Rapamycin and lifespan extension

Will a pill containing the immunosuppressant drug rapamycin someday extend human lifespan a few years? In spite of the hopeful research announcements that appeared a few days ago, I wouldn't recommend getting one's hopes up just yet.

This is a topic I've discussed before: Calorie restriction, TOR signaling, and aging. And for related stuff on mTOR: here.

The executive summary is that inhibition of mTOR signaling has been shown to extend lifespan in yeast, roundworms, and fruit flies. Mice can now be added to this list, in experiments that included rapamycin in their diet.

Here's the press release:

Easter Island Compound Extends Lifespan Of Old Mice: 28 To 38 Percent Longer Life (7/8/09)

On July 8, in the journal Nature, The University of Texas Health Science Center at San Antonio and two collaborating centers reported that the Easter Island compound – called "rapamycin" after the island's Polynesian name, Rapa Nui – extended the expected lifespan of middle-aged mice by 28 percent to 38 percent. In human terms, this would be greater than the predicted increase in extra years of life if cancer and heart disease were both cured and prevented.

Although rapamycin and some related compounds have been investigated as anti-cancer therapies, the hypothesized lifespan-extending benefits are thought to be related to the by now well-documented benefits of calorie restricted diets. (For very recent news on that front, see here, for example.)

Aging researchers currently acknowledge only two life-extending interventions in mammals: calorie restriction and genetic manipulation. Rapamycin appears to partially shut down the same molecular pathway as restricting food intake or reducing growth factors.

It does so through a cellular protein called mTOR (mammalian target of rapamycin), which controls many processes in cell metabolism and responses to stress.

A decade ago, Dr. [Dave] Sharp proposed to his colleagues that mTOR might be involved in calorie restriction. "It seemed like an off-the-wall idea at that time," Dr. Richardson said.

Experiments were performed in parallel at three separate research centers and consisted of feeding hundreds of mice, starting at an age of 20 months, a diet containing a special formulation of rapamycin designed to evade breakdown in the digestive system. It was found that the age at which 90% of mice had died rose from 1,078 days to 1,179 days in male mice, compared to controls, and from 1,094 days to 1,245 days in females. The total lifespan extension, on average, was therefore 9.4% in males and 13.8% in females.

Note that some accounts of the research claim lifespan extensions of 28% to 38%, but this is misleading, since those figures represent the extension of the "old age" period of mouse life beginning at 20 months. They do not mean that the mice lived up to almost 40% longer in total. (Some pretty shoddy reporting going on here....) And there was no particular evidence to indicate that extensions of such size would have occurred if the special diet began at an earlier age. However, in experiments still going on, there is evidence for some extension when addition of rapamycin to the diet begins for mice 270 days old.

Of course, even an extension of human lifespan in the 10% range – 7 or 8 years – would be quite an accomplishment, provided quality of life in the final years remained about where it is today. (Which is a big if.)

But there are various reasons to suspect that even a 10% extension in humans is rather optimistic. Some reasons:

1. Rapamycin is an immunosuppressant, currently used therapeutically to prevent organ transplant rejection. The experimental mice were maintained under conditions that carefully protected them from infection – conditions that would not be realistic for humans.
   
2. Although mice and humans are both mammals, their genetics are not all that similar. The complete sequence of the mouse genome was recently announced (see here), and it turns out that about 20% of mouse genes are different from human analogs, or not found in humans at all. (It's been 90 million years since the last common ancestor of mice and humans.)
   
3. Rapamycin is known to inhibit an important protein kinase called mTOR (mammalian target of rapamycin). mTOR plays a key role in regulating cell growth, proliferation, and survival, so it's not all that surprising that rapamycin might affect cell biology relevant to aging and longevity. This same property of rapamycin makes it interesting as an anti-cancer agent. Rapamycin and similar compounds that inhibit mTOR have in fact been found to have anti-cancer properties in animal models. Several analogs of rapamycin have been investigated as anti-cancer therapies, and one has even been approved for human use (Torisel). But even in the anti-cancer setting, mTOR inhibitors haven't yet been slam-dunk successes.
   
4. It is not clear that rapamycin in these experiments was working the same way as calorie restriction. None of the rapamycin-fed mice lost body weight, and calorie restriction usually works best when started relatively early in life.
   
5. Experimental mice that received rapamycin got a dose of 2.24 mg per kg of body weight. That's quite a lot – about 30 to 60 times (per kg) what would be given to a 60 kg human for immunosuppression.
   

The unfortunate truth is that cell signaling pathways that affect cell growth, proliferation, and survival are rather complicated, and any interventions in such pathways are very likely to not have the expected effects and/or to have various unexpected side-effects. Here's a diagram of just some of the important pathways mTOR is involved in. Imagine that were an electrical circuit and you made ad hoc changes to important components of the circuit.... Perhaps you can see how trying to affect mTOR in order either to control cancer or enhance longevity might be a dicey proposition.

In spite of all the reservations, there are still promising signs for the role of mTOR inhibition in lifespan extension. The mechanism of action need not be the same as calorie restriction, even though that hasn't been ruled out either. For example, TOR is known from yeast and nematode studies to promote protein production in ribosomes and to inhibit protein degradation via autophagy. Invertebrate studies have shown that reversal of these TOR effects can increase lifespan. And TOR signaling is also known to influence cell growth, cell-cycle progression, mitochondrial metabolism, and insulin-analog signaling.

Remember what we said about the diversity of effects of mTOR signaling? That's definitely a sword that can cut both ways – it's powerful, but hard to predict and control. We need to understand a lot more of the biological details – otherwise we're just swinging the sword in the dark.

Harrison, D., Strong, R., Sharp, Z., Nelson, J., Astle, C., Flurkey, K., Nadon, N., Wilkinson, J., Frenkel, K., Carter, C., Pahor, M., Javors, M., Fernandez, E., & Miller, R. (2009). Rapamycin fed late in life extends lifespan in genetically heterogeneous mice Nature DOI: 10.1038/nature08221

Further reading:

Tests raise life extension hopes (7/8/09) – BBC news story

Immune drug boosts lifespan (7/8/09) – TheScientist.com

Fountain of Youth on Easter Island? (7/8/09) – ScienceNOW

Cancer Drug Delays Aging in Mice (7/8/09) – Wired.com

A pill for longer life? (7/8/09) – Nature.com

Ageing: A midlife longevity drug? (7/8/09) – Nature.com PDF

Rapamycin extends life in mice, raising hopes of life-prolonging drug for humans (7/9/09) – The Times (UK)

What Does Life-Extending Drug Mean for Humans? (7/9/09) – Time

New clues in search for elixir of youth (7/9/09) – New Scientist

Antibiotic Delayed Aging in Experiments With Mice (7/8/09) – New York Times

Rapamycin: “An anti-aging drug today”? (3/6/07) – Ouroboros blog post

Tags: rapamycin, biogerontology, aging, longevity

New targeted therapy finds and eliminates deadly leukemia stem cells

Insecure people who are derisive or dismissive of technical scientific terminology (which they affectedly disdain as "jargon") can miss a lot of significant meaning.

Consider the medical term "leukemia", which is familiar to the public as referring to a form of blood cancer. It's related to the less familiar term "leukocyte", which refers to various kinds of white blood cells. (The prefix "leuko-" is derived from Greek leukos, meaning "white". The suffix, "-cyte" is also Greek: kytos, meaning "cell".)

Leukocytes were originally recognized as distinct from other types of cells in the blood, especially "red" blood cells, which derive their color from iron-containing hemoglobin. There are actually a number of different types of leukocytes – and different types of corresponding leukemias. One common subtype of leukemia involves myeloid cells (myelocytes), which are normally found in bone marrow and occur as precursors to several types of blood cells. Acute myeloid leukemia (AML, also known as acute myelogenous leukemia) is the most common example, and has several subtypes itself.

Leukocytes of many types are derived from myeloid cells, which are thus a type of stem cell. When such cells develop certain types of abnormalities they harmfully overproduce derived cells, effectively making them cancer (specifically, leukemia) stem cells. The most common type of abnormality is a type of cell surface receptor known as CD123. A receptor is simply a protein found on a cell surface which binds to external cell signaling proteins called cytokines. (There's the "cyto-" again. The "-kine" part is from Greek kinos, which refers to motion, as in "kinetic".)

Cytokines are often interpreted by cells as signals to divide and proliferate, usually in a helpful way, as normal with immune system cells. Certain immune-system cytokines are called interleukins, because they facilitate signaling among immune system leukocytes. CD123 receptors, in particular, are receptors for interleukin-3. Thus CD123 receptors have another name: interleukin-3 receptor, alpha.

CD123 is essential for the normal communication between immune system cells such as T cells. It must exist on the surfaces of cells that need to respond to interleukin-3, in order to have a proper immune system response to infection. You do not, however, want CD123 on stem cells, whose excessive proliferation results in leukemia.

And so it is that one promising treatment for acute myeloid leukemia involves the development of a novel antibody, called 7G3, that can block CD123 receptors without triggering proliferation. Of course, that might interfere with immune system function – but such interference is preferable to leukemia.

New Targeted Therapy Finds And Eliminates Deadly Leukemia Stem Cells (7/2/09)

Associate Professor Lock [senior study author] and colleagues exploited the fact that the molecule CD123 is expressed at very high levels on LSCs but not on normal blood cells. CD123 is part of the interleukin-3 receptor, a protein that interacts with a growth factor (called a cytokine) that influences cell survival and proliferation. The researchers created a therapeutic antibody that recognized and bound to CD123 with the hope that this antibody would selectively interfere with AML-LSC survival.

When AML-LSCs from human patients were transplanted into mice treated with the antibody, called 7G3, cytokine signaling in the tumor cells was blocked. Further, 7G3 impaired migration of the AML-LSCs to bone marrow and activated the innate immune system of the host mouse to destroy the AML-LSCs. Overall, treatment with 7G3 substantially improved mouse survival when compared with control groups. The researchers go on to report that a CD123-targeting antibody is currently being used in phase 1 clinical trials of advanced AML and that there are no signs of treatment-related toxicity.

Further reading:

New Drug Hits Leukemia Early (7/2/09) – Science News article

Monoclonal Antibody-Mediated Targeting of CD123, IL-3 Receptor α Chain, Eliminates Human Acute Myeloid Leukemic Stem Cells – Cell Stem Cell research article

Tags: cancer, cancer stem cell

Intermediate mass black holes

Black holes are controversial. (Just browse reader comments from partisans of various sorts of "alternative" astrophysical theories – which can be found at the end of many articles dealing with black holes that allow commenting by the general public.)

Nevertheless, very solid evidence has been accumulated over the years for the existence of two types of black holes: stellar-mass black holes with masses from 3 to several tens of solar masses (M_⊙), and supermassive black holes, which are vastly larger – generally millions to billions M_⊙. Concerning some of the evidence, see here.

Stellar-mass black holes are easy to explain as supernova remnants, while supermassive black holes seem to be an inseparable concomitant of the development of all galaxies.

Perhaps surprisingly, however, there has been very little evidence for the existence of black holes of intermediate mass. If such black holes exist at all, the processes that form them must be rather more unusual. Evidence for the existence of intermediate mass black holes has been reported in the past. (There's some discussion here of possible black holes of mass less than a million M_⊙.)

But because black holes, by their nature, are difficult to observe directly, and so their existence must be inferred indirectly, it has been difficult to come up with relatively unambiguous evidence. Now we have announcements of better evidence in two cases.

New Class Of Black Holes Discovered (7/1/09)

A new class of black hole, more than 500 times the mass of the Sun, has been discovered by an international team of astronomers.

The finding in a distant galaxy approximately 290 million light years from Earth is reported today in the journal Nature.

Until now, identified black holes have been either super-massive (several million to several billion times the mass of the Sun) in the centre of galaxies, or about the size of a typical star (between three and 20 Solar masses).

The new discovery is the first solid evidence of a new class of medium-sized black holes.

Important discoveries often don't come by themselves. Other researchers and teams tend to report related results at the same time. And this is no exception. The above reports concern a candidate object in a galaxy (ESO 243-49) about 290 million light-years away. But there's also a report of an object much closer, in the globular cluster M54 (more here), which is only about 87,000 light-years away. It's thought to belong, actually, not to the Milky Way itself, but rather to the Saggitarius Dwarf Elliptical Galaxy, a satellite of the Milky Way.

Density and kinematic cusps in M54 at the heart of the Sagittarius dwarf galaxy: evidence for a 10⁴ M_⊙ Black Hole?

We report the detection of a stellar density cusp and a velocity dispersion increase in the center of the globular cluster M54, located at the center of the Sagittarius dwarf galaxy (Sgr). The central line of sight velocity dispersion is 20.2 +/- 0.7 km/s, decreasing to 16.4 +/- 0.4 km/s at 2.5" (0.3 pc). Modeling the kinematics and surface density profiles as the sum of a King model and a point-mass yields a black hole (BH) mass of ~ 9400 M_⊙. However, the observations can alternatively be explained if the cusp stars possess moderate radial anisotropy.

M54

Further reading (ESO 243-49 candidate object):

Finally, an Average Black Hole (7/1/09) – ScienceNOW

New Candidates for Midsize Black Holes (7/3/09) – Sky and Telescope

An intermediate-mass black hole of over 500 solar masses in the galaxy ESO – Nature research article

XMM-Newton discovers a new class of black holes (7/1/09) – ESA press release

New Observations Suggest Mid-Size Black Holes Exist (7/1/09) – Space.com

Black holes: now available in size 'M' (7/2/09) – Cosmos magazine

Astronomers Discover Medium-Sized Class of Black Holes (7/1/09) – Universe Today

Intermediate-mass black hole (7/1/09) – Science Centric

Astronomers sniff intermediate mass black hole (7/2/09) – The Register

Astronomers Size Up a Candidate for Midsize Black Hole (7/1/09) – Scientific American

New Class of Black Holes Discovered (7/1/09) – Wired

X-rays are smoking gun for middleweight black holes (7/1/09) – New Scientist

A New Kind of Black Hole (7/2/09) – Smithsonian.com

Team May Have Found Intermediate Black Hole (7/6/09) – New York Times

Further reading (M54 candidate object):

Density and kinematic cusps in M54 at the heart of the Sagittarius dwarf galaxy: evidence for a 10^4 M_sun Black Hole? – Astrophysical Journal research article

Tags: black holes

Viroids

Perhaps you've thought that viruses are the simplest sort of "living" thing – if a virus can even be called "alive".

Well, maybe not. Viroids are even simpler. You're on your own as to whether you want to describe them as "alive".

Viroids are not a new discovery – they've been known since 1971. Viroids are found only in plant cells and don't seem to infect animals. They can cause plant pathology, apparently enough to be a serious economic problem.

A viroid consists entirely of a circular piece of RNA, that may be only a few hundred base units long. The smallest known viroid has only 220 units. None of this RNA codes for proteins – unlike virus RNA or DNA, which codes for proteins that (among other things) encapsulate the genetic material. The RNA or DNA of a virus is much larger than the RNA of a viroid. The smallest known virus capable of causing an infection by itself is about 2000 base units.

Viruses reproduce by co-opting machinery of the host cell. The DNA of a DNA virus, for example, is typically normal double-stranded DNA. In the virus life cycle, two separate processes are required (among others). The DNA itself has to be copied with a DNA polymerase enzyme, just as is used in making DNA copies during cell division. The proteins that the virus requires for its coat are also made in the normal way – using RNA polymerase enzyme to make messenger RNA, which can then be used to make proteins in a cell's ribosomes.

RNA viruses are trickier. Sometimes they work by using an enzyme called reverse transcriptase, which makes DNA from RNA. The HIV-1 virus responsible for AIDS is an example. Other RNA viruses, such as human polio viruses, use another enzyme, RNA replicase, which makes copies of RNA directly. RNA viruses usually encode the enzymes that they need for reproduction, to ensure a sufficient quantity of the enzyme.

So how does a viroid reproduce, given that it consists of RNA, but doesn't code for any special enzymes, or any proteins at all? The process isn't well understood, as the following explains:

Viroids: Molecular Vestiges Of The RNA World (5/17/09)

As opposed to plant viruses, which encode proteins that mediate their own replication and movement, viroids depend exclusively on host factors for these purposes. Viroids replicate through an RNA-based rolling circle mechanism with three steps: i) synthesis of longer-than-unit strands catalyzed by a host nuclear or chloroplastic RNA polymerase that reiteratively transcribes the initial circular template, ii) processing to unit-length, which remarkably is mediated by hammerhead ribozymes in the family Avsunviroidae, and iii) and circularization resulting from the action of an RNA ligase or from self-ligation.

Among the many pending issues, how viroids redirect the template specificity of certain host DNA-dependent RNA polymerases to transcribe RNA, is one of the most challenging. In addition, viroids must recruit host factors for their intracelular, cell-to-cell and long-distance movement within the plant. There are also pending questions in this context, the most appealing of which is how members of the family Avsunviridae gain access into the chloroplast; because essentially no other RNA has been reported to traffic inside this organelle, the answer to this question may reveal novel transport pathways in plant cells.

In order to understand what this is saying, the first fact needed is that viroid RNA comes in the form of a circle – no loose ends. In this respect, it is somewhat like bacterial DNA, which consists partly of circular loops of double-stranded DNA, called plasmids.

The interesting part is that viroids are apparently replicated by RNA polymerase, which normally produces RNA from a DNA template, rather than an RNA template. The process is called rolling circle replication, because the enzyme may travel around the loop a number of times, since there are no clear start and stop points. Later, in a separate operation, an RNA enzyme (ribozyme) of the host, cuts the multiply copied segments of viroid RNA back into unit segments, which join at the ends to form a circle again.

What's especially interesting about viroids is that they may give some insight into mechanisms that would be important in the RNA world hypothesis. This is the idea that before proteins existed, or even DNA itself, there was RNA – see here for some recent findings about how RNA itself may have originated.

RNA is capable of carrying genetic information just as DNA does – after all, that's what happens in RNA viruses. The main problem is how it was possible for RNA to reproduce itself. Viroids hardly give us a complete answer to this problem, since proteins (such as RNA polymerase) are still required for replication. But at least, in viroids, we have an example of a replicating entity that consists entirely of genetic information, with no proteins of its own.

Further reading:

Viroids and Virusoids

Hubble Photographs a Planetary Nebula

Hubble Photographs a Planetary Nebula to Commemorate Decommissioning of Super Camera

This planetary nebula is known as Kohoutek 4-55 (or K 4-55). It is one of a series of planetary nebulae that were named after their discoverer, Czech astronomer Lubos Kohoutek. A planetary nebula contains the outer layers of a red giant star that were expelled into interstellar space when the star was in the late stages of its life. Ultraviolet radiation emitted from the remaining hot core of the star ionizes the ejected gas shells, causing them to glow.

In the specific case of K 4-55, a bright inner ring is surrounded by a bipolar structure. The entire system is then surrounded by a faint red halo, seen in the emission by nitrogen gas. This multi-shell structure is fairly uncommon in planetary nebulae.

Kohoutek 4-55 – click for 946×710 image

More: here

Why Do We Rape, Kill and Sleep Around?

The "new" Newsweek is running an article on the evolutionary psychology debate that seems heavily slanted to one side. There seem to be some confusions in the article. They leave a bad impression of its objectivity.

Why Do We Rape, Kill and Sleep Around?

Over the years these arguments have attracted legions of critics who thought the science was weak and the message (what philosopher David Buller of Northern Illinois University called "a get-out-of-jail-free card" for heinous behavior) pernicious. But the reaction to the rape book was of a whole different order. Biologist Joan Roughgarden of Stanford University called it "the latest 'evolution made me do it' excuse for criminal behavior from evolutionary psychologists." Feminists, sex-crime prosecutors and social scientists denounced it at rallies, on television and in the press.

Such commentary is entirely political and nonscientific. It hardly merits a moment's response. Of course heinous behavior is not justified even by facts that are beyond dispute. The fact that humans have hands and arms that can wield weapons, or can even kill with bare hands, does not excuse murder. Likewise, behavioral traits that can be explained by evolution do not excuse rape and killing. (As for "sleeping around", that is in a different moral category entirely, if in any moral category at all.) Nothing more needs to be said about this kind of inanity that the article offers up.

So on to more substantive issues.

Scientific objectivity tends to be the victim of its own special kind of rape when "philosophers" enter the scene. Too bad "philosophers" don't stick to their own business and limit the damage to their own ranks. Philosophers (and their even more badly behaved kin, the "theologians") have certainly left enough carnage in other scientific topics, such as embryonic stem cells.

But read the article yourself, and then consider its shortcomings.

Exactly how was it decided that "evolutionary psychology" and "mental modules" are coextensive hypotheses? It seems to me that EP could easily be valid without the stronger hypothesis of modules. Who is it that's insisting the two ideas are inseparable?

Same question regarding "universal human nature". EP can easily explain traits that have context-dependent behavioral expression. Likewise, why does "universal human nature" have to be taken to rule out context-dependency of behavior?

Clearly, brain organization is very complex. From a programming perspective, it would be expected to involve a lot of conditional logic. Evolution nevertheless produced the organization the brain has now. Why would that be limited to only the most simplistic forms of organization - straight-line coding that has no alternative paths and data dependencies?

How hard is it to imagine that certain traits evolved in older stages of the human brain (or pre-human brain, for that matter), but that these traits have been partly been modified in later stages, with override switches when appropriate?

A nebulous "flexibility" is itself a debatable hypothesis, and it smells of the vacuousness that EP is accused of. It needs its own scientific evidence before being accepted. New social and physical conditions (for example, very high population densities, unlike any that humans have experienced over multiple generations) may require further evolutionary reprogramming when the supposed flexibility can't handle the changes.

Are straw man arguments being proposed to make EP look bad, or do most EP proponents really believe hypotheses that are obviously stronger than necessary?

Although the article makes valid points, it seem rather slanted to use these points as arguments against EP. The article has lots of spin and preoccupation with political agendas, not so much scientific objectivity.

Tags: evolutionary psychology

The impending demise of the university

Don Tapscott, who is a business executive, author of more than a dozen books on technology, president of a think tank, and a part-time professor in a university school of management, implies a fairly provocative claim in this article: The impending demise of the university.

Actually, he stops short of predicting outright the demise of universities, but he does begin with this:

For fifteen years, I've been arguing that the digital revolution will challenge many fundamental aspects of the University. I've not been alone. In 1998, none other than, Peter Drucker predicted that big universities would be "relics" within 30 years.

He cites various social, economic, and technological trends that could support such a prediction. I tend to agree with the idea that significant changes lie ahead for universities as we know them today – changes larger in magnitude than have occurred in the past 50 years, at least, even if not ultimately catastrophic ones.

There will probably, in 50 years, still be universities around not too unlike the ones we know now. However, I would guess they will probably provide education to a significantly smaller part of the population than they do today.

I won't outline all the details of the argument; they're in the article. I just want to focus on a few key points.

Tapscott is fairly critical of the model of professors lecturing to large halls full of students:

The broadcast model might have been perfectly adequate for the baby-boomers, who grew up in broadcast mode, watching 24 hours a week of television (not to mention being broadcast to as children by parents, as students by teachers, as citizens by politicians, and when then entered the workforce as employees by bosses). But young people who have grown up digital are abandoning one-way TV for the higher stimulus of interactive communication they find on the Internet. In fact television viewing is dropping and TV has become nothing more than ambient media for youth — akin to Muzak. Sitting mutely in front of a TV set — or a professor — doesn't appeal to or work for this generation. They learn differently best through non-sequential, interactive, asynchronous, multi-tasked and collaborative. [emphasis added]

(Aside: Tapscott clearly is not a master of English prose.)

In fact, Tapscott is not saying anything new or surprising here. It's true that young people today have grown up amid much more ambient media than existed, say, 50 years ago. However, large lectures were not especially appealing to most students even 50 years ago – or probably ever.

We should recall what has traditionally been considered a better model for higher education, as expressed a few years ago by the Provost of Drexel University:

When asked to describe his ideal of higher education, President James A. Garfield described it as then Williams College President Mark Hopkins sitting on one end of a log with his student sitting on the other end. This image of the learned professor imparting the wealth of knowledge of culture and history, arts and science, to his student and protégé evokes images of Aristotle and Plato and the Akademia in Athens. Akademia – to Plato a place, a city park, in ancient Athens. To us a word that describes what we are about, what we do for others and ourselves, and what we can be.

It's no accident that Plato depicted Socrates as teaching through dialogs with his students. Obviously, that has not been economically feasible in most lower division courses (or many graduate level courses) in universities for a long, long time. Tapscott does eventually point out that technology may be able to make something like this interactive model viable more broadly in the future.

Tapscott decries what he calls the "industrial model" of education:

The basic model of pedagogy is broken. "Broadcast learning" as I've called it is no longer appropriate for the digital age and for a new generation of students who represent the future of learning.

In the industrial model of student mass production, the teacher is the broadcaster. A broadcast is by definition the transmission of information from transmitter to receiver in a one-way, linear fashion. The teacher is the transmitter and student is a receptor in the learning process.

Here's a paper (PDF) that gives some background on what Tapscott means by "industrial model":

The academic profession and academic institutions, as they exist in America today, were born of the 19th-Century importation of the model of the "research university" from Germany. The founding of Johns Hopkins on the German model (1867) and the appointment of Charles William Eliot (a strong proponent of the model) as president of Harvard (1869) are usually cited as definitive events of this movement. This German model introduced the idea of the university as a site where knowledge is "produced," as a research "factory" or "powerhouse," and it embraced the advancement of knowledge – that is, scholarly productivity – in specialized fields of investigation as its central goal. The metaphors of production, manufacture, and power reflect the origin and location of this academic model in the industrialized society and economy of Western Europe.

Tapscott believes that the exposure young people have had to the Internet and pervasive media has motivated them to demand a different approach to education. It's possible that this is true, but most reasonably intelligent students for many decades have felt the same way. Quite possibly students are better prepared to handle a different approach now. Speaking of today's students, Tapscott says

They're used to multi-tasking, and have learned to handle the information overload. They expect a two-way conversation. What's more, growing up digital has encouraged this generation to be active and demanding enquirers. Rather than waiting for a trusted professor to tell them what's going on, they find out on their own on everything from Google to Wikipedia. [emphasis added]

Tapscott seems to think that it's professors themselves who prefer the broadcast lecture model. The truth is that some people do enjoy presenting lectures, and some of them are very good at it. However, most lecturers (in my experience) are not very good at it, even when experts in their field. They may talk too fast, or too slow, lack organization, and can be just plain boring. This is quite likely an indication that the professors themselves don't enjoy preparing and presenting lectures. They'd rather be doing research, or even interacting personally with students. However that may be, Tapscott offers this advice:

The professors who remain relevant will have to abandon the traditional lecture, and start listening and conversing with the students — shifting from a broadcast style and adopting an interactive one.

I suspect most professors wouldn't have much objection to this approach – if only their employers could afford to pay current salaries at a much lower student-teacher ratio.

Economics is really the crux of the matter. Universities could not afford to make the change, nor could students (or their parents) afford to bear the cost. So here's where technology comes in: The solution is for those teachers who most enjoy lecturing, and do the best job of it, to have their lectures digitally recorded and made available on the Internet. This is not rocket science, now that high-speed Internet is spreading rapidly (though not rapidly enough), and practically every student has (at least in Western countries) Internet access. The only barriers now are economic, and the willingness of universities to adapt.

It's true that students give up some interactivity with the lecturer when not physically present in the same room. But when professors are freed from the chore of preparing and presenting live lectures, they may instead use Internet tools to interact with their students in models that are much more like a Socratic dialogs or Mark Hopkins on a log.

Tapscott has some additional recommendations as to how professors should change their style:

Second, they should encourage students to discover for themselves, and learn a process of discovery and critical thinking instead of just memorizing the professor's store of information. Third, they need to encourage students to collaborate among themselves and with others outside the university. Finally, they need to tailor the style of education to their students' individual learning styles. [emphasis added]

Has the point about the benefits of collaboration among students, and between students and knowledgeable teachers and experts, been made enough yet? No? Then Tapscott makes it again:

Some leading educators are calling for this kind of massive change; one of these is Richard Sweeney, university librarian at the New Jersey Institute of Technology. He says the education model has to change to suit this generation of students. Smart but impatient, they like to collaborate and they reject one-way lectures, he notes.

And once more for good measure:

Another fixture of old-style learning is the assumption that students should learn on their own. Sharing notes in an exam hall, or collaborating on some of the essays and homework assignments, was strictly forbidden. Yet the individual learning model is foreign territory for most Net Geners, who have grown up collaborating, sharing, and creating together online. Progressive educators are recognizing this. Students start internalizing what they've learned in class only once they start talking to each other, says Seely Brown: "The whole notion of passively sitting and receiving information has almost nothing to do with how you internalize information into something that makes sense to you. Learning starts as you leave the classroom, when you start discussing with people around you what was just said. It is in conversation that you start to internalize what some piece of information meant to you."

In point of fact, collaboration among students on homework assignments was not always strictly forbidden in the past. Wise educators (which doesn't necessarily mean all educators) have (as far as I can tell) always been quite aware that good learning goes on when students confer with their peers – especially peers who may have achieved a better grasp of the subject – or when students get together in groups to work on assignments. Good educators have always encouraged such things. (Tests should eventually sort out who has really learned something and who hasn't.)

I think there are two ideas that pretty much sum up this whole discussion. One is multi-way interaction (as opposed to reliance solely on 1-to-many lecturing). The second, not unrelated, is collaboration among educators and students, and especially among students themselves.

I also think it's pretty clear some ways the modern Internet is able to facilitate the implementation of both these ideas. Namely, things like: video lecture series, social networking tools, constantly improving search tools, online and open-access books, journals, and reference materials, collaboratively made encyclopedias, and on, and on....

Let me conclude by referring to something I wrote about two months ago, that is Clay Shirky's diagnosis of the impending demise of traditional media journalism. (See here.) Near the end was this:

[T]here is one possible answer to the question “If the old model is broken, what will work in its place?” The answer is: Nothing will work, but everything might. Now is the time for experiments, lots and lots of experiments, each of which will seem as minor at launch as craigslist did, as Wikipedia did, as octavo volumes did.

Journalism has always been subsidized. Sometimes it’s been Wal-Mart and the kid with the bike. Sometimes it’s been Richard Mellon Scaife. Increasingly, it’s you and me, donating our time.

In other words: collaboration among consumers of information.

Interesting parallel, wouldn't you say?

Why Are Galaxies So Smooth?

Why Are Galaxies So Smooth? (5/1/09)

Using NASA's Spitzer Space Telescope, an international team of astronomers has discovered streams of young stars flowing from their natal cocoons in distant galaxies. These distant rivers of stars provide an answer to one of astronomy's most fundamental puzzles: how do young stars that form clustered together in dense clouds of dust and gas disperse to form the large, smooth distribution seen in the disks of spiral galaxies like the Milky Way? ...

"When you look at the disks of galaxies in the infrared they are remarkably smooth. All of the older stars are evenly distributed. But stars aren't born that way; they're born in clusters and associations like the Pleiades cluster, or the association of young stars in the Orion constellation of our own Milky Way galaxy. So the question is - why are the disks of galaxies so smooth?" said team leader David Block of the University of the Witwatersrand in South Africa.

"Our analysis now answers the grand puzzle. By finding a myriad of streams of young stars all over the disks of galaxies we studied, we see that the mechanism for pulling the clusters of young stars apart is shearing motions of the parent galaxy. These streams are the 'missing link' we needed to understand how the disks of galaxies evolve to look the way they do," said Block.

NGC 2841 – click for 1750×940 image

More: here, here

NASA's Galaxy Mission Celebrates Sixth Anniversary

NASA's Galaxy Mission Celebrates Sixth Anniversary

This image is a blend of the Galaxy Evolution Explorer's M33 image and another taken by NASA's Spitzer Space Telescope. M33, one of our closest galactic neighbors, is about 2.9 million light-years away in the constellation Triangulum, part of what's known as our Local Group of galaxies.

... This combined image shows in amazing detail the beautiful and complicated interlacing of the heated dust and young stars. In some regions of M33, dust gathers where there is very little far-ultraviolet light, suggesting that the young stars are obscured or that stars further away are heating the dust. In some of the outer regions of the galaxy, just the opposite is true: There are plenty of young stars and very little dust.

Far-ultraviolet light from young stars glimmers blue, near-ultraviolet light from intermediate age stars glows green, near-infrared light from old stars burns yellow and orange, and dust rich in organic molecules burns red. ... This image is a four-band composite that, in addition to the two ultraviolet bands, includes near infrared as yellow/orange and far infrared as red.

M33 – click for 450×699 image

More: here

Previous M33 image: here

Easily Grossed Out? You Might Be A Conservative!

Easily Grossed Out? You Might Be A Conservative! (6/5/09)

Are you someone who squirms when confronted with slime, shudders at stickiness or gets grossed out by gore? Do crawly insects make you cringe or dead bodies make you blanch?

If so, chances are you're more conservative -- politically, and especially in your attitudes toward gays and lesbians -- than your less-squeamish counterparts, according to two Cornell studies.

The results, said study leader David Pizarro, Cornell assistant professor of psychology, raise questions about the role of disgust -- an emotion that likely evolved in humans to keep them safe from potentially hazardous or disease-carrying environments -- in contemporary judgments of morality and purity.

This press release doesn't explain how the link between conservatism and feelings of disgust is based, at least in part, on theories of an academic in Virginia named Jonathan Haidt.

I've written about this guy before: Moral neuropolitics and ideology. His pet theory is that morality in general arises out of several human characteristics that can be explained by evolutionary psychology (EP). While it is true that EP can be taken too far in "explaining" human nature, I think it also has a lot of validity and if used carefully it can give real scientific explanations for some things.

The problem I have with Haidt's theories is not because of EP. Rather it's because he singles out three evolved traits that he believes influence conservative theories of morality yet are generally disregarded in liberal theories. One of these traits is a serious concern about "purity" – which sort of means an aversion to "disgusting" things, without an attempt to provide reasonable justification for the feeling in specific situations (such as homosexuality).

Haidt thinks this suggests liberal theories of morality are inadequate. I think that he's wrong. It does not seem to me that just because a trait evolved in humans (when social and physical conditions were vastly different from those of the present) it follows that such traits should be important influences on morality under current conditions.

Further, not only are these inherited traits unreliable guides for moral theories, but they are insufficient to provide good foundations for moral principles that are important in modern conditions – such as concern for the welfare of the environment, aversion to warfare, and the need for limitations on exploitative behavior of elites. However, all this is a discussion for another time.

Returning to the research described at the top, it's reassuring that the investigators shared my concerns about the role of "purity" in moral judgment:

Liberals and conservatives disagree about whether disgust has a valid place in making moral judgments, Pizarro noted. Conservatives have argued that there is inherent wisdom in repugnance; that feeling disgusted about something -- gay sex between consenting adults, for example -- is cause enough to judge it wrong or immoral, even lacking a concrete reason. Liberals tend to disagree, and are more likely to base judgments on whether an action or a thing causes actual harm. ...

The research speaks to a need for caution when forming moral judgments, Pizarro added. "Disgust really is about protecting yourself from disease; it didn't really evolve for the purpose of human morality," he said. "It clearly has become central to morality, but because of its origins in contamination and avoidance, we should be wary about its influences."