On 10 July 2000, a survey was conducted on the SLOAN-SLONE Discussion Group.  It was discovered that Sloans (all spellings) were dark, fair, tall, short, dark haired, blonds, and red heads.  All tend to be independant and stubborn!

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"Crooked Pinkie"
A suprising number of people have reported that a crooked little finger was a Sloan trait.  At this point, I'm not sure if this "Crooked Pinkie" trait is restricted to Sloans or is common everywhere.  So far it has been reported in these Sloan family lines:

David Sloan/Major, of Co. Down Ireland & Anderson Co. SC.
David Sloan/Watson line of Co. Antrim Ireland, & Wythe Co. Va.
Elizabeth Sloan/Morrison line of Lancaster Co. NC.
George Thomas Sloan line of Co. Cork Ireland & Laurens Co. SC.
James Sloan Jr./Brown line of Mecklenburg Co. NC.
John & Eleanor Sloan line of Pittsylvania Co. VA.
John Slone/Henry line of Va. & Gallia Co. Oh.
John Slone/Minix line of Tn. Al. & Coryell Co. Tx.
John Sloan/McNair line of Co. Artrim Ire./Laurens Co. SC.
John Sloan/Wilson line from possibly Killinchy, Co. Down Ireland
James Sloan/Montgomery line of Co. Antrim Ire. & Henry Co. IL.
James Slowan/Andrew of Dundonald, Ayrshire Co. Scotland
Jonathan Sloan/Jenkins line of Va. Jackson Co. Tn. & Simpkins Co. Ky.
Joseph Adam Sloan/McDonald line of Pa. & Meigs Co. Oh.
Samuel Sloan/Rutherford line of Mason Co. Il.
Shadrac & Winna Slone of Va. & Pike Co. Ky.
Thomas Sloan/Brock of Harlan & Clay Co. Ky.
William Sloan/Slown/Slowan/Kincaid line of Co. Antrim Ireland & Owen Co In.
William Slone/Sizemore{n.a.} line of Va. & Floyd Co. Ky.
William Harvey Sloan/Starr{n.a.} line of Ky. & McDonald Co. Mo.
William Wand Sloan/Guthrie line of Ire. & Chester Co. Pa.

Jonathan Sloan/Jenkins line of Va. Jackson Co. Tn. & Simpkins Co. Ky.
Joseph L. Sloan/Carter line of NC. & Hamlen Co. Tn.

I think this will be a common trait among the overweight baby-boomer generation!  f.e.m.

drop me a note: 

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? Sloane's Tooth ?
Crooked incisor tooth- it slightly overlaps the front tooth.
or
 Incisor (front bottom left) is set back a little from the other rows of teeth.

William Sloan/Slown/Kincaid line of Co. Antrim Ireland & Owen Co In.

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Hereditary Pancreatitis
This trait is more serious and the only one that has been documented.
If you descend from the Slone/Sloan/Sloane/Slown families of Eastern Kentucky, I highly recommend you visit this Hereditary Pancreatitis Website
original website w/article no longer available

David C. Whitcomb, MD, PhD Editoral
It takes a family

In 1972, two physicians at the University of Indiana, Robert McElroy and the late Philip Christiansen, published a paper in the American Journal of Medical Genetics on a large pedigree known as the 'S. family,' residing in the   neighbouring state of Kentucky, that was affected with a rare autosomal dominant form of a disease called     pancreatitis1. Affected individuals usually begin to show symptoms during childhood, suffering severe and     untreatable (although not usually life-threatening) bouts of epigastric pain. The sporadic form, which is diagnosed
more than 40,000 times each year in the United States, is usually attributable to diets rich in fatty foods or to
alcohol, as well as to stress. Hereditary pancreatitis had first been reported in the literature 20 years earlier, in
1952, but although the 'S. family' was one of the largest pedigrees with the disorder on record, the report by
McElroy and Christiansen was otherwise fairly unremarkable. The low prevalence and inability to treat the disease
did little to generate interest among fellow researchers, and an attempt to map the gene in the late 1970s failed.

But for the Slone family, the disease was anything but rare. Indeed, in large areas of Kentucky, their mysterious
ailment was known simply as 'Slone's disease,' reflecting the spread of the branches of the family tree. In 1989,
Kevin, then a teenager, became so sick that he was admitted to hospital suffering from blood clots in his pancreas
and kidney failure. He was officially diagnosed with hereditary pancreatitis, one of just a few hundred such
diagnoses in the United States each year. The attacks were so severe that he had to be fed intravenously, and was
not even allowed to suck ice chips. As Slone recently told the Wall Street Journal, "You don't realize how many
food commercials are on TV until you can't eat."2 Kevin's father, Bobby, began to compile a family tree, hoping to
chart the passage of the errant gene through his family. Likening himself to "a basketball player who throws the
ball inbounds," Slone contacted relatives and friends, slowly piecing together information about his extended family
and marking those who had suffered from the distinctive illness. The result was a pedigree of some 700 individuals
spanning nine generations2.

While Slone was researching his personal genealogy, researchers at the University of Pittsburgh, led by David
Whitcomb and Garth Ehrlich, decided to attempt to map and clone the gene for hereditary pancreatitis by
collecting suitable family material. Whitcomb was hoping that the hereditary disorder would provide a good model
for the more common (alcoholic) form of pancreatitis, and realised the project was feasible after Ehrlich localized
the gene for Crouzon syndrome in 1994. Whitcomb contacted one of his former colleagues, a gastroenterologist
named Lawrence Gates who had just set up a pancreatitis clinic at the University of Kentucky, and asked him to
keep an eye out for suitable patients. Not long afterwards, Bobby Slone entered the clinic clutching a
computerized print-out of his family tree. His son had just suffered another relapse, and had been admitted to
hospital suffering from chronic pancreatitis (more than three quarters of his pancreas was scar tissue). The timing
was especially fortunate, as Richard McElroy, the physician who had first worked with members of the Slone
family, had retired and just thrown away his records, thinking that after two decades, no-one would have any
need for them. The search for the S. family was over; the hunt for the gene was just beginning.

Eighteen months ago, Bobby Slone convened a family reunion at a park on the Kentucky­Virginia border, and
while 90 relatives swapped stories, doctors took blood samples. Progress was swift: by February this year, the
Pittsburgh team had successfully mapped the gene for hereditary pancreatitis3 to the long arm of chromosome 7.
A French group independently reached the same conclusion4. As luck would have it, the location not only
coincided with the known position of a pair of trypsinogen genes, but was also in the vicinity of the ß T-cell
receptor locus, the subject of a major sequencing effort by Lee Rowen and colleagues. Although their results5
were not yet published, much of the raw data had been deposited in GenBank, allowing the Pittsburgh team to
exclude a number of trypsinogen pseudogenes in their search. Less than three months after the gene had been
mapped, the gene had been found (see page 141)5.

Cationic trypsinogen is the precursor of trypsin, one of the digestive enzymes secreted by the pancreas. The
zymogen is activated in the intestine, setting in motion a feedback loop in which trypsin catalyses its own
conversion from the inactive precursor. Normally, a delicate balance of activation and enzymatic inhibition is
maintained, ensuring that activated trypsin does not damage its host tissue. But when Whitcomb et al.6 examined
the trypsinogen gene from affected members of the Slone family and four other pedigrees, they discovered an
arginine-to-histidine missense mutation that segregated perfectly in each case. Based on X-ray crystallography
data and good evidence that Arg 117 constitutes the main cleavage site during trypsin degradation, the authors
believe that the Arg-to-His mutation disrupts this important cleavage site. As a result, trypsin autoactivation would
probably proceed unchecked, and autodigestion of the pancreas thus ensues. Not all cases of hereditary
pancreatitis are explained so neatly, however. Ehrlich's group has recently identified a different mutation in one of
their families that seems to act somewhat differently.

One of the immediate benefits of the discovery is the opportunity to offer counselling to members of affected
families such as the Slones. Family members are being contacted and offered the opportunity to undergo genetic
testing, which many have indicated they would like to receive. With the basis for hereditary pancreatitis at least
partially understood, the possible association of trypsinogen variants with the sporadic disease can be examined.
Work is also in progress to produce valid mouse models of the hereditary disease, in the hope of developing some effective therapies where at present, there are none.

Since the first description of a family with hereditary pancreatitis in 1952, only about two families per year on
average have been recorded, perhaps explaining in part why study of this rare disease was never a priority for the
genetics community. Nevertheless, the identification of the gene offers yet another telling example of how rapidly
research can move from linkage to locus. The authors believe their success owes a great deal to the Human Genome Project and the welcome existence of hundreds of kilobases of genomic sequence in their candidate region. It also serves as a testimonial to the tireless cooperation of long-suffering families such as the Slones. After decades of cooperation with the research community, it would be fitting if they can finally reap some benefit.

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This Webpage is always looking for info, your corrections,comments and suggestions are welcome.
Franklin E. Mitchell
Apartado 0818-00117
Panama, Republic of Panama
Or E-mail: 
Last updated 2 Dec 2007

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