Internal and external carotid artery embolism following facial injection of autologous fat.

Autologous fat injection is a common aesthetic procedure for soft-tissue augmentation of the face. Although this procedure is generally regarded as safe, several patients have experienced acute visual loss or cerebral infarction after these injections. We describe a case of internal and external carotid artery fat embolism that occurred following injection of autologous fat into the face. It appeared that the injected fat entered a branch of the left external carotid artery and that the embolus likely migrated into the left internal carotid artery and distally into the left ophthalmic artery, left anterior artery, and middle cerebral artery. LEVEL OF EVIDENCE 5:

Stimulation of α7 nicotinic acetylcholine receptor by nicotine increases suppressive capacity of naturally occurring CD4+CD25+ regulatory T cells in mice in vitro.

α7 Nicotinic acetylcholine receptor (α7 nAChR) has been found in several non-neuronal cells and is described as an important regulator of cellular function. Naturally occurring CD4(+)CD25(+) regulatory T cells (Tregs) are essential for the active suppression of autoimmunity. The present study investigated whether naturally occurring Tregs expressed α7 nAChR and investigated the functionary role of this receptor in controlling suppressive activity of these cells. We found that CD4(+)CD25(+) Tregs from naive C57BL/6J mice positively expressed α7 nAChR, and its activation by nicotine enhanced the suppressive capacity of Tregs. Nicotine stimulation up-regulated the expression of cytotoxic T-lymphocyte-associated antigen (CTLA)-4 and forkhead/winged helix transcription factor p3 (Foxp3) on Tregs but had no effect on the production of interleukin (IL)-10 and transforming growth factor-ß1 by Tregs. In the supernatants of CD4(+)CD25(+) Tregs/CD4(+)CD25(-) T-cell cocultures, we observed a decrease in the concentration of IL-2 in nicotine-stimulated groups, but nicotine stimulation had no effect on the ratio of IL-4/interferon (IFN)-γ, which partially represented T-cell polarization. The above-mentioned effects of nicotine were reversed by a selective α7 nAChR antagonist, α-bungarotoxin. In addition, the ratio of IL-4/IFN-γ was increased by treatment with α-bungarotoxin. We conclude that nicotine might increase Treg-mediated immune suppression of lymphocytes via α7 nAChR. The effect is related to the up-regulation of CTLA-4 as well as Foxp3 expression and decreased IL-2 secretion in CD4(+)CD25(+) Tregs/CD4(+)CD25(-) T-cell coculture supernatants. α7 nAChR seems to be a critical regulator for immunosuppressive function of CD4(+)CD25(+) Tregs.

Construction of Multifunctional Nanoarchitectures in One Step on a Composite Fuel Catalyst through In Situ Exsolution of La0.5Sr0.5Fe0.8Ni0.1Nb0.1O3-δ.

Multifunctional nanoarchitecture (MNA) on catalysts has attracted great attention because of its capability to improve the performance, durability, and resistance to unwanted side reactions. Such structures, however, are conventionally prepared by deposition methods, which inherently suffer from costly and time-consuming drawbacks. Here, we report a simple one-step process to successfully construct a novel MNA with core-shell nanoparticles anchored at the heterointerface of dual-phase oxide substrates through a phase transition and in situ exsolution of perovskite La0.5Sr0.5Fe0.8Ni0.1Nb0.1O3-δ (LSFNNb0.1) in wet H2 (3% H2O) at 800 °C. The core-shell nanoparticles are composed of a Ni-Fe alloy core and a SrLaFeO4-type layered perovskite oxide shell (RP-Ruddlesden-Popper-layered perovskites), which synergistically improves the electrochemical activity and effectively suppresses aggregation and coarsening of the metallic core. The RP phase also covers the surface of perovskite bulk (SP-single perovskite), forming the heterointerface and preventing further decomposition of the SP phase. The RP/SP heterointerface may improve the kinetics of surface exchange of oxygen species, resulting in the enhancement of performance and durability of the reduced LSFNNb0.1 as an anode for solid oxide fuel cells (SOFCs). A doped zirconia electrolyte-supported single cell with the anode achieves the maximum power density (MPD) of 0.83 W cm-2 at 800 °C in wet H2, and the corresponding polarization resistance is as low as 0.15 Ω cm2. This work reveals the formation mechanism of the MNA by investigating the evolution of the crystal structure, composition and morphology of LSFNNb0.1, when changing reducing temperature and time in wet H2 and 5% H2-Ar. The oxygen vacancies and phase transitions are found to play important roles in the formation of the MNA. The construction of MNAs in one step opens a new opportunity to design and prepare high-performance and stable catalysts for applications in energy conversion and storage.

A self-assembled dual-phase composite as a precursor of high-performance anodes for intermediate temperature solid oxide fuel cells.

A durable high-performance anode with a unique microstructure of a hetero-structured surface layer and exsolved Fe-Cu bimetal nano-fibers is fabricated from a self-assembled dual-phase precursor consisting of a single perovskite (SP) and a Ruddlesden-Popper (RP) layered perovskite component. This work opens up new opportunities to fabricate high-performance anodes for IT-SOFCs.

Vagal Modulation of the Inflammatory Response in Sepsis.

The vagus nerve can sense peripheral inflammation and transmit action potentials from the periphery to the brainstem. Vagal afferent signaling is integrated in the brainstem, and efferent vagus nerves carry outbound signals that terminate in spleen and other organs. Stimulation of efferent vagus nerve leads to the release of acetylcholine in these organs. In turn, acetylcholine interacts with members of the nicotinic acetylcholine receptor (nAChR) family, particularly with the alpha7 nicotinic acetylcholine receptor (α7nAChR), which is expressed by macrophages and other cytokine-producing cells. Ultimately, the production of proinflammatory cytokines is markedly inhibited. This neuroimmune communication is termed "the inflammatory reflex". The uncontrolled inflammation as a result from sepsis can lead to multiple organ failure, and even death. Experimental data show that regulation of the inflammatory reflex appears to be a useful interventional strategy for septic response. Herein, we review recent advances in the understanding of the inflammatory reflex and discuss potential therapeutics that vagal modulation of the immune system for the treatment of severe sepsis and septic shock.

Novel Nano-composites SDC-LiNaSO4 as Functional Layer for ITSOFC.

As an ionic conductive functional layer of intermediate temperature solid oxide fuel cells (ITSOFC), samarium-doped ceria (SDC)-LiNaSO4 nano-composites were synthesized by a sol-gel method and their properties were investigated. It was found that the content of LiNaSO4 strongly affected the crystal phase, defect concentration, and conductivity of the composites. When the content of LiNaSO4 was 20 wt%, the highest conductivity of the composite was found to be, respectively, 0.22, 0.26, and 0.35 S cm-1 at temperatures of 550, 600, and 700 °C, which are much higher than those of SDC. The peak power density of the single cell using this composite as an interlayer was improved to, respectively, 0.23, 0.39, and 0.88 W cm-2 at 500, 600, and 700 °C comparing with that of the SDC-based cell. Further, the SDC-LiNaSO4(20 wt%)-based cell also displayed better thermal stability according to the performance measurements at 560 °C for 50 h. These results reveal that SDC-LiNaSO4 composite may be a potential good candidate as interlayer for ITSOFC due to its high ionic conductivity and thermal stability.

Advances in the management of acute liver failure.

Acute liver failure (ALF) is an uncommon but dramatic clinical syndrome characterized by hepatic encephalopathy and a bleeding tendency due to abrupt loss of liver function caused by massive or submassive liver necrosis in a patient with a previously healthy liver. The causes of ALF encompass a wide variety of toxic, viral, metabolic, vascular and autoimmune insults to the liver, and identifying the correct cause can be difficult or even impossible. Many patients with ALF develop a cascade of serious complications involving almost every organ system, and death is mostly due to multi-organ failure, hemorrhage, infection, and intracranial hypertension. Fortunately, the outcome of ALF has been improved in the last 3 decades through the specific treatment for the disease of certain etiology, and the advanced intensive care management. For most severely affected patients who fail to recover after treatment, rapid evaluation for transfer to a transplantation center and consideration for liver transplantation is mandatory so that transplantation can be applied before contraindications develop. This review focuses on the recent advances in the understanding of various contributing etiologies, the administration of etiology-specific treatment to alleviate the liver injury, and the management of complications (e.g., encephalopathy, coagulopathy, cardiovascular instability, respiratory failure, renal failure, sepsis and metabolic disturbance) in patients with ALF. Assessment of the need for liver transplantation is also presented.