Conservative and moderate grazing effects on Chihuahuan Desert wildlife sightings

Seasonal wildlife observations were made along transects on 2 pastures conservatively grazed (36% use of perennial grasses) and 2 pastures moderately grazed (47% use of perennial grasses) in south central New Mexico in non-drought (1997) and drought years (1998). Experimental pastures were similar in soils, terrain, spacing of watering points, and brush cover. Average ecological condition score for the conservatively grazed pastures was 60% compared with 64% for moderately grazed pastures. Throughout the study total standing vegetation understory herbage levels were higher ( P P > 0.05) between conservatively and moderately grazed pastures. Black-tailed jackrabbit ( Lepus californicus ) sightings were higher ( P Antilocapra americana ), scaled quail ( Callipepla squamata ), mourning doves ( Zenaida macroura ), and desert cottontails ( Sylvilagus auduboni ) showed no differences ( P > 0.05) between conservatively and moderately grazed pastures. Dry conditions in 1998 depressed total wildlife sightings by > 50% compared to 1997. Both songbird and gamebird (particularly mourning dove) sightings were severely reduced in the dry compared to wet year ( P < 0.05). Our results are consistent with Nelson et al. (1997) that livestock grazing at intermediate levels had no effect on most Chihuahuan Desert upland wildlife species, and that drought years severely depress wildlife sightings.     

Note on the occurrence of Siphlonurus autumnalis (Ephemeroptera: Siphlonuridae) in a Montana spring brook

The little-known mayfly Siphlonurus autumnalis McDunnough (Ephemeroptera: Siphlonuridae) was collected from several locations in its floodplain habitats along the Middle Fork of the Flathead River in western Montana. To confirm identification, nymphs were reared along with an associated species, S. occidentalis Eaton (Ephemeroptera: Siphlonuridae). Adults emerged from 6 September until 16 October. Habitats are described and the first photos of the 2 sexes are provided.     

Elevational changes in woody vegetation along three streams in Washington County, Utah

Patterns of change in the woody vegetation (trees and shrubs) of the riparian communities of three streams draining the slopes of the Pine Valley Mountains in Washington County, Utah, were examined. Thirty-nine study sites were established adjacent to the streams along an elevational gradient where vegetation, plant population, and species data were taken. Vegetation and species patterns varied with respect to elevation and geographical location. Vegetation of the high- and low-elevation areas was distinctly different, while that of the mid-elevations was transitional to both. Geographical patterns showed a north-south transition in vegetation between the Mojave and Great Basin deserts. Size-class distribution curves for 11 tree species showed varying degrees of survival with respect to age and location. Root sprouting was highly important in the reproductive effort of six of the trees. Species distribution patterns followed transriparian and intrariparian gradients within the riparian community.     

Genetic contributions to stability and change in intelligence from childhood to old age

Understanding the determinants of healthy mental ageing is a priority for society today. So far, we know that intelligence differences show high stability from childhood to old age and there are estimates of the genetic contribution to intelligence at different ages. However, attempts to discover whether genetic causes contribute to differences in cognitive ageing have been relatively uninformative. Here we provide an estimate of the genetic and environmental contributions to stability and change in intelligence across most of the human lifetime. We used genome-wide single nucleotide polymorphism (SNP) data from 1,940 unrelated individuals whose intelligence was measured in childhood (age 11 years) and again in old age (age 65, 70 or 79 years). We use a statistical method that allows genetic (co)variance to be estimated from SNP data on unrelated individuals. We estimate that causal genetic variants in linkage disequilibrium with common SNPs account for 0.24 of the variation in cognitive ability change from childhood to old age. Using bivariate analysis, we estimate a genetic correlation between intelligence at age 11 years and in old age of 0.62. These estimates, derived from rarely available data on lifetime cognitive measures, warrant the search for genetic causes of cognitive stability and change.     

Passenger deletions generate therapeutic vulnerabilities in cancer

Inactivation of tumour-suppressor genes by homozygous deletion is a prototypic event in the cancer genome, yet such deletions often encompass neighbouring genes. We propose that homozygous deletions in such passenger genes can expose cancer-specific therapeutic vulnerabilities when the collaterally deleted gene is a member of a functionally redundant family of genes carrying out an essential function. The glycolytic gene enolase 1 (ENO1) in the 1p36 locus is deleted in glioblastoma (GBM), which is tolerated by the expression of ENO2. Here we show that short-hairpin-RNA-mediated silencing of ENO2 selectively inhibits growth, survival and the tumorigenic potential of ENO1-deleted GBM cells, and that the enolase inhibitor phosphonoacetohydroxamate is selectively toxic to ENO1-deleted GBM cells relative to ENO1-intact GBM cells or normal astrocytes. The principle of collateral vulnerability should be applicable to other passenger-deleted genes encoding functionally redundant essential activities and provide an effective treatment strategy for cancers containing such genomic events.     

The Earth's 'hum' is driven by ocean waves over the continental shelves

Observations show that the seismic normal modes of the Earth at frequencies near 10 mHz are excited at a nearly constant level in the absence of large earthquakes. This background level of excitation has been called the 'hum' of the Earth, and is equivalent to the maximum excitation from a magnitude 5.75 earthquake. Its origin is debated, with most studies attributing the forcing to atmospheric turbulence, analogous to the forcing of solar oscillations by solar turbulence. Some reports also predicted that turbulence might excite the planetary modes of Mars to detectable levels. Recent observations on Earth, however, suggest that the predominant excitation source lies under the oceans. Here I show that turbulence is a very weak source, and instead it is interacting ocean waves over the shallow continental shelves that drive the hum of the Earth. Ocean waves couple into seismic waves through the quadratic nonlinearity of the surface boundary condition, which couples pairs of slowly propagating ocean waves of similar frequency to a high phase velocity component at approximately double the frequency. This is the process by which ocean waves generate the well known 'microseism peak' that dominates the seismic spectrum near 140 mHz (refs 11, 12), but at hum frequencies, the mechanism differs significantly in frequency and depth dependence. A calculation of the coupling between ocean waves and seismic modes reproduces the seismic spectrum observed. Measurements of the temporal correlation between ocean wave data and seismic data have confirmed that ocean waves, rather than atmospheric turbulence, are driving the modes of the Earth.     

Pathogenesis and therapy of psoriasis

Psoriasis is one of the most common human skin diseases and is considered to have key genetic underpinnings. It is characterized by excessive growth and aberrant differentiation of keratinocytes, but is fully reversible with appropriate therapy. The trigger of the keratinocyte response is thought to be activation of the cellular immune system, with T cells, dendritic cells and various immune-related cytokines and chemokines implicated in pathogenesis. The newest therapies for psoriasis target its immune components and may predict potential treatments for other inflammatory human diseases.     

A genome-wide association scan of tag SNPs identifies a susceptibility variant for colorectal cancer at 8q24.21

Much of the variation in inherited risk of colorectal cancer (CRC) is probably due to combinations of common low risk variants. We conducted a genome-wide association study of 550,000 tag SNPs in 930 familial colorectal tumor cases and 960 controls. The most strongly associated SNP (P = 1.72 x 10(-7), allelic test) was rs6983267 at 8q24.21. To validate this finding, we genotyped rs6983267 in three additional CRC case-control series (4,361 affected individuals and 3,752 controls; 1,901 affected individuals and 1,079 controls; 1,072 affected individuals and 415 controls) and replicated the association, providing P = 1.27 x 10(-14) (allelic test) overall, with odds ratios (ORs) of 1.27 (95% confidence interval (c.i.): 1.16-1.39) and 1.47 (95% c.i.: 1.34-1.62) for heterozygotes and rare homozygotes, respectively. Analyses based on 1,477 individuals with colorectal adenoma and 2,136 controls suggest that susceptibility to CRC is mediated through development of adenomas (OR = 1.21, 95% c.i.: 1.10-1.34; P = 6.89 x 10(-5)). These data show that common, low-penetrance susceptibility alleles predispose to colorectal neoplasia.     

Targeting microglia-mediated neurotoxicity: the potential of NOX2 inhibitors

Microglia are key sentinels of central nervous system health, and their dysfunction has been widely implicated in the progressive nature of neurodegenerative diseases. While microglia can produce a host of factors that are toxic to neighboring neurons, NOX2 has been implicated as a common and essential mechanism of microglia-mediated neurotoxicity. Accumulating evidence indicates that activation of the NOX2 enzyme complex in microglia is neurotoxic, both through the production of extracellular reactive oxygen species that damage neighboring neurons as well as the initiation of redox signaling in microglia that amplifies the pro-inflammatory response. More specifically, evidence supports that NOX2 redox signaling enhances microglial sensitivity to pro-inflammatory stimuli, and amplifies the production of neurotoxic cytokines, to promote chronic and neurotoxic microglial activation. Here, we describe the evidence denoting the role of NOX2 in microglia-mediated neurotoxicity with an emphasis on Alzheimer's and Parkinson's disease, describe available inhibitors that have been tested, and detail evidence of the neuroprotective and therapeutic potential of targeting this enzyme complex to regulate microglia.