The reliable detection and attribution of changes in vegetation growth is a prerequisite for the development of strategies for the sustainable management of ecosystems. This is an extraordinary challenge. To our knowledge, this study is the first to comprehensively detect and attribute a greening trend in China over the last three decades. We use three different satellite-derived Leaf Area Index (LAI) datasets for detection as well as five different process-based ecosystem models for attribution. Rising atmospheric CO 2 concentration and nitrogen deposition are identified as the most likely causes of the greening trend in China, explaining 85% and 41% of the average growing-season LAI trend (LAI GS ) estimated by satellite datasets (average trend of 0.0070 yr À1, ranging from 0.0035 yr À1 to 0.0127 yr À1 ), respectively. The contribution of nitrogen deposition is more clearly seen in southern China than in the north of the country. Models disagree about the contribution of climate change alone to the trend in LAI GS at the country scale (one model shows a significant increasing trend, whereas two others show significant decreasing trends). However, the models generally agree on the negative impacts of climate change in north China and Inner Mongolia and the positive impact in the Qinghai-Xizang plateau. Provincial forest area change tends to be significantly correlated with the trend of LAI GS (P < 0.05), and marginally significantly (P = 0.07) correlated with the residual of LAI GS trend, calculated as the trend observed by satellite minus that estimated by models through considering the effects of climate change, rising CO 2 concentration and nitrogen deposition, across different provinces. This result highlights the important role of China's afforestation program in explaining the spatial patterns of trend in vegetation growth.

Recent warming significantly advanced leaf onset in the northern hemisphere. This signal cannot be accurately reproduced by current models parameterized by daily mean temperature (Tmean). Here using in situ observations of leaf unfolding dates (LUDs) in Europe and the United States, we show that the interannual anomalies of LUD during 1982–2011 are triggered by daytime (Tmax) more than by nighttime temperature (Tmin). Furthermore, an increase of 1 °C in Tmax would advance LUD by 4.7 days in Europe and 4.3 days in the United States, more than the conventional temperature sensitivity estimated from Tmean. The triggering role of Tmax, rather than the Tmin or Tmean variable, is also supported by analysis of the large-scale patterns of satellite-derived vegetation green-up in spring in the northern hemisphere (>30°N). Our results suggest a new conceptual framework of leaf onset using daytime temperature to improve the performance of phenology modules in current Earth system models.

OBJECTIVECompelling epidemiological and clinical evidence has identified a specific cardiomyopathy in diabetes, characterized by early diastolic dysfunction and adverse structural remodeling. Activation of the insulin-like growth factor 1 (IGF-1) receptor (IGF-1R) promotes physiological cardiac growth and enhances contractile function. The aim of the present study was to examine whether cardiac-specific overexpression of IGF-1R prevents diabetes-induced myocardial remodeling and dysfunction associated with a murine model of diabetes.RESEARCH DESIGN AND METHODSType 1 diabetes was induced in 7-week-old male IGF-1R transgenic mice using streptozotocin and followed for 8 weeks. Diastolic and systolic function was assessed using Doppler and M-mode echocardiography, respectively, in addition to cardiac catheterization. Cardiac fibrosis and cardiomyocyte width, heart weight index, gene expression, Akt activity, and IGF-1R protein content were also assessed.RESULTSNontransgenic (Ntg) diabetic mice had reduced initial (E)-to-second (A) blood flow velocity ratio (E:A ratio) and prolonged deceleration times on Doppler echocardiography compared with nondiabetic counterparts, indicative markers of diastolic dysfunction. Diabetes also increased cardiomyocyte width, collagen deposition, and prohypertrophic and profibrotic gene expression compared with Ntg nondiabetic littermates. Overexpression of the IGF-1R transgene markedly reduced collagen deposition, accompanied by a reduction in the incidence of diastolic dysfunction. Akt phosphorylation was elevated ∼15-fold in IGF-1R nondiabetic mice compared with Ntg, and this was maintained in a setting of diabetes.CONCLUSIONSThe current study suggests that cardiac overexpression of IGF-1R prevented diabetes-induced cardiac fibrosis and diastolic dysfunction. Targeting IGF-1R–Akt signaling may represent a therapeutic target for the treatment of diabetic cardiac disease.

Atrial fibrillation (AF) is the most common sustained arrhythmia presenting at cardiology departments. A limited understanding of the molecular mechanisms responsible for the development of AF has hindered treatment strategies. The purpose of this study was to assess whether reduced activation of phosphoinositide 3-kinase (PI3K, p110␣) makes the compromised heart susceptible to AF. Risk factors for AF, including aging, obesity, and diabetes, have been associated with insulin resistance that leads to depressed/defective PI3K signaling. However, to date, there has been no link between PI3K(p110␣) and AF. To address this question, we crossed a cardiac-specific transgenic mouse model of dilated cardiomyopathy (DCM) with a cardiac-specific transgenic mouse expressing a dominant negative mutant of PI3K (dnPI3K; reduces PI3K activity). Adult (ϳ4.5 months) double-transgenic (dnPI3K-DCM), single-transgenic (DCM-Tg, dnPI3K-Tg), and nontransgenic mice were subjected to morphological, functional/ECG, microarray, and biochemical analyses. dnPI3K-DCM mice developed AF and had depressed cardiac function as well as greater atrial enlargement and fibrosis than DCM-Tg mice. AF was not detected in other groups. Aged DCM-Tg mice (ϳ15 months) with a similar phenotype to dnPI3K-DCM mice (4.5 months) did not develop AF , suggesting loss of PI3K activity directly contributed to the AF phenotype. Furthermore, increasing PI3K activity reduced atrial fibrosis and improved cardiac conduction in DCM-Tg mice. Finally, in atrial appendages from patients with AF, PI3K activation was lower compared with tissue from patients in sinus rhythm. These results suggest a link between PI3K(p110␣) and AF. (Am J Pathol

Multiple lines of evidence 1,2 have established the existence of a land carbon sink in the northern hemisphere, but its trend remains poorly understood 3,4 . Here we show from measurements of the atmospheric CO2 gradient between the stations of Mauna Loa (north) and of South Pole (south) since 1958 that the northern land sink remained rather stable between the 1960s and the late 1980s, but increased by 0.5 ± 0.4 Pg C yr -1 during the 1990s and further by 0.6 ± 0.5 Pg C yr -1 during the 2000s. The first increase of the northern land sink in the 1990s accounts for 65% of the increase in the global land flux during that period. The subsequent increase in the 2000s is larger than the increase of the global land flux, suggesting a coincident decrease of carbon uptake in southern regions. The decadal change in the northern land sink between the 1960s and the 1990s can be explained with a combination of rising atmospheric CO2, climate variability, and changes in land-cover as represented in an ensemble of terrestrial carbon cycle models 4 . The increase during the 2000s is however underestimated by all terrestrial models. Reducing uncertainties involve better consideration of changes in drivers such as land use change, diffuse light, and nitrogen deposition as well as denser observations to clarify the importance of different regions.Fossil fuel and land-use change emissions of CO2 into the atmosphere increased by a factor of three between 1960 and 2016, with a fast growth rate in the 1980s, a slower growth rate in the 1990s and a re-acceleration 5 in the 2000s. The global land and ocean carbon sinks increased proportionally with growing emissions 6 but their location and trends are incompletely understood. Northern Hemisphere (NH) lands make a dominant contribution to the global land carbon sink 1-4,7-8 . In the NH mid and high latitudes, vegetation greenness increased in the last 30 years 9 , and the seasonal amplitude of CO2 increased by 50% in the last 50 years 10 , suggesting an enhancement of ecosystem production.However, these observations are not proofs that the NH net carbon sink is increasing because of possible upward trends in soil respiration 11 and land-use emissions compensating for increased production.To gain insights on the long-term trend in the northern land sink over the last 50 years, we use the inter-hemispheric gradient of atmospheric CO2 (IG) defined as the observed difference of atmospheric CO2 between the Mauna-Loa (MLO) station located at 19°N, and South Pole (SPO).Both MLO and SPO record CO2 growth rates representative of the means in their respective hemisphere 12 . Here we examine the relationship between IG and fossil fuel and cement CO2 emissions (F) between 1958 and 2016, and recent changes during the 2000s, a period marked by the acceleration of global CO2 emissions, mainly from East and South Asia regions [13][14] .From 1958 to 2016 the IG grew proportional to F (Fig. 1; Fig. ED1) with a Pearson correlation coefficient (r) of 0.97 (p <0.01) and a mean regression slope 15 of 0.44± 0.01...

Background— Numerous molecular and biochemical changes have been linked with the cardioprotective effects of exercise, including increases in antioxidant enzymes, heat shock proteins, and regulators of cardiac myocyte proliferation. However, a master regulator of exercise-induced protection has yet to be identified. Here, we assess whether phosphoinositide 3-kinase (PI3K) p110α is essential for mediating exercise-induced cardioprotection, and if so, whether its activation independent of exercise can restore function of the failing heart. Methods and Results— Cardiac-specific transgenic (Tg) mice with elevated or reduced PI3K(p110α) activity (constitutively active PI3K [caPI3K] and dominant negative PI3K, respectively) and non-Tg controls were subjected to 4 weeks of exercise training followed by 1 week of pressure overload (aortic-banding) to induce pathological remodeling. Aortic-banding in untrained non-Tg controls led to pathological cardiac hypertrophy, depressed systolic function, and lung congestion. This phenotype was attenuated in non-Tg controls that had undergone exercise before aortic-banding. Banded caPI3K mice were protected from pathological remodeling independent of exercise status, whereas exercise provided no protection in banded dominant negative PI3K mice, suggesting that PI3K is necessary for exercise-induced cardioprotection. Tg overexpression of heat shock protein 70 could not rescue the phenotype of banded dominant negative PI3K mice, and deletion of heat shock protein 70 from banded caPI3K mice had no effect. Next, we used a gene therapy approach (recombinant adeno-associated viral vector 6) to deliver caPI3K expression cassettes to hearts of mice with established cardiac dysfunction caused by aortic-banding. Mice treated with recombinant adeno-associated viral 6-caPI3K vectors had improved heart function after 10 weeks. Conclusions— PI3K(p110α) is essential for exercise-induced cardioprotection and delivery of caPI3K vector can improve function of the failing heart.

Over the last century the Northern Hemisphere has experienced rapid climate warming, but this warming has not been evenly distributed seasonally, as well as diurnally. The implications of such seasonal and diurnal heterogeneous warming on regional and global vegetation photosynthetic activity, however, are still poorly understood. Here, we investigated for different seasons how photosynthetic activity of vegetation correlates with changes in seasonal daytime and night-time temperature across the Northern Hemisphere (>30°N), using Normalized Difference Vegetation Index (NDVI) data from 1982 to 2011 obtained from the Advanced Very High Resolution Radiometer (AVHRR). Our analysis revealed some striking seasonal differences in the response of NDVI to changes in day- vs. night-time temperatures. For instance, while higher daytime temperature (Tmax) is generally associated with higher NDVI values across the boreal zone, the area exhibiting a statistically significant positive correlation between Tmax and NDVI is much larger in spring (41% of area in boreal zone--total area 12.6×10(6) km2) than in summer and autumn (14% and 9%, respectively). In contrast to the predominantly positive response of boreal ecosystems to changes in Tmax, increases in Tmax tended to negatively influence vegetation growth in temperate dry regions, particularly during summer. Changes in night-time temperature (Tmin) correlated negatively with autumnal NDVI in most of the Northern Hemisphere, but had a positive effect on spring and summer NDVI in most temperate regions (e.g., Central North America and Central Asia). Such divergent covariance between the photosynthetic activity of Northern Hemispheric vegetation and day- and night-time temperature changes among different seasons and climate zones suggests a changing dominance of ecophysiological processes across time and space. Understanding the seasonally different responses of vegetation photosynthetic activity to diurnal temperature changes, which have not been captured by current land surface models, is important for improving the performance of next generation regional and global coupled vegetation-climate models.

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