Magneto-thermal convection in solar prominences

Coronal cavities are large low-density regions formed by hemispheric-scale magnetic flux ropes suspended in the Sun's outer atmosphere. They evolve over time, eventually erupting as the dark cores of coronal mass ejections. Although coronal mass ejections are common and can significantly affect planetary magnetospheres, the mechanisms by which cavities evolve to an eruptive state remain poorly understood. Recent optical observations of high-latitude 'polar crown' prominences within coronal cavities reveal dark, low-density 'bubbles' that undergo Rayleigh-Taylor instabilities to form dark plumes rising into overlying coronal cavities. These observations offered a possible mechanism for coronal cavity evolution, although the nature of the bubbles, particularly their buoyancy, was hitherto unclear. Here we report simultaneous optical and extreme-ultraviolet observations of polar crown prominences that show that these bubbles contain plasma at temperatures in the range (2.5-12)?×?10(5) kelvin, which is 25-120 times hotter than the overlying prominence. This identifies a source of the buoyancy, and suggests that the coronal cavity-prominence system supports a novel form of magneto-thermal convection in the solar atmosphere, challenging current hydromagnetic concepts of prominences and their relation to coronal cavities.     

Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis

Caspase-8 has two opposing biological functions--it promotes cell death by triggering the extrinsic pathway of apoptosis, but also has a survival activity, as it is required for embryonic development, T-lymphocyte activation, and resistance to necrosis induced by tumour necrosis factor-α (TNF-α) and related family ligands. Here we show that development of caspase-8-deficient mice is completely rescued by ablation of receptor interacting protein kinase-3 (RIPK3). Adult animals lacking both caspase-8 and RIPK3 display a progressive lymphoaccumulative disease resembling that seen with defects in CD95 or CD95-ligand (also known as FAS and FASLG, respectively), and resist the lethal effects of CD95 ligation in vivo. We have found that caspase-8 prevents RIPK3-dependent necrosis without inducing apoptosis by functioning in a proteolytically active complex with FLICE-like inhibitory protein long (FLIP(L), also known as CFLAR), and this complex is required for the protective function.     

Neurophysiology: Hodgkin and Huxley model--still standing?

Action potentials in cortical neurons show a variable threshold and a sudden rise in membrane potential at initiation. Naundorf et al. fail to explain these features using single- or double-compartment Hodgkin-Huxley-style models, suggesting instead that they could arise from cooperative opening of Na+ channels, although there is no direct biological evidence to support this. Here we show that these so-called unique features are to be expected from Hodgkin-Huxley models if the spatial geometry and spike initiation properties of cortical neurons are taken into account--it is therefore unnecessary to invoke exotic channel-gating properties as an explanation.     

Diets of sympatric bobcats and coyotes during years of varying rainfall in central Arizona

We collected fecal samples (scats) of sympatric bobcats ( Lynx rufus ) and coyotes ( Canis latrans ) between 2000 and 2003 in a 53,600-ha area of the Upper Sonoran Desert in central Arizona. Our objective was to investigate composition, diversity, and overlap of diets of bobcats and coyotes in relation to varying rainfall in the Sonoran Desert of central Arizona. In general, bobcats ate more rodents than did coyotes, and coyotes ate more lagomorphs, large prey, and fruit/seeds than did bobcats. Composition of bobcat diets was independent of differences among years in annual rainfall and seasonal rainfall during summer–autumn (May–October) and winter–spring (November–April). Composition of coyote diets also was independent of drought conditions among years during summer–autumn, but coyotes ate more large prey and fewer rodents during years with winter–spring drought. Seasonally, bobcats ate more rodents than did coyotes in summer–autumn and winter–spring, whereas coyotes ate more lagomorphs than did bobcats during winter– spring, and more large prey and fruit/seeds in both seasons. Coyotes ate more large prey and lagomorphs during winter–spring, when seasonal rainfall was higher, and more fruit/seeds in summer–autumn, when seasonal rainfall was lower. Diversity of diets was consistently higher for coyotes than for bobcats, and increased for bobcats but not for coyotes during winter–spring drought and during higher seasonal rainfall in winter–spring. Overlap of diets between predators was independent of rainfall levels. We suggest that bobcats in the Sonoran Desert are more selective, specialized predators and that coyotes are more generalist, opportunistic predators. We hypothesize that, although diversity of bobcat food items and composition of coyote diets differ with varying rainfall in the Sonoran Desert, patterns of feeding strategy are independent of seasonal differences in precipitation and effects of drought, and bobcats and coyotes partition food resources independently of varying rainfall.     

Red Butte Canyon Research Natural Area: history, flora, geology, climate, and ecology

Red Butte Canyon is a protected, near pristine canyon entering Salt Lake Valley, Utah. It contains a well-developed riparian zone and a perennial stream; hillside vegetation ranges from grasslands on the lower limits to Douglas-fir and aspen stands at the upper elevations. In this paper we describe the history of human impact, natural history aspects of climate, geology, and ecology, and faunal and floral information for key species in the canyon. The role and importance of Research Natural Areas is discussed, particularly with respect to the need to protect Red Butte Canyon:one of the few remaining undisturbed riparian ecosystems in the Intermountain West.     

Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome

Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by features reminiscent of marked premature ageing. Here, we present evidence of mutations in lamin A (LMNA) as the cause of this disorder. The HGPS gene was initially localized to chromosome 1q by observing two cases of uniparental isodisomy of 1q-the inheritance of both copies of this material from one parent-and one case with a 6-megabase paternal interstitial deletion. Sequencing of LMNA, located in this interval and previously implicated in several other heritable disorders, revealed that 18 out of 20 classical cases of HGPS harboured an identical de novo (that is, newly arisen and not inherited) single-base substitution, G608G(GGC > GGT), within exon 11. One additional case was identified with a different substitution within the same codon. Both of these mutations result in activation of a cryptic splice site within exon 11, resulting in production of a protein product that deletes 50 amino acids near the carboxy terminus. Immunofluorescence of HGPS fibroblasts with antibodies directed against lamin A revealed that many cells show visible abnormalities of the nuclear membrane. The discovery of the molecular basis of this disease may shed light on the general phenomenon of human ageing.     

Licensing of natural killer cells by host major histocompatibility complex class I molecules

Self versus non-self discrimination is a central theme in biology from plants to vertebrates, and is particularly relevant for lymphocytes that express receptors capable of recognizing self-tissues and foreign invaders. Comprising the third largest lymphocyte population, natural killer (NK) cells recognize and kill cellular targets and produce pro-inflammatory cytokines. These potentially self-destructive effector functions can be controlled by inhibitory receptors for the polymorphic major histocompatibility complex (MHC) class I molecules that are ubiquitously expressed on target cells. However, inhibitory receptors are not uniformly expressed on NK cells, and are germline-encoded by a set of polymorphic genes that segregate independently from MHC genes. Therefore, how NK-cell self-tolerance arises in vivo is poorly understood. Here we demonstrate that NK cells acquire functional competence through 'licensing' by self-MHC molecules. Licensing involves a positive role for MHC-specific inhibitory receptors and requires the cytoplasmic inhibitory motif originally identified in effector responses. This process results in two types of self-tolerant NK cells--licensed or unlicensed--and may provide new insights for exploiting NK cells in immunotherapy. This self-tolerance mechanism may be more broadly applicable within the vertebrate immune system because related germline-encoded inhibitory receptors are widely expressed on other immune cells.