Do Nonsteroidal Anti-Inflammatory Drugs Affect Bone Healing? A Critical Analysis

Nonsteroidal anti-inflammatory drugs (NSAIDs) play an essential part in our approach to control pain in the posttraumatic setting. Over the last decades, several studies suggested that NSAIDs interfere with bone healing while others contradict these findings. Although their analgesic potency is well proven, clinicians remain puzzled over the potential safety issues. We have systematically reviewed the available literature, analyzing and presenting the available in vitro animal and clinical studies on this field. Our comprehensive review reveals the great diversity of the presented data in all groups of studies. Animal and in vitro studies present so conflicting data that even studies with identical parameters have opposing results. Basic science research defining the exact mechanism with which NSAIDs could interfere with bone cells and also the conduction of well-randomized prospective clinical trials are warranted. In the absence of robust clinical or scientific evidence, clinicians should treat NSAIDs as a risk factor for bone healing impairment, and their administration should be avoided in high-risk patients

Macrophages are exploited from an innate wound healing response to facilitate cancer metastasis.

Tumour-associated macrophages (TAMs) play an important role in tumour progression, which is facilitated by their ability to respond to environmental cues. Here we report, using murine models of breast cancer, that TAMs expressing fibroblast activation protein alpha (FAP) and haem oxygenase-1 (HO-1), which are also found in human breast cancer, represent a macrophage phenotype similar to that observed during the wound healing response. Importantly, the expression of a wound-like cytokine response within the tumour is clinically associated with poor prognosis in a variety of cancers. We show that co-expression of FAP and HO-1 in macrophages results from an innate early regenerative response driven by IL-6, which both directly regulates HO-1 expression and licenses FAP expression in a skin-like collagen-rich environment. We show that tumours can exploit this response to facilitate transendothelial migration and metastatic spread of the disease, which can be pharmacologically targeted using a clinically relevant HO-1 inhibitor

Macrophages are exploited from an innate wound healing response to facilitate cancer metastasis

Tumour-associated macrophages (TAMs) play an important role in tumour progression, which is facilitated by their ability to respond to environmental cues. Here we report, using murine models of breast cancer, that TAMs expressing fibroblast activation protein alpha (FAP) and haem oxygenase-1 (HO-1), which are also found in human breast cancer, represent a macrophage phenotype similar to that observed during the wound healing response. Importantly, the expression of a wound-like cytokine response within the tumour is clinically associated with poor prognosis in a variety of cancers. We show that co-expression of FAP and HO-1 in macrophages results from an innate early regenerative response driven by IL-6, which both directly regulates HO-1 expression and licenses FAP expression in a skin-like collagen-rich environment. We show that tumours can exploit this response to facilitate transendothelial migration and metastatic spread of the disease, which can be pharmacologically targeted using a clinically relevant HO-1 inhibitor

Endothelin 1 levels in relation to clinical presentation and outcome of Henoch Schonlein purpura

<p>Abstract</p> <p>Background</p> <p>Henoch Schonlein purpura (HSP) is a common vasculitis of small vessels whereas endothelin-1 (ET-1) is usually reported elevated in vasculities and systematic inflammation. The aim of the present study was to investigate whether ET-1 levels are correlated with the clinical presentation and the outcome of HSP.</p> <p>Methods</p> <p>The study sample consisted of thirty consecutive patients with HSP. An equal number of healthy patients of similar age and the same gender were served as controls. The patients' age range was 2–12.6 years with a mean ± SD = 6.3 ± 3 years. All patients had a physical examination with a renal, and an overall clinical score. Blood and urinary biochemistry, immunology investigation, a skin biopsy and ET-1 measurements in blood and urine samples were made at presentation, 1 month later and 1 year after the appearance of HSP. The controls underwent the same investigation with the exception of skin biopsy.</p> <p>Results</p> <p>ET-1 levels in plasma and urine did not differ between patients and controls at three distinct time points. Furthermore the ET-1 were not correlated with the clinical score and renal involvement was independent from the ET-1 measurements. However, the urinary ET-1 levels were a significant predictor of the duration of the acute phase of HSP (HR = 0.98, p = 0.032, CI0.96–0.99). The ET-1 levels did not correlate with the duration of renal involvement.</p> <p>Conclusion</p> <p>Urinary ET-1 levels are a useful marker for the duration of the acute phase of HSP but not for the length of renal involvement.</p

A taste sensor device for unmasking admixing of rancid or winey-vinegary olive oil to extra virgin olive oil

Electrochemical sensor devices have gathered great attention in food analysis namely for olive oil evaluation. The adulteration of extra-virgin olive oil with lower-grade olive oil is a common worldwide fraudulent practice, which detection is a challenging task. The potentiometric fingerprints recorded by lipid polymeric sensor membranes of an electronic tongue, together with linear discriminant analysis and simulated annealing meta-heuristic algorithm, enabled the detection of extra-virgin olive oil adulterated with olive oil for which an intense sensory defect could be perceived, specifically rancid or winey-vinegary negative sensations. The homemade designed taste device allowed the identification of admixing of extra-virgin olive oil with more than 2.5% or 5% of rancid or winey-vinegary olive oil, respectively. Predictive mean sensitivities of 84±4% or 92±4% and specificities of 79±6% or 93±3% were obtained for rancid or winey-vinegary adulterations, respectively, regarding an internal-validation procedure based on a repeated K-fold cross-validation variant (4 folds×10 repeats, ensuring that the dataset was forty times randomly split into 4 folds, leaving 25% of the data for validation purposes). This performance was satisfactory since, according to the legal physicochemical and sensory analysis, the intentionally adulterated olive oil with percentages of 2.510%, could still be commercialized as virgin olive oil. It could also be concluded that at a 5% significance level, the trained panelists could not distinguish extra-virgin olive oil samples from those adulterated with 2.5% of rancid olive oil or up to 5% of winey-vinegary olive oil. Thus, the electronic tongue proposed in this study can be foreseen as a practical and powerful tool to detect this kind of worldwide common fraudulent practice of high quality olive oil.This work was financially supported by Project POCI-01–0145FEDER-006984 – Associate Laboratory LSRE-LCM, Project UID/QUI/ 00616/2013 – CQ-VR, Project UID/BIO/04469/2013 – CEB and strategic project PEst-OE/AGR/UI0690/2014 – CIMO all funded by FEDER - Fundo Europeu de Desenvolvimento Regional through COMPETE2020 - Programa Operacional Competitividade e Internacionalização (POCI) – and by national funds through FCT - Fundação para a Ciência e a Tecnologia, Portugal. Nuno Rodrigues thanks FCT, POPH-QREN and FSE for the Ph.D. Grant (SFRH/BD/104038/2014). Souheib Oueslati is also grateful for the support of the Tunisian Ministry of Agriculture.info:eu-repo/semantics/publishedVersio

Incomplete Kawasaki disease with intermittent fever and retropharyngeal inflammation

Kawasaki disease is a systemic vasculitis of unknown etiology, presenting typically in infants and young children. We report a rare case of incomplete Kawasaki disease in a 15-month-old male infant presenting with symptoms mimicking retropharyngeal abscess and intermittent fever. © 2012 by Lippincott Williams &amp; Wilkins