Monoclonal antibodies to human platelet glycoprotein IIb beta that initiate distinct platelet responses

Hybridomas secreting monoclonal antibodies (MoAbs) to human platelet membrane glycoprotein IIb (GPIIb) were prepared by fusing cells of a mouse myeloma line to spleen cells from a BALB/c mouse immunized with purified GPIIb. Six of the hybridomas secreted MoAbs that recognized epitopes on the 23,000-dalton, disulfide-linked subunit of GPIIb, GPIIb beta. All six of these MoAbs agglutinated platelets in the absence of calcium. The agglutination titers of three of the MoAbs, however, were enhanced between 2 and 6 log2 dilutions when titrated in the presence of mmol/L of calcium. The enhancement in titer was the result of MoAb- induced platelet activation followed by platelet aggregation, a reaction that could also be initiated by the monovalent Fab fragments prepared from one of the MoAbs. The MoAbs did not significantly agglutinate platelets from patients with Glanzmann's thrombasthenia, confirming biochemical evidence that there is a paucity of GPIIb beta in the membranes of these cells. Our results show that MoAbs to epitopes on GPIIb beta initiate distinct platelet responses; therefore, they should be useful for studying the ways in which regions of surface glycoproteins are involved in platelet-platelet interactions. In addition, these reagents may prove of value in diagnosing and typing patients with Glanzmann's thrombasthenia.     

The new consultation: developing doctor-patient communication. David Pendleton, Theo Schofield, Peter Tate, Peter Havelock (eds). (143 pages, {pound}19.95.) Oxford University Press, 2003. ISBN 0-19-263288

The consultation is the core of medicine. Consultations makeup more than two-thirds of the workload of a family doctor,but the number of books on the topic is surprisingly small.Those who have read these authors' first book     

Meningitis caused by Pseudomonas maltophilia.

A case of meningitis caused by Pseudomonas maltophilia is described, which was unusual in that it appeared to lack the predisposing factors commonly associated with this organism. Attention is drawn to the difficulties which may be encountered in the identification of Ps. maltophilia.     

Dietary chelators as antioxidant enzyme mimetics: implications for dietary intervention in neurodegenerative diseases

Following recent reviews on the role of metal ions in oxidative stress and neurodegenerative diseases, this article reports advances in the study of dietary components for the control of these conditions. Poor metal ion homeostasis is credited with pathological roles in the progression of a number of disorders including Alzheimer's disease, Parkinson's disease and multiple sclerosis. Synthetic metal ion chelators continue to show promise as a new therapeutic approach for neurodegenerative disorders. Dietary chelators, unlike most vitamins, are, however, capable of negating or even reversing the roles of metal ions by: (i) decorporation of metal ions, (ii) redox silencing, (iii) dissolution of deposits, and (iv) generation of an antioxidant enzyme mimetic. This review gives a critical evaluation of recent progress in, and potential for, dietary control of neurodegeneration on the basis of the formation of antioxidant enzyme mimetics.