In-situ measurements of oxygen, carbon monoxide and greenhouse gases from Ochsenkopf tall tower in Germany

We present 2.5 years (from June 2006 to December 2008) of in-situ measurements of CO2, O2, CH4, CO, N2O and SF6 mixing ratios sampled from 23, 90 and 163m above ground on the Ochsenkopf tower in the Fichtelgebirge range, Germany (50?0104900 N, 11?4803000 E, 1022ma.s.l.). In addition to the in-situ measurements, flask samples are taken at Ochsenkopf at approximately weekly intervals and are subsequently analysed for the mixing ratios of the same species, as well as H2, and the stable isotopes, ?13C, ?18O in CO2. The in-situ measurements of CO2 and O2 from 23m show substantial diurnal variations that are modulated by biospheric fluxes, combustion of fossil fuels, and by diurnal changes in the planetary boundary layer height. Measurements from 163m exhibit only very weak diurnal variability, as this height (1185ma.s.l.) is generally above the nocturnal boundary layer. CH4, CO, N2O and SF6 show little diurnal variation even at 23m owing to the absence of any significant diurnal change in the fluxes and the absence of any strong local sources or sinks. From the in-situ record, the seasonal cycles of the gas species have been characterized and the multi-annual trends determined. Because the record is short, the calculation of the trend is sensitive to inter-annual variations in the amplitudes of the seasonal cycles. However, for CH4 a significant change in the growth-rate was detected for 2006.5–2008.5 as compared with the global mean from 1999 to 2006 and is consistent with other recent observations of a renewed increasing global growth rate in CH4 since the beginning of 2007

Source attribution of air pollution by spatial scale separation using high spatial density networks of low cost air quality sensors

To carry out detailed source attribution for air quality assessment it is necessary to distinguish pollutant contributions that arise from local emissions from those attributable to non-local or regional emission sources. Frequently this requires the use of complex models and inversion methods, prior knowledge or assumptions regarding the pollution environment. In this paper we demonstrate how high spatial density and fast response measurements from low-cost sensor networks may facilitate this separation. A purely measurement-based approach to extract underlying pollution levels (baselines) from the measurements is presented exploiting the different relative frequencies of local and background pollution variations. This paper shows that if high spatial and temporal coverage of air quality measurements are available, the different contributions to the total pollution levels, namely the regional signal as well as near and far field local sources, can be quantified. The advantage of using high spatial resolution observations, as can be provided by low-cost sensor networks, lies in the fact that no prior assumptions about pollution levels at individual deployment sites are required. The methodology we present here, utilising measurements of carbon monoxide (CO), has wide applicability, including additional gas phase species and measurements obtained using reference networks. While similar studies have been performed, this is the first study using networks at this density, or using low cost sensor networks.The authors thank EPSRC (EP/E001912/1) for funding for the Message project. IH thanks the German National Academic Foundation for funding of MPhil degree.This is the final published version. It first appeared at http://www.sciencedirect.com/science/article/pii/S1352231015300583#

The Spin Structure of the Nucleon

We present an overview of recent experimental and theoretical advances in our understanding of the spin structure of protons and neutrons.Comment: 84 pages, 29 figure

A distal region of the human TGM1 promoter is required for expression in transgenic mice and cultured keratinocytes

BACKGROUND: TGM1(transglutaminase 1) is an enzyme that crosslinks the cornified envelope of mature keratinocytes. Appropriate expression of the TGM1 gene is crucial for proper keratinocyte function as inactivating mutations lead to the debilitating skin disease, lamellar ichthyosis. TGM1 is also expressed in squamous metaplasia, a consequence in some epithelia of vitamin A deficiency or toxic insult that can lead to neoplasia. An understanding of the regulation of this gene in normal and abnormal differentiation states may contribute to better disease diagnosis and treatment. METHODS: In vivo requirements for expression of the TGM1 gene were studied by fusing various lengths of promoter DNA to a reporter and injecting the DNA into mouse embryos to generate transgenic animals. Expression of the reporter was ascertained by Western blotting and immunohistochemistry. Further delineation of a transcriptionally important distal region was determined by transfections of progressively shortened or mutated promoter DNA into cultured keratinocytes. RESULTS: In vivo analysis of a reporter transgene driven by the TGM1 promoter revealed that 1.6 kilobases, but not 1.1 kilobases, of DNA was sufficient to confer tissue-specific and cell layer-specific expression. This same region was responsible for reporter expression in tissues undergoing squamous metaplasia as a response to vitamin A deprivation. Mutation of a distal promoter AP1 site or proximal promoter CRE site, both identified as important transcriptional elements in transfection assays, did not prevent appropriate expression. Further searching for transcriptional elements using electrophoretic mobility shift (EMSA) and transfection assays in cultured keratinocytes identified two Sp1 elements in a transcriptionally active region between -1.6 and -1.4 kilobases. While mutation of either Sp1 site or the AP1 site singly had only a small effect, mutation of all three sites eliminated nearly all the transcriptional activity. CONCLUSIONS: A distal region of the TGM1 gene promoter, containing AP1 and Sp1 binding sites, is evolutionarily conserved and responsible for high level expression in transgenic mice and in transfected keratinocyte cultures

Blood Flow and Glucose Metabolism in Stage IV Breast Cancer: Heterogeneity of Response During Chemotherapy

Objective: The purpose of the study was to compare early changes in blood flow (BF) and glucose metabolism (MRglu) in metastatic breast cancer lesions of patients treated with chemotherapy. Methods: Eleven women with stage IV cancer and lesions in breast, lymph nodes, liver, and bone were scanned before treatment and after the first course of chemotherapy. BF, distribution volume of water (Vd), MRglu/BF ratio, MRgluand its corresponding rate constants K1and k3were compared per tumor lesion before and during therapy. Results: At baseline, mean BF and MRgluvaried among different tumor lesions, but mean Vdwas comparable in all lesions. After one course of chemotherapy, mean MRgludecreased in all lesions. Mean BF decreased in breast and node lesions and increased in bone lesions. Vddecreased in breast and nodes, but did not change in bone lesions. The MRglu/BF ratio decreased in breast and bone lesions and increased in node lesions. In patients with multiple tumor lesions BF and MRgluresponse could be very heterogeneous, even within similar types of metastases. BF and MRgluincreased in lesions of patients who experienced early disease progression or showed no response during clinical follow-up. Conclusion: BF and MRgluchanges separately give unique information on different aspects of tumor response to chemotherapy. Changes in BF and MRgluparameters can be remarkably heterogeneous in patients with multiple lesions

Reconciling carbon-cycle concepts, terminology, and methods

Author Posting. © The Author(s), 2006. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Ecosystems 9 (2006): 1041-1050, doi:10.1007/s10021-005-0105-7.Recent patterns and projections of climatic change have focused increased scientific and public attention on patterns of carbon (C) cycling and its controls, particularly the factors that determine whether an ecosystem is a net source or sink of atmospheric CO2. Net ecosystem production (NEP), a central concept in C-cycling research, has been used to represent two different concepts by C-cycling scientists. We propose that NEP be restricted to just one of its two original definitions—the imbalance between gross primary production (GPP) and ecosystem respiration (ER), and that a new term—net ecosystem carbon balance (NECB)—be applied to the net rate of C accumulation in (or loss from; negative sign) ecosystems. NECB differs from NEP when C fluxes other than C fixation and respiration occur or when inorganic C enters or leaves in dissolved form. These fluxes include leaching loss or lateral transfer of C from the ecosystem; emission of volatile organic C, methane, and carbon monoxide; and soot and CO2 from fire. C fluxes in addition to NEP are particularly important determinants of NECB over long time scales. However, even over short time scales, they are important in ecosystems such as streams, estuaries, wetlands, and cities. Recent technological advances have led to a diversity of approaches to measuring C fluxes at different temporal and spatial scales. These approaches frequently capture different components of NEP or NECB and can therefore be compared across scales only by carefully specifying the fluxes included in the measurements. By explicitly identifying the fluxes that comprise NECB and other components of the C cycle, such as net ecosystem exchange (NEE) and net biome production (NBP), we provide a less ambiguous framework for understanding and communicating recent changes in the global C cycle. Key words: Net ecosystem production, net ecosystem carbon balance, gross primary production, ecosystem respiration, autotrophic respiration, heterotrophic respiration, net ecosystem exchange, net biome production, net primary production

An expression signature of syndecan-1 (CD138), E-cadherin and c-met is associated with factors of angiogenesis and lymphangiogenesis in ductal breast carcinoma in situ

INTRODUCTION: Heparan sulphate proteoglycan syndecan-1 modulates cell proliferation, adhesion, migration and angiogenesis. It is a coreceptor for the hepatocyte growth factor receptor c-met, and its coexpression with E-cadherin is synchronously regulated during epithelial-mesenchymal transition. In breast cancer, changes in the expression of syndecan-1, E-cadherin and c-met correlate with poor prognosis. In this study we evaluated whether coexpression of these functionally linked prognostic markers constitutes an expression signature in ductal carcinoma in situ (DCIS) of the breast that may promote cell proliferation and (lymph)angiogenesis. METHODS: Expression of syndecan-1, E-cadherin and c-met was detected immunohistochemically using a tissue microarray in tumour specimens from 200 DCIS patients. Results were correlated with the expression patterns of angiogenic and lymphangiogenic markers. Coexpression of the three prognostic markers was evaluated in human breast cancer cells by confocal immunofluorescence microscopy and RT-PCR. RESULTS: Coexpression and membrane colocalization of the three markers was confirmed in MCF-7 cells. E-cadherin expression decreased, and c-met expression increased progressively in more aggressive cell lines. Tissue microarray analysis revealed strong positive staining of tumour cells for syndecan-1 in 72%, E-cadherin in 67.8% and c-met in 48.6% of DCIS. E-cadherin expression was significantly associated with c-met and syndecan-1. Expression of c-met and syndecan-1 was significantly more frequent in the subgroup of patients with pure DCIS than in those with DCIS and a coexisting invasive carcinoma. Levels of c-met and syndecan-1 expression were associated with HER2 expression. Expression of c-met significantly correlated with expression of endothelin A and B receptors, vascular endothelial growth factor (VEGF)-A and fibroblast growth factor receptor-1, whereas E-cadherin expression correlated significantly with endothelin A receptor, VEGF-A and VEGF-C staining. CONCLUSION: Syndecan-1, E-cadherin and c-met constitute a marker signature associated with angiogenic and lymphangiogenic factors in DCIS. This coexpression may reflect a state of parallel activation of different signal transduction pathways, promoting tumour cell proliferation and angiogenesis. Our findings have implications for future therapeutic approaches in terms of a multiple target approach, which may be useful early in breast cancer progression

The Non-Catalytic Carboxyl-Terminal Domain of ARFGAP1 Regulates Actin Cytoskeleton Reorganization by Antagonizing the Activation of Rac1

The regulation of the actin cytoskeleton and membrane trafficking is coordinated in mammalian cells. One of the regulators of membrane traffic, the small GTP-binding protein ARF1, also activates phosphatidylinositol kinases that in turn affect actin polymerization. ARFGAP1 is a GTPase activating protein (GAP) for ARF1 that is found on Golgi membranes. We present evidence that ARFGAP1 not only serves as a GAP for ARF1, but also can affect the actin cytoskeleton.As cells attach to a culture dish foci of actin appear prior to the cells flattening and spreading. We have observed that overexpression of a truncated ARFGAP1 that lacks catalytic activity for ARF, called GAP273, caused these foci to persist for much longer periods than non-transfected cells. This phenomenon was dependent on the level of GAP273 expression. Furthermore, cell spreading after re-plating or cell migration into a previously scraped area was inhibited in cells transfected with GAP273. Live cell imaging of such cells revealed that actin-rich membrane blebs formed that seldom made protrusions of actin spikes or membrane ruffles, suggesting that GAP273 interfered with the regulation of actin dynamics during cell spreading. The over-expression of constitutively active alleles of ARF6 and Rac1 suppressed the effect of GAP273 on actin. In addition, the activation of Rac1 by serum, but not that of RhoA or ARF6, was inhibited in cells over-expressing GAP273, suggesting that Rac1 is a likely downstream effector of ARFGAP1. The carboxyl terminal 65 residues of ARFGAP1 were sufficient to produce the effects on actin and cell spreading in transfected cells and co-localized with cortical actin foci.ARFGAP1 functions as an inhibitor upstream of Rac1 in regulating actin cytoskeleton. In addition to its GAP catalytic domain and Golgi binding domain, it also has an actin regulation domain in the carboxyl-terminal portion of the protein