Vegetation dynamics and their response to freshwater inflow and climate variables in the Yellow River Delta, China

Based on SPOT Vegetation NDVI data, streamflow data and meteorological data, the variation of vegetation cover, measured by the Normalized Difference Vegetation Index (NDVI), and its response to freshwater inflow, precipitation and temperature in the Yellow River Delta and its buffer zones have been investigated for the period 1998-2009. The results show that NDVI has a remarkable regional and seasonal difference. The farther from the Yellow River Channel and the nearer to the Bohai Sea Coastline, the smaller the NDVI value, as influenced by the interaction between freshwater and saltwater on vegetation. Seasonally, high NDVI values appear in summer (August) and low in spring (April). From 1998 to 2009, growing season NDVI significantly increases in the Yellow River Delta. Summer and autumn NDVI have a similar trend pattern to growing season NDVI, while spring NDVI significantly decreases. NDVI shows different strengths of correlation with freshwater inflow, precipitation and temperature respectively and these correlations vary in different seasons and months. Freshwater inflow is a key factor for vegetation dynamics and NDVI variation. Climate features play a dominant role in seasonal variation in vegetation cover. However, the impacts of freshwater inflow and climate variables on vegetation have been greatly modified by a range of human activities such as land use pattern and land use change as well as water diversion from the Yellow River. Overall, the results of this study can be helpful for decision-making of regional ecological protection and economic development. (C) 2012 Elsevier Ltd and INQUA. All rights reserved.Based on SPOT Vegetation NDVI data, streamflow data and meteorological data, the variation of vegetation cover, measured by the Normalized Difference Vegetation Index (NDVI), and its response to freshwater inflow, precipitation and temperature in the Yellow River Delta and its buffer zones have been investigated for the period 1998-2009. The results show that NDVI has a remarkable regional and seasonal difference. The farther from the Yellow River Channel and the nearer to the Bohai Sea Coastline, the smaller the NDVI value, as influenced by the interaction between freshwater and saltwater on vegetation. Seasonally, high NDVI values appear in summer (August) and low in spring (April). From 1998 to 2009, growing season NDVI significantly increases in the Yellow River Delta. Summer and autumn NDVI have a similar trend pattern to growing season NDVI, while spring NDVI significantly decreases. NDVI shows different strengths of correlation with freshwater inflow, precipitation and temperature respectively and these correlations vary in different seasons and months. Freshwater inflow is a key factor for vegetation dynamics and NDVI variation. Climate features play a dominant role in seasonal variation in vegetation cover. However, the impacts of freshwater inflow and climate variables on vegetation have been greatly modified by a range of human activities such as land use pattern and land use change as well as water diversion from the Yellow River. Overall, the results of this study can be helpful for decision-making of regional ecological protection and economic development. (C) 2012 Elsevier Ltd and INQUA. All rights reserved

Microwave Assisted Hydrolysis Of Holocellulose Catalyzed With Sulfonated Char Derived From Lignin-Rich Residue

A microwave assisted green process has been developed for production of sugars through liquefying holocellulose catalyzed with sulfonated char derived from the lignin-rich residue produced during pretreatment of lignocellulose. Various reaction parameters including the hydrolysis temperature, hydrolysis time, catalyst content, and the ratio of water to feedstock were evaluated. The maximum sugars yield of 82.6% (based on the dry mass of holocellulose) was obtained under the optimum reaction conditions. The sulfonated char showed superior catalytic performance to that of dilute sulfuric acid in converting holocellulose into sugars under microwave irradiation

Inhibition of HSP90 promotes neural stem cell survival from oxidative stress through attenuating NF-κB/p65 activation

Stem cell survival post transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades of yeas. The engrafted stem cells face the damage of oxidative stress, inflammation and immune response at the lesion point in host. Among the pathology, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in detail mechanism of stem cell survival from oxidative stress has not revealed clearly. Here in this study, we used hydrogen peroxide (H2O2) to induced the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF-κB/p65 signalling pathways. Further application of the pharmacological inhibitors respectively targeting at each signalling indicated an upper streaming role of HSP90 upon NF-κB/p65 on NSCs survival. Pre-inhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF-κB/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF-κB mechanism provides a new evidence on rescuing NSCs from oxidative stress, and also promotes the stem cell application on CNS pathologies

Inhibition of HSP90 Promotes Neural Stem Cell Survival from Oxidative Stress through Attenuating NF- κ

Stem cell survival after transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades. The engrafted stem cells face the damage of oxidative stress, inflammation, and immune response at the lesion point in host. Among the damaging pathologies, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in-detail mechanism of stem cell survival from oxidative stress has not been revealed clearly. Here, in this study, we used hydrogen peroxide (H2O2) to induce the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF-κB/p65 signalling pathways. Further application of the pharmacological inhibitors, respectively, targeting at each signalling indicated an upper-stream role of HSP90 upon NF-κB/p65 on NSCs survival. Preinhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF-κB/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF-κB mechanism provides a new evidence on rescuing NSCs from oxidative stress and also promotes the stem cell application on CNS pathologies

Effects of Brain-Derived Neurotrophic Factor on Local Inflammation in Experimental Stroke of Rat

This study was aimed to investigate whether brain-derived neurotrophic factor (BDNF) can modulate local cerebral inflammation in ischemic stroke. Rats were subjected to ischemia by occluding the right middle cerebral artery (MCAO) for 2 hours. Rats were randomized as control, BDNF, and antibody groups. The local inflammation was evaluated on cellular, cytokine, and transcription factor levels with immunofluorescence, enzyme-linked immunosorbent assay, real-time qPCR, and electrophoretic mobility shift assay, respectively. Exogenous BDNF significantly improved motor-sensory, sensorimotor function, and vestibulomotor function, while BDNF did not decrease the infarct volume. Exogenous BDNF increased the number of both activated and phagocytotic microglia in brain. BDNF upregulated interleukin10 and its mRNA expression, while downregulated tumor necrosis factor α and its mRNA expression. BDNF also increased DNA-binding activity of nuclear factor-kappa B. BDNF antibody, which blocked the activity of endogenous BDNF, showed the opposite effect of exogenous BDNF. Our data indicated that BDNF may modulate local inflammation in ischemic brain tissues on the cellular, cytokine, and transcription factor levels

Metabolic Interaction of the Active Constituents of Coptis chinensis

Coptis chinensis is commonly used in traditional Chinese medicine. The study investigated metabolic interaction of the active constituents (berberine, coptisine, palmatine, and jatrorrhizine) of Coptis chinensis in human liver microsomes. After incubation of the four constituents of Coptis chinensis in HLMs, the metabolism of the four constituents was observed by HPLC. The in vitro inhibition experiment between the active constituents was conducted, and IC50 value was estimated. Coptisine exhibited inhibitions against the formation of the two metabolites of berberine with IC50 values of 6.5 and 8.3 μM, respectively. Palmatine and jatrorrhizine showed the weaker inhibitory effect on the formation of the metabolites of berberine. Berberine showed a weak inhibitory effect on the production of coptisine metabolite with an IC50 value of 115 μM, and palmatine and jatrorrhizine had little inhibitory effect on the formation of coptisine metabolite. Berberine, coptisine, and jatrorrhizine showed no inhibitory effect on the generation of palmatine metabolite (IC50 > 200 μM). The findings suggested that there are different degrees of metabolic interaction between the four components. Coptisine showed the strongest inhibition toward berberine metabolism

Single image super-resolution quality assessment: a real-world dataset, subjective studies, and an objective metric

Numerous single image super-resolution (SISR) algorithms have been proposed during the past years to reconstruct a high-resolution (HR) image from its low-resolution (LR) observation. However, how to fairly compare the performance of different SISR algorithms/results remains a challenging problem. So far, the lack of comprehensive human subjective study on large-scale real-world SISR datasets and accurate objective SISR quality assessment metrics makes it unreliable to truly understand the performance of different SISR algorithms. We in this paper make efforts to tackle these two issues. Firstly, we construct a real-world SISR quality dataset (i.e., RealSRQ ) and conduct human subjective studies to compare the performance of the representative SISR algorithms. Secondly, we propose a new objective metric, i.e., KLTSRQA , based on the Karhunen-Loéve Transform (KLT) to evaluate the quality of SISR images in a no-reference (NR) manner. Experiments on our constructed RealSRQ and the latest synthetic SISR quality dataset (i.e., QADS ) have demonstrated the superiority of our proposed KLTSRQA metric, achieving higher consistency with human subjective scores than relevant existing NR image quality assessment (NR-IQA) metrics. The dataset and the code will be made available at https://github.com/Zhentao-Liu/RealSRQ-KLTSRQA

Inhibition of HSP90 promotes neural stem cell survival from oxidative stress through attenuating NF-κB/p65 activation

Stem cell survival post transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades of yeas. The engrafted stem cells face the damage of oxidative stress, inflammation and immune response at the lesion point in host. Among the pathology, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in detail mechanism of stem cell survival from oxidative stress has not revealed clearly. Here in this study, we used hydrogen peroxide (H2O2) to induced the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF-κB/p65 signalling pathways. Further application of the pharmacological inhibitors respectively targeting at each signalling indicated an upper streaming role of HSP90 upon NF-κB/p65 on NSCs survival. Pre-inhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF-κB/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF-κB mechanism provides a new evidence on rescuing NSCs from oxidative stress, and also promotes the stem cell application on CNS pathologies