The multi-year contribution of Indo-China peninsula fire emissions to aerosol radiation forcing in southern China during 2013-2019.

Fire emissions in Southeast Asia transported to southern China every spring (March-May), influencing not only the air quality but also the weather and climate. However, the multi-year variations and magnitude of this impact on aerosol radiation forcing in southern China remain unclear. Here, we quantified the multi-year contributions of fire emissions in Indo-China Peninsula (ICP) region to aerosol radiation forcing in the various southern Chinese provinces during the fire season (March-May) of 2013-2019 combining the 3-dimension chemical transport model and the Column Radiation Model (CRM) simulations. The models' evaluations showed they reasonably capture the temporal and spatial distribution of surface aerosol concentrations and column aerosol optical properties over the study regions. The fire emissions over the ICP region were found to increase the aerosol optical depth (AOD) value by 0.1 (15 %) and reduce the single scattering albedo (SSA) in three southern regions of China (Yunnan-YN, Guangxi-GX, and Guangdong-GD from west to east), owing to increases in the proportions of black carbon (BC, 0.4 % ± 0.1 %) and organic carbon (OC, 3.0 % ± 0.9 %) within the aerosol compositions. The transported smoke aerosols cooled surface but heated the atmosphere in the southern China regions, with the largest mean reduction of -5 Wm-2 (-3 %) in surface shortwave radiation forcing and the maximum daily contributions of about -15 Wm-2 (-15 %) to the atmosphere radiation forcing in the GX region, followed by the GD and YN regions. The impacts of ICP fire emissions on aerosol optical and radiative parameters declined during 2013-2019, with the highest rate of 0.393 ± 0.478 Wm-2 yr-1 in the GX for the shortwave radiation forcing in the atmosphere. Besides, their yearly changes in the contribution were consistent with the annual fire emissions in the ICP region. Such strong radiative perturbations of ICP fire emissions were expected to influence regional meteorology in southern China and should be considered in the climate simulations.

Assessment of solar energy potential in China using an ensemble of photovoltaic power models.

Development of solar energy is one of the key solutions towards carbon neutrality in China. The output of solar energy is dependent on weather conditions and shows distinct spatiotemporal characteristics. Previous studies have explored the photovoltaic (PV) power potential in China but with single models and low-resolution radiation data. Here, we estimated the PV power potential in China for 2016-2019 using an ensemble of 11 PV models based on hourly solar radiation at the resolution of 5 km retrieved by the Himawari-8 geostationary satellite. On the national scale, the ensemble method revealed an annual average PV power potential of 242.79 kWh m-2 with the maximum in the west (especially the Tibetan Plateau) and the minimum in the southeast (especially the Sichuan Basin). The multi-model approach shows inter-model spreads of 6 %-7 % distributed uniformly in China, suggesting a robust spatial pattern predicted by these models. The seasonal variation in general shows the largest PV power generation in summer months except for Tibetan Plateau, where the peak value appears in spring because the high cloud coverage dampens the regional solar radiation in summer. On the national scale, the deseasonalized PV power potential shows a high correlation with cloud coverage (R2 = 0.71, p < 0.01) but a low correlation with aerosol optical depth (R2 = 0.08, p < 0.05). Sensitivity experiments show that national PV power potential increases by 0.55 % per 1 W m-2 increase of radiation and 0.79 % per 1 m s-1 increase of wind speed, but decreases by 0.46 % per 1 °C increase of air temperature. These sensitivities provide a solid foundation for the future projection of PV power potential in China under climate change.

Projections of fire emissions and the consequent impacts on air quality under 1.5 °C and 2 °C global warming.

Fire is a major source of atmospheric aerosols and trace gases. Projection of future fire activities is challenging due to the joint impacts of climate, vegetation, and human activities. Here, we project global changes of fire-induced particulate matter smaller than 2.5 µm (PM2.5) and ozone (O3) under 1.5 °C/2 °C warming using a climate-chemistry-vegetation coupled model in combination with site-level and satellite-based observations. Compared to the present day, fire emissions of varied air pollutants increase by 10.0%-15.4% at the 1.5 °C warming period and 15.1%-22.5% at the 2 °C warming period, with the most significant enhancements in Amazon, southern Africa, and boreal Eurasia. The warmer climate promotes fuel dryness and the higher leaf area index increases fuel availability, leading to escalated fire flammability globally. However, moderate declines in fire emissions are predicted over the Sahel region, because the higher population density increases fire suppressions and consequently inhibits fire activities over central Africa. Following the changes in fire emissions, the population-weighted exposure to fire PM2.5 increases by 5.1% under 1.5 °C warming and 13.0% under 2 °C warming. Meanwhile, the exposure to fire O3 enhances by 10.2% and 16.0% in response to global warming of 1.5 °C and 2 °C, respectively. As a result, limiting global temperature increase to 1.5 °C can greatly reduce the risks of exposure to fire-induced air pollution compared to 2 °C.

Global Perspective of Drought Impacts on Ozone Pollution Episodes.

Ozone (O3) pollution threatens global public health and damages ecosystem productivity. Droughts modulate surface O3 through meteorological processes and vegetation feedbacks. Unraveling these influences is difficult with traditional chemical transport models. Here, using an atmospheric chemistry-vegetation coupled model in combination with a suite of existing measurements, we investigate the drought impacts on global surface O3 and explore the main driving processes. Relative to the mean state, accelerated photochemical rates dominate the surface O3 enhancement during droughts except for eastern U.S. and western Europe, where reduced stomatal uptakes make comparable contributions. During 1990-2012, the simulated frequency of O3 pollution episodes in western Europe decreases greatly with a negative trend of -5.5 ± 6.6 days per decade following the reductions in anthropogenic emissions if meteorology is fixed. However, such decreased trend is weakened to -2.1 ± 3.8 days per decade, which is closer to the observed trend of -2.9 ± 1.1 days per decade when year-to-year meteorology is applied because increased droughts alone offset 43% of the effects from air pollution control. Our results highlight that more stringent controls of O3 precursors are necessary to mitigate the higher risks of O3 pollution episodes by more droughts in a warming world.

Identifying the dominant climate-driven uncertainties in modeling gross primary productivity.

Accurate simulation of gross primary productivity (GPP) is essential for estimating the global carbon budget. However, GPP modeling is subject to various sources of uncertainties, among which the impacts of biases in climate forcing data have not been well quantified. Here, using a well-validated vegetation model, we compare site-level simulations using either ground-based meteorology or assimilated reanalyses to identify climate-driven uncertainties in the predicted GPP at 91 FLUXNET sites. Simulations yield the lowest root mean square errors (RMSE) in GPP relative to observations when all site-level meteorology and CO2 concentrations are used. Sensitivity tests conducted with Modern-Era Retrospective Analysis (MERRA) reanalyses increase GPP RMSE by 30%. Replacement of site-level CO2 with global annual average values provides limited contributions to these changes. In contrast, GPP uncertainties increase almost linearly with the biases in meteorology. Among all factors, photosynthetically active radiation (PAR), especially diffuse PAR, plays dominant roles in modulating GPP uncertainties. Simulations using all MERRA forcings but with site-level diffuse PAR help reduce over 50% of the climate-driven biases in GPP. Our study reveals that biases in meteorological forcings, especially the variabilities at diurnal to seasonal time scales, can induce significant uncertainties in the simulated GPP at FLUXET sites. We suggest cautions in simulating global GPP using climate reanalyses for dynamic global vegetation models and urgent improvements in climatic variability in reanalyses data, especially for diffuse radiation.

Presence of White Matter Lesions Associated with Diabetes-Associated Cognitive Decline in Male Rat Models of Pre-Type 2 Diabetes.

BACKGROUND The aim of this study was to determine the association between white matter lesions (WML) and diabetes-associated cognitive decline (DACD) in rat models of type 2 diabetes (T2DM). MATERIAL AND METHODS Sixty Sprague-Dawley male rats were divided into 4 groups: control, control+metformin, T2DM, and T2DM+metformin groups. The T2DM groups were fed a diet high in fat and glucose to induce impaired glucose tolerance (IGT) and then were injected with streptozotocin to induce T2DM. The Morris water maze test was used to evaluate cognitive function. Brain diffusion tensor imaging scans were performed for WML. The expression of myelin basic protein (MBP), oligodendrocyte transcription factor 1 (OLIG1), and OLIG2 (markers of brain damage and repair) was determined using immunofluorescence. After IGT, the fractional anisotropy (FA) values of the right thalamus area were significantly lower in both T2DM groups compared with controls. RESULTS Eight weeks after streptozotocin injection, the FA values of the thalamus were lower in the T2DM (bilateral thalamus) group and T2DM+metformin (left thalamus) group than in controls, while the FA values in the left thalamus area were lower in the T2DM+metformin group than in the control and control+metformin groups. The maze escape latency was longer and the number of rats passing through the platform was smaller in the T2DM and T2DM+metformin groups than in the control group. MBP levels were lower and OLIG1 and OLIG2 levels were higher in both T2DM groups than in controls. CONCLUSIONS WML is associated with DACD and appears before the onset of T2DM and signs of DACD and plays a role in diabetes-associated cognitive decline. Metformin reduces WMLs but does not rescue cognitive dysfunction.

High sucrose/fat diet and isosorbide mononitrate increase insulin resistance, nitric oxide production and myocardial apoptosis in a hypertensive rat model.

The present study aimed to investigate the association between insulin resistance (IR), nitric oxide (NO) production and myocardial apoptosis in a background of coexisting hypertension in a rodent animal model. A hypertensive rat model was established by feeding Wistar and spontaneously hypertensive rats (SHR) with a high sucrose/fat (HSF) diet for 12 weeks, in conjunction with isosorbide mononitrate (ISMN). Increased IR, NO content, apoptotic gene and protein expression, and morphological alterations within rat myocardium were evaluated. Following a total of 12 weeks of feeding with HSF and ISMN resulted in increased IR and NO content within the myocardial tissue of Wistar and SHR rats. HSF and ISMN activated myocardial apoptosis by downregulating the gene transcription and protein expression levels of the anti­apoptotic B­cell lymphoma 2 (Bcl­2), and increasing the pro­apoptotic Bcl­2 associated X protein. Apoptosis was demonstrated by DNA fragmentation in terminal deoxynucleotidyl­transferase­mediated dUTP nick end labelling assay. In all experiments, the combination of HSF and ISMN was associated with more pronounced effects, indicating the possible synergistic effects. In addition, the correlation analysis in the Wistar rats fed with HSF only, revealed a positive association between NO production and IR. The results of the present study indicated that HSF and ISMN simultaneously increased IR, NO production and myocardial apoptosis in the hypertensive rat model, and may therefore contribute to investigations into the long­term clinical use of ISMN in hypertensive patients.

C1qTNF-related protein 1 improve insulin resistance by reducing phosphorylation of serine 1101 in insulin receptor substrate 1.

C1qTNF-related protein 1 (CTRP1) is independently associated with type 2 diabetes. However, the relationship between CTRP1 and insulin resistance is still not established. This study aimed to explore the role of CTRP1 under the situation of insulin resistance in adipose tissue. Plasma CTRP1 level was investigated in type 2 diabetic subjects (n = 35) and non-diabetic subjects (n = 35). The relationship between CTRP1 and phosphorylation of multi insulin receptor substrate 1 (IRS-1) serine (Ser) sites was further explored. Our data showed that Plasma CTRP1 was higher and negative correlation with insulin resistance in diabetic subjects (r = -0.283, p = 0.018). Glucose utilisation test revealed that the glucose utilisation rate of mature adipocytes was improved by CTRP1 in the presence of insulin. CTRP1 was not only related to IRS-1 protein, but also negatively correlated with IRS-1 Ser1101 phosphorylation (r = -0.398, p = 0.031). Furthermore, Phosphorylation levels of IRS-1 Ser1101 were significantly lower after incubation with 40 ng/mL CTRP1 in mature adipocytes than those with no intervention (p < 0.05). There was no significant correlation between CTRP1 and other IRS-1 serine sites (Ser302, Ser307, Ser612, Ser636/639, and Ser789). Collectively, our results suggested that CTRP1 might improve insulin resistance by reducing the phosphorylation of IRS-1 Ser1101, induced in the situation of insulin resistance as a feedback adipokine.

Role of PI3K p110ß in the differentiation of human embryonic stem cells into islet-like cells.

To investigate the effects of the PI3K inhibitors on the differentiation of insulin-producing cells derived from human embryonic stem cells. Here, we report that human embryonic stem cells induced by phosphatidylinositol-3-kinase (PI3K) p110ß inhibitors could produce more mature islet-like cells. Findings were validated by immunofluorescence analysis, quantitative real-time PCR, insulin secretion in vitro and cell transplantation for the diabetic SCID mice. Immunofluorescence analysis revealed that unihormonal insulin-positive cells were predominant in cultures with rare polyhormonal cells. Real-time PCR data showed that islet-like cells expressed key markers of pancreatic endocrine hormones and mature pancreatic ß cells including MAFA. Furthermore, this study showed that the expression of most pancreatic endocrine hormones was similar between groups treated with the LY294002 (nonselective PI3K inhibitor) and TGX-221 (PI3K isoform selective inhibitors of class 1ß) derivatives. However, the level of insulin mRNA in TGX-221-treated cells was significantly higher than that in LY294002-treated cells. In addition, islet-like cells displayed glucose-stimulated insulin secretion in vitro. After transplantation, islet-like cells improved glycaemic control and ameliorated the survival outcome in diabetic mice. This study demonstrated an important role for PI3K p110ß in regulating the differentiation and maturation of islet-like cells derived from human embryonic stem cells.

Elevated circulating levels of CTRP1, a novel adipokine, in diabetic patients.

Complement C1q tumor necrosis factor-related protein 1 (CTRP1), an adipose tissue-derived adipokine has been shown to decrease blood glucose levels and to improve metabolism of glucose in mice. In addition, CTRP1 has exhibited significant association with BMI, adiponectin and TNF-α in diabetic animal models. However, there are no published studies addressing CTRP1 levels in type 2 diabetic patients. Therefore, it was of interest to evaluate plasma CTRP1 levels and associated clinical parameters and biomarkers in patients with type 2 diabetes. 135 subjects were recruited to this study, including 62 type 2 diabetic patients (DM group) and 73 healthy subjects (control group). We measured biochemical parameters, CTRP1, TNF-α and adiponectin using enzyme-linked immunosorbent assay (ELISA). Plasma CTRP1 levels showed a significant difference between the DM group and the control group (646.3 ± 154.4 ng/mL vs. 442.6 ± 165.4 ng/mL, p < 0.01). In addition, CTRP1 was strongly positively associated with BMI, glucose levels, HbA1c, HOMA-IR and TNF-α in diabetic patients. CTRP1 showed negative correlation with adiponectin. In Multivariate regression analysis, CTRP1 was strongly independently associated with diabetes when CTRP1 levels were analyzed by both as a continuous variable and quartile (OR: 1.009, 95% CI: 1.004-1.015, p < 0.05; OR: 2.443, 95% CI: 1.379-4.182, p < 0.01, respectively). Increased plasma CTRP1 was independently associated with type 2 diabetes. Profiling of plasma adipokines such as CTRP1 is particularly important to obtain a greater understanding of their contribution to the type 2 diabetic state.

Tubulin as a binding partner of the heag2 voltage-gated potassium channel.

The aim of this work was to investigate interactions of the human ether-a-go-go channel heag2 with human brain proteins. For this, we used heag2-GST fusion proteins in pull-down assays with brain proteins and mass spectrometry, as well as coimmunoprecipitation. We identified tubulin and heat shock 70 proteins as binding to intracellular C-terminal regions of the channel. To study functional effects, heag2 channels were expressed in Xenopus laevis oocytes for two-electrode voltage clamping. Coexpression of alpha-tubulin or the application of colchicine significantly prolonged channel activation times. Application at different times of colchicine gave similar results. The data suggest that colchicine application and tubulin expression do not affect heag2 trafficking and that tubulin may associate with the channel to cause functional effects. Coexpression of heat shock 70 proteins had no functional effect on the channel. The role of tubulin in the cell cytoskeleton suggests a link for the heag2 channel in tubulin-dependent physiological functions, such as cellular proliferation.