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M Bessler

Publications and source records attributed to M Bessler.

75 records · Page 5Linked to original sources

Ultrathin coating by plasma polymerization applied to corneal contact lens.

Plasma coating (deposition of polymer under the influence of plasma) is utilized to modify the surface properties of corneal contact lens. An ultrathin layer (thickness of roughly 200 A) of plasma polymer of acetylene/H20/N2 is applied to poly(methyl methacrylate) (PMMA) corneal contact lenses. The surface becomes highly wettable with water compared to uncoated lens. When coated and uncoated contact lenses are placed on rabbit eyes, a remarkable difference in accumulation of mucous matter is observed. With the control lenses, the accumulation of mucous matter in a week is sufficient to affect the optical clarity of the lenses, whereas the coated lenses show no change after three months continuous wearing. The comparative degree of adhesion of the corneal epithelium cells onto glass, modified glass, PMMA, and coated PMMA surfaces is studied using tissue cultures and phase contrast microscopy. The coated PMMA surface exhibits a degree of tissue adhesion lower than that of control PMMA and higher than that of glass surface, and no sign of toxicity of the coated surface is observed by the tissue cultures.

Acetylene↗

Transluminal aortic valve placement. A feasibility study with a newly designed collapsible aortic valve.

Percutaneous stents are used in vascular applications in conjunction with angioplasty and in combination with graft material for repair of abdominal aneurysms. The authors have designed a collapsible bioprosthetic aortic valve for placement by a transluminal catheter technique. This trileaflet stent valve is composed of stainless steel and bovine pericardium. Stent valves, 23 and 29 mm, were tested in a pulse duplicator system with rigid rings from 21 to 31 mm in 2 mm increments. At a mean flow of 3.1 L/min (+/-0.7), normal systemic aortic pressure was generated with a transvalvular gradient of 14.9 +/- 7 mmHg (mean +/- SD). Regurgitation fraction ranged from 10 to 18% (mean 13.8 +/- 3%) in the best ring size. Valves with the best hemodynamic profile were used for implantation in three 70 kg pigs in an open chest model. The valve was collapsed in a 24 Fr catheter designed to allow slow, controlled release. After resection of the native leaflets, the new valve was placed in the subcoronary position. No additional sutures were used for securing the valve. Two animals were successfully weaned from cardiopulmonary bypass and maintained systemic pressures of 100/45 (+/-10) and 116/70 (+/-15) mmHg, respectively. Intraoperative color echocardiography revealed minimal regurgitation, central flow, full apposition of all leaflets, and no interference with coronary blood flow. Both animals were sacrificed after being off bypass for 2 hr. Postmortem examination revealed the valves to be securely anchored. The third animal was weaned from cardiopulmonary bypass but developed refractory ventricular fibrillation because of valve dislodgment due to structural failure. Although long term survival data are needed, development of a hemodynamically acceptable prosthetic aortic valve for transluminal placement is feasible.

Animals↗

Factor V Leiden mutation investigated by amplification created restriction enzyme site (ACRES) in PNH patients with and without thrombosis.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired chronic hemolytic anemia characterized by intravascular hemolysis, often associated with neutropenia and thrombocytopenia. Venous thrombosis, including the Budd-Chiari syndrome, is one of the major complications of PNH, but not all PNH patients develop thrombosis. The basis for the high risk of thrombosis in PNH is not known. Recent reports have shown that Factor V Leiden mutation is a common cause of increased tendency to develop thrombosis. Fifty-six PNH patients were tested for Factor V Leiden mutation using Amplification Created Restriction Enzyme Site methods. PNH patients do not show an increased frequency of Factor V Leiden mutations.

Factor V↗