Philippians: Paul\u27s Handbook on Conflict Management

Much of my life has been devoted to bringing together people and concepts which did not seem to belong together. In my high school days, I delighted in hosting parties to which I intentionally invited students from very different social groups. As a pastor, I have worked hard to bring the various cliques of small churches together in a sense of: unity. As a seminary student, I have striven to combine the highest academic standards with a concern for the relevance of each academic activity to the every-day pastorate. This thesis is a further step towards developing a minstry of bridge-building. First, it is a study of the techniques of developing unity and cooperation within the local church. But on a second level, this thesis is an attempt to bring together the best of sociological studies on conflict management with the best of Biblical studies on the subject. It is my prayer that it will be useful ln encouraging others to become bridge-builders

A survey of debris trails from short-period comets

We observed 34 comets using the 24 micron camera on the Spitzer Space Telescope. Each image contains the nucleus and covers at least 10^6 km of each comet's orbit. Debris trails due to mm-sized or larger particles were found along the orbits of 27 comets; 4 comets had small-particle dust tails and a viewing geometry that made debris trails impossible to distinguish; and only 3 had no debris trail despite favorable observing conditions. There are now 30 Jupiter-family comets with known debris trails, of which 22 are reported in this paper for the first time. The detection rate is >80%, indicating that debris trails are a generic feature of short-period comets. By comparison to orbital calculations for particles of a range of sizes ejected over 2 yr prior to observation, we find that particles comprising 4 debris trails are typically mm-sized while the remainder of the debris trails require particles larger than this. The lower-limit masses of the debris trails are typically 10^11 g, and the median mass loss rate is 2 kg/s. The mass-loss rate in trail particles is comparable to that inferred from OH production rates and larger than that inferred from visible-light scattering in comae.Comment: accepted by Icarus; figures compressed for astro-p

Mutagenesis in Drosophila Melanogaster. I. Scheduled Synthesis of Nuclear and Mitochondrial Dna and Unscheduled Dna Synthesis. II. Dosimetry Studies Using Phosphorus-33. IIi. Molecular Analysis of Induced Mutations at the Adh Locus (Alcohol Dehydrogenase, Restriction, Cloning, Southern, Blotting).

Presented here are three distinct, but interwoven areas of mutation research and molecular genetics using Drosophila melanogaster as the test organism. The first section describes the characterization of the DNA replication process and DNA repair in the oocyte. This involved sex-linked recessive lethal tests on ethyl methanesulfonate (EMS) treated females and unscheduled DNA synthesis (UDS) studies involving EMS, methyl methanesulfonate (MMS) and N-ethyl-N-nitrosourea (ENU). Oocytes were positive for UDS with EMS and MMS in a DNA repair competent strain and negative in excision repair deficient strains. ENU was negative in a DNA repair competent strain. Since UDS is not quantitative the development of a molecular dosimetry assay for oocytes is a necessity. The second section describes equilibrium labeling of Drosophila with (\u2733)P. This technique relies on the theory that Drosophila, living their life on media with (\u2733)P, will reach an equilibrium between the (\u2733)P and unlabeled phosphorus in the media, leading to a uniform labeling of the DNA. This has been achieved and may eventually replace ((\u2714)C-dT) deoxythymidine as a DNA label. Analysis of the types of mutations makes up the third section and involves the study of x-ray induced mutations at the Alcohol dehydrogenase (Adh) locus. Only two of the eight mutants (25%) analyzed here or two out of the original 31 (6%) induced mutants produced a detectable protein using the O\u27Farrell two-dimensional gel technique. Restriction endonuclease and Southern blot studies showed five out of the eight (63%) of the mutants previously determined not to be large deletions had an altered DNA restriction pattern, including one spontaneous mutant. These alterations were all outside of the Adh structural gene region. Only one of these produced a detectable ADH protein. Of the three normal appearing mutants after restriction endonuclease and Southern blot analysis only one made a detectable ADH protein. All of the mutants made a normal sized mature mRNA which hybridized to the genomic probe. These alterations in the five mutants not producing a detectable ADH protein may be due to very small deletions resulting in frameshifts

Pancreatic Cancer Center: Providing the Research Tools Necessary to Advance Pancreatic Cancer Patient Care

poster abstractThere were approximately 43,000 new cases of pancreatic ductal adenocarcinoma (PDAC) in the U.S. in 2010, and approximately 37,000 deaths. PDAC thus constitutes the fourth leading cause of cancer deaths, and PDAC patients have a dismal 5-year survival rate of 6%; approximately 75% of patients die within the first year after diagnosis. PDAC is notoriously resistant to chemotherapy and radiation and even with our best treatment options, a complete margin-negative surgical resection, few patients achieve long-term survival. Despite these statistics, surprisingly only a small number of NCI-designated cancer centers have a specialized pancreatic cancer program. The creation of the IUPUI Signature Center for Pancreatic Cancer Research has been the foundation for putting IUPUI, the IU School of Medicine, Purdue University and the IU Simon Cancer Center at the forefront of pancreatic cancer treatment and research across the nation. The Signature Center, comprised of basic, translational and clinical researchers, represents the continuum of the disease from biological / molecular investigation to clinical trials. Funding from the Signature Center Initiative is being utilized to develop genetically engineered mouse models, generate orthotopic pancreatic cancer mouse models as well as provide funding for peer reviewed pilot projects. Establishment and characterization of these in vivo models provides the groundwork to be used by all members in their translational research projects; support of pilot projects provides preliminary data and identification of projects to be used in a SPORE application. Additionally, work has begun on a web portal to promote and educate both patients and clinicians about the IUSCC Pancreas Cancer Clinic which became operational in 2010. Taken together these activities provide the infrastructure to support pancreas cancer research at IU across the continuum of bench to bedside to practice. The availability of these resources to all members promotes inter-disciplinary collaborations aimed at increasing our understanding of pancreatic cancer so that advancements can be made in diagnosis, prevention and treatment of this malignancy

DNA Repair Proteins as Molecular Targets for Cancer Therapeutics

Cancer therapeutics include an ever-increasing array of tools at the disposal of clinicians in their treatment of this disease. However, cancer is a tough opponent in this battle and current treatments which typically include radiotherapy, chemotherapy and surgery are not often enough to rid the patient of his or her cancer. Cancer cells can become resistant to the treatments directed at them and overcoming this drug resistance is an important research focus. Additionally, increasing discussion and research is centering on targeted and individualized therapy. While a number of approaches have undergone intensive and close scrutiny as potential approaches to treat and kill cancer (signaling pathways, multidrug resistance, cell cycle checkpoints, anti-angiogenesis, etc.), much less work has focused on blocking the ability of a cancer cell to recognize and repair the damaged DNA which primarily results from the front line cancer treatments; chemotherapy and radiation. More recent studies on a number of DNA repair targets have produced proof-of-concept results showing that selective targeting of these DNA repair enzymes has the potential to enhance and augment the currently used chemotherapeutic agents and radiation as well as overcoming drug resistance. Some of the targets identified result in the development of effective single-agent anti-tumor molecules. While it is inherently convoluted to think that inhibiting DNA repair processes would be a likely approach to kill cancer cells, careful identification of specific DNA repair proteins is increasingly appearing to be a viable approach in the cancer therapeutic cache