Granulomatous lesions developed in the spleens and livers of control animals, as opposed to a widespread infiltration of mononuclear cells seen in the organs of anti-IL-12-treated mice. In the latter (heavily infected), salmonellae were seen within mononuclear cells, indicating an impairment of the bactericidal or bacteriostatic ability of the phagocytes in the absence of biologically active IL-12. Gamma interferon (IFN-gamma) levels were reduced in the sera and tissue homogenates from anti-IL-12-treated mice compared to those in control animals. Furthermore, fluorescence-activated cell sorter analysis on spleen cells showed that IL-12 neutralization impaired the upregulation of I-Ad/I-Ed antigens on macrophages from infected mice. Inducible nitric oxide synthase and IFN-gamma mRNA production was down-regulated in anti-IL-12-treated mice, which also showed an increased production of IL-10 mRNA and a decrease in nitric oxide synthase activity in the tissues. Administration of recombinant IFN-gamma to anti-IL-12-treated mice was able to restore host resistance, granuloma formation, and expression of major histocompatibility complex class II antigens in F4/80(+) and CD11b+ spleen cells.