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One of the first steps in treating hepatitis C is preventing patients from transmitting the virus. Although the best way to do that is with the most effective therapy, that doesn’t always happen; even with a cure, hepatitis C is still deadly. So now, we need a way to detect infection. Most commercial laboratories use polymerase chain reaction to test for the virus, but the analysis typically takes a week and costs $175. The CDC estimates that in 2014, more than 3 million Americans were infected with hepatitis C, a disease that causes liver damage, liver failure, and cancer.
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A small team led by Jennifer Ray, an assistant professor of chemical engineering at the University of Delaware and of chemistry and biochemistry at Medstar Georgetown University Hospital, has shown that a new type of electrochemical sensor can fulfill all three roles. With the electrical readout, the test could be performed on site. And because the new technology is very specific, it can pinpoint the presence of a particular virus.
The sensors are made of a single piece of glass coated with gold or silver. When a solution containing the sample
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Google Translate: The Language Installer for Windows Free Installer detects the language of your computer and gets the installer automatically installed in. Cadence.OrCAD.v16.5 Hotfix.SPB16.50.028 Setup Free.Effects of genipin on the structural integrity, viability, and antioxidant activity of human lung fibroblasts in the presence of simulated airway fluid.
Pulmonary alveolar proteinosis (PAP) is a potentially life-threatening lung disease with a rising prevalence in the industrialized world and no accepted treatment. Pulmonary alveolar proteinosis is characterized by accumulation of surfactant in the alveoli, leading to respiratory insufficiency. The mechanism for intracellular surfactant retention and how to reverse this accumulation is not fully understood. Genipin, a natural compound from the gardenia tree, has been shown to be a potent inhibitor of protein phosphatase 2B. In this study, we investigated whether genipin was able to protect normal human lung fibroblasts from lipid peroxidation induced by a fluid similar to that found in PAP. Our results demonstrate that genipin (0.25-2.0 mM) inhibits lipid peroxidation by 20-40% in these cells exposed to the fluid. The underlying mechanism of protection was assessed at the cellular level. Viability assays revealed that cells exposed to genipin showed no adverse effects. Furthermore, genipin was shown to protect these cells against an ethanol/alkaline exposure, a treatment which induces lipid peroxidation. Analysis of membrane structural integrity using lactate dehydrogenase (LDH) release and flow cytometry showed that exposure of fibroblasts to the fluid for 12 h increased membrane permeability by 50%. Treatment with 2 mM genipin inhibited the induced membrane damage in a dose-dependent manner. Analysis of the antioxidant activity of fibroblasts exposed to the fluid showed that the antioxidant activities of both ferric reducing ability of plasma (FRAP), and of the superoxide dismutase mimic, 2,2′-azinobis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS), were significantly lowered in these cells. Preincubation with 2 mM genipin increased antioxidant activities in a dose-dependent manner. The present results indicate that genipin can protect normal human lung fibroblasts against the negative effects of an airway fluid similar to