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- Saarikangas, J, et al.
(author)
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Missing-in-metastasis MIM/MTSS1 promotes actin assembly at intercellular junctions and is required for integrity of kidney epithelia
- 2011
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In: Journal of cell science. - : The Company of Biologists. - 1477-9137 .- 0021-9533. ; 124:8Pt 8, s. 1245-1255
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Journal article (peer-reviewed)abstract
- MIM/MTSS1 is a tissue-specific regulator of plasma membrane dynamics, whose altered expression levels have been linked to cancer metastasis. MIM deforms phosphoinositide-rich membranes through its I-BAR domain and interacts with actin monomers through its WH2 domain. Recent work proposed that MIM also potentiates Sonic hedgehog (Shh)-induced gene expression. Here, we generated MIM mutant mice and found that full-length MIM protein is dispensable for embryonic development. However, MIM-deficient mice displayed a severe urinary concentration defect caused by compromised integrity of kidney epithelia intercellular junctions, which led to bone abnormalities and end-stage renal failure. In cultured kidney epithelial (MDCK) cells, MIM displayed dynamic localization to adherens junctions, where it promoted Arp2/3-mediated actin filament assembly. This activity was dependent on the ability of MIM to interact with both membranes and actin monomers. Furthermore, results from the mouse model and cell culture experiments suggest that full-length MIM is not crucial for Shh signaling, at least during embryogenesis. Collectively, these data demonstrate that MIM modulates interplay between the actin cytoskeleton and plasma membrane to promote the maintenance of intercellular contacts in kidney epithelia.
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- Sainio, M. T., et al.
(author)
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Neurofilament Light Regulates Axon Caliber, Synaptic Activity, and Organelle Trafficking in Cultured Human Motor Neurons
- 2022
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In: Frontiers in Cell and Developmental Biology. - : Frontiers Media SA. - 2296-634X. ; 9
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Journal article (peer-reviewed)abstract
- Neurofilament light (NFL) is one of the proteins forming multimeric neuron-specific intermediate filaments, neurofilaments, which fill the axonal cytoplasm, establish caliber growth, and provide structural support. Dominant missense mutations and recessive nonsense mutations in the neurofilament light gene (NEFL) are among the causes of Charcot-Marie-Tooth (CMT) neuropathy, which affects the peripheral nerves with the longest axons. We previously demonstrated that a neuropathy-causing homozygous nonsense mutation in NEFL led to the absence of NFL in patient-specific neurons. To understand the disease-causing mechanisms, we investigate here the functional effects of NFL loss in human motor neurons differentiated from induced pluripotent stem cells (iPSC). We used genome editing to generate NEFL knockouts and compared them to patient-specific nonsense mutants and isogenic controls. iPSC lacking NFL differentiated efficiently into motor neurons with normal axon growth and regrowth after mechanical axotomy and contained neurofilaments. Electrophysiological analysis revealed that motor neurons without NFL fired spontaneous and evoked action potentials with similar characteristics as controls. However, we found that, in the absence of NFL, human motor neurons 1) had reduced axonal caliber, 2) the amplitude of miniature excitatory postsynaptic currents (mEPSC) was decreased, 3) neurofilament heavy (NFH) levels were reduced and no compensatory increases in other filament subunits were observed, and 4) the movement of mitochondria and to a lesser extent lysosomes was increased. Our findings elaborate the functional roles of NFL in human motor neurons. NFL is not only a structural protein forming neurofilaments and filling the axonal cytoplasm, but our study supports the role of NFL in the regulation of synaptic transmission and organelle trafficking. To rescue the NFL deficiency in the patient-specific nonsense mutant motor neurons, we used three drugs, amlexanox, ataluren (PTC-124), and gentamicin to induce translational read-through or inhibit nonsense-mediated decay. However, the drugs failed to increase the amount of NFL protein to detectable levels and were toxic to iPSC-derived motor neurons.
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- Bijnens, J., et al.
(author)
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Pion-pion scattering at low energy
- 1997
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In: Nuclear Physics B. - 0550-3213. ; 508:1-2, s. 263-310
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Journal article (peer-reviewed)abstract
- We present technical details of the evaluation of the elastic ππ scattering amplitude to two loops in chiral perturbation theory. In particular, we elaborate on the renormalization procedure at the two-loop order and on the evaluation of the relevant Feynman diagrams that can all be expressed in terms of elementary functions. For the sake of clarity, we discuss these matters both in the N-component φ4 theory (in its symmetric phase) and in chiral perturbation theory. Estimates for the relevant low-energy constants of O(p6) are presented. Threshold parameters and phase shifts are then calculated for two sets of O(p4) coupling constants and compared with experiment. We comment on the extraction of threshold parameters from phase shift data.
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- Zucca, M., et al.
(author)
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Metrology for Inductive Charging of Electric Vehicles (MICEV)
- 2019
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In: 2019 AEIT International Conference of Electrical and Electronic Technologies for Automotive (AEIT AUTOMOTIVE). ; , s. 1-6
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Conference paper (peer-reviewed)abstract
- The European Union funded project MICEV aims at improving the traceability of electrical and magnetic measurement at charging stations and to better assess the safety of this technology with respect to human exposure. The paper describes some limits of the instrumentation used for electrical measurements in the charging stations, and briefly presents two new calibration facilities for magnetic field meters and electric power meters. Modeling approaches for the efficiency and human exposure assessment are proposed. In the latter case, electromagnetic computational codes have been combined with dosimetric computational codes making use of highly detailed human anatomical phantoms in order to establish human exposure modeling real charging stations. Detailed results are presented for light vehicles where, according to our calculations, the concern towards human exposure is limited. Currently, the project has reached half way point (about 18 months) and will end in August 2020.
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| 10. |
- Alenius, M, et al.
(author)
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Cognitive Performance among Cognitively Healthy Adults Aged 30-100 Years
- 2019
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In: Dementia and geriatric cognitive disorders extra. - : S. Karger AG. - 1664-5464. ; 9:1, s. 11-23
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Journal article (peer-reviewed)abstract
- <b><i>Background/Aims:</i></b> To detect cognitive decline in older adults, measures of verbal fluency and verbal memory are widely used. Less is known about performance in these measures in younger persons or according to education level and gender. We investigated cognitive performance according to age, education and gender among cognitively healthy adults aged 30–100 years. <b><i>Methods:</i></b> The study population comprised 4,174 cognitively healthy persons participating in the nationally representative Finnish Health 2011 survey. Cognitive assessment included verbal fluency, word list memory, word list recall and word list savings from the Consortium to Establish a Registry for Alzheimer’s Disease neuropsychological battery. <b><i>Results:</i></b> Total variance in the cognitive test performance explained by age, education and gender varied from 12.3 to 31.2%. A decreasing trend in cognitive performance existed in all subtests by advancing age, with differences appearing between 50 and 55 years. Persons with the highest-education level performed best for all measures. For the participants < 55 years, education explained part of the variance, while age and gender did not. <b><i>Conclusions:</i></b> When assessing cognition, age and education should be accounted for in more detail in research and clinical practice. Additionally, the cohort effect and its potential impact on the renewal cycle of future normative values for cognitive tests should be considered.
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