The Rewards of Repetitive Cruelty: A look at Stuart Zola-Morgan,
the newly appointed director of the Yerkes National Primate Research
Center, and the implied public message in his appointment.
August 1, 2001
researcher was studying grasshoppers. She sat a grasshopper
on the sterile white counter and said, "Jump grasshopper!
She carefully recorded the distance the insect had jumped,
and pulled off one of the grasshopper's legs. Then, once
again, "Jump grasshopper! Jump!"
Another measurement, another recording, and another leg;
"Jump grasshopper! Jump!"
This went on again and again.
One leg left. "Jump grasshopper! Jump!" the
researcher sternly demanded. She recorded: "Grasshopper
with one leg: .002cm"
Finally, the grasshopper is lying on the counter, on her
back with no legs. "Jump grasshopper! Jump!"
Nothing. Disappointed, this time slapping the table next
to the twitching critter, the researcher screamed as loudly
as she could, "Jump grasshopper! Jump!"
And she records: Grasshopper with no legs: Cannot hear."
Anonymous old joke
Yerkes may be the best known and perhaps the most prestigious primate-based
research facility in the nation. The decisions made concerning Yerkes
choice of research and directorship is closely watched by the National
Institutes of Health (NIH) and the rest of the vivisecting community.
The person chosen for the position probably has the approval of the
senior NIH staff. The choice of director may be viewed as a statement
by the NIH regarding what research methods are desirable. The directors
own research will be seen as an example of high caliber research and
will set the tone as he assumes the role of spokesperson for this
flagship facility. Of interest is the fact that the previous director,
Tom Insel, lost his position after being caught in less than factual
statements on national television as he tried to discredit a child
who had an encounter with an escaped monkey on her front porch. This
public relations blunder, coupled with the cover-up surrounding the
death a young lab worker at the facility, was too large an embarrassment
for Yerkes and NIH. Insel was reassigned.
The choice of Stuart Zola-Morgan to head Yerkes makes two strong interrelated
statements. The first concerns the nature, quality and methodology
of research that NIH finds worthy of high reward and showcasing. The
second concerns the public face being put on the research occurring
in the nations taxpayer-funded primate-based experimental programs.
This second reason for choosing Zola-Morgan is directly related to
the escalating battle between those suckling at the public teat who
are engaged in research that is being increasingly questioned on grounds
of ethics and efficacy and those calling the research into question.
Zola-Morgans research will be examined first.
Stuart Zola-Morgan has spent the last twenty years destroying various
parts of monkeys brains and then testing them to determine whether
they could still learn and whether they could remember what they had
Zola-Morgan explains his research:
|The resolution of many
issues surrounding the neuropsychology of memory depends
significantly on knowing the specific brain structures
that, when damaged, cause amnesia. During the course of
our work, we have successfully established a model of
human amnesia in the monkey, and we have been able to
identify a neural system of memory in the temporal lobe
that includes the hippocampal region (i.e., dentate gyrus,
the hippocampus proper, and subicular complex) and adjacent
cortical regions, i.e., entorhinal, perirhinal, and parahippocampal
cortices. Identification of the specific sites important
for memory has opened the way for more detailed neurobiological
investigations. Our work is relevant to issues of how
memory is organized in the brain and to issues of memory
impairment associated with a wide range of human conditions,
e.g., aging, Alzheimer's disease, and stroke.1
Zola-Morgans initial premise is illogical. Though damaging an
area of the brain associated with memory may result in amnesia, it
is illogical to assume that any amnesia arising from any brain injury
is an indication that the area damaged is involved in a direct way
with the phenomena of memory. Consider a much simpler system: an automobile.
Someone seeking to understand how an automobile works could, following
Zola-Morgans methods, destroy various components of a car, the
key for instance, and make various inferences. A naïve observer
might come to the conclusion that the key is a critical component.
Deep and careful study of the key itself would offer little insight
into the mechanics of internal combustion engines or modern transmissions.
The same observer might come to the conclusion that the seatbelt interlock
is important for the car to function when in actuality, the seatbelt,
the key, the gear shift lever, the parking brake, and other peripheral
devices are only marginally associated with the basic functions of
Further, even if one did determine that destroying the spark plugs,
for instance, interfered with the operation of the engine, one would
have little understanding of what the spark plugs do, or of course,
how to repair them once they were destroyed. In fact, Zola-Morgan
has acknowledged as much. The degree of memory loss in humans due
to brain injury is directly related to the size as much as the location
of the injury. In other words, if you have a small injury you dont
lose as much memory as you would if you had a larger injury. This
suggests that memory may be a widely dispersed dynamic phenomena rather
than a storing of experiences in discrete neural compartments. Zola-Morgan
|One idea that has emerged
from this work is that the severity of memory impairment
might increase as more components of the medial temporal
lobe are damaged. We have evaluated this idea directly
by examining behavioral data from 30 monkeys (ten normal
monkeys and 20 monkeys with bilateral lesions involving
structures within the medial temporal lobe) that have
completed testing on our standard memory battery during
the last 10 years. The main finding was that the severity
of memory impairment depended on the locus and extent
of damage to the medial temporal lobe. Specifically, damage
limited to the hippocampal region produced a mild memory
impairment. More severe memory impairment was produced
when the damage was increased to include the adjacent
entorhinal and parahippocampal cortices (the H+ lesion).
Finally, memory impairment was even more severe when the
H+ lesion was extended forward to include the anterior
entorhinal cortex and the perirhinal cortex (H++ lesion).
Taken together, these findings suggest that, whereas damage
to the hippocampal region produces measurable memory impairment,
a substantial part of the severe memory impairment produced
by large medial temporal lobe lesions in humans and monkeys
can be attributed to damage to entorhinal, perirhinal,
and parahippocampal cortices adjacent to the hippocampal
Most troubling is the fact that Zola-Morgan is not destroying various
parts of a car; he is methodically destroying parts of living monkeys
brains. To fully understand the unsettling nature of Zola-Morgans
experiments, it is necessary to first understand who his victims are.
Monkeys have been increasingly understood to possess complex minds
and emotions. Monkeys are used in experiments specifically because
they are capable of abstract thought3,
display emotion4, exhibit altruism5,
and maintain highly complex social relationships6.
These well-known characteristics should compel a basic ethical and
moral reconsideration of the experimental manipulations of these beings,
but the contrary is true among the primate experimentation community.
The close similarities of the most fundamental aspects of human-ness
and monkey-ness mind and emotion have been magnets for
exploitation by those without moral rudders; Zola-Morgan is an exemplar
of this phenomena.
Early in Zola-Morgans career he began destroying parts of monkeys
brains and pointing out that the resultant impairments were similar
to impairments seen in humans with similar brain damage. In 1981,
in the first of two
experiments, we compared the behavioral effects of inferotemporal
cortical lesions with those of either hippocampus, entorhinal
area, or fornix, using a visual concurrent discrimination
task. Monkeys with either hippocampal or entorhinal ablations
were impaired, while those with fornix sections were not.
However, ablations of hippocampus included inadvertent
damage of the inferotemporal cortex. Therefore, in the
second experiment, behavioral effects of inferotemporal
lesions were compared with those of hippocampus (without
additional inferotemporal damage) on the concurrent task
in both visual and tactual modalities. In the visual mode,
monkeys with hippocampal removals were as impaired as
those with inferotemporal ablations. In the tactual mode,
however, hippocampal, but no inferotemporal, ablations
were followed by a deficit. Our results, taken together
with other existing evidence, emphasize the role of the
hippocampus in mediating associative learning in more
than one modality. These results, obtained with non-human
primates, are in line with clinical findings.7
From this passage it is clear that Zola-Morgans methods are
less than precise. He says, ablations of hippocampus included
inadvertent damage of the inferotemporal cortex. Indeed, this
messiness and imprecision suggest that his results are suspect. In
1991, Zola-Morgan as much as admitted that variation between individual
monkeys brain physiology makes precision in locating brain structures
problematic. He wrote:
|A technique is described
for producing accurate stereotaxic lesions of the hippocampus
in monkeys. This technique overcomes the problem that
the size and shape of the brain can vary considerably
from monkey to monkey. Magnetic resonance imaging (MRI)
is used to create an individual brain atlas for each monkey.
The atlas is then used to derive coordinates for making
stereotaxic radio frequency lesions of the hippocampus.8
Yerkes and the rest of the NIH Regional Primate Research Center system
make the claim that they are sacrificing monkeys for the sake of human
health. Yerkes explains its mission:
| Long recognized as one
of the leading centers for biomedical and behavioral research
with non-human primates, Yerkes is focused on the following
To conduct a research program focused on scientific problems
relevant to human health and the mission of the National
Institutes of Health9
So it must be assumed that Yerkes and NIH see Zola-Morgans research
as fitting neatly into, perhaps exemplifying, this goal. Is Zola-Morgans
research actually relevant to human health? Of course he says it is
when he makes the claim: Our work is relevant to issues of how
memory is organized in the brain and to issues of memory impairment
associated with a wide range of human conditions, e.g., aging, Alzheimer's
disease, and stroke.10 But
this claim requires substantiation.
Zola-Morgan has investigated the loss of tactile amnesia in monkeys
whose brains he has injured. Tactile memory or amnesia refers to the
recollection (or loss of ability to recollect) of the physical feel
of an object. In other words, when you feel a coin in your pocket
do you remember that it is a coin? Is this question relevant to human
NIH maintains an online database of medical journals:
|PubMed, available via the
NCBI Entrez retrieval system, was developed by the National
Center for Biotechnology Information (NCBI) at the National
Library of Medicine (NLM), located at the National Institutes
of Health (NIH). The PubMed database was developed in
conjunction with publishers of biomedical literature as
a search tool for accessing literature citations and linking
to full-text journal articles at web sites of participating
This database is used by researchers as they seek to ascertain whether
their work is redundant and as a source for scientific information.
A search for cancer results in a list of 1,355,509 citations.
This is unsurprising due to the prevalence of the malady and the research
effort associated with it. Likewise, arteriosclerosis
results in over 56,000 citations and stroke over 65,000
citations. On the other hand, amnesia results in 6,999
(as of July 30, 2001) and tactile AND amnesia results
in 17 citations.
Of these seventeen citations, seven refer to the temporary and often
desirable amnesia associated with anesthesia and sedatives. Of the
remaining ten, one is a paper published in 1970, and six others published
in the years 1979, 1980, 1982, 1983, 1984, and 1990. A study of rats
with experimental brain damage induced tactile amnesia was published
in 1991, and single papers in 1993 and 2000.
It must be inferred that the study of tactile amnesia is of little
interest in the medical community, not perhaps out of a lack of compassion,
but more likely due to the rarity of the condition. Undoubtedly, there
must be a few doctors and researchers with an interest in the topic,
but its relevance as compared with the major human ailments must be
considered to be very low.
It is precisely this inconsequential and logically flawed research
that NIH and Yerkes have chosen to highlight by choosing Zola-Morgan
to head the most visible of all the nations primate laboratories.
To gain a better understanding of what it is that Zola-Morgan does
in his laboratory one need only consult his published work.12
Twenty-eight male cynomolgus monkeys (Macaca fascicularis)
were tested, all weighing between 3.1 kg and 5.2 kg at
the start of the experiment. Five monkeys received bilateral
lesions of the perirhinal cortex (PR group). Five monkeys
received bilateral lesions of inferotemporal cortical
area TE (TE group). The remaining eighteen monkeys comprised
unoperated control groups used in the individual experiments.
Monkeys were anesthetized using Isofluorane gas and placed
in a stereotaxic headholder that allowed unobstructed
access to the temporal portion of the skull. The temporal
muscles were exposed and fully retracted, and the zygomatic
arches were removed. Bilateral openings were made in the
skull to expose the anterior and ventrolateral portions
of the temporal lobe, and the dura was opened. The pial
surface over the intended lesions was first cauterized,
and the cauterized tissue together with the underlying
cortical tissue was then removed by suction using a glass
pipette with an angled tip. Cortical tissue was removed
slowly until the white matter was visualized. The dura
was then sewn, and the wound was closed in anatomical
Prior to the brain surgeries, the monkeys had been trained to reach
over a visual barrier and feel an object. If it was the correct object,
and they tugged on it thee times, they received a food reward (a raisin).
The monkeys learned which objects when tugged on resulted in a food
After their brains were damaged, they were again tested.
| BEHAVIORAL TESTING
All testing was conducted in the Wisconsin General Testing
Apparatus (WGTA; Harlow and Bromer 1938). In this
apparatus, the experimenter and monkey face opposite sides
of a testing tray that has three food wells. A sliding
opaque door separates the monkey from the testing tray,
and a sliding door with a one-way mirror separates the
experimenter from the tray. The one-way mirror allows
the experimenter to observe the monkey but prevents the
monkey from seeing the experimenter. During a trial, the
experimenter lowers the one-way mirror and raises the
opaque door, allowing the monkey to respond to the objects
on the testing tray.
Each operated group was allowed 6-8 weeks of recovery
prior to the start of behavioral testing. During four
to six daily sessions of pretraining, operated monkeys
and control monkeys learned to obtain food by displacing
objects that covered any of three food wells located on
a stimulus tray in front of the testing chamber.
In summary, the present findings demonstrate the distinct
functions of the perirhinal cortex and area TE. The deficits
following lesions of area TE are consistent with an impairment
of visual perception. Lesions of area TE produced a unimodal
visual impairment in visual recognition memory (experiment
1), an impairment in visual recognition even at very short
delays (experiment 2), and an impairment in relatively
complex visual discrimination learning together with sparing
of simple visual object discrimination learning (experiment
3). In contrast, the impairment following perirhinal lesions
is best described as a memory impairment. Lesions of perirhinal
cortex produced a multimodal impairment in recognition
memory (experiment 1), spared short-term memory and impaired
long-term memory (experiments 1 and 2), and impaired simple
object discrimination learning while sparing more complex
visual discrimination learning (experiment 3).
One way to judge the value of a researchers work is to look
at the number of times it has been referred to in subsequent research
by other scientists. If a scientist publishes a paper and no one pays
attention, it can mean that others deem the work unimportant. In animal-based
studies, it is the norm for researchers to claim that the work they
are engaged in will have value for human health at some later date.
The paper excerpted above was published at the end of 1999, or a year
and a half ago at the time of this writing. To date, according to
the journals publishers, the paper has been cited in ten subsequent
papers.14 Two of those papers are
Zola-Morgan citing his own work. Two of the papers have to do with
experiments on rats, and five of the papers are by other monkey users.
Only one is from a human study, and this is a German clinical study
on brain plasticity related to language after cochlear implants.
But perhaps a year and a half is simply too short a time for clinical
researchers to have taken note of Zola-Morgans work. Another
paper15 published over ten years
ago has been cited much more frequently. The publisher reports that
the paper has been cited forty-one times. Of these: three are Zola-Morgan
citing his own work; one is a Guinea pig-based study; two are experiments
using cats; ten are rat-based studies; fifteen are by other researchers
destroying monkeys brains; one is based on an unnamed species;
one is a general article rather than a research report; and seven
are human related.
Of these seven human related studies, one16
is coauthored by one of Zola-Morgans own regular co-authors,
David Amaral, himself a monkey brain experimenter at the California
RPRC in Davis. The rest cite Zola-Morgan when noting that the parahippocampus
may be involved in memory. But none of the clinical papers seem to
actually build on Zola-Morgans work.
It would be unreasonable to claim that Zola-Morgans work has
in any way been trail blazing or otherwise exemplary.
Zola-Morgan has, however, blazed a trail to the bank. He explains
why he should keep being paid from the public trough:
|This is our second competing
continuation for a project begun in 1983. Work during
the most recent funding period (1987-present) has resulted
in 27 publications that lay out the steps that have established
an animal model of amnesia in the monkey and in identifying
the anatomical components of the medial temporal lobe
memory system. These developments allow us to now address
a fundamental issue concerning memory function, that is,
how individual structures of this system contribute to
memory. The present proposal involves detailed behavioral
and anatomic analyses of a group of normal monkeys and
seven operated groups of monkeys including those with
damage to components of the medial temporal lobe memory
system and to area TE.17
Over the past decade Zola-Morgan has received nearly $2 million in
taxpayer funding: 1992 - $48,203; 1993 - $158,227; 1994 - $156,011;
1995 - $162,657; 1996 - $169,303; 1997 none listed; 1998 -
$306,105; 1999 - $315,128; 2000 - $324,580; 2001 - $334,321.18
The second reason that Zola-Morgan is likely to have been selected
to head Yerkes is his strong and outspoken opposition to the critics
of vivisection. On Thursday, May 14, 1998, Zola-Morgan testified before
the U.S. House of Representatives Committee on Sciences
National Science Policy Hearing. His talk was titled: Communicating
Science and Engineering in a Sound-Bite World. His speech was couched
in reasonable terms and he assured the Committee members that his
research was helping find answers to Alzheimer's Disease (AD), encephalitis,
head trauma, chronic stress and the memory problems associated with
He went on to claim that the reason the public was increasingly critical
of using animals in research was due to their scientific illiteracy.
| The claims about animal
research and about the process of science in general that
were being made by the animal activists seemed not unreasonable
on the surface. And because they were not being effectively
disputed by the scientific community, the distortions
and untruths about science and the scientific process
were often accepted without question by the general public
Moreover, claims of abuse of animals were often being
accepted at face value by the general public and by legislators,
who were beginning to generate legislation that would
further regulate research using animals.
And such legislation would impact on Zola-Morgans freedom to
scramble monkeys brains. He continued:
| As a result, in the mid
1980s I became interested in the issue of communicating
science to the general public and to legislators, as well.
I was, at that time, Chair of the Animal Subjects Committee
at UCSD and I knew that we ranked very high in our science
(UCSD is consistently in the top 10 or 12 institutions
in the country in terms of grant funding received) and
in our humane treatment of animals.
UCSD ranked sixteenth in terms of grant funding in Fiscal 200018.
Johns Hopkins was number one with NIH grants totaling over four hundred
million dollars. UCSD received one hundred ninety million dollars.
In terms of the humane treatment of animals facilities
are not ranked. This claim was simple posturing before the Congressional
Committee. In addition, Zola-Morgans position as chair of the
Animal Subjects Committee gave him great power to deflect any internal
criticism of his own work, and when the committee chair is involved
in such blatantly pointless and cruel experiments, it tends to open
the door for others who might otherwise be under greater constraints.
| A small group of individuals
at UCSD began to develop counter arguments to the claims
of the activists, and to speak out at animal rights gatherings
in San Diego. However, it soon became clear that in terms
of educating people about science, it was not the animal
rights activists whom we should target. Their views were
unlikely to be changed by us. Instead, we determined that
we should focus on the general public, and on legislators.
And this is likely at the core of Emory Universitys and the
NIHs decision to see Zola-Morgan assume the leadership there.
Local anti-cruelty activists have been recently successful in having
legislators ask pointed questions of the facility. The need to deflect
the likely outcome of acknowledging that you have been wasting millions
of dollars and thousands of lives has motivated them to seek out someone
with a good track record of pubic relations. And clearly, if Zola-Morgan
can spin his own experiments in ways that will mollify lawmakers,
Yerkes might assume that he might be able to shield them as well.
But it seems that the Yerkes administration and NIH have failed to
do their homework. An anti-cruelty activist from the San Diego area
| During the period around
l988-90 there were concerted efforts underway in San Diego
to end the contract between UCSD and the county Department
of Animal Control. "Pound seizure" had been
in place for about 30 years at that point, with UCSD taking
hundreds of dogs and cats annually for experimentation.
San Diego Animal Advocates and a group called Stop Taking
Our Pets went from city council to city council, persuading
them to put a clause in their animal control contracts
that would forbid the county from selling (or giving away)
animals, who were picked up in that city, to the university
for research. In a number of cities we were successful.
While the cities still contracted with the county for
animal control services, the clause was inserted to protect
strays from research.
Zola Morgan and colleague, Dr. Patrick Cleveland from
the Veterans Administration Hospital, showed up at these
meetings as well, to argue their case that all medical
advances on the planet were dependent on the use of pound
animals. They specifically insisted that pound animals
were preferable to purpose-bred animals because of the
desirability of the unknown genetic backgrounds!
During this time frame San Diego Animal Advocates held
a big demonstration on what was then known as World Day
for Laboratory Animals, in April. We presented a mock
"vivisector of the year" award each year to
someone from UCSD known for a grisly experiment. Both
Zola-Morgan and his buddy Cleveland called our animal
rights information line and left messages on the recorder.
Each one claimed that he should win the award instead
of the other, because he used more animals or did more
experiments, or had been doing them longer, etc.
They found this very amusing until we took the tapes
to the city council meetings and played them. The first
time we brought out the tape recorder, Zola-Morgan was
on his feet protesting that it was inappropriate, but
it was allowed nevertheless. The callous attitude toward
the animals was very apparent and he was very embarrassed
and angered. That city was Solana Beach and they passed
our proposal that evening.
On another occasion, San Diego Animal Advocates testified
at the county Board of Supervisors meeting about the
pound seizure issue. One of the supervisors was Pam
Slater, who was very favorable to the abolition of pound
seizure, although not opposed to all animal research.
After the hearing, Zola-Morgan went up to her and angrily
demanded to know why she had been so critical of UCSD
research. He said, You know us you have
worked with us. (She had been a lab assistant
there at one time, unbeknownst to us.) She answered
that it was precisely because of what she had seen in
Zola-Morgan's own laboratory that she was against pound
seizure. I don't know if he used any dogs or cats in
his experiments, I think it was mostly primates, but
whatever she saw made her unwilling to let former companion
animals end up at UCSD.19
The effects of Zola-Morgans appointment remain to be seen. What
does seem clear is that the vivisecting community has escalated their
defense of experimenting on animals. The battle is joined, and now
we must all decide whether we stand on the side of kindness and compassion,
or with the Zola-Morgans who claim the unfettered right to appease
any and every curiosity.
Note: A few years ago Zola-Morgan dropped the -Morgan from his name.
He now goes by Stuart M. Zola.
1 From Zola-Morgan's profile at the University of California San Diego
2 Zola-Morgan S, Squire LR, Ramus SJ. 1994. Severity of memory impairment
in monkeys as a function of locus and extent of damage within the
medial temporal lobe memory system. Hippocampus. Aug;4(4):483-95.
Comment in: Hippocampus. 1995;5(3):232-9.
3 Wallis J, Anderson K, Miller E. 2001. Single Neurons in prefrontal
cortex encode abstract rules. Nature: 953-956.
4 Barbas H. 2000.Connections underlying the synthesis of cognition,
memory, and emotion in primate prefrontal cortices. Brain Res Bull.
5 Masserman J, Wechkin S, and Terris W. 1964. 'Altruistic' behavior
in rhesus monkeys. American Journal of Psychiatry vol. 121. pp. 584-585.]
6 Bachevalier J, Alvarado MC, Malkova L. 1999. Memory and socioemotional
behavior in monkeys after hippocampal damage incurred in infancy or
in adulthood. Biol Psychiatry. Aug 1;46(3):329-39.
7 Moss M, Mahut H, Zola-Morgan S. 1981. Concurrent discrimination
learning of monkeys after hippocampal, entorhinal, or fornix lesions.
J Neurosci: Mar;1(3):227-40.
8 Alvarez-Royo P, Clower RP, Zola-Morgan S, Squire LR. 1991. Stereotaxic
lesions of the hippocampus in monkeys: determination of surgical coordinates
and analysis of lesions using magnetic resonance imaging. J Neurosci
Methods: Jul; 38(2-3):223-32.
9 From the Yerkes homepage: [http://www.emory.edu/WHSC/YERKES/about_mission.html].
10 See note 1.
11 PubMed Overview [http://www.ncbi.nlm.nih.gov:80/entrez/query/static/overview.html].
12 Buffalo EA, Ramus SJ, Clark RE, Teng E, Squire LR, Zola MS. 1999.
Dissociation Between the Effects of Damage to Perirhinal Cortex and
Area TE. Learning and Memory: Vol. 6, No. 6, pp. 572-599, November/December.
13 Harlow H, and Bromer. 1938. A test-apparatus for monkeys. Psychol.
Rev: 19: 434-438.
14 Learning and Memory: 6:572-599.
15 Zola-Morgan S, Squire LR, Amaral DG and Suzuki WA. 1989. Lesions
of perirhinal and parahippocampal cortex that spare the amygdala and
hippocampal formation produce severe memory impairment Journal of
Neuroscience: Vol 9, 4355-4370.
16 Corkin S, Amaral DG, González RG., Johnson KA, Hyman BT.
1997. H. M.'s Medial Temporal Lobe Lesion: Findings from Magnetic
Resonance Imaging. J. Neurosci: 17: 3964-3979.
17 NIH Grant Number: 5R01MH58933-15; Neurology of Memory. Project
Start: 01-Mar-83; Project End: 31-Jan-03. National Institutes of Mental
18 National institutes of Health Office of Extramural Research Award
19 Cartmil, J. San Diego Animal Advocates. Private correspondence
with the author. August, 2001.