10 research outputs found
Plasmon-Induced Conductance Enhancement in Single-Molecule Junctions
The effect of surface plasmons on the conductance of single-molecule
junctions is studied using a squeezable break junction setup. We show
that the conductance of 2,7-diaminofluorene single-molecule junctions
can be enhanced upon laser irradiation. Our experimental approach
enables us to show that this enhancement is due to the plasmon-induced
oscillating field within the nanoscale metal gap of the junctions.
The effective plasmon field enhancement within the gap is calculated
to be âź1000. The experimental procedure presented in this work,
which enables one to explore the coupling between plasmons and molecular
excitations via transport measurements, could potentially become a
valuable tool in the field of plexcitonics
Molecular pathways of senescence regulate placental structure and function
The placenta is an autonomous organ that maintains fetal growth and development. Its multinucleated syncytiotrophoblast layer, providing fetal nourishment during gestation, exhibits characteristics of cellular senescence. We show that in human placentas from pregnancies with intrauterine growth restriction, these characteristics are decreased. To elucidate the functions of pathways regulating senescence in syncytiotrophoblast, we used dynamic contrast-enhanced MRI in mice with attenuated senescence programs. This approach revealed an altered dynamics in placentas of p53-/- , Cdkn2a-/- , and Cdkn2a-/- ;p53-/- mice, accompanied by histopathological changes in placental labyrinths. Human primary syncytiotrophoblast upregulated senescence markers and molecular pathways associated with cell-cycle inhibition and senescence-associated secretory phenotype. The pathways and components of the secretory phenotype were compromised in mouse placentas with attenuated senescence and in human placentas from pregnancies with intrauterine growth restriction. We propose that molecular mediators of senescence regulate placental structure and function, through both cell-autonomous and non-autonomous mechanisms