157 research outputs found

    The Hybrid SPECT/CT as an Additional Lymphatic Mapping Tool in Patients with Breast Cancer

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    Background Conventional lymphoscintigraphy does not always define the exact anatomic location of a sentinel node. The lymphatic drainage pattern may be unusual or may not be shown at all. The recently introduced hybrid SPECT/CT imaging could help overcome these difficulties. SPECT is a tomographic version of conventional lymphoscintigraphy and the images have better contrast and resolution. When fused with the anatomical details provided by CT into one image, a meaningful surgical ā€˜ā€˜roadmapā€™ā€™ can be created. So far, there is little literature on the use of hybrid SPECT/CT in lymphatic mapping in patients with breast cancer. The purpose of this review was to report on these publications, including our own experience, focusing on patient selection, SPECT/CT settings, anatomic localization, and the detection of additional sentinel nodes. Methods The majority of investigators did not formulate indications for additional SPECT/CT after conventional imaging but scanned all patients eligible for sentinel node biopsy. The SPECT/CT settings used in the studies of this review were mostly similar, but the methods used for conventional imaging were more variable. Results All studies demonstrated an improved anatomical localization by performing additional SPECT/CT; sentinel nodes outside the axilla or nodes close to the injection sit

    A review of global ocean temperature observations: Implications for ocean heat content estimates and climate change

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    The evolution of ocean temperature measurement systems is presented with a focus on the development and accuracy of two critical devices in use today (expendable bathythermographs and conductivityā€temperatureā€depth instruments used on Argo floats). A detailed discussion of the accuracy of these devices and a projection of the future of ocean temperature measurements are provided. The accuracy of ocean temperature measurements is discussed in detail in the context of ocean heat content, Earth's energy imbalance, and thermosteric sea level rise. Upā€toā€date estimates are provided for these three important quantities. The total energy imbalance at the top of atmosphere is best assessed by taking an inventory of changes in energy storage. The main storage is in the ocean, the latest values of which are presented. Furthermore, despite differences in measurement methods and analysis techniques, multiple studies show that there has been a multidecadal increase in the heat content of both the upper and deep ocean regions, which reflects the impact of anthropogenic warming. With respect to sea level rise, mutually reinforcing information from tide gauges and radar altimetry shows that presently, sea level is rising at approximately 3ā€‰mmā€‰yrāˆ’1 with contributions from both thermal expansion and mass accumulation from ice melt. The latest data for thermal expansion sea level rise are included here and analyzed

    Modulation of calcification of vascular smooth muscle cells in culture by calcium antagonists, statins, and their combination

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    Background Vascular calcification is an organized process in which vascular smooth muscle cells (VSMCs) are implicated primarily. The purpose of the present study was to assess the effects of calcium antagonists and statins on VSMC calcification inĀ vitro. Methods VSMC calcification was stimulated by incubation in growth medium supplemented with 10Ā mmol/l Ī²-glycerophosphate, 8Ā mmol/l CaCl2, 10Ā mmol/l sodium pyruvate, 1Ā Ī¼mol/l insulin, 50Ā Ī¼g/ml ascorbic acid, and 100Ā nmol/l dexamethasone (calcification medium). Calcification, proliferation, and apoptosis of VSMCs were quantified. Results Calcium deposition was stimulated dose-dependently by Ī²-glycerophosphate, CaCl2, and ascorbic acid (all PĀ <Ā 0.01). Addition of amlodipine (0.01ā€“1Ā Ī¼mol/l) to the calcification medium did not affect VSMC calcification. However, atorvastatin (2ā€“50Ā Ī¼mol/l) stimulated calcium deposition dose-dependently. Combining treatments stimulated calcification to a degree similar to that observed with atorvastatin alone. Both atorvastatin and amlodipine inhibited VSMC proliferation at the highest concentration used. Only atorvastatin (50Ā Ī¼mol/l) induced considerable apoptosis of VSMCs. Conclusion InĀ vitro calcification of VSMCs is not affected by amlodipine, but is stimulated by atorvastatin at concentrations ā‰„10Ā Ī¼mol/l, which could contribute to the plaque-stabilizing effect reported for statins
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