An EPR methodology for measuring the London penetration depth for the ceramic superconductors

The use is discussed of electron paramagnetic resonance (EPR) as a quick and easily accessible method for measuring the London penetration depth, lambda for the high T(sub c) superconductors. The method utilizes the broadening of the EPR signal, due to the emergence of the magnetic flux lattice, of a free radical adsorbed on the surface of the sample. The second moment, of the EPR signal below T(sub c) is fitted to the Brandt equation for a simple triangular lattice. The precision of this method compares quite favorably with those of the more standard methods such as micro sup(+)SR, Neutron scattering, and magnetic susceptibility

Microwave (EPR) measurements of the penetration depth measurements of high-Tc superconductors

The use is discussed of electron paramagnetic resonance (EPR) as a quick and easily accessible method for measuring the London penetration depth, lambda for the high T sub c superconductors. The method uses the broadening of the EPR signal, due to the emergence of the magnetic flux lattice, of a free radical adsorbed on the surface of the sample. The second moment, of the EPR signal below T sub c is fitted to the Brandt equation for a simple triangular lattice. The precision of this method compares quite favorably with those of the more standard methods such as micro sup(+)SR, neutron scattering, and magnetic susceptibility

Direct measurement of astrophysically important resonances in ^(38)K(p,γ)^(39)Ca

Background: Classical novae are cataclysmic nuclear explosions occurring when a white dwarf in a binary system accretes hydrogen-rich material from its companion star. Novae are partially responsible for the galactic synthesis of a variety of nuclides up to the calcium (A∼40) region of the nuclear chart. Although the structure and dynamics of novae are thought to be relatively well understood, the predicted abundances of elements near the nucleosynthesis endpoint, in particular Ar and Ca, appear to sometimes be in disagreement with astronomical observations of the spectra of nova ejecta. Purpose: One possible source of the discrepancies between model predictions and astronomical observations is nuclear reaction data. Most reaction rates near the nova endpoint are estimated only from statistical model calculations, which carry large uncertainties. For certain key reactions, these rate uncertainties translate into large uncertainties in nucleosynthesis predictions. In particular, the ^(38)K(p,γ)^(39)Ca reaction has been identified as having a significant influence on Ar, K, and Ca production. In order to constrain the rate of this reaction, we have performed a direct measurement of the strengths of three candidate ℓ=0 resonances within the Gamow window for nova burning, at 386±10 keV, 515±10 keV, and 689±10 keV. Method: The experiment was performed in inverse kinematics using a beam of unstable ^(38)K impinged on a windowless hydrogen gas target. The ^(39)Ca recoils and prompt γ rays from ^(38)K(p,γ)^(39)Ca reactions were detected in coincidence using a recoil mass separator and a bismuth-germanate scintillator array, respectively. Results: For the 689 keV resonance, we observed a clear recoil-γ coincidence signal and extracted resonance strength and energy values of 120^(+50)_(−30)(stat.)^(+20)_(−60)(sys.)meV and 679^(+2)_(−1)(stat.)±1(sys.)keV, respectively. We also performed a singles analysis of the recoil data alone, extracting a resonance strength of 120±20(stat.)±15(sys.) meV, consistent with the coincidence result. For the 386 keV and 515 keV resonances, we extract 90% confidence level upper limits of 2.54 meV and 18.4 meV, respectively. Conclusions: We have established a new recommended ^(38)K(p,γ)^(39)Ca rate based on experimental information, which reduces overall uncertainties near the peak temperatures of nova burning by a factor of ∼250. Using the rate obtained in this work in model calculations of the hottest oxygen-neon novae reduces overall uncertainties on Ar, K, and Ca synthesis to factors of 15 or less in all cases

Persistent DNA Damage after High Dose In Vivo Gamma Exposure of Minipig Skin

Exposure to high doses of ionizing radiation (IR) can lead to localized radiation injury of the skin and exposed cells suffer dsDNA breaks that may elicit cell death or stochastic changes. Little is known about the DNA damage response after high-dose exposure of the skin. Here, we investigate the cellular and DNA damage response in acutely irradiated minipig skin.IR-induced DNA damage, repair and cellular survival were studied in 15 cm(2) of minipig skin exposed in vivo to ~50 Co-60 γ rays. Skin biopsies of control and 4 h up to 96 days post exposure were investigated for radiation-induced foci (RIF) formation using γ-H2AX, 53BP1, and active ATM-p immunofluorescence. High-dose IR induced massive γ-H2AX phosphorylation and high 53BP1 RIF numbers 4 h, 20 h after IR. As time progressed RIF numbers dropped to a low of <1% of keratinocytes at 28-70 days. The latter contained large RIFs that included ATM-p, indicating the accumulation of complex DNA damage. At 96 days most of the cells with RIFs had disappeared. The frequency of active-caspase-3-positive apoptotic cells was 17-fold increased 3 days after IR and remained >3-fold elevated at all subsequent time points. Replicating basal cells (Ki67+) were reduced 3 days post IR followed by increased proliferation and recovery of epidermal cellularity after 28 days.Acute high dose irradiation of minipig epidermis impaired stem cell replication and induced elevated apoptosis from 3 days onward. DNA repair cleared the high numbers of DBSs in skin cells, while RIFs that persisted in <1% cells marked complex and potentially lethal DNA damage up to several weeks after exposure. An elevated frequency of keratinocytes with persistent RIFs may thus serve as indicator of previous acute radiation exposure, which may be useful in the follow up of nuclear or radiological accident scenarios

Prioritizing Risks and Uncertainties from Intentional Release of Selected Category A Pathogens

This paper synthesizes available information on five Category A pathogens (Bacillus anthracis, Yersinia pestis, Francisella tularensis, Variola major and Lassa) to develop quantitative guidelines for how environmental pathogen concentrations may be related to human health risk in an indoor environment. An integrated model of environmental transport and human health exposure to biological pathogens is constructed which 1) includes the effects of environmental attenuation, 2) considers fomite contact exposure as well as inhalational exposure, and 3) includes an uncertainty analysis to identify key input uncertainties, which may inform future research directions. The findings provide a framework for developing the many different environmental standards that are needed for making risk-informed response decisions, such as when prophylactic antibiotics should be distributed, and whether or not a contaminated area should be cleaned up. The approach is based on the assumption of uniform mixing in environmental compartments and is thus applicable to areas sufficiently removed in time and space from the initial release that mixing has produced relatively uniform concentrations. Results indicate that when pathogens are released into the air, risk from inhalation is the main component of the overall risk, while risk from ingestion (dermal contact for B. anthracis) is the main component of the overall risk when pathogens are present on surfaces. Concentrations sampled from untracked floor, walls and the filter of heating ventilation and air conditioning (HVAC) system are proposed as indicators of previous exposure risk, while samples taken from touched surfaces are proposed as indicators of future risk if the building is reoccupied. A Monte Carlo uncertainty analysis is conducted and input-output correlations used to identify important parameter uncertainties. An approach is proposed for integrating these quantitative assessments of parameter uncertainty with broader, qualitative considerations to identify future research priorities

Abraham model correlations for solute partitioning into o-xylene, m-xylene and p-xylene from both water and the gas phase

Article on Abraham model correlations for solute partitioning into o-xylene, m-xylene and p-xylene from both water and the gas phase

How long do nosocomial pathogens persist on inanimate surfaces? A systematic review

BACKGROUND: Inanimate surfaces have often been described as the source for outbreaks of nosocomial infections. The aim of this review is to summarize data on the persistence of different nosocomial pathogens on inanimate surfaces. METHODS: The literature was systematically reviewed in MedLine without language restrictions. In addition, cited articles in a report were assessed and standard textbooks on the topic were reviewed. All reports with experimental evidence on the duration of persistence of a nosocomial pathogen on any type of surface were included. RESULTS: Most gram-positive bacteria, such as Enterococcus spp. (including VRE), Staphylococcus aureus (including MRSA), or Streptococcus pyogenes, survive for months on dry surfaces. Many gram-negative species, such as Acinetobacter spp., Escherichia coli, Klebsiella spp., Pseudomonas aeruginosa, Serratia marcescens, or Shigella spp., can also survive for months. A few others, such as Bordetella pertussis, Haemophilus influenzae, Proteus vulgaris, or Vibrio cholerae, however, persist only for days. Mycobacteria, including Mycobacterium tuberculosis, and spore-forming bacteria, including Clostridium difficile, can also survive for months on surfaces. Candida albicans as the most important nosocomial fungal pathogen can survive up to 4 months on surfaces. Persistence of other yeasts, such as Torulopsis glabrata, was described to be similar (5 months) or shorter (Candida parapsilosis, 14 days). Most viruses from the respiratory tract, such as corona, coxsackie, influenza, SARS or rhino virus, can persist on surfaces for a few days. Viruses from the gastrointestinal tract, such as astrovirus, HAV, polio- or rota virus, persist for approximately 2 months. Blood-borne viruses, such as HBV or HIV, can persist for more than one week. Herpes viruses, such as CMV or HSV type 1 and 2, have been shown to persist from only a few hours up to 7 days. CONCLUSION: The most common nosocomial pathogens may well survive or persist on surfaces for months and can thereby be a continuous source of transmission if no regular preventive surface disinfection is performed