
Peripheral sensitization indicates increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation, which usually occurs after peripheral tissue injury and inflammation.As an integral part of pain, peripheral sensitization and its mechanisms have received much attention, and numerous types of neurotransmitters and chemicals related to peripheral sensitization were investigated.We developed an animal model of peripheral sensitization, and it provides evidence that some neurotransmitters, such as glutamate and substance P, release from adjacent peripheral nerves contributing to the peripheral sensitization of pathological pain.In this chapter, we reviewed the advances in peripheral sensitization, and it will provide a basis for new targets to attenuate pain of peripheral origin.
Clinical and Experimental DermatologyVolume 1, Issue 1 p. 37-50 Original article Pityriasis rubra pilaris-an historical approach 2 CLINICAL FEATURES W.A.D. GRIFFITHS, W.A.D. GRIFFITHS Department of Dermatology, Liverpool Royal Infirmary, Pembroke Place, Liverpool L3 5POSearch for more papers by this author W.A.D. GRIFFITHS, W.A.D. GRIFFITHS Department of Dermatology, Liverpool Royal Infirmary, Pembroke Place, Liverpool L3 5POSearch for more papers by this author First published: March 1976 https://doi.org/10.1111/j.1365-2230.1976.tb01397.xCitations: 52AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume1, Issue1March 1976Pages 37-50 RelatedInformation
In Sézary's syndrome (SS), cutaneous manifestations are associated with an abnormal mononuclear cell in the blood. Clinically, the differential diagnosis with Mycosis fungoides is impossible. However, some of the symptoms are more in favor of SS, such as leonin face, palm and sole hyperkeratosis and changes in pigmentation. The diagnosis of SS rests upon the identification on ordinary blood smears of a lymphocytic cell, the size of which is variable and which exhibits a grooved, folded and lobulated nucleus. This cell is negative for both esterases and peroxydases. It is not a monocyte. Large cells have big nuclei with tetraploid DNA values, whereas small variants have near diploid values. Chromosome analysis may reveal near hypertetraploid, hyper or hypodiploid counts. Marker chromosomes have been seen which could be common to all types. However, many cases are known in which the karyotype was normal. In addition, there are cases in which chromosome analysis was impossible due to poor responses of the Sézary cells to PHA. As regards surface markers, there is general agreement that Sézary's cells are non-B lymphocytes. In some cases, the cells had both T markers (antigen and E-rosettes), whereas in others, only one (antigen) was expressed. In still other cases, the abnormal blood cell had neither B nor T markers. In at least one case, the cells had both B and T surface receptors. The diversity of the Sézary's cell would be explained by the immunologic pressure exerted upon skin lymphocytes by the epidermis due to a change in the antigenicity of this tissue in relation to ageing or to the presence of exogenous chemicals, or to physically induced mutations. Recent studies from this laboratory, using autoradiography after incorporation of tritiated thymidine, have shown labelled lymphocytes in the skin of three out of four cases of SS. These results suggest that cutaneous manifestations in SS, as well as in Mycosis fungoides, are comparable to a chronic Graft-Versus-Host reaction (GVH).