Quantitative metrics for assessing plan quality

Despite many studies over the last 3 decades that have attempted to explicitly quantify the decision-making process for radiotherapy treatment plan evaluation, judgments of an individual plan's degree of quality are still largely subjective and can show inter- and intra-practitioner variability even if the clinical treatment goals are the same. Several factors conspire to confound the full quantification of treatment plan quality, including uncertainties in dose response of cancerous and normal tissue, the rapid pace of new technology adoption, and the human component of treatment planning. However, new developments in clinical informatics and automation are lowering the bar for developing and implementing quantitative metrics into the treatment planning process. This review discusses general strategies for using quantitative metrics in the treatment planning process and presents a case study in intensity-modulated radiation therapy planning whereby control was established on a variable system via such techniques.     

Perhentidines A-C: macroline-macroline bisindoles from Alstonia and the absolute configuration of perhentinine and macralstonine

Three new bisindole alkaloids of the macroline-macroline type, perhentidines A-C (1-3), were isolated from the stem-bark extract of Alstonia macrophylla and Alstonia angustifolia. The structures of these alkaloids were established on the basis of NMR and MS analyses. The absolute configurations of perhentinine (4) and macralstonine (5) were established by X-ray diffraction analyses, which facilitated assignment of the configuration at C-20 in the regioisomeric bisindole alkaloids perhentidines A-C (1-3). A potentially useful method for the determination of the configuration at C-20 based on comparison of the NMR chemical shifts of the bisindoles and their acetate derivatives, in these and related bisindoles with similar constitution and branching of the monomeric units, is also presented.     

Portal Vein Embolisation for Extended Hepatectomy: Single-Centre Experience

Background  

Portal vein embolisation (PVE) induces contra-lateral liver hypertrophy to facilitate an extended hepatectomy.     

Enhanced inflammatory response via activation of NF-kappaB in acute experimental diabetic neuropathy subjected to ischemia-reperfusion injury

Reperfusion following ischemia increases ischemic fiber degeneration (IFD) in diabetic nerves compared to control normoglycemic nerves. The mechanism of this excessive susceptibility is unclear. Since reperfusion injury results in an inflammatory response, we tested the hypothesis that the diabetic state increases the inflammatory cascade. We used an animal model of unilateral ischemia-reperfusion (IR) injury to streptozotocin (STZ)-induced diabetic nerve to evaluate the density and localization of mediators of the inflammatory response using selective immunolabeling methods (for nuclear factor kappa B (NF-kappaB), intercellular adhesion molecule-1 (ICAM-1), cytokines and inflammatory cells). We studied a 1-month diabetic group and an age-matched control group (n=6 each). The right limb underwent 3 h ischemia at 35 degrees C and 7 days reperfusion. This was achieved by ligating the supplying arteries and collaterals to the right sciatic-tibial nerve for 3 h, followed by releasing the ties. Immunohistochemistry was performed on proximal sciatic and mid tibial nerves. NF-kappaB expression in diabetic sciatic endothelial cell and Schwann cell (SC) was significantly increased over that of controls subjected to identical IR injury. We observed a nearly 2-fold increase in density of NF-kappaB and ICAM-1 expression in microvessels of diabetic nerve compared with control nerve. Extensive infiltration of monocyte macrophages (1C7) was observed in the endoneurium of diabetic nerves, while only mild infiltration of granulocytes (HIS 48) occurred in the endoneurium of diabetic tibial nerves. This study provides evidence for an enhanced inflammatory response in diabetic nerves subjected to IR injury apparently via NF-kappaB activation.