Global patient outcomes after elective surgery: prospective cohort study in 27 low-, middle- and high-income countries.

BACKGROUND: As global initiatives increase patient access to surgical treatments, there remains a need to understand the adverse effects of surgery and define appropriate levels of perioperative care. METHODS: We designed a prospective international 7-day cohort study of outcomes following elective adult inpatient surgery in 27 countries. The primary outcome was in-hospital complications. Secondary outcomes were death following a complication (failure to rescue) and death in hospital. Process measures were admission to critical care immediately after surgery or to treat a complication and duration of hospital stay. A single definition of critical care was used for all countries. RESULTS: A total of 474 hospitals in 19 high-, 7 middle- and 1 low-income country were included in the primary analysis. Data included 44 814 patients with a median hospital stay of 4 (range 2-7) days. A total of 7508 patients (16.8%) developed one or more postoperative complication and 207 died (0.5%). The overall mortality among patients who developed complications was 2.8%. Mortality following complications ranged from 2.4% for pulmonary embolism to 43.9% for cardiac arrest. A total of 4360 (9.7%) patients were admitted to a critical care unit as routine immediately after surgery, of whom 2198 (50.4%) developed a complication, with 105 (2.4%) deaths. A total of 1233 patients (16.4%) were admitted to a critical care unit to treat complications, with 119 (9.7%) deaths. Despite lower baseline risk, outcomes were similar in low- and middle-income compared with high-income countries. CONCLUSIONS: Poor patient outcomes are common after inpatient surgery. Global initiatives to increase access to surgical treatments should also address the need for safe perioperative care. STUDY REGISTRATION: ISRCTN5181700

Defect reduced selectively grown GaN pyramids as template for green InGaN quantum wells

We report the growth of green emitting InGaN quantum wells (QWs) by metal-organic vapor-phase epitaxy (MOVPE) on three-dimensional GaN templates. The {10 (1) over bar1} facets of GaN pyramids, fabricated by selective-area growth (SAG), reduce the influence of the quantum-confined Stark effect (QCSE) on the emission properties of the QW. The luminescence properties of a QW are a good indicator for the crystalline quality of the GaN layer beneath. Especially the presence of voids inside the pyramids, as well as stacking faults (SFs) and threading dislocations (TDs) in the wing region strongly influence the strain situation and the incorporation of In into the overlying InGaN layer. Thus, the crystal quality of the GaN pyramid has a strong influence on the efficiency and the emission properties of the active region. Therefore, a low-temperature nucleation on the GaN buffer in conjunction with a decreasing Ga-flux taking the decreasing c-plane growth surface of the pyramid into account was introduced. The low-temperature photoluminescence (PL) properties of the InGaN QW reveal the differences between the standard formation of the pyramid and this modified growth. Cathodoluminescence (CL) and transmission electron microscopy (TEM) measurements confirm the differences between the two growth modes in the crystal quality of the inner part of the pyramid. (C) 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinhei

Medin co-aggregates with vascular amyloid-β in Alzheimer’s disease.

Aggregates of medin amyloid (a fragment of the protein MFG-E8, also known as lactadherin) are found in the vasculature of almost all humans over 50 years of age1,2, making it the most common amyloid currently known. We recently reported that medin also aggregates in blood vessels of ageing wild-type mice, causing cerebrovascular dysfunction3. Here we demonstrate in amyloid-β precursor protein (APP) transgenic mice and in patients with Alzheimer’s disease that medin co-localizes with vascular amyloid-β deposits, and that in mice, medin deficiency reduces vascular amyloid-β deposition by half. Moreover, in both the mouse and human brain, MFG-E8 is highly enriched in the vasculature and both MFG-E8 and medin levels increase with the severity of vascular amyloid-β burden. Additionally, analysing data from 566 individuals in the ROSMAP cohort, we find that patients with Alzheimer’s disease have higher MFGE8 expression levels, which are attributable to vascular cells and are associated with increased measures of cognitive decline, independent of plaque and tau pathology. Mechanistically, we demonstrate that medin interacts directly with amyloid-β to promote its aggregation, as medin forms heterologous fibrils with amyloid-β, affects amyloid-β fibril structure, and cross-seeds amyloid-β aggregation both in vitro and in vivo. Thus, medin could be a therapeutic target for prevention of vascular damage and cognitive decline resulting from amyloid-β deposition in the blood vessels of the brain