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James M Anderson

Publications and source records attributed to James M Anderson.

64 records · Page 4Linked to original sources
PubMed2002

New suppressor technology improves trace level anion analysis with carbonate-hydrogencarbonate mobile phases.

Sodium carbonate-hydrogencarbonate mobile phases are preferred over sodium hydroxide for anion analysis by suppressor-based ion chromatography (IC). Unlike hydroxide, carbonate-hydrogencarbonate has strong eluting power and its buffering capacity can be used as a selectivity tool for controlling separations. However, carbonate-hydrogencarbonate mobile phases fell out of favor for trace level analysis because the carbonic acid suppressor effluent has some background conductivity, which reduces sensitivity compared to sodium hydroxide. This paper describes a new suppressor technology that improved anion analysis with carbonate-hydrogencarbonate mobile phases. In addition to converting the carbonate-hydrogencarbonate buffer to carbonic acid like other traditional IC suppressors, the new DS-Plus suppressor also removed carbonic acid from the suppressor effluent. Anions are now detected in water background, just like when using sodium hydroxide as the mobile phase. The lower background conductivity improves sensitivity and reduces detection limits. The water-dip often seen with conventional suppressors is greatly reduced, improving fluoride quantification.

Anions↗
PubMed2002

Surface modification of liposomes for selective cell targeting in cardiovascular drug delivery.

Cardiovascular disease processes such as atherosclerosis, restenosis, and inflammation are typically localized to discrete regions of the vasculature, affording great opportunity for targeted pharmacological treatment. Liposomes are potentially advantageous targeted drug carriers for such intravascular applications. To facilitate their use as drug delivery vehicles, we have considered three components of liposome design: (i) identification of candidate cell surface receptors for targeting; (ii) identification of ligands that maintain binding specificity and affinity; and (iii) prevention of rapid nonspecific clearance of liposomes into the reticuloendothelial organs. In this report, we describe our work in developing liposomal surface modifications that address both targeting and clearance. An arginine-glycine-aspartic acid (RGD) containing peptide was used as a model ligand to target liposomes to the integrin GPIIb-IIIa on activated platelets. Additionally, oligodextran surfactants incorporated into liposomes provided insight into the effect of vesicle perturbations on liposome clearance, and the importance of molecular geometry in designing oligosaccharide surface modifications. Together these studies demonstrate the feasibility of using peptides to guide liposomes to desired receptors, and illustrate the influence of vesicle stability on liposome interactions in vivo. Furthermore, they underscore the importance of simultaneously considering both targeting specificity and vesicle longevity in the design of effective targeted drug delivery systems.

Animals↗
PubMed2002

Shear stress and material surface effects on adherent human monocyte apoptosis.

Monocytes play a critical role as both phagocytes and mediators of inflammatory responses in the prevention of cardiovascular device-related infections. However, persistent infection of these devices still occurs and may be attributed to deleterious cellular alterations resulting from monocyte interactions with a foreign material in an environment of dynamic flow. Thus, the effects of both shear stress and adhesion to material surfaces on human monocyte apoptosis were investigated. A rotating disk system generated physiologically relevant shear stress levels (0-14 dyn/cm(2)), and shear-related apoptosis occurring in adherent monocytes was characterized. Using annexin V analysis, apoptosis of polyurethane-adherent monocytes under shear for 4 h increased to levels >70% with increasing shear in a near-linear fashion (r2 = 0.713). It was qualitatively confirmed using confocal microscopy that filamentous (F)-actin distribution was altered, that DNA fragmentation occurred, and that activated caspases were involved in shear-induced apoptosis. Static studies determined that spontaneous apoptosis was material-dependent over 72 h by demonstrating marked differences between apoptosis of monocytes adherent to a polyurethane compared to an alkyl-modified glass. Treatment with TNF-alpha augmented this material dependency in a dose-dependent fashion over time. F-actin content of TNF-alpha-treated cells decreased to <62% of untreated cells. We conclude that concomitant effects from both material surfaces and dynamic flow mediate human monocyte apoptosis and may have serious implications in the context of implanted cardiovascular device infection.

Actins↗
PubMed2002

Activation of caspase 3 during shear stress-induced neutrophil apoptosis on biomaterials.

Within the complex environment of an implanted cardiovascular device comprised of dynamic flow and foreign materials, phagocytic neutrophils may be ineffective in combating infection due to cellular responses to shear stress. This may be explained, in part, by our recent reports of apoptosis of biomaterial-adherent leukocytes induced through exposure to shear stress. Here we utilize a rotating disk system to generate physiologically relevant shear stress levels (0-18 dynes/cm(2)) at the surface of a polyetherurethane urea (PEUU) and investigate neutrophil intracellular pathways involved in shear-induced apoptosis. In situ detection of activated caspases, the enzymatic mediators of the apoptosis cascade, showed qualitatively that these proteases participate in shear-induced apoptosis and are activated in a shear-dependent manner. The involvement of caspase 3 was confirmed through immunoprecipitation and immunoblotting of extracted neutrophil proteins. Comparative studies with neutrophils adherent under static conditions demonstrated time-dependent activation of caspases in TNF-alpha/cycloheximide-induced apoptosis, for which caspase-3 also was implicated. These findings are the first steps toward elucidation of the mechanisms behind the inappropriate induction of apoptosis by adhesion to biomaterials, which may contribute to the development and persistence of device-related infections.

Apoptosis↗
PubMed2002

Adhesion behavior of monocytes, macrophages, and foreign body giant cells on poly (N-isopropylacrylamide) temperature-responsive surfaces.

Monocyte and macrophage adhesion and foreign body giant cell (FBGC) formation has been observed on surfaces with a wide range of properties. In this study we have utilized novel, temperature-responsive surfaces (TRS) with dynamic surface properties to investigate inflammatory cell adhesion behavior. With temperature changes, grafted chains of poly-N-isopropylacrylamide pass through their lower critical solution temperature (LCST) and can either extend (hydrate), creating a hydrophilic surface at 20 degrees C, or contract (dehydrate), creating a hydrophobic surface at 37 degrees C. Isolated human monocytes and monocyte-derived macrophages were able to adhere, spread, and form FBGC on the hydrophobic surface. Decreasing the temperature below the lower critical solution temperature induced a change in the surface wettability, creating a hydrophilic surface, that induced a differential detachment of adherent cells that decreased with time, ranging from 98% after 2 h of culture to 30% at day 10. These detached cells remained viable, and were recultured onto TCPS for 3, 7, and 10 days. These novel surfaces allow investigation of the adhesive behavior of adherent inflammatory cells in a temporal manner, and the effects of surface conformation and wettability changes on cell adhesion and detachment.

Cell Adhesion↗
PubMed2002

Beta1 and beta2 integrins mediate adhesion during macrophage fusion and multinucleated foreign body giant cell formation.

An in vitro system of interleukin (IL)-4-induced human monocyte-derived macrophage fusion was used to investigate the cell/substrate adhesive mechanisms that support multinucleated foreign body giant cell (FBGC) formation. Monocytes were cultured for 3 days and IL-4 was added to induce macrophage fusion and FBGC formation by day 7. Functionally defined anti-integrin antibodies demonstrated that initial monocyte adhesion is mediated by beta2 integrins, whereas during the induction of macrophage fusion by IL-4, an additional dependence on beta1 integrins is acquired. The combination of anti-beta1 plus anti-beta2 was most effective, reducing macrophage/FBGC adhesion to 10% of controls. Consistent with integrin-mediated signaling, the tyrosine kinase inhibitor genistein and the phosphatidylinositol-3-kinase inhibitors wortmannin and LY294002 also attenuated macrophage/FBGC adhesion. Confocal microscopic analysis revealed that beta2 integrins are present on monocytes after initial adhesion and are strongly expressed on fusing macrophages, particularly in peripheral cell areas, and on FBGCs. In contrast, beta1 integrins are not detected on monocytes but begin to appear during macrophage development and are strongly expressed on fusing macrophages and FBGCs. For the first time, these results demonstrate the IL-4-induced acquisition of cooperation between beta1 and beta2 integrins in the cell/substrate adhesive interactions that are required for multinucleated FBGC formation.

Amino Acid Sequence↗
PubMed2002

Adherent endotoxin mediates biological responses of titanium particles without stimulating their phagocytosis.

Aseptic loosening of orthopaedic implants is thought to be primarily due to stimulation of cytokine production by wear particles from the implants. The cytokines increase osteoclast differentiation, leading to osteolysis and implant loosening. Accumulating evidence indicates that adherent endotoxin mediates the biological responses induced by the wear particles. One mechanism by which adherent endotoxin may act is by increasing phagocytosis of the wear particles. To test this hypothesis, the effect of adherent endotoxin on phagocytosis of titanium particles was determined. First, we developed reliable confocal and fluorescence microscopy methods to examine both the attachment and internalization steps of phagocytosis. Use of these methods showed that adherent endotoxin does not detectably alter the rate or the extent of phagocytosis of titanium particles by RAW 264.7 cells. Despite this lack of an effect on phagocytosis, adherent endotoxin dramatically increases the ability of RAW 264.7 cells to produce TNF-alpha and induce osteoclast differentiation. Thus, adherent endotoxin mediates these biological responses by a mechanism that does not rely on increased phagocytosis. These results also demonstrate that phagocytosis is not sufficient to induce cytokine production and osteoclast differentiation but do not rule out the possibility that phagocytosis is required for induction of these responses by titanium particles with adherent endotoxin.

Animals↗
PubMed2002

Interleukin-4 inhibits tumor necrosis factor-alpha-induced and spontaneous apoptosis of biomaterial-adherent macrophages.

Biocompatibility of implanted materials is determined by the host foreign-body response, which is comprised of cellular (adherent monocytes and macrophages) and soluble (secreted cytokines) components. Modulating the presence, activity or both of adherent macrophages may increase or decrease the biocompatibility of implants because these cells remain adherent to the implant surface and fuse to form foreign-body giant cells (FBGCs), leading to failure of the implant. An attractive mechanism of eliminating these cells is through the induction of apoptosis; therefore ways of inducing or inhibiting apoptosis of biomaterial-adherent inflammatory cells are being investigated. We hypothesized that interleukin-4 (IL-4) promotes macrophage survival by inhibiting tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis. We found that TNF-alpha induces apoptosis in a time- and dose-dependent manner, whereas IL-4 inhibits TNF-alpha-induced and spontaneous apoptosis of biomaterial-adherent macrophages. Blocking experiments and evaluation of shedding of soluble TNF receptor type I (TNF-RI) demonstrated that endogenous TNF-alpha production is responsible for spontaneous apoptosis of biomaterial-adherent cells and that IL-4 inhibits this apoptosis by increasing levels of shedding of soluble TNF-RI. These findings suggest that TNF-alpha and IL-4 play key roles in determining the fate of biomaterial-adherent cells and that fusion of macrophages into FBGCs is a mechanism for promoting inflammatory-cell survival on implanted materials.

Adult↗
PubMedDate not supplied

Intestinal malrotation in children: a problem-solving approach to the upper gastrointestinal series.

Intestinal malrotation, which is defined by a congenital abnormal position of the duodenojejunal junction, may lead to midgut volvulus, a potentially life-threatening complication. An evaluation for malrotation is part of every upper gastrointestinal (GI) tract examination in pediatric patients, particularly neonates and infants. Although the diagnosis of malrotation is often straightforward, the imaging features in approximately 15% of upper GI tract examinations are equivocal and lead to a false-positive or false-negative interpretation. The clinical manifestations and upper GI tract findings of malrotation in older children and adults are less specific than are those in younger patients, and for this reason diagnosis of the condition may be more difficult. Successful differentiation between a normal variant and malrotation requires the use of optimal techniques in acquiring and interpreting the upper GI series. Familiarity with the upper GI series appearance of both normal and abnormal anatomic variants allows the radiologist to increase both diagnostic accuracy and confidence in the diagnosis of malrotation.

Diagnosis, Differential↗