Solid-Phase Synthesis of Fluorinated Analogues of Glycosyl 1-Phosphate Repeating Structures from Leishmania using the Phosphoramidite Method.

Bacterial and protozoan sugar chains contain glycosyl 1-phosphate repeating structures; these repeating structures have been studied for vaccine development. The fluorinated analogues of [ß-Gal-(1→4)-α-Man-(1→6)-P-] n , which are glycosyl 1-phosphate repeating structures found in Leishmania, were synthesised using the solid-phase phosphoramidite method. This method has been less extensively studied for the synthesis of glycosyl 1-phosphate units than H-phosphonate chemistry. A stepwise synthesis of a compound containing five such repeating units has been conducted using the phosphoramidite method herein, which is the longest glycosyl 1-phosphate structures to be chemically constructed in a stepwise manner.

English version of the concluding report published in 2001 by the Advisory Committee on Atopic Dermatitis Severity Classification Criteria of the Japanese Dermatological Association.

The Japanese Dermatological Association established an advisory committee in 1995 to develop a severity scoring system for atopic dermatitis (AD). Its interim and concluding reports were published in Japanese in the Japanese Journal of Dermatology (108: 1491-1496, 1998 and 111: 2023-2033, 2001). Because of the strong demand for an English version, we have decided to publish the reports in English. This manuscript is the English version of the concluding report. The interim report suggested that eruption components such as erythema, papule, erosion, crust, excoriation and lichenification with extent of involved areas in five body regions, including the head and neck, anterior and posterior trunks, and upper and lower limbs, were important items for assessing AD severity. Additionally, it was recommended that streamlining of eruption components was mandatory for improving the statistical validity and reliability. The committee members subsequently concentrated their efforts on this task, and finally proposed an Atopic Dermatitis Severity Classification Criteria of the Japanese Dermatological Association.

Detection, epitope-mapping and function of anti-Fas autoantibody in patients with silicosis.

Dysregulation of apoptosis through the Fas-Fas ligand pathway is associated with the onset of autoimmune disease. Since autoantibodies directed against unknown antigens are present in the sera of these patients, sera samples were examined for the presence of autoantibodies directed against the Fas molecule. Using Western blotting and a ProteinChip analysis, autoantibodies against Fas were detected in patients with silicosis, systemic lupus erythematosus (SLE) and systemic sclerosis (SSc), and weakly detected in healthy individuals. Using epitope mapping employing 12-amino-acid polypeptides with the SPOTs system, a minimum of four epitopes and a maximum of 10 epitopes were found. Several amino acid residues involved in binding FasL, such as C66, R87, L90, E93 and H126, were presented within the epitopes. Serum containing a large amount of anti-Fas autoantibody from silicosis patients inhibited the growth of a Fas-expressing human cell line, but did not inhibit the growth of a low Fas-expresser nor a Fas-expresser in which the Fas gene had been silenced by small interference RNA. All epitopes in the intracellular region of Fas were located in the death domain. The possible roles of anti-Fas autoantibody detected in healthy volunteers and patients with silicosis or autoimmune diseases are discussed here.

Koebner phenomenon in lupus erythematosus with special consideration of clinical findings.

The isomorphic response of Koebner can be observed not only in psoriasis, but also in other diseases, such as lichen planus and some systemic diseases including LE (lupus erythematosus) or sarcoidosis. Several clinical findings in LE skin were presented and discussed in this review. The mutually-interactive-, negative-, and internal-Koebner phenomena were introduced and discussed with some speculative views. Many forms of environmental stress on the skin were reported as provocating factors of the Koebner phenomenon, including trauma, scratching, UV-exposure, and various types of dermatitis. Clinical observations of the nature, localization, and movement of lesions should be carefully made. The pathophysiology of the Koebner phenomenon may be classified into two steps. A first non-specific inflammatory step and a second disease-specific step. The inflammatory products released from the first step would be targeted in the second step. In the first step, there could be many substances including cytokines, stress proteins, adhesion molecules, or autoantigens translocated from intra-cellular areas. In the second step after latent periods, there may be disease-specific reactions, including ones by T-cells, B-cells, autoantibodies, and immune deposits, under the restriction of genetic backgrounds. The Koebner phenomenon may prove useful in understanding the pathophysiology of diseases of unknown origin.