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Biomedical subjects

J M Anderson

Publications and source records attributed to J M Anderson.

At least 91 records · Page 5Linked to original sources
PubMed1999

Human agency and the process of healing: lessons learned from women living with a chronic illness--'re-writing the expert'.

In this paper we examine the notion of human agency in the context of women experiencing a chronic illness. Based on two qualitative studies conducted with Canadian women of Chinese- and Anglo-descent living with diabetes, we unmask the complex power relations inherent in patient-practitioner interactions, and problematize the privileging of healthcare providers as knowers and experts on the patient's body. Specifically, we analyse the meanings that women ascribe to their illness experience. We discuss how women experience the loss of agency in healthcare encounters, how they resist patienthood by reclaiming agency, and how healthcare providers foster agency in their interactions with women. Rather than suggesting that biomedical experts should be 'written out', we propose to rewrite healthcare providers as 'reflexive practitioners' through the construction of transformative knowledge. We argue that praxis-oriented practice, which is based on transformative knowledge, will provide the space for women and healthcare providers to enter into a new dialogue and a relation in which women can sustain a sense of self, and begin the journey of healing.

Adaptation, Psychological↗
PubMed1999

Cyclic strain effects on human monocyte interactions with endothelial cells and extracellular matrix proteins.

Human vascular endothelial cells (ECs) are exposed to various levels of hemodynamic forces, cyclic strain, and shear stress in vivo. Here, we examined the in vitro effects of the various levels (0-6%, 7-16%, and 17-25%) of strain at 60, 30, and 15 cycles per minute (cpm) on human monocyte adherence to endothelial cells and extracellular matrix protein preabsorbed surfaces. Monocyte adhesion to endothelial cells under cyclic strain significantly increased. At both 30 and 60 cpm, ECs under strains of 7-16% and 17-25% showed >52% and >117% higher monocyte adhesion than endothelial cells under static condition when monocytes were added for 0.5 h. This increase in monocyte adhesion to ECs under cyclic strain remained significantly higher even after 24 h of incubation. Human monocyte adhesion to extracellular matrix protein preabsorbed surfaces differed depending on the specific extracellular matrix protein. Monocytes adhered to collagen type I and fibronectin preabsorbed surfaces >50% under 0-6% strain, >23% under 7-16% strain, and >52% under 17-25% strain at 15 and 30 cpm compared to the collagen type V preabsorbed surface. However, when extracellular protein preabsorbed surfaces under cyclic strain were compared to the control static condition, monocyte adhesion did not significantly change on most of other surfaces. These results suggest that cyclic strain may play a role in the regulation of monocyte-endothelial cells/extracellular matrix interactions in vivo.

Cell Adhesion↗
PubMed1999

Disruption of filamentous actin inhibits human macrophage fusion.

The foreign body reaction to implanted biomaterials, characterized by the presence of macrophages and foreign body giant cells (FBGC), can result in structural and functional failure of the implant. Recently, we have shown that interleukin-4 and interleukin-13 can independently induce human macrophage fusion to form FBGC via a macrophage mannose receptor (MR) -mediated pathway. The MR is believed to mediate both endocytosis of glycoproteins and phagocytosis of microorganisms, which bear terminal mannose, fucose, N-acetylglucosamine, or glucose residues. Polarization of microfilaments to closely apposed macrophage membranes as observed with fluorescence confocal microscopy led us to ask whether MR-mediated fusion occurred via a filamentous actin-dependent pathway. Cytochalasins B and D and latrunculin-A, agents that disrupt microfilaments, inhibited macrophage fusion in a concentration-dependent manner. The concentrations of cytochalasins D and B that inhibited fusion did not significantly decrease macrophage adhesion, spreading, or motility but did inhibit internalization of Candida albicans during interleukin-13-enhanced, MR-mediated phagocytosis. Very low concentrations of cytochalasin B (< 2 microM) induced a slight enhancement of macrophage fusion. Taken together, the results of this study suggest that cytokine-induced, MR-mediated macrophage fusion requires an intact F-actin cytoskeleton and that the mechanism of fusion is similar to phagocytosis.--DeFife, K. M., Jenney, C. R., Colton, E., Anderson, J. M. Disruption of filamentous actin inhibits human macrophage fusion.

Actins↗
PubMed1999

Developmental stuttering and Parkinson's disease: the effects of levodopa treatment.

The effects of dopamine on developmental stuttering was studied in a 44 year old man with developmental stuttering and Parkinson's disease during three levodopa "on" periods and three "off" periods. When compared with the "off" periods, during the "on"' periods he demonstrated an increase of speech dysfluencies. These findings lend support to the dopamine hypothesis of developmental stuttering.

Adult↗
PubMed1999

Photochemically immobilized polymer coatings: effects on protein adsorption, cell adhesion, and leukocyte activation.

Amphiphilic chains of 4-benzoylbenzoic acid moieties and polymer were photochemically immobilized onto silicone rubber to ask whether the covalently coupled polymers would passivate the silicone rubber by inhibiting protein adsorption and subsequent cell adhesion and activation. Three groups of polymers were utilized: the hydrophilic synthetic polymers of polyacrylamide, polyethylene glycol, and polyvinylpyrrolidone; the glycosaminoglycan, hyaluronic acid; and poly(glycine-valine-glycine-valine-proline), a polypeptide derived from the sequence of elastin. Each coating variant decreased the adsorption of fibrinogen and immunoglobulin G compared to uncoated silicone rubber. All except the methoxy-polyethylene glycol coating nearly abolished fibroblast growth, but none of the coating variants inhibited monocyte or polymorphonuclear leukocyte adhesion. Interleukin-1beta, interleukin-1 receptor antagonist, and tumor necrosis factor-alpha secretion by leukocytes were not statistically different between any of the coating variants and uncoated silicone rubber. However, the methoxy-polyethylene glycol and elastin-based polypeptide coatings, which supported the highest numbers of adherent monocytes, also elicited the lowest levels of proinflammatory cytokine secretion. When these in vitro data were collectively evaluated, the coating that most effectively passivated silicone rubber was the polypeptide derived from elastin.

Acrylic Resins↗
PubMed1999

Cytoskeletal and adhesive structural polarizations accompany IL-13-induced human macrophage fusion.

During the inflammatory response to an implanted biomaterial, monocytes undergo a striking phenotypic progression of differentiation into macrophages, which may subsequently fuse to form foreign body giant cells (FBGCs). Taking advantage of an in vitro system of cytokine-induced FBGC formation together with the optical slicing capabilities of a confocal microscope, we investigated the cytoskeletal reorganization and adhesive structure development during this dramatic morphological progression. Human monocytes demonstrated diffuse cytoplasmic staining of adhesive structural proteins. Punctate filamentous (F)-actin structures appeared along the ventral cell membrane of macrophages and were identified as the core of podosome adhesive structures by the distinctive ring staining of vinculin, talin, and paxillin around the F-actin. Cytokine-induced FBGCs were characterized by a restriction of podosomes to the extreme periphery of the ventral cell surface. Although macrophages and FBGC contained equivalent amounts of F-actin, significantly more F-actin was located within 1 micron of the ventral plasma membrane in FBGCs compared to macrophages. Taken together, these results provide new information on the dynamic cytoskeletal reorganization and adhesive structure development that occur during phenotypic progression from human monocytes to macrophages to FBGC. Furthermore, they suggest the acquisition of functional specializations on FBGC formation, which may enhance our understanding of chronic inflammatory processes.

Actins↗
PubMed1999

VAP-33 localizes to both an intracellular vesicle population and with occludin at the tight junction.

Tight junctions create a regulated intercellular seal between epithelial and endothelial cells and also establish polarity between plasma membrane domains within the cell. Tight junctions have also been implicated in many other cellular functions, including cell signaling and growth regulation, but they have yet to be directly implicated in vesicle movement. Occludin is a transmembrane protein located at tight junctions and is known to interact with other tight junction proteins, including ZO-1. To investigate occludin's role in other cellular functions we performed a yeast two-hybrid screen using the cytoplasmic C terminus of occludin and a human liver cDNA library. From this screen we identified VAP-33 which was initially cloned from Aplysia by its ability to interact with VAMP/synaptobrevin and thus was implicated in vesicle docking/fusion. Extraction characteristics indicated that VAP-33 was an integral membrane protein. Antibodies to the human VAP-33 co-localized with occludin at the tight junction in many tissues and tissue culture cell lines. Subcellular fractionation of liver demonstrated that 83% of VAP-33 co-isolated with occludin and DPPIV in a plasma membrane fraction and 14% fractionated in a vesicular pool. Thus, both immunofluorescence and fractionation data suggest that VAP-33 is present in two distinct pools in the cells. In further support of this conclusion, a GFP-VAP-33 chimera also distributed to two sites within MDCK cells and interestingly shifted occludin's localization basally. Since VAP-33 has previously been implicated in vesicle docking/fusion, our results suggest that tight junctions may participate in vesicle targeting at the plasma membrane or alternatively VAP-33 may regulate the localization of occludin.

Animals↗
PubMed1999

Transmembrane proteins in the tight junction barrier.

Three types of transmembrane proteins have been identified within the tight junction, but it remains to be determined how they provide the molecular basis for regulating the paracellular permeability for water, solutes, and immune cells. Several of these proteins localize specifically within the continuous cell-to-cell contacts of the tight junction. One of these, occludin, is a cell adhesion molecule that has been demonstrated to influence ion and solute permeability. The claudins are a family of four-membrane spanning proteins; unexpectedly, other members of this family have already been characterized without recognizing their relationship to tight junctions. Junction adhesion molecule, the most recently identified tight junction component, is a member of the Ig superfamily and influences the paracellular transmigration of immune cells. A plaque of cytoplasmic proteins under the junction may be responsible for scaffolding the transmembrane proteins, creating a link to the perijunctional actin cytoskeleton and transducing regulatory signals that control the paracellular barrier.

Animals↗
PubMed1999

The female athlete triad: disordered eating, amenorrhea, and osteoporosis.

The Female Athlete Triad is a common clinical entity amongst female athletes. The physician caring for such athletes needs to keep the symptoms of the triad in mind and recognize their potential severity. Still more needs to be done in the areas of prevention, early detection, and early treatment. Education efforts should be focused on junior high and early high school girls because the rapid bone formation during puberty will be necessary to carry them for the rest of their lives. It is also important to note that the female athlete triad should not be used as a reason to disqualify otherwise healthy female athletes from athletic participation. Athletic participation and exercise are good and healthy, if done appropriately. Women have made great strides in the athletic realm, and it would be inappropriate to imply that they should not participate because of the risk or presence of the Female Athlete Triad.

Adolescent↗
PubMed1998

Bacterial surface properties of clinically isolated Staphylococcus epidermidis strains determine adhesion on polyethylene.

The role of surface physiochemical properties of Staphylococcus epidermidis strains in adhesion to polyethylene (PE) was investigated under physiological flow conditions in phosphate buffered saline (PBS) and 1% platelet poor plasma (PPP). Four clinically isolated strains were divided into two groups: low and high relative hydrophobicity, and the F1198 and RP62A strains showing significantly greater hydrophobicity than the F21 and F1018 strains. In PBS, adhesion of all S. epidermidis strains was shear dependent from 0 to 15 dyn/cm2, after which adhesion becomes shear independent. Strains with higher surface hydrophobicity showed higher adhesion to PE, demonstrating the influence of bacterial surface hydrophobicity in nonspecific adhesion. Bacterial adhesion correlated well with bacterial surface hydrophobicity at low shear stresses (0-8 dyn/cm2). In 1% PPP, adhesion of all strains dramatically decreased and we found no correlation between bacterial surface hydrophobicity and adhesion. The presence of plasma proteins reduced nonspecific adhesion. S. epidermidis surface charge did not correlate with bacterial adhesion in either test media. The results suggested that S. epidermidis surface hydrophobicity may mediate nonspecific adhesion to PE at low shear stresses in protein-free media.

Bacterial Adhesion↗
PubMed1998

The tight junction protein ZO-1 establishes a link between the transmembrane protein occludin and the actin cytoskeleton.

The tight junction protein ZO-1 belongs to a family of multidomain proteins known as the membrane-associated guanylate kinase homologs (MAGUKs). ZO-1 has been demonstrated to interact with the transmembrane protein occludin, a second tight junction-specific MAGUK, ZO-2, and F-actin, although the nature and functional significance of these interactions is poorly understood. To further elucidate the role of ZO-1 within the epithelial tight junction, we have introduced epitope-tagged fragments of ZO-1 into cultured MDCK cells and identified domains critical for the interaction with ZO-2, occludin, and F-actin. A combination of in vitro and in vivo binding assays indicate that both ZO-2 and occludin interact with specific domains within the N-terminal (MAGUK-like) half of ZO-1, whereas the unique proline-rich C-terminal half of ZO-1 cosediments with F-actin. Consistent with these observations, we found that a construct encoding the N-terminal half of ZO-1 is specifically associated with tight junctions, whereas the unique C-terminal half of ZO-1 is distributed over the entire lateral surface of the plasma membrane and other actin-rich structures. In addition, we have identified a 244-amino acid domain within the N-terminal half of ZO-1, which is required for the stable incorporation of ZO-1 into the junctional complex of polarized MDCK cells. These observations suggest that one functional role of ZO-1 is to organize components of the tight junction and link them to the cortical actin cytoskeleton.

Actins↗
PubMed1998

Human CASK/LIN-2 binds syndecan-2 and protein 4.1 and localizes to the basolateral membrane of epithelial cells.

In Caenorhabditis elegans, mutations in the lin-2 gene inactivate the LET-23 receptor tyrosine kinase/Ras/MAP kinase pathway required for vulval cell differentiation. One function of LIN-2 is to localize LET-23 to the basal membrane domain of vulval precursor cells. LIN-2 belongs to the membrane-associated guanylate kinase family of proteins. We have cloned and characterized the human homolog of LIN-2, termed hCASK, and Northern and Western blot analyses reveal that it is ubiquitously expressed. Indirect immunofluorescence localizes CASK to distinct lateral and/or basal plasma membrane domains in different epithelial cell types. We detect in a yeast two-hybrid screen that the PDZ domain of hCASK binds to the heparan sulfate proteoglycan syndecan-2. This interaction is confirmed using in vitro binding assays and immunofluorescent colocalization. Furthermore, we demonstrate that hCASK binds the actin-binding protein 4.1. Syndecans are known to bind extracellular matrix, and to form coreceptor complexes with receptor tyrosine kinases. We speculate that CASK mediates a link between the extracellular matrix and the actin cytoskeleton via its interaction with syndecan and with protein 4.1. Like other membrane-associated guanylate kinases, its multidomain structure enables it to act as a scaffold at the membrane, potentially recruiting multiple proteins and coordinating signal transduction.

Animals↗
PubMed1998

Adhesion of Staphylococcus epidermidis and transposon mutant strains to hydrophobic polyethylene.

Staphylococcus epidermidis capsular polysaccharide adhesin (PS/A) and slime were studied as possible mediators of bacterial adhesion to NHLBI polyethylene (PE) under dynamic flow. This putative interaction was examined by quantifying the adhesion of M187 (PS/A+, slime+) parent strain and isogenic transposon mutant strain sn3 (PS/A-, slime-) to polyethylene (PE) under a range of physiologic shear stress conditions in both phosphate-buffered saline (PBS) and 1% platelet poor plasma (PPP). No significant differences in adhesion were noted between the M187 and sn3 strains in either test medium. However, adhesion of both strains in 1% PPP was decreased 75-95% compared to adhesion in PBS. In PBS, adhesion was shear stress dependent from 0-15 dyne/cm2, after which adhesion was comparatively shear stress independent. Adhesion in 1% PPP was independent of shear stress. Epifluorescent imaging of both strains labeled for slime confirmed the presence of slime on the surface of M187 and suggested that PS/A and slime promote the formation of large aggregates, as aggregates were totally absent in the images of the sn3 strain. The results suggest that PS/A and slime do not mediate S. epidermidis adhesion to bare PE or PE with adsorbed plasma proteins, but may be necessary for intercellular adhesion, which is important for biofilm formation.

Bacterial Adhesion↗
PubMed1998

Detection of bacterial adherence on biomedical polymers.

The ability to adhere to materials and promote formation of a biofilm is an important feature of the pathogenicity of some organisms, most notably the coagulase negative staphylococci. Various methods to detect bacterial adherence are available, but detection of adherence to nontransparent materials can be difficult. It was the purpose of this study to establish the suitability of a dye elution technique to detect adherence. The technique involves fixing the bacterial film with formalin, staining with crystal violet, eluting the dye with ethanol, and determining the optical density of the solution using 96-well plates and an enzyme immunosorbent assay reader with a 540-nm filter. This technique distinguished a known adherent from a known nonadherent organism and demonstrated that the presence of protein can inhibit adherence, and that adherence of different organisms to different biomedically important polymers can be measured. The dye elution technique was used to evaluate the adherence of known slime-producing polysaccharide antigen-positive (PSA+) and known nonslime-producing polysaccharide antigen-negative (PSA-) Staphylococcus epidermidis organisms to implant grade materials (polyethylene, expanded polytetrafluoroethylene, Dacron, silicone, and collagen) as well as to polystyrene.

Bacterial Adhesion↗