Low oxygen saturation and mortality in an adult cohort; the Tromsø Study

Published version, also available at http://dx.doi.org/10.1186/s12890-015-0003-5Background: Oxygen saturation has been shown in risk score models to predict mortality in emergency medicine. The aim of this study was to determine whether low oxygen saturation measured by a single-point measurement by pulse oximetry (SpO2) is associated with increased mortality in the general adult population. Methods: Pulse oximetry was performed in 5,152 participants in a cross-sectional survey in Tromsø, Norway, in 2001–2002 (“Tromsø 5”). Ten-year follow-up data for all-cause mortality and cause of death were obtained from the National Population and the Cause of Death Registries, respectively. Cause of death was grouped into four categories: cardiovascular disease, cancer except lung cancer, pulmonary disease, and others. SpO2 categories were assessed as predictors for all-cause mortality and death using Cox proportional-hazards regression models after correcting for age, sex, smoking history, body mass index (BMI), C-reactive protein level, self-reported diseases, respiratory symptoms, and spirometry results. Results: The mean age was 65.8 years, and 56% were women. During the follow-up, 1,046 (20.3%) participants died. The age- and sex-adjusted hazard ratios (HRs) (95% confidence intervals) for all-cause mortality were 1.99 (1.33–2.96) for SpO2 ≤ 92% and 1.36 (1.15–1.60) for SpO2 93–95%, compared with SpO2 ≥ 96%. In the multivariable Cox proportional-hazards regression models that included self-reported diseases, respiratory symptoms, smoking history, BMI, and CRP levels as the explanatory variables, SpO2 remained a significant predictor of all-cause mortality. However, after including forced expiratory volume in 1 s percent predicted (FEV1% predicted), this association was no longer significant. Mortality caused by pulmonary diseases was significantly associated with SpO2 even when FEV1% predicted was included in the model. Conclusions: Low oxygen saturation was independently associated with increased all-cause mortality and mortality caused by pulmonary diseases. When FEV1% predicted was included in the analysis, the strength of the association weakened but was still statistically significant for mortality caused by pulmonary diseases

Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to 300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m 2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

Canagliflozin and renal outcomes in type 2 diabetes and nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to &lt;90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], &gt;300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of &lt;15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P&lt;0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P&lt;0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

Tropical tree growth driven by dry-season climate variability

Interannual variability in the global land carbon sink is strongly related to variations in tropical temperature and rainfall. This association suggests an important role for moisture-driven fluctuations in tropical vegetation productivity, but empirical evidence to quantify the responsible ecological processes is missing. Such evidence can be obtained from tree-ring data that quantify variability in a major vegetation productivity component: woody biomass growth. Here we compile a pantropical tree-ring network to show that annual woody biomass growth increases primarily with dry-season precipitation and decreases with dry-season maximum temperature. The strength of these dry-season climate responses varies among sites, as reflected in four robust and distinct climate response groups of tropical tree growth derived from clustering. Using cluster and regression analyses, we find that dry-season climate responses are amplified in regions that are drier, hotter and more climatically variable. These amplification patterns suggest that projected global warming will probably aggravate drought-induced declines in annual tropical vegetation productivity. Our study reveals a previously underappreciated role of dry-season climate variability in driving the dynamics of tropical vegetation productivity and consequently in influencing the land carbon sink.We acknowledge financial support to the co-authors provided by Agencia Nacional de Promoción Científica y Tecnológica, Argentina (PICT 2014-2797) to M.E.F.; Alberta Mennega Stichting to P.G.; BBVA Foundation to H.A.M. and J.J.C.; Belspo BRAIN project: BR/143/A3/HERBAXYLAREDD to H.B.; Confederação da Agricultura e Pecuária do Brasil - CNA to C.F.; Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES, Brazil (PDSE 15011/13-5 to M.A.P.; 88881.135931/2016-01 to C.F.; 88887.199858/2018-00 to G.A.-P.; Finance Code 001 for all Brazilian collaborators); Conselho Nacional de Desenvolvimento Científico e Tecnológico - CNPq, Brazil (ENV 42 to O.D.; 1009/4785031-2 to G.C.; 311874/2017-7 to J.S.); CONACYT-CB-2016-283134 to J.V.-D.; CONICET to F.A.R.; CUOMO FOUNDATION (IPCC scholarship) to M.M.; Deutsche Forschungsgemeinschaft - DFG (BR 1895/15-1 to A.B.; BR 1895/23-1 to A.B.; BR 1895/29-1 to A.B.; BR 1895/24-1 to M.M.); DGD-RMCA PilotMAB to B.T.; Dirección General de Asuntos del Personal Académico of the UNAM (Mexico) to R.B.; Elsa-Neumann-Scholarship of the Federal State of Berlin to F.S.; EMBRAPA Brazilian Agricultural Research Corporation to C.F.; Equatorian Dirección de Investigación UNL (21-DI-FARNR-2019) to D.P.-C.; São Paulo Research Foundation FAPESP (2009/53951-7 to M.T.-F.; 2012/50457-4 to G.C.; 2018/01847‐0 to P.G.; 2018/24514-7 to J.R.V.A.; 2019/08783-0 to G.M.L.; 2019/27110-7 to C.F.); FAPESP-NERC 18/50080-4 to G.C.; FAPITEC/SE/FUNTEC no. 01/2011 to M.A.P.; Fulbright Fellowship to B.J.E.; German Academic Exchange Service (DAAD) to M.I. and M.R.; German Ministry of Education, Science, Research, and Technology (FRG 0339638) to O.D.; ICRAF through the Forests, Trees, and Agroforestry research programme of the CGIAR to M.M.; Inter-American Institute for Global Change Research (IAI-SGP-CRA 2047) to J.V.-D.; International Foundation for Science (D/5466-1) to M.I.; Lamont Climate Center to B.M.B.; Miquelfonds to P.G.; National Geographic Global Exploration Fund (GEFNE80-13) to I.R.; USA’s National Science Foundation NSF (IBN-9801287 to A.J.L.; GER 9553623 and a postdoctoral fellowship to B.J.E.); NSF P2C2 (AGS-1501321) to A.C.B., D.G.-S. and G.A.-P.; NSF-FAPESP PIRE 2017/50085-3 to M.T.-F., G.C. and G.M.L.; NUFFIC-NICHE programme (HEART project) to B.K., E.M., J.H.S., J.N. and R. Vinya; Peru ‘s CONCYTEC and World Bank (043-2019-FONDECYT-BM-INC.INV.) to J.G.I.; Peru’s Fondo Nacional de Desarrollo Científico, Tecnológico y de Innovación Tecnológica (FONDECYT-BM-INC.INV 039-2019) to E.J.R.-R. and M.E.F.; Programa Bosques Andinos - HELVETAS Swiss Intercooperation to M.E.F.; Programa Nacional de Becas y Crédito Educativo - PRONABEC to J.G.I.; Schlumberger Foundation Faculty for the Future to J.N.; Sigma Xi to A.J.L.; Smithsonian Tropical Research Institute to R. Alfaro-Sánchez.; Spanish Ministry of Foreign Affairs AECID (11-CAP2-1730) to H.A.M. and J.J.C.; UK NERC grant NE/K01353X/1 to E.G.Peer reviewe

First Sagittarius A* Event Horizon Telescope Results. II. EHT and Multiwavelength Observations, Data Processing, and Calibration

We present Event Horizon Telescope (EHT) 1.3 mm measurements of the radio source located at the position of the supermassive black hole Sagittarius A* (Sgr A*), collected during the 2017 April 5-11 campaign. The observations were carried out with eight facilities at six locations across the globe. Novel calibration methods are employed to account for Sgr A*'s flux variability. The majority of the 1.3 mm emission arises from horizon scales, where intrinsic structural source variability is detected on timescales of minutes to hours. The effects of interstellar scattering on the image and its variability are found to be subdominant to intrinsic source structure. The calibrated visibility amplitudes, particularly the locations of the visibility minima, are broadly consistent with a blurred ring with a diameter of similar to 50 mu as, as determined in later works in this series. Contemporaneous multiwavelength monitoring of Sgr A* was performed at 22, 43, and 86 GHz and at near-infrared and X-ray wavelengths. Several X-ray flares from Sgr A* are detected by Chandra, one at low significance jointly with Swift on 2017 April 7 and the other at higher significance jointly with NuSTAR on 2017 April 11. The brighter April 11 flare is not observed simultaneously by the EHT but is followed by a significant increase in millimeter flux variability immediately after the X-ray outburst, indicating a likely connection in the emission physics near the event horizon. We compare Sgr A*'s broadband flux during the EHT campaign to its historical spectral energy distribution and find that both the quiescent emission and flare emission are consistent with its long-term behavior