Critical Assessment of the Use of Excess Lead Iodide in Lead Halide Perovskite Solar Cells.

It is common practice in the lead halide perovskite solar cell field to add a small molar excess of lead iodide (PbI2) to the precursor solution to increase the device performance. However, recent reports have shown that an excess of PbI2 can accelerate performance loss. In addition, PbI2 is photoactive (band gap ∼2.3 eV), which may lead to parasitic absorption losses in a solar cell. Here we show that devices using small quantities of excess PbI2 exhibit better device performance as compared with stoichiometric devices, both initially and for the duration of a stability test under operating conditions, primarily by enhancing the charge extraction. However, the photolysis of PbI2 negates the beneficial effect on charge extraction by leaving voids in the perovskite film and introduces trap states that are detrimental for device performance. We propose that although excess PbI2 provides a good template for enhanced performance, the community must continue to seek other additives or synthesis routes that fulfill the same beneficial role as excess PbI2, but without the photolysis that negates these beneficial effects under long-term device operation

Prenatal and Early, but Not Late, Postnatal Exposure of Mice to Sidestream Tobacco Smoke Increases Airway Hyperresponsiveness Later in Life

Background Cigarette smoke exposure in utero and during early postnatal development increases the incidence of asthma and airway hyperresponsiveness (AHR) later in life, suggesting that a possible critical period of developmental sensitivity exists in the prenatal and early postnatal periods. Objective We investigated mechanisms of susceptibility during critical developmental periods to sidestream smoke (SS) exposure and evaluated the possible effects of SS on neural responses. Methods We exposed three different age groups of mice to either SS or filtered air (FA) for 10 consecutive days beginning on gestation day (GD) 7 by maternal exposure or beginning on postnatal day (PND) 2 or PND21 by direct inhalation. Lung function, airway substance P (SP) innervation, and nerve growth factor (NGF) levels in broncho alveolar lavage fluid were measured after a single SS exposure on PND59. Results Methacholine (MCh) dose response for lung resistance (RL) was significantly elevated, and dynamic pulmonary compliance (Cdyn) was significantly decreased, in the GD7 and PND2 SS exposure groups compared with the FA groups after SS exposure on PND59. At the same time points, the percent area of SP nerve fibers in tracheal smooth muscle and the levels of NGF were significantly elevated. MCh dose–response curves for RL and Cdyn, SP nerve fiber density, and the level of NGF were not significantly changed in the PND21 exposure group after SS exposure on PND59. Conclusions These results suggest that a critical period of susceptibility to SS exposure exists in the prenatal and early postnatal period of development in mice that results in increased SP innervation, increased NGF levels in the airway, and enhanced MCh AHR later in life

Prenatal and Early, but Not Late, Postnatal Exposure of Mice to Sidestream Tobacco Smoke Increases Airway Hyperresponsiveness Later in Life

Background Cigarette smoke exposure in utero and during early postnatal development increases the incidence of asthma and airway hyperresponsiveness (AHR) later in life, suggesting that a possible critical period of developmental sensitivity exists in the prenatal and early postnatal periods. Objective We investigated mechanisms of susceptibility during critical developmental periods to sidestream smoke (SS) exposure and evaluated the possible effects of SS on neural responses. Methods We exposed three different age groups of mice to either SS or filtered air (FA) for 10 consecutive days beginning on gestation day (GD) 7 by maternal exposure or beginning on postnatal day (PND) 2 or PND21 by direct inhalation. Lung function, airway substance P (SP) innervation, and nerve growth factor (NGF) levels in broncho alveolar lavage fluid were measured after a single SS exposure on PND59. Results Methacholine (MCh) dose response for lung resistance (RL) was significantly elevated, and dynamic pulmonary compliance (Cdyn) was significantly decreased, in the GD7 and PND2 SS exposure groups compared with the FA groups after SS exposure on PND59. At the same time points, the percent area of SP nerve fibers in tracheal smooth muscle and the levels of NGF were significantly elevated. MCh dose–response curves for RL and Cdyn, SP nerve fiber density, and the level of NGF were not significantly changed in the PND21 exposure group after SS exposure on PND59. Conclusions These results suggest that a critical period of susceptibility to SS exposure exists in the prenatal and early postnatal period of development in mice that results in increased SP innervation, increased NGF levels in the airway, and enhanced MCh AHR later in life

Early postnatal ozone exposure alters rat nodose and jugular sensory neuron development

Sensory neurons originating in nodose and jugular ganglia that innervate airway epithelium (airway neurons) play a role in inflammation observed following exposure to inhaled environmental irritants such as ozone (O3). Airway neurons can mediate airway inflammation through the release of the neuropeptide substance P (SP). While susceptibility to airway irritants is increased in early life, the developmental dynamics of afferent airway neurons are not well characterized. The hypothesis of this study was that airway neuron number might increase with increasing age, and that an acute, early postnatal O3 exposure might increase both the number of sensory airway neurons as well as the number SP-containing airway neurons. Studies using Fischer 344 rat pups were conducted to determine if age or acute O3 exposure might alter airway neuron number. Airway neurons in nodose and jugular ganglia were retrogradely labeled, removed, dissociated, and counted by means of a novel technique employing flow cytometry. In Study 1, neuron counts were conducted on postnatal days (PD) 6, 10, 15, 21, and 28. Numbers of total and airway neurons increased significantly between PD6 and PD10, then generally stabilized. In Study 2, animals were exposed to O3 (2 ppm) or filtered air (FA) on PD5 and neurons were counted on PD10, 15, 21, and 28. O3-exposed animals displayed significantly less total neurons on PD21 than FA controls. This study shows that age-related changes in neuron number occur, and that an acute, early postnatal O3 exposure significantly alters sensory neuron development

The 1<z<5 Infrared Luminosity Function of Type I Quasars

We determine the rest-frame 8 micron luminosity function of type I quasars over the redshift range 1<z<5. Our sample consists of 292 24 micron sources brighter than 1 mJy selected from 7.17 square degrees of the Spitzer Space Telescope MIPS survey of the NOAO Deep Wide-Field Survey Bootes field. The AGN and Galaxy Evolution Survey (AGES) has measured redshifts for 270 of the R<21.7 sources and we estimate that the contamination of the remaining 22 sources by stars and galaxies is low. We are able to select quasars missed by ultra-violet excess quasar surveys, including reddened type I quasars and 2.2<z<3.0 quasars with optical colors similar to main sequence stars. We find reddened type I quasars comprise 20% of the type I quasar population. Nonetheless, the shape, normalization, and evolution of the rest-frame 8 micron luminosity function is comparable to that of quasars selected from optical surveys. The 8 micron luminosity function of type I quasars is well approximated by a power-law with index -2.75(+/-0.14). We directly measure the peak of the quasar space density to be at z=2.6(+/-0.3).Comment: Accepted for publication in the ApJ, 19 pages, 12 figure

Hadronic Regge Trajectories: Problems and Approaches

We scrutinized hadronic Regge trajectories in a framework of two different models --- string and potential. Our results are compared with broad spectrum of existing theoretical quark models and all experimental data from PDG98. It was recognized that Regge trajectories for mesons and baryons are not straight and parallel lines in general in the current resonance region both experimentally and theoretically, but very often have appreciable curvature, which is flavor-dependent. For a set of baryon Regge trajectories this fact is well described in the considered potential model. The standard string models predict linear trajectories at high angular momenta J with some form of nonlinearity at low J.Comment: 15 pages, 9 figures, LaTe

RNA polymerase II stalling promotes nucleosome occlusion and pTEFb recruitment to drive immortalization by Epstein-Barr virus

Epstein-Barr virus (EBV) immortalizes resting B-cells and is a key etiologic agent in the development of numerous cancers. The essential EBV-encoded protein EBNA 2 activates the viral C promoter (Cp) producing a message of ~120 kb that is differentially spliced to encode all EBNAs required for immortalization. We have previously shown that EBNA 2-activated transcription is dependent on the activity of the RNA polymerase II (pol II) C-terminal domain (CTD) kinase pTEFb (CDK9/cyclin T1). We now demonstrate that Cp, in contrast to two shorter EBNA 2-activated viral genes (LMP 1 and 2A), displays high levels of promoter-proximally stalled pol II despite being constitutively active. Consistent with pol II stalling, we detect considerable pausing complex (NELF/DSIF) association with Cp. Significantly, we observe substantial Cp-specific pTEFb recruitment that stimulates high-level pol II CTD serine 2 phosphorylation at distal regions (up to +75 kb), promoting elongation. We reveal that Cp-specific pol II accumulation is directed by DNA sequences unfavourable for nucleosome assembly that increase TBP access and pol II recruitment. Stalled pol II then maintains Cp nucleosome depletion. Our data indicate that pTEFb is recruited to Cp by the bromodomain protein Brd4, with polymerase stalling facilitating stable association of pTEFb. The Brd4 inhibitor JQ1 and the pTEFb inhibitors DRB and Flavopiridol significantly reduce Cp, but not LMP1 transcript production indicating that Brd4 and pTEFb are required for Cp transcription. Taken together our data indicate that pol II stalling at Cp promotes transcription of essential immortalizing genes during EBV infection by (i) preventing promoter-proximal nucleosome assembly and ii) necessitating the recruitment of pTEFb thereby maintaining serine 2 CTD phosphorylation at distal regions

Mid-Infrared Selection of Active Galaxies

Mid-infrared photometry provides a robust technique for identifying active galaxies. While the ultraviolet to mid-infrared continuum of normal galaxies is dominated by the composite stellar black body curve and peaks at approximately 1.6 microns, the ultraviolet to mid-infrared continuum of active galaxies is dominated by a power law. Consequently, with sufficient wavelength baseline, one can easily distinguish AGN from stellar populations. Mirroring the tendency of AGN to be bluer than galaxies in the ultraviolet, where galaxies (and stars) sample the blue, rising portion of stellar spectra, AGN tend to be redder than galaxies in the mid-infrared, where galaxies sample the red, falling portion of the stellar spectra. We report on Spitzer Space Telescope mid-infrared colors, derived from the IRAC Shallow Survey, of nearly 10,000 spectroscopically identified sources from the AGN and Galaxy Evolution Survey. Based on this spectroscopic sample, we find that simple mid-infrared color criteria provide remarkably robust separation of active galaxies from normal galaxies and Galactic stars, with over 80% completeness and less than 20% contamination. Considering only broad-lined AGN, these mid-infrared color criteria identify over 90% of spectroscopically identified quasars and Seyfert 1s. Applying these color criteria to the full imaging data set, we discuss the implied surface density of AGN and find evidence for a large population of optically obscured active galaxies.Comment: 13 pages, 3 figures; submitted to the Astrophysical Journal Letter

Myeloid-specific Asxl2 deletion limits diet-induced obesity by regulating energy expenditure

We previously established that global deletion of the enhancer of trithorax and polycomb (ETP) gene, Asxl2, prevents weight gain. Because proinflammatory macrophages recruited to adipose tissue are central to the metabolic complications of obesity, we explored the role of ASXL2 in myeloid lineage cells. Unexpectedly, mice without Asxl2 only in myeloid cells (Asxl2ΔLysM) were completely resistant to diet-induced weight gain and metabolically normal despite increased food intake, comparable activity, and equivalent fecal fat. Asxl2ΔLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine gene expression. Energy expenditure and brown adipose tissue metabolism in Asxl2ΔLysM mice were protected from the suppressive effects of HFD, a phenomenon associated with relatively increased catecholamines likely due to their suppressed degradation by macrophages. White adipose tissue of HFD-fed Asxl2ΔLysM mice also exhibited none of the pathological remodeling extant in their control counterparts. Suppression of macrophage Asxl2 expression, via nanoparticle-based siRNA delivery, prevented HFD-induced obesity. Thus, ASXL2 controlled the response of macrophages to dietary factors to regulate metabolic homeostasis, suggesting modulation of the cells\u27 inflammatory phenotype may impact obesity and its complications