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- Lauwers, E., et al.
(author)
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Potential human transmission of amyloid beta pathology: surveillance and risks
- 2020
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In: Lancet Neurology. - 1474-4422 .- 1474-4465. ; 19:10, s. 872-878
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Journal article (peer-reviewed)abstract
- Studies in experimental animals show transmissibility of amyloidogenic proteins associated with prion diseases, Alzheimer's disease, Parkinson's disease, and other neurodegenerative diseases. Although these data raise potential concerns for public health, convincing evidence for human iatrogenic transmission only exists for prions and amyloid beta after systemic injections of contaminated growth hormone extracts or dura mater grafts derived from cadavers. Even though these procedures are now obsolete, some reports raise the possibility of iatrogenic transmission of amyloid beta through putatively contaminated neurosurgical equipment. Iatrogenic transmission of amyloid beta might lead to amyloid deposition in the brain parenchyma and blood vessel walls, potentially resulting in cerebral amyloid angiopathy after several decades. Cerebral amyloid angiopathy can cause life-threatening brain haemorrhages; yet, there is no proof that the transmission of amyloid can also lead to Alzheimer's dementia. Large, long-term epidemiological studies and sensitive, cost-efficient tools to detect amyloid are needed to better understand any potential routes of amyloid beta transmission and to clarify whether other similar proteopathic seeds, such as tau or alpha-synuclein, can also be transferred iatrogenically.
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- Thorslund, Sara E, et al.
(author)
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The RACK1 signaling scaffold protein selectively interacts with Yersinia pseudotuberculosis virulence function
- 2011
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In: PLOS ONE. - San Francisco : Public Library of Science. - 1932-6203. ; 6:2, s. e16784-
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Journal article (peer-reviewed)abstract
- Many Gram-negative bacteria use type III secretion systems to translocate effector proteins into host cells. These effectors interfere with cellular functions in a highly regulated manner resulting in effects that are beneficial for the bacteria. The pathogen Yersinia can resist phagocytosis by eukaryotic cells by translocating Yop effectors into the target cell cytoplasm. This is called antiphagocytosis, and constitutes an important virulence feature of this pathogen since it allows survival in immune cell rich lymphoid organs. We show here that the virulence protein YopK has a role in orchestrating effector translocation necessary for productive antiphagocytosis. We present data showing that YopK influences Yop effector translocation by modulating the ratio of the pore-forming proteins YopB and YopD in the target cell membrane. Further, we show that YopK that can interact with the translocators, is exposed inside target cells and binds to the eukaryotic signaling protein RACK1. This protein is engaged upon Y. pseudotuberculosis-mediated beta1-integrin activation and localizes to phagocytic cups. Cells with downregulated RACK1 levels are protected from antiphagocytosis. This resistance is not due to altered levels of translocated antiphagocytic effectors, and cells with reduced levels of RACK1 are still sensitive to the later occurring cytotoxic effect caused by the Yop effectors. Further, a yopK mutant unable to bind RACK1 shows an avirulent phenotype during mouse infection, suggesting that RACK1 targeting by YopK is a requirement for virulence. Together, our data imply that the local event of Yersinia-mediated antiphagocytosis involves a step where YopK, by binding RACK1, ensures an immediate specific spatial delivery of antiphagocytic effectors leading to productive inhibition of phagocytosis.
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- Edgren, Aina, 1995, et al.
(author)
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High temperature deformation of polycrystalline C40 Mo(Si,Al) 2
- 2022
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In: Materials Science & Engineering A: Structural Materials: Properties, Microstructure and Processing. - : Elsevier BV. - 0921-5093. ; 849
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Journal article (peer-reviewed)abstract
- Polycrystalline Mo(Si,Al)2 with C40 crystal structure was deformed in compression with a strain rate of 10−4 s−1 at 1300 °C. The specimens were deformed to a strain of 10%–15% and showed maximum stresses around 150 MPa prior to pronounced softening. No crack formation or significant increase in porosity could be observed. Post-test microstructure analysis revealed that the material was inhomogeneously deformed on both inter- and intragranular levels. Dynamic recrystallization occurred alongside low angle grain boundary formation in highly deformed grains. Furthermore, complex intragranular deformation fields suggest that slip systems other than 21̄1̄0[0001] may be active during deformation.
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