This article highlights the summary of five articles that mainly focuses on the use of polymers in the body and how it affects the body. It highlights several topics such as new technology for biomedical polymers, polymers and inflammation, analyzing the interactions between plasma protein and commercial protein, developing and validating an HPLC method to quantify camptothecin in polymeric nanocapsule suspension and the development and application of molecularly imprinted polymers as solid-phase sorbents for erythromycin extraction.
This article highlights the use of the SAMEs, short for Self-Assembling Monolayer End; which is a new and upcoming two-dimensional nanotechnology which can be used to control surface properties of polymer-made medical devices. Apart from that, the article also emphasizes on the fact that surface chemistry does have a biological interaction when at the surface of a medical device. The article also described the new technology that allowed polymer to be built onto by engineers to use on a particular device.
Apart from that, it also explores this technology and the way it operates and also explores its potential to be used in disposables, implantables and prostheses. The article concludes by exploring the future research of SAMEs technology which includes developing sophisticated polymer based medical devices as it is able to modify the surface during the process of manufacturing and therefore provides a more robust and built-in chemistry surface. Polymers and inflammation: disease mechanisms of the serpinopathies (Gooptu, B & Lomas, D. A, 2008)
The article discusses on the serpin(serine proteinase inhibitor) members which engages in a vital role in taking control of inflammatory, coagulation and fibrinolytic cascades. Besides that, it is noted that point mutations may be the basis for abnormal conformational transitions in the protein that may be disease generating. Furthermore, this article focuses on incorporating these three mechanisms which were defined by recent studies as a pathway to cause tissue damage, to be in a new model of pathogenesis of emphysema which are caused by mutations in the serpin 1-antitrypsin.
The evidence concluded that the both uncontrolled proteolytic activity did contribute to the pathogenesis of emphysema. New therapies were suggested for ai-antitrypsin deficiency. One of the therapies that were suggested was to redefine versions of these molecules in order to block the protein polymerization without any affect of its inhibitory activity. Another suggestion was to activate neutrophilis by blocking the ability of polymers. This therefore would reinstate the nonnal migration pathway of neutro- phils from the circulation to the alveoli. Apart from that, another strategy was to target the downstream effect rather than the polymer.