BEGIN:VCALENDAR VERSION:2.0 PRODID:-//jEvents 2.0 for Joomla//EN CALSCALE:GREGORIAN METHOD:PUBLISH BEGIN:VTIMEZONE TZID:America/Denver BEGIN:STANDARD DTSTART:20141102T010000 RDATE:20150308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20151101T010000 RDATE:20160313T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20161106T010000 RDATE:20170312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20171105T010000 RDATE:20180311T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20181104T010000 RDATE:20190310T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20191103T010000 RDATE:20200308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20201101T010000 RDATE:20210314T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20211107T010000 RDATE:20220313T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20221106T010000 RDATE:20230312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20231105T010000 RDATE:20240310T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20241103T010000 RDATE:20250309T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20251102T010000 RDATE:20260308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20261101T010000 RDATE:20270314T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20271107T010000 RDATE:20280312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20281105T010000 RDATE:20290311T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20291104T010000 RDATE:20300310T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20301103T010000 RDATE:20310309T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20311102T010000 RDATE:20320314T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20321107T010000 RDATE:20330313T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20331106T010000 RDATE:20340312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20341105T010000 RDATE:20350311T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20351104T010000 RDATE:20360309T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20361102T010000 RDATE:20370308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20371101T010000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:DAYLIGHT DTSTART:20140525T070000 RDATE:20141102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20150308T030000 RDATE:20151101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20160313T030000 RDATE:20161106T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20170312T030000 RDATE:20171105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20180311T030000 RDATE:20181104T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20190310T030000 RDATE:20191103T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20200308T030000 RDATE:20201101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20210314T030000 RDATE:20211107T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20220313T030000 RDATE:20221106T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20230312T030000 RDATE:20231105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20240310T030000 RDATE:20241103T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20250309T030000 RDATE:20251102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20260308T030000 RDATE:20261101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20270314T030000 RDATE:20271107T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20280312T030000 RDATE:20281105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20290311T030000 RDATE:20291104T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20300310T030000 RDATE:20301103T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20310309T030000 RDATE:20311102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20320314T030000 RDATE:20321107T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20330313T030000 RDATE:20331106T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20340312T030000 RDATE:20341105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20350311T030000 RDATE:20351104T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20360309T030000 RDATE:20361102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20370308T030000 RDATE:20371101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT END:VTIMEZONE BEGIN:VEVENT UID:468b0935d7b7307db1303cb9cc0abb53 CATEGORIES:LSDM CREATED:20150523T101039 SUMMARY:Shawnie Bray DESCRIPTION:  \n  \n  \n    "I believed I was living a truncated life... so, I never took a new day for granted."   Travis Bray Founder, FAPFoundation     Above:  Travis Bray speaks to La Societe Deux Magots (LSDM) on 18 Feb 2014, Wasatch Bagel, Park City, UT.   Travis H. Bray is a third ge neration familial adenomatours polyposis (F.A.P) survivor and understands f irsthand the long-reaching physical and emotional effects living with this disease has on both the patient and their loved ones. By drawing upon both personal experiences with F.A.P. and those of his extended family, he is mo tivated to developing a support net for those born or affected by F.A.P. Tr avis graduate with top honors for his graduate work in Actinide Chemistry a t Auburn University in 2008. He continued his research for two years as the Berkeley Actinide Postdoctoral Fellow at Lawrence Berkeley National Labora tory, and a third year of post-doctoral research at Argonne National Labora tory. Travis stepped away from his career as a chemistry researcher (June, 2012) to found the F.A.P. Foundation.   Hat tip: Event     Abo ve:  Travis Bray presses a point as he educates LSDM members on familial ad enomatours polyposis, a congenital colon cancer.  Wasatch Bagel, 18 Februar y 2014.     http://ghr.nlm.nih.gov/condition/familial-adenomatous-pol yposis (http://ghr.nlm.nih.gov/condition/familial-adenomatous-polyposis) What is familial adenomatous polyposis? Familial adenomatou s polyposis (FAP) is an inherited disorder characterized by cancer of the l arge intestine (colon) and rectum. People with the classic type of familial adenomatous polyposis may begin to develop multiple noncancerous (benign) growths (polyps) in the colon as early as their teenage years. Unless the c olon is removed, these polyps will become malignant (cancerous). The averag e age at which an individual develops colon cancer in classic familial aden omatous polyposis is 39 years. Some people have a variant of the disorder, called attenuated familial adenomatous polyposis, in which polyp growth is delayed. The average age of colorectal cancer onset for attenuated familial adenomatous polyposis is 55 years.\n In people with classic famili al adenomatous polyposis, the number of polyps increases with age, and hund reds to thousands of polyps can develop in the colon. Also of particular si gnificance are noncancerous growths called desmoid tumors. These fibrous tu mors usually occur in the tissue covering the intestines and may be provoke d by surgery to remove the colon. Desmoid tumors tend to recur after they a re surgically removed. In both classic familial adenomatous polyposis and i ts attenuated variant, benign and malignant tumors are sometimes found in o ther places in the body, including the duodenum (a section of the small int estine), stomach, bones, skin, and other tissues. People who have colon pol yps as well as growths outside the colon are sometimes described as having Gardner syndrome.\n A milder type of familial adenomatous polyposis , called autosomal recessive familial adenomatous polyposis, has also been identified. People with the autosomal recessive type of this disorder have fewer polyps than those with the classic type. Fewer than 100 polyps typica lly develop, rather than hundreds or thousands. The autosomal recessive typ e of this disorder is caused by mutations in a different gene than the clas sic and attenuated types of familial adenomatous polyposis.\n Ho w common is familial adenomatous polyposis? The reported incid ence of familial adenomatous polyposis varies from 1 in 7,000 to 1 in 22,00 0 individuals.\n What genes are related to familial adenomatous polyposis? Mutations in the APC gene cause both classic and at tenuated familial adenomatous polyposis. These mutations affect the ability of the cell to maintain normal growth and function. Cell overgrowth result ing from mutations in the APC gene leads to the colon polyps seen in famili al adenomatous polyposis. Although most people with mutations in the APC ge ne will develop colorectal cancer, the number of polyps and the time frame in which they become malignant depend on the location of the mutation in th e gene.\n Mutations in the MUTYH gene cause autosomal recessive fam ilial adenomatous polyposis (also called MYH-associated polyposis). Mutatio ns in this gene prevent cells from correcting mistakes that are made when D NA is copied (DNA replication) in preparation for cell division. As these m istakes build up in a person's DNA, the likelihood of cell overgrowth incre ases, leading to colon polyps and the possibility of colon cancer.\n Read more about the APC (http://ghr.nlm.nih.gov/gene/APC) and MUTYH (http ://ghr.nlm.nih.gov/gene/MUTYH) genes.\n How do people inherit fa milial adenomatous polyposis? Familial adenomatous polyposis c an have different inheritance patterns.\n When familial adenomatous polyposis results from mutations in the APC gene, it is inherited in an au tosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person has one parent with the condition.\n When familial adenomatous pol yposis results from mutations in the MUTYH gene, it is inherited in an auto somal recessive pattern, which means both copies of the gene in each cell h ave mutations. Most often, the parents of an individual with an autosomal r ecessive condition each carry one copy of the mutated gene, but do not show signs and symptoms of the condition.\n     Takeaways...   One cure.  Total colonectomy.    33% of those contracting are de nov o... ie. gene mutation in parent.   In last 90 days, six individual s with F.A.P. have died.   2013. 144k deaths from colon cancer... o f which, 5% are hereditary (1% F.A.P.).   Travis diagnosed at 15 years of age.  Colon removed replaced by "J patch" fashioned by removed section of small intestine.  "J patch" is one of seven surgical procedures used for disease.   In his early 30's Travis relapsed... effects of the cancer spread to duodenum.    "I believed I was living a truncated life... so, I never took a new day for granted."    Travis left a promising career in chemical and nuclear research to form FAPFoundation.  http://www.hcctak esguts.org/ (http://www.hcctakesguts.org/)   Travis, a trained research er, was amazed at the significant amount of scientific research on F.A.P.  But, none of the research was available in easy to understand, synthesized form for the average afflicted person.  Because of the diseases rarity, the average physician had little knowledge.  The condition was often diagnosed as hemorrhoids or some such...   Drawn from Argonne National Laborator y in Illinois, to Huntsman Cancer Center, Salt Lake City where the world's top experts in F.A.P. work... Randy Burt, Deb Meckelson... they have connec ted F.A.P. "to the 5th gene..."  they are the best at hereditary cancers in the world.  Their scientific progress was facilitated by their extensive u se of LDS church familial and hereditary records.   "I learned from Mec kelson that there was no reason I couldn't live a long life. I was virtuall y given a new life by my connection with the people at Huntsman.   "I have found my niche."   FAPFoundation is located in Park City, UT and is run by Travis and his wife.   Supporters of FAPFoundation are 60% individu als and 40% corporations.  We have a good network of friends and family.   The National Society of Genetic Counselors has 700 members.  We work cl osely to educate genetic counselors on F.A.P.   Five scientists/researc hers at Huntsman are on the board of FAPFoundation.     Thank-you.   LSDM thanks Travis Bray for his very informative presentation about the little understood colon affliction, familial adenomatours polyposis, and c ongratulates him for his dedication making this affliction better known.     La Societe Deux Magots (LSDM) is a non-partisan ROMEO (retired old men eating out) group which meets daily, at 7:00 AM at Wasatch Bagel in Par k City, UT. LSDM members are the rightful intellectual heirs of a group of authors (Hemingway, Sartre, Camus, deBouvoir) who met daily at Cafe Deux Ma gots, in Paris, France in the 1930's.    \n  \n  \n La Societe Deux Ma gots (LSDM) is a non-partisan ROMEO (retired old men eating out) group whic h meets daily, at 7:00 AM at Wasatch Bagel in Park City, UT. LSDM members a re the rightful intellectual heirs of a group of authors (Hemingway, Sartre , Camus, deBouvoir) who met daily at Cafe Deux Magots, in Paris, France in the 1930's.) www.lsdm-parkcity.com (http://www.lsdm-parkcity.c om/)\n   X-ALT-DESC;FMTTYPE=text/html:

 

 

 

  
< strong>"I believed I was living a truncated life... so, I never took a new day for granted."
 
Travis Bray
Founder, FAPFoundation
 
 
Above:  Travis B ray speaks to La Societe Deux Magots (LSDM) on 18 Feb 2014, Wasatch Bagel, Park City, UT.
 
Travis H. Bray is a third generation familial adenomatours polypo sis (F.A.P) survivor and understands firsthand the long-reac hing physical and emotional effects living with this disease has on both th e patient and their loved ones. By drawing upon both personal experiences w ith F.A.P. and those of his extended family, he is motivated to developing a support net for those born or affected by F.A.P. Travis graduate with top honors for his graduate work in Actinide Chemistry at Auburn University in 2008. He continued his research for two years as the Berkeley Actinide Pos tdoctoral Fellow at Lawrence Berkeley National Laboratory, and a third year of post-doctoral research at Argonne National Laboratory. Travis stepped a way from his career as a chemistry researcher (June, 2012) to found the F.A .P. Foundation.
 
Hat tip: Event
 
 
Above:  Travis Bray presses a point as he educates LSDM members on familial adenomatours polypo sis, a congenital colon cancer.  Wasatch Bagel, 18 February 2014.
 
 
http://ghr.nlm.nih.gov/condition/familial-ade nomatous-polyposis

What is familial adenomatous polyposis?

Familial adenomato us polyposis (FAP) is an inherited disorder characterized by cancer of the large intestine (colon) and rectum. People with the classic type of familia l adenomatous polyposis may begin to develop multiple noncancerous (benign) growths (polyps) in the colon as early as their teenage years. Unless the colon is removed, these polyps will become malignant (cancerous). The avera ge age at which an individual develops colon cancer in classic familial ade nomatous polyposis is 39 years. Some people have a variant of the disorder, called attenuated familial adenomatous polyposis, in which polyp growth is delayed. The average age of colorectal cancer onset for attenuated familia l adenomatous polyposis is 55 years.

In people with classic familial adenomatous polyposi s, the number of polyps increases with age, and hundreds to thousands of po lyps can develop in the colon. Also of particular significance are noncance rous growths called desmoid tumors. These fibrous tumors usually occur in t he tissue covering the intestines and may be provoked by surgery to remove the colon. Desmoid tumors tend to recur after they are surgically removed. In both classic familial adenomatous polyposis and its attenuated variant, benign and malignant tumors are sometimes found in other places in the body , including the duodenum (a section of the small intestine), stomach, bones , skin, and other tissues. People who have colon polyps as well as growths outside the colon are sometimes described as having Gardner syndrome.

A milder type of fa milial adenomatous polyposis, called autosomal recessive familial adenomato us polyposis, has also been identified. People with the autosomal recessive type of this disorder have fewer polyps than those with the classic type. Fewer than 100 polyps typically develop, rather than hundreds or thousands. The autosomal recessive type of this disorder is caused by mutations in a different gene than the classic and attenuated types of familial adenomatou s polyposis.

How common is familial adenomatous polyposis?

The reported inc idence of familial adenomatous polyposis varies from 1 in 7,000 to 1 in 22, 000 individuals.

What genes are related to familial adenomatous polyposis?< /h2>

Mutat ions in the APC  gene cause both classic and attenuated familial adenomatous polyposis. Thes e mutations affect the ability of the cell to maintain normal growth and fu nction. Cell overgrowth resulting from mutations in the APC gene leads to the colon polyps seen in familial adenomatous polyposis. Although most people with mutations in the APC gene will develop colorectal cancer, the number of polyps and the time frame in which they become malignant depend on the location of the mutation in the gene.

Mutation s in the MUTYH g ene cause autosomal recessive familial adenomatous polyposis (also called M YH-associated polyposis). Mutations in this gene prevent cells from correct ing mistakes that are made when DNA is copied (DNA replication) in preparat ion for cell division. As these mistakes build up in a person's DNA, the li kelihood of cell overgrowth increases, leading to colon polyps and the poss ibility of colon cancer.

Read more about the APC and MUTYH genes.

How do people inheri t familial adenomatous polyposis?

Familial adenomatous polyposis can have differ ent inheritance patterns.

When familial adenomatous polyposis results from mutations in t he APC gene, it is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most case s, an affected person has one parent with the condition.

When familial adenomatous polypo sis results from mutations in the MUTYH gene, it is inherited in an autosomal recessive pat tern, which means both copies of the gene in each cell have mutations. Most often, the parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but do not show signs and symptoms of the condition.

 
 
Takeaways...
 
One cure.  Total colonectomy. 
 
33% of those contracting are de novo... ie. gene mutation in parent.< /div>
 
In last 90 days, six individuals with F.A.P . have died.
 
2013. 144k deaths from colon c ancer... of which, 5% are hereditary (1% F.A.P.).
 
Travis diagnosed at 15 years of age.  Colon removed replaced by " J patch" fashioned by removed section of small intestine.  "J patch" is one of seven surgical procedures used for disease.
 
In his early 30's Travis relapsed... effects of the cancer spread to duode num. 
 
"I believed I was living a truncated life ... so, I never took a new day for granted." 
 
T ravis left a promising career in chemical and nuclear research to form FAPF oundation.  http://www.hcctakesguts.org/
 
T ravis, a trained researcher, was amazed at the significant amount of scient ific research on F.A.P.  But, none of the research was available in easy to understand, synthesized form for the average afflicted person.  Because of the diseases rarity, the average physician had little knowledge.  The cond ition was often diagnosed as hemorrhoids or some such...
 
Drawn from Argonne National Laboratory in Illinois, to Huntsman C ancer Center, Salt Lake City where the world's top experts in F.A.P. work.. . Randy Burt, Deb Meckelson... they have connected F.A.P. "to the 5th gene. .."  they are the best at hereditary cancers in the world.  Their scientifi c progress was facilitated by their extensive use of LDS church familial an d hereditary records.
 
"I learned from Meckelson that there was no reason I couldn't live a long life. I was virtually give n a new life by my connection with the people at Huntsman.   "I have found my niche."
 
FAPFoundation is located in Park Cit y, UT and is run by Travis and his wife.
 
Suppor ters of FAPFoundation are 60% individuals and 40% corporations.  We have a good network of friends and family.
 
The Nationa l Society of Genetic Counselors has 700 members.  We work closely to educat e genetic counselors on F.A.P.
 
Five scientists/ researchers at Huntsman are on the board of FAPFoundation.
 
 
Thank-you.
 
LSDM thanks Travis Bray for his very informat ive presentation about the little understood colon affliction, familial ade nomatours polyposis, and congratulates him for his dedication making this a ffliction better known.
 
 
La Societe Deux Magots (LSDM) is a non-partisan ROMEO (retired old men eating out) group wh ich meets daily, at 7:00 AM at Wasatch Bagel in Park City, UT. LSDM members are the rightful intellectual heirs of a group of authors (Hemingway, Sart re, Camus, deBouvoir) who met daily at Cafe Deux Magots, in Paris, France i n the 1930's.
 

 

 

 

La Societe Deux Magots ( LSDM) is a non-partisan ROMEO (retired old men eating out) group which meet s daily, at 7:00 AM at Wasatch Bagel in Park City, UT. LSDM members are the rightful intellectual heirs of a group of authors (Hemingway, Sartre, Camu s, deBouvoir) who met daily at Cafe Deux Magots, in Paris, France in the 19 30's.)
< div>  
DTSTAMP:20260424T140624 DTSTART;TZID=America/Denver:20150526T070000 DTEND;TZID=America/Denver:20150526T080000 SEQUENCE:0 TRANSP:OPAQUE END:VEVENT END:VCALENDAR