Waterlogging control for improved water and land use efficiencies: a systematic analysis

Submitted to Office of Water Research and Technology, U.S. Dept. of the Interior; December 1980.Bibliography: pages 135-138.OWRT project 14-34-0001-6211-C-7144

No increase in radiation-induced chromosome aberration complexity detected by m-FISH after culture in the presence of 5’-bromodeoxyuridine

The thymidine analogue, 5’-bromodeoxyuridine (BrdU), is a known mutagen that is routinely introduced into culture media for subsequent Harlequin stain analysis and determination of cell cycle status. Previously, we examined the induction of chromosome aberrations in human peripheral blood lymphocytes (PBL) known to be in their 1st cell division following exposure to a low dose (0.5 Gy, average one -particle per cell) of high-LET α-particles. We found complex chromosome aberrations to be characteristic of exposure to high-LET radiation and suggested the features of complex exchange to reflect qualitatively the spatial deposition of this densely ionising radiation. To exclude the possibility that BrdU addition post-irradiation influenced the complexity of chromosomal damage observed by m-FISH, the effect of increasing BrdU concentration on aberration complexity was investigated. Comparisons between BrdU concentration (0, 10, and 40 M) and between sham- and α-particle irradiated PBL, were made both independently and in combination to enable discrimination between BrdU and high-LET radiation effects. Aberration type, size, complexity and completeness were assessed by m-FISH, and the relative progression through cell division was evaluated. We found no evidence of any qualitative difference in the complexity of damage as visualized by m-FISH but did observe an increase in the frequency of complex exchanges with increasing BrdU concentration indicative of altered cell cycle kinetics. The parameters measured here are consistent with findings from previous in vitro and in vivo work, indicating that each complex aberration visualised by m-FISH is characteristic of the structure of the high-LET α-particle track and the geometry of cell irradiated

The Nature of LINERs

We present $J$-band ($1.15-1.35 \mu$m) spectroscopy of a sample of nine galaxies showing some degree of LINER activity (classical LINERs, weak-[O {\sc i}] LINERs and transition objects), together with $H$-band spectroscopy for some of them. A careful subtraction of the stellar continuum allows us to obtain reliable [Fe {\sc ii}]$1.2567 \mu$m/Pa$\beta$ line ratios. We conclude that different types of LINERs (i.e., photoionized by a stellar continuum or by an AGN) cannot be easily distinguished based solely on the [Fe {\sc ii}]$1.2567 \mu$m/Pa$\beta$ line ratio. The emission line properties of many LINERs can be explained in terms of an aging starburst. The optical line ratios of these LINERs are reproduced by a model with a metal-rich H {\sc ii} region component photoionized with a single stellar temperature $T_* = 38,000$K, plus a supernova remnant (SNR) component. The [Fe {\sc ii}] line is predominantly excited by shocks produced by SNRs in starbursts and starburst-dominated LINERs, while Pa$\beta$ tracks H {\sc ii} regions ionized by massive young stars. The contribution from SNRs to the overall emission line spectrum is constrained by the [Fe {\sc ii}]$1.2567 \mu$m/Pa$\beta$ line ratio. Although our models for aging starbursts are constrained only by these infrared lines, they consistently explain the optical spectra of the galaxies also. The LINER-starburst connection is tested by predicting the time dependence of the ratio of the ionizing luminosity ($L_{\rm ion}$) to the supernova rate (SNr), $L_{\rm ion}$/(SNr). We predict the relative number of starbursts to starburst-dominated LINERs (aging starbursts) and show that it is in approximate agreement with survey findings for nearby galaxies.Comment: Accepted in ApJ (19 pages, 8 figures, uses emulateapj.sty

The formation, properties and impact of secondary organic aerosol: current and emerging issues

Secondary organic aerosol (SOA) accounts for a significant fraction of ambient tropospheric aerosol and a detailed knowledge of the formation, properties and transformation of SOA is therefore required to evaluate its impact on atmospheric processes, climate and human health. The chemical and physical processes associated with SOA formation are complex and varied, and, despite considerable progress in recent years, a quantitative and predictive understanding of SOA formation does not exist and therefore represents a major research challenge in atmospheric science. This review begins with an update on the current state of knowledge on the global SOA budget and is followed by an overview of the atmospheric degradation mechanisms for SOA precursors, gas-particle partitioning theory and the analytical techniques used to determine the chemical composition of SOA. A survey of recent laboratory, field and modeling studies is also presented. The following topical and emerging issues are highlighted and discussed in detail: molecular characterization of biogenic SOA constituents, condensed phase reactions and oligomerization, the interaction of atmospheric organic components with sulfuric acid, the chemical and photochemical processing of organics in the atmospheric aqueous phase, aerosol formation from real plant emissions, interaction of atmospheric organic components with water, thermodynamics and mixtures in atmospheric models. Finally, the major challenges ahead in laboratory, field and modeling studies of SOA are discussed and recommendations for future research directions are proposed

Molecular Hydrogen and [FeII] in Active Galactic Nuclei

(Abridge) Near-infrared spectroscopy is used to study the kinematics and excitation mechanisms of the H2 and [FeII] gas in a sample of AGN. The H2 lines are unresolved in all objects in which they were detected while the [FeII] lines have widths implying gas velocities of up to 650 km/s. This suggests that, very likely, the H2 and [FeII] emission does not originate from the same parcel of gas. Molecular H2 were detected in 90% of the sample, including PG objects, indicating detectavel amounts of molecular material even in objects with low levels of circumnuclear starburst activity. The data favors thermal excitation for the H2 lines. Indeed, in NGC3227, Mrk766, NGC4051 and NGC4151, the molecular emission is found to be purely thermal. This result is also confirmed by the rather similar vibrational and rotational temperatures in the objects for which they were derived. [FeII] lines are detected in all of the AGN. The [FeII] 1.254mu/Pa-beta ratio is compatible with excitation of the [FeII] by the active nucleus, but in Mrk 766 it implies a stellar origin. A correlation between H2/Br-gamma and [FeII]/Pa-beta is found. We confirm that it is a useful diagnostic tool in the NIR to separate emitting line objects by their level of nuclear activity. X-ray excitation models are able to explain the observed H2 and part of the [FeII] emission. Most likely, a combination of X-ray heating, shocks driven by the radio jet, and circumnuclear star formation contributes, in different proportions, to the H2 and [FeII] emission. In most of our spectra, the [FeII] 1.257mu/1.644mu ratio is found to be 30% lower than the intrinsic value based on current atomic data. This implies either than the extinction towards the [FeII] emitting clouds is very similar in most objects or there are possible inaccuracies in the A-values in the [FeII] transitions.Comment: 18 pages, 6 figures, Accepted for publication in Astronomy & Astrophysic

Mycolactone-dependent depletion of endothelial cell thrombomodulin is strongly associated with fibrin deposition in Buruli ulcer lesions

A well-known histopathological feature of diseased skin in Buruli ulcer (BU) is coagulative necrosis caused by the Mycobacterium ulcerans macrolide exotoxin mycolactone. Since the underlying mechanism is not known, we have investigated the effect of mycolactone on endothelial cells, focussing on the expression of surface anticoagulant molecules involved in the protein C anticoagulant pathway. Congenital deficiencies in this natural anticoagulant pathway are known to induce thrombotic complications such as purpura fulimans and spontaneous necrosis. Mycolactone profoundly decreased thrombomodulin (TM) expression on the surface of human dermal microvascular endothelial cells (HDMVEC) at doses as low as 2ng/ml and as early as 8hrs after exposure. TM activates protein C by altering thrombin's substrate specificity, and exposure of HDMVEC to mycolactone for 24 hours resulted in an almost complete loss of the cells' ability to produce activated protein C. Loss of TM was shown to be due to a previously described mechanism involving mycolactone-dependent blockade of Sec61 translocation that results in proteasome-dependent degradation of newly synthesised ER-transiting proteins. Indeed, depletion from cells determined by live-cell imaging of cells stably expressing a recombinant TM-GFP fusion protein occurred at the known turnover rate. In order to determine the relevance of these findings to BU disease, immunohistochemistry of punch biopsies from 40 BU lesions (31 ulcers, nine plaques) was performed. TM abundance was profoundly reduced in the subcutis of 78% of biopsies. Furthermore, it was confirmed that fibrin deposition is a common feature of BU lesions, particularly in the necrotic areas. These findings indicate that there is decreased ability to control thrombin generation in BU skin. Mycolactone's effects on normal endothelial cell function, including its ability to activate the protein C anticoagulant pathway are strongly associated with this. Fibrin-driven tisischemia could contribute to the development of the tissue necrosis seen in BU lesions

Paid work is associated with improved health-related quality of life in patients with rheumatoid arthritis

Numerous patients with rheumatoid arthritis (RA) end their working career due to consequences of the disease. No publication has reported whether there is an independent association between patients' health-related quality of life (HRQOL) and employment status. The objective of the study was to investigate the association of paid work and HRQOL in patients with RA whilst controlling for demographics and disease severity. This was a cross-sectional study. Three hundred and ten patients were consecutively recruited from two Norwegians hospitals when commencing disease modifying anti-rheumatic drug treatment. Data on demographics, employment status, disease activity (DAS28-3), physical functioning, pain, tiredness, and HRQOL (SF-36) were collected. HRQOL were compared between 123 patients working full- or part-time and 187 patients not working due to disability pension, retirement, being students or “home workers”. The regression analyses showed an independent positive association between paid work and the physical (p = 001) and the mental component (p = 012) of the SF-36 when controlling for demographics and disease severity. Paid work was statistically significantly associated with better HRQOL in patients with RA. The positive association of performing paid work and HRQOL imply that health care providers should thoroughly evaluate the possibilities for the patients to continue with paid work

A functional genetic screen defines the AKT-induced senescence signaling network

Exquisite regulation of PI3K/AKT/mTORC1 signaling is essential for homeostatic control of cell growth, proliferation, and survival. Aberrant activation of this signaling network is an early driver of many sporadic human cancers. Paradoxically, sustained hyperactivation of the PI3K/AKT/mTORC1 pathway in nontransformed cells results in cellular senescence, which is a tumor-suppressive mechanism that must be overcome to promote malignant transformation. While oncogene-induced senescence (OIS) driven by excessive RAS/ERK signaling has been well studied, little is known about the mechanisms underpinning the AKT-induced senescence (AIS) response. Here, we utilize a combination of transcriptome and metabolic profiling to identify key signatures required to maintain AIS. We also employ a whole protein-coding genome RNAi screen for AIS escape, validating a subset of novel mediators and demonstrating their preferential specificity for AIS as compared with OIS. As proof of concept of the potential to exploit the AIS network, we show that neurofibromin 1 (NF1) is upregulated during AIS and its ability to suppress RAS/ERK signaling facilitates AIS maintenance. Furthermore, depletion of NF1 enhances transformation of p53-mutant epithelial cells expressing activated AKT, while its overexpression blocks transformation by inducing a senescent-like phenotype. Together, our findings reveal novel mechanistic insights into the control of AIS and identify putative senescence regulators that can potentially be targeted, with implications for new therapeutic options to treat PI3K/AKT/mTORC1-driven cancers.Peer reviewe