Self-adaptive integrated photonic receiver for turbulence compensation in free space optical links.

In Free Space Optical (FSO) communication systems, atmospheric turbulence distorts the propagating beams, causing a random fading in the received power. This perturbation can be compensated using a multi-aperture receiver that samples the distorted wavefront on different points and adds the various signals coherently. In this work, we report on an adaptive optical receiver that compensates in real time for scintillation in FSO links.

Design, evolution, and experience with the candy plug device for endovascular false lumen occlusion of chronic aortic dissections.

Introduction: The management of the false lumen (FL) when dealing with aortic dissection is a crucial aspect since inducing its thrombosis is necessary in order to achieve aortic remodeling. One of the pitfalls of endovascular treatment of aortic dissection (AD) is retrograde distal FL perfusion and pressurization, which prevents FL thrombosis and thus aortic remodeling, while being associated with aneurysmal degeneration of the FL and poor long-term outcomes.

Areas Covered: Currently, there is no CE/FDA approved device for FL closure, however different techniques and devices have been proposed to overcome this challenge, the most known of which is the Candy Plug (CP).

Plug-Based Embolization Techniques of Aortic Side Branches during Standard and Complex Endovascular Aortic Repair.

Vascular plugs are an evolving family of vessel occluders providing a single-device embolization system for large, high-flow arteries. Nitinol mesh plugs and polytetrafluoroethylene membrane plugs are available in different configurations and sizes to occlude arteries from 3 to 20 mm in diameter. Possible applications during complex endovascular aortic procedures are aortic branch embolization to prevent endoleak or to gain an adequate landing zone, directional branch occlusion, and false lumen embolization in aortic dissection.

APOE2 gene therapy reduces amyloid deposition and improves markers of neuroinflammation and neurodegeneration in a mouse model of Alzheimer disease.

Epidemiological studies show that individuals who carry the relatively uncommon APOE ε2 allele rarely develop Alzheimer disease, and if they do, they have a later age of onset, milder clinical course, and less severe neuropathological findings than people without this allele. The contrast is especially stark when compared with the major genetic risk factor for Alzheimer disease, APOE ε4, which has an age of onset several decades earlier, a more aggressive clinical course and more severe neuropathological findings, especially in terms of the amount of amyloid deposition. Here, we demonstrate that brain exposure to APOE ε2 via a gene therapy approach, which bathes the entire cortical mantle in the gene product after transduction of the ependyma, reduces Aβ plaque deposition, neurodegenerative synaptic loss, and, remarkably, reduces microglial activation in an APP/PS1 mouse model despite continued expression of human APOE ε4.