The Hanging of Goodwife Knapp in 1653

Roger Knapp was born about 1618 in England and came to New England in the early 1640s. He eventually settled in Fairfield in the colony of New Haven in 1644 (now Connecticut). Not much is known about Roger Knapp except that he is listed as a farmer and an Indian trader.

His wife is known only as "Goodwife" Knapp—a title that’s equivalent to "Mrs." Knapp in modern times. (Sometimes shortened to “Goody”. Women with a higher status in society were referred to as “Mistress.”) In 1653 Goodwife Knapp was accused and convicted of witchcraft and executed by hanging in Try’s field outside the village of Fairfield. (None of the witches executed in New England were burned at the stake.)

Nothing is known of the trial of Goodwife Knapp or what she was accused of. This was right in the middle of the epidemic of witch trials and executions in England and Scotland and the phenomenon naturally made its way to the new colonies. Typically, the witch was accused of associating with the Devil, sometimes intimately. The “evidence” was usually a series of unusual happenings that occurred in the presence of the accused, or strange behavior that was deemed to be inappropriate. In many cases, the accused women seem to be rather more outspoken than others—in other words, they didn’t know their proper place.

Men who were accused of witchcraft were also people who were not satisfied with the status quo.

One of the books put on line by Googel is The Salem Witch Trials: a Reference Guide (by K. David Goss). It recounts the trial of Anne Hibbins who was hanged in 1656.

Anne Hibbins (1656) was censured by Boston church leaders for her contentious behavior in repeatedly accusing a local craftsman of overcharging for his labor. She was furthermore charged with supplanting her husband’s position in dealing with this problem, violating the puritan belief that wives should submit themselves to the leadership of their husbands. For this offense, she was unrepentant. She was removed from membership in the Boston church and found guilty of witchcraft in 1654 after the death of her husband. Although the magistrates denied the initial vedict, a second trial was held before the Massachusetts Great and General Court. Anne Hibbins was convicted a second time of witchcraft and executed in 1656. In his assessment of this tragedy, Governor Thomas Hutchinson, in his "History of Massachusetts," places the blame for this conviction upon the people of Boston who disliked Anne Hibbin’s contentious nature. He wrote that the trial and the condemnation of Anne Hibbins for withcraft was "a most remarkable occurrence in the colony," for he found tha is was her temper and argumentative nature that caused he neighbors to accuse he of being a wtich.

It’s very likely that Goodwife Knapp was hung for the same reasons three years earlier in Fairfield in the New Haven Colony.

The remarkable thing about the Goodwife Knapp execution is not the trial itself but the aftermath. Roger Ludlow, the Deputy Governor of Connecticut, had been fighting on and off for several years with his neighbor Mary Staples (wife of Thomas Staples, also known as Staplies). In 1651 Ludlow won a suit against Mary Staples for slander but this did not put and end to their dispute.

During the trial and imprisonment of Goodwife Knapp, Roger Ludlow and his supporters tried to get her to affirm that Mary Staples was a witch but Knapp refused. Just before the execution, Ludlow claimed that Goodwife Knapp came down the ladder and whispered in his ear that Mary Staples was, indeed, a witch.

Ludlow told this story to his friends, Rev. John Davenport and his wife, and it soon spread to the entire village of Fairfield. Accusing someone of witchcraft was a very serious charge—especially just after Goodwife Knapp had been hanged. When Thomas Staples heard that Ludlow was making these accusations against his wife he filed a defamation suit against Roger Ludlow.

The trail took place in May, 1654. There are several accounts on the internet taken from books that have recently been scanned. The best and most readable is from The Witchcraft Delusion in Colonial Connecticut by John M. Taylor. This is from the trial records and some of the descriptions are quite graphic, particularly the account of the examination of Goodwife Knapp’s body for witch’s teates.

There’s another good account in Witch-Hunting in Seventeenth-Century New England: A Documentary History 1638 ... by David D. Hall.

The role of the Sherwood family in the trial is described in A Changing America: Seen Through One Sherwood Family Line 1634-2006.

The reason for my interest in this trial is that many of my ancestors lived in Fairfield at the time and their names are mentioned in the account. Some of my ancestors were friends of the Staples and defended Mary Staples while others sided with Roger Ludlow. Ludlow lost the case and he left Fairfield the following year (1654), making his way eventually back to England and then to Ireland where he remained for the rest of his life.

By an extraordinary coincidence, my good friend and former best man at my wedding, Charles Beach, is a descendant of Mary Staples and Thomas Staples. Their daughter, Mary Nicol Staples (1630-1677) married John Beach (1623-1677).

My living relatives might be interested in our connections to the trial: here they are.

These are ancestors of Isabelle Hooper Burns (1862-1923) the mother of my maternal grandfather. More specifically, they are direct ancestors of her mother’s mother, Esther Treen (1807-~1891).

Here are the names of people mentioned in the defamation lawsuit. Our direct ancestors are underlined. (Some of these have subsequently been proven to be incorrect = strikeout.)

John Banks (1619-1684), attorney for Thomas Staples. (He is my great⁹-grandfather. Most of the others are from this generation or one generation earlier: great¹⁰)

Witnesses Andrew Ward (1597-1659) and his wife Hester Ward = Hester Sherman (1606-1666).

Witnesses: Goodwife Barlow = Ann Ward (?-1684) and her husband John Barlow (1599-1674)

Witness: Goodwife Sherwood = Mary Onge? second wife of Thomas Sherwood (1586-1655). Thomas' first wife, my ancestor, was Alice Tiler¹ (1585-1635).

Witness: Goodwife Odell (Odill) daughter-in-law of John Odell (1574) and Joan Bingley (1581-1640).

Witness: Mr. Jones is John Jones (1591-1665).

Witness: Goodwife Lockwood is Susan (Susanna) Norman (1616-1661) wife of Robert Lockwood (1600-1658).

Witness: Deborah Lockwood (1636-?), 17 years old at the time of the trial and my great⁹-grandmother. She is the daughter of Robert Lockwood and Susanna Lockwood.

Witness: Thomas Lyon (1621-1690).

Witness: Rebecca (Rebecka) Hull is Rebecca Jones, wife of Cornelius Hull and daughter of John Jones (1591-1665) and Sarah UNKNOWN (1599-1650).

Witness: Thomas Barlow was the second husband of Rose Sherwood, daughter of Thomas Sherwood (1586-1655) and Alice Tiler¹ (1585-1655).

Goodwife Pell is not an ancestor of mine but she has an interesting connection. She is Lucy Pell, wife of Thomas Pell who later founded Pelham, in what is now the Bronx, New York City [The Involvement of Thomas Pell's Family in the Witchcraft Persecution of Goody Knapp].

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1. Usually given as Alice Seabrook but this is almost certainly wrong according to A Changing America: Seen Through One Sherwood Family Line 1634-2006, Volume 1 By Frank P. Sherwood.

The drawing of the hanging of Ann Hibbins and the map of the colonies in 1650 are from the HTY277 website of the University of Maine at Farmington.

More Junk DNA Fallacies

 
BiOpinionated is a blog written by a molecular biologist named Nils Reinton. He tries to see every side of an argument but there are times when this attempt goes astray.

The "debate" over junk DNA is an example. Here's how Nils responed to claims by Ryan Gregory and me that most of our genome is junk [How to have your cake, eat it, and then complain].

First: State that most of our genome is junk.

Second: When more and more promoters, enhancers, repressors and other regulatory elements are discovered, claim that this of course was not included in the definition of “most of the genome”. The perfect excuse because it means you’ll never be wrong.

Last: Complain when the press does not understand that “most of our DNA” actually meant “much of our DNA , but with a lot of exceptions” and that science reporters don’t intuitively know which exceptions these are.

Post written using the zpen in dire agony over extremely poor science communication from the same persons who most eagerly criticize science communication from others.[see the original article for links - LAM]

Oh dear. There's so much wrong with the logic of this posting that I hardly know where to begin.

Nils is mostly upset about a recent posting on Genomicron: The Junk DNA myth strikes again (next up: media hype). This isn't very complicated so let me give you the short version.

Most of our genome is junk. That does not mean that all of our genome is junk and it certainly never meant (among intelligent scientists) that all of our non-coding DNA is junk. Here's a short list of non-coding DNA that is absolutely essential in our genome: all genes that produce functional RNAs instead of proteins; all regulatory sequences including enhancers; sequences that control splicing and other RNA processing events such as capping and polyadenylation; some 5′-leaders and 3′-tails of mRNA; chromatin domain markers (regulatory); scaffold attachment sites (SARs); some recombination hotspots; origins of replication; centromeres; telomeres.

Ryan was complaining about a paper that's about to be published in Molecular Biology and Evolution. The authors say this in their abstract.

Protein-coding sequences make up only about 1% of the mammalian genome. Much of the remaining 99% has been long assumed to be junk DNA, with little or no functional significance.

I agree with Ryan Gregory that this is extremely misleading. It implies that there are legitimate scientists who think that all non-coding DNA is junk. It would be far better to say something like this ...

Genes that encode proteins, and other genes, make up only a few percent of our genome. If you add in all of the other DNA sequences that are known to be essential you still can only account for no more than 5% of our genome. Most of the rest is thought to be junk DNA with no biological function. There are no respectable scientists who think that none of it will ever be shown to have a function but the general consensus among the defenders of junk DNA is that the vast majority of these DNA sequences, consisting mostly of defective transposons and pseudogenes, will turn out to have no function.

The authors of the paper go on to present evidence that about 5.4% of non-coding DNA has a function.

Big deal. That's not much more than what the textbooks have been saying for several decades.

Nils, there's an interesting debate going on about the amount of junk DNA in our genome. You're welcome to participate but please make sure you understand the issue and, please, don't spread false information. When we say that most of our genome is junk that does not mean that some of what we now consider to be junk DNA won't turn out to have a function. We're not that stupid—please don't imply that we are.

What we're saying is that the vast majority of DNA sequence in our genome is junk. I think the amount of junk is going to be >90%. That still leaves room for discovering a function for about twice as much DNA as we already know to be functional.

Get back to me when someone publishes solid evidence that more than 10% of our genome is essential.

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Monday's Molecule #137

 
Today's "molecule" is actually several molecules, one of which is shown in a diagram below the electron micrograph. You have enough clues to identify this virus. As soon as you get the right answer it will lead you directly to one or more Nobel Laureates.

The first person to describe the "molecule" and name the Nobel Laureate wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only three ineligible candidates for this week's reward: Maria Altshuler of the University of Toronto, Philip Johnson of the University of Toronto and Ben Morgan of the University of North Carolina at Chapel Hill.

All of the recent winners are in a position to accept their prize so there haven't been any recent winners who donated the free lunch to a deserving undergraduate. Consequently, I do not have an extra free lunch for a deserving undergraduate so I'm not going to continue to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch. If you can't make it for lunch then please consider donating it to someone who can in the next round.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

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The "yuck factor"

 
We live in a society that values change and innovation¹ but some changes are too much to stomach. An example might be the proposal to eliminate pain and suffering in cattle raised in feedlots or chickens confined to huge barns (or cages).

"What's wrong with that?", you might ask. You might think that eliminating feedlots is a good thing, but that's not what's being proposed. Instead, the proposal is to genetically modify animals so they quite literally "feel no pain" (Shriver 2009).

The author of this proposal, Adam Shriver, is a philosopher and the suggestion should be treated as a thought experiment and not as a feat of genetic engineering that's about to be implemented by a major meatpacking company. Shriver is a vegetarian so he's familiar with the main arguments against eating meat.

One of those arguments is that the animals we eat are often raised under inhumane conditions where they suffer pain and psychological stress. If we can genetically eliminate pain and stress, then one of the main arguments against meat eating disappears. The logic is impeccable.

Vegans and vegetarians are not about to throw steaks on the BBQ. That's because the "pain and stress" argument isn't really behind their decision to avoid meat.² There are other, far more important, reasons behind their choice of food. What a thought experiment will do, hopefully, is get rid of illogical arguments and focus more attention on the real ethical questions that divide vegetarians and omnivores.

Which brings us to the "yuck factor." I don't read the journal Neuroethics where the Shriver paper was published. I learned about it in the September 5-11 issue of New Scientist [Pain-free animals could take suffering out of farming]. An editorial in that issue points out that in spite of rationality "... there is something deeply unsettling about an animal engineered to be pain free" [Pain-free animals would not be guilt-free].

Sometimes it's not easy to explain why something is unsettling. This is called the "yuck factor" in the editorial. The yuck factor is not always a reliable indicator of real ethical problem.

Some conservative commentators argue that the yuck factor is a reliable indicator that a moral Rubicon has been crossed. Yet all too often such distaste is irrational and a barrier to progress. Progressive thought often comes from ignoring such reactions and thinking things through logically instead.

The editorial argues that opposition to pain-free animals is not irrational. The "real" debate is whether factory farming is acceptable in the first place. It's perfectly respectable to oppose the development of genetically modified (GM) animals, according to the editors of New Scientist.

Maybe, maybe not, that's not the point. As Shriver points out, if you use the argument of pain and suffering then you are bound by rationality to support GM animals. Taking that argument off the table does not mean that you favor factory farms and meat-eating.

The arguments between vegetarians and omnivores often boil down to arguments based on emotions versus arguments based on rationality. I usually side with rationality (but not always).

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1. Sometimes this causes problems, such as when we get confused about the difference between "change" and "improvement." They are not synonyms.

2. And neither is the "ecology" argument. If we could prove tomorrow that raising free-range cattle on scrubland was more energy-efficient than trying to grow wheat on that same land, it wouldn't convert a single vegetarian.

Shriver, A. (2009) Knocking Out Pain in Livestock: Can Technology Succeed Where Morality has Stalled? Neuroethics published online Aug. 21, 2009 [SpringerLink] [doi: 10.1007/s12152-009-9048-6]

An Entire Generation Is Being Brainwashed

 
Kirk Cameron warns us that an entire generation is being brainwashed. You might be surprised at who gets the blame ...

You'll also be surprised at some of the other claims in this video. Have you ever wondered why we call them IDiots? Here's why ...

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How Bad Papers Get Published in Good Journals

 
Donald Williamson used to be a marine biologist. He has some strange ideas about evolution. He thinks, for example, that the reason why butterflies have distinct larval and adult stages is because they arose from the fusion of two separate species—a larva-like species and a butterfly-like species.

Lots of us have crazy ideas but it's a real challenge to get them published in the peer-reviewed literature, and that's how it should be. The reason why science is so successful as a way of knowing is, in part, because it's dominated by skepticism and a requirement for evidence-based rational thought. The system sometimes impedes the acceptance of real innovative ideas but not for long. What is does do successfully, however, is weed out the kooks. But even that doesn't work all the time.

The Proceedings of the National Academy of Sciences (PNAS) is a prestigious journal that's run by the National Academy of Sciences. Once elected to the academy, members have some special privileges when it comes to publishing in the journal. They can "contribute" one of their own papers, in which case they can have a great deal of influence on choosing reviewers, or they can "communicate" the paper of a friend or colleague, in which case they choose the reviewers and send the reviews to the editor of the journal.

It's easy to see the potential for abuse but the remarkable thing is that the process actually works quite well. The quality of papers "contributed" or "communicated" is, in general, no worse than that of papers published in other front-line journals. Two of my own papers were "contributed by" my former Ph.D. supervisor and the process was a rigorous as any other.

But when the system fails, it fails spectacularly.

Lynn Margulis is a member of the National Academy. She "communicated" a paper by Donald Williamson on his strange idea about butterfly evolution (Williamson 2009). That's when the excrement hit the fan.

The editor of PNAS, Randy Schekman, has announced that the "communicated by" option for members will end in July 2010 [PNAS Nixes Special Privileges for (Most) Papers] The Science article reporting on this change in policy leaves little doubt about what prompted it.

An example of alleged gamesmanship popped up online 28 August in PNAS. Lynn Margulis, the noted biologist at the University of Massachusetts, Amherst, communicated a paper by Donald Williamson, a retired marine biologist in the United Kingdom. In it, Williamson promoted his longheld, intriguing—and, say most other biologists, almost certainly misguided—theory about the origins of caterpillars and butterflies. Current biological theory argues that they were always a single species and that each stage evolved via natural selection. Williamson argues instead that two distinct species (one caterpillar-like, one butterfly-like) somehow fused into a hybrid way back when. One species' sperm must have fertilized the other's eggs, transferring genes laterally across species in a non-Mendelian fashion.

Margulis was unavailable for comment, but Williamson says, "Lynn Margulis is prepared to put her name and reputation on the line" to prove that "genome mergers" occur in evolution, a position his paper supports. He also says he knows that Margulis sent his paper to a half-dozen academy reviewers. Williamson says that he thinks they were all positive reviews, but Margulis told Scientific American last week that she canvassed six or seven reviewers to find the two positive reviews necessary to push the paper through.

Shame on you, Lynn Margulis, You've made some outstanding contributions to biology over the years—endosymbioisis being the best example—but it's time to hang up your hat and retire gracefully. Your latest ideas are totally wacky and your inability to distinguish between science and fantasy—as evidenced in your promotion of the Williamson paper—is an embarrassment to those of us who, for several decades, have been holding you up as an example of a successful and creative scientist.

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Williamson, D.I. (2009) Caterpillars evolved from onychophorans by hybridogenesis. Proc. Natl. Acad. Sci. (USA) Aug 28, 2009 [Epub ahead of print] [PubMed] [doi: 10.1073/pnas.0908357106]

Monday's Molecule #136: Winner!

 
This is the Golgi apparatus. It's responsible for sorting and targeting proteins that have to be secreted or localized to internal vesicles. These proteins are inserted into the lumen of the endoplasmic reticulum (ER) during protein biosynthesis and from there they are partially modified and shuffled off to the Gorgi in small vesicles that bud off the ER and fuse with the membrane stacks shown in the image. While in the Gogi the proteins are further modified and targeted to the cell surface or peroxisomes or lysozomes. They travel to those locations in vesicles that bud off the edges of the Golgi disks.

The Nobel Laureate is Camillo Golgi who discovered the Golgi apparatus over 115 years ago.

This week's winner is Ben Ryan, an undergraduate from the University of North Carolina at Chapel Hill. He's the son of an old friend who's now the Managing Editor of American Scientist. It's scary when you realize that people who you remember as toddlers are now university students who can correctly answer Monday's Molecule. I'm hoping that Ben will be able to visit Toronto and collect his prize. I have stories to tell him that I can't put in writing.

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Today's "molecule" is an easy one in celebration of the start of a new academic year for many university students. Name this structure and provide a very brief description of it's function.

The Nobel Laureate should be obvious.

The first person to describe the "molecule" and name the Nobel Laureate wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.

There are only three ineligible candidates for this week's reward: Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany, Maria Altshuler of the University of Toronto, and Philip Johnson of the University of Toronto.

I have an extra free lunch for a deserving undergraduate so I'm going to continue to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow.

Comments will be blocked for 24 hours. Comments are now open.

---

Oct. 28-30: Reserve These Dates!

 

THE GAIRDNER FOUNDATION 50TH
ANNIVERSARY TORONTO SYMPOSIUM:

Wednesday, October 28- Friday, October 30, 2009

WEDNESDAY, OCTOBER 28, 2009

Gairdner 50^th Anniversary Symposium on Stem Cells, Disease Mechanisms and Future Therapies in collaboration with the McEwen Centre for Regenerative Medicine.

Location: Macleod Auditorium, University of Toronto

Time: 9am -12:45pm

Co-Chairs: Dr. Janet Rossant, Sick Kids Hospital, Toronto, ON
Dr. Gordon Keller,Director, McEwen Centre for Regenerative Medicine, UHN, Toronto

Introduction: Dr. John Dirks, President and Scientific Director,
the Gairdner Foundation

9.00-9:30
Shinya Yamanaka, Professor, Department of Stem
Cell Biology, Institute for Frontier Medical Sciences, Kyoto University, Japan

Induction of pluripotency by defined factors

9.30-10:00
Gordon Keller, Director, McEwen Centre for Regenerative Medicine, Toronto, ON.

Directed differentiation of pluripotent stem cells to functional tissues

10.00-10:30
Andras Nagy, Senior Investigator Samuel Lunenfeld Research Institute, and Canada Research Chair in Stem Cells and Regeneration ,Toronto, ON

Transposon-mediated reprogramming provides a powerful exploratory tool for understanding stem cell induction

10.30-10:45 Break

10.45-11:15
Mario Cappechi, Distinguished Professor of Human Genetics and Biology, University of Utah School of Medicine, Salt Lake City, Utah

Stem cells of the intestine

11.15-11:45
Phillip Sharp,Institute Professor, Massachusetts Institute of Technology, Boston MA

The roles of small RNAs in stem cells

11.45-12:15
Samuel Weiss, University of Calgary, AB

Adult neurogenesis and the formation of social memories

12.15-12:45
Oliver Smithies, Excellence Professor of Pathology and Laboratory Medicine, University of North Caroline, Chapel Hill, NC

On being a scientist for 60 years

12.45 Reception

1:15-4:45 - Gairdner Global Health Symposium

Location: Dalla Lana School of Public Health, University of Toronto, 155 College Street, 6^th Floor, Toronto, ON M5T 3M7 Canada,

1:15-1:25

Introduction: Dr. John Dirks, President & Scientific Director, The Gairdner Foundation

Welcome: Dr. Jack Mandel, Director, Dalla Lana School of Public Health, University of Toronto

The Global Health Stage

Chair: Kiyoshi Kurokawa, Professor, National Graduate Institute for Policy Studies, Tokyo

1:25-1:40
Jeff Koplan, Director of Global Health, Emory University

What's global health and why is it important?

1: 40-1:55
Tachi Yamada, President of Global Health Program, Gates Foundation

Innovation and access in global health

1:55-2:10Mark Walport,Director, Wellcome Trust.
Building capacity

2:10-2:25
Peter Singer, Director, McLaughlin-Rotman Centre
for Global Health, University Health Network and University of Toronto

Global health: why Canada should care and what Canada should
do.

2:25-2:45
Discussion

2:45-3:00 Break

The Challenge of Chronic
Disease

Chair:Alan Bernstein, Executive Director, Global HIV Vaccine Enterprise

3:00-3:20
Nubia Munoz, Inaugural Canada Gairdner Global Health award recipient

Burden of cancer associated with infectious agents in developing countries.

3:20-3:35
John Sulston, Cambridge, UK
What is Science for anyway?

3:35 -3:50
Margaret G. McGlynn, President, Merck Vaccines, Merck and Company Inc.
The evolving global vaccine landscape

3:50-4:05 Prabhat Jha, Director, Centre for Global Health Research, University of Toronto
Death and tobacco taxes

4:05-4:20
Richard Peto,Professor of Medical Statistics and Epidemiology, Co-Director, CTSU, Oxford University
Halving adult mortality worldwide

4:20-4:40 Discussion

4:40-4:45 Conclusion

Dr. John Dirks, President and Scientific Director, the Gairdner Foundation

1:30-4:45 -The Cell: An Endless Frontier

Location: Macleod auditorium,
University of Toronto

1:30-1:40 Introduction

1:40-2:00pm
Elizabeth Blackburn, Morris Herzstein Endowed Professor in Biology & Physiology, Department of Biochemistry & Biophysics University of California, San Francisco
How cells - and organisms - respond to perturbing their telomere maintenance

2:00-2:20pm
Ulrich Hartl, Max- Planck Institute for Biochemistry, Martinsried, Germany

The cellular machinery of protein folding: Molecular chaperones in health and disease

2:20-2:40
Avram Hershko, Technion Institute of Technology, Haifa

Roles of ubiquitin-mediated protein degradation in cellular regulation

2:40-2:55 Coffee Break

2:55-3:15pm
Bob Horvitz, David H. Koch Professor of Biology, Massachusetts Institute of Technology, Boston and Investigator, Howard Hughes Medical Institute

Genetic control of programmed cell death in C. elegans

3:15-3:35pm
Victor Ambros,Professor, Department of Molecular Medicine, University of Massachusetts Medical School, Worcester, MA

Small RNAs in every corner of the cell

3:35- 3:55
Gary Ruvkun,Professor of Genetics, Harvard Medical School

A C. elegans endocrine system that couples detection of xenobiotic drugs to regulation of reproduction and longevity

3:55 - 4:15
Robert G. Roeder, Arnold and Mabel Beckman
Professor, Laboratory of Biochemistry and Molecular Biology, Rockefeller University, NY

Transcriptional regulatory mechanisms in animal cells

4:15- 4:35pm Richard Axel, Investigator, Howard Hughes Medical Institute and University Professor, Columbia University, NY
Topic TBA

4:35pm Concluding Remarks

THURSDAY, OCTOBER 29, 2009

7:15 - 9:00am -
Gairdner Industry Breakfast, Unclogging the Pipeline: Rejuvenating drug discovery
Location: MaRS Centre, MaRS Collaboration Centre Auditorium


Moderator:Cal Stiller, Chair, Genome Canada/Bioquest Innovations Inc. /Ontario Institute for Cancer Research and Professor Emeritus, University of Western Ontario; Toronto, ON


Speakers:
Philip Sharp, Institute Professor, Massachusetts Institute of Technology; Cambridge, MA

Corey Goodman, Past President, Biotherapeutics and Bioinnovation Center, Pfizer Inc.; San Francisco, CA
David Baltimore, President Emeritus, Robert Andrews Millikan Professor of Biology, California Institute of Technology; Pasadena, CA

Please RSVP by email tothegairdner@gairdner.org, include the first and last name of the total number of guests attending.

9:00 - 3:00 -2009 Canada Gairdner Recipients' Lectures, The Charles Hollenberg Symposium

Location: JJR Macleod auditorium, University of Toronto

9:00am Dr John Dirks, Welcoming remarks

9:15 -9:45am Dr. Peter Walter, Professor, Department of Biochemistry, University of California, San Francisco Investigator of the Howard Hughes Medical Institute, CA,
Protein homeostasis in health and
disease

9:45-10:15am Dr. Kazutoshi Mori, Professor, Department of Biophysics, Graduate School of Science, Kyoto University, Japan
The unfolded protein response: To
mammals and beyond

10:15-10:30 Coffee Break

10:30-11:00am Dr. Lucy Shapiro, Director, Beckman Center for Molecular and Genetic Medicine,Professor, Developmental Biology, Stanford University School of Medicine, Stanford, CA
The systems architecture of the bacterial cell cycle

11:00-11:30am Dr. Richard Losick, Professor, Microbial Development and Gene Regulation, Harvard University, Cambridge, MA
Developmental biology of a simple organism

11:30-12:00pm Dr. David Sackett, Professor Emeritus, Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, ON
On the tribulations of not performing
randomized trials

12:00-1:00pm Lunch Break

1:00-1:05 John Dirks, Introduction of the Inaugural Canada Gairdner Global Health Award

1:05-1:45 Dr. Nubia Munoz, Emeritus Professor, National Cancer Institute, Bogota, Colombia and Visiting Scientist, Catalan Institute of Oncology, Barcelona
From causality to prevention: the case of cervical cancer

1:45-2:15 Dr. Shinya Yamanka, Professor, Department of Stem Cell Biology, Institute for Frontier Medical Sciences, Kyoto University, Japan
Induction of pluripotency by defined factors

2:15- 2:45 Dr. Sydney Brenner, Distinguished Professor, The Salk Institute, San Diego
Humanity's genes

FRIDAY OCTOBER 30, 2009

8:45-3:00-Gairdner/Nobel and Gairdner Laureate Forums

Location: Convocation Hall, University of Toronto
All sessions will present a moderated panel discussion,
followed by Q&A from the audience.

Friday's events are free but registration is required.
Click here.

8:45-10:15amAttack and Repulsions: Infections and the Immune System

Dr. David Baltimore (Moderator), Robert Andrews Millikan Professor of Biology, California Institute of Technology, CA

Dr. Ralph Steinman, Henry G. Kunkel Professor & Sr. Physician, The Rockefeller University, New York

Dr. Emil Unanue, Paul & Ellen Lacy Professor, Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO

Dr. Rolf Zinkernagel, University of Zurich, Zurich, Switzerland


10:30-12:00pm The Metabolome: Food and Fuel for Thought

Dr. Joe Goldstein (Moderator), Julie and Louis A. Beecherl Distinguished Chair in Biomedical Science, Southwestern Medical Center, University of Dallas, TX

Dr. Jeff Friedman, Marilyn M. Simpson Professor, The Rockefeller University, New York

Dr. Tony Pawson, University Professor, Program in Molecular Biology &Cancer, Samuel Lunenfeld Research Institute, Toronto

Dr. Michael Brown, Paul J. Thomas Chair in Medicine, Southwestern Medical Center, University of Texas, Dallas, TX

Dr. Ron Evans, Professor, Salk Institute for Biological Studies, La Jolla California

2:00-3:30pm Cancer: Can New Insights into Biology Yield Better Results?

Dr. Michael Bishop (Moderator) Chancellor, University of California, San Francisco

Dr.Harald zur Hausen, Professor Emeritus, German Cancer Research institute, Heidelberg, Germany

Dr.Dennis Slamon, Chief, Department of Hematology, Oncology, University of California, Los Angeles

Dr. Bob Weinberg, Professor of Biology, Member, Whitehead Institute, MIT, Cambridge, MA

Dr. Barry Marshall, International Research Foundation for Helicobacter and
Intestinal Immunology, Virginia

7:00- 8:30pm
The Personalized Genome: Do I Want to Know?

Dr. Michael Hayden, Director and Senior Scientist, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver

Dr. Sydney Brenner, Distinguished Professor, The Salk Institute, San Diego

Charles Sabine, Award winning NBC News correspondent and carrier of the gene for Huntington's Disease

If you need more information please contact Sheila Robinson at

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Oklahoma Museum of Natural History vs. The Discovery Institute

 
The anti-science movie Darwin's Dilemma is an attempt to discredit evolution by pointing to "problems" with the evolution of animals during the early to mid-Cambrian.

The IDiots who promote this movie were clever enough to have arranged for a showing at the Sam Nobel Oklahoma Museum of Natural History, a museum associated with the University of Oklahoma. The IDiot IDEA Club of the university knew full well that the museum is legally obligated to host public lectures regardless of how unscientific they might be.

Here's a brief description of Student's IDEA Clubs from their website.

Intelligent Design and Evolution Awareness (IDEA) Clubs are student-initiated clubs on high school and college campuses where students can promote scientific evidence that supports intelligent design. IDEA Clubs are a growing network of student-led clubs on university and high school campuses around the United States, and worldwide.

Today there is a great inequality in the science classroom. Students in most public or private high schools and universities are not exposed to the full range of scientific evidence and opinions about how living organisms arose and diversified. IDEA Clubs help fill the gaps in science education by providing the opportunity for students to educate their fellow students, friends, and even faculty about scientific evidence for intelligent design theory and problems with evolutionary theory. By this, people are naturally challenged by the metaphysical implications of the scientific evidence.

Naturally, the scientists at the museum are upset about this. It prompted the Museum Director, Michael A. Mares, to issue a disclaimer on the museum's website: An Open Letter from Dr. Michael A. Mares, Museum Director.

The Sam Noble Oklahoma Museum of Natural History is dedicated to science and to elucidating the remarkable evolutionary history of life on Earth. The museum actively engages in public programs, undergraduate and graduate education, outreach education, and other efforts to increase the scientific literacy of visitors to the museum and the people of Oklahoma.

Although the museum does not support unscientific views masquerading as science, such as those espoused by the Discovery Institute, the museum does respect the religious beliefs of all people. Moreover, the museum is obligated to rent its public space to any organization that is engaged in lawful activities, free speech and open discourse. The museum does not discriminate against recognized campus organizations based on their religious beliefs, political philosophy, scientific literacy, or any other factors.

We invite everyone interested in an accurate description of how life developed over the last four billion years to visit our galleries. The well-organized and scientifically accurate exhibits illustrate – through real specimens and scientific methods – the fact of evolution by natural selection as first described by Charles Darwin and continually supported by all branches of science ever since that time. The museum also recommends that people interested in evolutionary science review the more than 1,000 publications by our curators and professional staff that are based in evolutionary biology.

The museum's many galleries will be open for free before and after the showing of the Discovery Institute’s film "Darwin’s Dilemma" on Sept. 29 so the public can see that there is no scientific controversy in evolutionary science's explanation of the development and history of Earth's biodiversity.

This calendar year – the 150th anniversary of the publication of Darwin’s On the Origin of Species – the museum, in partnership with OU departments of Zoology, the Department of Botany and Microbiology, the Department of Anthropology, and the History of Science and History of Science Collections of the OU Library, has presented more than 15 public education programs related to evolution, with many more on the calendar ahead. We encourage the public to take part in these programs, many of which are free, to educate themselves about the true nature of the science of evolutionary biology.

Well said, and opening up the museum free of charge before and after the movie is a brilliant move.

Now the next question is, when are the IDiots actually going to get around to fulfilling their promise to present real evidence for Intelligent Design Creationism? So far, all we've seen is scientifically amateurish attempts to discredit evolution.^1.

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1. While the attempts are scientifically at a kindergarten level, they are often dressed up in all the glitz and glamor of a Hollywood production. Most people aren't fooled by this, right? Please tell me I'm right.

Mary Travers (1937 - 2009)

 
The first video is an anti-war protest in Washington in March 1971. The second is a very special appearance of Peter, Paul, & Mary with John Denver singing Leaving on a Jet Plane.

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Darwin's Dilemma

 
The students in my class have to read Icons of Evolution by Jonathan Wells. (Nobody said university was going to be fun!)

One of the "icons" is Chapter 3: Darwin's Tee of Life where he discusses the Cambrian explosion and why it refutes evolution. Scientists know this isn't true but the IDiots persist in their attmepts to use any means possible to challenge evolution.

The latest attempt is Darwin's Dilemma, a movie that's promoted on the IDiot web sites [Darwin's Dilemma, New Intelligent Design Film, Due Out Sept. 15]. It's about to be released. If you pay good money to buy the DVD then make sure you take something to settle your stomach. Oh yes, don't forget that if you see the movie in public, you mustn't laugh out loud, that's not polite.

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A Good Example of Framing?

 
This video is making the rounds on all the commie liberal blogs. It deserves to be seen by everyone—that's why I'm piling on. I wonder if our "framer" friends think it's the right way to promote social change?

Will a message like this ever be seen on television in the other countries that need to hear it?

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Chromosomes, Drift, and Demes

One of the characteristics of evolution is change in chromosome number and organization. These large-scale changes are often associated with speciation events although it would be a mistake to assume that there's a causal relationship.

One particular chromosomal rearrangement has been getting a lot of press recently because it has been featured on blogs and in some recent trade books on evolution.

Humans (H) have only 23 pairs of chromosomes while most other apes, such as the chimpanzee (C), have 24 pairs. Evidence for a fusion of two of these ancestral chromosomes into a single chromosome 2 in humans has been well supported by genome sequence data. Our fusion chromosome contains remnants of telomeres at the fusion point and it has another centromere-like region at just the right position.

Intelligent design proponents have a hard time explaining this event. They don't propose an explanation based on their concept of intelligent design—that would be too ridiculous—instead they concentrate on raising questions about evolutionary explanations. One of the common objections is that the new fusion chromosome would screw up mitosis and meiosis because it would initially have two centromeres. According to them, the chromosomal rearrangement would be detrimental and could never be fixed by natural selection.

As it turns out, the latter part of this statement is correct. Natural selection is not responsible for this kind of evolution. But no serious scientist would suggest otherwise.

The first part of the statement isn't as serious as the IDiots would like to think. Rearrangements of this sort aren't much of a problem. Many species are heterozygous for such rearrangements and we can see that it has little effect on the viability of dividing cells. Nevertheless, a newly rearranged chromosome is unlikely to be completely neutral. It's probably slightly deleterious with respect to the ancestral chromosome(s).

So, how does a slightly deleterious mutation become fixed in a population? The answer, of course, is random genetic drift. But in order to understand the importance of random genetic drift you have to understand the substructure of species. Species are usually subdivided into many smaller, locally inbreeding, populations or "demes." Slightly deleterious (nearly neutral) mutations can easily become fixed in a deme by accident.

Over at Panda's Thumb, Dave Wisker Arthur Hunt has been writing about chromosomal rearrangements and how they become fixed in a species. His latest essay talks about how fixation within a deme can lead to fixation by random genetic drift in the entire population: The Rise of Human Chromosome 2: Beyond the Deme.

This is a nice, short, explanation of a very important mechanism of evolution. I urge everyone to get on over to Panda's Thumb and read it right now.

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[Image Credit: This drawing is from: Chromosome Fusion: Chance or Design?. I don't know the original source.

The Old Cavendish Laboratory: Maxwell to Watson & Crick

 
For scientists, some places are more "holy" than others. Here's the story of one such place. "The moral of the story is that 'place matters'."

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How Granting Agencies Destroy Young Scientists

 
Peter Lawrence has an article in the latest issue of PLoS Biology: Real Lives and White Lies in the Funding of Scientific Research.

He's not saying anything we don't already know but he says it so well. Peter describes the typical example of a young researcher (K.) who is frustrated and discouraged by the way science is funded in the UK. The details may differ but it's the same basic story at universities in North America and everywhere else.

He then describes his own experience and highlights the problem.

After more than 40 years of full-time research in developmental biology and genetics, I wrote my first grant and showed it to those experienced in grantsmanship. They advised me my application would not succeed. I had explained that we didn't know what experiments might deliver, and had acknowledged the technical problems that beset research and the possibility that competitors might solve problems before we did. My advisors said these admissions made the project look precarious and would sink the application. I was counselled to produce a detailed, but straightforward, program that seemed realistic—no matter if it were science fiction. I had not mentioned any direct application of our work: we were told a plausible application should be found or created. I was also advised not to put our very best ideas into the application as it would be seen by competitors—it would be safer to keep those ideas secret.

The peculiar demands of our granting system have favoured an upper class of skilled scientists who know how to raise money for a big group [3]. They have mastered a glass bead game that rewards not only quality and honesty, but also salesmanship and networking. A large group is the secret because applications are currently judged in a way that makes it almost immaterial how many of that group fail, so long as two or three do well. Data from these successful underlings can be cleverly packaged to produce a flow of papers—essential to generate an overlapping portfolio of grants to avoid gaps in funding.

Thus, large groups can appear effective even when they are neither efficient nor innovative. Also, large groups breed a surplus of PhD students and postdocs that flood the market; many boost the careers of their supervisors while their own plans to continue in research are doomed from the outset. The system also helps larger groups outcompete smaller groups, like those headed by younger scientists such as K. It is no wonder that the average age of grant recipients continues to rise [4]. Even worse, sustained success is most likely when risky and original topics are avoided and projects tailored to fit prevailing fashions—a fact that sticks a knife into the back of true research [5]. As Sydney Brenner has said, “Innovation comes only from an assault on the unknown” [6].

You know, what's really puzzling about this phenomenon is not that we are unaware of the problem—it's that we haven't done anything about it. If the system isn't working then let's fix it.

There are several innovations that could fix the problem. Peter suggests that only the best papers from a lab should be evaluated and that young investigators could be interviewed by the granting agencies to evaluate promise. Others suggest that funds could be given to departments and the departments could distribute the money in the most efficient and effective manor.

Many scientists advocate shorter grant proposals with more of an emphasis on past productivity than on what's in the actual proposal. If you've been successful in the past then you will probably be successful in the future. It's time to stop rewarding grantsmanship and start rewarding science.

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