8 research outputs found
The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension
Background: Elevation of intracranial pressure in idiopathic intracranial hypertension induces an edema of the prelaminar section of the optic nerve (papilledema). Beside the commonly observed optic nerve sheath distention, information on a potential pathology of the retrolaminar section of the optic nerve and the short-term effect of normalization of intracranial pressure on these abnormalities remains scarce.
Methods: In this exploratory study 8 patients diagnosed with idiopathic intracranial hypertension underwent a MRI scan (T2 mapping) as well as a diffusion tensor imaging analysis (fractional anisotropy and mean diffusivity). In addition, the clinical presentation of headache and its accompanying symptoms were assessed. Intracranial pressure was then normalized by lumbar puncture and the initial parameters (MRI and clinical features) were re-assessed within 26 h.
Results: After normalization of CSF pressure, the morphometric MRI scans of the optic nerve and optic nerve sheath remained unchanged. In the diffusion tensor imaging, the fractional anisotropy value was reduced suggesting a tissue decompression of the optic nerve after lumbar puncture. In line with these finding, headache and most of the accompanying symptoms also improved or remitted within that short time frame.
Conclusion: The findings support the hypothesis that the elevation of intracranial pressure induces a microstructural compression of the optic nerve impairing axoplasmic flow and thereby causing the prelaminar papilledema. The microstructural compression of the optic nerve as well as the clinical symptoms improve within hours of normalization of intracranial pressure
Organic room-temperature polariton condensate in a higher-order topological lattice
Organic molecule exciton-polaritons in photonic lattices are a versatile
platform to emulate unconventional phases of matter at ambient conditions,
including protected interface modes in topological insulators. Here, we
investigate bosonic condensation in the most prototypical higher-order
topological lattice: a 2D-version of the Su-Schrieffer-Heeger (SSH) model,
supporting both 0D and 1D topological modes. We study fluorescent
protein-filled, structured microcavities defining a staggered photonic trapping
potential and observe the resulting first- and higher-order topologically
protected modes via spatially resolved photoluminescence spectroscopy. We
account for the spatial mode patterns by tight-binding calculations and
theoretically characterize the topological invariants of the lattice. Under
strong optical pumping, we observe bosonic condensation into the topological
modes. Via interferometric measurements, we map the spatial first-order
coherence in the protected 1D modes extending over 10 microns. Our findings
pave the way towards organic on-chip polaritonics using higher-order topology
as a tool for the generation of robustly confined polaritonic lasing states.Comment: 23 pages, 7 figure
Angle- and polarization-resolved luminescence from suspended and hexagonal boron nitride encapsulated MoSe2 monolayers
The polarized photoluminescence from atomically thin transition metal dichalcogenides is a frequently applied tool to scrutinize optical selection rules and valley physics, yet it is known to sensibly depend on a variety of internal and external material and sample properties. In this work, we apply combined angle- and polarization-resolved spectroscopy to explore the interplay of excitonic physics and phenomena arising from the commonly utilized encapsulation procedure on the optical properties of atomically thinMoSe2.We probe monolayers prepared in both suspended and encapsulated manners.We show that the hBN encapsulation significantly enhances the linear polarization of exciton photoluminescence emission at large emission angles. This degree of linear polarization of excitons can increase up to ∼17% in the hBN encapsulated samples. As we confirm by finite-difference time-domain simulations, it can be directly connected to the optical anisotropy of the hBN layers. In comparison, the linear polarization at finite exciton momenta is significantly reduced in a suspendedMoSe2 monolayer, and becomes notable only in cryogenic conditions. This phenomenon strongly suggests that the effect is rooted in the k-dependent anisotropic exchange coupling inherent in2Dexcitons.Our results have strong implications on further studies on valley contrasting selection rules and valley coherence phenomena using standard suspended and encapsulated samples
Spatial coherence of room-temperature monolayer WSe exciton-polaritons in a trap
The emergence of spatial and temporal coherence of light emitted from
solid-state systems is a fundamental phenomenon, rooting in a plethora of
microscopic processes. It is intrinsically aligned with the control of
light-matter coupling, and canonical for laser oscillation. However, it also
emerges in the superradiance of multiple, phase-locked emitters, and more
recently, coherence and long-range order have been investigated in bosonic
condensates of thermalized light, as well as in exciton-polaritons driven to a
ground state via stimulated scattering. Here, we experimentally show that the
interaction between photons in a Fabry-Perot microcavity and excitons in an
atomically thin WSe layer is sufficient such that the system enters the
hybridized regime of strong light-matter coupling at ambient conditions. Via
Michelson interferometry, we capture clear evidence of increased spatial and
temporal coherence of the emitted light from the spatially confined system
ground-state. The coherence build-up is accompanied by a threshold-like
behaviour of the emitted light intensity, which is a fingerprint of a polariton
laser effect. Valley-physics is manifested in the presence of an external
magnetic field, which allows us to manipulate K and K' polaritons via the
Valley-Zeeman-effect. Our findings are of high application relevance, as they
confirm the possibility to use atomically thin crystals as simple and versatile
components of coherent light-sources, and in valleytronic applications at room
temperature.Comment: 13 pages, 4 figure
Depletion and activation of microglia impact metabolic connectivity of the mouse brain
AimWe aimed to investigate the impact of microglial activity and microglial FDG uptake on metabolic connectivity, since microglial activation states determine FDG-PET alterations. Metabolic connectivity refers to a concept of interacting metabolic brain regions and receives growing interest in approaching complex cerebral metabolic networks in neurodegenerative diseases. However, underlying sources of metabolic connectivity remain to be elucidated.Materials and methodsWe analyzed metabolic networks measured by interregional correlation coefficients (ICCs) of FDG-PET scans in WT mice and in mice with mutations in progranulin (Grn) or triggering receptor expressed on myeloid cells 2 (Trem2) knockouts ((-/-)) as well as in double mutant Grn(-/-)/Trem2(-/-) mice. We selected those rodent models as they represent opposite microglial signatures with disease associated microglia in Grn(-/-) mice and microglia locked in a homeostatic state in Trem2(-/-) mice;however, both resulting in lower glucose uptake of the brain. The direct influence of microglia on metabolic networks was further determined by microglia depletion using a CSF1R inhibitor in WT mice at two different ages. Within maps of global mean scaled regional FDG uptake, 24 pre-established volumes of interest were applied and assigned to either cortical or subcortical networks. ICCs of all region pairs were calculated and z-transformed prior to group comparisons. FDG uptake of neurons, microglia, and astrocytes was determined in Grn(-/-) and WT mice via assessment of single cell tracer uptake (scRadiotracing).ResultsMicroglia depletion by CSF1R inhibition resulted in a strong decrease of metabolic connectivity defined by decrease of mean cortical ICCs in WT mice at both ages studied (6-7 m;p = 0.0148, 9-10 m;p = 0.0191), when compared to vehicle-treated age-matched WT mice. Grn(-/-), Trem2(-/-) and Grn(-/-)/Trem2(-/-) mice all displayed reduced FDG-PET signals when compared to WT mice. However, when analyzing metabolic networks, a distinct increase of ICCs was observed in Grn(-/-) mice when compared to WT mice in cortical (p < 0.0001) and hippocampal (p < 0.0001) networks. In contrast, Trem2(-/-) mice did not show significant alterations in metabolic connectivity when compared to WT. Furthermore, the increased metabolic connectivity in Grn(-/-) mice was completely suppressed in Grn(-/-)/Trem2(-/-) mice. Grn(-/-) mice exhibited a severe loss of neuronal FDG uptake (- 61%, p < 0.0001) which shifted allocation of cellular brain FDG uptake to microglia (42% in Grn(-/-) vs. 22% in WT).ConclusionsPresence, absence, and activation of microglia have a strong impact on metabolic connectivity of the mouse brain. Enhanced metabolic connectivity is associated with increased microglial FDG allocation
Deciphering sources of PET signals in the tumor microenvironment of glioblastoma at cellular resolution
Various cellular sources hamper interpretation of positron emission tomography (PET) biomarkers in the tumor microenvironment (TME). We developed an approach of immunomagnetic cell sorting after in vivo radiotracer injection (scRadiotracing) with three-dimensional (3D) histology to dissect the cellular allocation of PET signals in the TME. In mice with implanted glioblastoma, translocator protein (TSPO) radiotracer uptake per tumor cell was higher compared to tumor-associated microglia/macrophages (TAMs), validated by protein levels. Translation of in vitro scRadiotracing to patients with glioma immediately after tumor resection confirmed higher single-cell TSPO tracer uptake of tumor cells compared to immune cells. Across species, cellular radiotracer uptake explained the heterogeneity of individual TSPO-PET signals. In consideration of cellular tracer uptake and cell type abundance, tumor cells were the main contributor to TSPO enrichment in glioblastoma;however, proteomics identified potential PET targets highly specific for TAMs. Combining cellular tracer uptake measures with 3D histology facilitates precise allocation of PET signals and serves to validate emerging novel TAM-specific radioligands