Intratemporal vascular tumors: detection with CT and MR imaging

The diagnostic contributions of computed tomography (CT) and magnetic resonance (MR) imaging were compared in 12 patients with benign intratemporal vascular tumors (hemangioma or vascular malformation). The tumors included six in the internal acoustic canal and six in the geniculate ganglion region. Clinical and histologic correlations were made. Two of the six patients with tumors in the internal acoustic canal underwent CT, and both required gas cisternography to show the tumor. Five patients in that group underwent MR imaging, and all five studies showed the tumor. All six patients with geniculate ganglion tumors underwent CT. Results in one study were questionable, and five showed the tumor. Five patients in this group underwent MR imaging, but the MR findings were positive in only two cases. MR imaging should therefore be performed before CT in the evaluation of facial nerve dysfunction, as it demonstrated all tumors in the internal acoustic canal and some in the geniculate ganglion region. If MR findings are negative, CT should then be performed to rule out a possible geniculate ganglion lesion.     

Lps Genotype in the C57 Black Mouse Blackground and its Influence on the Interleukin-6 Response to E. coli Urinary Tract Infection

The present study examined the influence of the mouse Lps genotype on the interleukin-6 (IL-6) and polymorphonuclear leucocyte (PMN) responses to mucosal Escherichia coli infection. Lipopolysaccharide (LPS) responder C57BL/6J (Lpsn, Lpsn) and LPS non-responder C57BL/10ScCr (Lpsd, Lpsd) mice were inoculated intravesically with Escherichia coli Hu734. The secretion of IL-6, the recruitment of PMNs into urine, and the bacterial clearance from the kidneys and bladders were compared between the two mouse strains at 2, 6 and 24 h after infection. The C57BL/6J mice showed a high PMN response and rapid clearance of bacteria from the kidneys and bladders. In the C57BL/10ScCr mice the PMN response was low and infection remained. This supported a role of the Lps genotype in these events. The IL-6 levels remained low after infection in both LPS responder and non-responder mice, but became elevated in the animals which were accidentally traumatized during infection. The IL-6 response to trauma alone was independent of Lps genotype, but the response to trauma and infection combined differed between the mouse strains. The IL-6 response to trauma and infection was more rapid in the C57BL/6J than in the C57B1/10ScCr mice. The traumatized and infected animals did not clear the infection as efficiently as the non-injured animals in both backgrounds. The difference in PMN recruitment and susceptibility of infection between LPS responder and non-responder mice in the C57 Black background followed the pattern previously seen in the C3H mouse background and suggested that these events were under Lps gene control. An effect of the Lps locus on the IL-6 response could be detected only in traumatized and infected animals.     

Blood donation behavior of Hispanics in the lower Rio Grande Valley

This study was designed to determine the blood donation behavior and attitudes of Hispanic residents of the Lower Rio Grande Valley for the purpose of developing promotional and educational approaches to enhance levels of donor participation. Personal interviews of 545 respondents were conducted in English and Spanish using quota sampling and standard intercept techniques at lower- and middle-income supermarkets in five cities during a payday weekend. A number of research hypotheses were established to test for demographic, behavioral, and attitudinal differences that were observed in donors and nondonors using chi-square analysis and multiple discriminant analysis. After analyzing the difference between Hispanics and non-Hispanics for blood donation rates, all non-Hispanics were eliminated from analysis, and the remaining 419 Hispanics were evaluated on the basis of their donor behavior. Donation among Hispanics was most likely to be by better- educated, English-speaking, higher-job-status individuals who had participated in a blood donation drive. Donors tend to have parent(s) who were donors, and they were also more likely to carry an organ donor card. Donors were found to vary in their behaviors as well as their attitudes and beliefs. Perceptions of a lack of safety in donating, the risk of contracting acquired immune deficiency syndrome, and the financial motivation of donors were most pronounced among Hispanics, which indicated a need for improved education on these issues.     

Escherichia coli induces transuroepithelial neutrophil migration by an intercellular adhesion molecule-1-dependent mechanism.

During bacterial infections at mucosal sites, neutrophils migrate to the mucosa and cross the epithelial barrier. We have examined neutrophil migration across Escherichia coli-stimulated uroepithelial cell layers in an attempt to more fully understand this process. Stimulation of uroepithelial cells with E. coli or interleukin-1 alpha (IL-1 alpha) induced transepithelial neutrophil migration in a time- and stimulant dose-dependent manner. Uroepithelial cell lines and nontransformed uroepithelial cells expressed intercellular adhesion molecule-1 (ICAM-1) but not ICAM-2, E-selectin, or P-selectin. Epithelial ICAM-1 expression was enhanced after stimulation with E. coli or IL-1 alpha. Anti-ICAM-1 antibody reduced transepithelial neutrophil migration by 61 to 85%, indicating that neutrophils bound ICAM-1 on the epithelial surface. Antibodies to CD18 and CD11b reduced migration by 70 to 79%, suggesting that CD11b/CD18 (Mac-1) was acting as the neutrophil receptor for ICAM-1 in this process. Anti-CD11a antibodies had no effect on neutrophil migration. In conclusion, E. coli induced ICAM-1- and Mac-1-dependent transepithelial neutrophil migration. Previous studies have shown that urinary tract epithelial cells secrete IL-8 when exposed to E. coli or IL-1 alpha. These observations suggest that epithelial cells play an active role in neutrophil migration during urinary tract infections.     

Human leukocyte antigen matching and fetal loss: results of a 10 year prospective study

The role that maternal and fetal human leukocyte antigen (HLA) genes play in pregnancy is unknown, but it has been suggested that fetuses whose HLA alleles do not differ from maternal alleles (i.e. histocompatible fetuses) are more likely to be aborted than fetuses with HLA alleles that differ from maternal alleles (i.e. histoincompatible fetuses). To elucidate the role of HLA compatibility in pregnancy, we tested the hypothesis that couples who match for HLA alleles or haplotypes would have reduced fertility because only these couples could produce histocompatible fetuses. We conducted a 10 year prospective study of HLA matching and pregnancy outcome in 111 Hutterite couples, providing information on 251 pregnancies. A logistic regression analysis was performed to determine the effects of HLA matching at HLA regions and loci on pregnancy outcome (fetal loss versus delivery). Significantly increased fetal loss rates were observed among couples matching for the entire 16-locus haplotype (P = 0.002). Among the individual loci, loss rates were increased among couples matching for HLA-B (P = 0.019), HLA-C (P = 0.033) and the complement component, C4 (P = 0.043). We interpret these results as evidence that matching for the entire 16-locus haplotype and/or alleles at an HLA-B-linked locus confers significant risk for fetal loss.      

Ly6C expression differentiates plasma cells from other B cell subsets in mice.

Plasma cell differentiation is induced in vitro by lipopolysaccharide (LPS) stimulation but can be blocked by including anti-CD40 antibodies. Using subtractive cDNA hybridization we have identified the cell surface protein Ly6C as differentially expressed on B cells stimulated with LPS only. Ly6C has been shown to be expressed on certain T cell subsets and on subsets of macrophages and NK cells, but not on resting B cells. We show that Ly6C is up-regulated upon LPS stimulation of B cells in vitro and that this up-regulation is blocked by anti-CD40 or anti-Ig antibodies. Furthermore, ELISPOT analysis of cells sorted by magnetic-activated cell sorting show that Ly6C is expressed on ex vivo plasma cells from the spleen and bone marrow. Flow cytometric analysis showed that Ly6C is expressed on splenic plasma cells as well as on lamina propria plasma cells. Finally, Ly6C cross-linking positively up-regulated the amount of immunoglobulin produced by LPS-stimulated splenic B cells in vitro.     

Selective cytokine production by epithelial cells following exposure to Escherichia coli.

This study compared the repertoire of cytokines produced by epithelial cell lines and human peripheral blood monocytes in response to Escherichia coli. The A-498 and J82 urinary tract epithelial cell lines and human peripheral blood monocytes were exposed to E. coli Hu734. The cytokine content of single cells was detected by indirect immunofluorescence using monoclonal antibodies to interleukin-1 alpha (IL-1 alpha), IL-1 beta, tumor necrosis factor alpha (TNF-alpha), TNF-beta, IL-6, IL-8, and granulocyte macrophage-colony-stimulating factor, and the number of positive cells was used to quantitate the response. The J82 bladder cell line stained positive for IL-6, IL-8, and IL-1 alpha. The IL-8 and IL-6 response peaked at 2 h, while the number of IL-1 alpha-positive cells reached a peak 6 h after E. coli stimulation. The A-498 kidney cell line stained for IL-8 with a peak at 2 h and IL-6 with a peak at 6 h after E. coli stimulation. Peripheral blood monocytes stained for the cytokines IL-1 alpha, IL-1 beta, IL-8, IL-6, and TNF-alpha but not for TNF-beta and granulocyte macrophage-colony-stimulating factor after stimulation with E. coli. The results demonstrated that bacteria activated a cytokine response in the epithelial cell lines and monocytes. The epithelial cell lines had a more limited cytokine response profile than circulating monocytes, which may serve to limit the consequences of microbial exposure at the mucosal surface and help maintain the integrity of other tissue compartments.     

Marrow regeneration after mechanical depletion

The origin of marrow regeneration after mechanical depletion was reinvestigated in mouse chimeras. The results were compatible with the local origin of stem cells from remnants of incompletely removed marrow, but not with their origin from a common precursor of both bone and hemopoietic cell lines. In transplanted femurs depleted by a modified technique of in vivo evacuation of marrow, hemopoietic regeneration failed to occur. The presence of hemopoietic stem cells in the Haversian canals was thus excluded. The demonstration of ample hemopoiesis with minimal bone formation in nondepleted controls in which bone marrow initially became necrotic provided new evidence that osteogenesis was not a prerequisite of hemopoietic regeneration.     

First-time anterior shoulder dislocations: should they be arthroscopically stabilised?

The glenohumeral joint is inherently unstable because the large humeral head articulates with the small shadow glenoid fossa. Traumatic anterior dislocation of the shoulder is a relatively common athletic injury, and the high frequency of recurrent instability in young athletes after shoulder dislocation is discouraging to both the patient and the treating physician. Management of primary traumatic shoulder dislocation remains controversial. Traditionally, treatment involves initial immobilisation for 4–6 weeks, followed by functional rehabilitation. However, in view of the high recurrence rates associated with this traditional approach, there has been an escalating interest in determining whether immediate surgical intervention can lower the rate of recurrent shoulder dislocation, improving the patient’s quality of life. This review article aims to provide an overview of the nature and pathogenesis of first-time primary anterior shoulder dislocations, the widely accepted management modalities, and the efficacy of primary surgical intervention in first-time primary anterior shoulder dislocations.