Identify sectors’ role on the embedded CO2 transfer networks through China’s regional trade

This study developed a framework for combining multi-regional input-output analysis and network indicators to assess the interregional CO₂ flows in China. The interregional CO₂ flows of eight regions were calculated and visualized based on a multiregional input-output (MRIO) model for China. The focus of the research was intermediate use. The results of the network indicators showed that refined petroleum, coke, nuclear fuel and chemical products (07), and basic metals and fabricated metal sectors (09) played key roles in the complex networks. and these sectors in most regions controlled a large share of CO₂ transfer by functioning as key hubs and authorities. They along with commerce, transport, storage, and post (16) acted as agents that brokered the CO₂ flows within and between regions. The roles of some other industrial sectors were also identified, e.g., construction (15) functioned as the largest authority. The results demonstrated the importance and effectiveness of network indicators for identifying the characteristics of CO₂ emissions embedded in the domestic supply chain, and provided new information relevant to policy implementation.     

mAbs’s communication networks

Since its start in 2009, mAbs has actively contributed to the communication networks among our readers. One way we achieve this is by publishing highly detailed reports of numerous meetings, conferences, summits, forums and congresses focused on antibody research and development (R&D) that are held in the US and Europe. The meetings serve critical informational and educational functions and are valuable networking opportunities, and mAbs is pleased to serve the antibody community by providing published records of the proceedings. PDFs of the meeting reports are generously made open access by the publisher of mAbs.     

Is there a role for CEA in innate immunity in the colon?

Carcinoembryonic antigen (CEA) is a well known tumor marker associated with the progression of colorectal tumors. The CEA family of glycoproteins has been fully characterized and the function of some of its members is now beginning to be understood. Here, we advance the hypothesis that, rather than functioning in cell adhesion as has been suggested previously, CEA plays a role in protecting the colonic mucosa from microbial invasion. This hypothesis is based on new microscopic, molecular, phylogenetic and microbiological evidence.     

Dung beetle-megafauna trophic networks in Singapore’s fragmented forests

We investigated trophic networks between dung beetles and megafauna species in five forest fragments in Singapore varying in size and isolation. We found that Singapore's dung beetle communities were attracted to extant and extinct dung types from different dietary groups. All forest fragment networks were similar and displayed high generalism and high nestedness.     

New insights into the role of TREM2 in Alzheimer’s disease

Alzheimer’s disease (AD) is the leading cause of dementia. The two histopathological markers of AD are amyloid plaques composed of the amyloid-β (Aβ) peptide, and neurofibrillary tangles of aggregated, abnormally hyperphosphorylated tau protein. The majority of AD cases are late-onset, after the age of 65, where a clear cause is still unknown. However, there are likely different multifactorial contributors including age, enviornment, biology and genetics which can increase risk for the disease. Genetic predisposition is considerable, with heritability estimates of 60–80%. Genetic factors such as rare variants of TREM2 (triggering receptor expressed on myeloid cells-2) strongly increase the risk of developing AD, confirming the role of microglia in AD pathogenesis. In the last 5 years, several studies have dissected the mechanisms by which TREM2, as well as its rare variants affect amyloid and tau pathologies and their consequences in both animal models and in human studies. In this review, we summarize increases in our understanding of the involvement of TREM2 and microglia in AD development that may open new therapeutic strategies targeting the immune system to influence AD pathogenesis.     

Regulatory role of Vγ1 γδ T cells in tumor immunity through IL-4 production

It has been demonstrated that the two main subsets of peripheral γδ T cells, Vγ1 and Vγ4, have divergent functions in many diseases models. Recently, we reported that Vγ4 γδ T cells played a protective role in tumor immunity through eomesodermin-controlled mechanisms. However, the precise roles of Vγ1 γδ T cells in tumor immunity, especially whether Vγ1 γδ T cells have any interaction with Vγ4 γδ T cells, remain unknown. We demonstrated in this paper that Vγ1 γδ T cells suppressed Vγ4 γδ T cell-mediated antitumor function both in vitro and in vivo, and this suppression was cell contact independent. Using neutralizing anti-IL-4 Ab or IL-4(-/-) mice, we determined the suppressive factor derived from Vγ1 γδ T cells was IL-4. Indeed, treatment of Vγ4 γδ T cells with rIL-4 significantly reduced expression levels of NKG2D, perforin, and IFN-γ. Finally, Vγ1 γδ T cells produced more IL-4 and expressed significantly higher level of GATA-3 upon Th2 priming in comparison with Vγ4 γδ T cells. Therefore, to our knowledge, our results established for the first time a negative regulatory role of Vγ1 γδ T cells in Vγ4 γδ T cell-mediated antitumor immunity through cell contact-independent and IL-4-mediated mechanisms. Selective depletion of this suppressive subset of γδ T cells may be beneficial for tumor immune therapy.     

Does the mitochondrial genome play a role in the etiology of Alzheimer’s disease?

We report here the analyses of complete mtDNA coding region sequences from more than 270 Alzheimer’s disease (AD) patients and normal controls to determine if inherited mtDNA mutations contribute to the etiology of AD. The AD patients and normal individuals were carefully screened and drawn from two populations of European descent in an effort to avoid spurious effects due to local population anomalies. Overall, there were no significant haplogroup associations in the combined AD and normal control sequence sets. Reduced median network analysis revealed that the AD mtDNA sequences contained a higher number of substitutions in tRNA genes, and that there was an elevated frequency of replacement substitutions in the complex I genes of the control sequences. Analysis of the replacement substitutions indicated that those arising in the AD mtDNAs were no more deleterious, on average, than those in the control mtDNAs. The only evidence for the synergistic action of mutations was the presence of both a rare non-conservative replacement substitution and a tRNA mutation in 2 AD mtDNAs, from a total of 145, whereas such a combination of mutations was not observed in the control sequences. Overall, the results reported here indicate that pathogenic inherited mtDNA mutations do not constitute a major etiological factor in sporadic AD. At most, a small proportion of AD patients carry a pathogenic mtDNA mutation and a small proportion of cognitively normal aged individuals carry a mtDNA mutation that reduces the risk of AD.Electronic Supplementary Material Supplementary material is available for this article at and is accessible for authorized users.     

Ubiquitin-protein ligase parkin and its role in the development of Parkinson’s disease

Parkin is a protein encoded by the corresponding parkin gene. It exhibits ubiquitin-protein ligase activity. In this review, we analyze domain structure, substrate specificity, subcellular localization of parkin, and regulation of its activity. Then we discuss data on the effects of various mutations in the parkin gene on structure and functions of this protein and results obtained with parkin knock-out animals. Better understanding of parkin biochemistry, its compartmentalization, functions, and altered functions would help the development of new approaches for the treatment of both inherited and sporadic cases of Parkinson’s disease. Published in Russian in Biokhimiya, 2006, Vol. 71, No. 8, pp. 1050–1061.     

Cities through the Prism of People’s Spending Behavior

Scientific studies of society increasingly rely on digital traces produced by various aspects of human activity. In this paper, we exploit a relatively unexplored source of data–anonymized records of bank card transactions collected in Spain by a big European bank, and propose a new classification scheme of cities based on the economic behavior of their residents. First, we study how individual spending behavior is qualitatively and quantitatively affected by various factors such as customer’s age, gender, and size of his/her home city. We show that, similar to other socioeconomic urban quantities, individual spending activity exhibits a statistically significant superlinear scaling with city size. With respect to the general trends, we quantify the distinctive signature of each city in terms of residents’ spending behavior, independently from the effects of scale and demographic heterogeneity. Based on the comparison of city signatures, we build a novel classification of cities across Spain in three categories. That classification exhibits a substantial stability over different city definitions and connects with a meaningful socioeconomic interpretation. Furthermore, it corresponds with the ability of cities to attract foreign visitors, which is a particularly remarkable finding given that the classification was based exclusively on the behavioral patterns of city residents. This highlights the far-reaching applicability of the presented classification approach and its ability to discover patterns that go beyond the quantities directly involved in it.