University of Bedfordshire

About: University of Bedfordshire is a education organization based out in Luton, Bedford, United Kingdom. It is known for research contribution in the topics: Population & Context (language use). The organization has 3860 authors who have published 6079 publications receiving 143448 citations. The organization is also known as: University of Luton.

Frey's syndrome after parotid surgery.

Abstract: The operative records of seventy-one patients who had parotid surgery carried out in the ten year period from 1964 to 1973 were reviewed. Forty-one (67%) of the operations were suprafacial parotidectomies. Of the fifty patients who agreed to reassessment in a special clinic, seventeen had a noticeable degree of Frey's syndrome, and of these fourteen were submitted to further investigations. Minor's test in these fourteen patients showed the greater auricular nerve to be involved in six patients, the ariculotemporal nerve in four, and both nerves in two. The results in two patients were inconclusive. Because the starch test reveals only the distribution of the gustatory sweating, a useful adjunct is described for investigating Frey's syndrome. By blocking of the contralateral greater auricular nerve in the neck and mapping out of the anesthetized area, its sensory distribution is demonstrated. We conclude that it is manifestly unwise to avulse the auriculotemporal nerve if the sweating occurs in the distribution of the greater auricular nerve.

Spleen Tyrosine Kinase Inhibition Attenuates Autoantibody Production and Reverses Experimental Autoimmune GN

Abstract: Spleen tyrosine kinase (SYK) has an important role in immunoreceptor signaling, and SYK inhibition has accordingly attenuated immune-mediated injury in several in vivo models. However, the effect of SYK inhibition on autoantibody production remains unclear, and SYK inhibition has not been studied in an autoimmune model of renal disease. We, therefore, studied the effect of SYK inhibition in experimental autoimmune GN, a rodent model of antiglomerular basement membrane disease. We show glomerular SYK expression and activation by immunohistochemistry in both experimental and clinical disease, and we show that treatment with fostamatinib, a small molecule kinase inhibitor selective for SYK, completely prevents the induction of experimental autoimmune GN. In established experimental disease, introduction of fostamatinib treatment led to cessation of autoantibody production, reversal of renal injury, preservation of biochemical renal function, and complete protection from lung hemorrhage. B cell ELISpot and flow cytometric analysis suggest that short-term fostamatinib treatment inhibits the generation and activity of antigen-specific B cells without affecting overall B-cell survival. Additionally, fostamatinib inhibited proinflammatory cytokine production by nephritic glomeruli ex vivo and cultured bone marrow-derived macrophages in vitro, suggesting additional therapeutic effects independent of effects on autoantibody production that are likely related to inhibited Fc receptor signaling within macrophages in diseased glomeruli. Given these encouraging results in an in vivo model that is highly applicable to human disease, we believe clinical studies targeting SYK in GN are now warranted.