Abstract. Accurate assessment of anthropogenic carbon dioxide (CO2) emissions and their redistribution among the atmosphere, ocean, and terrestrial biosphere is important to better understand the global carbon cycle, support the development of climate policies, and project future climate change. Here we describe datasets and a methodology to quantify all major components of the global carbon budget, including their uncertainties, based on the combination of a range of data, algorithms, statistics and model estimates and their interpretation by a broad scientific community. We discuss changes compared to previous estimates consistency within and among components, alongside methodology and data limitations. CO2 emissions from fossil-fuel combustion and cement production (EFF) are based on energy statistics, while emissions from Land-Use Change (ELUC), including deforestation, are based on combined evidence from land-cover change data, fire activity in regions undergoing deforestation, and models. The global atmospheric CO2 concentration is measured directly and its rate of growth (GATM) is computed from the annual changes in concentration. The mean ocean CO2 sink (SOCEAN) is based on observations from the 1990s, while the annual anomalies and trends are estimated with ocean models. The variability in SOCEAN is evaluated for the first time in this budget with data products based on surveys of ocean CO2 measurements. The global residual terrestrial CO2 sink (SLAND) is estimated by the difference of the other terms of the global carbon budget and compared to results of Dynamic Global Vegetation Models. All uncertainties are reported as ± 1 sigma, reflecting the current capacity to characterise the annual estimates of each component of the global carbon budget. For the last decade available (2003–2012), EFF was 8.6 ± 0.4 GtC yr−1, ELUC 0.8 ± 0.5 GtC yr−1, GATM 4.3 ± 0.1 GtC yr−1, SOCEAN 2.6 ± 0.5 GtC yr−1, and SLAND 2.6 ± 0.8 GtC yr−1. For year 2012 alone, EFF grew to 9.7 ± 0.5 GtC yr−1, 2.2% above 2011, reflecting a continued trend in these emissions; GATM was 5.2 ± 0.2 GtC yr−1, SOCEAN was 2.9 ± 0.5 GtC yr−1, and assuming and ELUC of 0.9 ± 0.5 GtC yr−1 (based on 2001–2010 average), SLAND was 2.5 ± 0.9 GtC yr−1. GATM was high in 2012 compared to the 2003–2012 average, almost entirely reflecting the high EFF. The global atmospheric CO2 concentration reached 392.52 ± 0.10 ppm on average over 2012. We estimate that EFF will increase by 2.1% (1.1–3.1%) to 9.9 ± 0.5 GtC in 2013, 61% above emissions in 1990, based on projections of World Gross Domestic Product and recent changes in the carbon intensity of the economy. With this projection, cumulative emissions of CO2 will reach about 550 ± 60 GtC for 1870–2013, 70% from EFF (390 ± 20 GtC) and 30% from ELUC (160 ± 55 GtC). This paper is intended to provide a baseline to keep track of annual carbon budgets in the future. All data presented here can be downloaded from the Carbon Dioxide Information Analysis Center (10.3334/CDIAC/GCP_2013_v1.1).

These results indicate that the inactivation of ECRG 4 gene by hypermethylation is a frequent molecular event in ESCC and may be involved in the carcinogenesis of this cancer.

SummaryDegeneration of basal forebrain cholinergic neurons (BFCNs) is associated with cognitive impairments of Alzheimer’s disease (AD), implying that BFCNs hold potentials in exploring stem cell-based replacement therapy for AD. However, studies on derivation of BFCNs from embryonic stem cells (ESCs) are limited, and the application of ESC-derived BFCNs remains to be determined. Here, we report on differentiation approaches for directing both mouse and human ESCs into mature BFCNs. These ESC-derived BFCNs exhibit features similar to those of their in vivo counterparts and acquire appropriate functional properties. After transplantation into the basal forebrain of AD model mice, ESC-derived BFCN progenitors predominantly differentiate into mature cholinergic neurons that functionally integrate into the endogenous basal forebrain cholinergic projection system. The AD mice grafted with mouse or human BFCNs exhibit improvements in learning and memory performances. Our findings suggest a promising perspective of ESC-derived BFCNs in the development of stem cell-based therapies for treatment of AD.

The Greenland ice sheet is expected lose at least 90% of its current volume if ice sheet summer temperatures warm by around 1.8°C above pre-industrial. Geoengineering by stratospheric sulfate aerosol injection might slow Greenland ice sheet melting and sea level rise by reducing summer temperature and insolation; however, such schemes could also reduce precipitation and affect large-scale climate drivers such as the Atlantic Meridional Over-turning Circulation (AMOC). Earlier work found that AMOC increased under geoengineering and that might lead to greater mass loss from Greenland than under greenhouse gas forcing alone. We simulated Greenland ice sheet climates using four Earth system models running the stratospheric sulfate aerosol injection experiment GeoMIP G4 and the CMIP RCP4.5 and RCP8.5 greenhouse gas scenarios that were then used to drive the surface energy and mass balance model, SEMIC. Simulated runoff is 20% lower under G4 than RCP4.5, while under RCP8.5 it is 17% higher. The mechanism is through increased Arctic sea ice concentration and reduced humidity leading to surface cooling of the ablation zone. Reduced absorption of outgoing longwave radiation caused by hydrological cycle weakening dominates associated decreases in precipitation under geoengineering and stronger AMOC than under RCP4.5. An ice dynamics model simulates 15% lower ice losses under G4 than RCP4.5. Thus, total sea level rise by 2070 from the Greenland ice sheet under G4 geoengineering is about 15-20% lower than under the RCP4.5 scenario. Plain Language SummaryMass loss from the Greenland ice sheet is expected to raise sea levels by tens of centimeters this century and far more in the further future. Rising seas are one of the most damaging aspects of the warming climate, affecting hundreds of millions, and costing $ trillions by 2100, and geoengineering might be one approach that could be used against this threat. But the North Atlantic climate is a complex region where the flux of warm tropical waters is being reduced by greenhouse warming, which geoengineering would reverse. Hence, how Greenland would likely respond is a key factor in deciding the potential utility of doing geoengineering. We examine the impact of stratospheric aerosol geoengineering on both the surface ice sheet water runoff (which accounts for half of present-day ice loss) and the dynamic loss of ice from fast-flowing glaciers that are being accelerated by warming ocean currents (accounting for the other half). We find that aerosol injection equivalent to about ¼ Pinatubo volcanic eruption per year can slow mass loss from Greenland by 15-20% compared with greenhouse gas forcing alone, mainly due to reduced surface melting.

SummaryAlzheimer's disease (AD) is characterized by memory impairments in its earliest clinical phase. The synaptic loss and dysfunction leading to failures of synaptic networks in AD brain directly cause cognitive deficits of patient. However, it remains unclear whether the synaptic networks in AD brain could be repaired. In this study, we generated functional human induced neural progenitor/stem cells (iNPCs) that had been transplanted into the hippocampus of immunodeficient wild-type and AD mice. The grafted human iNPCs efficiently differentiated into neurons that displayed long-term survival, progressively acquired mature membrane properties, formed graft-host synaptic connections with mouse neurons and functionally integrated into local synaptic circuits, which eventually reinforced and repaired the neural networks of host hippocampus. Consequently, AD mice with human iNPCs exhibited enhanced synaptic plasticity and improved cognitive abilities. Together, our results suggest that restoring synaptic failures by stem cells might provide new directions for the development of novel treatments for human AD.

To develop a comprehensive approach for the study of oxytocin (OT) and vasopressin (VP) gene expression in the rat hypothalamus, we first developed an intronic riboprobe to measure OT heteronuclear RNA (hnRNA) levels by in situ hybridization histochemistry (ISHH). Using this 84-bp riboprobe, directed against intron 2 of the OT gene, we demonstrate strong and specific signals in neurons confined to the supraoptic (SON) and paraventricular (PVN) nuclei of the rat hypothalamus. We used this new intronic OT probe, together with other well-established intronic and exonic OT and VP probes, to reevaluate OT and VP gene expression in the hypothalamus under two classical physiological conditions, acute osmotic stimulation, and lactation. We found that magnocellular neurons in 7- to 8-day lactating female rats exhibit increased OT but not VP hnRNA. Since VP mRNA is increased during lactation, this suggests that decreased VP mRNA degradation during lactation may be responsible for this change. In contrast, whereas there was the expected large increase in VP hnRNA after acute salt loading, there was no change in OT hnRNA, suggesting that acute hyperosmotic stimuli produce increased VP but not OT gene transcription. Hence, the use of both exon- and intron-specific probes, which distinguish the changes in hnRNA and mRNA levels, respectively, can provide insight into the relative roles of transcription and mRNA degradation processes in changes in gene expression evoked by physiological stimuli.

In recent decades, there have been a number of debates on climate warming and its driving forces. Based on an extensive literature review, we suggest that (1) climate warming occurs with great uncertainty in the magnitude of the temperature increase;(2) both human activities and natural forces contribute to climate change, but their relative contributions are difficult to quantify; and (3) the dominant role of the increase in the atmospheric concentration of greenhouse gases (including CO 2 ) in the global warming claimed by the Intergovernmental Panel on Climate Change (IPCC) is questioned by the scientific communities because of large uncertainties in the mechanisms of natural factors and anthropogenic activities and in the sources of the increased atmospheric CO 2 concentration. More efforts should be made in order to clarify these uncertainties. carbon emissions, climate change, global warming, human activities, natural forces, uncertainty Citation: Fang J Y, Zhu J L, Wang S P, et al. Global warming, human-induced carbon emissions, and their uncertainties.

We have previously cloned and identified a novel esophageal cancer related gene 2 (ECRG2; GenBank Accession Number AF268198), which is down-regulated in esophageal squamous cell carcinoma (ESCC) and involved in the induction of the apoptosis in esophageal cancer cell lines. In the present study, we have found a short tandem repeat (STR) polymorphism in the noncoding region of the exon 4 of the ECRG2 gene by using PCR-denaturing high-performance liquid chromatography (DHPLC Esophageal cancer, with a 5-year survival rate Ͻ10%, is one of the most common fetal cancers worldwide and occurs at very high frequencies in certain areas of China, Iran, South Africa, Uruguay, France and Italy. 1 Fifty percent of esophageal cancer cases in the world occur in China. Among high-risk areas of esophageal squamous cell carcinoma (ESCC), Linxian County in Henan Province has the highest age-adjusted mortality rate of this cancer. 2 Epidemiological studies have revealed that the incidence of ESCC is associated with several factors, such as N-nitrosamines, which have been shown to be involved in the etiology of ESCC in Linxian. 3 However, studies in high-risk areas have demonstrated a strong tendency towards familial aggregation or clustering of cases within families, suggesting that genetic susceptibility factors may also play an important role in the etiology of ESCC.Previous studies have shown that several genetic abnormalities including amplification of C-myc, Int-2 and Hst, 4,5 mutation and/or deletion of p53 and Rb 2 and allelic deletion 6 have frequently occurred in human ESCC and esophageal cancer cell lines. However, the genetic events that lead to the development of esophageal cancer are not clear yet. In recent years, many studies of esophageal cancer are focused on the cloning and identification of novel esophageal cancer-related genes, which might play an important role in the carcinogenesis and development of the cancer. [7][8][9] Recently, we have cloned and identified a novel ESCC-related gene, ECRG2 (Genbank Accession Number AF 268198), from human normal esophageal epithelia. Firstly, we obtained an EST fragment by mRNA differential display techniques from 3 normal esophageal epithelia and 2 primary ESCC tissues from high incidence families in Linxian County and named it ECRG2. The RT-PCR detection results demonstrated that the expression of ECRG2 was down-regulated in ESCC as well as colon and brain tumors. 10 Secondly, we obtained the 569 bp full-length cDNA of the ECRG2 gene by SMARTTM RACE technique. We found that the gene contains 4 exons, spans about 3,540 bp on chromosome 5q32-33 and has a 258 bp open reading frame encoding an 85-amino acids polypeptide. 11 Analysis by bioinformatics has shown that 97% of the amino acid sequences of ECRG2 are homologous to a tumor associated KAZAL-type serine protease inhibitor that may play a central role in the protection of esophageal mucosa. 12 Thirdly, we studied the function of the ECRG2 gene by yeast 2-hybrid system and identified that the ECRG2 gene interacts directly ...