Beyond guts, a great business plan, and friends with deep pockets, clean energy entrepreneurs will need patience and perhaps most of all, a favorable policy environment to succeed. Fortune magazine editor Brian Dumaine leads a discussion with panelists from the worlds of venture capital, academia and industry on “how to build a winning green tech company.”

Nancy Floyd sees talented and practical entrepreneurs “solving problems we see in front of us.” Some of these may be “game changers,” although they are “certainly not science experiments.” Her firm insists that investment-worthy renewable energy ventures must not pose an additional cost premium, which means that projects must be “at grid parity or below.” She also dismisses the notion that a great idea will be totally disruptive, completely upending or bypassing current powers in the energy and utility industries. “I think that’s a stupid strategy…You need to engage those incumbents in a smart way. That’s the only way to get companies launched here.” The good news is that there are “many, many companies requiring less than $50 million that may have a huge impact on core technologies.”

Kevin Surace’s company replaced 6,500 windows on the Empire State Building with new energy efficient glass, saving the owner $410 thousand per year. Green tech, he passionately believes, “has to pay back, and pay back fast, or cost less up front.” Government subsidies for energy conservation, and public incentives for consumers to buy green don’t last forever, so entrepreneurs need to create a cost-saving product that will sell itself. Surace sees market-friendly green tech as vital to turning around the U.S. economy, bringing manufacturing back home, and reducing the nation’s $16 trillion debt. But while he believes that “the best business plans don’t require government intervention,” Surace acknowledges not only the necessity of government backing in such giant energy startups as solar installations, but a wholesale shift in the regulatory environment. “The solution to all of this nobody wants to talk about is a carbon tax.”

“We need an ecosystem for energy that is more developed,” agrees Scott Stern, who worries that the U.S. has squandered its global leadership role in addressing climate change, and is currently in political gridlock around comprehensive energy and climate change legislation. In spite of this paralysis, Stern recommends that entrepreneurs look ahead and invent for the future. “Right now, we have bad prices for carbon … We must think down the road: How will the institutional environment for paying for energy change over time, and how will the institutional environment for supporting energy infrastructure change?” Stern suggests that eventually, society will recognize that the cost of emitting carbon will be more expensive than a carbon tax. This is a long-term challenge that poses an opportunity to entrepreneurs to develop “a range of technical options.” Stern hopes that some of these new energy products might eventually diffuse through the market and become universally adopted, as did semiconductors and the Internet.

Physicist and art collector Walter Lewin shares his personal insights into major works of art from the first quarter of the 20th century.

Known in the hallways of building 37 for his famous art contests, Lewin succumbs to pressure from students and colleagues to give this lecture as part of an IAP event in advance of trips to the Museum of Fine Arts and the Fogg Art Museum. This talk is centered on pioneering artists whose work changed the world.

Lewin begins by providing a framework to understand pioneering art, by dispelling the myth of “beauty” in the artwork. An excerpt follows:

“At the turn of the century we’ve reached a point that beauty is no longer an issue. Now you may find some of these works beautiful, but the intention of the artists that you’ve just seen, was definitely not to paint something that was beautiful. They wanted to introduce a new way of looking at the world, and they did that in different ways. The reason why you may now find many of these works beautiful is that their new way of seeing—their new way of looking at the world which they invented has become your world—your way of seeing. Our ideas of beauty evolve. What is plain ugly a hundred years ago can now be beautiful.

And I want to show you today how in the first quarter of the 20th century, this process of removing constraints—of breaking the handcuffs of tradition—was completed in less than 25 years. It was a period that led to total artistic liberation.

If you still think that the goal of 20th century art is to create something beautiful you might as well leave now. It’s one of the greatest misconceptions of people who are not educated in art. To appreciate 20th century art you must abandon the idea of beauty. Pioneering art is a new way of looking at the world, and those works of art can be very interesting, they can sometimes be stunning, and sometimes they can knock me out, but I prefer not to use the word ‘beautiful’. It can be very confusing. The beauty of a pioneering work of art, no matter how ugly, is in the meaning.”

Physicist and art collector Walter Lewin shares his personal insights into major works of art from the first quarter of the 20th century.

Known in the hallways of building 37 for his famous art contests, Lewin succumbs to pressure from students and colleagues to give this lecture as part of an IAP event in advance of trips to the Museum of Fine Arts and the Fogg Art Museum. This talk is centered on pioneering artists whose work changed the world.

Lewin begins by providing a framework to understand pioneering art, by dispelling the myth of “beauty” in the artwork. An excerpt follows:

“At the turn of the century we’ve reached a point that beauty is no longer an issue. Now you may find some of these works beautiful, but the intention of the artists that you’ve just seen, was definitely not to paint something that was beautiful. They wanted to introduce a new way of looking at the world, and they did that in different ways. The reason why you may now find many of these works beautiful is that their new way of seeing—their new way of looking at the world which they invented has become your world—your way of seeing. Our ideas of beauty evolve. What is plain ugly a hundred years ago can now be beautiful.

And I want to show you today how in the first quarter of the 20th century, this process of removing constraints—of breaking the handcuffs of tradition—was completed in less than 25 years. It was a period that led to total artistic liberation.

If you still think that the goal of 20th century art is to create something beautiful you might as well leave now. It’s one of the greatest misconceptions of people who are not educated in art. To appreciate 20th century art you must abandon the idea of beauty. Pioneering art is a new way of looking at the world, and those works of art can be very interesting, they can sometimes be stunning, and sometimes they can knock me out, but I prefer not to use the word ‘beautiful’. It can be very confusing. The beauty of a pioneering work of art, no matter how ugly, is in the meaning.”

In his introduction, moderator Ian Condry advocates utilizing the expertise and innovation of all disciplines in order to best explore new directions in the humanities. He suggests that the challenge of discovery may ultimately be useful as theoretical exploration, which incorporates the transformative power of art as well.

What would it mean, Lev Manovich asks, to "be stupid?" That is, what would it mean to take risks and start creating artifacts, interpretations and analysis that reach beyond language? To begin analyzing patterns in massive cultural data sets, Manovich uses computer-based techniques, already commonly employed in the sciences, for quantitative analysis and interactive visualization. "An image is worth thousand words. An interface is worth a thousand images. Why not have both?" he asks.

Manovich sorts visual media analysis into one of two categories: 'direct visualization' and 'visualization without quantification."

In the first technique, images are manipulated to produce new images, which reveal patterns. The image grid made up of thousands of Time magazine covers reveals a gradual evolution in the design and content of the magazine: black & white imagery doesn't become color immediately; there is a gradual shift. Waves of color are apparent over time, as are patterns of cultural content.

Manovich demonstrates the 'visualization without quantification' technique by using the same data set (Time covers), but visualizing contrast & saturation. In contrast to 'direct visualization,' this technique "allows you to see the variability of cultural data. We get this wonderful cloud of history," he explains.

Manovich introduces cultural analytics as interpreted on the HIPerSpace Wall (Highly Interactive Parallelized Display Wall) at Calit2, a high-capacity tool generally used for earth science research. The demonstration explores a set of more than 150 Mark Rothko paintings. "Graphs developed from features of paintings – texture, brightness, number of shapes, saturation – can be used to explore trends in this painter's life and work."

Finally, Manovich looks at a dataset of a million pages of manga represented in a scatterplot matrix; a "manga universe." The position of each page is determined by level of contrast (on the x axis) and level of grayscale (on the y axis). Visualizations such as this provide a unique way of describing culture in all its complexity and variability. He concludes with his hope that visualization will continue to emerge as a source of new and powerful questions leading to more revealing interpretations of culture.

In his introduction, moderator Ian Condry advocates utilizing the expertise and innovation of all disciplines in order to best explore new directions in the humanities. He suggests that the challenge of discovery may ultimately be useful as theoretical exploration, which incorporates the transformative power of art as well.

What would it mean, Lev Manovich asks, to "be stupid?" That is, what would it mean to take risks and start creating artifacts, interpretations and analysis that reach beyond language? To begin analyzing patterns in massive cultural data sets, Manovich uses computer-based techniques, already commonly employed in the sciences, for quantitative analysis and interactive visualization. "An image is worth thousand words. An interface is worth a thousand images. Why not have both?" he asks.

Manovich sorts visual media analysis into one of two categories: 'direct visualization' and 'visualization without quantification."

In the first technique, images are manipulated to produce new images, which reveal patterns. The image grid made up of thousands of Time magazine covers reveals a gradual evolution in the design and content of the magazine: black & white imagery doesn't become color immediately; there is a gradual shift. Waves of color are apparent over time, as are patterns of cultural content.

Manovich demonstrates the 'visualization without quantification' technique by using the same data set (Time covers), but visualizing contrast & saturation. In contrast to 'direct visualization,' this technique "allows you to see the variability of cultural data. We get this wonderful cloud of history," he explains.

Manovich introduces cultural analytics as interpreted on the HIPerSpace Wall (Highly Interactive Parallelized Display Wall) at Calit2, a high-capacity tool generally used for earth science research. The demonstration explores a set of more than 150 Mark Rothko paintings. "Graphs developed from features of paintings – texture, brightness, number of shapes, saturation – can be used to explore trends in this painter's life and work."

Finally, Manovich looks at a dataset of a million pages of manga represented in a scatterplot matrix; a "manga universe." The position of each page is determined by level of contrast (on the x axis) and level of grayscale (on the y axis). Visualizations such as this provide a unique way of describing culture in all its complexity and variability. He concludes with his hope that visualization will continue to emerge as a source of new and powerful questions leading to more revealing interpretations of culture.

In his introduction, moderator Ian Condry advocates utilizing the expertise and innovation of all disciplines in order to best explore new directions in the humanities. He suggests that the challenge of discovery may ultimately be useful as theoretical exploration, which incorporates the transformative power of art as well.

What would it mean, Lev Manovich asks, to "be stupid?" That is, what would it mean to take risks and start creating artifacts, interpretations and analysis that reach beyond language? To begin analyzing patterns in massive cultural data sets, Manovich uses computer-based techniques, already commonly employed in the sciences, for quantitative analysis and interactive visualization. "An image is worth thousand words. An interface is worth a thousand images. Why not have both?" he asks.

Manovich sorts visual media analysis into one of two categories: 'direct visualization' and 'visualization without quantification."

In the first technique, images are manipulated to produce new images, which reveal patterns. The image grid made up of thousands of Time magazine covers reveals a gradual evolution in the design and content of the magazine: black & white imagery doesn't become color immediately; there is a gradual shift. Waves of color are apparent over time, as are patterns of cultural content.

Manovich demonstrates the 'visualization without quantification' technique by using the same data set (Time covers), but visualizing contrast & saturation. In contrast to 'direct visualization,' this technique "allows you to see the variability of cultural data. We get this wonderful cloud of history," he explains.

Manovich introduces cultural analytics as interpreted on the HIPerSpace Wall (Highly Interactive Parallelized Display Wall) at Calit2, a high-capacity tool generally used for earth science research. The demonstration explores a set of more than 150 Mark Rothko paintings. "Graphs developed from features of paintings – texture, brightness, number of shapes, saturation – can be used to explore trends in this painter's life and work."

Finally, Manovich looks at a dataset of a million pages of manga represented in a scatterplot matrix; a "manga universe." The position of each page is determined by level of contrast (on the x axis) and level of grayscale (on the y axis). Visualizations such as this provide a unique way of describing culture in all its complexity and variability. He concludes with his hope that visualization will continue to emerge as a source of new and powerful questions leading to more revealing interpretations of culture.

As an undergraduate at MIT, Robert Horvitz did not take a biology course until his senior year. But after only six weeks into his first class with professor Cy Leventhal, he realized this was the field for him. He boldly asked for a recommendation as part of his application to grad school—in biology. “Is it too late?” he wanted to know. Professor Leventhal explained that his own undergraduate and graduate degrees had been in physics and that Horvitz would, in fact, be “starting early.”

It was his work in Cambridge, England, however, that set the stage for the discoveries for which he would receive the Nobel Prize in 2002. Here he worked with Sidney Brenner and John Sulston on a phenomenon called “programmed cell death” or apoptosis. Cell death occurs naturally as part of the genetic program of every cell—a tadpole loses its tail as it turns into a frog, a bird that doesn’t need webbed feet loses the webbing as it develops. But for many years biologists ignored this behavior thinking that they must be doing something wrong when cells they were studying died.

When Horvitz first began work on the analysis of programmed cell death, he didn’t study human or animal diseases. Instead, he relied on a tiny nematode—C. elegans—only 1mm in length and comprised of exactly 959 cells. He had been warned that C. elegans was obscure and that using it would be a “scientific dead end.” Nonetheless, this creature proved to be the perfect “research subject” for the genetic and molecular work he did in understanding apoptosis. “It’s very easy to study an organism . . . that simple.”

Today cell death—cellular suicide—is recognized as a normal part of the development and biology of animal cells. Disease, on the other hand, is seen as an abnormality in the regulation of programmed cell death. According to Horvitz, diseases come in “two flavors”—cells in which there is too little programmed cell death (cells that should die, instead live) and cells in which there is too much programmed cell death (cells that should live, instead die).

Horvitz also emphasizes the importance of basic research and the importance of federal funding for that work. “If all funding is targeted to specific areas, then out-of-the-box discoveries wouldn’t happen and progress would be much slower.”

As an undergraduate at MIT, Robert Horvitz did not take a biology course until his senior year. But after only six weeks into his first class with professor Cy Leventhal, he realized this was the field for him. He boldly asked for a recommendation as part of his application to grad school—in biology. “Is it too late?” he wanted to know. Professor Leventhal explained that his own undergraduate and graduate degrees had been in physics and that Horvitz would, in fact, be “starting early.”

It was his work in Cambridge, England, however, that set the stage for the discoveries for which he would receive the Nobel Prize in 2002. Here he worked with Sidney Brenner and John Sulston on a phenomenon called “programmed cell death” or apoptosis. Cell death occurs naturally as part of the genetic program of every cell—a tadpole loses its tail as it turns into a frog, a bird that doesn’t need webbed feet loses the webbing as it develops. But for many years biologists ignored this behavior thinking that they must be doing something wrong when cells they were studying died.

When Horvitz first began work on the analysis of programmed cell death, he didn’t study human or animal diseases. Instead, he relied on a tiny nematode—C. elegans—only 1mm in length and comprised of exactly 959 cells. He had been warned that C. elegans was obscure and that using it would be a “scientific dead end.” Nonetheless, this creature proved to be the perfect “research subject” for the genetic and molecular work he did in understanding apoptosis. “It’s very easy to study an organism . . . that simple.”

Today cell death—cellular suicide—is recognized as a normal part of the development and biology of animal cells. Disease, on the other hand, is seen as an abnormality in the regulation of programmed cell death. According to Horvitz, diseases come in “two flavors”—cells in which there is too little programmed cell death (cells that should die, instead live) and cells in which there is too much programmed cell death (cells that should live, instead die).

Horvitz also emphasizes the importance of basic research and the importance of federal funding for that work. “If all funding is targeted to specific areas, then out-of-the-box discoveries wouldn’t happen and progress would be much slower.”

As an undergraduate at MIT, Robert Horvitz did not take a biology course until his senior year. But after only six weeks into his first class with professor Cy Leventhal, he realized this was the field for him. He boldly asked for a recommendation as part of his application to grad school—in biology. “Is it too late?” he wanted to know. Professor Leventhal explained that his own undergraduate and graduate degrees had been in physics and that Horvitz would, in fact, be “starting early.”

It was his work in Cambridge, England, however, that set the stage for the discoveries for which he would receive the Nobel Prize in 2002. Here he worked with Sidney Brenner and John Sulston on a phenomenon called “programmed cell death” or apoptosis. Cell death occurs naturally as part of the genetic program of every cell—a tadpole loses its tail as it turns into a frog, a bird that doesn’t need webbed feet loses the webbing as it develops. But for many years biologists ignored this behavior thinking that they must be doing something wrong when cells they were studying died.

When Horvitz first began work on the analysis of programmed cell death, he didn’t study human or animal diseases. Instead, he relied on a tiny nematode—C. elegans—only 1mm in length and comprised of exactly 959 cells. He had been warned that C. elegans was obscure and that using it would be a “scientific dead end.” Nonetheless, this creature proved to be the perfect “research subject” for the genetic and molecular work he did in understanding apoptosis. “It’s very easy to study an organism . . . that simple.”

Today cell death—cellular suicide—is recognized as a normal part of the development and biology of animal cells. Disease, on the other hand, is seen as an abnormality in the regulation of programmed cell death. According to Horvitz, diseases come in “two flavors”—cells in which there is too little programmed cell death (cells that should die, instead live) and cells in which there is too much programmed cell death (cells that should live, instead die).

Horvitz also emphasizes the importance of basic research and the importance of federal funding for that work. “If all funding is targeted to specific areas, then out-of-the-box discoveries wouldn’t happen and progress would be much slower.”

Lily and Yuh-Nung Jan have been pioneers in the field of molecular neurobiology for more than 30 years, and their genetic studies of fruit flies and mice have provided major insights into many different aspects of brain function and development. In this joint lecture, they summarize their recent work on the genetic control of neuronal shape and of electrical properties, including many implications for human brain disorders.

The brain’s extraordinary wiring complexity is largely due to dendrites, the elaborate branched structures through which neurons receive incoming signals. In the first part of their joint lecture, Yuh-Nung Jan summarizes the genetic mechanisms that control the shapes of these elaborate structures.

Jan describes how dendrites recognize and avoid other dendrites of the same neuron, while ignoring dendrites from adjacent neurons. The key to this self/non-self discrimination ability is a remarkable gene called dsCAM, which encodes some 38,000 different splice variants. Each neuron is believed to express a different subset of these variants, giving it a unique molecular identity. Genetic studies are also starting to reveal how dendritic arbor size is regulated. Like a well- pruned tree, dendritic arbors are dynamic structures in which new growth and branch removal are kept in precise balance. Jan estimates that around 100 genes are involved in this process, and he argues that mutations in these genes could contribute significantly to many human brain disorders.

Studies of dendritic structure are providing insights into neurodegenerative diseases such as Huntington’s disease. Jan shows that over-expression of the human mutant protein in fruit fly neurons causes systematic changes to their dendrites, making these flies an ideal system in which to study the disease mechanism and identify new therapeutic strategies.

The Jans have been pioneers in the study of potassium channels (K channels), the most abundant class of ion channels in the brain. In the second part of their joint presentation, Lily Jan examines the complex regulatory mechanisms by which K channels regulate brain’s activity.

To function properly, K channels must be targeted to the correct part of the neuron. Jan describes how this is accomplished for a prototypical mouse K channel known as Kv1, with the help of two associated proteins that are responsible for transporting the channel molecules along axons.

Kv1 is also present in dendrites but it gets there via a different mechanism. Rather than transporting the protein, as happens in axons, the RNA encoding the channel is localized to dendrites, where its translation is controlled locally by electrical activity at synaptic sites. Jan describes the pathway by which this happens, which appears to constitute a positive feedback loop – synaptic activity suppresses the synthesis of Kv1.1, thus increasing activity levels still further. She then shows how disruptions to this feedback pathway could contribute to autism and pervasive developmental disorder.

In the final part of the talk, Jan describes the regulation of another class of K channels known as GIRKs. Unlike the voltage-gated Kv channels, which open and close rapidly in response to electrical activity, the GIRK channels open more slowly (seconds rather than milliseconds) in response to chemical signals between neurons. GIRK channels were recently found to be concentrated at excitatory synapses within the brain, and Jan presents evidence that GIRK channels may play a fundamental role in controlling synaptic plasticity and learning.

Lily and Yuh-Nung Jan have been pioneers in the field of molecular neurobiology for more than 30 years, and their genetic studies of fruit flies and mice have provided major insights into many different aspects of brain function and development. In this joint lecture, they summarize their recent work on the genetic control of neuronal shape and of electrical properties, including many implications for human brain disorders.

The brain’s extraordinary wiring complexity is largely due to dendrites, the elaborate branched structures through which neurons receive incoming signals. In the first part of their joint lecture, Yuh-Nung Jan summarizes the genetic mechanisms that control the shapes of these elaborate structures.

Jan describes how dendrites recognize and avoid other dendrites of the same neuron, while ignoring dendrites from adjacent neurons. The key to this self/non-self discrimination ability is a remarkable gene called dsCAM, which encodes some 38,000 different splice variants. Each neuron is believed to express a different subset of these variants, giving it a unique molecular identity. Genetic studies are also starting to reveal how dendritic arbor size is regulated. Like a well- pruned tree, dendritic arbors are dynamic structures in which new growth and branch removal are kept in precise balance. Jan estimates that around 100 genes are involved in this process, and he argues that mutations in these genes could contribute significantly to many human brain disorders.

Studies of dendritic structure are providing insights into neurodegenerative diseases such as Huntington’s disease. Jan shows that over-expression of the human mutant protein in fruit fly neurons causes systematic changes to their dendrites, making these flies an ideal system in which to study the disease mechanism and identify new therapeutic strategies.

The Jans have been pioneers in the study of potassium channels (K channels), the most abundant class of ion channels in the brain. In the second part of their joint presentation, Lily Jan examines the complex regulatory mechanisms by which K channels regulate brain’s activity.

To function properly, K channels must be targeted to the correct part of the neuron. Jan describes how this is accomplished for a prototypical mouse K channel known as Kv1, with the help of two associated proteins that are responsible for transporting the channel molecules along axons.

Kv1 is also present in dendrites but it gets there via a different mechanism. Rather than transporting the protein, as happens in axons, the RNA encoding the channel is localized to dendrites, where its translation is controlled locally by electrical activity at synaptic sites. Jan describes the pathway by which this happens, which appears to constitute a positive feedback loop – synaptic activity suppresses the synthesis of Kv1.1, thus increasing activity levels still further. She then shows how disruptions to this feedback pathway could contribute to autism and pervasive developmental disorder.

In the final part of the talk, Jan describes the regulation of another class of K channels known as GIRKs. Unlike the voltage-gated Kv channels, which open and close rapidly in response to electrical activity, the GIRK channels open more slowly (seconds rather than milliseconds) in response to chemical signals between neurons. GIRK channels were recently found to be concentrated at excitatory synapses within the brain, and Jan presents evidence that GIRK channels may play a fundamental role in controlling synaptic plasticity and learning.

Lily and Yuh-Nung Jan have been pioneers in the field of molecular neurobiology for more than 30 years, and their genetic studies of fruit flies and mice have provided major insights into many different aspects of brain function and development. In this joint lecture, they summarize their recent work on the genetic control of neuronal shape and of electrical properties, including many implications for human brain disorders.

The brain’s extraordinary wiring complexity is largely due to dendrites, the elaborate branched structures through which neurons receive incoming signals. In the first part of their joint lecture, Yuh-Nung Jan summarizes the genetic mechanisms that control the shapes of these elaborate structures.

Jan describes how dendrites recognize and avoid other dendrites of the same neuron, while ignoring dendrites from adjacent neurons. The key to this self/non-self discrimination ability is a remarkable gene called dsCAM, which encodes some 38,000 different splice variants. Each neuron is believed to express a different subset of these variants, giving it a unique molecular identity. Genetic studies are also starting to reveal how dendritic arbor size is regulated. Like a well- pruned tree, dendritic arbors are dynamic structures in which new growth and branch removal are kept in precise balance. Jan estimates that around 100 genes are involved in this process, and he argues that mutations in these genes could contribute significantly to many human brain disorders.

Studies of dendritic structure are providing insights into neurodegenerative diseases such as Huntington’s disease. Jan shows that over-expression of the human mutant protein in fruit fly neurons causes systematic changes to their dendrites, making these flies an ideal system in which to study the disease mechanism and identify new therapeutic strategies.

The Jans have been pioneers in the study of potassium channels (K channels), the most abundant class of ion channels in the brain. In the second part of their joint presentation, Lily Jan examines the complex regulatory mechanisms by which K channels regulate brain’s activity.

To function properly, K channels must be targeted to the correct part of the neuron. Jan describes how this is accomplished for a prototypical mouse K channel known as Kv1, with the help of two associated proteins that are responsible for transporting the channel molecules along axons.

Kv1 is also present in dendrites but it gets there via a different mechanism. Rather than transporting the protein, as happens in axons, the RNA encoding the channel is localized to dendrites, where its translation is controlled locally by electrical activity at synaptic sites. Jan describes the pathway by which this happens, which appears to constitute a positive feedback loop – synaptic activity suppresses the synthesis of Kv1.1, thus increasing activity levels still further. She then shows how disruptions to this feedback pathway could contribute to autism and pervasive developmental disorder.

In the final part of the talk, Jan describes the regulation of another class of K channels known as GIRKs. Unlike the voltage-gated Kv channels, which open and close rapidly in response to electrical activity, the GIRK channels open more slowly (seconds rather than milliseconds) in response to chemical signals between neurons. GIRK channels were recently found to be concentrated at excitatory synapses within the brain, and Jan presents evidence that GIRK channels may play a fundamental role in controlling synaptic plasticity and learning.

Tools developed by Martin Wattenberg and his associate Fernanda Viégas, have changed the way people look at and use visualizations, by empowering and equipping users with the methodology needed to ask different questions. Wattenberg, whose background is in math and computer science, asks how the humanities have influenced the evolution of data visualization and then answers with several examples from his own work.

Web Seer compares Google's "auto-suggest" feature in one-to-one, weighted comparisons such as "why doesn't he…" and "why doesn't she…" The resultant text image uses the size of arrows and words to reflect frequency, demonstrating how text can impart meaning.

Another Wattenberg/Viégas collaboration is Many Eyes, a social media tool and Web site that has "democratized" powerful visualization systems by putting them in the hands of general audiences. This tool lets users visualize data in numerous ways, from scatterplots and bar charts to tree maps and stack graphs.

Word Tree, a visualization technique that lets users pick a word or phrase from a data set, shows the different contexts in which it appears via a tree-like branching structure. Chimera takes care of the "boilerplate problem" by examining large collections of text, such as contracts, and pointing out identical phrases. Seeing results arranged in faux 3D "skyscrapers" clearly illustrates levels of recurrence. Although Word Tree and Chimera are fundamentally repetition searches, they are important tools for semantic analysis: simple, but revealing.

The idea behind Phrase Net is to expose a text's underlying network; this visualization tool diagrams the relationships between different words used in a text. It uses a simple form of pattern matching to provide multiple views of the concepts contained a book, speech, or poem.

Another Wattenberg/ Viégas collaboration is Fleshmap, "an inquiry into human desire." The relationship between the body and its visual and verbal representation are explored in a series of artistic studies employing song lyrics and body imagery. Flickr Flow, Wattenberg explains, is an experiment whose materials are color and time. Software calculated the relative proportions of different colors seen in photos of Boston taken during each month of the year and plotted those colors on a wheel creating a "river of meaning."

Wattenberg addresses questions regarding the impact of race in personified visualizations, and his subjective motives in selecting particular data for analysis. He admits that his "hard drive is loaded with failed visualizations," but emphasizes that the visualization process should be one of trial and error. As for encouraging the development of visual literacy, Wattenberg concludes, "as visualization becomes part of the discourse and people realize, 'this is something that's powerful, it can help me make my case in life,' they'll learn… I'm hoping for education and good, old-fashioned human brain power."

Tools developed by Martin Wattenberg and his associate Fernanda Viégas, have changed the way people look at and use visualizations, by empowering and equipping users with the methodology needed to ask different questions. Wattenberg, whose background is in math and computer science, asks how the humanities have influenced the evolution of data visualization and then answers with several examples from his own work.

Web Seer compares Google's "auto-suggest" feature in one-to-one, weighted comparisons such as "why doesn't he…" and "why doesn't she…" The resultant text image uses the size of arrows and words to reflect frequency, demonstrating how text can impart meaning.

Another Wattenberg/Viégas collaboration is Many Eyes, a social media tool and Web site that has "democratized" powerful visualization systems by putting them in the hands of general audiences. This tool lets users visualize data in numerous ways, from scatterplots and bar charts to tree maps and stack graphs.

Word Tree, a visualization technique that lets users pick a word or phrase from a data set, shows the different contexts in which it appears via a tree-like branching structure. Chimera takes care of the "boilerplate problem" by examining large collections of text, such as contracts, and pointing out identical phrases. Seeing results arranged in faux 3D "skyscrapers" clearly illustrates levels of recurrence. Although Word Tree and Chimera are fundamentally repetition searches, they are important tools for semantic analysis: simple, but revealing.

The idea behind Phrase Net is to expose a text's underlying network; this visualization tool diagrams the relationships between different words used in a text. It uses a simple form of pattern matching to provide multiple views of the concepts contained a book, speech, or poem.

Another Wattenberg/ Viégas collaboration is Fleshmap, "an inquiry into human desire." The relationship between the body and its visual and verbal representation are explored in a series of artistic studies employing song lyrics and body imagery. Flickr Flow, Wattenberg explains, is an experiment whose materials are color and time. Software calculated the relative proportions of different colors seen in photos of Boston taken during each month of the year and plotted those colors on a wheel creating a "river of meaning."

Wattenberg addresses questions regarding the impact of race in personified visualizations, and his subjective motives in selecting particular data for analysis. He admits that his "hard drive is loaded with failed visualizations," but emphasizes that the visualization process should be one of trial and error. As for encouraging the development of visual literacy, Wattenberg concludes, "as visualization becomes part of the discourse and people realize, 'this is something that's powerful, it can help me make my case in life,' they'll learn… I'm hoping for education and good, old-fashioned human brain power."

Tools developed by Martin Wattenberg and his associate Fernanda Viégas, have changed the way people look at and use visualizations, by empowering and equipping users with the methodology needed to ask different questions. Wattenberg, whose background is in math and computer science, asks how the humanities have influenced the evolution of data visualization and then answers with several examples from his own work.

Web Seer compares Google's "auto-suggest" feature in one-to-one, weighted comparisons such as "why doesn't he…" and "why doesn't she…" The resultant text image uses the size of arrows and words to reflect frequency, demonstrating how text can impart meaning.

Another Wattenberg/Viégas collaboration is Many Eyes, a social media tool and Web site that has "democratized" powerful visualization systems by putting them in the hands of general audiences. This tool lets users visualize data in numerous ways, from scatterplots and bar charts to tree maps and stack graphs.

Word Tree, a visualization technique that lets users pick a word or phrase from a data set, shows the different contexts in which it appears via a tree-like branching structure. Chimera takes care of the "boilerplate problem" by examining large collections of text, such as contracts, and pointing out identical phrases. Seeing results arranged in faux 3D "skyscrapers" clearly illustrates levels of recurrence. Although Word Tree and Chimera are fundamentally repetition searches, they are important tools for semantic analysis: simple, but revealing.

The idea behind Phrase Net is to expose a text's underlying network; this visualization tool diagrams the relationships between different words used in a text. It uses a simple form of pattern matching to provide multiple views of the concepts contained a book, speech, or poem.

Another Wattenberg/ Viégas collaboration is Fleshmap, "an inquiry into human desire." The relationship between the body and its visual and verbal representation are explored in a series of artistic studies employing song lyrics and body imagery. Flickr Flow, Wattenberg explains, is an experiment whose materials are color and time. Software calculated the relative proportions of different colors seen in photos of Boston taken during each month of the year and plotted those colors on a wheel creating a "river of meaning."

Wattenberg addresses questions regarding the impact of race in personified visualizations, and his subjective motives in selecting particular data for analysis. He admits that his "hard drive is loaded with failed visualizations," but emphasizes that the visualization process should be one of trial and error. As for encouraging the development of visual literacy, Wattenberg concludes, "as visualization becomes part of the discourse and people realize, 'this is something that's powerful, it can help me make my case in life,' they'll learn… I'm hoping for education and good, old-fashioned human brain power."

In 1906, when Alois Alzheimer first described the disease that bears his name, it was a rarity; life expectancy in the US was around 50 years, and few people lived long enough to develop Alzheimer’s disease (AD). But as life expectancies have risen around the world, AD has become vastly more prevalent, and it is now one of the major public health problems of our time. In this lecture, Steven Paul, former Executive Vice President at Lilly, reviews our current understanding of the pathological mechanisms and implications for future treatments of this disease.

People with AD experience a progressive loss of memory and other cognitive abilities, the result of slow degeneration within the brain. Postmortem examination of patients’ brains reveals myriad deposits known as amyloid plaques and neurofibrillary tangles, especially within the forebrain areas that underlie memory and higher cognitive functions.

The behavioral signs of AD usually appear in the 70’s or later, and the risk of the disease rises sharply with age. But it now thought that the pathological process begins many years earlier, before the condition is diagnosed. The aim of therapy, Paul argues, should be to slow the process and thus delay onset of symptoms; even a five-year delay in onset would reduce the prevalence of the disease by 50%, a huge public benefit.

Clues to the mechanisms that may cause AD have come from genetic studies, especially of rare early-onset cases. These cases are caused by mutations in any of several genes, all of which lead to increased production of a peptide known as Abeta42 (Aβ42), the major component of amyloid plaques.

But these mutations are rare and cannot account for most cases of AD. By far the most important genetic risk factor is a gene known as ApoE, of which there are three common variants in the human population. The variant known as ApoE4 increases risk, especially in people who inherit two copies. The ApoE3 variant is intermediate, and the ApoE2 version has the lowest risk.

Paul and his colleagues were able to replicate this effect in transgenic mice genetically engineered to develop AD, and to express one or more of the human ApoE variants that either worsen or alleviate the disease. Their results support the idea that the protective E2 version of the protein is expressed at higher levels than the other versions, and that raising the expression of the gene in humans might be beneficial. Lilly has developed a compound that does this, and which is currently being tested in mice.

The ApoE protein is involved in cholesterol transport within the blood, but its role in the brain is less well understood. Paul presents evidence that ApoE works in microglial cells to clear Aβ42 from the brain before it can accumulate to form damaging plaques.

Paul ends his talk by discussing what these insights may mean for the prospects of new therapies. By the time a person is diagnosed with AD, the accumulation of Abeta may already be complete. So even if a therapy could prevent such accumulation, it may be too late to be effective. Instead, Paul argues, we need biomarkers that predict at an earlier age who is at risk for the disease, and then treat these people preventatively -- perhaps in their 50s or earlier, as is done with statins for cholesterol and cardiovascular disease. He is optimistic that current research will lead to strong predictive biomarkers; the main challenge now is to develop drugs that can be given safely over long periods to prevent the accumulation of Abeta aggregates within the brain.

In 1906, when Alois Alzheimer first described the disease that bears his name, it was a rarity; life expectancy in the US was around 50 years, and few people lived long enough to develop Alzheimer’s disease (AD). But as life expectancies have risen around the world, AD has become vastly more prevalent, and it is now one of the major public health problems of our time. In this lecture, Steven Paul, former Executive Vice President at Lilly, reviews our current understanding of the pathological mechanisms and implications for future treatments of this disease.

People with AD experience a progressive loss of memory and other cognitive abilities, the result of slow degeneration within the brain. Postmortem examination of patients’ brains reveals myriad deposits known as amyloid plaques and neurofibrillary tangles, especially within the forebrain areas that underlie memory and higher cognitive functions.

The behavioral signs of AD usually appear in the 70’s or later, and the risk of the disease rises sharply with age. But it now thought that the pathological process begins many years earlier, before the condition is diagnosed. The aim of therapy, Paul argues, should be to slow the process and thus delay onset of symptoms; even a five-year delay in onset would reduce the prevalence of the disease by 50%, a huge public benefit.

Clues to the mechanisms that may cause AD have come from genetic studies, especially of rare early-onset cases. These cases are caused by mutations in any of several genes, all of which lead to increased production of a peptide known as Abeta42 (Aβ42), the major component of amyloid plaques.

But these mutations are rare and cannot account for most cases of AD. By far the most important genetic risk factor is a gene known as ApoE, of which there are three common variants in the human population. The variant known as ApoE4 increases risk, especially in people who inherit two copies. The ApoE3 variant is intermediate, and the ApoE2 version has the lowest risk.

Paul and his colleagues were able to replicate this effect in transgenic mice genetically engineered to develop AD, and to express one or more of the human ApoE variants that either worsen or alleviate the disease. Their results support the idea that the protective E2 version of the protein is expressed at higher levels than the other versions, and that raising the expression of the gene in humans might be beneficial. Lilly has developed a compound that does this, and which is currently being tested in mice.

The ApoE protein is involved in cholesterol transport within the blood, but its role in the brain is less well understood. Paul presents evidence that ApoE works in microglial cells to clear Aβ42 from the brain before it can accumulate to form damaging plaques.

Paul ends his talk by discussing what these insights may mean for the prospects of new therapies. By the time a person is diagnosed with AD, the accumulation of Abeta may already be complete. So even if a therapy could prevent such accumulation, it may be too late to be effective. Instead, Paul argues, we need biomarkers that predict at an earlier age who is at risk for the disease, and then treat these people preventatively -- perhaps in their 50s or earlier, as is done with statins for cholesterol and cardiovascular disease. He is optimistic that current research will lead to strong predictive biomarkers; the main challenge now is to develop drugs that can be given safely over long periods to prevent the accumulation of Abeta aggregates within the brain.

In 1906, when Alois Alzheimer first described the disease that bears his name, it was a rarity; life expectancy in the US was around 50 years, and few people lived long enough to develop Alzheimer’s disease (AD). But as life expectancies have risen around the world, AD has become vastly more prevalent, and it is now one of the major public health problems of our time. In this lecture, Steven Paul, former Executive Vice President at Lilly, reviews our current understanding of the pathological mechanisms and implications for future treatments of this disease.

People with AD experience a progressive loss of memory and other cognitive abilities, the result of slow degeneration within the brain. Postmortem examination of patients’ brains reveals myriad deposits known as amyloid plaques and neurofibrillary tangles, especially within the forebrain areas that underlie memory and higher cognitive functions.

The behavioral signs of AD usually appear in the 70’s or later, and the risk of the disease rises sharply with age. But it now thought that the pathological process begins many years earlier, before the condition is diagnosed. The aim of therapy, Paul argues, should be to slow the process and thus delay onset of symptoms; even a five-year delay in onset would reduce the prevalence of the disease by 50%, a huge public benefit.

Clues to the mechanisms that may cause AD have come from genetic studies, especially of rare early-onset cases. These cases are caused by mutations in any of several genes, all of which lead to increased production of a peptide known as Abeta42 (Aβ42), the major component of amyloid plaques.

But these mutations are rare and cannot account for most cases of AD. By far the most important genetic risk factor is a gene known as ApoE, of which there are three common variants in the human population. The variant known as ApoE4 increases risk, especially in people who inherit two copies. The ApoE3 variant is intermediate, and the ApoE2 version has the lowest risk.

Paul and his colleagues were able to replicate this effect in transgenic mice genetically engineered to develop AD, and to express one or more of the human ApoE variants that either worsen or alleviate the disease. Their results support the idea that the protective E2 version of the protein is expressed at higher levels than the other versions, and that raising the expression of the gene in humans might be beneficial. Lilly has developed a compound that does this, and which is currently being tested in mice.

The ApoE protein is involved in cholesterol transport within the blood, but its role in the brain is less well understood. Paul presents evidence that ApoE works in microglial cells to clear Aβ42 from the brain before it can accumulate to form damaging plaques.

Paul ends his talk by discussing what these insights may mean for the prospects of new therapies. By the time a person is diagnosed with AD, the accumulation of Abeta may already be complete. So even if a therapy could prevent such accumulation, it may be too late to be effective. Instead, Paul argues, we need biomarkers that predict at an earlier age who is at risk for the disease, and then treat these people preventatively -- perhaps in their 50s or earlier, as is done with statins for cholesterol and cardiovascular disease. He is optimistic that current research will lead to strong predictive biomarkers; the main challenge now is to develop drugs that can be given safely over long periods to prevent the accumulation of Abeta aggregates within the brain.

A focus on designing technologies that allow the "visualization of things not visible" has been at the center of Ben Shneiderman’s work over the past two decades. He advocates the discovery of temporal patterns, relationships and clusters via an empowering user experience which enables discovery at a customizable pace and depth.

Shneiderman makes a clear distinction between high-resolution presentation (ala Edward Tufte) and discovery, which he defines as "the dynamics of interaction." Noting that different patterns will be interesting to different people, he suggests that the capacity to quickly test out a viewpoint, to ask a large number of questions in a short amount of time…is an "enriching gift."

Shneiderman cites several different projects which utilize various methodologies of user exploration and empowerment, principles applicable to the scientific and technical world, as well as the humanities and arts. The best known of these is Spotfire, a commercial application of visual data mining and information visualization. (User control – via dynamic query sliders, for example - directs the rapid updating of a display containing color- and size-coded points.)

He describes other methodologies – including treemaps (space-constrained visualizations of hierarchical structures), TimeSearcher (a visual analysis tool for time series data), FeatureLens (interactive visualization of text patterns) and Social Action (for social network data, now incorporated into NodeXL) – as capable of giving "answers to questions you didn't know you had."

Questions from the audience address the challenges of visualizing uncertainty and the notion of a "user" as a participant whose contributions and engagement actually reshape the very conditions of the system. Shneiderman emphasizes a desire to not only empower users but to alert them to potential hazards of interpretation and make them more cautious users, readers and/or participants.

Additionally, Shneiderman encourages an information visualization approach through which selection strategies allow "treasures to rise to the surface" from vast databases. Noting ongoing constraints of time and budget, he emphasizes the processes of categorization and prioritization, and supports courage of ownership for decisions made.

A focus on designing technologies that allow the "visualization of things not visible" has been at the center of Ben Shneiderman’s work over the past two decades. He advocates the discovery of temporal patterns, relationships and clusters via an empowering user experience which enables discovery at a customizable pace and depth.

Shneiderman makes a clear distinction between high-resolution presentation (ala Edward Tufte) and discovery, which he defines as "the dynamics of interaction." Noting that different patterns will be interesting to different people, he suggests that the capacity to quickly test out a viewpoint, to ask a large number of questions in a short amount of time…is an "enriching gift."

Shneiderman cites several different projects which utilize various methodologies of user exploration and empowerment, principles applicable to the scientific and technical world, as well as the humanities and arts. The best known of these is Spotfire, a commercial application of visual data mining and information visualization. (User control – via dynamic query sliders, for example - directs the rapid updating of a display containing color- and size-coded points.)

He describes other methodologies – including treemaps (space-constrained visualizations of hierarchical structures), TimeSearcher (a visual analysis tool for time series data), FeatureLens (interactive visualization of text patterns) and Social Action (for social network data, now incorporated into NodeXL) – as capable of giving "answers to questions you didn't know you had."

Questions from the audience address the challenges of visualizing uncertainty and the notion of a "user" as a participant whose contributions and engagement actually reshape the very conditions of the system. Shneiderman emphasizes a desire to not only empower users but to alert them to potential hazards of interpretation and make them more cautious users, readers and/or participants.

Additionally, Shneiderman encourages an information visualization approach through which selection strategies allow "treasures to rise to the surface" from vast databases. Noting ongoing constraints of time and budget, he emphasizes the processes of categorization and prioritization, and supports courage of ownership for decisions made.