SUMMARYWe set out to examine if the IgG-producing cells in the colonic mucosa in UC are committed to tropomyosin isoform 5 (hTM5), a putative autoantigen in UC. Lamina propria mononuclear cells (LPMC) were isolated from colonoscopic biopsy specimens from recto-sigmoid and proximal colon. Twenty-three patients with UC, eight with Crohn's colitis (CC), and 10 non-inflammatory bowel disease (non-IBD) controls were included. The ELISPOT assays were used to quantify lamina propria B cells producing total immunoglobulin (IgA, IgG, IgM), IgG, IgA, as well as IgG against hTM5 isoform. The median value of percentage of total IgG-producing lymphocytes was similar in UC (12%) and CC (11%), but was significantly (P , 0´0002) higher than non-IBD controls (6%). However, in UC, but not in CC and non-IBD, a large number of lamina propria B cells produced IgG against hTM5 (median values: UC 42%, CC 2´5%, non-IBD 0%). This difference in UC when compared with CC and non-IBD was highly significant (P , 0´00001). Twenty-one of 23 (91%) patients with UC had percentage of antihTM5 IgG-producing immunocytes more than 2 s.d. above the mean for non-UC patients. In UC but not in CC and non-IBD controls, the increased number of IgG-producing cells are largely committed to produce IgG against hTM5-related epitope(s).

SUMMARYColonic administration of a hapten, 2,4,6-trinitrobenzene sulphonic acid (TNBS) has been shown to induce colitis in rats. We are using this model to investigate the role of colonic antigens in the immunopathology. In this study, we show that colitis can be suppressed by oral administration of haptenized colonic antigens prior to the TNBS enema. Moreover, our data suggest that haptenization of the colonic antigens is not essential because oral feeding of non haptenized colonic antigens too protects rats from TNBS-induced colitis. Thus, unmodified colonic antigens may be involved in the induction of oral tolerance, and possibly in the pathogenesis in this model of colitis. Further, we show that the protective immunity or oral tolerance induced by non haptenized colonic antigens can be passively transferred to naõ Ève rats by mesenteric T lymphocytes. Interestingly, oral feeding of small intestinal antigens, haptenized and non haptenized, does not protect rats from colitis, suggesting a specific role for colonic antigens. These data underscore the usefulness of this rat model in the identification of pathogenic antigens in colitis and in the development of therapeutic strategies based on oral tolerance.

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In this study, the authors discuss unsupervised separation of two speakers from single microphone recording using empirical mode decomposition (EMD) and Hilbert transform (HT) generally known as Hilbert-Huang transform. A two-stage separation procedure is proposed for single-channel (SC) speech separation. Initial stage of separation is done using EMD, HT and instantaneous frequencies. EMD decomposes the mixed signal into oscillatory functions known as intrinsic mode functions (IMFs). Suitable IMFs are selected using successive EMD decomposition and HT is applied to extract the instantaneous frequencies. The speech frames are grouped into two speakers using correlation of instantaneous frequencies between mixed signal and selected IMFs. Second-stage separation is done by further decomposing the estimated speakers into IMFs and finding the instantaneous amplitudes using HT. A ratio of instantaneous amplitudes of mixed speech and stage 1 recovered speech signal is computed for both speakers. Histogram of the ratio obtained can be used to estimate the ideal binary mask for each speaker. These masks are applied to the speech mixture and the underlying speakers are estimated. The proposed method was compared with the existing unsupervised SC source separation algorithms. The results show significant improvement in objective measures.

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