Photometric Variability in Earthshine Observations

The identification of an extrasolar planet as Earth-like will depend on the detection of atmospheric signatures or surface non-uniformities. In this paper we present spatially unresolved flux light curves of Earth for the purpose of studying a prototype extrasolar terrestrial planet. Our monitoring of the photometric variability of earthshine revealed changes of up to 23 % per hour in the brightness of Earth's scattered light at around 600 nm, due to the removal of specular reflection from the view of the Moon. This variability is accompanied by reddening of the spectrum, and results from a change in surface properties across the continental boundary between the Indian Ocean and Africa's east coast. Our results based on earthshine monitoring indicate that specular reflection should provide a useful tool in determining the presence of liquid water on extrasolar planets via photometric observations.Comment: To appear in Astrobiology 9(3). 17 pages, 3 figures, 1 tabl

Mastitis in Chinese Breastfeeding Mothers: A Prospective Cohort Study

Introduction: Mastitis is a common problem encountered by breastfeeding mothers. This study investigated the incidence and risk factors of lactation mastitis among Chinese women. Subjects and Methods: A prospective cohort study on infant feeding practices was conducted during 2010 and 2011 in Jiangyou, Sichuan Province, China. Poisson regression analysis was performed to determine factors influencing the incidence of mastitis within 6 months postpartum. Results: Of the 670 Chinese mothers who were breastfeeding at discharge, 42 women (6.3%) experienced at least one episode of mastitis during the first 6 months after delivery. The cumulative incidence of mastitis was 10.3%. Mothers with a cracked and sore nipple (incidence rate ratio 2.24; 95% confidence interval 1.38, 3.63) and those who felt stressed (incidence rate ratio 3.15; 95% confidence interval 1.56, 6.37) appeared to sustain more episodes of mastitis. Conclusions: The incidence of lactation mastitis was low among Chinese mothers. To further reduce the risk of mastitis, instructions on the correct positioning of the baby during breastfeeding should be emphasized. Providing new mothers with guidance on how to cope with stress may also prevent the recurrence of the condition

The influence of N-acetyl-L-cysteine on oxidative stress and nitric oxide synthesis in stimulated macrophages treated with a mustard gas analogue

Background: Sulphur mustard gas, 2, 2′-dichlorodiethyl sulphide (HD), is a chemical warfare agent. Both mustard gas and its monofunctional analogue, 2-chloroethyl ethyl sulphide (CEES), are alkylating agents that react with and diminish cellular thiols and are highly toxic. Previously, we reported that lipopolysaccharide (LPS) significantly enhances the cytotoxicity of CEES in murine RAW 264.7 macrophages and that CEES transiently inhibits nitric oxide (NO) production via suppression of inducible NO synthase (iNOS) protein expression. NO generation is an important factor in wound healing. In this paper, we explored the hypotheses that LPS increases CEES toxicity by increasing oxidative stress and that treatment with N-acetyl-L-cysteine (NAC) would block LPS induced oxidative stress and protect against loss of NO production. NAC stimulates glutathione (GSH) synthesis and also acts directly as a free radical scavenger. The potential therapeutic use of the antibiotic, polymyxin B, was also evaluated since it binds to LPS and could thereby block the enhancement of CEES toxicity by LPS and also inhibit the secondary infections characteristic of HD/CEES wounds. Results: We found that 10 mM NAC, when administered simultaneously or prior to treatment with 500 μM CEES, increased the viability of LPS stimulated macrophages. Surprisingly, NAC failed to protect LPS stimulated macrophages from CEES induced loss of NO production. Macrophages treated with both LPS and CEES show increased oxidative stress parameters (cellular thiol depletion and increased protein carbonyl levels). NAC effectively protected RAW 264.7 cells simultaneously treated with CEES and LPS from GSH loss and oxidative stress. Polymyxin B was found to partially block nitric oxide production and diminish CEES toxicity in LPS-treated macrophages. Conclusion: The present study shows that oxidative stress is an important mechanism contributing to CEES toxicity in LPS stimulated macrophages and supports the notion that antioxidants could play a therapeutic role in preventing mustard gas toxicity. Although NAC reduced oxidative stress in LPS stimulated macrophages treated with CEES, it did not reverse CEES-induced loss of NO production. NAC and polymyxin B were found to help prevent CEES toxicity in LPS-treated macrophages

Inhibition of Inducible Nitric Oxide Synthase by a Mustard Gas Analog in Murine Macrophages

Background: 2-Chloroethyl ethyl sulphide (CEES) is a sulphur vesicating agent and an analogue of the chemical warfare agent 2,2′-dichlorodiethyl sulphide, or sulphur mustard gas (HD). Both CEES and HD are alkylating agents that influence cellular thiols and are highly toxic. In a previous publication, we reported that lipopolysaccharide (LPS) enhances the cytotoxicity of CEES in murine RAW264.7 macrophages. In the present investigation, we studied the influence of CEES on nitric oxide (NO) production in LPS stimulated RAW264.7 cells since NO signalling affects inflammation, cell death, and wound healing. Murine macrophages stimulated with LPS produce NO almost exclusively via inducible nitric oxide synthase (iNOS) activity. We suggest that the influence of CEES or HD on the cellular production of NO could play an important role in the pathophysiological responses of tissues to these toxicants. In particular, it is known that macrophage generated NO synthesised by iNOS plays a critical role in wound healing. Results: We initially confirmed that in LPS stimulated RAW264.7 macrophages NO is exclusively generated by the iNOS form of nitric oxide synthase. CEES treatment inhibited the synthesis of NO (after 24 hours) in viable LPS-stimulated RAW264.7 macrophages as measured by either nitrite secretion into the culture medium or the intracellular conversion of 4,5-diaminofluorescein diacetate (DAF-2DA) or dichlorofluorescin diacetate (DCFH-DA). Western blots showed that CEES transiently decreased the expression of iNOS protein; however, treatment of active iNOS with CEES in vitro did not inhibit its enzymatic activity. Conclusion: CEES inhibits NO production in LPS stimulated macrophages by decreasing iNOS protein expression. Decreased iNOS expression is likely the result of CEES induced alteration in the nuclear factor kappa B (NF-κB) signalling pathway. Since NO can act as an antioxidant, the CEES induced down-regulation of iNOS in LPS-stimulated macrophages could elevate oxidative stress. Since macrophage generated NO is known to play a key role in cutaneous wound healing, it is possible that this work has physiological relevance with respect to the healing of HD induced skin blisters

Inhibition of inducible Nitric Oxide Synthase by a mustard gas analog in murine macrophages

BACKGROUND: 2-Chloroethyl ethyl sulphide (CEES) is a sulphur vesicating agent and an analogue of the chemical warfare agent 2,2'-dichlorodiethyl sulphide, or sulphur mustard gas (HD). Both CEES and HD are alkylating agents that influence cellular thiols and are highly toxic. In a previous publication, we reported that lipopolysaccharide (LPS) enhances the cytotoxicity of CEES in murine RAW264.7 macrophages. In the present investigation, we studied the influence of CEES on nitric oxide (NO) production in LPS stimulated RAW264.7 cells since NO signalling affects inflammation, cell death, and wound healing. Murine macrophages stimulated with LPS produce NO almost exclusively via inducible nitric oxide synthase (iNOS) activity. We suggest that the influence of CEES or HD on the cellular production of NO could play an important role in the pathophysiological responses of tissues to these toxicants. In particular, it is known that macrophage generated NO synthesised by iNOS plays a critical role in wound healing. RESULTS: We initially confirmed that in LPS stimulated RAW264.7 macrophages NO is exclusively generated by the iNOS form of nitric oxide synthase. CEES treatment inhibited the synthesis of NO (after 24 hours) in viable LPS-stimulated RAW264.7 macrophages as measured by either nitrite secretion into the culture medium or the intracellular conversion of 4,5-diaminofluorescein diacetate (DAF-2DA) or dichlorofluorescin diacetate (DCFH-DA). Western blots showed that CEES transiently decreased the expression of iNOS protein; however, treatment of active iNOS with CEES in vitro did not inhibit its enzymatic activity CONCLUSION: CEES inhibits NO production in LPS stimulated macrophages by decreasing iNOS protein expression. Decreased iNOS expression is likely the result of CEES induced alteration in the nuclear factor kappa B (NF-κB) signalling pathway. Since NO can act as an antioxidant, the CEES induced down-regulation of iNOS in LPS-stimulated macrophages could elevate oxidative stress. Since macrophage generated NO is known to play a key role in cutaneous wound healing, it is possible that this work has physiological relevance with respect to the healing of HD induced skin blisters

Effect of Iodine Doping on Bi2_{2}Sr2_{2}Ca1_{1}Cu2_{2}Ox_{x}: Charge Transfer or Interlayer Coupling?

A comparative study has been made of iodine-intercalated Bi$_{2}$Sr$_{2}$Ca$_{1}$Cu$_{2}$O$_{x}$ single crystal and 1 atm O$_{2}$ annealed Bi$_{2}$Sr$_{2}$Ca$_{1}$Cu$_{1}$O$_{x}$ single crystal using AC susceptibility measurement, X-ray photoemission (XPS) and angle-resolved ultraviolet photoemission spectroscopy (ARUPS). AC susceptibility measurement indicates that O$_{2}$-doped samples studied have T$_{c}$ of 84 $^{o}$K, whereas T$_{c}$ of Iodine-doped samples studied are 80 $^{o}$K. XPS Cu 2p core level data establish that the hole concentration in the CuO$_{2}$ planes are essentially the same for these two kinds of samples. ARUPS measurements show that electronic structure of the normal states near the Fermi level has been strongly affected by iodine intercalation. We conclude that the dominant effect of iodine doping is to alter the interlayer coupling.Comment: LBL 9 pages, APS_Revtex. 5 Figures, available upon request. UW-Madison preprin

Scenario for Ultrarelativistic Nuclear Collisions: Space--Time Picture of Quantum Fluctuations and the Birth of QGP

We study the dynamics of quantum fluctuations which take place at the earliest stage of high-energy processes and the conditions under which the data from e-p deep-inelastic scattering may serve as an input for computing the initial data for heavy-ion collisions at high energies. Our method is essentially based on the space-time picture of these seemingly different phenomena. We prove that the ultra-violet renormalization of the virtual loops does not bring any scale into the problem. The scale appears only in connection with the collinear cut-off in the evolution equations and is defined by the physical properties of the final state. In heavy-ion collisions the basic screening effect is due to the mass of the collective modes (plasmons) in the dense non-equilibrium quark-gluon system, which is estimated. We avoid the standard parton phenomenology and suggest a dedicated class of evolution equations which describe the dynamics of quantum fluctuations in heavy-ion collisions.Comment: 54 pages, 11 Postscript figures, uses RevTe

T-Bet and Eomes Regulate the Balance between the Effector/Central Memory T Cells versus Memory Stem Like T Cells

Memory T cells are composed of effector, central, and memory stem cells. Previous studies have implicated that both T-bet and Eomes are involved in the generation of effector and central memory CD8 T cells. The exact role of these transcription factors in shaping the memory T cell pool is not well understood, particularly with memory stem T cells. Here, we demonstrate that both T-bet or Eomes are required for elimination of established tumors by adoptively transferred CD8 T cells. We also examined the role of T-bet and Eomes in the generation of tumor-specific memory T cell subsets upon adoptive transfer. We showed that combined T-bet and Eomes deficiency resulted in a severe reduction in the number of effector/central memory T cells but an increase in the percentage of CD62LhighCD44low Sca-1+ T cells which were similar to the phenotype of memory stem T cells. Despite preserving large numbers of phenotypic memory stem T cells, the lack of both of T-bet and Eomes resulted in a profound defect in antitumor memory responses, suggesting T-bet and Eomes are crucial for the antitumor function of these memory T cells. Our study establishes that T-bet and Eomes cooperate to promote the phenotype of effector/central memory CD8 T cell versus that of memory stem like T cells. © 2013 Li et al