7 research outputs found
Enhanced generation of VUV radiation by four-wave mixing in mercury using pulsed laser vaporization
The efficiency of a coherent VUV source at 125 nm, based on 2-photon resonant
four-wave mixing in mercury vapor, has been enhanced by up to 2 orders of
magnitude. This enhancement was obtained by locally heating a liquid Hg surface
with a pulsed excimer laser, resulting in a high density vapor plume in which
the nonlinear interaction occurred. Energies up to 5 μJ (1 kW peak power)
have been achieved while keeping the overall Hg cell at room temperature,
avoiding the use of a complex heat pipe. We have observed a strong saturation
of the VUV yield when peak power densities of the fundamental beams exceed the
GW/cm2 range, as well as a large intensity-dependant broadening (up to ~30
cm-1) of the two-photon resonance. The source has potential applications for
high resolution interference lithography and photochemistry
Autophagy in major human diseases
Autophagy is a core molecular pathway for the preservation of cellular and organismal homeostasis. Pharmacological and genetic interventions impairing autophagy responses promote or aggravate disease in a plethora of experimental models. Consistently, mutations in autophagy-related processes cause severe human pathologies. Here, we review and discuss preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders
Autophagy gene Atg16L1 prevents lethal T cell alloreactivity mediated by dendritic cells
Atg16L1 mediates the cellular degradative process of autophagy and is considered a critical regulator of inflammation based on its genetic association with inflammatory bowel disease. Here we find that Atg16L1 deficiency leads to an exacerbated graft-versus-host disease (GVHD) in a mouse model of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Atg16L1-deficient allo-HSCT recipients with GVHD displayed increased T cell proliferation due to increased dendritic cell (DC) numbers and costimulatory molecule expression. Reduced autophagy within DCs was associated with lysosomal abnormalities and decreased amounts of A20, a negative regulator of DC activation. These results broaden the function of Atg16L1 and the autophagy pathway to include a role in limiting a DC-mediated response during inflammatory disease, such as GVHD