Galileo data shows Jupiter's lightning associated with low-pressure regions

MADISON, Wisconsin—Images of Jupiter's night side taken by the Galileo spacecraft reveal that the planet's lightning is controlled by the large-scale atmospheric circulation and is associated with low-pressure regions.

The new findings were reported October 13, 1998 by Andrew Ingersoll at the 30th annual meeting of the American Astronomical Society's Division for Planetary Sciences.

"Lightning is an indicator of convection and precipitation," says Ingersoll, a professor of planetary science at the California Institute of Technology and member of the Galileo Imaging Team. "These processes are the main sources of atmospheric energy, both on Earth and on Jupiter."

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In a terrestrial hurricane, Ingersoll explains, the low pressure at the center draws air in along the ocean surface, where it picks up moisture. Energy is relased when the moisture condenses and falls out as rain.

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On Jupiter, energy is transferred from the warm interior of the planet to the visible atmosphere in a similar process. The new findings show that lightning occurs in the low-pressure regions on Jupiter, too.

"On both planets, the air spins counterclockwise around a low in the northern hemisphere and clockwise around a low in the southern hemisphere," Ingersoll says. "The lows are called cyclones and the highs are called anticyclones."

On Jupiter the cyclones are amorphous, turbulent regions that are spread out in the east-west direction. In the Voyager movies they spawn rapidly expanding bright clouds that look like huge thunderstorms. The Galileo lightning data confirm that convection is occurring there.

"We even caught one of these bright clouds on the day side and saw it flashing away on the night side less than two hours later," says Ingersoll.

In contrast, the Jovian anticyclones tend to be long-lived, stable, and oval-shaped. The Great Red Spot is the best example (it is three times the size of Earth and has been around for at least 100 years), but it has many smaller cousins. No lightning was seen coming from the anticyclones.

"That probably means that the anticyclones are not drawing energy from below by convection," says Ingersoll. "They are not acting like Jovian hurricanes."

Instead, the anticyclones maintain themselves by merging with the smaller structures that get spun out of the cyclones. "That's what we see in the Voyager movies, and the Galileo lightning data bear it out. Whether the precipitation is rain or snow is uncertain," says Ingersoll.

"Models of terrestrial lightning suggest that to build up electrical charge, both liquid water and ice have to be present. Rain requires a relatively wet Jupiter, and that's a controversial subject.

"Water is hard to detect from the outside because it is hidden below the ammonia clouds. And the Galileo probe hit a dry spot where we didn't expect much water."

Fortunately the Galileo imaging system caught glimpses of a cloud so deep it has to be water, according to findings to be reported at the conference by Dr. Don Banfield of Cornell University and an imaging team affiliate. Banfield showed images of the water cloud near the convective centers in the cyclonic regions.

These results appear in the September issue of Icarus, the International Journal of Solar System Studies.

"We know the water is there, and we know where it's raining," says Ingersoll. "This is a big step toward understanding how Jupiter's weather gets its energy."

 

Writer: 
Robert Tindol
Writer: 

Caltech Question of the Month: Is there any such thing as "earthquake weather"?

Submitted by Maureen Castro, Oakland, California, and answered by Kate Hutton, Seismologist, Caltech.

There is a popular notion that earthquakes happen more often in certain kinds of weather. Unfortunately, the description of the preferred weather varies geographically and with the person providing the description.

Traditionally, earthquake weather was still and sultry. According to Aristotle, earthquakes were caused by winds trapped underground. Less wind above the surface must mean more below, and hence earthquakes were more likely. In California, however, which frequently has hot weather, earthquakes are often associated with the Santa Ana condition. In particular, the Northridge quake, "the earthquake" that is currently on people's minds, happened on an unseasonably warm day. Case proven, right?

In actuality, earthquakes are caused by the accumulation of strain in the crust due to the motion of tectonic plates. Most hypocenters (the place where the quake starts, directly below the epicenter) occur at least five miles below the surface, for large quakes. What is going on in the atmosphere simply does not affect conditions at that depth. Weather doesn't even affect the temperature in a well-designed wine cellar!

Besides, we have to remember that Alaska has several times the number of earthquakes that we do here. In Alaska, earthquake weather is cold and snowy!

As an aside, weather could very easily influence the scale of the disaster caused by an earthquake. Consider the effect of Santa Ana winds on fires and the effect of rain on the ubiquitous California mudslide in your worst-case planning scenarios.

Crust of Tibetan Plateau is being squeezed by India and Asia, new study shows

PASADENA—Geophysicists have discovered why there are high plains and mountains in the Himalayas for trekkers to trek on. According to new data, the soft crust of the Tibetan Plateau is being squeezed like an accordion between the harder crusts of India and Asia.

According to Caltech professor of geophysics Donald Helmberger and his doctoral student Lupei Zhu, the results show for the first time that a portion of crust can be squeezed and thickened if plate tectonics is forcing a harder section of crust into another hard section. Before the current study, geophysicists were unsure whether the plateau was formed by actions in the mantle or more shallow movements of the crust.

In the August 21 issue of the journal Science, the researchers show that the northward tectonic motion of India is forcing the softer and younger crust of the Tibetan Plateau into the Qaidam Basin to the north. Like India, the crust of the Qaidam Basin is also old and hard.

Since the seismic data shows there is a dramatic change in the thickness of the crust at the edge of the Qaidam Basin, the researchers infer that the softer crust is being literally forced into a hard vertical wall beneath the surface.

Therefore, the crust of the Tibetan Plateau is being crammed up and thickened in the collision. In addition to providing uplift, the action is also grinding the materials laterally. The horizontal fault lines observed in the region also support this interpretation.

"This gives a different perception about how strong an old crust can be," says Helmberger. "There's a very sharp change in the thickness of the crust, from about 40 kilometers at the Qaidam Basin to about 60 kilometers at the Tibetan Plateau.

"Physically, this means the crust beneath the Qaidam Basin is like a solid wall," he adds. "This thing below the basin is cold and old and very tough."

Zhu and Helmberger's results come from raw data collected by the Institute of Geophysics at Beijing and the University of South Carolina during the joint PASSCAL project in the early 1990s. Zhu did some of the field work before entering Caltech in 1993 as a graduate student.

Zhu says he would like to return to Tibet for additional data at other sites, and both he and Helmberger think the work could herald a new understanding of how the crust figures into plate tectonics. 

Writer: 
Robert Tindol
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Mechanism of cell suicide determined by Caltech, MIT researchers

PASADENA—Biologists at MIT and Caltech have uncovered the chemical details of a mechanism that cells use to commit suicide. The work appears in the August 28 issue of the journal Science.

According to David Baltimore, president of Caltech and a Nobel Prize-winning biologist, his lab at MIT has succeeded in describing how roundworms known as nematodes kill off unwanted cells. The work is especially interesting, Baltimore says, because human beings have very similar proteins to those causing cell suicide in nematodes and, in fact, his lab can often substitute human proteins for the same results.

"All cells contain the machinery to commit suicide," Baltimore said prior to publication of the paper. "You can see this in a wide variety of events, such as a tadpole's resorption of its tail, local ischemia in a stroke victim's brain, and tissue destruction after a heart attack.

"Cell suicide is also one of the great protections against cancer." According to the current paper in Science, a common type of apoptosis, or cell suicide, involves three stable proteins found in nematode cells. These proteins are normally quiet, but can be readily triggered by death signals in such a way that the cell digests itself.

The three proteins are known as CED-3, CED-4, and CED-9. None of these proteins alone will kill cells, the research shows, but the three interact in such a way that CED-4 can signal CED-3 to begin the destruction process, while CED-9 acts as an inhibitor to CED-4.

The general outline of this particular pathway of apoptosis was discovered by MIT professor Robert Horvitz some years ago, but the details have never been understood until now, Baltimore says.

"We did all of this with proteins from a nematode where the pathway was first found, but the proteins all have human homologs," Baltimore says. These are Apaf-1, which is very similar to CED-4; Bcl-2, which is a homolog of CED-9; and mammalian cysteine protease zymogens that are analogous to CED-3.

Therefore, the cascade of reactions in nematode cells could very well resemble the manner in which the human body can cause cancerous cells to self-destruct. The work was supported by the National Institutes of Health. In addition to Baltimore, the authors are Xiaolu Yang and Howard Y. Chang. Yang is currently at the University of Pennsylvania.

Writer: 
Robert Tindol
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New Study Shows How Axons Find Their Way Home

Pasadena--Like a commuter trying to get to work during rush hour, a growing axon must thread its way through a throng of other axons that are headed in many different directions in the developing brain. Axons are the wire like extensions of nerve cells that carry electrical signals from one place to another in the brain, and during development they must navigate across long distances (many centimeters) to reach their correct address within the brain. If the axon gets lost, brain circuits cannot form normally, and, like the commuter showing up at the wrong office, the axon may not be able to do its job. So how do axons find their way? A report published in the July 24 issue of the journal Science. by Drs. Susan Catalano and Carla Shatz of the University of California at Berkeley, sheds light on how axons home in on their correct targets.

Traditionally, scientists studying the mechanisms of axon navigation thought in terms of molecular guidance cues. Molecules located in specific places in the brain can tell a growing axon "grow here," "don't grow there," or "make a left turn here." The collective distribution of these molecules in the developing brain forms a pathway that the axon can follow to get to the right place. But Catalano and Shatz suspected that the situation might be more complicated than that. The brain is too complicated, and the genome too small, for there to be a molecular address at every possible target location in the brain. They suspected that there might be another potential source of guidance cues for the growing axons: electrical activity itself. They decided to block electrical activity within the developing brain with a neurotoxin made by the Japanese puffer fish, and their suspicions were confirmed: in the absence of activity many axons fail to find their way to the correct address. Instead they become confused and wander into other regions they normally bypass. Dr. Susan Catalano, now at the California Institute of Technology, offers this analogy: "If the growing axon is like a car, then the highway pavement and traffic signals would be like the guidance molecules. Demonstrating that neural activity is critical for axon navigation is like adding a Global Positioning System into the mix; its a whole new level of information that the axon can potentially use to guide its way toward the appropriate target."

Catalano and Shatz studied axons that grow out from nerve cells located in a brain structure called the thalamus. During development these axons must navigate toward their correct target, the neocortex. The thalamus is a vital way station within the brain; all of the information coming from the sensory organs (such as the eyes, ears, and skin surface) passes through the thalamus on its way to the neocortex. The neocortex is the highly folded layer of neurons on the surface of the brain that is responsible for such functions as language processing; in other words, it is the brain structure that makes us uniquely human. The connections from the thalamus to the cortex are not randomly organized: specific groups of nerve cells within the thalamus (called nuclei) connect up to specific areas of the neocortex. This precise organization, or "map", is critical for proper brain function. In order to form this circuit correctly during development, groups of axons coming from specific places within the thalamus must navigate across the vast expanse of neocortex. They must bypass incorrect areas of the neocortex and choose just the right area to connect with, but without electrical activity, the axons become lost.

How might electrical activity produce this effect? While that is not currently known, clues can be found in studies of other regions in the brain. Previous work from Dr. Shatz's lab has shown that very early in development when the axons from the eye are still navigating toward their targets in the brain, waves of electrical activity sweep across the retina. This means that axons that are nearest neighbors are electrically active at the same time. Simultaneous activity could alter the molecular environment of the pathway through which the axons grow and allow cohorts of axons to keep together during navigation.

Ever since the pioneering work of Nobel laureates David Hubel and Torsten Wiesel, it has been known that the pattern of electrical activity carried by different sets of axons can influence the physical shape of the axons themselves. During the last phases of development, axons from the thalamus form many branches as they spread out through the neocortex to make their final sets of connections. These branches are literally shaped like the branches of a tree, and hence are called the "terminal arbor." Changes in the axon's pattern of electrical activity can change the shape of the tree that forms; less activity results in a shrunken, knarled axon tree. Surrounding axons with normal levels of activity form many more branches that grow into the shrunken tree's territory, just like their counterparts in nature that grow into the sunlit space created when a neighbor falls.

While the role of electrical activity in the final stages of thalamic axon branch formation had been well established, the possibility that the same process might be crucial in early development during axon navigation remained uninvestigated until now. The clinical implications of this are potentially alarming: drugs such as nicotine, which can affect electrical activity within the brain, have the potential to disrupt circuit formation in a developing infant's brain at very early stages, when the major circuits of the brain are being formed. The possibility that developing brains are vulnerable to disruption by activity-altering agents at such early times suggests important areas for future research.

Brain cells attuned to visual nearness and farness interact to allow judgments of size, research shows

PASADENA—Evolution has been benevolent to humans and other primates in providing us with eyes that can judge the size of nearby objects.

With a visual feature known as "size constancy," we can pretty accurately judge whether the furry thing walking across our field of view is the size of a mouse or the size of a lion, regardless of its distance and whether we recognize the object. Where survival of the species is concerned, the advantage of having size constancy is pretty obvious: it helps us identify dinner, but at the same time helps us stay off someone else's menu.

But the precise neurological nature of size constancy has never been well understood. If we are seeing our very first lion and the lion is walking away from us, then his image in our field of vision is getting smaller and smaller. Distance cues and stereoscopic vision are at play, but what is really happening in our brains? Is the third dimension added on at a late stage in visual processing, or are the images of lions at varying distances actually analyzed at the very first stage of visual perception?

New research from the California Institute of Technology shows that the latter is the case. Our brains need information for object and three-dimensional scaling, and this information is common to all visual cortical areas of the brain.

In the July 24 issue of Science, Caltech biology professor John Allman and his colleagues write that brain cells involved in vision tend to be apportioned to picking up farness or nearness. In working with rhesus monkeys trained to follow dots of varying size on a moving TV monitor, the researchers have found that the monkeys use their nearness and farness cells in tandem.

"The perception of depth is the product of the interaction of the two opposed tendencies, near and far," says Allman. "There are many systems in the body, and several in the visual system, which work by the precise counterbalancing of two opposed tendencies.

"For color perception, for example, you have opposition between black and white, red and green, and blue and yellow," he adds. "So our results show that depth perception is also a fundamental opposition."

Thus, the basic idea is that ability to judge the size of objects is embedded in the primary visual center as a code of opposed interaction of "nearness" and "farness" cells. Therefore, the neurons are pooled for depth perception; lab work with monkeys earning rewards for correct depth identification bears this out.

In addition to Allman, the authors are Jozsef Fiser of the University of Southern California; and Allan C. Dobbins and Richard M. Jeo of the Caltech Division of Biology.

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Robert Tindol
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Caltech Question of the Month: What is really happening when we have aftershocks after an earthquake?

Submitted by Gloria Hughes, Pasadena, California, and answered by Lucile M. Jones, Seismologist, U.S. Geological Survey/Visiting Research Associate, Caltech.

Earthquakes occur in clusters. In any cluster, the earthquake with the largest magnitude is called the mainshock, anything before it is a foreshock, and anything after it is an aftershock. A mainshock will be redefined as a foreshock if a subsequent event has a larger magnitude. Aftershock sequences follow predictable patterns as a group, although the individual earthquakes are random and unpredictable.

Aftershocks usually occur geographically near the mainshock. The stress on the mainshock's fault changes drastically during the mainshock and that fault produces most of the aftershocks. Sometimes the change in stress caused by the mainshock is great enough to trigger aftershocks on other, nearby faults, and for a very large mainshock sometimes even farther away. As a rule of thumb, we call earthquakes aftershocks if they are at a distance from the mainshock's fault no greater than the length of that fault. For example, the fault rupture length was 15 km (10 miles) in the 1994 Northridge (M6.7) earthquake, and 430 km (270 miles) in the 1906 San Francisco (M7.8) earthquake.

An earthquake large enough to cause damage will probably be followed by several felt aftershocks within the first hour. The rate of aftershocks dies off quickly: the decrease is proportional to the inverse of time since the mainshock. This means the second day has about 1/2 the number of aftershocks of the first day and the tenth has about 1/10 the number of the first day. These patterns describe only the mass behavior of aftershocks; the actual times, numbers and locations of the aftershocks are random. We call an earthquake an aftershock as long as the rate at which earthquakes occur in that region is greater than the rate before the mainshock. How long this lasts depends on the size of the mainshock (bigger earthquakes have more aftershocks) and how active the region was before the mainshock (if the region was seismically quiet before the mainshock, the aftershocks continue above the previous rate for a longer time). It can be weeks or decades.

Bigger earthquakes have more and larger aftershocks. The bigger the mainshock, the bigger the largest aftershock will be, on average. The difference in magnitude between the mainshock and largest aftershock ranges from 0.1 to 3 or more, but averages 1.2 (a M5.5 aftershock to a M6.7 mainshock, for example). There are more small aftershocks than large ones. Aftershocks of all magnitudes die off at the same rate, but because the large aftershocks are already less frequent, the decay can be noticed more quickly. We have large aftershocks months or even years after the mainshock.

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Robert Tindol
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Parent that takes care of offspring tends to outlive the other parent, study shows

PASADENA--The parent who stays home to take care of the kids may be getting a good deal healthwise. New primate research from the California Institute of Technology shows that a primary caregiver tends to live longer than the other parent.

In a statistical study of 10 primate species, including humans, apes, and various Old and New World monkeys, the Caltech researchers show that the parent that cares for the offspring is significantly longer lived than the mate, regardless of gender. Titi monkey males of South America, for example, which take care of the baby after the mother has given birth, outlive their mates by 20 percent.

"The numbers show that if there is a difference in role, the sex doing the bulk of the care is likely to survive longer," says John Allman, a Caltech biology professor who is lead author of the study.

"This follows from the fact that it takes a lot of energy to raise a big-brained offspring like a human or an ape or a monkey," he adds. "The sex not caring for the infants will not be as crucial for the survival of the species."

The size of the brain is the key, Allman says. Species with big brains mature slowly and have only one baby at time, and these babies depend on their parents for a long time.

"Big brains are very expensive," Allman says. "They are costly in terms of time, energy and anatomical complexity. This reduces the reproductive potential of the parents because extra-special care must be provided to insure that this reduced number survive to reproductive age."

In an article appearing in the current issue of the journal Proceedings of the National Academy of Science, Allman and his coauthors outline their data from the 10 species of primates. To determine the lifespans of males and females that have borne offspring, the researchers analyzed the data from zoo populations, field studies, laboratory research, and human historical and demographic documents.

The researchers were especially interested in reviewing field studies as well as zoo data to ensure that artificial effects were not skewing the data. However there is also data from natural populations of primates that supports this hypothesis.

"Female gorillas, orangutans, and chimpanzees have a proportionally larger survival advantage than human females," Allman says. But the advantage of female gorillas is not so pronounced, and this could very well have to do with the fact that male gorillas play with their offspring and take on certain other nurturing duties.

In fact, the Caltech hypothesis is not only that the caregiver who takes care of the offspring tends to outlive his/her mate, but also that the effect disappears when parents share in caregiving more or less equally.

Perhaps for this reason human males and females also have lifespans that are fairly similar in length. The current figure is about 8 percent, but does not take into consideration the fact that medical care has significantly reduced the death rate from childbirth. Swedish demographic data from the late 1700s, by contrast, shows that females lived about 5 percent longer than their mates in those days, when childbirth was a leading cause of death in women.

The demographic data of the 10 primate species shows remarkable conformity to the hypothesis. In all of the primates studied in which females are the primary caregivers-spider monkeys, gibbons, orangutans and gorillas-females live significantly longer than males. Human female live longer than males, but the difference is smaller than in these primates and the male role is larger although less than the female role in childrearing.

In the two primates studied in which females and males share caregiving more or less equally, there is no difference between the survival rates of the sexes. In the two primate studies in which males have a larger role in caring for offspring, the owl monkey and the titi monkey, males live longer than females. The effect is significant for the owl monkeys, but not for titi monkeys because of the smaller sample available for these animals.

Allman acknowledges that the results are somewhat counterintuitive: many people think that child raising is quite stressful, and if anything should shorten the life of a harried parent. But just the opposite is true.

"There's probably not one single reason that the caregiver outlives the other parent," he says. "Risk taking in males and estrogen in females are probably factors, and there may even be a beneficial hormonal or chemical change that occurs through extending care to another.

"There's evidence that greater longevity can also coincide with the taking care of an elderly parent or even a pet," he concludes.

"So it could be that taking care of others is just good for you."

The other authors of the paper are Andrea Hasenstaub, a junior majoring in mathematics and engineering at Caltech; Aaron Rosin, a former Caltech student who graduated with a degree in biology; and Roshan Kumar, another Caltech graduate, who is now a researcher at the Scripps Research Institute in La Jolla, California.

Writer: 
Robert Tindol
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Biologists discover fundamental genetic principle governing blood vessel formation

PASADENA--An unsuspected but fundamental genetic rule governing the formation of the cardiovascular system has been uncovered by biologists at the California Institute of Technology. The discovery could influence the development of therapies for both cardiovascular disease and cancer.

According to Caltech biology professor and Howard Hughes Medical Institute Investigator David Anderson, the new findings arrive amid an explosion of new information about the molecular basis of blood vesveins "have to 'talk' to each other to develop properly," says Anderson. The findings may help explain how an intact circulatory system, with the correct proportion of arteries and veins, can be put into place before the heart even begins to beat. The research appears in the current issue of the journal Cell.

By "talking," Anderson is referring to the major finding of the study, which is that complementary molecules found on surfaces of primitive arteries and veins must interact with each other for proper blood vessel formation to occur.

The findings may have broad implications, Anderson suggests. "One should reconsider the molecular biology, pathology, and drug therapies of the vascular system in terms of the molecular differences between arteries and veins." It is likely, says Anderson, that arteries and veins will differ in their expression of many other genes that have yet to be discovered. Such genes may lead to the development of new artery- or vein-specific drugs, or may help to target known drugs specifically to either arteries or veins. Such advances could potentially enhance the efficacy or specificity of blood vessel-directed anticancer drugs such as those discovered by Dr. Folkman. They could also aid in the treatment of diseases that selectively affect either arteries or veins.

Specifically, the Anderson team found that a molecule known as ephrin-B2, present on developing arteries, must communicate with its receptor Eph-B4, present on developing veins. These proteins are expressed by endothelial cells, the first cells that form primitive vessel-like tubules in the embryo and that go on to form the inner lining of arteries or veins. This process appears to be a fundamental interaction for the development of the embryo. If it fails to occur, embryonic development is blocked almost as soon as the heart begins to beat.

The discovery actually occurred when Anderson's graduate student, Hai Wang, was performing a gene knockout experiment to see if the ephrin-B2 gene is essential for the development of the nervous system. When Wang eliminated the gene that codes for ephrin-B2 in mouse embryos, he found no nervous system defects, but did notice that there were defects in the forming vascular system and heart.

The procedure involved the substitution of a "marker" gene that makes cells turn blue where the ephrin-B2 gene would normally be turned on. The result revealed, surprisingly, that the ephrin-B2 gene was expressed in arteries but not veins. Wang then showed that the receptor for ephrin-B2, Eph-B4, was expressed on veins but not arteries. Eph-B4 and ephrin-B2 fit together in a lock-and-key-like manner, signaling each cell that the other has been engaged. This complementarity was seen on vessels throughout the developing embryo. The fact that elimination of the ephrin-B2 gene caused defects in both arteries and veins suggests that not only do arteries send a signal to veins via ephrin-B2, but that veins must also signal back to arteries. The fact that both ephrin-B2 and Eph-B4 span the cell membrane suggests that each protein may be involved in both sending and receiving a signal.

Writer: 
Robert Tindol
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Posthumous Paper by Gene Shoemaker Details Evidence of Comet Shower That Pummeled Earth 36 Million Years Ago

PASADENA—Geochemical evidence from a rock quarry in northern Italy indicates that a shower of comets hit Earth about 36 million years ago.

The findings not only account for the huge craters at Popagai in Siberia and at Chesapeake Bay in Maryland, but posit that they were but a tiny fraction of the comets active during a period of two or three million years during the late Eocene period. The work provides indirect evidence that a gravitational perturbation of the Oort comet cloud outside the orbit of Pluto was responsible for sending a wave of comets swarming toward the center of the solar system.

In a paper published today in the journal Science, a group from the California Institute of Technology, the U.S. Geological Survey Flagstaff office, and the Coldigioco Geological Observatory in Italy, report their evidence of a very large increase in the amount of extraterrestrial dust hitting Earth in the late Eocene period. The writers include the husband-and-wife team of Gene and Carolyn Shoemaker. Gene Shoemaker died in a car crash last year while the research was in progress.

According to lead author Ken Farley, a geochemist at Caltech, the contribution of Shoemaker was especially crucial in the breakthrough.

"Basically, Gene saw my earlier work and recognized it as a new way to test an important question: are large impact craters on Earth produced by collisions with comets or asteroids," Farley says.

"He suggested we study a quarry near Massignano, Italy, where seafloor deposits record debris related to the large impact events 36 million years ago. He said that if there had been a comet shower, the technique I've been working on might show it clearly in these sediments."

Carolyn Shoemaker said that she and her husband went to Italy last year to perform field work in support of the paper.

"Gene was pretty excited about the work Ken was doing," she said. "He was glad Ken was taking it on. It's exciting work, and it's a rather new type of work."

The matter involved detecting the helium isotope known as 3He, which is rare on Earth but common in extraterrestrial materials. 3He is very abundant in the sun, and some of it is ejected from the sun as solar wind throughout the solar system. The helium is easily picked up and carried along by extraterrestrial objects such as asteroids and comets and their associated dust particles.

Thus, arrival of extraterrestrial matter on Earth's surface can be detected by measuring its associated 3He. And even this material is unlikely to include large objects like asteroids and comets. Because these heavy, solid objects fall into the atmosphere with a high velocity, they melt or vaporize, giving their helium up to the atmosphere. This 3He never falls below very high altitudes, and soon reenters space.

But tiny particles entering the atmosphere are another story. These particles can pass through the atmosphere at low temperatures, and so retain helium. These particles accumulate on the seafloor, and seafloor sediments provide an archive of these particles going back hundreds of millions of years.

Elevated levels of 3He would suggest an unusually dusty inner solar system, possibly because of enhanced abundances of active comets. Such an elevated abundance of comets might arise when a passing star or other gravity anomaly kicks a huge number of comets from the Oort cloud into elliptical, sun-approaching orbits.

When Farley took Shoemaker's suggestion and traveled to the Italian quarry, he discovered that there was indeed an elevated flux of 3He-laced materials in a sedimentary layer some 50 feet beneath the surface. Because this region of Italy was submerged in water until about 10 million years ago, the comet impacts and microscopic debris had accumulated on the ocean bed, and this debris was preserved because dying organisms had cooperatively covered the debris over the eons.

The depth of the sedimentary layer suggested to the researchers that the 3He had been deposited about 36 million years ago. This corresponds to the dating of the craters at Popagai and Chesapeake Bay.

More precisely, the 3He measurements show enhanced solar system dustiness associated with the impacts 36 million years ago, but with the dustiness beginning 0.5 million years before the impacts and continuing for about 1.5 million years after. The conclusion is that there were a large number of Earth-crossing comets and much dust from their tails for a period of about 2.5 million years.

In addition to Gene and Carolyn Shoemaker and Ken Farley, the paper was cowritten by Alessandro Montanari, who holds joint appointments at the Coldigioco Geological Observatory in Apiro, Italy, and the School of Mines in Paris.

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Robert Tindol
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