Comparison of AFITPAC versus NOS and a Packet Radio Network Design

This thesis encompasses two themes: (1) A comparison of the Network Operating System (NOS) software package, developed by Phil Karn and others, and AFITPAC, written by Marsh and Geier at the Air Force Institute of Technology. The comparison is based on the Air Force Logistics Command\u27s requirements for the development of a Packet Radio Network program. The results of the comparison are a recommendation that use of the NOS package be pursued because it can meet all twelve of the requirements and compiles with five of the Military Standard Protocols. (2) The design of a personal computer Packet Radio Network Simulator used to analyze the network performance of AFITPAC and NOS is proposed. The proposal concludes with a discussion of problems in development of the simulation which used MODSIM IITM, C++, and a 80386/25Mhz personal computer. Recommendations are made for pursuing the simulation effort on other hardware platforms and for improvements to the design

Ultradeep Sequencing of a Human Ultraconserved Region Reveals Somatic and Constitutional Genomic Instability

Ultradeep sequencing of genomes permits the detection of very low-level genomic instability in non-neoplastic tissues of patients with the most common form of inherited colorectal cancer

Interleukin-1 regulates CXCL8 release and influences disease outcome in response to streptococcus pneumoniae, defining intercellular cooperation between pulmonary epithelial cells and macrophages

The success of Streptococcus pneumoniae (the pneumococcus) as a pulmonary pathogen is related to its restriction of innate immune responses by respiratory epithelial cells. The mechanisms used to overcome this restriction are incompletely elucidated. Pulmonary chemokine expression involves complex cellular and molecular networks, involving the pulmonary epithelium, but the specific cellular interactions and the cytokines that control them are incompletely defined. We show that serotype 2 or 4 pneumococci induce only modest levels of CXCL8 expression from epithelial cell lines, even in the absence of a polysaccharide capsule. In contrast, coculture of A549 cells with the macrophage-like THP-1 cell line, differentiated with vitamin D, or monocyte-derived macrophages enhanced CXCL8 release. Supernatants from the THP-1 cell line prime A549 cells to release CXCL8 at levels similar to cocultures. Interleukin-1Ra (IL-1Ra) inhibits CXCL8 release from cocultures and reduces the activity of macrophage-conditioned media, but inhibition of tumor necrosis factor alpha (TNF-alpha) had only a minimal effect on CXCL8 release. Release of IL-1 beta but not TNF-alpha was upregulated in cocultures. IL-1 type 1 receptor knockout C57BL/6 and BALB/c mice confirmed the importance of IL-1 signaling in CXC chemokine expression and neutrophil recruitment in vivo. In fulminant disease, increased IL-1 signaling resulted in increased neutrophils in the airway and more invasive disease. These results demonstrate that IL-1 is an important component of the cellular network involving macrophages and epithelial cells, which facilitates CXC chemokine expression and aids neutrophil recruitment during pneumococcal pneumonia. They also highlight a potential clinical role for anti-IL-1 treatment to limit excessive neutrophilic inflammation in the lung