Storage phosphor digital mammography

Digital mammography using storage phosphor CR is still in the investigational stage. It is the only digital mammography system that has been tested in preliminary clinical trials with promising early results. Further clinical studies are needed to assess the impact of the limited spatial resolution of storage phosphor technology on its application as a digital screening mammography system. Further studies also are needed to determine the optimum image processing parameters needed in digital mammography.     

Identification of two genetic markers that distinguish pathogenic and nonpathogenic strains of Acanthamoeba spp.

Species-level identification of Acanthamoeba isolates is difficult and gives little or no indication of the isolate's pathogenicity. We identified two amplification-based genetic markers that were highly correlated with pathogenicity in Acanthamoeba spp. One marker, designed to amplify a 485-bp fragment of the small-subunit ribosomal RNA gene (ssrDNA), was preferentially amplified from the nonpathogenic strains; amplifications from the pathogenic strains yielded anomalous fragments of 650 and 900?bp. A second marker was developed on the basis of the anomalous 650-bp fragment. Primers to this sequence preferentially amplified a noncoding locus (called Ac6) only from the pathogenic strains. These two genetic markers may be useful for identification of pathogenic Acanthamoeba spp. strains.     

Cholera Toxin B-Mediated Targeting of Lipid Vesicles Containing Ganglioside GM1 to Mucosal Epithelial Cells

Purpose. To determine whether the non-toxic pentameric B subunit of Cholera toxin (CTB) binding to ganglioside GM1 on both the lipid vesicles and epithelial cells may provide a means to target lipid vesicles to mucosal cells expressing surface GM1. Methods. Sonicated lipid vesicles containing ganglioside GM1 were prepared. Inter-vesicle cross-linking due to pentameric CTB binding to these GM1 vesicles was determined with a sub-micron particle analyzer. Association of CTB to GM1 vesicles was analyzed with continuous sucrose gradient centrifugation. CTB-mediated binding of GM1 vesicles to human mucosal epithelial cells (Caco-2 and HT-29), mucous membranes of mouse trachea, and nasal tissues were detected with fluorescent labeled vesicles. Results. An increase in lipid particle size due to binding of CTB to lipid vesicles and inter-vesicles cross-linking was detected. At a 30-to-1 mole ratio of membrane-bound GMl-to-CTB, optimum increase in GM1 vesicle aggregation, was detected. Under such conditions, all the added CTB molecules were associated with GM1 vesicles. Time course analysis showed that inter-vesicles cross linking by CTB was detectable within 10 min. and reached a maximum value at 60 min. CTB associated GM1-vesicles bind to mucosal epithelial cells HT-29 and Caco-2 with similar affinity [K_d = 7.8 × 10^–4 M lipid (Caco-2) and 7.6 × 10^–4 M lipid (HT-29)]. GM1 mediated binding specificity was demonstrated by blocking with anti-GMl antibody and the insignificant degree of CTB-associated GM1 vesicle binding to GM1 deficient C6 cells. Conclusions. The CTB-mediated GM1 binding to multiple membrane surfaces provides selective localization of GM1 vesicles to GM1 expressing mucosal cells and tissues. The strategy may be useful in localizing drugs and proteins to gut and respiratory tract mucosa.     

Internal fixation of children's fractures of the lower extremity

Lower grade fractures are by definition stable and almost always treated with casting or functional splinting. The best kind of fixation for the higher grade fractures, however, differs between adults and children. Appropriate treatments are discussed, and case-study illustrations are provided. Background on the anatomy of the tibia and femur is included.     

Production of reactive oxygen species by tubular epithelial cells in culture

Reactive oxygen species (ROS) have been implicated in the pathogenesis of toxic, ischemic and immunologically-mediated renal injury. Although substantial evidence exists for the production of ROS by glomerular cells, little is known about production of these reactive oxygen metabolites by renal tubular cells. We examined the ability of cultured cells from different segments of the rabbit nephron to elaborate ROS. Under basal conditions, cells of the proximal tubule, cortical collecting duct, and papillary collecting duct produced superoxide anion and hydrogen peroxide. Exposure to opsonized zymosan or heat-aggregated gamma globulin significantly increased ROS production by all three tubular cell types. The production of superoxide anion and hydrogen peroxide was time dependent and increased with increasing concentrations of the stimulating factors. These experiments indicate that renal tubular cells have the potential to participate in renal injury via elaboration of highly-reactive oxygen metabolites.     

Embryonic and maternal heat shock responses to a teratogenic hyperthermic insult

Exposing embryos to elevated temperatures both in vivo and in vitro has been shown to result in the production of offspring with severe congenital abnormalities. While a direct effect of heat cannot be excluded, recent interest has been focused on the possible role that the induction of the heat shock response may have in the etiology of the observed congenital defects. In the present study, mouse embryos from inbred strains known to differ in terms of their sensitivity to heat-induced exencephaly were treated in vivo and their heat shock response determined using SDS-PAGE electrophoretic techniques. Further, the embryonic responses were compared with a maternal cell type. We observed excellent agreement between the two test systems following exposure to a teratogenic hyperthermic insult. Both the embryonic and maternal cells underwent a reduction in total protein synthesis and an enhanced synthesis of four heat shock proteins migrating with the molecular weights of 68, 70, 97, and 110 kDa. The results failed to indicate any strong correlation between the heat shock response and enhanced genetic sensitivity to hyperthermia-induced neural tube defects.     

The role of hemoglobin in arterial narrowing after subarachnoid hemorrhage

A porcine model for subarachnoid hemorrhage has been developed to allow the selective application of blood and its components to cerebral arteries. Whole blood was centrifuged to produce two fractions consisting of washed erythrocytes (red blood cells, RBC's) and white blood cells (WBC) plus platelet-rich plasma (PRP); the RBC fraction was subsequently separated into hemoglobin (Hb)-containing cytosol and erythrocyte membranes. Each fraction was selectively applied to the middle cerebral artery (MCA) of pigs for 10 days; after which, vessels were perfusion-fixed and examined by light and transmission electron microscopy and immunohistochemical studies. By morphometric analysis, a marked reduction in the MCA lumen cross-sectional area was observed after selective application of RBC's or Hb/cytosol but not of WBC/PRP or erythrocyte membranes. In both RBC- and Hb/cytosol-treated vessels, luminal narrowing was associated with a differential increase in vessel wall thickness of the ventral (subarachnoid) compared to the dorsal (brain) aspect of the artery, but no significant change in cross-sectional area of the vessel wall. After 10 days of exposure to RBC's or Hb/cytosol, there was a spectrum of ultrastructural changes in the vessel wall comparable to those seen after periadventitial application of whole blood. Selective application of commercially available Hb to MCA produced similar structural and morphometric changes. The degree of luminal narrowing after exposure to whole blood or RBC's was proportional to the volume of the erythrocyte mass adjacent to the vessel at sacrifice. These data suggest that arterial narrowing after SAH is mediated by mechanisms related to prolonged exposure of the vessel wall to hemoglobin or its catabolites from lysing subarachnoid erythrocytes.