| 41. |
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| 42. |
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| 43. |
- Sanmun, D, et al.
(författare)
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Involvement of a functional NADPH oxidase in neutrophils and macrophages during programmed cell clearance: implications for chronic granulomatous disease
- 2009
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Ingår i: American journal of physiology. Cell physiology. - : American Physiological Society. - 1522-1563 .- 0363-6143. ; 297:3, s. C621-C631
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Tidskriftsartikel (refereegranskat)abstract
- Resolution of inflammation requires clearance of activated neutrophils by macrophages in a manner that prevents injury to adjacent tissues. Surface changes, including phosphatidylserine (PS) exposure, may target neutrophils for phagocytosis. In this study, we show that externalization of PS is defective in phorbol myristate acetate (PMA)-activated neutrophils obtained from chronic granulomatous disease (CGD) patients with mutations in components of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Moreover, activated neutrophils from CGD patients failed to undergo clearance upon cocultivation with macrophages from normal donors. In line with these results, treatment of donor neutrophils with diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase, blocked PMA-induced PS oxidation and externalization and prevented their engulfment by macrophages. Furthermore, primary macrophages from CGD patients or human gp91phox-deficient PLB-985 cells differentiated into macrophage-like cells were defective for engulfment of apoptotic target cells. Pretreatment of normal macrophages with DPI also suppressed the subsequent ingestion of PS-positive target cells. Together, these data demonstrate that NADPH oxidase plays an important role in the process of macrophage disposal of target cells (programmed cell clearance). Thus we speculate that the lack of a functional NADPH oxidase results in impaired neutrophil clearance and the exaggerated inflammation that is characteristic for CGD.
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| 44. |
- Schejbel, L, et al.
(författare)
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Molecular basis of hereditary C1q deficiency-revisited: identification of several novel disease-causing mutations
- 2011
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Ingår i: GENES AND IMMUNITY. - : Springer Science and Business Media LLC. - 1466-4879 .- 1476-5470. ; 12:8, s. 626-634
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Tidskriftsartikel (refereegranskat)abstract
- C1q is the central pattern-recognition molecule in the classical pathway of the complement system and is known to have a key role in the crossroads between adaptive and innate immunity. Hereditary C1q deficiency is a rare genetic condition strongly associated with systemic lupus erythematosus and increased susceptibility to bacterial infections. However, the clinical symptoms may vary. For long, the molecular basis of C1q deficiency was ascribed to only six different mutations. In the present report, we describe five new patients with C1q deficiency, present the 12 causative mutations described till now and review the clinical spectrum of symptoms found in patients with C1q deficiency. With the results presented here, confirmed C1q deficiency is reported in 64 patients from at least 38 families.
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| 45. |
- Westergard, R, et al.
(författare)
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Sliding wear and friction of Si3N4-SiC-based ceramic composites containing hexagonal boron nitride
- 1998
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Ingår i: PROCEEDINGS OF THE INSTITUTION OF MECHANICAL ENGINEERS PART J-JOURNAL OF ENGINEERING TRIBOLOGY. - : PROFESSIONAL ENGINEERING PUBLISHING LTD. - 1350-6501. ; 212:J5, s. 381-387
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- The friction and wear behaviour of a series of new Si3N4-SiC-based ceramic composites, intended for face seal applications, has been investigated with cylinder-on-disc equipment. In particular, the influence of water and vapour on the friction, wear and t
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| 46. |
- Zduniak, K., et al.
(författare)
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Nuclear osteopontin-c is a prognostic breast cancer marker
- 2015
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Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 112:4, s. 729-738
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Tidskriftsartikel (refereegranskat)abstract
- Background: Although Osteopontin has been known as a marker for cancer progression, the elevated production of this cytokine is not specific for cancer. We have identified the splice variant Osteopontin-c as being absent from healthy tissue but associated with about 75% of breast cancer cases. However, in previous studies of Osteopontin-c, follow-up information was not available. Methods: Here we have analysed 671 patients, comprising a cohort of 291 paraffin blocks plus a population-based case-control study of 380 arrayed breast tumor tissues. Results: We find that high staining intensity of nuclear Osteopontin-c is strongly associated with mortality in patients with early breast cancer. Cytosolic staining for exon 4, reflective of Osteopontin-a and -b also predicts poor outcome. By contrast, total Osteopontin does not correlate with prognosis. These diverse assessments of Osteopontin also do not correlate with each other, suggesting distinct expression patterns for the variant forms. Consistent with its role in tumor progression, not tumor initiation, Osteopontin-c is not correlated with proliferation markers (Ki-67, cyclin A, cyclin B, cyclin E and cyclin D), neither is it correlated with ER, PR or HER2. Conclusions: The addition of Osteopontin-c immunohistochemistry to standard pathology work-ups may have prognostic benefit in early breast cancer diagnosis.
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