Is Accused Murderer Dr. Amy Bishop An Academic Fraud, Delusional or Both?

Dr. Amy Bishop faces capital murder charges for three deaths when she reportedly opened fire during a faculty meeting at the University of Alabama-Huntsville last Friday. Three other colleagues were also shot and are hospitalized, at least two in critical condition. Early speculation says Dr. Bishop may have been motivated because she was reportedly denied tenure.

According to attorney and employment law expert Jayne Cucchiara, "tenure is the Holy Grail in academia. It is perceived as a guarantee of job security. While tenured professors can be removed for cause, proving sufficient cause to discharge a tenured professor is almost always a very difficult burden to meet."

"Most universities have a defined tenure application process," employment lawyer Jayne Cucchiara explained. She said "the process typically begins with an application package prepared and  submitted by a professor seeking tenure. The application package details teaching, research, publishing and institutional and community accomplishments that the tenure applicant believes warrant tenure. The tenure decision of the applicant's Department Chair is generally given substantial deference when reviewed by a Dean level appointee in a university's administration."

According to Attorney Cucchiara, "in order to have a realistic chance of challenging a department's decision to deny tenure, the non-tenured professor must at a minimum be able to demonstrate a level and record of academic accomplishment comparable with those being granted tenure both in her department and at a university wide level."  Attorney Cucchiara explained, "in academia, there is saying which is very true: publish or perish."  She said, "student evaluations are considered, but generally much greater weight is placed on an established and consistent record of scholarly research published in peer reviewed journals."

An anonymous Commentor to this Blog, identifying himself as a UAH faculty member for the past 15 years, shed further light on the tenure review process at UAH:

Anonymous said...

As a faculty member at UAH, I would like to make two comments. First, in response to another anonymous comment, politics are not the most important issue at UAH. I have been here 15 years and have served on tenure review committees at every level at the university. I can tell you that we have denied tenure for really popular people who did not cut muster with regard to research, and we have granted tenure to people with excellent records, even though they had less desirable personality issues. Our tenure process is about as fair and objective as I can imagine. Second, the process at UAH involves 5 stages: departmental review, Dean review, college level tenure committee review, university-level review board, and the Provost. I have seen cases where one or more of these levels voted no, but the person ultimately recieved tenure, and I have also seen the opposite situation where multiple people said yes, but the Provost said no. So, it would not be unc! ommon for the department chair to be overruled after voting yes for tenure. The beauty of the tenure review process here is that no one person can kill your tenure if they happen to dislike you. 

A review of the archived web pages of Dr. Bishop on the University of Alabama Department of Biological Sciences' website discloses numerous red flags that may well be the reason Dr. Bishop was denied tenure.  In fact, after studying and comparing Dr. Bishop's archived web pages over the five plus years she was at UAH, one is left with an abiding and growing suspicion that Dr. Bishop is either an academic fraud or totally delusional in the same vein as the Jack Nicholson' character in Stephen King's The Shining, who believed he was writing the next great American novel only for his wife to discover he had been typing the same sentence over and over and over all ! winter long.

Maybe we will discover that Dr. Bishop is just a run of the mill sociopath for whom killing those in her way, whether they be colleagues or family, registers no greater blip on her emotional chart than, say, severing the spines of live animals to determine if she can induce neuron recovery by first subjecting the soon to be paralyzed animals to varying doses of nitric oxide, which, but the way, is fatal when overdosed, and which just so happens to be a fair restatement of Nos. 8 and 9 on Dr. Bishop's essentially static "research plan" since she arrived at UAH.

Put aside my obvious and impossible to disguise disgust with scientific research predicated on torturing animals. What still remains is that Dr. Bishop has been regurgitating the same static research plan for years:

Here is verbatim Dr.  Bishop's December 11, 2003 published "Research Plan": 

The overall goal of my laboratory will be to explore resistance to nitro-oxidative stress in CNS cells. The specific aims are to: 

1. Determine if the adaptive resistance extends to other oxidants and other CNS cell types.
2. Determine which cellular targets of NO-mediated damage are protected by HO1 induction
and induced adaptive resistance.
3. Characterize NO-mediated signal transduction pathways that induce HO1.
4. Characterize the NO-mediated increase of HO1 mRNA stability and/or transcriptional
induction of HO1.
5. Determine what other genes are turned/off by HO1 induction and whether their
induction/inhibition is necessary for the induced adaptive resistance.
6. Characterize the role of HO-1, HO-1-mediated heme metabolism and iron in induced
adaptive resistance.
7. Characterize of the role of cytostasis and differentiation in NO resistance.
8. Eventually use whole animals for studies of induced adaptive resistance in the CNS.
9. Whole animal studies of induced recovery from spinal transection.
10. Study the influence of the low gravity/high radiation environment of space flight on
resistance mechanisms to oxidative stress in the CNS.

Here is verbatim Dr.  Bishop's June 14, 2008 UAH  "Research Plan":

The overall goal of my laboratory will be to explore resistance to nitro-oxidative stress in CNS cells. The specific aims are to:  

1. Determine if the adaptive resistance extends to other oxidants and other CNS cell types.
2. Determine which cellular targets of NO-mediated damage are protected by HO1 induction and induced adaptive resistance.
3. Characterize NO-mediated signal transduction pathways that induce HO1.
4. Characterize the NO-mediated increase of HO1 mRNA stability and/or transcriptional induction of HO1.
5. Determine what other genes are turned/off by HO1 induction and whether their induction/inhibition is necessary for the induced adaptive resistance.
6. Characterize the role of HO-1, HO-1-mediated heme metabolism and iron in induced adaptive resistance.
7. Characterize of the role of cytostasis and differentiation in NO resistance.
8. Eventually use whole animals for studies of induced adaptive resistance in the CNS.
9. Whole animal studies of induced recovery from spinal transection.
10. Study the influence of the low gravity/high radiation environment of space flight on resistance mechanisms to oxidative stress in the CNS.

It is difficult sometimes when reading technical jargon to do comparisons, but whether you understand the jargon or not, when you compare Dr. Bishop's two "Research Plans," which are five years apart,  side by side, line by line, you do not need to be a Harvard trained geneticist to conclude that her plan never changes.

2003:  1. Determine if the adaptive resistance extends to other oxidants and other CNS cell types.
2008:  1. Determine if the adaptive resistance extends to other oxidants and other CNS cell types.

2003: 2. Determine which cellular targets of NO-mediated damage are protected by HO1 induction
and induced adaptive resistance.
2008:  2. Determine which cellular targets of NO-mediated damage are protected by HO1 induction and induced adaptive resistance.

2003: 3. Characterize NO-mediated signal transduction pathways that induce HO1.
2008: 3. Characterize NO-mediated signal transduction pathways that induce HO1.

2003: 4. Characterize the NO-mediated increase of HO1 mRNA stability and/or transcriptional
induction of HO1
2008: 4. Characterize the NO-mediated increase of HO1 mRNA stability and/or transcriptional induction of HO1.

2003: 5. Determine what other genes are turned/off by HO1 induction and whether their
induction/inhibition is necessary for the induced adaptive resistance.
2008: 5. Determine what other genes are turned/off by HO1 induction and whether their induction/inhibition is necessary for the induce

2003: 6. Characterize the role of HO-1, HO-1-mediated heme metabolism and iron in induced adaptive resistance.
2008: 6. Characterize the role of HO-1, HO-1-mediated heme metabolism and iron in induced adaptive resistance.

2003: 7. Characterize of the role of cytostasis and differentiation in NO resistance.
2008: 7. Characterize of the role of cytostasis and differentiation in NO resistance.

2003: 8. Eventually use whole animals for studies of induced adaptive resistance in the CNS.
2008: 8. Eventually use whole animals for studies of induced adaptive resistance in the CNS.

2003: 9. Whole animal studies of induced recovery from spinal transection.
2008: 9. Whole animal studies of induced recovery from spinal transection.

2003: 10. Study the influence of the low gravity/high radiation environment of space flight on
resistance mechanisms to oxidative stress in the CNS.
2008: 10. Study the influence of the low gravity/high radiation environment of space flight on resistance mechanisms to oxidative stress in the CNS.

As demonstrated, you do not need to understand biology, to easily see that Dr. Bishop has not changed a word of her plan in five years. If you are not yet flashing back to Jack Nicholson's novel pages in the Shining  -- All work and no play makes Jack a dull boy. All work and no play makes Jack a dull boy. All work and no play makes Jack a dull boy. All work and no play makes Jack a dull boy. All work and no play makes Jack a dull bo! y. All work and no play makes Jack a dull boy -- then you didn't see the movie. 

One anonymous Commentor to this Blog has suggested, "[a]s for the research plan being the same in 2003 and 2008, that could simply mean that she didn't care about her departmental web page. You ask professors to put something online, like their course syllabi or an NSF-style bio, and they will often do the bare minimum copy and pasting necessary to comply---it is, after all, a distraction from their job." This observation seems both reasonable and plausible in general terms. However, when you consider that 2003 was Dr. Bishop's first year at UAH and 2008 would have been a critical year in the tenure review process for her, it seems prudent to do than more than the 'bare minimum' these two pivotal years.

In addition to turning in the same boiler plate "Research Plan" year after year after year, with not a single step of research progression documented, when the tenure application process was upon her, Dr. Bishop engaged in what could fairly be described as  a form of academic fraud.   

According to her last UAH Department web page,  Dr. Bishop's claims three publications in 2009:

1. Anderson, L. B., Anderson P. B., Anderson T. B., Bishop A., Anderson J., Effects of selective serotonin reuptake inhibitors on motor neuron survival (2009) International Journal of General Medicine. In press
2. Bishop A., Green-Hobbs K., Eguchi A., Pennie C., Anderson J.E., Estévez A. Differential sensitivity of oligodendrocytes and motor neurons to reactive nitrogen species: a new paradigm for the etiology of Multiple Sclerosis (2009). Journal of Neurochemistry. (109) 93-104.
3. 

Bishop A, Gooch R, Green-Hobbs K, Cashman N. R., Demple B., Anderson J. E., Estévez A.,. Mitigation of nitrotyrosine formation in motor neurons adapted to nitrooxidative stress. (2009) Journal of Neurochemistry. (109) 74-84.  



The first article "Effects of selective serotonin reuptake inhibitors on motor neuron survival" claims to have been written by "Anderson, L. B., Anderson P. B., Anderson T. B., Bishop A., Anderson J." and going to press in the "International Journal of General Medicine."  If you track the article down what you discover is that the authors full names are Lily B Anderson, Phaedra B Anderson, Thea B Anderson,  James Anderson and Dr. Bishop. Another way to describe the purported authors are that they are Dr. Bishop, her husban! d James 'Jimmy' Anderson and three of their children.  Mr. Anderson and his children are all identified as employees of "Cherokee Labsystems" in Huntsville. 

The website for  Cherokee Labsystems --  www.cherokeelabsystems.com -- has a notice "Please stand by. We are currently updating our site and will be on-line shortly" and also shows the web address defaults to http://cherokeelabs.com/ 

According to the wayback machine this web address -- http://cherokeelabs.com/  -- was only active October 16, 2003 through January 30, 2005, but all the archived pages for that period show a website that relates to Cherokee Labrador dogs,  not a genetic research laboratory.  
 
Moreover, googling with street view the claimed address for Cherokee Labsystems -  2103 McDowling Dr. SE, Huntsville, AL - shows a residential home and not a laboratory allegedly involved in genetic research:

 

If pawning off your family as co-authors employed at a bogus genetic research lab located in a residential home is not fraud, then how about paying to have your alleged research published by an online vanity press that admits in its marketing materials that its idea of peer review "is that any paper that has interest to the readers and is reasonably written will be published. Thus the Editor is looking for reasons to publish your paper, NOT reject it."  The other two articles 'published' by Dr. Bishop in 2009, include among the purported authors Dr. Bishop's husband "J.E. Anderson," whom she characterizes as her "Research Consultant, Cherokee Labsystems" in her June 2008 UAH webpage.


On her 2008 UAH faculty page, Dr. Bishop claimed:

My laboratory’s goal will be to continue in our effort to develop a neural computer, the Neuristor™, using living neurons. This computer will exploit all of the advantages of neurons. Specifically, neurons rich with the nitric oxide (NO) dependent learning receptor, N Methyl D Aspartate receptor (NMDAR), will be utilized. These have previously been studied in the context of induced adaptive resistance to NO (IAR). For the Neuristor™ we will take advantage of the IAR phenomena since it has been demonstrated that IAR neurons express more learning and memory receptors (NMDAR) as well as increased neurite outgrowth. The neurons that we are currently using are mammalian motor neurons. We are exploring the possibility of using neurons derived from adult stem cells, and from bony fishes provided by Bruce Stallsmith Ph.D. This laboratory has created a portable cell culture incubator, the Cell Drive™ that is an ideal support structure for the Neuri! stor™.

With respect to the Cell Drive, at seeming odds with Dr. Bishop's claim that her UAH lab  "created a portable cell culture incubator, the Cell Drive™," on August 26, 2008 a TradeMark application for the name "CELLDRIVE" to be used for "laboratory equipment and supplies, namely, incubators" was filed by the claimed "Owner (Applicant) Cherokee Labsystems Jimmy E. Anderson...[who identified himself as] SOLE PROPRIETOR." Once again, the McDowling Drive address referenced above was given for Cherokee Labsystems.

An archived article accessible through the wayback machine depicts a "Press Release" about Dr. Bishop which  reports that on March 10, 2009,  Dr. Bishop's "Neuron Research Lab Launches Experiment in Space." The "launch" was on par with the Balloon Boy's purported takeoff, only with less drama and coverage. Also, while Dr. Bishop more than once mentions NASA on her web page, the March 2009 'launch' was handled by UAH Space Hardware Club, not NASA. Cherokee Labsystems, however, was purportedly involved; Dr. Bishop credited Cherokee with "payload support development." The payload -- live neuron cells from Dr. Bishop's lab secured in what looks to be a jury rigged contraption she calls the "'incubation chamber" purportedly designed to maintain temperature and pressure as the balloon ascended.

 

 While the 'launching' of the balloon may have been a fun exercise for the students involved, the drafting of an amateur press release about the excursion hardly qualifies as published scholarly research.

Dr. Bishop's most startling claim in the 2008 UAH web page is her claim that her "laboratory’s goal will be to continue in our effort to develop a neural computer, the Neuristor™, using living neurons." 

The Neuristor Trademark is registered to a Japanese company Eisai Company.  None of Dr. Bishop's publications, even the one published in the online vanity journal, describe any research pertaining to neural computers or the Neuristor.  It may well be that Dr. Bishop was contemplating taking her interest in neuron research into the sci-fi frontier of developing a neural computer, but it also seems logical that if this were, in truth, a new direction Dr. Bishop intended to pursue she would have revamped her published research plan to identify logical steps toward such a goal. 

There is no question that Dr. Bishop is smart. But it also seems very evident that she suffers delusions of genuis. Far from establishing  a record of accomplishment warranting the grant of tenure, since joining UAH Dr. Bishop took a long nap on her one true laurel -- her affiliation with Harvard .

Evidence strongly suggests that Dr. Bishop used her husband, her family and by all appearances the sham 'Cherokee Labsystems' to fabricate a record of recent accomplishments. Her use of essentially an online vanity publisher further diminishes her professional stature.  

It should have been no surprise to Dr. Bishop that the University easily saw through the smoke and mirrors and that she would not receive tenure. But an oversized ego can be blinding.

It seems clear that Dr. Bishop re-wrote the rules for herself. Rather than face the reality that she needed to conduct real research and publish substantial, scholarly work in peer reviewed journals, Dr. Bishop tried to cheat her way to tenure. And, when that failed, it appears Dr. Bishop premeditated a new plan: if you don't accept what I publish, you will perish.


 


  

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Note: If you'd like some background and history on how this whole thing got started, see here -- Le Nature's stands AGAINST FREE SPEECH



My condolences to the people who's sweat and labor held up this company while it crumbled from the top down. Some of your fellow coworkers have already spoken up about their experiences. Whether you worked for Le Nature's or with Le Nature's, I invite you, as a worker, to express yourself here. Yo! u can do so anonymously. Whether you have good or bad things to say, you can speak up here without fearing.

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The Dalmation Crossbreeding Project...

It is not only the red setter that has undergone a restoration by utilizing crossbreeding as a mechanism to bring the needed genetics into the breed. The Dalmation Heritage Project is an ongoing project by a group of dedicated Dalmation breeders, who are using crossbreeding to English Pointers (the closest relative to the Dalmation), as well as other breeding and health-positive techniques, to improve the quality and health of their breed. As most of you who read this blogsite are well aware, I am a staunch opponant of strictly closed registries such as the AKC. I am also a strong advocate of revam! ping our registries to modernize them and make them better aligned with contemporary advances in canine and population genetics. The Dalmation Heritage Project is a perfect example of how genetics, breeding, and pedigree registration can be blended to present a useful and functional tool for recording breed records, yet also act as a helpful guide for breeding healthy working dogs.

Be sure to visit the website of the Dalmation Heritage Project at http://www.dalmatianheritage.com/index.htm

A Special thanks to James Seltzer for providing permission to post this information on our blogsite. Please feel free to copy and paste to anyone with an interest in breeding healthy working dogs.

!

A n Overview of the Backcross Project
June 2006
By James E Seltzer, Ph.D.

The uric-acid stone problem is a principal genetic defect in the Dal breed. Since at least 1938 we have known the inheritance pattern of this defect. It behaves like a simple autosomal recessive. (This is the same sort of genetic trait as the one that determines whether a Dal will have black spots or liver spots.)
It is essential that we keep in mind that the defective trait we are talking about is the very high urinary uric acid (UUA) concentration in Dals. The relationship between UUA and the actual formation of stones is not linear. I will go into this latter point in more detail after the fundamentals are out of the way.
Let's be perfectly clear: The mode of inheritance of the uric acid defect in Dalmatians is not in dispute.
First, let's make sure we understand the fundamentals. A good ! place to start is at the web page of the American College of Veterinary Surgeons, ACVS http://www.acvs.org/flash.html
Overview
Urolithiasis (urinary stones) is a common condition responsible for lower urinary tract disease in dogs and cats. The formation of bladder stones is associated with precipitation and crystal formation of a variety of minerals (magnesium ammonium phosphate hexahydrate, calcium oxalate, urates, and others).
Causes and Risk FactorsWhat causes urinary stones? Several factors are responsible for the formation of urinary stones. The understanding of these processes is important for the treatment and prevention of urinary stones. In general, conditions that contribute to stone formation include:* a high concentr! ation of salts in urine* retention of these salts and crystals! for per iods of time in the urinary tract* an optimal pH that favors salt crystallization* a scaffold for crystal formation* a decrease in the body's natural inhibitors of crystal formation.
The Backcross project is primarily concerned with the first of these since this is directly related to the uniquely Dalmatian genetic defect mentioned above (Trimble, HC, and CE Keeler. 1938. The inheritance of "high uric acid excretion" in dogs. J. Heredity, 29, 280-289.)
The other contributing factors to the urinary stone problem are interesting and worthy of discussion, but we should not confuse these with what the Backcross project is about.
In this overview I will try to explain:
How one introduces a normal version of the gene into the Dalmatian breed.
How one identifies and isolates that gene in the progeny.
How one insures that the normal gene is passed on to succeeding generations.
How one validates that the Dalmatian uric acid defect has been corrected! .
Current status of the Backcross project and location of the defective gene in the Dalmatian genome.
Alternative approaches for dealing with the uric acid defect (such as pedigree analysis and selective breeding).
How one introduces a normal version of the gene into the Dalmatian breed.
To anticipate and avoid arguments about inviolability of pure breeds and racial purity, I need to say up front that pure canine breeds exist primarily in the minds of the dog fancy and are simply paperwork exercises codified in the registries of the various national kennel clubs. They do not exist in the flesh and blood reality of dogs living in the real world. Dog registries and closed stud books are a recent invention of today's dog fancy - originating only a little more than a century ago. The partnership between man and dog reaches back much further. Robert K. Wayne of the University of California, Los Angeles and his colleagues now have evidence that dogs could have! been domesticated 100,000 years ago -- if not earlier. http://www.sciencenews.org/pages/sn_arc97/6_28_97/ bob1.htm
What comprises a breed is not a unique set of genes, neatly packaged with clear boundaries that identify what is and what is not a member of the breed. AKC registration is not especially meaningful for defining the attributes of the Dalmatian. Even a cursory visit to Sue MacMillan's coat color web pages will quickly shatter such an illusion. http://www.geocities.com/~paisleydals/color.html
Purebred Dalmatians, presumably AKC registered, can be fo! und in brindle, lemon, orange, blue, tri-color, and sable. Dals share these genes with other pure breeds. In Dals, these alleles are fairly uncommon; in other breeds they are both common and in many cases desired. There is no doubt that genes that control other conformational attributes (e.g., ears, height, tail set, etc.) are also shared with the other so-called pure breeds.
What distinguishes one breed from another is the relative allele frequencies of the aggregate set of genes that serve as blueprints for the breeds of dogs. Dalmatians, for example, have a higher frequency for the extreme white piebald allele (sw) and the ticking allele (T) than the cocker spaniel -- but Dals do not have exclusive ownership of either of these alleles. Dals just have these alleles in greater abundance.
Most breeds of dogs have a normal gene for uric acid excretion, and, compared with Dals, rarely have problems with urate stones. The ancestor to the Dalmatian also had such a nor! mal gene, but that gene got lost in the shuffle as the breed w! as propa gated and artificial selection was taking place. The normal gene may have been closely linked (on the same chromosome) with another gene that was considered a desirable characteristic by the early breeders. On the other hand, the normal gene may simply have become victim to random genetic drift and got lost along the way, which is not unusual when the number of dogs being bred is small. However it occurred, to the best of our knowledge, there were no Dalmatians anywhere that still carried the normal uric acid excretion gene prior to the Backcross project.
Since that normal gene did not exist within the Dal breed, it was not possible to use breeder selection methods to increase the normal allele frequency and thereby diminish the incidence of urate stone disease in Dals. (Which answers the question of why we can't reestablish the normal gene in the same way that we can establish a true-breeding, liver-spotted line of Dals.)
To find the normal gene it was necessary t! o turn the clock back to the point in time before the Dalmatian breed branched off from its kin at their common origins and followed its own path. We don't know exactly what the common ancestor(s) was at that early branch point, but we can surmise what its progeny probably look like today even though they followed different selection paths during the intervening generations. Considering a broad array of phenotypic attributes, and the likelihood of a not-too-distant common ancestor, Dr. Bob Schaible selected the Pointer as a probable descendent of that closest common ancestor.
When a Dalmatian was mated to a Pointer, all the cross-bred pups carried one copy of the normal uric acid excretion gene that it got from its Pointer sire. Since, according to the early work by Trimble and Keeler, we already know that the uric acid defect is a simple autosomal (not sex-linked) recessive gene, all the first-generation pups excreted normal levels of urinary uric acid (UUA) as was pr! edicted by the autosomal recessive model. The first-generation! pups, o f course, did not much look like Dalmatians.
In order to refine the line it was necessary to cross-breed back to a purebred Dalmatian, hence the name Backcross project. The second generation pups, although they began to look more like purebred Dalmatians, did not all carry a gene for normal UUA. Only about 1/2 of these pups got the normal gene. The best of those carrying a copy of the normal UUA gene, i.e., those that most closely resembled Dalmatians, were selected for further breeding in the Backcross project. The other pups found loving homes and lived out their lives as pets.
The process continued to select pups 1. for normal UUA, and 2. for proper Dalmatian conformational attributes. The Backcross project has continued to the point that the latest generation pups are tenth generation descendents of the one original Pointer. The lucky one's still carry that Pointer's genetic bequest: a gene for normal UUA. Most of their other genes are derived from their Dalmat! ian dam, their Dalmatian grandam, their Dalmatian great-grandam, etc.
These pups are still heterozygous for the normal UUA gene. The decision not to breed a homozygous-normal UUA line (yet) has been intentional and relates to the necessity to avoid a genetic bottleneck and all the concomitant headaches that ensue when a line is closely line-bred.
How one identifies and isolates that [normal UUA] gene in the progeny.
The Backcross project started with a Pointer that had normal uric acid excretion (10-60 mg of uric acid in his urine per day) that was mated to a Dalmatian dam with high uric acid excretion (400-600 mg of uric acid per day in her urine). There is no overlap in these numbers; there is no mistaking one for the other. A veterinary lab technician provided an unlabeled urine sample from the sire and a urine sample from the dam could easily tell you which sample came from the Pointer and which sample came from the Dalmatian. (Canine and Feline Nephrolog! y and Urology, Osborne & Finco, 1995, p824)
It is imp! ortant t hat we understand the hereditary pattern for the Dalmatian defect before we can develop a reasonable protocol for progeny testing. The UUA defect in the Dalmatian is transmitted as an autosomal recessive. Trimble and Keeler (1938) crossed Dalmatians to Collies, and through subsequent crosses determined that the genetic defect in Dalmatians was an autosomal recessive trait.
When a carrier for the defect (one normal gene and one defective gene) from the Backcross line is mated to a purebred Dalmatian (two defective genes), the expected ratio of carriers to defectives in the resulting litter is 1:1, i.e., we expect approximately 1/2 of the pups to be UUA normal and 1/2 to be UUA defective. This is the distribution of the defect that could be expected by the second generation and for all subsequent generations of puppies.
As early as 1968 a method for screening for abnormal levels of uric acid in humans had been published: J Pediatr. 1968 Oct;73(4):583-92., "Urine uric! acid to creatinine ratio--a screening test for inherited disorders of purine metabolism. Phosphoribosyltransferase (PRT) deficiency in X-linked cerebral palsy and in a variant of gout."
Another paper that was published many years after the Backcross project had been initiated questioned the use of the UUA:CR ratio test to estimate the 24-hour total uric acid excretion in healthy Beagles. Am J Vet Res. 1994, 55:472-476, Bartges, JW; CA Osborne; LJ Felice; LK Unger; KA Bird; LA Koebler; M Chen, "Reliability of single urine and serum samples for estimation of 24-hour urinary uric acid excretion in six healthy Beagles."The authors of the 1994 paper found that some spot samples of urine and creatine taken during the day did not correlate well with the 24-hour UUA excretions, and they attributed that "to differences in urinary uric acid and creatinine excretions after digestion, absorption, and metabolism of the diets."
Yet another paper published in 2004, questioned t! he use of single 24-hour urinary uric acid excretion measureme! nts in h ealthy humans since uric acid excretion levels fluctuate widely over even longer periods. Rheumatology 2004 3(12):1541-1545; doi:10.1093/rheumatology/keh379, K.-H. Yu, S.-F. Luo, W.-P. Tsai and Y.-Y. Huang "Intermittent elevation of serum urate and 24-hour urinary uric acid excretion."
The authors of the 2004 paper conclude: "The data presented here demonstrate individual variations in serum urate levels and 24-h urinary uric acid excretions in healthy men with serial measurement. Transient hyperuricaemia and hyperuricosuria are more common than expected, and both transitory and monthly variations are important factors to consider when evaluating the influence of other factors upon serum urate levels and urinary uric acid excretion."
Needless to say, this puts the veterinary clinician who is trying to manage urinary uric acid problems in his patients on the horns of a dilemma. The UUA:CR test, it is claimed, is invalid, because of diurnal fluctuations. The 24-hour ! urine collections are no good because urinary uric acid excretions are found to vary widely when monthly measurements are compared. Further, these monthly variations are not insignificant: median 623, range 389–1565. http://rheumatology.oxfordjournals.org/cgi/content/abstract/ 43/12/1541
Fortunately, the fluctuations in UUA excretions are of far less concern to the geneticist who is armed with foreknowledge that the pups produced in the Backcross line will segregate into two distinctly different classes according to their levels of UUA excretion. If he can demonstrate that whichever test he uses differentiates between a normal UUA level and a high UUA level, and that the two classes do not over! lap, then his objective of matching the pups to the class carr! ying the normal gene and the class of those that are homozygous for the defective gene is solved.
The Dalmatian Backcross project has used and continues to use the UUA:CR ratio test for puppy classification purposes only. When I get to the urinary excretion test results and the correlations of these results with a specific genetic microsatellite marker, I will discuss this matter in greater detail.
I add as a footnote that other recent studies have also used UUA:CR ratio tests. Urology. 2003 Sep;62(3):566-70. Carvalho M, Lulich JP, Osborne CA, Nakagawa Y. "Role of urinary inhibitors of crystallization in uric acid nephrolithiasis: Dalmatian dog model."
I will have more to say about the role of urinary crystallization inhibitorst. It is relevant to the discussion because such inhibitors have been postulated as a reason why, though all Dalmatians excrete high levels of uric acid, not all Dalmatians form urate stones.
How one insures that the normal gene is passed o! n to succeeding generations.
I have already discussed the use of various urinary uric acid testing procedures and briefly discussed their weaknesses. I observed that the job of the geneticist working on the Backcross project is considerably easier than that of the veterinary clinician treating stone forming Dalmatians. Nonetheless, the Backcross geneticist must select for further breeding, with a high degree of confidence only those Dals that carry the normal UUA gene.
Let us assume that there are 8 puppies produced in a litter where the sire carries one copy the normal UUA gene and the dam is homozygous for the defective UUA gene. The pups should segregate into two classes: a low-UUA class and a high-UUA class, and the most probable split is 4 of each. Of course, getting that exact ratio is not guaranteed. In fact, all 8 pups might fall into the one class or the other -- though that outcome is unlikely (about 4 chances in a thousand for either extreme).
The ! Backcross breeder will use the computed UUA:CR ratios for each! pup in the litter and can plot these values as points along the x-axis on a graph. Examining the plot almost certainly identifies the puppies that belong to each of the two classes, since the human eye has great power to recognize patterns in data.
However, a statistician (even a blind statistician) can analyze the data using a simple algorithm that defines each class on the basis of a minimum variance algorithm. The details are interesting to me, but probably to no one else, so I will not go into them here. I will, however, give you the UUA:CR ratios as they were provided to me for one set of Backcross pups, Topper X Twyla litter, Aug, 2005, 8 pups:
UUA:CR ratios (mg/dl uric acid per mg/dl creatinine)0.2660.2820.2940.3190.3762.032.342.77
Is it possible that anyone looking at these data could fail to identify the high and low UUA classes? As far as puppy classifications are concerned, there is no mystery , there is no uncertainty begging further clarification, there ! is no skulduggery. The class boundaries are self-evident.
How one validates that the Dalmatian uric acid defect has been corrected.
It is important to reiterate: the genetic defect being addressed in the Backcross project is the high urinary uric acid excretion which predisposes Dalmatians to urate and uric acid stones.
-- Non-Dalmatian normal uric acid excretion (10-60 mg of uric acid per day)-- Dalmatian range for uric acid excretion (400-600 mg of uric acid per day)
Data already exist that place urinary uric acid concentrations for the low-UUA Backcross Dalmatian class in the same range as urinary uric acid samples taken from healthy Beagles. Without correcting for diurnal variations (which are influenced by digestion, absorption, and metabolism of their diets), direct comparisons of the uric acid concentration samples for Beagles and the Backcross Dals are impossible using the existing data set.
Let me be perfectly clear in this. I am referring ! to quantitative assessments of urinary uric acid excretions. I! am not questioning the legitimacy of the UUA:CR ratios as a discriminant used to classify the puppies from the Backcross litters according to whether or not they carry the normal UUA Pointer gene. I will have more to say on that matter later.
Although the 24-hour uric acid excretion values were used by Trimble and Keeler (1938) and have been discussed in Osborne and Finco (1995), they suffer to some degree from the same problem as the UUA:CR sample data. That is they do not reveal peak daily uric acid concentrations, nor do they account for the long-term, monthly fluctuations in uric acid excretion levels. However, from a purely practical standpoint, the 24-hour uric acid excretion values for a set of Backcross Dalmatians can be informative.
Without outlining at this time a detailed protocol for such a validation test (although a fairly straightforward blinded test can easily be worked out), I merely indicate that I, for one, believe that a limited set of 24-hour tests is! entirely appropriate and achievable.
Current status of the Backcross project and location of the defective gene in the Dalmatian genome.
For me this topic is the probably the most fascinating of any that I have covered in this discussion. First, I want to draw your attention to a very recent publication:
Mammalian Genome. 2006 Apr;17(4):340-5. Epub 2006. Linkage analysis with an interbreed backcross maps Dalmatian hyperuricosuria to CFA03., Safra N, Schaible RH, Bannasch DL. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&list _uids=3059479&dopt=Abstract
"Dalmatians, like humans, excrete uric acid in their ! urine. All other dogs and most mammals excrete allantoin, a wa! ter-solu ble compound that is further along the purine degradation pathway. Excretion of uric acid at high concentrations (hyperuricosuria) predisposes Dalmatians to the formation of urinary urate calculi. Hyperuricosuria (huu) is found in all Dalmatians tested and is inherited as an autosomal recessive trait. A genome scan and linkage analysis performed on a Dalmatian x Pointer interbreed backcross detected a single linked marker, REN153P03, located on CFA03. Haplotype analysis of the region around this marker defined a 3.3-Mb interval flanked by single recombination events. This interval, which contains the huu mutation, is estimated to include 24 genes."
What this means is that a team of geneticists at UC Davis and Dr. Bob Schaible have successfully narrowed the search for the defective UUA Dalmatian gene to a fairly small region containing only about 24 genes on canine chromosome 3. (Dogs have 39 chromosomes with a total of about 30,000 genes.) So the search for the defectiv! e gene is rapidly closing in on its prey.
A marker on that chromosome, REN153P03, is close enough to the actual gene so that the marker can be used to flag the presence or absence of the normal UUA gene. If you are curious you can look at the marker map for canine chromosome 3 (CFA03) at: http://research.nhgri.nih.gov/dog_genome /guyon2003/ guyonmaps_data/cfa03.pdf You will find the marker, REN153P03, in the lower (magenta) depiction on that map.
A lot of information can be found both on the web and in various publications about the use of markers to aid the breeder in the selection of dogs for breeding and the elimination of hereditary diseases. A good foundational book on the subject is the AKCCHF publication, Future Dog, Breeding for Genet! ic Soundness, by Patricia J. Wilkie.
The significance of ! the REN1 53P03 marker to the Backcross project is that its use allows a breeder to identify Dals that carry the normal UUA gene by DNA analysis. Urinary uric acid excretion tests still remain as a valuable alternative. However, the DNA test has the advantage of distinguishing between a carrier and a homozygous normal condition.
How well do the DNA tests correlate with the UUA:CR tests? One of the investigators at UC Davis states: "We have never encountered a discrepancy between our [DNA] molecular testing and these phenotypes (low or high uric acid/creatinine)." So the correlation to date is perfect. Markers do not always give perfect correlations unless they lie very close to the defective gene, so this is very encouraging.
Summing up the progress on the project:
The normal UUA gene from the Pointer has been successfully integrated into the genome of the Dalmatian Backcross line.
The Dalmatian defective UUA gene, as expected, behaves like an autosomal recessive g! ene as reported by Trimble and Keeler in 1938.
The UUA:CR ratio test unambiguously discriminates between puppies that are carriers for the Pointer gene and those that do not carry the gene.
A gene marker has been located on canine chromosome 3 that can be used to identify Dals that carry the normal UUA gene and will also be able to identify Dals that are homozygous for that gene when they are produced.
The gene marker, REN153P03, correlates perfectly with the classifications of Backcross puppies based on the UUA:CR ratio test. IMO, this deserves a double smiley. :-) :-)
Alternative approaches for dealing with the uric acid defect
In this section. I will attempt here to look at other approaches to attacking the Dalmatian urate stone problem that afflicts far too many of our spotted companions.
Care and managementThis approach essentially maintains the status quo. Recommended methods for minimizing the risk for urinary stones include (1) adequate! hydration (there is some evidence that bottled, especially di! stilled, water can be beneficial), (2) provide ample opportunities for urination, (3) limit purine intake, (3) use pH test strips to monitor urine acidity, (4) use allopurinol under veterinary supervision to prevent recurrence.These basic Dalmatian husbandry procedures can help, but the underlying hereditary defect of high UUA excretion remains. Periods of stress, especially when accompanied by chronic diarrhea, can lead to acidification of urine and the formation of uric acid stones. http://www.urostonecenter.com/anatomy.aspFurther, unless uric acid levels are carefully monitored, treatment of stone-forming Dals with allopurinol can result in the formation of xanthine stones. http://www.marvistavet.com/html/body _uric_acid_stones_in_dalmatians.html
Gene implantationNow that the gene that causes the high UUA excretion in Dals is in the boresight of the researchers, some have suggested that high-tech gene splicing should be able to solve the Dalmatian defect without resorting to a crossbreeding to install the normal gene. Perhaps some day, but not in the foreseeable future."Gene transfer can be targeted to somatic (body) or germ (egg and sperm) cells. In somatic gene transfer the recipient's genome is changed, but the change is not passed on to the next generation. In germline gene transfer, the parents' egg and sperm cells are changed with the goal of passing on the changes to their offspring."Obviously, Dal breeders want to use germline gene transfer since they want the normal gene that is implanted to be passed on to the puppies."Germlin! e gene transfer is not being actively investigated, at least i! n larger animals and humans, although a great deal of discussion is being conducted about its value and desirability..." http://www.genome.gov/10004764There are so many intrinsic technical difficulties and risks associated with germline gene transfer, that the process is unlikely to offer a practical alternative for many years.
Selective breedingIt has been suggested that even though all Dals excrete high levels of uric acid, not all form stones. Therefore factors other than the uric acid defect must be involved. The reasoning continues: If breed lines that consistently produce Dals that do not form stones can be identified and the environmental and subsidiary genetic factors that mitigate the stone problem understood, then selective breeding should produce stone-free Dals. Although appealing at first, there are serious problems with this line of reasoning.First, we should note that environmental factors, which were briefly mentioned under 1., above, are not refined by selectiv! e breeding. If selective breeding is to prove useful, it must deal with identifiable hereditary traits. Such traits should have a reasonably high heritability to be amenable to artificial selection methods. Further, it must be possible to identify dogs that carry the desirable traits during the period of their lives that they are used for breeding. Unfortunately, the trait "does not form stones" can only be assigned with certainty after the dog's death.Second, we should recognize, particularly in light of Dr. Susanne Hughes ultrasound study, that the category "does not form stones" might be better classified as "has not yet formed stones."Nonetheless, recent studies with both Dalmatians and humans have identified a number of substances commonly found in urine that are known to inhibit crystal formation and the growth of urinary stones. One of the most studied is the naturally occurring Tamm-Horsfall protein which is a thick mucous material produced in the kidneys. This prot! ein is also known to provide some protection against bacterial! infecti on in the urinary tract.Carvalho M., and others at the University of Chicago found that the amounts of Tamm-Horsfall protein (THP), and glycosaminoglycans (GAGs) were lower in Dalmatians that formed stones when compared with Dalmatians that did not form stones. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd= Retrieve&dopt=abstract&list_uids=12946778& query_hl=7&itool =pubmed_docsumIf it can be demonstrated that the Tam-Horsfall protein gene in Dalmatians has several variants, and if the correlation between these genetic variants and the stone-forming status of Dalmatians is shown to be high, then selective breeding might help to minimize the ! stone-forming proclivity of Dalmatians in a carefully selected breeding line. A cautionary note must be inserted here. Inhibitors of urinary stone formation do not prevent crystals from being formed and growing. These inhibitors only increase the uric acid concentrations that are maintained in solution before saturation occurs and crystals are produced -- that is the reason they are called "inhibitors" rather than "preventatives."
This concludes my abbreviated foray into the rationale for and science of the Backcross project. It was my desire to turn away from Dalmatian club politics so that the merits of the Backcross project could be evaluated independently of the current ballot issue. I believe that at least to some degree I have succeeded
I may at times have appeared to act as a cheer leader for the project, and I must confess to being attracted to the idea of finally doing something positive and of lasting value for the genetic health of a popular canine bree! d. Except for providing advice, I am not affiliated with the B! ackcross project.
I am tired of reading articles like Stephen Budiansky's "The Truth about Dogs" which you will remember from the 1999 Atlantic Monthly. We really can make a difference.

Dr. Seltzer first shared this information with members of ShowDals, an online list for Dalmatian breeders and owners, in June 2006.
Dr. Seltzer has been a member of the Dalmatian Club of America since 1976. He bred Dalmatians under the Willowind kennel name. The Willowwind website can be found at: http://users.nbn.net/jseltzer/

the problems with cross breeding

Perm url with updates: http://xahlee.org/js/css2.html

CSS1 And CSS2 Differences

Xah Lee, 2005-11, ..., 2010-08-21

This page shows the primary features in CSS2 not in CSS1. If you are not familiar with CSS, see: CSS Basics. If you know the basics and want a practical examples of css tag matching supported by all current versions of browsers, see: CSS Tag Matching (Selector) Syntax.

CSS1 is published in 1996. CSS2 is published in 1998. As of today, all major browsers supports pratically 99.9% of CSS2. CSS3 is in works but not out yet.

Note: there's no way to specify a CSS version number in your HTML markup. Just test with browsers if you must use new features.

Tag Matching

CSS2 provides more powerful ways to associate styles with tags.

“*” matches any tag.

 /* make everything red */ * {color:red} 

“>” means parent-child relationship.

 /* p inside div of class header inside body */ body > div.header > p {color:red} 

Space can be used to specify that a tag must have other tags as its ancestor.

 /* make any div.x inside table red */ table div.x {color:red} 

“+” can be used to specify some restriction on same level tags.

 /* if p comes immediately after img, make the text red */ img + p {color:red}

Pseudo-class: link, hovering, focus, first child...

There are special syntax to match some mouse hovering, focusing, behaviors. (these “:xxx” forms are called pseudo-class.)

 a:link {color:red} a:visited {color:green} a:hover {color:yellow}  div.myButtonX:hover {color:red} div.myButtonX:active {color:green} div.myButtonX:focus {color:yellow} 

“:first-child” can be used to match a tag only if it is the first child.

 /* make first line of list red */ li:first-child {color:red} 

“:first-letter” and “:first-line” can be used. e.g.

 p:first-letter {color:red} p:first-line {color:blue} 

For detail, see: CSS “first-letter” and “first-line” Example.

Matching Tags with Attributes

Existance of a Attribute

You can match the existance of a attribute, by the syntax “tagName[attributeName]”.

 /* if a link has a “title” attribute, render the link red */ a[title] {color:red} 

Matching Attribute Values

You can match a tag's attribute's value, using the syntax “tagName[attributeName="valueString"]”.

/* if a image's alt attribute is “icon”, set a red border */ img[alt="icon"] {border:solid thin red} 

Matching a Word in the Attribute's Value

A word in the value of a attribute can be matched, by using the operator “~=”.

 /* if a image's alt text has the word “house” in it, set a red border */ img[alt~="house"] {border:solid thin red} 

Layout, Layers, Tabular Format, and Text Flow

A very important feature in CSS2 is the ability to do layout and with layers.

Layout and Layers

Layout is to specify the position of each item, in a absolute coordinate or relative to its parent. In HTML, It is often done in practice by using Table tag with width attribute.

In CSS2, layout are done with attributes “display” and “position”. The value fo “position” can be “absolute” or “relative”. There's also attributes “top”, “bottom”, “left”, “right”, and each's value is a length unit. Example:

 AAA {display:block;} BBB {display:block; position:absolute; top:300px, left:50px} CCC {display:block; position:relative; left:100px} 

Examples: CSS Layout and Layers

Example: Fixed Widget with Cascading Style Sheet

CSS2 allows one to specify which element should be displayed on top of another (hiding the one behind). This is done with the “z-index” attribute. The parameter for z-index are integers. The larger the integer, the more front it is.

 BBB {display:block; position:absolute; top:300px; z-index:50} CCC {display:block; position:absolute; top:300px; z-index:2} 

Another useful directive is the “visibility” attribute. It can be set to “visible” or “hidden”, giving more control of CSS2's layout capabilities. This can be used in conjunction with javascript to fruitful effects. For example, if you have tabs on a page, clicking a tab can automatically make the main area content associated with that tab visible, while make all content associated with other tabs hidden.

The CSS2's layering and layout feature is used to implement pop-up tooltips.

Tabular Format

• CSS2 has the ability to specify a table format. This in conjunction with “position” and “z-index” can achieve may web-design effects. For example:

 * {border: solid} AAA {display: table} BBB {display: table-row} CCC {display: table-cell} DDD {display: table-cell} 

will render the following XML code:

 <AAA>   <BBB>     <CCC>ccc1</CCC>     <DDD>ddd1</DDD>   </BBB>   <BBB>     <CCC>ccc2</CCC>     <DDD>ddd2</DDD>   </BBB>   <BBB>     <CCC>ccc3</CCC>     <DDD>ddd3</DDD>   </BBB> </AAA> 

like a table as in HTML:

 <table border="1">   <tr>    <td>ccc1</td>    <td>ddd1</td>   </tr>   <tr>     <td>ccc2</td>     <td>ddd2</td>   </tr>   <tr>     <td>ccc3</td>     <td>ddd3</td>   </tr> <table> 

See a example here: Tabular Formatting with CSS2

“white-space” has a new behavior spec: nowrap. Example:

 BBB {white-space: normal} CCC {white-space: pre} DDD {white-space: nowrap} 

Example: CSS Text Wrapping.

Changing Content

Text can be inserted at the beginning or end of specified tag, using “:before” and “:after”. e.g.

 AA:before {content:'Proof: '} AA:after {content:'End of Proof.'} 

for element such as:

 <AA>because 1+1 is 2, therefore I win.</AA> 

will become

 <AA>Proof: because 1+1 is 2, therefore I win. End of Proof.</AA> 

Example: css_before_after.html

Color, Background image, Tex decoration, Font

CSS2 supports color names of Browser's GUI. For Example:

 A {color:AppWorkspace} B {color:ButtonFace} C {color: ButtonHighlight} D {color:ButtonText} E {color:CaptionText} F {color:Highlight} G {color:HighlightText} 

Example: CSS2's System Colors.

Several features are new in CSS2 for background image. It can be repeated, or just horizontally or vertically. It can also be fixed, so that scrolling doesn't move it. Example:

 AAA {background-image:url("some.gif")} AAA {background-repeat:repeat-x} AAA {background-position: top} AAA {background-attachment: fixed} 

A new tag text-shadow can have size and color.

 BBB {text-shadow: 5px 12px red} 

Font can now be specified based on Browser's setup. e.g.

 AAA {font:caption} BBB {font:small-caption} CCC {font:status-bar} 

Mouse Pointer or Cursor's shape can be specified. e.g.

 AAA {cursor: crosshair} BBB {cursor: pointer} CCC {cursor: move} DDD {cursor: e-resize} EEE {cursor: text} FFF {cursor: wait} help {cursor: help} uri {cursor: url(".../pointer.gif")} 

• CSS “position” Tutorial
• CSS Example of Text over Image
• Centering with CSS
• Flowing List Items

tabular format example

Tutor For Statistics Can Help Students Master This Tricky Subject

Statistics can be a tricky subject. I know, because my job involves a lot of it! I went through 9 years of undergraduate and graduate-level engineering courses, and it included a lot of statistics. But even now, I am stumped by some arcane aspect of the subject that I evidently did not pay enough attention to when I should have!

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