Quantification of Mycophenolic Acid in Plasma by High Performance Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS).

Mycophenolate mofetil (MMF) and sodium mycophenolate are commonly prescribed immunosuppressive drugs for patients who have undergone solid organ transplant. Therapeutic drug monitoring (TDM) of these drugs is performed by assessing mycophenolic acid (MPA) in plasma. Due to the large inter-individual variability and narrow therapeutic range, the precise determination of systemic MPA concentration carries great clinical significance.

Interlaboratory validation of an improved method for detection of Cyclospora cayetanensis in produce using a real-time PCR assay.

A collaborative validation study was performed to evaluate the performance of a new U.S. Food and Drug Administration method developed for detection of the protozoan parasite, Cyclospora cayetanensis, on cilantro and raspberries.

Reliability and group differences in quantitative cervicothoracic measures among individuals with and without chronic neck pain.

Background: Clinicians frequently rely on subjective categorization of impairments in mobility, strength, and endurance for clinical decision-making; however, these assessments are often unreliable and lack sensitivity to change. The objective of this study was to determine the inter-rater reliability, minimum detectable change (MDC), and group differences in quantitative cervicothoracic measures for individuals with and without chronic neck pain (NP).

Methods: Nineteen individuals with NP and 20 healthy controls participated in this case control study.

Comparison of pulse oximetry measures in a healthy population.

In this study finger and ear oximetry readings of 89 healthy persons were compared. The findings do not support the common nursing practice of using a finger sensor to obtain a pulse oximetry reading from an individual's ear if the finger is not usable.

National animal health surveillance: Return on investment.

A weighted benefit-cost analysis (BCA) supports prioritization of animal health surveillance activities to safeguard animal agriculture industries and reduce the impact of disease on the national economy. We propose to determine the value of investment in surveillance by assessing benefits from: avoiding disease incursion and expansion modified by the probability of occurrence of the disease event, the sensitivity of systems to detect it, and the degree to which we can mitigate disease impact when detected. The weighted benefit-cost ratio is the modified value of surveillance as laid out above divided by the cost of surveillance.

Innate immune evasion by hepatitis C virus and West Nile virus.

Antiviral immunity in mammals involves several levels of surveillance and effector actions by host factors to detect viral pathogens, trigger alpha/beta interferon production, and to mediate innate defenses within infected cells. Our studies have focused on understanding how these processes are regulated during infection by hepatitis C virus (HCV) and West Nile virus (WNV). Both viruses are members of the Flaviviridae and are human pathogens, but they each mediate a very different disease and course of infection.

Functional and therapeutic analysis of hepatitis C virus NS3.4A protease control of antiviral immune defense.

Chronic hepatitis C virus (HCV) infection is a major global public health problem. HCV infection is supported by viral strategies to evade the innate antiviral response wherein the viral NS3.4A protease complex targets and cleaves the interferon promoter stimulator-1 (IPS-1) adaptor protein to ablate signaling of interferon alpha/beta immune defenses.

Regulation of innate antiviral defenses through a shared repressor domain in RIG-I and LGP2.

RIG-I is an RNA helicase containing caspase activation and recruitment domains (CARDs). RNA binding and signaling by RIG-I are implicated in pathogen recognition and triggering of IFN-alpha/beta immune defenses that impact cell permissiveness for hepatitis C virus (HCV). Here we evaluated the processes that control RIG-I signaling.

RalB GTPase-mediated activation of the IkappaB family kinase TBK1 couples innate immune signaling to tumor cell survival.

The monomeric RalGTPases, RalA and RalB are recognized as components of a regulatory framework supporting tumorigenic transformation. Specifically, RalB is required to suppress apoptotic checkpoint activation, the mechanistic basis of which is unknown. Reported effector proteins of RalB include the Sec5 component of the exocyst, an octameric protein complex implicated in tethering of vesicles to membranes.

Viral and therapeutic control of IFN-beta promoter stimulator 1 during hepatitis C virus infection.

Viral signaling through retinoic acid-inducible gene-I (RIG-I) and its adaptor protein, IFN promoter-stimulator 1 (IPS-1), activates IFN regulatory factor-3 (IRF-3) and the host IFN-alpha/beta response that limits virus infection. The hepatitis C virus (HCV) NS3/4A protease cleaves IPS-1 to block RIG-I signaling, but how this regulation controls the host response to HCV is not known. Moreover, endogenous IPS-1 cleavage has not been demonstrated in the context of HCV infection in vitro or in vivo.

CARD games between virus and host get a new player.

A growing family of cellular proteins encoding the caspase activation and recruitment domain (CARD) has a crucial role in immunity by sensing virus infection and signaling antiviral immune defenses. Four independent studies have identified a novel CARD-containing protein, variously called IPS-1, MAVS, VISA and Cardif, which is an essential signaling adaptor of the host defense mediating CARD-CARD interactions with retinoic acid inducible gene-I (RIG-I) and melanoma differentiation-associated gene 5 (MDAS), sensors of virus infection. Disruption of this novel signaling pathway by hepatitis C virus (HCV) might provide a foundation for viral persistence.

Control of antiviral defenses through hepatitis C virus disruption of retinoic acid-inducible gene-I signaling.

Hepatitis C virus (HCV) is a major human pathogen that infects 170 million people. A hallmark of HCV is its ability to establish persistent infections reflecting the evasion of host immunity and interference with alpha/beta-IFN innate immune defenses. We demonstrate that disruption of retinoic acid-inducible gene I (RIG-I) signaling by the viral NS3/4A protease contributes to the ability of HCV to control innate antiviral defenses.