PubMed Health⌕ Search

Biomedical subjects

I W Wang

Publications and source records attributed to I W Wang.

9 recordsLinked to original sources
PubMed1999

Platelet-derived microparticles on synthetic surfaces observed by atomic force microscopy and fluorescence microscopy.

Platelet activation on a thrombogenic surface includes the release of membrane-derived microparticles that provide catalytic sites for blood coagulation factors. Here, we describe a quantitative investigation on the production and dimensions of platelet-derived microparticles observed on glass and polyethylene under aqueous conditions, using atomic force microscopy (AFM) and complementary fluorescence microscopy. The results show that contact-activated platelet microparticles are not evenly distributed over a thrombogenic surface, but in clusters in close proximity to adherent platelets. The microparticles are localized near the platelet periphery, and in some cases appear to emanate from platelet pseudopodia, suggesting that formation may result from vesiculation of the pseudopodia. The microparticles measured 125 +/- 21 nm (n = 73) in the x-y dimensions and 5.2 +/- 3.6 nm in height. The results compared closely with 125 +/- 22 nm width and 4.1 +/- 1.6 nm height obtained for control preparations of thrombin activated microparticles, that were filtered and deposited on glass. Large differences between the measured widths and heights of adsorbed microparticles suggest that platelet microparticles may undergo spreading after attachment to a surface. The adsorbed microparticles expressed platelet membrane receptor GPIIb/IIIa, and many expressed the platelet activation marker P-selectin as determined by fluorescence microscopy. The high number distribution of procoagulant microparticles per unit area of surface compared with platelets suggests that platelet-derived microparticles provide a mechanistic route for amplifying thrombus formation on a thrombogenic surface.

Biocompatible Materials↗
PubMed1999

Vitamin K reduces bleeding in left ventricular assist device recipients.

BACKGROUND: Despite advances in left ventricular assist device (LVAD) design that permit support without anticoagulation, LVAD recipients often suffer profound bleeding complications. This bleeding diathesis may be attributable to pre-operative right-ventricular failure with concomitant hepatic dysfunction. The purpose of this study was to characterize coagulation abnormalities in LVAD recipients and determine the impact of pre-operative vitamin K administration on the incidence of postoperative bleeding. METHODS: Hemostatic and liver function profiles were obtained in 66 recipients of the Heartmate LVAD; 39 of these patients received perioperative vitamin K. RESULTS: During LVAD support, hepatic synthetic function improved as evidenced by increases in clotting factors II, V, VII, XI. There was ongoing fibrinolysis with elevation of fibrinopeptide A and D-dimers and diminution of fibrinogen; however, plasminogen levels did not decline suggesting that systemic disseminated intravascular coagulation (DIC) did not occur. Bleeding requiring re-exploration more than 48 hours postimplantation occurred in 9 of 66 patients (13.6%). Prior to implantation, patients that bled had decreased levels of factor II (52.2 +/- 27.1% vs 69.7 +/- 26.6%; p = 0.048) and prolonged prothrombin times (16.5 +/- 2.4 seconds vs 13.8 +/- 3.1 seconds; p = 0.005) compared to patients that did not bleed. Seven of 27 patients (25.9%) not treated with vitamin K bled, while only 2 of 39 (5.1%) patients treated with vitamin K required re-exploration for bleeding (p = 0.026). CONCLUSIONS: We conclude that: (1) Liver synthetic function improves during LVAD support resulting in increased levels of circulating coagulation factors; (2) ongoing fibrinolysis occurs but likely only represents remodeling of fibrin on the LVAD surface; (3) perioperative vitamin K reduces nonsurgical bleeding in LVAD recipients.

Disseminated Intravascular Coagulation↗
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↗
PubMed1995

Adhesion of Staphylococcus epidermidis to biomedical polymers: contributions of surface thermodynamics and hemodynamic shear conditions.

Adhesion studies of Staphylococcus epidermidis RP62A were conducted using a rotating disk system to determine the roles of surface physicochemistry and topographies under physiologic shear conditions. Six materials were investigated: biomedical reference polyethylene and polydimethylsiloxane; argon plasma-treated reference polyethylene (Ar-PE); Silastic; expanded polytetrafluoroethylene; and woven Dacron. All of the polymers except Dacron demonstrated reduced bacterial adhesion with increasing shear stress. Argon plasma treatment of polyethylene reduced the level of staphylococcal adhesion. Adsorption of human plasma proteins effected significantly lower numbers of adherent bacteria. The lowest adhesion was observed for Ar-PE in 1% human plasma protein solution, whereas Dacron had the highest number of adherent bacteria. The high adhesion on Dacron was attributed to increased bacterial flux caused by topography-induced turbulent flow and physical entrapment of the bacteria in the fiber interstices. The results indicate that the driving force for S. epidermidis adhesion is strongly influenced by substrate physicochemistry, but this may be dominated by physical forces such as shear and turbulence.

Bacterial Adhesion↗
PubMed1993

Platelet-mediated adhesion of Staphylococcus epidermidis to hydrophobic NHLBI reference polyethylene.

The effects of platelets and plasma proteins on the adhesion of Staphylococcus epidermidis strain RP62A to hydrophobic NHLBI reference polyethylene was quantitatively studied using a rotating disk system to generate well-defined shear conditions simulating the hemodynamics of human blood circulation. Bacterial adhesion was quantified by adhesive coefficient, the percentage of bacteria transported to the surface that becomes adherent. The results showed that surface modification by adsorption of plasma proteins reduced the adhesion of S epidermidis as compared to the bare polymer surface. This surface modification was not sufficient to eliminate completely bacterial adhesion, even at the highest physiologic shear stress level. S epidermidis did adhere strongly to polyethylene surface modified by platelets. This is readily evident as approximately 50% of the adherent S epidermidis were bound to contact-activated platelets which occupied only 4% of the surface area. Adhesive coefficients to platelets were significantly greater than to the protein-adsorbed polyethylene surface by at least one order of magnitude (P < or = .01) across the range of physiological shear conditions investigated. These studies show that it is biologic surface modification by contact-activated platelets, and not plasma proteins, which mediates S epidermidis adhesion to polyethylene.

Bacterial Adhesion↗
PubMed1993

Staphylococcus epidermidis adhesion to hydrophobic biomedical polymer is mediated by platelets.

A quantitative investigation on the effects of plasma proteins and platelets on the adhesion of Staphylococcus epidermidis RP62A to a hydrophobic biomedical polymer (National Heart, Lung, and Blood Institute reference polyethylene) was carried out under well-defined shear conditions approximating human blood circulation by using a rotating disk system. The results showed that contact-activated platelets mediated S. epidermidis adhesion to the polymer surface. In the range of physiologic shear conditions, the adhesive coefficient (ratio of bacteria per unit area to the product of bacterial flux and the duration of the experiment) to platelets was significantly greater than to the protein-adsorbed polyethylene surface by at least one order of magnitude (P < or = .01). The presence of absorbed plasma proteins on polyethylene reduced the adhesion of S. epidermidis compared with that seen with the bare polymer surface. These studies show that S. epidermidis adhesion to polyethylene is mediated by contact-activated platelets, not absorbed plasma proteins.

Adsorption↗
PubMedDate not supplied

Hemostatic profiles of HeartMate ventricular assist device recipients.

Candidates for ventricular assist devices often have hepatic dysfunction and concomitant coagulation abnormalities. Factors II, V, VII, XI, plasminogen, fibrinopeptide A (FpA), and D-dimers were measured in 19 HeartMate (ThermoCardiosystems, Inc., Woburn, MA) patients before device implantation; at 6 hr, 24 hr, and 2 weeks postimplantation; and before explantation. Ten patients had entry hepatic dysfunction (total bilirubin > 2 mg/dl; aspartate and alanine aminotransferases > 60 U/L); nine had normal hepatic function. All except one patient received perioperative aprotinin; all received only aspirin and dipyridamole after surgery. At preimplant, both patient groups had subnormal factor II, V, VII, XI, and plasminogen with elevated FpA and D-dimer. By 2 weeks postimplant, these factor levels had normalized, except for FpA and D-dimer levels, which suggest ongoing remodeling of fibrin deposits on the device surfaces. No statistically significant differences in the assayed hemostatic markers were observed between the two patient groups. Clinically, 15/19 (79%) patients survived to cardiac transplantation; 3/19 (16%) patients required reoperation for early bleeding. All three had low factor VII and XI; two of three also had hepatic dysfunction and subnormal levels of factor II and V. Most patients with entry hepatic dysfunction improve after device implantation; all four deaths were in patients with persistent hepatic dysfunction despite circulatory support.

Blood Coagulation Factors↗