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Biomedical subjects

D K Han

Publications and source records attributed to D K Han.

45 records · Page 3Linked to original sources
PubMedDate not supplied

Bacterial adhesion on PEG modified polyurethane surfaces.

Polyurethane surface was modified with poly(ethylene glycol) (mol. wt. 1000, PEG1k) carrying terminal hydroxyl, amino and sulfonate groups, poly(ethylene glucol) (mol. wt. 3350, PEG3.4k) and PEG3.4k-Heparin, respectively. These surfaces were investigated for bacterial adhesion using S. epidermidis and E. coli in tryptic soya broth (TSB), brain heart infusion (BHI), and human plasma. All PEG modified surfaces reduced bacterial adhesion significantly and the adhesion level differs depending on surfaces as well as media. In the case of PEG1k surfaces, no reduction of S. epidermidis adhesion was demonstrated in TSB media, regardless of terminal functional groups of PEG1k. However, adhesion in plasma was reduced to the different degree, depending on terminal groups of PEG1k (least adhesion on sulfonated PEG surface). Relatively longer PEG surface (PEG3.4k) and PEG3.4k-heparin surface minimized bacterial adhesion in both media. In the case of E. coli adhesion, significant reduction in adherent bacteria was observed on all PEG1k, PEG3.4k, and PEG-heparin surfaces in both media compared to controls. In contrast, no reduction in bacterial adhesion was demonstrated on poly(propylene glycol) (PPG1k) grafted PU surface as compared to control PU. These results suggest that surface modification with PEG1k-SO3, PEG3.4k and PEG3.4k-heparin seems to be effective for prevention of bacterial adhesion and subsequent infection.

Animals↗
PubMedDate not supplied

Chemical modification of implantable biologic tissue for anti-calcification.

Biologic porcine tissue was modified by coupling sulfonated polyethyl-eneoxide (PEO-SO3) and the effect of modification on calcification was evaluated in vitro and in vivo. The modification process involves grafting PEO-SO3 to porcine valve leaflet either by carbodiimide (EDC) activation or by direct coupling using glutaraldehyde. Thermal property, measured by differential scanning calorimetry, showed that the shrinkage temperature of modified tissue increased compared with control tissue and fresh tissue, suggesting increased thermal stability. Resistance to collagenase digestion revealed that modified tissues have greater resistance to enzyme digestion than do control tissues. In vitro calcification showed that modified tissues have less calcium deposition than do control tissues. In vivo calcification, using a rat subcutaneous implantation model, also showed less calcification of modified tissue than that of control. The resistance of modified tissue to collagenase, higher shrinkage temperature, and reduced calcification, when compared with control tissue, attest to the usefulness of this chemical modification for implantable biologic tissue.

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PubMedDate not supplied

Transition of apoptotic resistant vascular smooth muscle cells to troptotic sensitive state is correlated with downregulation of c-FLIP.

Fas and its ligand, FasL, are a receptor-ligand pair identified as promoting cell death in several tissues. Vascular smooth muscle cells (VSMCs) are resistant to FasL or anti-Fas antibody (Ab) signal, and a number of in vitro studies show that VSMC death can only be induced by anti-Fas Ab or FasL in the presence of protein inhibitor or additional inflammatory mediators. It remains to be clarified whether known, constitutively expressed cytoprotective molecules are reduced by protein inhibitor, thereby accounting for sensitization to cell death by Fas/FasL signaling. We found that Fas mRNA and protein exist in several primary VSMCs, as previously reported. We also demonstrated (1) that critical death-signaling molecules, such as FADD, caspase-1/ICE, and caspase-3/YAMA, are present in these VSMCs, (2) that human VSMCs contain high concentrations of c-FLIP (3) and that following treatment with the protein inhibitor, CHX, cell extracts showed a decrease in c-FLIP protein that was dose- and time-dependent on the degree of apoptosis and inversely correlated with both caspase-8 and -3 activity. In contrast, there was neither a change nor an even modest upregulation of Bcl-2 family, even after 12 h of treatment with CHX. Taken together, these results may provide a novel insight into atherogenesis and suggest that c-FLIP may contribute to an apoptosis-resistant state of VSMC, and that a downregulation of c-FLIP may render VSMCs susceptible to apoptosis.

Apoptosis↗
PubMedDate not supplied

Antithrombotic activity of a lumbrokinase immobilized polyurethane surface.

Six fractions of strong and novel fibrinolytic enzymes (lumbrokinase, LK) were extracted from the earthworm Lumbricus rubellus. The enzymes in these fractions appeared to be very stable and showed greater antithrombotic activity than other currently used antithrombotics. The authors immobilized an LK fraction that shows the most potent fibrinolytic activity on a polyurethane (PU) surface to investigate its enzymatic and antithrombotic activity. The methanol extracted PU surface was treated with a 3% (wt/vol) maleic anhydride methylvinyl ether copolymer (MAMEC) solution and finally incubated in an LK solution in PBS (pH 7.4). The immobilized LK activity was estimated by the fibrin plate method and caseinolytic activity assay. The antithrombotic activity was evaluated by in vitro 125I-fibrinogen adsorption in fresh whole blood and 99mTc platelet adhesion tests. In addition, the occlusion time was determined through ex vivo rabbit A-A shunt experiments. The content and unit activity of immobilized LK were found to be 24 micrograms/cm2 and 18 IU/cm2, respectively. The relative activity ratio of immobilized LK to soluble LK was found to be approximately 34%. Immobilized LK was stable within a various pH range and resistant to inhibitors and thermal inactivation. Less fibrinogen was adsorbed and fewer platelets adhered on an LK-immobilized surface than on PU and PU-MAMEC controls. The ex vivo occlusion time of untreated PU and PU-MAMEC surfaces were only 32 and 42 minutes, respectively. But that of LK-immobilized PU was extended to 140 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The fluid dynamic effect on protein adsorption in left ventricular assist devices.

Plasma protein adsorption onto an artificial surface is strongly influenced by not only the surface characteristics of materials, but also by the fluid dynamics inside the blood pump, and it would influence subsequent platelet adhesion or activation, which plays a major role in the initiation of thrombus formation at the blood-material interface in vivo. In vitro flow visualization of an electrohydraulic LVAD was performed by a video camera (CCD, Hitachi) and an image processor (PC VISION PLUS) with an IBM PC. The electrohydraulic LVADs were implanted in mongrel dogs of approximately 20 kg. The authors sectioned the blood contacted ventricle after animal death according to the level of shear rate. Because analysis of adsorbed protein might be influenced by the size of the ventricle segment, the number of segments was limited to eight per ventricle. Platelet adhesion and its morphology were observed by scanning electron microscopy (SEM). Adsorbed plasma proteins (fibrinogen, albumin, and IgG) on each segment were quantified by enzyme linked immunosorbent assay (ELISA). The specimens were soaked in 2% (wt/vol) SDS/PBS for 2 days and the released protein concentration assessed. A well developed large vortex was observed at the center of the artificial ventricle. Polyurethane blood pumps displayed different degrees of protein adsorption and subsequent platelet adhesion on each segment.

Adsorption↗
PubMedDate not supplied

In vivo canine studies of a Sinkhole valve and vascular graft coated with biocompatible PU-PEO-SO3.

PU-PEO-SO3 was applied as a coating material over a newly designed Sinkhole bileaflet PU heart valve and a porous PU vascular graft. Performance and biocompatibility were evaluated using an in vivo canine shunt system between the right ventricle and pulmonary artery. The survival periods in three implantations were 14, 24, and 39 days, during which no mechanical failure occurred in any Sinkhole valve or vascular graft. Scanning electron microscopy (SEM) studies demonstrated much less platelet adhesion and thrombus formation on PU-PEO-SO3 grafts than on PU vascular grafts. Cracks in the valve leaflet were occasionally observed on PU surfaces, but not on PU-PEO-SO3. After a 39 day implantation, calcium deposition on vascular grafts was decreased as compared with valve leaflets, and calcification on PU-PEO-SO3 was much lower than on PU. These results suggest that Sinkhole valves and vascular grafts are promising, and PU-PEO-SO3 as a coating material is more blood compatible, biostable, and calcification resistant in vivo than in untreated PU.

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