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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current strategies to limit macrophage adhesion, fusion and fibrous capsule formation in the foreign body response have focused on modulating material surface properties. We hypothesize that topography close to biological scale, in the micron and nanometric range, provides a passive approach without bioactive agents to modulate macrophage behavior. In our study, topography-induced changes in macrophage behavior was examined using parallel gratings (250 nm-2 mum line width) imprinted on poly(epsilon-caprolactone) (PCL), poly(lactic acid) (PLA) and poly(dimethyl siloxane) (PDMS). RAW 264.7 cell adhesion and elongation occurred maximally on 500 nm gratings compared to planar controls over 48 h. TNF-alpha and VEGF secretion levels by RAW 264.7 cells showed greatest sensitivity to topographical effects, with reduced levels observed on larger grating sizes at 48 h. In vivo studies at 21 days showed reduced macrophage adhesion density and degree of high cell fusion on 2 mum gratings compared to planar controls. It was concluded that topography affects macrophage behavior in the foreign body response on all polymer surfaces examined. Topography-induced changes, independent of surface chemistry, did not reveal distinctive patterns but do affect cell morphology and cytokine secretion in vitro, and cell adhesion in vivo particularly on larger size topography compared to planar controls.
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PMID:Characterization of topographical effects on macrophage behavior in a foreign body response model. 2013 63

Bee stings are a health concern in the Americas, where fatal envenomings due to massive attacks by Africanized honeybees have been documented in the last decades. Most studies on the toxic effects of honeybee venom in experimental animals have been performed using the intravenous or intraperitoneal injection routes. The aim of this study was to develop a mouse model that would better resemble a massive honeybee attack by using the subcutaneous (s.c.) route to induce a severe, sublethal systemic envenoming. An array of acute venom effects were characterized, including biochemical, hematological, histological, and inflammatory alterations, after the s.c. injection of 0.5 median lethal dose of venom. Rapid increases in serum alanine (ALT) and aspartate (AST) transaminases, creatinine, urea nitrogen, uric acid, sodium and chloride electrolytes, and creatine kinase (CK) were recorded, indicating damage to liver, kidneys, and skeletal muscle. Also, coagulation disturbances (fibrinogen decrease, and moderate delay in prothrombin and partial thromboplastin times) were demonstrated. Circulating platelet and leukocyte numbers remained unaltered, but a hemoconcentration effect (hematocrit and hemoglobin increase) was observed. This effect might be related to the marked edema induced by the venom. In addition, this inflammatory response included a systemic increase in cytokines (IL-1 beta, IL-6, TNF-alpha), together with an elevation of serum malondialdehyde and nitric oxide. The myotoxic effects of venom, melittin, and phospholipase A(2) were demonstrated after injection by s.c. route. No synergistic myotoxicity between melittin and PLA(2) was observed. Moreover, these two components, when injected at equivalent concentrations to those present in venom, induced a lower increase in serum CK than venom, suggesting that other components also contribute to its strong systemic toxicity towards skeletal muscle. The model here presented may be useful in preclinical studies to assess therapeutic antivenoms developed to cope with the problem of massive bee attacks.
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PMID:Acute physiopathological effects of honeybee (Apis mellifera) envenoming by subcutaneous route in a mouse model. 2063


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