Kamis, 30 April 2009
This fish lives in waters well below freezing and only just above the freezing point of salt water (about -2C). If you went swimming in water this cold wearing a Speedo then, as Lewis Pugh discovered, your cells would freeze and consequently suffer quite serious damage. If you stayed in more than a few minutes you would die.
So how does the ice-fish survive? The answer is that it has evolved an antifreeze glycoprotein in its blood. The glycoprotein molecules bind to ice crystals and prevent them from growing to a size where they would damage the fish’s body. Although this has been known since the 1960's work continues in this area, for example this paper, One-pot synthesis of cyclic antifreeze glycopeptides from earlier this year.
Of greater relevance to today's lecture is the strange clear, almost transparent, appearance of the fish. They are sometimes referred to as 'white blooded' because their blood contains no hemoglobin. Lots of antifreeze and no hemoglobin! So how do the fish survive? Well, remember that solubility of oxygen increases as temperature decreases. So the frigid waters of the Antarctic have considerably more oxygen in solution. Furthermore the blood plasma can hold more oxygen at low temperatures (for the same reason) and the animal's metabolic rate is lower. So the icefish can deliver sufficient oxygen to their cells in the plasma without requiring hemoglobin as a specific oxygen-carrying molecule. Cool.
It is not known whether there is any link between these two phenomena. It is not actually necessary for there to be a selective advantage to the loss of hemoglobin to explain its dissapearance (remember genetic drift?) but I can't help but wonder whether there is a link. For example if the presence of hemoglobin reduces the efficiency of the antifreeze.
If you want to read more then this 2006 paper will get you into the literature: When bad things happen to good fish: the loss of hemoglobin and myoglobin expression in Antarctic icefishes.
Rabu, 29 April 2009
Posting a reference to Tim Noakes yesterday reminded me of his recent work with Lewis Gordon Pugh, a British 'Environmentalist, Explorer and Swimmer.'
Pugh is most famous for his cold water swims which he usually does to publicize global warming and the melting ice-caps. These swims are done without a wetsuit, in water as cold as zero degrees centigrade (because of the salt seawater freezes a couple of degrees below zero).
An article in New Scientist magazine a few months ago reveals some of the science behind Pugh's remarkable ability. Most interesting was the discovery by his trainer, the aforementioned Tim Noakes, that Pugh is able to consciously raise his body temperature.
As the swim gets closer, he psychs himself up by listening to music by the likes of Eminem and P. Diddy. In the minutes before entering the water, Pugh recalls these emotions and is able to raise his core temperature, without doing any physical exercise, to 38.4 °C. That's an extraordinary 1.4 °C above his normal body temperature. Such "anticipatory thermogenesis" has been observed before, but not to such a high degree.
You can read the actual paper in the appropriately named 'Journal of Thermal Biology': Body temperatures during three long-distance polar swims in water of 0–3 °C.
Pugh appears to have reached some of the limits of the human body:
In 2007 he swam 1 kilometre in the coldest water yet - a glacial -1.7 °C - at the geographic North Pole.
"When I went below 0 °C the cells in my fingers started to freeze. It took another four months before I could feel my hands again," he says. After reaching his goal of swimming both in the Arctic and in Antarctica, Pugh has for now hung up his towel.
Selasa, 28 April 2009
There's a simple answer, the heart doesn't have the same type of pain receptors as the muscles, but a fuller answer is much more interesting and shows some surprising gaps in our knowledge.
There are two types of muscle 'pain' associated with exercise. There is fatigue during exercise, and we don't really know what causes that, and there is pain after exercise (DOMS or Delayed Onset muscle Soreness), and we don't really know what causes that! The cause of fatigue is a pretty hot topic. One theory is that it is caused by a problem with the calcium flow inside muscle cells. One of the functions of calcium is to help control muscle contractions. Recent research published in PNAS found that after extended high-intensity exercise, small channels in the muscle cells begin to leak calcium, which leads to weakened muscle contractions. This leaked calcium also stimulates an enzyme that attacks muscle fibers and also leads to fatigue. It is really surprising to me that such a basic phenomenon is still fairly unknown.
DOMS is thought to be caused by a breakdown of muscle fibers and microscopic tears in muscle tissue that occurs as a result of exercise. This typically occurs 1 to 2 days after exercise, particularly if the exercise is new or extreme. There is also evidence that DOMS is more extreme if the muscle movement is eccentric - that is the muscle elongates whilst under tension (eg lowering a weight, starting out with your hand by your shoulder and gradually lowering the weight will produce an eccentric contraction of the biceps muscle).
It used to be thought that lactic acid was involved in both these phenomena but recent evidence suggests that lactic acid may have been unfairly blamed for years and that it may play a more useful role.
In both these cases actual pain is probably caused primarily by swelling which puts pressure on nerves and produces the sensation of muscle pain.
Although the heart does not have the same type of stretch receptor that registers this type of pain it does have some pain receptors. Strangely enough it has the same type of nerve receptors that register the burning sensation from the capsaicin in hot peppers. These are the receptors that are thought to cause the sensation of chest pain from a heart attack. The heart may be less vulnerable to DOMS since it does not undergo eccentric contraction.
All of this is somewhat complicated by the role of the brain. Obviously it is in your interest to stop exercising before damage occurs to your muscles, and, in particular, to your heart. Tim Noakes, a South African sports scientist, has renewed interest in a rather old theory, that Noakes calls the 'Central Governor Model', that the brain is the primary organ that dictates how fast, how long, and how hard humans can exercise.
As you can tell I find this whole intersection of physiology and exercise very interesting. So I have bitten the bullet and next quarter (ie Fall 2009) I will be teaching a CCS class on Endurance Physiology. This will be a seminar format class where we read and discuss papers very much like those listed above and look critically at the evidence for and against various theories and the implications these have for the way people train for what I have generally termed endurance events (swimming, cycling, and running or, for those crazy enough, all three). Loosely inspired by the fact that for the first time in over 25 years Santa Barbara will have a large Marathon event in the fall of 2009.
Senin, 27 April 2009
For many years, I have told students, “Do not do what I do; rather, take whatever I have to offer and do with it what I could never imagine doing and then come back and tell me about it.” My hope is that colleges and universities will be shaken out of their complacency and will open academia to a future we cannot conceive.
"Plant-insect interactions in tropical rain forest canopies - 10 million or 100 million species?"
Dr Lowman is Professor of Biology and Environmental Studies and Director of Environmental Initiatives, New College of Florida. Meg pioneered the science of forest canopy ecology, helping to develop the current techniques for canopy access and using them to study processes that maintain biodiversity in tropical forest canopies. Her most recent work focuses on environmental education and outreach, the role of science in environmental policy, and the development of research coordination networks (especially NEON).
Minggu, 26 April 2009
The answer is “NO”! This is a classic case of the common misunderstanding about the relationship between correlation and causation. Yes, there is a clear correlation between breast-feeding and a lower risk of diabetes and heart disease later in life, according to the study. But that is not proof that the act of breast-feeding is what reduces the risk. What if women who breast-fed their children are just more health conscious overall throughout life? What if they exercise more often, or have healthier diets?
A more correct headline would be “Breast-Feeding May Benefit Mothers, Study Suggests”. Indeed, the article itself goes on to say that some experts are cautioning that an association (between breast-feeding and health benefits) does not prove a causal relationship, and that more research would be needed to determine the exact cause of the effect (lower risk).
Jumat, 24 April 2009
Llama blood may one day be able to help soldiers, scientists and city officials set up an early-warning system against the tiniest weapons of terror--biological agents like anthrax and smallpox. Authorities have long worried that, were these diseases to get loose, it would be difficult to know anything was wrong until innocent people started dying. Llama blood might provide a better detection method.
How? Antibodies, the tiny molecules that float around in the bloodstreams of people and almost all animals. Antibodies keep a sort of "memory" of all the diseases, allergens and other foreign invaders your body has come into contact with. If the same infiltrator shows up again, the antibodies can match it up with their stored records and immediately know how to fight it.
For a while now, scientists have used genetically altered antibodies to help ID and treat specific diseases. But these techniques always ran into a common problem: Antibodies were just too delicate to be of much use outside a lab or hospital setting. Enter the llama.
According to news stories about the research, llamas have extraordinarily tough and hardy antibodies, capable of sustaining exposure to temperatures as high as 200 degrees F. This discovery gave the researchers the idea to develop sensors, based on llama antibodies, that could be distributed to soldiers in a war, or around cities back home. Modified to be specifically on the lookout for likely-to-be-weaponized diseases, these sensors could pick up signs of a biochemical attack before victims started arriving at the hospital.
Kamis, 23 April 2009
News articles on the upcoming change appeared in most major papers yesterday, including the Los Angeles Times.
Jessica Tyler from the Department of Biochemistry and Molecular Genetics University of Colorado School of Medicine - and a faculty recruitment candidate - will be speaking today (Thursday) at 3:30 in the Rathmann Auditorium in LSB on:
"Epigenetic Regulation of Gene Expression, DNA repair, aging and cancer"
Rabu, 22 April 2009
It's only a couple of steps from there to linking together all your equipment, adding in some simple algorithms for how the scientific process works, and you can go hang out on a beach whilst your lab equipment does its own experiments.
Sounds a bit futuristic? Nope, a recent paper in Science entitled 'The Automation of Science' describes just such a scenario. Scientists in England developed a robot named Adam to identify genes involved in yeast metabolism. Adam formulates hypotheses about the origins of enzymes for which scientists have been unable to identify the encoding genes. The robot then plans and executes experiments to test its hypotheses--selecting yeast mutants from a collection, incubating cells, and measuring their growth rates. Adam came up with 20 hypotheses about genes encoding 13 enzymes, 12 of which it confirmed.
There's a commentary on the paper in Science, the story was picked up by the media, but the best comment is in a New Scientist report:
'Will Bridewell, an artificial intelligence researcher at Stanford University in Palo Alto, California, says Adam is operating only at the level of a graduate student. '
Selasa, 21 April 2009
We will finish at ~9.50 so that you can attend Oliver Sack's talk in the Old Little Theater.
If you haven't read any of is work, take a look around his website and check out a couple of interesting recent articles, one in wired magazine on hallucinations, one from the New Yorker about music and amnesia, and an interview in Discover magazine: Your Brain on Music, Magnets, and Meth.
Senin, 20 April 2009
The UCSB brown-bag forum on spatial thinking Presents:
Kevin D. Lafferty, US Geological Survey
Marine Science Institute, University of California, Santa Barbara
Spatial and Temporal trends in global malaria: How do climate change and economics interact?
Ellison Hall 6824, 12:00 p.m. Wednesday, 22 April 2009
Abstract. Malaria is the most important infectious disease facing humans. Although it is largely a concern in tropical developing countries, a century ago its distribution extended well into upper latitudes presently occupied by developing countries. Because temperature and precipitation affect mosquito vectors and the plasmodium disease agent, transmission depends on climate. Projected climate changes may therefore alter where malaria will be a problem in the future. The discussion will briefly describe the ways that geographers have used spatial data to project future climate envelopes for infectious disease. It will then consider the relative importance of covariates that help explain a portion of the variation in transmission. By analogy, a paper by Kuhn (PNAS 2002) shows that wetland destruction and cattle farming do a better job explaining historical temporal variability in malaria in Britain than does climate variability. The main purpose of the discussion will be to pose the question of how to partition the effects of climate and economics on the spatial and temporal variation in malaria at the global scale. Knowing the relative roles of these factors would greatly help explain current patterns of transmission as well as identify future challenges and opportunities for diseases control.
Minggu, 19 April 2009
One percent per year is not fast enough for the heart to repair itself under natural conditions after a heart attack. But the fact that it occurs at all is giving researchers new hope. If future research were to improve our understanding of how cardiac muscle cell replacement is regulated, perhaps new drugs or treatments could be developed that would jump-start the process after a heart attack.
It could be decades before any patients are actually helped by the new findings, but that’s the way science goes…..a little breakthrough here, a little breakthrough there, and pretty soon there’s real progress!
Jumat, 17 April 2009
Sex chromosomes have evolved independently many times in both animals and plants from ordinary chromosomes. Much research on sex chromosome evolution has focused on the degeneration and loss of genes from the Y chromosome. Here, we describe another principle of sex chromosome evolution: bursts of adaptive fixations on a newly formed X chromosome.
UC Berkeley had a press release that summarizes the work quite nicely.
There were a number of relevant posts last year on the whole sex/mating/development issue:
- Haplodiploidy in social insects
- Question of the day
- Girls will be boys
- Channel 4
- Sniff and swim
- Miracle of life
- How do biologists ever reproduce?
Kamis, 16 April 2009
In this figure the parent cell has two homologous pairs of chromosomes (2n=4). This is shown in the diagram with two short lines and two longer lines. Each homologous pair is not identical because one was obtained from the mother and one from the father.
During the very first stage of meiosis the chromosomes replicate - each producing genetically identical sister chromatids that remain attached together at the centromere. These are not counted as separate chromosomes. So the chromosome number of the cell as it enters meiosis (second line) is still 2n=4. It is only during the second meiotic division, the last line on the figure, that they finally are separated and distributed into separate cells. However as soon as the joined chromatids are separated they are no longer called sisters because they are no longer connected to each other. Instead they are now called unreplicated chromosomes.
Next, virgin birth in Komodo dragons. Here's an interesting paper from Nature that answers most scientific questions on the phenomenon, and here are some press reports.
Speaking of hormones, which I think we were, Friday's Psychology Neuroscience & Behavior colloquium series talk will be by Dr. Laurence Tecott (UCSF) entitled
"BRAIN SEROTONIN SYSTEM REGULATION OF ENERGY BALANCE AND "LIFESTYLE" IN THE MOUSE"
The seminar will be held in Psychology 1523 on Friday April 17th at 4pm.
No one knows for sure. But well-meaning climate scientists who believe in tipping points warn of doomsday scenarios in an effort to get people to do something about global warming before it is too late. You’ve heard it all before - the Amazon rainforest will become grasslands; the polar ice caps will melt; the seas will rise several meters, flooding most of Earth’s populated areas; ecosystems will be disrupted. Some climate scientists worry that talk of tipping points could backfire. If a tipping point doesn’t happen within the next couple of decades, will people quit worrying about global warming altogether and decide it’s not worth doing anything about? Yawn! I’m bored with this whole subject…….
The best climate models can’t tell us yet whether or not there are tipping points. And therein lies the danger - there may actually be tipping points. Perhaps more likely is that lots of little tipping points in Earth’s complex climate system will add up to acceleration of global warming the higher the temperatures get.
For a recent news article on the subject, see “Among Climate Scientists, a Dispute Over ‘Tipping Points’”, The New York Times, Mar. 29, 2009.
Rabu, 15 April 2009
When original and interesting research is distorted to garner additional attention, both the work in question and previous studies can be shortchanged. Here, I will describe a recent and notable case from the journal Science in which the perceived novelty and importance of a study were significantly enhanced.
Selasa, 14 April 2009
How do the various processes that affect stomatal opening and closure coordinate their actions? What happens if the stomata get conflicting signals?
I just started to do some reading on this when I came across this amazing paper from 2006 describing how stomata close upon detection of potential microbial pathogens to prevent the infection of the leaf interior. That's pretty cool but they also show how pathogenic bacteria have evolved strategies to suppress the closure of stomata! This appears to be brand new research and I think it is both the first demonstration of the defensive role of stomata as well as the first demonstration of bacteria overcoming this defense.
The journal editors obviously thought was pretty cool too since there's a nice preview of the research.
Plant Stomata Function in Innate Immunity against Bacterial Invasion
Cell, Volume 126, Issue 5, 8 September 2006, Pages 969-980
Maeli Melotto, William Underwood, Jessica Koczan, Kinya Nomura and Sheng Yang He
Senin, 13 April 2009
In August three groups of plant molecular biologists finally pinned down the identity of florigen, a signal that initiates the seasonal development of flowers. The signal is the messenger RNA of a gene called FT. When days get long enough, this RNA moves from leaves to the growth tip, where the FT protein interacts with a growth tip-specific transcription factor, FD.
However if you click on the original article then you may notice the sentence 'This article has been retracted.'
After the first author (T.H.) left the Umeå Plant Science Centre for another position, analysis of his original data revealed several anomalies. It is apparent from these files that data from the real-time RT-PCR were analyzed incorrectly. Certain data points were removed, while other data points were given increased weight in the statistical analysis. When all the primary real-time RT-PCR data are subjected to correct statistical analysis, most of the reported significant differences between time points disappear. Because of this, we are retracting the paper in its entirety.
In new experiments, we have reproduced the floral induction caused by a heat-shock induction of FT in a single leaf, but we have failed to detect movement of the transgenic FT mRNA from leaf to shoot apex. We therefore retract the conclusion that FT mRNA is part of the floral inductive signal moving from leaf to shoot apex.Curious. After 70 years of elusivity (is that a word?) Florigen is not ready to give in yet.
Jumat, 10 April 2009
Not an athletic event, the Grunion Run is a remarkable annual occurrence where the little grunion fish comes ashore to spawn. Peak spawning season typically occurs from April through early June and the grunion runs occur late at night, twice a month, after the highest tides associated with a full or new moon.
Now you too can be a part of this:
A professor at Pepperdine collects data on grunion runs on California beaches and organizes "grunion greeters" to help collect the data. Members of our Bio departments have been involved every year thus far and will be involved this year as well. If you're interested in watching grunion runs and reporting what you see, Dr. Karen Martin will be coming to campus next Wednesday evening (April 15) to conduct a volunteer workshop in MSRB. Check out the flyer for more information.
Kamis, 09 April 2009
A comparative study of the effectiveness of the new DNA test (HPV test) versus the Pap smear (cytologic test) in preventing cervical cancer deaths was conducted in India with funds provided by the Bill and Belinda Gates Foundation. After just eight years, the study showed that the DNA test reduced cervical cancer deaths by nearly 50% compared to the Pap test. Significantly, not one woman whose DNA test for HPV was negative died of cervical cancer during the study period.
Watch the video here.
I think this is more of a commentary on teaching than it is a criticism of these students, or students in general.
Rabu, 08 April 2009
From 'The Adulthood' section
So you're in your early 20s and your brain has finally reached adulthood. Enjoy it while it lasts. The peak of your brain's powers comes at around age 22 and lasts for just half a decade. From there it's downhill all the way.
This long, slow decline begins at about 27 and runs throughout adulthood, although different abilities decline at different rates. Curiously, the ones that start to go first - those involved with executive control, such as planning and task coordination - are the ones that took the longest to appear during your teens. These abilities are associated with the prefrontal and temporal cortices, which are still maturing well into your early 20s.
Episodic memory, which is involved in recalling events, also declines rapidly, while the brain's processing speed slows down and working memory is able to store less information.
So just how fast is the decline? According to research by Art Kramer, a psychologist at the University of Illinois in Urbana-Champaign, and others, from our mid-20s we lose up to 1 point per decade on a test called the mini mental state examination
That all sounds rather depressing, but there is an upside. The abilities that decline in adulthood rely on "fluid intelligence" - the underlying processing speed of your brain. But so-called "crystallised intelligence", which is roughly equivalent to wisdom, heads in the other direction. So even as your fluid intelligence sags, along with your face and your bottom, your crystallised intelligence keeps growing along with your waistline. The two appear to cancel each other out, at least until we reach our 60s and 70s.
There's another reason to be cheerful. Staying mentally and physically active, eating a decent diet and avoiding cigarettes, booze and mind-altering drugs seem to slow down the inevitable decline.
Although some might find this depressing I was really quite excited by this article. I'd assumed I was getting senile MUCH quicker than this......
Selasa, 07 April 2009
Although innovative programs like the HeroRats organization can greatly speed up demining, there is a clear need for multiple tools to manage the growing problem. The Nitrogen dioxide detecting plants, RedDetect, I mentioned in class are now being developed by Aresa - a non-profit organization in Wallonia, a part of Belgium. Although Arabidopsis plants were originally used it was decided that, although they grow quickly, they were not visible enough from a distance (kind of important if you want to stand well back). Therefore the same technqiue has been applied to tobacco plants. The tobacco plant was chosen as it is known to grow well in a wide range of environmental conditions and any changes in colour can easily be seen because of its large leaves. The tobacco plants were transformed in the same way as the Arabidopsis with an activation gene from the snapdragon plant, which enables them to detect nitrogen dioxide, a by-product of landmines, in contaminated soil. This releases anthocyanin, a natural red plant pigment, into the leaves.
As of April 2009 the plants have already been successfully tested in laboratories and greenhouses and are now undergoing field trials in Serbia and South Africa. The plants only detect the mines of course, someone still needs to physically remove them...
One of the guys that took us into the minefield has stepped on 6 landmines. The first landmine blew off his foot. The next landmine took off half his leg. The next 4 blew his prosthetic leg to pieces, and he hopped down to the NGO for a replacement. Yet, he keeps going back into the minefields to illegally cut down trees that he can sell to the Thais for $5 a piece. This is how he feeds his family. And that is the life of a village de-miner.
From Adam Katz's blog entry about a visit to a Cambodian minefield.
Senin, 06 April 2009
In flowering plants, fertilization is unique because it involves two pairs of male and female gametes, a process known as double fertilization. Here, we provide an overview of the field and a detailed review of the outstanding recent advances, including in vivo imaging of double fertilization and the identification of a signaling pathway controlling the release of the male gametes and of a protein involved in gamete membrane fusion. These recent results are stepping stones for further research; our knowledge of double fertilization is expanding as newly discovered molecular pathways are explored and new mutants are characterized. Controlling plant fertilization is essential for seed production, and molecular understanding of double fertilization will provide the tools to improve crops and breeding programs.
Jumat, 03 April 2009
In 2005 scientists hit upon an ingenious method that takes advantage of a dark period in recent world history - the above-ground testing of nuclear weapons between the mid-1950s and 1963. Nuclear weapons testing resulted in a sharp spike in carbon-14 levels worldwide. The levels peaked in 1967 and have since declined as carbon-14 diffused and equilibrated with the atmosphere, the oceans, and the biosphere. Carbon is incorporated into the chemical components of all new cells, of course, including DNA. It turns out that the carbon-14 levels in nuclear DNA correspond very closely to the atmospheric levels at the time the DNA was synthesized. So by comparing the cells’ nuclear DNA carbon-14 levels to a chart of atmospheric cabon-14 levels each year, one can determine the cells’ birth date.
How does this help us determine cell turnover? Think about it: if all of the cells in a piece of tissue are the same age as the individual, then cells are not being replaced throughout life. But if the average cell age is much younger than the individual, then cell turnover must be relatively high. The scientists who developed the cell-dating technique report that neurons in the cerebral cortex (the most highly developed area of the brain) do not undergo significant replacement throughout life - you’re born with all the cortical brainpower you’re ever going to have. In contrast, cells lining the intestine are replaced frequently.
Reference: "Retrospective Birth Dating of Cells in Humans". Cell 122:133-143, 2005.
Costs of Changing Sex Do Not Explain Why Sequential Hermaphroditism Is Rare
The RR Warner in the acknowledgements and numerous citations is, of course, UCSB's Bob Warner who works, amongst other things, on sequential hermaphroditism in fish
Also, if you'd like to read the original Nature paper describing the Papaya story I mentioned you can find it here:
A primitive Y chromosome in papaya marks incipient sex chromosome evolution
Kamis, 02 April 2009
Extreme longevity in proteinaceous deep-sea corals
The "gold coral" Gerardia and the black coral Leiopathes both grow several meters tall at depths of up to 500 meters on the Hawaiian seabed. They grow when each succeeding coral polyp secretes a thin layer of calcium carbonate onto the base of the "cups" in which they live.
Previous studies had guessed their age at a few hundred years but the PNAS study by Brendan Roark and colleagues argues that what were previously counted as annual growth rings actually take much longer to form. Using high-resolution radiocarbon dating, Roark's team studied the corals' outermost shell for traces of "bomb carbon" - radioactive carbon produced during nuclear tests in the 1950s. They found it was present in only the upper 10 micrometres of the coral skeleton, suggesting this tiny slice took decades to build up. Further carbon dating of layers down at the corals' base revealed the oldest Gerardia to be about 2742 years old and the Leiopathes 4265 years old.
Rabu, 01 April 2009
Spring seminar series on Channel Island Restoration
Monday nights: 6-7pm, CCBER: Harder South, Rm 1013.
This series is supported in part by the students of UCSB through the
March 30th : Chris Still (UCSB Geography): Setting the Stage:
Background Geography of Channel Islands
April 6: Brad Keitt (Island Conservation): Protecting seabird
biodiversity by conserving islands: an integrated regional approach
April 13: Ken Owen & Duke McPherson (Channel Islands Restoration):
Invasive Plant Control on the Channel Islands
(Followed by pizza and discussion)
April 20^th : Kathryn McEachern (USGS): Rare Plant Research and
Restoration: California Channel Islands
April 27^th : Emily Howe (SERG, SDSU): Restoration on San Clemente Island
May 4^th : Lisa Stratton (CCBER): Limiting Factors to Oak Restoration
on Santa Catalina Island
May 11: Sarah Chaney (NPS Channel Islands): Weed Control and
Restoration on Anacapa Island
May 18^th : Steve Junak (Santa Barbara Botanic Garden): Rare Plant
Recovery on San Clemente Island
(Followed by snacks and discussion)
June 1: Final Discussion
Natalie R. Doerr PhD seminar
Wednesday, April 1, 2009 at 4:00pm Horvath Conference Room, Bio Sci 2 Bldg, Rm 6141
"Climate change and aquatic ecosystems on the west coast: Can we forecast responses and prepare for impacts?"
Daniel Schindler, University of Washington
Monday, April 6th, MSI Auditorium
Daniel is a broad community ecologist. However, he perhaps best known for his research looking at how climate change impacts fisheries, with an emphasis on salmon populations in Alaska.
From his website: My current research activities are focused generally on understanding the causes and consequences of dynamics in aquatic ecosystems. Of particular interest are (1) the effects of changing climate on trophic interactions and ecosystem services provided by aquatic ecosystems, (2) fisheries as large-scale drivers of ecosystem organization, (3) importance of anadromous fishes for linking marine ecosystems to coastal aquatic and riparian systems, and (4) the importance of aquatic-terrestrial coupling in the organization of aquatic ecosystems.