Geosensing systems engineering for ocean security and sustainable coastal zone management

<正>Three major threats to ocean security and coastal zone sustainability - global warming,the loss of ocean biodiversity,and pollution - are combining to threaten the ecological integrity of our marine environment and life support systems.We put forward a geomatics-based systems engineering architecture to identify the location and extent of oil spills,thereby improving the ecological integrity of the world's oceans and helping contingency planners to determine required assets,personnel and other resources.This real-time,event-based and cost effective emergency management decision support system can aid in the classification,detection,and monitoring of oil spills in the marine environment.The developed Synthetic-Aperture Radar(SAR) processing and calibration techniques efficiently monitor environmental changes in inaccessible ocean regions,characterize oil spill scenarios,and help to identify spill sources.The system is used to improve emergency management in the Gulf of Mexico,with application to oil spills arising from Hurricane Katrina.     

对抗感染 动物有高招

<正>人类在一刻不停地与疾病作战。我们朝细菌发射抗生素导弹,向病毒投掷疫苗形状的手雷,把抗菌肥皂和洗手液做成的炸弹扔到所有能扔到的东西上。人类和寄生物(这是个涵盖了病毒、细菌以及大得多的寄生生物的统称)之间的斗争有着古老的根源。和猎食者、干旱或者饥荒一样,这种斗争对演化施加着强大的力量。其他物种当然也面临着类似的威胁,一说起人     

Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17

Frontotemporal dementia (FTD) is the second most common cause of dementia in people under the age of 65 years. A large proportion of FTD patients (35-50%) have a family history of dementia, consistent with a strong genetic component to the disease. In 1998, mutations in the gene encoding the microtubule-associated protein tau (MAPT) were shown to cause familial FTD with parkinsonism linked to chromosome 17q21 (FTDP-17). The neuropathology of patients with defined MAPT mutations is characterized by cytoplasmic neurofibrillary inclusions composed of hyperphosphorylated tau. However, in multiple FTD families with significant evidence for linkage to the same region on chromosome 17q21 (D17S1787-D17S806), mutations in MAPT have not been found and the patients consistently lack tau-immunoreactive inclusion pathology. In contrast, these patients have ubiquitin (ub)-immunoreactive neuronal cytoplasmic inclusions and characteristic lentiform ub-immunoreactive neuronal intranuclear inclusions. Here we demonstrate that in these families, FTD is caused by mutations in progranulin (PGRN) that are likely to create null alleles. PGRN is located 1.7 Mb centromeric of MAPT on chromosome 17q21.31 and encodes a 68.5-kDa secreted growth factor involved in the regulation of multiple processes including development, wound repair and inflammation. PGRN has also been strongly linked to tumorigenesis. Moreover, PGRN expression is increased in activated microglia in many neurodegenerative diseases including Creutzfeldt-Jakob disease, motor neuron disease and Alzheimer's disease. Our results identify mutations in PGRN as a cause of neurodegenerative disease and indicate the importance of PGRN function for neuronal survival.     

A stem batrachian from the Early Permian of Texas and the origin of frogs and salamanders

The origin of extant amphibians (Lissamphibia: frogs, salamanders and caecilians) is one of the most controversial questions in vertebrate evolution, owing to large morphological and temporal gaps in the fossil record. Current discussions focus on three competing hypotheses: a monophyletic origin within either Temnospondyli or Lepospondyli, or a polyphyletic origin with frogs and salamanders arising among temnospondyls and caecilians among the lepospondyls. Recent molecular analyses are also controversial, with estimations for the batrachian (frog-salamander) divergence significantly older than the palaeontological evidence supports. Here we report the discovery of an amphibamid temnospondyl from the Early Permian of Texas that bridges the gap between other Palaeozoic amphibians and the earliest known salientians and caudatans from the Mesozoic. The presence of a mosaic of salientian and caudatan characters in this small fossil makes it a key taxon close to the batrachian (frog and salamander) divergence. Phylogenetic analysis suggests that the batrachian divergence occurred in the Middle Permian, rather than the late Carboniferous as recently estimated using molecular clocks, but the divergence with caecilians corresponds to the deep split between temnospondyls and lepospondyls, which is congruent with the molecular estimates.     

Structure and mechanism of the M2 proton channel of influenza A virus

The integral membrane protein M2 of influenza virus forms pH-gated proton channels in the viral lipid envelope. The low pH of an endosome activates the M2 channel before haemagglutinin-mediated fusion. Conductance of protons acidifies the viral interior and thereby facilitates dissociation of the matrix protein from the viral nucleoproteins--a required process for unpacking of the viral genome. In addition to its role in release of viral nucleoproteins, M2 in the trans-Golgi network (TGN) membrane prevents premature conformational rearrangement of newly synthesized haemagglutinin during transport to the cell surface by equilibrating the pH of the TGN with that of the host cell cytoplasm. Inhibiting the proton conductance of M2 using the anti-viral drug amantadine or rimantadine inhibits viral replication. Here we present the structure of the tetrameric M2 channel in complex with rimantadine, determined by NMR. In the closed state, four tightly packed transmembrane helices define a narrow channel, in which a 'tryptophan gate' is locked by intermolecular interactions with aspartic acid. A carboxy-terminal, amphipathic helix oriented nearly perpendicular to the transmembrane helix forms an inward-facing base. Lowering the pH destabilizes the transmembrane helical packing and unlocks the gate, admitting water to conduct protons, whereas the C-terminal base remains intact, preventing dissociation of the tetramer. Rimantadine binds at four equivalent sites near the gate on the lipid-facing side of the channel and stabilizes the closed conformation of the pore. Drug-resistance mutations are predicted to counter the effect of drug binding by either increasing the hydrophilicity of the pore or weakening helix-helix packing, thus facilitating channel opening.     

Adult hippocampal neurogenesis buffers stress responses and depressive behaviour

Glucocorticoids are released in response to stressful experiences and serve many beneficial homeostatic functions. However, dysregulation of glucocorticoids is associated with cognitive impairments and depressive illness. In the hippocampus, a brain region densely populated with receptors for stress hormones, stress and glucocorticoids strongly inhibit adult neurogenesis. Decreased neurogenesis has been implicated in the pathogenesis of anxiety and depression, but direct evidence for this role is lacking. Here we show that adult-born hippocampal neurons are required for normal expression of the endocrine and behavioural components of the stress response. Using either transgenic or radiation methods to inhibit adult neurogenesis specifically, we find that glucocorticoid levels are slower to recover after moderate stress and are less suppressed by dexamethasone in neurogenesis-deficient mice than intact mice, consistent with a role for the hippocampus in regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Relative to controls, neurogenesis-deficient mice also showed increased food avoidance in a novel environment after acute stress, increased behavioural despair in the forced swim test, and decreased sucrose preference, a measure of anhedonia. These findings identify a small subset of neurons within the dentate gyrus that are critical for hippocampal negative control of the HPA axis and support a direct role for adult neurogenesis in depressive illness.     

Herpesvirus latency confers symbiotic protection from bacterial infection

All humans become infected with multiple herpesviruses during childhood. After clearance of acute infection, herpesviruses enter a dormant state known as latency. Latency persists for the life of the host and is presumed to be parasitic, as it leaves the individual at risk for subsequent viral reactivation and disease. Here we show that herpesvirus latency also confers a surprising benefit to the host. Mice latently infected with either murine gammaherpesvirus 68 or murine cytomegalovirus, which are genetically highly similar to the human pathogens Epstein-Barr virus and human cytomegalovirus, respectively, are resistant to infection with the bacterial pathogens Listeria monocytogenes and Yersinia pestis. Latency-induced protection is not antigen specific but involves prolonged production of the antiviral cytokine interferon-gamma and systemic activation of macrophages. Latency thereby upregulates the basal activation state of innate immunity against subsequent infections. We speculate that herpesvirus latency may also sculpt the immune response to self and environmental antigens through establishment of a polarized cytokine environment. Thus, whereas the immune evasion capabilities and lifelong persistence of herpesviruses are commonly viewed as solely pathogenic, our data suggest that latency is a symbiotic relationship with immune benefits for the host.     

Genetic variation increases during biological invasion by a Cuban lizard

A genetic paradox exists in invasion biology: how do introduced populations, whose genetic variation has probably been depleted by population bottlenecks, persist and adapt to new conditions? Lessons from conservation genetics show that reduced genetic variation due to genetic drift and founder effects limits the ability of a population to adapt, and small population size increases the risk of extinction. Nonetheless, many introduced species experiencing these same conditions during initial introductions persist, expand their ranges, evolve rapidly and become invasive. To address this issue, we studied the brown anole, a worldwide invasive lizard. Genetic analyses indicate that at least eight introductions have occurred in Florida from across this lizard's native range, blending genetic variation from different geographic source populations and producing populations that contain substantially more, not less, genetic variation than native populations. Moreover, recently introduced brown anole populations around the world originate from Florida, and some have maintained these elevated levels of genetic variation. Here we show that one key to invasion success may be the occurrence of multiple introductions that transform among-population variation in native ranges to within-population variation in introduced areas. Furthermore, these genetically variable populations may be particularly potent sources for introductions elsewhere. The growing problem of invasive species introductions brings considerable economic and biological costs. If these costs are to be mitigated, a greater understanding of the causes, progression and consequences of biological invasions is needed.