Road freight transportation accounts for around 7% of total world energy-related carbon dioxide emissions. With the appropriate incentives, energy savings and emissions reductions can be achieved by shifting freight to rail or water modes, both of which are far more efficient than road. We briefly introduce five general strategies for decarbonizing freight transportation, and then focus on the literature and data relevant to estimating the global decarbonization potential through modal shift. We compare freight activity (in tonne-km) by mode for every country where data are available. We also describe major intraregional freight corridors, their modal structure, and their infrastructure needs. We find that the current world road and rail modal split is around 60:40. Most countries are experiencing strong growth in road freight and a shift from rail to road. Rail intermodal transportation holds great potential for replacing carbon-intense and fast-growing road freight, but it is essential to have a targeted design of freight systems, particularly in developing countries. Modal shift can be promoted by policies targeting infrastructure investments and internalizing external costs of road freight, but we find that not many countries have such policies in place. We identify research needs for decarbonizing the freight transportation sector both through improvements in the efficiency of individual modes and through new physical and institutional infrastructure that can support modal shift.

BackgroundArrest of metastasising lung cancer cells to the brain microvasculature maybe mediated by interactions between ligands on circulating tumour cells and endothelial E-selectin adhesion molecules; a process likely to be regulated by the endothelial glycocalyx. Using human cerebral microvascular endothelial cells and non-small cell lung cancer (NSCLC) cell lines, we describe how factors secreted by NSCLC cells i.e. cystatin C, cathepsin L, insulin-like growth factor-binding protein 7 (IGFBP7), vascular endothelial growth factor (VEGF) and tumour necrosis factor-alpha (TNF-α), damage the glycocalyx and enhance initial contacts between lung tumour and cerebral endothelial cells.MethodsEndothelial cells were treated with tumour secreted-proteins or lung tumour conditioned medium (CM). Surface levels of E-selectin were quantified by ELISA. Adhesion of A549 and SK-MES-1 cells was examined under flow conditions (1 dyne/cm2). Alterations in the endothelial glycocalyx were quantified by binding of fluorescein isothiocyanate-linked wheat germ agglutinin (WGA-FITC).ResultsA549 and SK-MES-1 CM and secreted-proteins significantly enhanced endothelial surface E-selectin levels after 30 min and 4 h and tumour cell adhesion after 30 min, 4 and 24 h. Both coincided with significant glycocalyx degradation; A549 and SK-MES-1 CM removing 55 ± 12 % and 58 ± 18.7 % of WGA-FITC binding, respectively. Inhibition of E-selectin binding by monoclonal anti-E-selectin antibody completely attenuated tumour cell adhesion.ConclusionThese data suggest that metastasising lung cancer cells facilitate their own adhesion to the brain endothelium by secreting factors that damage the endothelial glycocalyx, resulting in exposure of the previously shielded adhesion molecules and engagement of the E-selectin-mediated adhesion axis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-015-0223-9) contains supplementary material, which is available to authorized users.

Epithelial ovarian cancer (EOC) metastasizes transcoelomically to the peritoneum and omentum, and despite surgery and chemotherapy, recurrent disease is likely. Metastasis requires the induction of proangiogenic changes in the omental microenvironment and EOC-induced omental angiogenesis is currently a key therapeutic target. In particular, antiangiogenic therapies targeting the vascular endothelial growth factor A (VEGFA) pathway are commonly used, although, with limited effects. Here, using human omental microvascular endothelial cells (HOMECs) and ovarian cancer cell lines as an in vitro model, we show that factors secreted from EOC cells increased proliferation, migration, and tube-like structure formation in HOMECs. However, EOC-induced angiogenic tube-like formation and migration were unaffected by inhibition of tyrosine kinase activity of VEGF receptors 1 and 2 (Semaxanib; SU5416) or neutralization of VEGFA (neutralizing anti-VEGFA antibody), although VEGFA165-induced HOMEC migration and tube-like structure formation were abolished. Proteomic investigation of the EOC secretome identified several alternative angiogenesis-related proteins. We screened these for their ability to induce an angiogenic phenotype in HOMECs, i.e., proliferation, migration, and tube-like structure formation. Hepatocyte growth factor (HGF) and insulin-like growth factor binding protein 7 (IGFBP-7) increased all three parameters, and cathepsin L (CL) increased migration and tubule formation. Further investigation confirmed expression of the HGF receptor c-Met in HOMECs. HGF- and EOC-induced proliferation and angiogenic tube structure formation were blocked by the c-Met inhibitor PF04217903. Our results highlight key alternative angiogenic mediators for metastatic EOC, namely, HGF, CL, and IGFBP-7, suggesting that effective antiangiogenic therapeutic strategies for this disease require inhibition of multiple angiogenic pathways.

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Renewable natural gas (RNG) sources are being considered in future energy strategy discussions as potential replacements for fossil natural gas (FNG). While today’s supply of RNG resources is insufficient to meet U.S. demands, there is significant interest in its viability to supplement and decarbonize the natural gas supply. However, the studies compare the life cycle global warming potential (GWP) of various RNG production pathways are lacking and focus mostly on a singular pathway. This effort is an attempt to close this gap and provide a comparison between the life cycle GWP of three major RNG pathways and the FNG pathway. The three RNG pathways evaluated are anaerobic digestion (AD), thermal gasification (TG), and power-to-gas (P2G) using various feedstocks. The functional unit is 1 MJ of compressed RNG ready for injection into the natural gas transmission network. The results show that RNG production is not always carbon neutral or negative. Depending on the pathway, the GWP impact of RNG production can range from −229 to 27 g CO2e/MJ compressed RNG, with AD of animal manure and AD of municipal solid waste being the least and the most impactful pathways, respectively, compared to the 10.1 g CO2e/MJ impact for compressed FNG.

The risk of venous thromboembolism (VTE) is increased in patients with cancer. However, the role of tumor markers as potential indicators of increased risk of VTE is still undetermined. In this retrospective observational case control study, levels of the tumor markers CEA, CA 19-9 and CA 125 in patients with colorectal, pancreatic, and ovarian cancer respectively, who were admitted to two community hospitals between January 2001 and December 2011, were compared between patients who were VTE positive and those who were VTE negative. The primary goal of this study was to determine whether VTE positive cancer patients had higher tumor marker levels compared to VTE negative cancer patients. In our study, 66.7% (48/72) of patients who were positive for VTE had elevated tumor markers while 65.3% (66/101) of patients who were negative for VTE had low (normal) tumor markers, indicating an association of high tumor marker levels with the diagnosis of VTE. This was statistically significant with an odds ratio of 3.77 and p-value of <0.0001 (95% CI of 1.99-7.14). When the VTE group was further divided into DVT and PE groups, 70.2% (40/57) of patients in the DVT positive group had high tumor markers with a p value of <0.0001 and an odds ratio of 3.99 (95% CI of 2.02 to 7.89) while 57.9% (11/19) of patients in pulmonary embolism positive group had high tumor markers; this was, however, not statistically significant (p-value of 0.35 and a CI of 0.59 to 4.10). In this retrospective study of 173 individuals with a diagnosis of either colorectal, pancreatic, or ovarian Cancer, higher tumor marker levels (CEA, CA 19-9, and CA 125 respectively) were associated with an increased risk of VTE, either DVT or PE. However, when further divided into either DVT or PE groups, the association remained statistically significant only for DVT but not for PE.