Diabetic neuropathies, affecting the autonomic, sensory, and motor peripheral nervous system, are among the most frequent complications of diabetes. The symptoms of diabetic polyneuropathies are multi-faceted; the etiology and the underlying mechanisms are as yet unclear. Clinical studies established a significant correlation between the control of the patients' blood glucose level and the severity of the damage to the peripheral nervous system. Recent in vitro studies suggest that elevated glucose levels induced dysfunction and apoptosis in cultured cells of neuronal origin, possibly through the formation of reactive oxygen species (ROS). Based on these results, we hypothesized that elevated glucose levels impair neuronal survival and function via ROS dependent intracellular signaling pathways. In order to test this hypothesis, we cultured neural crest-derived PC12 pheochromocytoma cells under euglycemic (5 mM) and hyperglycemic (25 mM) conditions. Continuous exposure of undifferentiated PC12 cells for up to 72 h to elevated glucose induced the enhanced generation of ROS, as assessed from the increase in the cell-associated fluorescence of the ROS-sensitive fluorogenic indicator, 2,7-dichlorodihydrofluorescein diacetate. In cells cultured in high glucose, both basal and secretagogue-stimulated catecholamine release were enhanced. Furthermore, high glucose, reduced (by ca. 30%) the rate of cell proliferation and enhanced the occurrence of apoptosis, as assessed by DNA fragmentation, TUNEL assay and the activation of an apoptosis-specific protease, caspase CCP32. Elevated glucose levels significantly attenuated nerve growth factor (NGF)-induced neurite extension, as quantitated by computer-aided image analysis. Culturing PC12 cells in high glucose resulted in alterations in basal and NGF-stimulated mitogen-activated protein kinase (MAPK) signaling pathways, specifically in a switch from the neuronal survival/differentiation-associated MAPK ERK to that of apoptosis/stress-associated MAPK p38 and JNK. Based on our results we present a model in which the prolonged, excess formation of ROS represents a common mechanism for hyperglycemia-induced damage to neuronal cells. We propose that this simple in vitro system might serve as an appropriate model for evaluating some of the effects of elevated glucose on cultured cells of neuronal origin.

The lung is a complex structure that is interdigitated with immune cells. Understanding the 4-dimensional process of normal and defective lung function and immunity has been a centuries-old problem. Challenges intrinsic to the lung have limited adequate microscopic evaluation of its cellular dynamics in real time, until recently. Because of emerging technologies, we now recognize alveolar-to-airway transport of inhaled antigen. We understand the nature of neutrophil entry during lung injury and are learning more about cellular interactions during inflammatory states. Insights are also accumulating in lung development and the metatastatic niche of the lung. Here we assess the developing technology of lung imaging, its merits for studies of pathophysiology and areas where further advances are needed.

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Objectives Describe at least four available billing codes covering palliative care services. Describe four or more payment arrangements that can be used by any palliative care team, along with their pros and cons. Describe at least three primary interests of payers in provider contracting for their seriously ill members. Despite political uncertainties, the drive towards payment reform continues unabated, and palliative care providers have strong opportunities for sustainable payment. This session will help attendees to understand the opportunities better, as well as destroy some prevailing myths about alternative payment. First, this session will review the scope of successful payment arrangements that now exist for palliative care programs, both under Medicare and with private payers. This payment arrangement review will cover both important fee-for-service changes and alternative payments, drawing on interviews and market research conducted under the CAPC Payment Accelerator. Next, the session turns to a frank discussion with a health plan on their goals as a payer and the practical considerations they face in negotiating provider payments. It also covers how a health plan can compensate a palliative care team both directly and indirectly, turning a medical group or ACO into the palliative care team's payer. Finally, presenters will review why the palliative care field must think broadly about payment opportunities and suggest next steps.