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Biomedical subjects

L McKeown

Publications and source records attributed to L McKeown.

8 recordsLinked to original sources

The discourse of dental hygiene practice in Canada.

Recently the discourse in Canada relating to dental hygiene practice has changed. While dentistry still exercises controlling power over the public's oral cavity, dental hygienists have made inroads through legislative changes. A description of Canadian dental hygiene practice is provided to set the stage for a discussion about current discourse in the dental hygiene profession. Although power is often perceived as a shifting changing set of relations, these can be frozen in abstraction. It is rather like taking a photo of a single moment or event in an ongoing activity. This moment provides a starting point, an event that can be analysed. Four such events are evident in Canadian dental hygiene practice; they include, education, recognition of dental hygienists as primary care providers, the culture of dental hygiene and self-regulation. While all the events are important, self-regulation is critical to the viability and development of the profession. It is the central event that provides the backdrop for effecting change. With self-regulation comes responsibility and accountability for professional actions. It also provides possibilities for changing the discourse in oral care. As oral health care discourse is transformed through legislation and public awareness, the public will, hopefully, be able to directly access dental hygiene services, and dental hygienists themselves might increasingly recognise their importance as contributors in the health care system.

Canada↗

Social relations and breath odour.

In this retrospective qualitative study, the researcher reviewed 55 client records of The Breath Odour Clinic. The purpose was to determine if individuals attended a clinic specialised in treating oral malodour for medical or social reasons. The study focused on the psychosocial and breath odour history. Clients had agreed to the use of information for research purposes. Society uses odour as a means to define and interact with the world. The olfactory, smelling experience is intimate, emotionally charged and connects us with the world. It follows that the smell from mouth breath odour can connect or disconnect a person from their social environment and intimate relationships. How one experiences one's own body is very personal and private but also very public. Breath odour is public as it occurs within a social and cultural context and personal as it affects one's body image and self-confidence. Body image, self-image and social relations mesh, interact and impact upon each other. Breath odour is a dynamic and interactive aspect of the self-image. In addition, breath odour may be value-coded as 'bad'. In 75% of the cases reviewed, decreased self-confidence and insecurity in social and intimate relations led clients to seek treatment at the specialised breath odour clinic. Their doctor, dental hygienist or dentist had treated medical and oral conditions but not resolved their breath odour problem. When a person perceives a constant bad breath problem, she/he uses defence techniques, and may avoid social situations and social relations. This affects a person's well-being.

Adolescent↗

Basal joint arthritis: trapeziectomy with ligament reconstruction and tendon interposition arthroplasty.

This article provides a qualitative and quantitative outcomes assessment of a consecutive series of 27 patients (30 thumbs) with basal joint arthritis of the thumb undergoing ligament reconstruction and tendon interposition arthroplasty. Outcome analysis revealed that 24 (89%) patients were satisfied with the relief of pain provided by the arthroplasty and 23 (87%) would undergo surgery again. Eighteen (67%) thumbs were noted to have improvement in the ability to perform activities of daily living. Significant improvements were noted in web space measurements and in grip and pinch strength determination. X-ray film assessment using the trapezial space ratio averaged 0.33 +/- 0.08 in preoperative x-ray films of thumbs with stage III and IV degenerative arthritis and 0.23 +/- 0.07 in thumbs following basal joint arthroplasty. This represents a total decrease of 51% in the trapezial space ratio following arthroplasty compared to the normal values obtained in previous studies and 33% compared to the preoperative values obtained in this study. Outcomes assessment at a mean of 42 months after surgery showed that there was no significant correlation between maintenance of trapezial height and both objective and subjective clinical outcomes. Although ligament reconstruction consistently failed to restore trapezial height, primary and secondary clinical outcomes following basal joint arthritis were almost uniformly satisfactory.

Activities of Daily Living↗

Platelet adhesion to collagen in individuals lacking glycoprotein IV.

The Naka isoantigen is expressed on glycoprotein (GP) IV (CD36), a platelet membrane GP that has been identified as having a role in platelet interactions with collagen and thrombospondin and in binding Plasmodium falciparum-infected erythrocytes to endothelial cells and melanoma cells. We have studied normal platelets and Naka- platelets from two Japanese donors that have 1% of GPIV by concentration-dependent antibody binding and flow cytometry. We studied the adherence of normal and Naka- platelets to types I, III, and IV collagen in static and to type I collagen in flowing systems at high shear force. We have also studied aggregation of normal and Naka- platelets to type I collagen. Naka- platelets showed normal or increased aggregation to type I collagen and normal adhesion to types I, III, and IV collagen in the presence of Mg++ or EDTA. Platelet aggregation and adhesion were inhibited by the anti-alpha 2 beta 1 antibody 176D7 to the same extent in Naka- as in normal platelets. We also studied endogenous thrombospondin surface expression and found that thrombin-stimulated Naka- platelets expressed the same amount of thrombospondin as did normal platelets. From our studies with Naka- platelets, we cannot identify a definitive role for GPIV in platelet aggregation, in adhesion to types I, III, and IV collagen, or in endogenous thrombospondin binding to platelets.

Antigens, CD↗

Platelet adhesion to collagen types I through VIII under conditions of stasis and flow is mediated by GPIa/IIa (alpha 2 beta 1-integrin).

Platelet adhesion to fibrillar collagens (types I, II, III, and V) and nonfibrillar collagens (types IV, VI, VII, and VIII) was investigated in the presence of physiologic concentrations of divalent cations under conditions of stasis and flow. Under static conditions, platelet adhesion was observed to collagen types I through VII but not to type VIII. Under flow conditions, platelet adhesion to collagen types I, II, III, and IV was almost independent of shear rates above 300/s. Collagen type V was nonadhesive. Platelet adhesion to collagen type VI was shear rate-dependent and optimal at a rate of 300/s. Collagen types VII and VIII showed minor reactivity and supported platelet adhesion only between shear rates 100 to 1,000/s. Monoclonal antibody (MoAb) 176D7, directed against platelet membrane glycoprotein Ia (GPIa; very late antigen [VLA]-alpha 2 subunit), completely inhibited platelet adhesion to all collagens tested, under conditions of both stasis and flow. Platelet adhesion to collagen type III at shear rate 1,600/s was only inhibited for 85%. The concentration of antibody required for complete inhibition of platelet adhesion was dependent on the shear rate and the reactivity of the collagen. An MoAb directed against GPIIa (VLA-beta subunit) partially inhibited platelet adhesion to collagen. These results show that GPIa-IIa is a major and universal platelet receptor for eight unique types of collagen.

Antibodies, Monoclonal↗

A monomeric von Willebrand factor fragment, Leu-504--Lys-728, inhibits von Willebrand factor interaction with glycoprotein Ib-IX [corrected].

von Willebrand factor interaction with glycoprotein Ib alpha (GPIb alpha) plays a critical role in the initial phase of platelet adhesion at high shear rates, and it may also play a role in platelet thrombus formation in partially occluded arteries. Previous studies have indicated that two peptides, Cys-474--Pro-488 (peptide 153) and Ser-692--Pro-708 (peptide 154), inhibit von Willebrand factor--GPIb alpha interaction. We have expressed a recombinant fragment of von Willebrand factor, Leu-504--Lys-728 [corrected], with a single intrachain disulfide bond linking residues Cys-509--Cys-695 and examined its ability to inhibit von Willebrand factor--GPIb alpha interactions and platelet adhesion at high shear forces. This recombinant fragment, named VCL, inhibits ristocetin-induced, botrocetin-induced, and asialo-von Willebrand factor-induced platelet aggregation and binding to platelets at an IC50 = 0.011-0.260 microM, significantly lower than the IC50 of peptide 153 or 154, IC50 = 86-700 microM. Peptides 153 and 154 did not result in any inhibition of platelet adhesion (IC50 greater than 500 microM). In contrast, VCL inhibited 50% of platelet adhesion at 0.94 microM and at 7.6 microM inhibited greater than 80% of platelet adhesion to human umbilical artery subendothelium at high shear forces. VCL inhibited the contact and spreading of platelets and also caused a marked decrease in thrombus formation. These studies indicate that VCL may be an effective antithrombotic agent in preventing arterial thrombus formation in areas of high shear force.

Amino Acid Sequence↗

Endogenous platelet fibrinogen: its modulation after surface expression is related to size-selective access to and conformational changes in the bound fibrinogen.

Platelet stimulation results in the release of endogenous platelet fibrinogen which binds to the platelet surface. Previous studies have demonstrated that plasma fibrinogen bound to activated platelets becomes inaccessible to a variety of probes. We have studied endogenous platelet fibrinogen binding to activated platelets by employing an immunopurified polyclonal anti-fibrinogen antibody and F26, a monoclonal anti-fibrinogen antibody, which recognizes fibrinogen only when it is bound to a surface. Employing the Ig or F(ab')2 of the poly- or monoclonal antibody we found a marked decrease of fibrinogen accessibility 30-60 min after platelet activation. In contrast, platelet-bound fibrinogen remains accessible to the Fab fragment of F26 at a constant level for 30 min and increases at 60 min. The reduction of the polyclonal Fab fragment binding at 30 and 60 min is similar to the F26 Ig. These results indicate that the decreased accessibility of bound fibrinogen is related to two mechanisms; (1) that the access route to fibrinogen in size selective for the antibody probes and only small antibody probes, e.g. Fab fragments, can gain access to fibrinogen and (2) fibrinogen undergoes a conformational change(s) after binding which exposes at least one neo-epitope in the D domain of fibrinogen and which may decrease or mask the reactivity of other fibrinogen domains. Only the F26 Fab probe has full access to and identifies fibrinogen present on the platelet surface 60 min after stimulation.

Antibodies, Monoclonal↗

Endogenous platelet fibrinogen surface expression on activated platelets.

Intracellular platelet fibrinogen surface expression was studied in arabinogalactan-purified, resting, and thrombin-stimulated platelets. Platelet fibrinogen is derived from endocytosis of plasma fibrinogen by megakaryocytes. Like a variety of other adhesive proteins, it is stored in the platelet alpha-granule. Platelet fibrinogen surface expression was studied by using the antigen-binding fragments of a murine monoclonal antibody to platelet fibrinogen, F26, and an immunopurified polyclonal antifibrinogen antibody. Studies correlating platelet fibrinogen surface expression with the presence of the glycoprotein IIb-IIIa (GPIIb-IIIa) complex showed that in the presence of ethylene glycol tetraacetic acid (EGTA) at 37 degrees C, neither the GPIIb-IIIa complex nor platelet fibrinogen was expressed on the surface of thrombin-activated platelets. Similar experiments performed in the presence of EGTA and calcium showed proportional expression of the GPIIb-IIIa complex and platelet fibrinogen. The addition of Arg-Gly-Asp-Ser-containing peptides, the pentadecapeptide of the fibrinogen gamma-chain carboxy terminus, or the monoclonal antibody 10E5, when directed against the GPIIb-IIIa complex before thrombin activation, inhibited 65% to 94% of the platelet fibrinogen expression, as determined with the polyclonal and monoclonal antigen-binding fragments. When these same inhibitory agents were added immediately after or 5 minutes after thrombin, the amount of inhibition decreased significantly. Similar studies with a washed platelet system revealed that when the inhibitors of platelet fibrinogen expression were added before thrombin stimulation, the degree of inhibition observed was only 24% to 38%. This suggests that the major portion of platelet fibrinogen expression involves the release of platelet fibrinogen and its subsequent binding to GPIIb-IIIa. This binding may occur within the open canalicular system or on the platelet surface; in either case, wherever the site of released platelet fibrinogen binding occurs, it can be markedly inhibited by the RGD-containing peptides and the gamma-chain fibrinogen peptides. Approximately 10% to 30% of platelet fibrinogen may be expressed prebound to a platelet receptor, or else it is released and binds to a platelet receptor other than the GPIIb-IIIa complex.

Amino Acid Sequence↗