| 1. |
- Aad, G, et al.
(författare)
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- 2015
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swepub:Mat__t
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| 2. |
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| 3. |
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| 4. |
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| 5. |
- Zumla, A, et al.
(författare)
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Towards host-directed therapies for tuberculosis
- 2015
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Ingår i: Nature reviews. Drug discovery. - : Springer Science and Business Media LLC. - 1474-1784 .- 1474-1776. ; 14:8, s. 511-
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Tidskriftsartikel (refereegranskat)
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| 6. |
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| 7. |
- Kumar, Rajiv, et al.
(författare)
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Effect of chromium and aluminum addition on anisotropic and microstructural characteristics of ball milled nanocrystalline iron
- 2016
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Ingår i: Journal of Alloys and Compounds. - : Elsevier BV. - 0925-8388 .- 1873-4669. ; 671, s. 164-169
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Tidskriftsartikel (refereegranskat)abstract
- Prior studies on synthesis of nanocrystalline elements have discussed the effect of ball milling on lattice parameter, crystallite size, and micro-strain. For elemental milled powders, the anisotropic peak broadening does not change with increasing milling time. However, the effect of alloying addition on the anisotropic behavior of ball milled nanocrystalline powders remains an unexplored area. Here we report the effect of chromium and aluminum addition on the anisotropic behavior of iron in nanocrystalline Fe–20Cr–5Al (wt%) alloy powders synthesized by ball milling. The experimental results show that the anisotropic behavior of iron changes towards isotropic with milling. This change was also correlated to the theoretically calculated anisotropic factor from the change in elastic constant of iron due to milling. Addition of alloying elements exhibited a monotonic rise in the lattice parameter with crystallite size, which was attributed to the excess grain boundary interfacial energy and excess free volume at grain boundaries. Transmission electron microscopy image confirmed the crystallite size and nature of dislocation obtained using modified Williamson-Hall method.
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| 8. |
- Maertzdorf, Jeroen, et al.
(författare)
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Human gene expression profiles of susceptibility and resistance in tuberculosis
- 2011
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Ingår i: Genes and Immunity. - London, UK : Nature Publishing Group. - 1466-4879 .- 1476-5470. ; 12:1, s. 15-22
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Tidskriftsartikel (refereegranskat)abstract
- Tuberculosis (TB) still poses a profound burden on global health, owing to significant morbidity and mortality worldwide. Although a fully functional immune system is essential for the control of Mycobacterium tuberculosis infection, the underlying mechanisms and reasons for failure in part of the infected population remain enigmatic. Here, whole-blood microarray gene expression analyses were performed in TB patients and in latently as well as uninfected healthy controls to define biomarkers predictive of susceptibility and resistance. Fc gamma receptor 1B (FCGRIB)was identified as the most differentially expressed gene, and, in combination with four other markers, produced a high degree of accuracy in discriminating TB patients and latently infected donors. We determined differentially expressed genes unique for active disease and identified profiles that correlated with susceptibility and resistance to TB. Elevated expression of innate immune-related genes in active TB and higher expression of particular gene clusters involved in apoptosis and natural killer cell activity in latently infected donors are likely to be the major distinctive factors determining failure or success in controlling M. tuberculosis infection. The gene expression profiles defined in this study provide valuable clues for better understanding of progression from latent infection to active disease and pave the way for defining predictive correlates of protection in TB.
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| 9. |
- Naeem, Aishath, et al.
(författare)
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Pirtobrutinib targets BTK C481S in ibrutinib-resistant CLL but second-site BTK mutations lead to resistance
- 2023
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Ingår i: Blood Advances. - : American Society of Hematology. - 2473-9529 .- 2473-9537. ; 7:9, s. 1929-1943
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Tidskriftsartikel (refereegranskat)abstract
- Covalent inhibitors of Bruton tyrosine kinase (BTK) have transformed the therapy of chronic lymphocytic leukemia (CLL), but continuous therapy has been complicated by the development of resistance. The most common resistance mechanism in patients whose disease progresses on covalent BTK inhibitors (BTKis) is a mutation in the BTK 481 cysteine residue to which the inhibitors bind covalently. Pirtobrutinib is a highly selective, noncovalent BTKi with substantial clinical activity in patients whose disease has progressed on covalent BTKi, regardless of BTK mutation status. Using in vitro ibrutinib-resistant models and cells from patients with CLL, we show that pirtobrutinib potently inhibits BTK-mediated functions including B-cell receptor (BCR) signaling, cell viability, and CCL3/CCL4 chemokine production in both BTK wild-type and C481S mutant CLL cells. We demonstrate that primary CLL cells from responding patients on the pirtobrutinib trial show reduced BCR signaling, cell survival, and CCL3/CCL4 chemokine secretion. At time of progression, these primary CLL cells show increasing resistance to pirtobrutinib in signaling inhibition, cell viability, and cytokine production. We employed longitudinal whole-exome sequencing on 2 patients whose disease progressed on pirtobrutinib and identified selection of alternative-site BTK mutations, providing clinical evidence that secondary BTK mutations lead to resistance to noncovalent BTKis.
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