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Biomedical subjects

J Lindon

Publications and source records attributed to J Lindon.

10 recordsLinked to original sources
PubMed1994

A multi-dimensional model of groupwork for adolescent girls who have been sexually abused.

This paper describes a treatment approach for sexually abused adolescent girls using a group work model. The model incorporates three treatment modalities: a skills component, a psychotherapeutic component, and an educative component. The group ran for 16 sessions over a 6-month period and each girl was assessed prior to joining the group. The girls were again assessed at the end of treatment and a 6-months follow-up; all of them showed improvement on self-statements (outcome) and on behavioral measures assessed by others (follow-up). Girls who had been sexually abused demonstrated difficulties in many areas of their lives following abuse. These problems related to their feelings of guilt and helplessness in relation to both themselves and their abuser. Sexually abused children often have poor knowledge of sexual matters and demonstrate confusion over their own body image. Using a multidimensional model the problems following abuse can be addressed.

Adaptation, Psychological↗
PubMed1993

Effects of free and macromolecular-bound TXA2 receptor antagonist BM 13.505 on U46619-induced platelet aggregation.

The goal of this study was to synthesize a macromolecular probe of the TXA2 receptor antagonist BM13.505 which is unable to penetrate the platelet membrane for localization and characterization of the TXA2 receptor. The active NHS-ester of BM13.505 was synthesized and purified. It was used for covalent coupling of BM13.505 to bovine serum albumin, a macromolecular carrier. Inhibitory effects of free and macromolecular bound BM13.505 on aggregatory properties of U46619-stimulated platelets were measured and compared to TXA2 generation in platelets, as determined by TXB2 radioimmunoassay. No inhibitory effects of free and macromolecular-bound BM13.505 on ADP- or thrombin-induced platelet aggregation were observed. Equimolar concentrations of free or macromolecular bound BM13.505 inhibited U46619-induced platelet aggregation and TXA2 generation with equal potency. IC50-values for platelet aggregation inhibition by free and macromolecular bound BM13.505 were 64 nM and 96 nM respectively. It appears that the TXA2 receptor ligand binding site is located close to the outer membrane surface of platelets. Interaction of macromolecular bound BM13.505 with the platelet thromboxane receptor does not depend on the availability of the free carboxyl residue in BM13.505. The method for coupling a TXA2 receptor antagonist to a macromolecule will aid in constructing probes for the localization and characterization of the TXA2 receptor.

Adenosine Diphosphate↗
PubMed1989

Activity toward thrombin-antithrombin of heparin immobilized on two hydrogels.

Commercially obtained (Diosynth) heparin was covalently bonded to poly (vinyl alcohol) (PVA) hydrogels and to polyethylene oxide (PEO) hydrogels activated by tresyl chloride. We found that as tresyl chloride activation of PVA increased, the specific activity of the bound heparin toward thrombin and antithrombin decreased by nearly a factor of 10 and that commercial heparin bound to PEO had nearly ten-fold greater activity than when bound to PVA at comparable concentrations. These findings suggest that the long 'leash' provided by PEO hydrogels may give the heparin more access to the thrombin-antithrombin pair than the tight bond to PVA, and that crowding of heparin units on a surface limits access of the thrombin-antithrombin pair.

Antithrombins↗
PubMed1986

Crosslinked polyether/polysiloxane networks for blood-interfacing applications.

The interaction of blood with new artificial surfaces is an area of continual medical interest. In this study, a series of polyether/polysiloxane networks were synthesized, characterized in terms of both bulk and surface compositions, and evaluated for blood compatibility. The crosslinked networks were produced by reacting the epoxy groups of polyglycidoxy propyl methyl siloxane (PGPMS) with the hydroxyl end groups of polypropylene glycol (PPG). Blood compatibility was evaluated using an in vitro platelet retention test and fibrinogen adsorption experiments from human plasma and buffered saline. The PPG/PGPMS networks exhibit low fibrinogen adsorption and low platelet activation. Such properties make the networks potentially attractive as materials for blood-interfacing applications.

Adsorption↗
PubMed1986

Fibrinogen adsorption and platelet adhesion at the surface of modified polypropylene glycol/polysiloxane networks.

The protein film adsorbed at an artificial surface ultimately affects platelet adhesion and activation. This study examines the role of fibrinogen in platelet adhesion at the surface of crosslinked polypropylene glycol (PPG)/polyglycidoxy propyl methyl siloxane (PGPMS) networks which contain polyethylene glycol monomethyl ether (PEGME) chains. These crosslinked networks were produced by reacting the epoxy groups of PGPMS with the hydroxyl groups of the polyethers. PEGME chains were attached covalently to the network at only one end while PPG chains were attached at both ends. The incorporation of PEGME resulted in a substantial reduction in fibrinogen adsorption as compared to the model network (PPG + PGPMS only), but the expected concomitant decrease in platelet adhesion was not observed.

Adsorption↗
PubMed1984

Interactions of human platelets with insoluble anticoagulant modified polystyrene resins.

The interactions of two insoluble anticoagulant polystyrene derivatives with human platelets were studied in an in vitro system similar to a chromatography column. Blood was pumped through the column and platelets were counted before and after passage through the column. Interaction of platelets with the beads led to retention of platelets in the column. The same experiment was performed with several donors. Different pretreatments were assayed and compared for both materials: platelet poor plasma, antithrombin III-depleted platelet poor plasma and an antithrombin III solution. Platelet retention depends on the polymer composition: the material containing glutamic acid sulphamide groups, which has a larger anticoagulant activity in plasma than the materials only substituted by sulphonate groups, is always less reactive towards platelets. The differences in the effects of pretreatment on both materials can be correlated with the variations of antithrombin adsorption on the synthetic surfaces.

Anticoagulants↗
PubMed1981

Platelets and artificial surfaces: the effects of drugs.

Contact of blood with a foreign surface activates platelets and leads to their consumption. This property is shared by most non-biological materials, including air, but can be reduced by an optimal balance of hydrophobicity and hydrophilicity, minimal capacity for hydrogen bonding, avoidance of crystallinity, maintenance of polymer backbone mobility, and other manipulations of the chemistry of the polymer. None the less, no totally non-thrombogenic artificial surface has been developed. Attention has therefore turned to suppression of platelet-surface interaction by drugs that alter platelet function. Agents that block cyclo-oxygenase inhibit surface-induced secretion and aggregation but have no effect on platelet adhesion. Drugs that increase platelet cyclic AMP levels have a dose-related effect, which at high concentrations can eliminate adhesion to surfaces. The most successful agent, prostacyclin, has achieved total protection of platelets during cardiopulmonary bypass, with preservation of normal platelet number and function. Associated vasodilatation is a notable side effect, and hypotension may prove to be a significant problem in clinical practice. The development of more selective analogues with minimal vasodepressor activity is to be encouraged.

Acrylates↗
PubMed1978

Interaction of human platelets with heparinized agarose gel.

Platelet interaction with surfaces to which heparin had been covalently bonded was investigated with a chromatographic technique employing agarose gel beads heparinized via a cyanogen bromide reaction. Heparinization significantly increased platelet retention by the gel. Platelet retention was unchanged after pretreatment of the heparinized gel with albumin but increased after pretreatment with fibrinogen. Pretreatment with plasma or purified AT III decreased platelet retention. Reduction in platelet retention was correlated with the amount of AT III removed from plasma. Plasma with decreased levels of AT III was less effective in surface passivation. Pretreatment of heparinized gel with PF4 or protamine sulfate did not decrease platelet retention, but subsequent exposure to plasma did. The results suggest that a surface with covalently bonded heparin is reactive toward platelets but can be passivated by formation of a heparin/AT III complex.

Albumins↗