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Institution

Purdue Pharma

CompanyPickering, Ontario, Canada
About: Purdue Pharma is a company organization based out in Pickering, Ontario, Canada. It is known for research contribution in the topics: Buprenorphine & Chronic pain. The organization has 622 authors who have published 691 publications receiving 31545 citations. The organization is also known as: Purdue Pharmaceuticals L.P..


Papers
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Journal ArticleDOI
TL;DR: Whether or not Plugge and Van Der Vlies' method, based on their proposed statistic or on MD, could be accepted today, is examined.
Abstract: pared. At the time Plugge and Van Der Vlies developed their method, no reference guidelines for NIR were in place to use in evaluating their method. Therefore, this paper examines the question of whether or not such a method, based on their proposed statistic or on MD, could be accepted today.

14 citations

Journal ArticleDOI
TL;DR: The authors call on nurses to assess and manage acute pain in accordance with evidence-based guidelines, expert consensus reports, and position statements from professional nursing organizations in order to minimize the likelihood of its becoming chronic.
Abstract: Acute pain, which is usually sudden in onset and time limited, serves a biological protective function, warning the body of impending danger. However, while acute pain often resolves over time with normal healing, unrelieved acute pain can disrupt activities of daily living and transition to chronic pain. This article describes the effects of unrelieved acute pain on patients and clinical outcomes. The authors call on nurses to assess and manage acute pain in accordance with evidence-based guidelines, expert consensus reports, and position statements from professional nursing organizations in order to minimize the likelihood of its becoming chronic.

14 citations

Patent
07 Apr 2015
TL;DR: The Invention as mentioned in this paper provides indole derivatives of Formula I: and pharmaceutically acceptable salts and solvates thereof, wherein R 1e, R 1f, A, X, Y, Z, and W 4 are defined as set forth in the specification.
Abstract: The Invention provides indole derivatives of Formula I: and pharmaceutically acceptable salts and solvates thereof, wherein R 1e , R 1f , A, X, Y, Z, and W 4 are defined as set forth in the specification. The Invention also provides the use of compounds of Formula I and the pharmaceutically acceptable salts and solvates thereof to treat pain. In certain embodiments, the Compounds of the Invention are effective in treating a disorder responsive to blockade of one or more sodium channels.

14 citations

Journal ArticleDOI
TL;DR: This analysis demonstrates that ODIC may contain misinformation and HCPs and consumers should be aware of the potential for misinformation and consider more than 1 drug information resource to obtain unbiased, accurate, and complete product-specific drug information to help support the safe and effective use of prescription drug products.
Abstract: Background: Online drug information compendia (ODIC) are valuable tools that health care professionals (HCPs) and consumers use to educate themselves on pharmaceutical products. Research suggests that these resources, although informative and easily accessible, may contain misinformation, posing risk for product misuse and patient harm. Objective: Evaluate drug summaries within ODIC for accuracy and completeness and identify product-specific misinformation. Methods: Between August 2014 and January 2015, medical information (MI) specialists from 11 pharmaceutical/biotechnology companies systematically evaluated 270 drug summaries within 5 commonly used ODIC for misinformation. Using a standardized approach, errors were identified; classified as inaccurate, incomplete, or omitted; and categorized per sections of the Full Prescribing Information (FPI). On review of each drug summary, content-correction requests were proposed and supported by the respective product’s FPI. Results: Across the 270 drug summarie...

14 citations

Journal ArticleDOI
TL;DR: It is suggested that central neuronal circuitry in mammals could affect Vth in a mechanism similar to that of veratridine, by inducing a negative shift in the activation voltage of sodium channels.
Abstract: Previous work has shown that motoneurone excitability is enhanced by a hyperpolarization of the membrane potential at which an action potential is initiated (V(th)) at the onset, and throughout brainstem-evoked fictive locomotion in the adult decerebrate cat and neonatal rat. Modeling work has suggested the modulation of Na(+) conductance as a putative mechanism underlying this state-dependent change in excitability. This study sought to determine whether modulation of voltage-gated sodium channels could induce V(th) hyperpolarization. Whole-cell patch-clamp recordings were made from antidromically identified lumbar spinal motoneurones in an isolated neonatal rat spinal cord preparation. Recordings were made with and without the bath application of veratridine, a plant alkaloid neurotoxin that acts as a sodium channel modulator. As seen in HEK 293 cells expressing Nav1.2 channels, veratridine-modified channels demonstrated a hyperpolarizing shift in their voltage-dependence of activation and a slowing of inactivation that resulted in an enhanced inward current in response to voltage ramp stimulations. In the native rat motoneurones, veratridine-modified sodium channels induced a hyperpolarization of V(th) in all 29 neonatal rat motoneurones examined (mean hyperpolarization: -6.6 ± 4.3 mV). V(th) hyperpolarization was not due to the effects on Ca(2+) and/or K(+) channels as blockade of these currents did not alter V(th). Veratridine also significantly increased the amplitude of persistent inward currents (PICs; mean increase: 72.5 ± 98.5 pA) evoked in response to slow depolarizing current ramps. However, the enhancement of the PIC amplitude had a slower time course than the hyperpolarization of V(th), and the PIC onset voltage could be either depolarized or hyperpolarized, suggesting that PIC facilitation did not mediate the V(th) hyperpolarization. We therefore suggest that central neuronal circuitry in mammals could affect V(th) in a mechanism similar to that of veratridine, by inducing a negative shift in the activation voltage of sodium channels. Furthermore, this shift appears to be independent of the enhancement of PICs.

14 citations


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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20218
202013
201915
201819
201750
201640