@article{12702,
  abstract     = {Hydrocarbon mixtures are extremely abundant in the Universe, and diamond formation from them can play a crucial role in shaping the interior structure and evolution of planets. With first-principles accuracy, we first estimate the melting line of diamond, and then reveal the nature of chemical bonding in hydrocarbons at extreme conditions. We finally establish the pressure-temperature phase boundary where it is thermodynamically possible for diamond to form from hydrocarbon mixtures with different atomic fractions of carbon. Notably, here we show a depletion zone at pressures above 200 GPa and temperatures below 3000 K-3500 K where diamond formation is thermodynamically favorable regardless of the carbon atomic fraction, due to a phase separation mechanism. The cooler condition of the interior of Neptune compared to Uranus means that the former is much more likely to contain the depletion zone. Our findings can help explain the dichotomy of the two ice giants manifested by the low luminosity of Uranus, and lead to a better understanding of (exo-)planetary formation and evolution.},
  author       = {Cheng, Bingqing and Hamel, Sebastien and Bethkenhagen, Mandy},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  publisher    = {Springer Nature},
  title        = {{Thermodynamics of diamond formation from hydrocarbon mixtures in planets}},
  doi          = {10.1038/s41467-023-36841-1},
  volume       = {14},
  year         = {2023},
}

@article{11143,
  abstract     = {Dravet syndrome is a neurodevelopmental disorder characterized by epilepsy, intellectual disability, and sudden death due to pathogenic variants in SCN1A with loss of function of the sodium channel subunit Nav1.1. Nav1.1-expressing parvalbumin GABAergic interneurons (PV-INs) from young Scn1a+/− mice show impaired action potential generation. An approach assessing PV-IN function in the same mice at two time points shows impaired spike generation in all Scn1a+/− mice at postnatal days (P) 16–21, whether deceased prior or surviving to P35, with normalization by P35 in surviving mice. However, PV-IN synaptic transmission is dysfunctional in young Scn1a+/− mice that did not survive and in Scn1a+/− mice ≥ P35. Modeling confirms that PV-IN axonal propagation is more sensitive to decreased sodium conductance than spike generation. These results demonstrate dynamic dysfunction in Dravet syndrome: combined abnormalities of PV-IN spike generation and propagation drives early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology.},
  author       = {Kaneko, Keisuke and Currin, Christopher and Goff, Kevin M. and Wengert, Eric R. and Somarowthu, Ala and Vogels, Tim P and Goldberg, Ethan M.},
  issn         = {2211-1247},
  journal      = {Cell Reports},
  number       = {13},
  publisher    = {Elsevier},
  title        = {{Developmentally regulated impairment of parvalbumin interneuron synaptic transmission in an experimental model of Dravet syndrome}},
  doi          = {10.1016/j.celrep.2022.110580},
  volume       = {38},
  year         = {2022},
}

@article{10530,
  abstract     = {Cell dispersion from a confined area is fundamental in a number of biological processes,
including cancer metastasis. To date, a quantitative understanding of the interplay of single
cell motility, cell proliferation, and intercellular contacts remains elusive. In particular, the role
of E- and N-Cadherin junctions, central components of intercellular contacts, is still
controversial. Combining theoretical modeling with in vitro observations, we investigate the
collective spreading behavior of colonies of human cancer cells (T24). The spreading of these
colonies is driven by stochastic single-cell migration with frequent transient cell-cell contacts.
We find that inhibition of E- and N-Cadherin junctions decreases colony spreading and average
spreading velocities, without affecting the strength of correlations in spreading velocities of
neighboring cells. Based on a biophysical simulation model for cell migration, we show that the
behavioral changes upon disruption of these junctions can be explained by reduced repulsive
excluded volume interactions between cells. This suggests that in cancer cell migration,
cadherin-based intercellular contacts sharpen cell boundaries leading to repulsive rather than
cohesive interactions between cells, thereby promoting efficient cell spreading during collective
migration.
},
  author       = {Zisis, Themistoklis and Brückner, David and Brandstätter, Tom and Siow, Wei Xiong and d’Alessandro, Joseph and Vollmar, Angelika M. and Broedersz, Chase P. and Zahler, Stefan},
  issn         = {0006-3495},
  journal      = {Biophysical Journal},
  keywords     = {Biophysics},
  number       = {1},
  pages        = {P44--60},
  publisher    = {Elsevier},
  title        = {{Disentangling cadherin-mediated cell-cell interactions in collective cancer cell migration}},
  doi          = {10.1016/j.bpj.2021.12.006},
  volume       = {121},
  year         = {2022},
}