High-resolution computed tomography of the major salivary glands: current status.

At our institution, computed tomography is the procedure of choice for evaluation of suspected mass lesions of the major salivary glands. It affords exact anatomic localization of a mass and allows simultaneous examination of the contralateral gland and other regional structures of importance in salivary gland disease. Intravenous contrast medium enhancement is always utilized; however, concomitant sialography has never been necessary. Regional anatomy of the salivary glands with respect to computed tomography imaging and clinical material demonstrating its efficacy are presented. The neoplastic and nonneoplastic diseases affecting the salivary glands are reviewed.

High resolution computed tomography, Part 2: The salivary glands and oral cavity.

High resolution computed tomography (CT) has been of extraordinary value in all areas of the head and neck. Previous communications have indicated its effectiveness in the evaluation of the temporal bone and soft tissues of the neck. This current communication illustrates and discusses the anatomy and pathology of the salivary glands and oral cavity as seen on CT.

High resolution computed tomography, Part 1: Soft tissues of the neck.

Normal and pathologic anatomy of the soft tissues of the neck is clearly delineated with high resolution computed tomography (CT). The CT densities of soft tissues, fat, and enhanced blood vessels are strikingly different from each other and, therefore, mass lesions are clearly discernable. Often, a histologic diagnosis may be suggested with a high level of confidence based on the location and tissue characteristics.

Comparison of superior vena cava and antecubital vein as DSA injection site.

A prospective study in 47 patients was undertaken to determine which of the two major sites for injection of contrast material, superior vena cava or antecubital vein, produces digital subtraction images of higher quality. Both injection sites were used to obtain images of the carotid and aortic arch areas in each patient. The two injection sites were also compared for ease of performance of the study, patient acceptance, and incidence of complications and motion artifacts. It was determined that the degree of vessel conspicuity is not affected by injection site when equal volumes of contrast material are injected. No significant differences in overall image quality attributable to injection site were found, except for carotid images obtained in the anteroposterior projection; for these images, the antecubital vein injection site produced significantly better images. Vessel conspicuity was not the major determinant of overall image quality as judged by radiologists.

Gallium localization in peritonitis. Two case reports.

Diffuse abdominal localization of gallium was found in two patients with peritonitis, one due to M. tuberculosis and the other presumably pyogenic. Gallium scanning may be useful in the diagnosis of peritonitis and perhaps of other serosal infections.

Differential activation of resident macrophage subsets with two sources of lymphokine preparations.

Resident murine macrophages were separated into subsets by Percoll density gradient centrifugation before treatment with lipopolysaccharide-stimulated lymphocytes or different lymphokine preparations. The lymphokines used were culture supernatants from lymphocytes obtained from lipopolysaccharide-injected mice or from purified protein derivative-treated lymphocytes from mice bearing an active BCG infection. The macrophage subsets were activated by the stimulated lymphocytes or lymphokine preparations to express C3b receptor-mediated ingestion or to inhibit the intracellular replication of Toxoplasma gondii or both. The results showed that the macrophage subsets were heterogeneous with respect to ingestion and T. gondii inhibition when activated with lipopolysaccharide-stimulated lymphocytes or lipopolysaccharide-derived lymphokines but were all homogeneous when activated with lymphokines from purified protein derivative-stimulated lymphocytes. When the macrophage subsets were allowed to remain in vitro for various times before lymphokine treatment, the relative pattern of subset activation changed when treated with lipopolysaccharide-derived lymphokines. In contrast, the macrophage subsets remained equally activated throughout the in vitro period when treated with the lymphokines from purified protein derivative-stimulated lymphocytes. The results suggested that functional macrophage heterogeneity depends not only on the nature of the activating signal but also on a state of receptivity of that signal by the macrophage population.

Dissociation of innate susceptibility to Salmonella infection and endotoxin responsiveness in C3HeB/FeJ mice and other strains in the C3H lineage.

Studies of various mouse strains in the C3H lineage have shown that there is no correlation between innate susceptibility to Salmonella infection and sensitivity to the toxic or mitogenic effects of lipopolysaccharide (LPS). C3H/HeNCrlBR mice were Salmonella resistant, but sensitive to the toxic and mitogenic effects of LPS, whereas C3HeB/FeJ mice were Salmonella susceptible as the C3H/HeJ mice, yet were mitogenically responsive to LPS and sensitive to its lethal effects. Furthermore, other mouse strains (C3H/HeTex and C3H/HeDub) displayed intermediate susceptibility to Salmonella infection and were responders to the mitogenic and toxic effects of LPS. These results are interpreted to mean that endotoxemia cannot be a major factor in the pathogenesis of Salmonella infection and provide evidence for the involvement of multiple factors in the control of innate resistance to Salmonella infection in mice of the C3H lineage.

The increase of a normally occurring K cell population during progressive tumor growth in mice.

K cell activity of the spleen cells from normal and tumor-bearing mice was compared using an antibody-dependent cellular cytotoxicity assay. The K cell activity increased with progressive tumor growth (syngeneic) compared to the K cell activity of normal mice. The increase in K cell activity most likely reflected an increase in the numbers of K cells normally present in nontumor-bearing mice rather than the emergence of a distinct population of K cells induced by the growing tumor.

Induction of C3b-mediated phagocytosis in macrophages by distinct populations of lipopolysaccharide-stimulated lymphocytes.

Unelicited resident peritoneal macrophages do not significantly ingest erythrocytes coated with C3b. However, these resident macrophages can be induced to ingest via the C3b receptor when cocultured with peritoneal or splenic nonadherent cells obtained from mice previously injected with lipopolysaccharide. In this study, the extent of ingestion induced in resident macrophages was dependent on the number of stimulated nonadherent cells cocultured with the macrophages as well as on the amount of lipopolysaccharide injected in the mice from which the nonadherent cells were obtained. The ability of the stimulated nonadherent cells to convert resident macrophages to a state of C3b receptor-mediated ingestion was not abrogated by the inclusion of polymyxin B in the cocultivation medium. To further characterize these nonadherent cells, different lipopolysaccharide-stimulated cells were obtained by either nylon-wool filtration, depletion of C3b receptor-bearing cells, or depletion of Thy 1.2-positive cells. None of these populations by themselves were capable of inducing resident macrophages to ingest via the C3b receptor, whereas unfractionated cells were. However, coculture of resident macrophages with recombinations of splenic nylon-wool effluent (T cell-enriched) or bound (B cell-enriched) nonadherent cells from lipopolysaccharide-injected mice reconstituted the ability to induce ingestion via the C3b receptor. Taken together, these results suggest that one means by which lipopolysaccharide can induce C3b receptor-mediated ingestion by macrophages is through the cooperative effects of stimulated T and B lymphocytes.

Requirement for a radiosensitive lymphoid cell in the generation of lipopolysaccharide-induced rejection of a murine tumor allograft.

Lipopolysaccharide-initiated rejection of a tumor allograft requires the cooperation of a radiosensitive nonadherent lymphoid cell population and an adherent cell, presumably a macrophage.

Tumor inhibition in mice by lipopolysaccharide-induced peritoneal cells and an induced soluble factor.

Lipopolysaccharide (LPS) was shown to prevent tumor growth in BALB/c mice when administered either prior to or after the inoculation of lethal doses of tumor cells. An attempt to elucidate the mechanism of this phenomenon utilizing in vivo protocols was made by the adoptive transfer of tumor protection with peritoneal cells as well as with cell-free peritoneal fluids obtained from non-tumor-bearing, LPS-stimulated syngeneic mice. The in vivo-activated peritoneal cells from LPS-treated mice were capable of adoptively transferring tumor protection at peritoneal cell to tumor cell ratios ranging from 1,000:1 to 100:1. Experiments were also performed that indicate that: (i) LPS exerts no direct toxic or inhibitory effect on the tumor cells, and (ii) that residual LPS present in cell and fluid preparations was not responsible for such protection.

Biologic activities of rabbit immunoglobulin G in relation to domains of the Fc region.

Biologic properties of antibodies are known to be mediated by the Fc portion of the H chains. In the present study such properties as complement fixation, cutaneous anaphylaxis, and macrophage cytophilia were examined in relation to the CH2 and CH3 domains of rabbit IgG. Fragments containing but one of these domains were prepared from plasmin and papain digests. Facb fragments of anti-DNP antibodies, together with the antigen DNP-BSA, were able to fix complement by the classical pathway, a result which implicates the CH2 domain; however, guinea pig Fab fragments directed to regions of the rabbit antibody molecule other than CH2 were able to inhibit complement fixation. Facb fragments were unable to mediate PCA or reverse PCA reactions in guinea pigs, nor were CH3 fragments active in tests of reverse PCA or inhibition of PCA. These results suggest that the entire Fc region is needed for cutaneous anaphylaxis. The ability to bind to guinea pig lung macrophages was studied with a rosette technique. Facb fragments were active whereas CH3 fragments failed to inhibit. It is suggested that although some effector functions of antibodies can be assigned to individual domains, others require the entire Fc region.

Complement-dependent release of immune complexes from the lymphocyte membrane.

Soluble antigen-antibody-complement complexes bound to mouse B lymphocytes are rapidly released from the cell membrane in the presence of normal serum from several mammalian species. The release is not the result of antigen-antibody dissociation or extensive degradation of the complexes. However, the released complexes have been altered because they will no longer bind to fresh lymphocytes. The release is not the result of lymphocyte damage mediated by complement. It is complement-dependent, and is generated either preferentially or exclusively via the alternate pathway, since it occurs in C4-deficient serum, is Mg(++) but not Ca(++) dependent, and requires C3 proactivator. C3 inactivator is not involved. The release activity of the serum, once generated, is unstable at 37 degrees C. The release of complexes from the lymphocyte membrane by serum provides a convenient assay for the functioning of the alternate pathway in the mouse and in other species.