232 research outputs found

    Multifractal magnetic susceptibility distribution models of hydrothermally altered rocks in the Needle Creek Igneous Center of the Absaroka Mountains, Wyoming

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    International audienceMagnetic susceptibility was measured for 700 samples of drill core from thirteen drill holes in the porphyry copper-molybdenum deposit of the Stinkingwater mining district in the Absaroka Mountains, Wyoming. The magnetic susceptibility measurements, chemical analyses, and alteration class provided a database for study of magnetic susceptibility in these altered rocks. The distribution of the magnetic susceptibilities for all samples is multi-modal, with overlapping peaked distributions for samples in the propylitic and phyllic alteration class, a tail of higher susceptibilities for potassic alteration, and an approximately uniform distribution over a narrow range at the highest susceptibilities for unaltered rocks. Samples from all alteration and mineralization classes show susceptibilities across a wide range of values. Samples with secondary (supergene) alteration due to oxidation or enrichment show lower susceptibilities than primary (hypogene) alteration rock. Observed magnetic susceptibility variations and the monolithological character of the host rock suggest that the variations are due to varying degrees of alteration of blocks of rock between fractures that conducted hydrothermal fluids. Alteration of rock from the fractures inward progressively reduces the bulk magnetic susceptibility of the rock. The model introduced in this paper consists of a simulation of the fracture pattern and a simulation of the alteration of the rock between fractures. A multifractal model generated from multiplicative cascades with unequal ratios produces distributions statistically similar to the observed distributions. The reduction in susceptibility in the altered rocks was modelled as a diffusion process operating on the fracture distribution support. The average magnetic susceptibility was then computed for each block. For the purpose of comparing the model results with observation, the simulated magnetic susceptibilities were then averaged over the same interval as the measured data. Comparisons of the model and data from drillholes show good but not perfect agreement

    Outcome of postoperative critically ill patients with heparin-induced thrombocytopenia: an observational retrospective case-control study

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    INTRODUCTION: Heparin-induced thrombocytopenia (HIT) is described as a decrease in platelet count associated with heparin administration and is an immune-mediated adverse drug reaction that can cause both arterial and venous thromboses. It can be a life-threatening complication of heparin exposure. Little data concerning incidence, predisposing factors, or outcome in critically ill surgical patients are available. METHODS: All critically ill, postoperative patients admitted between January 1, 2000, and December 31, 2001, to a surgical intensive care unit (SICU) who tested positive by an enzyme-linked immunosorbent assay for the HIT antibody (HPIA; Diagnostica Stago, Inc., Parsippany, NJ, USA) were identified. Patient risk factors and outcomes were abstracted retrospectively from the medical record and compared with those from control patients matched for age, gender, diagnosis, severity of illness, and date of SICU admission. RESULTS: Two hundred and ten patients out of 2,046 patients (10%) admitted to the SICU had HIT assays performed. Nineteen patients (0.9% of admissions; 9% of tested individuals) had positive tests. HIT-antibody-positive patients, compared with 19 matched controls, had an increased risk of death or major thrombotic complications (37% versus 10%; P < 0.05) and prolonged length of intensive care unit (ICU) stay (20 days versus 10 days; P < 0.05). Exposure to heparin via intravascular flushes alone was sufficient to generate HIT antibodies in 12 of 19 (63%) patients. Five patients received platelet transfusions after the diagnosis of HIT was known; four of these patients died. CONCLUSION: Heparin flushes were the most common cause of HIT in this study. HIT-antibody-positive patients had an increased risk of death or major complications and a prolonged length of ICU stay. Platelet transfusions often were administered despite a positive HIT test result and were associated with a high mortality rate. Treatment algorithms that minimize exposure to heparin and contraindicate platelet transfusions merit further study

    An introductory overview of open-source and commercial software options for the analysis of forensic sequencing data

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    The top challenges of adopting new methods to forensic DNA analysis in routine laboratories are often the capital investment and the expertise required to implement and validate such methods locally. In the case of next-generation sequencing, in the last decade, several specifically forensic commercial options became available, offering reliable and validated solutions. Despite this, the readily available expertise to analyze, interpret and understand such data is still perceived to be lagging behind. This review gives an introductory overview for the forensic scientists who are at the beginning of their journey with implementing next-generation sequencing locally and because most in the field do not have a bioinformatics background may find it difficult to navigate the new terms and analysis options available. The currently available open-source and commercial software for forensic sequencing data analysis are summarized here to provide an accessible starting point for those fairly new to the forensic application of massively parallel sequencing

    Pharmacological inhibitors of the cystic fibrosis transmembrane conductance regulator exert off-target effects on epithelial cation channels

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    The cystic fibrosis transmembrane conductance regulator (CFTR) anion channel and the epithelial Na+ channel (ENaC) play essential roles in transepithelial ion and fluid transport in numerous epithelial tissues. Inhibitors of both channels have been important tools for defining their physiological role in vitro. However, two commonly used CFTR inhibitors, CFTRinh-172 and GlyH-101, also inhibit non-CFTR anion channels, indicating they are not CFTR specific. However, the potential off-target effects of these inhibitors on epithelial cation channels has to date not been addressed. Here, we show that both CFTR blockers, at concentrations routinely employed by many researchers, caused a significant inhibition of store-operated calcium entry (SOCE) that was time-dependent, poorly reversible and independent of CFTR. Patch clamp experiments showed that both CFTRinh-172 and GlyH-101 caused a significant block of Orai1-mediated whole cell currents, establishing that they likely reduce SOCE via modulation of this Ca2+ release-activated Ca2+ (CRAC) channel. In addition to off-target effects on calcium channels, both inhibitors significantly reduced human αβγ-ENaC-mediated currents after heterologous expression in Xenopus oocytes, but had differential effects on δβγ-ENaC function. Molecular docking identified two putative binding sites in the extracellular domain of ENaC for both CFTR blockers. Together, our results indicate that caution is needed when using these two CFTR inhibitors to dissect the role of CFTR, and potentially ENaC, in physiological processes
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