| 1. |
|
|
| 2. |
- Akselsson, Roland, et al.
(författare)
-
Multidisciplinary Research on Integration of Human Factors and Production Concepts such as TQM - A Participatory Discussion Session
- 1999
-
Ingår i: Proceedings of the Conference on TQM and Human Factors. - 9172195207 ; 2, s. 439-448
-
Konferensbidrag (refereegranskat)abstract
- A discussion session where the conference participants are invited to participate is planned. One topic for the session is to discuss experiences of multidisciplinary research on integration of human factors and different production concepts applied in change processes within Swedish companies. An important question that the discussion will focus on is: How to get high quality in multidisciplinary research? Another topic is to discuss how people from different disciplines in the companies interact with each other and with the researchers. Researchers from the centre Change@Work at Lund University in Sweden will present some of their experiences from several years of multidisciplinary research in companies. As a background the research questions within Change@Work are presented below. Discussions during the workshop will be performed according to methods used by the researchers in their research in the companies. All discussion will be documented and later sent to all workshop participants.
|
|
| 3. |
|
|
| 4. |
- Ohlsson, Jörgen, et al.
(författare)
-
Structure–activity relationships of galabioside derivatives as inhibitors of E. coli and S. suis adhesins: nanomolar inhibitors of S. suis adhesins
- 2005
-
Ingår i: Organic and Biomolecular Chemistry. - : Royal Society of Chemistry (RSC). - 1477-0539 .- 1477-0520. ; 3:5, s. 886-900
-
Tidskriftsartikel (refereegranskat)abstract
- Four collections of Gal1-4Gal derivatives were synthesised and evaluated as inhibitors of the PapG class II adhesin of uropathogenic Escherichia coli and of the PN and PO adhesins of Streptococcus suis strains. Galabiosides carrying aromatic structures at C1, methoxyphenyl O-galabiosides in particular, were identified as potent inhibitors of the PapG adhesin. Phenylurea derivatisation at C3 and methoxymethylation at O2 of galabiose provided inhibitors of the S. suis strains type PN adhesin with remarkably high affinities (30 and 50 nM, respectively). In addition, quantitative structure–activity relationship models for E. coli PapG adhesin and S. suis adhesin type PO were developed using multivariate data analysis. The inhibitory lead structures constitute an advancement towards high-affinity inhibitors as potential anti-adhesion therapeutic agents targeting bacterial infections.
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
- Aoun, M., et al.
(författare)
-
Antigen-presenting autoreactive B cells activate regulatory T cells and suppress autoimmune arthritis in mice
- 2023
-
Ingår i: Journal of Experimental Medicine. - Stockholm : Karolinska Institutet, Dept of Medical Biochemistry and Biophysics. - 0022-1007 .- 1540-9538. ; 220:11
-
Tidskriftsartikel (refereegranskat)abstract
- B cells undergo several rounds of selection to eliminate potentially pathogenic autoreactive clones, but in contrast to T cells, evidence of positive selection of autoreactive B cells remains moot. Using unique tetramers, we traced natural autoreactive B cells (C1-B) specific for a defined triple-helical epitope on collagen type-II (COL2), constituting a sizeable fraction of the physiological B cell repertoire in mice, rats, and humans. Adoptive transfer of C1-B suppressed arthritis independently of IL10, separating them from IL10-secreting regulatory B cells. Single-cell sequencing revealed an antigen processing and presentation signature, including induced expression of CD72 and CCR7 as surface markers. C1-B presented COL2 to T cells and induced the expansion of regulatory T cells in a contact-dependent manner. CD72 blockade impeded this effect suggesting a new downstream suppressor mechanism that regulates antigen-specific T cell tolerization. Thus, our results indicate that autoreactive antigen-specific naive B cells tolerize infiltrating T cells against self-antigens to impede the development of tissue-specific autoimmune inflammation.
|
|
| 9. |
|
|
| 10. |
|
|
