The time‐of‐flight method has been used to study the effect of P3HT molecular weight (Mn = 13–121 kDa) on charge mobility in pristine and PCBM blend films using highly regioregular P3HT. Hole mobility was observed to remain constant at 10−4 cm2V−1s−1 as molecular weight was increased from 13–18 kDa, but then decreased by one order of magnitude as molecular weight was further increased from 34–121 kDa. The decrease in charge mobility observed in blend films is accompanied by a change in surface morphology, and leads to a decrease in the performance of photovoltaic devices made from these blend films.

Activated macrophages avidly consume arginine via the action of inducible nitric oxide synthase (iNOS) and/or arginase. In contrast to our knowledge regarding macrophage iNOS expression, the stimuli and mechanisms that regulate expression of the cytosolic type I (arginase I) or mitochondrial type II (arginase II) isoforms of arginase in macrophages are poorly defined. We show that one or both arginase isoforms may be induced in the RAW 264.7 murine macrophage cell line and that arginase expression is regulated independently of iNOS expression. For example, 8-bromo-cAMP strongly induced both arginase I and II mRNAs but not iNOS. Whereas interferon-γ induced iNOS but not arginase, 8-bromo-cAMP and interferon-γ mutually antagonized induction of iNOS and arginase I mRNAs. Dexamethasone, which did not induce either arginase or iNOS, almost completely abolished induction of arginase I mRNA by 8-bromo-cAMP but enhanced induction of arginase II mRNA. Lipopolysaccharide (LPS) induced arginase II mRNA, but 8-bromo-cAMP plus LPS resulted in synergistic induction of both arginase I and II mRNAs. In all cases, increases in arginase mRNAs were sufficient to account for the increases in arginase activity. These complex patterns of expression suggest that the arginase isoforms may play distinct, although partially overlapping, functional roles in macrophage arginine metabolism.

In this paper, an indicator of network resilience is defined that quantifies the ability of an intermodal freight transport network to recover from disruptions due to natural or human-caused disaster. The indicator considers the network's inherent ability to cope with the negative consequences of disruptions as a result of its topological and operational attributes. Furthermore, the indicator explicitly accounts for the impact of potential recovery activities that might be taken in the immediate aftermath of the disruption to meet target operational service levels while adhering to a fixed budget. A stochastic mixed-integer program is proposed for quantifying network resilience and identifying an optimal postevent course of action (i.e., set of activities) to take. To solve this mathematical program, a technique that accounts for dependencies in random link attributes based on concepts of Benders decomposition, column generation, and Monte Carlo simulation is proposed. Experiments were conducted to illustrate the resilience concept and procedure for its measurement, and to assess the role of network topology in its magnitude.

No abstract

In the developing brain, differentiation of neural precursors into neurons or glial cells occurs in response to neurotrophic factors acting on the cell surface. Intracellular signaling mechanisms that relay information to initiate differentiative responses of neural precursor cells are poorly understood. To investigate whether stimulation of the cAMP-dependent signaling pathway participates in differentiative responses of cells in the developing CNS, we performed experiments using both conditionally immortalized neural precursor cells (RC2.E10 cells) and primary cultures of cells from developing rat cortex. Initially, we determined that RC2.E10 cells retain phenotypic features of neural precursors after inactivation of the immortalizing oncogene, a temperature-sensitive mutant of the simian virus 40 large-T antigen (SV40T). We found that, once SV40T is inactivated, RC2.E10 cells cease to divide and die. However, RC2.E10 cells can proliferate in the presence of basic fibroblast growth factor.In addition, they express nestin, a marker of neural precursor cells. Both RC2.E10 cells and primary cortical precursor cells undergo astroglial differentiation in response to cAMP stimulation by treatment with 8-bromo-cAMP. In both cases, cAMPinduced astrocyte differentiation is characterized by morphological changes, stimulation of glial fibrillary acidic protein expression, downregulation of nestin expression, and decreased proliferation. No increases in the expression of neuronal or oligodendrocytic markers were observed. Our results support the notion that the developing CNS contains neural precursor cells with the capacity of undergoing astrocyte differentiation in response to increased intracellular cAMP concentrations.