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Biomedical subjects

S Bowry

Publications and source records attributed to S Bowry.

8 recordsLinked to original sources
PubMed2001

Nanoscale modulation of the pore dimensions, size distribution and structure of a new polysulfone-based high-flux dialysis membrane.

Current haemodialysis therapy modalities such as haemodiafiltration enhance the removal of larger uraemic solutes from the blood of patients on end-stage renal disease. A number of clinical investigations have demonstrated the clinical benefits of such therapies in contributing towards better patient survival rates and an improved quality of life. A fundamental prerequisite to the application of convective treatment modalities is the availability of appropriate, technologically-advanced high-flux dialysis membranes that are able to eliminate larger uraemic substances with high efficiency but without causing an excessive leakage of useful proteins. A new membrane, Helixone, has been developed specifically to meet the present-day requirements of high-flux dialysis and haemodiafiltration therapies involving large substitution rates. The application of nanotechnology fabrication principles and procedures has enabled the development of a membrane having highly-defined inner, separating layer surface structures that offer minimal resistance to the removal of large molecular weight substances across the membrane; for the first time, pore size dimensions, pore size distribution and pore geometry have been modulated and controlled at the nanoscale level for Helixone. This paper describes the characterisation of the essential structure- and permeation-related parameters of the new membrane using a number of physical analytical techniques.

Biocompatible Materials↗
PubMed1994

In vitro biocompatibility evaluation of a heparinizable material (PUPA), based on polyurethane and poly(amido-amine) components.

The biocompatibility of a new heparinizable material based on polyurethane and poly(amido-amine) (PUPA) was evaluated both in the heparinized and non-heparinized forms. The quantity of heparin present on the material was measured using radiolabelled heparin and biological tests. Heparin release in plasma from heparinized PUPA was investigated using in vitro methods. The behaviour of PUPA towards cellular and plasmatic blood components was studied. The influence of sterilization on the cytocompatibility response of both heparinized and non-heparinized PUPA was investigated; gamma-rays were found to be a suitable method of sterilization as no toxic response was noticed.

Animals↗
PubMed1986

Method for the determination of fast acting plasminogen activator inhibitor capacity (PAI-cap) in plasma, platelets and endothelial cells.

A titration assay for the determination of the fast acting plasminogen activator inhibitor capacity (PAI-cap) was developed. Most of the hitherto published assays for fast acting PAI are reported to have the disadvantage of non-parallel titration curves of tissue plasminogen activator (t-PA) in buffer and plasma. In the assay reported here, this problem has been overcome by adequate predilution of the samples, thus achieving parallel titration curves regardless of the individual PAI-cap of a sample. Provided that values are calculated from parallel titration curves, reproducible PAI-cap values at different dilutions of a sample are obtained. This assay can be applied for the determination of PAI-cap in plasma, serum and other biological fluids as platelet releasates and endothelial cell conditioned medium. PAI-cap of plasma of 10 healthy male volunteers ranged from 15.3 to 32.3 arbitrary inhibitor units AU/ml (24.5 +/- 5.2, mean +/- SD). The alternative use of three different anticoagulants (citrate, EDTA, heparin) had no influence on PAI-cap determinations. Serum generated from blood contained a mean of PAI-cap of 129% in comparison to the plasma of the same donor indicating the release of PAI from cells during clotting. Plasma PAI-cap changed during the day with a constant decrease from the highest levels in the morning (100%) to low levels in the evening (62.9%). Platelets aggregated by thrombin released plasminogen activator inhibitor amounting to a mean PAI-cap of 4.33 +/- 2.98 AU per 2.5 X 10(8) cells.

Anticoagulants↗
PubMed1975

Cirrhosis of choline deficiency in the Rhesus Monkey. Possible role of dietary cholesterol (38541).

One of five rhesus monkeys fed a diet deficient in choline and protein for 31 mo developed signs of cirrhosis at 26 mo. Five other monkeys were fed the same diet for 14 mo, at which time cholesterol comprising 2% of the diet was added. Three followed a sharp rise in hepatic lipids. One monkey developed marked hypercholesterolemia and showed signs of cirrhosis 2 mo after cholesterol supplementation. The findings indicate that the rhesus monkey is susceptible to choline-deficiency cirrhosis. They suggest that cholestrol supplementation accelerates this process.

Animals↗