Interview of John J. Rooney, Ph.D.

Dr. John J. Rooney was born in 1923 to a working class family in South Philadelphia. He went to primarily Catholic schools and during his childhood, witnessed three World Series from his house. He started attending La Salle University in 1940, majoring in chemistry. During World War II, he left school to join the Navy as a flight instructor. He came back to La Salle and graduated in 1946. From there, he went to Temple University to get a master’s and then Ph.D. in psychology. During this time, he simultaneously went to school, taught first chemistry and then psychology at La Salle, and was director of the counseling program. After receiving his Ph.D., he became a permanent professor at La Salle. He taught classes until 1983, during which time he witnessed many changes in both the school and the psychology department, including a change from commuter to resident students and the introduction of female students. After he retired from teaching, he became the director of the Master’s in counseling program, a position he has maintained up until the present. He has been active in a number of La Salle and professional organizations

Modulation of the F-actin cytoskeleton by c-Abl tyrosine kinase in cell spreading and neurite extension

The nonreceptor tyrosine kinase encoded by the c-Abl gene has the unique feature of an F-actin binding domain (FABD). Purified c-Abl tyrosine kinase is inhibited by F-actin, and this inhibition can be relieved through mutation of its FABD. The c-Abl kinase is activated by physiological signals that also regulate the actin cytoskeleton. We show here that c-Abl stimulated the formation of actin microspikes in fibroblasts spreading on fibronectin. This function of c-Abl is dependent on kinase activity and is not shared by c-Src tyrosine kinase. The Abl-dependent F-actin microspikes occurred under conditions where the Rho-family GTPases were inhibited. The FABD-mutated c-Abl, which is active in detached fibroblasts, stimulated F-actin microspikes independent of cell attachment. Moreover, FABD-mutated c-Abl stimulated the formation of F-actin branches in neurites of rat embryonic cortical neurons. The reciprocal regulation between F-actin and the c-Abl tyrosine kinase may provide a self-limiting mechanism in the control of actin cytoskeleton dynamics

CHRPR Operations Manual

1.0 Overview The TSA systems VM-250AGN portal monitor is a set of two pillars made to detect nuclear material in a vehicle. Each pillar contains two polyvinyl toluene (PVT) plastic gamma ray detectors and four 3He neutron detectors, as well as a power supply and electronics to process the output from these detectors. Pacific Northwest National Laboratory has designed and built a continuous high-resolution PVT readout (CHRPR) for the TSA portal to allow spectral readout from the gamma and neutron detectors. The CHRPR helps differentiate between different types of radioactive material through increased spectroscopic capability and associated developments. The TSA VM-250AGN continually monitors the natural neutron and gamma ray background which occurs around the pillars. When the system is installed, the two pillars are placed on either side of a roadway, and a vehicle presence sensor records the passage of cars between them. When radiation measurements exceed a preset alarm threshold, the system alarms to let the user know that a radioactive material is present. Time-stamped measurements are continually sent to a computer, where they can be recorded via a Windows terminal or the TSA RAVEN software. For each pillar in the original TSA model, output from each detector is amplified and shaped by a single channel analyzer, the SCA-775. Information from both SCA-775’s are passed to the SC-770 in the master pillar. This is the detector interface module and main data processor. It counts electrical pulses and uses program software to output total readings to the computer, as well as trigger any appropriate alarms. The CHRPR allows a parallel approach to recording radiation readings from the TSA system. After installing the CHRPR system, all TSA power and signal connections are unchanged. The CHRPR captures electrical pulses containing detector and occupancy sensor information from the SCA-775 on either side. These pulses are converted to a signal with a time width proportional to the amplitude, via voltage to pulse width converters (VPW). These time widths are then digitized by a field programmable gate array (FPGA) and transmitted over Ethernet to a data acquisition computer. The CHRPR records the magnitude of each pulse to a continuous event mode file on or each detector and occupancy sensor This manual begins with CHRPR installation instructions, then a section on CHRPR software. Afterward is a brief overview of how the TSA system works, then an explanation of the CHRPR. This manual is meant as a supplement to the TSA VM-250AGN manual, which can be found at http://tsasystems.com/library/manuals/pm700agn-vm250agn_manual.pdf . That manual is the manufacturer’s guide for the installation, programming, and maintenance of the portal system

Telomere Position Effect (TPE) Regulates DUX4 in Human Facioscapulohumeral Muscular Dystrophy (FSHD)

Telomeres may regulate human disease by at least two independent mechanisms. 1) Replicative senescence occurs once short telomeres generate DNA damage signals that produce a barrier to tumor progression. 2) Telomere Position Effect (TPE) can change gene expression at intermediate telomere lengths in cultured human cells. We here report a human disease, facioscapulohumeral muscular dystrophy (FSHD) where telomere length may well contribute to its pathogenesis. FSHD is age-related and genetically only 25-60 kb from the end of chromosome 4q. We used a floxable telomerase to generate isogenic clones with different telomere lengths from patients and their unaffected siblings. DUX4, the primary candidate for FSHD pathogenesis, is upregulated >10-fold in FSHD myoblasts-myotubes with short versus long telomeres, and its expression is inversely proportional to telomere length. FSHD may represent a human disease in which TPE contributes to its age-related phenotype

c-Abl phosphorylates Dok1 to promote filopodia during cell spreading

Filopodia are dynamic F-actin structures that cells use to explore their environment. c-Abl tyrosine kinase promotes filopodia during cell spreading through an unknown mechanism that does not require Cdc42 activity. Using an unbiased approach, we identified Dok1 as a specific c-Abl substrate in spreading fibroblasts. When activated by cell adhesion, c-Abl phosphorylates Y361 of Dok1, promoting its association with the Src homology 2 domain (SH2)/SH3 adaptor protein Nck. Each signaling component was critical for filopodia formation during cell spreading, as evidenced by the finding that mouse fibroblasts lacking c-Abl, Dok1, or Nck had fewer filopodia than cells reexpressing the product of the disrupted gene. Dok1 and c-Abl stimulated filopodia in a mutually interdependent manner, indicating that they function in the same signaling pathway. Dok1 and c-Abl were both detected in filopodia of spreading cells, and therefore may act locally to modulate actin. Our data suggest a novel pathway by which c-Abl transduces signals to the actin cytoskeleton through phosphorylating Dok1 Y361 and recruiting Nck

Properties of ion implanted Ti-6Al-4V processed using beamline and PSII techniques

The surface of Ti-6Al-4V (Ti64) alloy has been modified using beamline implantation of boron. In separate experiments, Ti64 has been implanted with nitrogen using a plasma source ion implantation (PSII) technique utilizing either ammonia (NH{sub 3}), nitrogen (N{sub 2}), or their combinations as the source of nitrogen ions. Beamline experiments have shown the hardness of the N-implanted surface saturates at a dose level of {approximately} 4 {times} 10{sup 17} at/cm{sup 2} at {approximately} 10 GPa. The present work makes comparisons of hardness and tribological tests of (1) B implantation using beamline techniques, and (2) N implanted samples using ammonia and/or nitrogen gas in a PSII process. The results show that PSII using N{sub 2} or NH{sub 3} gives similar hardness as N implantation using a beamline process. The presence of H in the Ti alloy surface does not affect the hardness of the implanted surface. Boron implantation increased the surface hardness by as much as 2.5x at the highest dose level. Wear testing by a pin-on-disk method indicated that nitrogen implantation reduced the wear rate by as much as 120x, and boron implantation reduced the wear rate by 6.5x. Increased wear resistance was accompanied by a decreased coefficient of friction