11 research outputs found
Epidermal growth factor receptor, p16, cyclin D1, and p53 staining patterns for inverted papilloma
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/101829/1/alr21215.pd
Enhancement of Inducible Nitric Oxide Synthase Activity by Low Molecular Weight Peptides Derived from Protamine: A Potential Therapy for Chronic Rhinosinusitis
Nitric oxide (NO) is a key immune
defense agent that is produced
from l-arginine in the airways by leukocytes and airway epithelial
cells, primarily via inducible nitric oxide synthase (iNOS). Deficiencies
in nasal NO levels have been associated with diseases such as primary
ciliary dyskinesia and chronic rhinosinusitis. Herein, we demonstrate
a proof-of-concept regarding a potential new therapeutic approach
for such disorders. We show that arginine-rich low molecular weight
peptides (LMWPs) derived from the FDA-approved protamine (obtained
from salmon sperm) are effective at significantly raising NO production
in both RAW 264.7 mouse macrophage and LA4 mouse epithelial cell lines.
LMWP is produced using a stable, easily produced immobilized thermolysin
gel column followed by size-exclusion purification. Monomeric l-arginine induces concentration-dependent increases in NO production
in stimulated RAW 264.7 and LA4 cells, as measured by stable nitrite
in the cell media. In stimulated RAW 264.7 cells, LMWP significantly
increases iNOS expression and total NO production 12â24 h post-treatment
compared to cells given equivalent levels of monomeric l-arginine.
For stimulated LA4 cells, LMWPs are effective in significantly increasing
NO production compared to equivalent l-arginine monomer concentrations
over 24 h but do not substantially enhance iNOS expression. The use
of the arginase inhibitor S-boronoethyl-l-cysteine in combination
with LMWPs results in even higher NO production by stimulated RAW
264.7 cells and LA4 cells. Increases in NO due to LMWPs, compared
to l-arginine, occur only after 4 h, which may be due to
iNOS elevation rather than increased substrate availability
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International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis
BackgroundCritical examination of the quality and validity of available allergic rhinitis (AR) literature is necessary to improve understanding and to appropriately translate this knowledge to clinical care of the AR patient. To evaluate the existing AR literature, international multidisciplinary experts with an interest in AR have produced the International Consensus statement on Allergy and Rhinology: Allergic Rhinitis (ICAR:AR).MethodsUsing previously described methodology, specific topics were developed relating to AR. Each topic was assigned a literature review, evidence-based review (EBR), or evidence-based review with recommendations (EBRR) format as dictated by available evidence and purpose within the ICAR:AR document. Following iterative reviews of each topic, the ICAR:AR document was synthesized and reviewed by all authors for consensus.ResultsThe ICAR:AR document addresses over 100 individual topics related to AR, including diagnosis, pathophysiology, epidemiology, disease burden, risk factors for the development of AR, allergy testing modalities, treatment, and other conditions/comorbidities associated with AR.ConclusionThis critical review of the AR literature has identified several strengths; providers can be confident that treatment decisions are supported by rigorous studies. However, there are also substantial gaps in the AR literature. These knowledge gaps should be viewed as opportunities for improvement, as often the things that we teach and the medicine that we practice are not based on the best quality evidence. This document aims to highlight the strengths and weaknesses of the AR literature to identify areas for future AR research and improved understanding
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Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/1/ICARPrimaryAuthorCOIForms1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/2/ICARSecondaryAuthorCOIForms.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/3/ICARPrimaryAuthorCOIForms2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/4/ICARAuthorCOI2017.8.15.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/5/alr22073_c.pd