63 research outputs found
Biological and Non-Biological Methods for Lignocellulosic Biomass Deconstruction
Owing to their abundance and cost-effectiveness, lignocellulosic materials have
attracted increasing attention in clean energy technologies over the last decade.
However, the complex polymer structure in these residues makes it difficult to extract
the fermentable sugars. Therefore, various pretreatment regimes have been used
resulting in the breaking of lignocelluloses’ physical and chemical structures, thereby
enhancing the availability of the polysaccharides which are subsequently hydrolysed
into different biocommodities. This chapter provides an evaluation of some of the latest
exploited methodologies that are used in the pretreatment of lignocellulosic materials.
Moreover, the chapter discusses the advantages and disadvantages of each method
Deep peri-implantitis: Two cases treated with implant apicoectomy with follow-up of at least 7 years
Aim: Deep periimplantitis is a lesion located in the periapical region of an osseointegtated implant. The aim of this study was to present 2 cases of this feature treated with apicoectomy. Materials and methods: Two cases of deep periimplantitis located in the maxillary premolar region are presented in this report. Both the lesions were situated in the apical segment of otherwise osseointegrated and long (15mm) implants. They were treated with surgical debridement, apicoectomy, bone substitute and antibiotics. Results: Bone overheating, proximity to periapical lesions or previous inflammation seem to be the three possible causes of the lesions in the cases presented. The follow-up period of 7 and 10 years indicates that implant apicoectomy is a safe and reliable treatment choice. Conclusions: The treatment of choice for deep periimplantitis is implant apicoectomy, unless the implant is mobile, where implant removal is preferable. © 2015 The British Association of Oral Surgeons and John Wiley & Sons Ltd
Recommended from our members
Susceptibility to ozone-induced airway inflammation is associated with decreased levels of surfactant protein D.
BackgroundOzone (O3), a common air pollutant, induces exacerbation of asthma and chronic obstructive pulmonary disease. Pulmonary surfactant protein (SP)-D modulates immune and inflammatory responses in the lung. We have shown previously that SP-D plays a protective role in a mouse model of allergic airway inflammation. Here we studied the role and regulation of SP-D in O3-induced inflammatory changes in the lung.MethodsTo evaluate the effects of O3 exposure in mouse strains with genetically different expression levels of SP-D we exposed Balb/c, C57BL/6 and SP-D knockout mice to O3 or air. BAL cellular and cytokine content and SP-D levels were evaluated and compared between the different strains. The kinetics of SP-D production and inflammatory parameters were studied at 0, 2, 6, 12, 24, 48, and 72 hrs after O3 exposure. The effect of IL-6, an O3-inducible cytokine, on the expression of SP-D was investigated in vitro using a primary alveolar type II cell culture.ResultsOzone-exposed Balb/c mice demonstrated significantly enhanced acute inflammatory changes including recruitment of inflammatory cells and release of KC and IL-12p70 when compared with age- and sex-matched C57BL/6 mice. On the other hand, C57BL/6 mice had significantly higher levels of SP-D and released more IL-10 and IL-6. Increase in SP-D production coincided with the resolution of inflammatory changes. Mice deficient in SP-D had significantly higher numbers of inflammatory cells when compared to controls supporting the notion that SP-D has an anti-inflammatory function in our model of O3 exposure. IL-6, which was highly up-regulated in O3 exposed mice, was capable of inducing the expression of SP-D in vitro in a dose dependent manner.ConclusionOur data suggest that IL-6 contributes to the up-regulation of SP-D after acute O3 exposure and elevation of SP-D in the lung is associated with the resolution of inflammation. Absence or low levels of SP-D predispose to enhanced inflammatory changes following acute oxidative stress
- …