Medtronic. Dr. Nead has received personal fees from Medtronic. Dr. Bowling has received personal fees from Medtronic. Dr. Murgu has received personal fees from Medtronic, Boston Scientific, Pinnacle Biologics, Olympus, Cook, Auris Robotics, and Elsevier; and has stock ownership in Concordia, Boston Scientific, and Merck. Dr. Krimsky has received personal fees from Medtronic, Innovital Systems, Gala Therapeutic, SOC, and Peytant; has stock ownership with Innovital Systems and CSA Medical; and has patents pending with Medtronic and Merit. Dr. Murillo has received support from Medtronic. Dr. LeMense has received personal fees from Medtronic. Dr. Minnich has received personal fees from Medtronic. Dr. Bansal has received personal fees from Medtronic, Pinnacle Biologics, Sunovion, and Veran Medical. Dr. Ellis has received support from Medtronic. Dr. Mahajan has received personal fees from Medtronic. Dr. Gildea has received personal fees from Medtronic. Dr. Bechara has received support from Medtronic. Dr. Sztejman has received support from Medtronic. Dr. Flandes has received grants from BTG-PneumRx and Ambu; and personal fees from Medtronic, BTG-PneumRx, Olympus, Ambu, PulmonX, and Boston Scientific. Dr. Rickman has received personal fees from Medtronic, Veran Medical, BD, Olympus, and Abbvie. Dr. Benzaquen has received support from Medtronic. Dr. Hogarth has received personal fees from Medtronic, Auris Surgical Robotics, Boston Scientific, Grifols, Shire, and CSL; and has stock ownership with Auris Surgical Robotics. Dr. Linden has received support from Medtronic. Dr. Wahidi has received personal fees from Medtronic and Veran Medical. Dr. Mattingley has received personal fees from Medtronic and is current employee of Medtronic (employment began after completion of enrollment). Dr. Hood is an employee with stock ownership at Medtronic; and has stock ownership with Boston Scientific. Ms. Lin and Ms. Wolvers are employees with stock ownership at Medtronic. Dr. Khandar has received personal fees from Medtronic.

The newly refined CPRL-4 is safe and yields an R0 resection with complete lymph node removal. It has lower morbidity, mortality, shorter hospital stay, and better quality of life than rib- and nerve-sparing thoracotomy. Technical advances are possible to shorten and improve the operation.

Dendritic cells (DCs) play a key role in critical illness and are depleted in spleens from septic patients and mice. To date, few studies have characterized the systemic effect of sepsis on DC populations in lymphoid tissues. We analyzed the phenotype of DCs and Th cells present in the local (mesenteric) and distant (inguinal and popliteal) lymph nodes of mice with induced polymicrobial sepsis (cecal ligation and puncture). Flow cytometry and immunohistochemical staining demonstrated that there was a significant local (mesenteric nodes) and partial systemic (inguinal, but not popliteal nodes) loss of DCs from lymph nodes in septic mice, and that this process was associated with increased apoptosis. This sepsis-induced loss of DCs occurred after CD3+CD4+ T cell activation and loss in the lymph nodes, and the loss of DCs was not preceded by any sustained increase in their maturation status. In addition, there was no preferential loss of either mature/activated (MHCIIhigh/CD86high) or immature (MHCIIlow/CD86low) DCs during sepsis. However, there was a preferential loss of CD8+ DCs in the local and distant lymph nodes. The loss of DCs in lymphoid tissue, particularly CD8+ lymphoid-derived DCs, may contribute to the alterations in acquired immune status that frequently accompany sepsis.

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