The Emerging Scientific Discipline of Aeroecology

In the history of science and technology, there is an infrequent combination of empirical discoveries, theories and technology developments converge that make it possible to recognize a new discipline. Past examples include marine biology, biomechanics and astrobiology with more recent developments of nanotechnology and bioinformatics – all disciplines that are now well established in the lexicon of modern science and technology.

Aeroecology is one such emerging discipline, says Thomas Kunz, Boston University professor of biology and director of the Center of Ecology and Conservation Biology and the lead author of "Aeroecology: probing and modeling the aerosphere," a research report in Integrative and Comparative Biology, based on a symposium sponsored by the Society for Integrative and Comparative Biology.

Kunz, who is best known for his extensive research on bats, explains that aeroecology embraces and integrates the domains of atmospheric science, earth science, geography, ecology, computer science, computational biology, and engineering.

The unifying concept that underlies aeroecology is its focus on the planetary boundary layer of the Earth's atmosphere, or aerosphere, which supports the myriad of airborne organisms that, in large part, depend upon this natural environment for their existence. Organisms that use the aerosphere, specifically arthropods, birds and bats, are also influenced by an increasing number of anthropogenic or man-made conditions and structures, notably lighted towns and cities, air pollution, skyscrapers, aircraft, radio and television towers, plus a recent proliferation of communication towers and wind turbines that dot the Earth's landscape.

In addition, human-altered landscapes increasing are characterized by deforestation, intensive agriculture, urbanization, and assorted industrial activities that are rapidly and irreversibly transforming the quantity and quality of available terrestrial and aquatic habitats which airborne organisms rely upon. These conditions are known to influence navigational cues, sources of food, water, nesting and roosting habitats--factors that can, in turn, alter the structure and function of terrestrial and aquatic ecosystems and the assemblages of organisms.

Similarly, "climate change and its expected increase in global temperatures, altered circulation of air masses, and effects on local and regional weather patterns are expected to have profound impacts on the foraging and migratory behavior of insects, birds and bats," noted Kunz.

"In contrast to organisms that depend strictly on terrestrial or aquatic existence, those that routinely use the aerosphere are almost immediately influenced by changing atmospheric conditions ( e.g. winds, air density, precipitation, air temperature) sunlight, polarized light, moonlight and geomagnetic and gravitational forces," the report states.

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Alzheimer's-associated Enzyme Can Disrupt Brain Activity

An enzyme involved in the formation of the amyloid-beta protein associated with Alzheimer’s disease can also alter the mechanism by which signals are transmitted between brain cells, the disruption of which can cause seizures. These findings from researchers at the MassGeneral Institute for Neurodegenerative Disorders (MGH-MIND) may explain the increased incidence of seizures in Alzheimer’s patients and suggest that potential treatments that block this enzyme – called beta-secretase or BACE – may alleviate their occurrence. The report will appear in the journal Nature Cell Biology and is receiving early online release.

“We have found a molecular pathway by which BACE can modulate the activity of sodium channels on neuronal cell membranes,” says study leader Dora Kovacs, director of the Neurobiology of Disease Laboratory in the Genetics and Aging Research Unit at MGH-MIND. “That implies that elevated BACE activity may be responsible for the seizures frequently observed in Alzheimer’s patients.”

Alzheimer's disease is characterized by plaques within the brain of the toxic amyloid-beta protein. Amyloid-beta is formed when the larger amyloid precursor protein (APP) is clipped by two enzymes – BACE and gamma-secretase – which releases the amyloid-beta fragment.
Signaling impulses in nerve cells are transmitted via voltage-gated sodium channels, structures on the cell membrane that transmit electrochemical signal by admitting charged sodium particles into the cell’s interior. Sodium channels consist of an alpha subunit, which makes up the body of the channel, and one or two beta subunits that help to regulate the channels’ activity.

Previous studies from Kovacs’ team and others showed that the BACE and gamma-secretase enzymes that release amyloid-beta from APP also act on the beta2 subunit of neuronal sodium channels. The current study was designed to examine how this processing of the beta2 subunit may alter neuronal function.

Lead author Doo Yeon Kim, and colleagues first confirmed that the beta2 subunit, similar to APP, can be acted on by BACE and gamma-secretase, releasing a portion of the beta2 molecule from the cell membrane. A series of experiments using brain tissue from animal models and from Alzheimer’s patients revealed the following series of cellular events: Elevated levels of the free beta2 segment within the cell appear to increase production of the alpha subunits, but those molecules are not incorporated into new sodium channels on the cell surface. The resulting deficit of membrane sodium channels inhibits the passage of neuronal signals into and through the cells.

Neuronal sodium-channel dysfunction is known to cause seizures in both mice and humans. In a supplement to the current paper the investigators present evidence that sodium channel metabolism is altered in the brains of Alzheimer’s patients compared with non-demented individuals of similar age.

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Teen Risk-Taking May Be Biologically Driven and Inevitable, Research Says

While the government spends billions of dollars on educational and prevention programs to persuade teens not to do things like smoke, drink or do drugs, a Temple University psychologist suggests that competing systems within the brain make adolescents more susceptible to engaging in risky or dangerous behavior, and that educational interventions alone are unlikely to be effective.

Laurence Steinberg, distinguished university professor and the Laura H. Carnell professor of psychology at Temple, outlines his argument in, “Risk Taking in Adolescence: New Perspectives from Brain and Behavioral Science,” in the April issue of the journal, Current Directions in Psychological Science.

“While it is probably not fair to say that none of the programs we have developed works, most of the educational efforts to persuade kids to not smoke or to not use drugs or alcohol, to engage in safe sex or to drive more safely have not been effective,” says Steinberg, director of the John D. and Catherine T. MacArthur Foundation Research Network on Adolescent Development and Juvenile Justice. “There is a program here or there that works, but, by and large, we have spent billions of dollars on initiatives that have not really had much of an impact.”



Steinberg says that over the past 10 years there has been a great deal of new research on adolescent brain development that he believes sheds light on why kids engage in risky and dangerous behavior, and why the educational programs or interventions that have been developed have not been especially effective.



According to Steinberg, heightened risk taking in adolescence is the result of competition between two very different brain systems, the socioemotional and cognitive-control networks, that are undergoing maturation during adolescence, but along very different timetables. During the adolescence, the socioemotional system becomes more assertive during puberty, while the cognitive-control system gains strength only gradually and over a longer period of time.
The socioemotional system, which processes social and emotional information, becomes very active during puberty allowing adolescents to become more easily aroused and experience more intense emotion, and to become more sensitive to social influence.



Conversely, says Steinberg, the cognitive-control system is the part of the brain that regulates behavior and makes the ultimate decisions, but is still maturing during adolescence and into a person’s mid-20s at least.



In the article, Steinberg says that the socioemotional network is not in a state of constantly high activation during adolescence. When the socioemotional network is not highly activated -- for example, when individuals are not emotionally excited or are alone -- the cognitive-control network is strong enough to impose regulatory control over impulsive and risky behavior, even in early adolescence.



In the presence of peers, however, or in situations where emotions run high, the socioemotional network becomes sufficiently activated to diminish the regulatory effectiveness of the cognitive-control network.


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First Glimpse of Influenza Replication Machine

In 1918, 50 million people died during a worldwide influenza pandemic caused by mutation of a bird-specific strain of the influenza virus. Recently H5N1, another highly infectious avian strain has caused outbreaks of bird flu around the world. There is great concern that this virus might also mutate to allow human-to-human transmission and cause another catastrophic pandemic.

Specific mutations in a viral protein, the polymerase, contribute to the ability of the bird virus to jump the species barrier to humans.

Researchers from the European Molecular Biology Laboratory (EMBL) in Grenoble and Heidelberg, the Institut de Biologie Structurale (IBS) and the Unit of Virus Host Cell Interactions (UVHCI), both in Grenoble, have now produced the first three-dimensional image of part of this key protein. The study, which is published in the current issue of Nature Structural and Molecular Biology, investigates the structure and function of the protein and sheds light on how polymerase mutations contribute to transmission of avian flu to humans.

Upon infection the influenza virus starts multiplying in the cells of an infected host. The polymerase is crucial in this process because it copies the viral genome and directs the production of its proteins. Interfering with polymerase function would prevent the virus replicating, thereby reducing the spread of the virus and the severity of the infection.

"For many years scientists have tried to understand the flu polymerase and to look for weak points that could be targeted by drugs," says Darren Hart, whose team participated in the research at EMBL Grenoble. "But no one could get enough protein to analyse its structure. We developed a way to use robots to screen tens of thousands of experimental conditions and discovered a piece of the influenza polymerase that we could work with. It is a small part of the entire protein, but it provides interesting insights into how the protein works and how mutations may affect host range."

Together with scientists at the IBS they visualized the atomic structure of the protein and discovered a previously overlooked signal that labels it for transport to the human nucleus where the genetic material of the virus is replicated. Cell microscopy studies at EMBL Heidelberg revealed that the human nuclear transport protein, importin alpha, recognises this signal and shuttles the polymerase into the nucleus. To find out how the polymerase and importin interact, Stephen Cusack, head of EMBL Grenoble, and collaborators at the UVHCI, used the high intensity X-ray source of the European Synchrotron Radiation Facility to generate a high-resolution image of the two proteins interacting with each other.

The image revealed that mutations known to play a role in the transmission of avian influenza virus to mammals were located within, or close to, this site of interaction. This suggests that mutations may affect the efficiency of nuclear transport and through this the ability of the virus to replicate in different species.

"Interfering with polymerase function could provide new ways to treat or prevent flu," says Cusack, "but this will require a detailed picture of the rest of the polymerase. This is what we are aiming for in our new FLUPOL project. In a joint effort with other European laboratories, and with financial support by the European Commission, we will explore both structure and function of this key drug target and try to characterise other mutations implicated in bird-to-human transmission."

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