The concentrations of ozone, nitrogen oxides, and nonmethane hydrocarbons measured near the surface in a variety of urban, suburban, rural, and remote locations are analyzed and compared in order to elucidate the relationships between ozone, its photochemical precursors, and the sources of these precursors. While a large gradient is found among remote, rural, and urban/suburban nitrogen oxide concentrations, the total hydrocarbon reactivity in all continental locations is found to be comparable. Apportionment of the observed hydrocarbon species to mobile and stationary anthropogenic sources and biogenic sources suggests that present-day emission inventories for the United States underestimate the size of mobile emissions. The analysis also suggests a significant role for biogenic hydrocarbon emissions in many urban/suburban locations and a dominant role for these sources in rural areas of the eastern United States. As one moves from remote locations to rural locations and then from rural to urban/suburban locations, ozone and nitrogen oxide concentrations tend to increase in a consistent manner while total hydrocarbon reactivity does not. hydrocarbon concentrations in four chemically distinct regimes of the atmospheric boundary layer, each having a distinct mix of anthropogenic and natural hydrocarbon and NOx emissions. These regimes are: I, the urban/suburban atmosphere, which is the regime most strongly impacted by anthropogenic emissions; II, the rural atmosphere, which is somewhat less impacted by anthropogenic emissions and more impacted by natural emissions than that of the urban atmosphere; III, the atmosphere over the remote, tropical forest which is essentially free of anthropogenic volatile organic compounds (VOC) and NOx emissions and strongly influenced by natural emissions; and IV, the remote, marine atmosphere, which is not only free of anthropogenic emissions but is also characterized by relatively small biogenic sources of VOC and NO x. Because we are most interested in the conditions that foster ozone episodes, our analysis concentrates on observations made during the daylight hours of the summer months.In the sections below we first briefly summarize the fundamentals of the photochemical smog mechanism and the nonlinearities inherent in this system and then discuss the concentrations of 03, NOx, and hydrocarbons typically observed in the four regimes listed above. PHOTOCHEMICAL SMOGWhile uncertainties remain in our understanding of tropospheric photochemistry, the basic set of reactions that lead to 03 production have been identified. These reactions, commonly referred to in the aggregate as the "photochemical smog" mechanism, involve the oxidation of hydrocarbons and other volatile organic compounds in the presence of nitrogen oxides (NOx) and sunlight [Haagen-Srnit, 1952; $einfeld, 1988]. Typical of this mechanism are reactions (R1) through (R7),RH + OH--> R + H20 (R2) R + 02 + M--> RO2 + M (R3) RO 2 + NO--> RO + NO 2 (R4) RO + 0 2 --> HO 2 + RCHO 6037
Chromosome 4q deletion syndrome (4q- syndrome) is a rare condition, with an estimated incidence of 1 in 100,000. Although variable, the clinical spectrum commonly includes craniofacial, developmental, digital, skeletal, and cardiac involvement. Data on the genotype-phenotype correlation within the 4q arm are limited. We present detailed clinical and genetic information by array CGH on 20 patients with 4q deletions. We identified a patient who has a ∼465 kb deletion (186,770,069-187,234,800, hg18 coordinates) in 4q35.1 with all clinical features for 4q deletion syndrome except for developmental delay, suggesting that this is a critical region for this condition and a specific gene responsible for orofacial clefts and congenital heart defects resides in this region. Since the patients with terminal deletions all had cleft palate, our results provide further evidence that a gene associated with clefts is located on the terminal segment of 4q. By comparing and contrasting our patients' genetic information and clinical features, we found significant genotype-phenotype correlations at a single gene level linking specific phenotypes to individual genes. Based on these data, we constructed a hypothetical partial phenotype-genotype map for chromosome 4q which includes BMP3, SEC31A, MAPK10, SPARCL1, DMP1, IBSP, PKD2, GRID2, PITX2, NEUROG2, ANK2, FGF2, HAND2, and DUX4 genes.
We identified individuals with variations in ACTL6B, a component of the chromatin remodeling machinery including the BAF complex. Ten individuals harbored bi-allelic mutations and presented with global developmental delay, epileptic encephalopathy, and spasticity, and ten individuals with de novo heterozygous mutations displayed intellectual disability, ambulation deficits, severe language impairment, hypotonia, Rett-like stereotypies, and minor facial dysmorphisms (wide mouth, diastema, bulbous nose). Nine of these ten unrelated individuals had the identical de novo c.1027G>A (p.Gly343Arg) mutation. Human-derived neurons were generated that recaptured ACTL6B expression patterns in development from progenitor cell to post-mitotic neuron, validating the use of this model. Engineered knock-out of ACTL6B in wild-type human neurons resulted in profound deficits in dendrite development, a result recapitulated in two individuals with different bi-allelic mutations, and reversed on clonal genetic repair or exogenous expression of ACTL6B. Wholetranscriptome analyses and whole-genomic profiling of the BAF complex in wild-type and bi-allelic mutant ACTL6B neural progenitor cells and neurons revealed increased genomic binding of the BAF complex in ACTL6B mutants, with corresponding transcriptional changes in several genes including TPPP and FSCN1, suggesting that altered regulation of some cytoskeletal genes contribute to altered dendrite development. Assessment of bi-alleic and heterozygous ACTL6B mutations on an ACTL6B knock-out human background demonstrated that bi-allelic mutations mimic engineered deletion deficits while heterozygous mutations do not, suggesting that the former are loss of function and the latter are gain of function. These results reveal a role for ACTL6B in neurodevelopment and implicate another component of chromatin remodeling machinery in brain disease.
Habitat loss, electrocution on power poles and persecution by humans are the main threats to birds of prey. Nevertheless, the effects of human disturbance on endangered species are becoming notorious due to the increasing recreational use of the natural environment. We evaluated the effects of human disturbances on Egyptian vulture Neophron percnopterus breeding success and developed conservation measures based on minimum distance of effect and buffer areas in a high human density area of northern Spain. A total of 100 breeding attempts of 15 breeding pairs were monitored over 8 years. Human disturbances affected 42 of the breeding attempts. Those disturbances related to and originating in forestry work had the most severe effect on breeding success, being associated with the loss of 100% of 13 breeding attempts, while human disturbances related to free-time activities caused 44% failures in 25 breeding attempts by four pairs, two of them within Natural Parks. The breeding success was significantly less in territories affected by disturbances than in those free of disturbances. Some pairs affected by disturbances changed their nest site, increasing breeding success. Adults were prevented from entering the nest to feed chicks when anyone was detected at an average distance of 307 m, while an average distance of 837.5 m allowed them access. The maximum alert distance was estimated at 605 m and the buffer area was 57 ha. We discuss the application of our results for management schemes and conservation of this species.
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