A general framework and review of scatter correction methods in cone beam CT. Part 2: scatter estimation approaches

The main components of scatter correction procedures are scatter estimation and a scatter compensation algorithm. This paper completes a previous paper where a general framework for scatter compensation was presented under the prerequisite that a scatter estimation method is already available. In the current paper, the authors give a systematic review of the variety of scatter estimation approaches. Scatter estimation methods are based on measurements, mathematical-physical models, or combinations of both. For completeness they present an overview of measurement-based methods, but the main topic is the theoretically more demanding models, as analytical, Monte-Carlo, and hybrid models. Further classifications are 3D image-based and 2D projection-based approaches. The authors present a system-theoretic framework, which allows to proceed top-down from a general 3D formulation, by successive approximations, to efficient 2D approaches. A widely useful method is the beam-scatter-kernel superposition approach. Together with the review of standard methods, the authors discuss their limitations and how to take into account the issues of object dependency, spatial variance, deformation of scatter kernels, external and internal absorbers. Open questions for further investigations are indicated. Finally, the authors refer on some special issues and applications, such as bow-tie filter, offset detector, truncated data, and dual-source CT.     

A pilot study to assess the effects of combining fluticasone propionate/salmeterol and tiotropium on the airflow obstruction of patients with severe-to-very severe COPD

The aim of this pilot study was to explore the relative efficacy in terms of improvement in symptoms and lung function of combining fluticasone propionate/salmeterol combination (FSC) and tiotropium in patients with severe-to-very severe stable COPD. Ninety patients were randomized to receive 3 months of treatment in one of three treatment groups: (1) FSC 500/50 microg Diskus, 1 inhalation twice daily+placebo Handihaler 1 inhalation once-daily daily; (2) tiotropium 18 microg Handihaler, 1 inhalation once daily+placebo Diskus, 1 inhalation twice daily; (3) FSC 500/50 microg Diskus, 1 inhalation twice daily+tiotropium 18 microg Handihaler, 1 inhalation once-daily daily. Patients attended the clinic before and after 1 month, 2 months, and 3 months of treatment for evaluations of pulmonary function, and dyspnea, which was assessed using a visual analog scale (VAS). Also the supplemental salbutamol use was measured. Eighty-one patients completed the 3-month treatment period: 26 patients receiving FSC, 26 patients receiving tiotropium, and 29 patients receiving FSC+tiotropium. Patients were withdrawn for COPD exacerbation. Improvements in trough FEV(1) with all treatments medications were observed by the first month when trough FEV(1) had improved significantly above baseline by 74 mL (p<0.05) in the tiotropium group, by 117 mL (p<0.05) in the FSC group and by 115 mL (p<0.05) in FSC+tiotropium group. At the end of the study, trough FEV(1) had improved significantly above baseline by 141 mL (p<0.05) in the tiotropium group, by 140 mL (p<0.05) in the FSC group and by 186 mL (p<0.05) in FSC+tiotropium group. The difference between FSC and tiotropium appeared to decrease, that between FSC and FSC+tiotropium appeared to increase and that between tiotropium and FSC+tiotropium remained almost similar with study duration. Our results suggest that adding FSC and tiotropium may provide benefits in symptomatic patients with severe-to-very severe stable COPD.     

Single dose of MDMA causes extensive decrement of serotoninergic fibre density without blockage of the fast axonal transport in Dark Agouti rat brain and spinal cord

Prolonged neurotoxicity of the recreational drug, MDMA (3,4-methylenedioxymethamphetamine) on serotoninergic axon terminals has been suggested. The effect of a single (15 mg/kg) dose of intraperitoneally administered MDMA on serotoninergic fibre density, defined by tryptophan hydroxylase (TpH) and serotonin transporter (5-HTT) immunoreactivity, has been evaluated in the spinal cord and brain areas in Dark Agouti rats, 7 and 180 days after MDMA applications. Immunostaining for amyloid precursor protein (APP) has been performed to examine possible defects of the fast axonal transport, and 5-HTT mRNA expressions were quantified in neurones of medullary raphe nuclei. Seven days after MDMA treatment, a substantial decrease in the density of TpH-immunoreactive fibres was detectable in the frontal cortex, the caudate-putamen, the CA1 region of the hippocampus, and marked decreases were found in the spinal cord. These changes in TpH density showed a high correlation with 5-HTT densities. In contrast, APP-immunoreactive axonal bulbs were not detected in any of the brain regions studied. Seven days after MDMA administrations, significantly elevated 5-HTT mRNA expressions were found in the raphe pallidus and obscurus. Our results suggest that a single dose of MDMA elicits widespread depletion of TpH and 5-HTT immunoreactivity in serotoninergic axons without morphological sign of the blockage of the fast anterograde axonal transport. Our results do not support the notion of MDMA-induced axotomy of serotoninergic neurones. The up-regulation of 5-HTT mRNA expressions 1 week after MDMA injections might indicate the potential recovery of the serotonin system.     

Right hepatic lobe agenesis. Where is the gallbladder?

Anomalies of the liver are infrequent. Agenesis of the right hepatic lobe is an uncommon, usually asymptomatic, entity that is diagnosed through new imaging techniques or during surgery. We present the case of a 51-year-old woman with right hepatic lobe agenesis who underwent technically difficult cholecystectomy for symptomatic gallstones. We discuss the diagnosis and technical difficulties that can be encountered during cholecystectomy when there is right hepatic lobe agenesis.     

CUTANEOUS MERCURY GRANULOMA

Mercury poisoning arising from cutaneous mercury deposition is highly unusual. The diagnosis is difficult to make when no history of a penetrating injury is given. We report such a case and discuss investigation and management. Other cutaneous manifestations of mercury exposure are outlined.