A Family Blog for Family & Friends
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On December 5th, we as a family were given unimaginable news, our father
and husband, Steve, has Creutzfeldt-Jakob Disease (CJD.) We knew it was a
possibility but were ever hopeful it was not this tragic news. Knowing the
disease is rapidly progressive and always fatal was heartbreaking. Though we are
grateful for every moment we still have left with him, seeing a man of his
brilliance, sense of humor and love deteriorate is horribly painful for family,
friends, and co-workers. We cannot express how thankful we are to the hundreds
of well-wishes, meals, donations, prayers, thoughts, etc we have received from
the community. It has been an overwhelming amount of support that we will be
forever thankful for. We still have a difficult road ahead of us and we hope to
keep dad’s community from CDC to basketball, to family and friends, aware of
what is happening through the main website and this blog.
December 30, 2012 by teamthacker Posted in UncategorizedTagged CJD,
Creutzfeldt-Jakob, Stephen B. Thacker, ThackerLeave a reply
About Team Thacker In December 2012, Stephen B. Thacker, MD, MSc, RADM/ASG
(ret.), USPHS, father and husband, was diagnosed with Creutzfeldt-Jakob Disease
(CJD.) Classic CJD is a human prion disease. It is a neurodegenerative disorder
with characteristic clinical and diagnostic features. This disease is rapidly
progressive and always fatal. Infection with this disease leads to death usually
within 1 year of onset of illness.
Dr. Thacker passed away on Friday, February 15, 2013 from complications of
CJD. We encourage you to visit the family website to learn more www.teamthacker.com.
Leadership Office of the Director
Stephen B. Thacker, MD, MSc, USPHS Director
Dr. Stephen B. Thacker is the Director of the Centers for Disease Control
and Prevention′s Office of Science, Epidemiology and Laboratory Services
(OSELS). In this role, Dr. Thacker provides critical leadership in the
application of information, computer science, and technology to improve public
health practice, research, and learning.
Prior to assuming this post, he was the Director of the Office of Workforce
and Career Development (OWCD), where he served since June 2004. As Director of
OWCD, Dr. Thacker lead the CDC program responsible for improving health outcomes
by ensuring a competent and sustainable workforce through excellence and
innovation in workforce and career development.
Dr. Thacker served as director of the Epidemiology Program Office (EPO),
CDC in August 1989 through June 2004. As director of EPO, Dr. Thacker led the
CDC program responsible for domestic and international training and consultation
in epidemiology, statistics, and applied public health, as well as scientific
communications.
Dr. Thacker served as acting director of the Center for Injury Prevention
and Control (NCIPC) from September 1999 through November 2000. As acting
director of NCIPC, Dr. Thacker led the CDC Program responsible for preventing
and controlling the incidence, severity, and adverse outcomes of injury related
to both violent and unintentional causes through research, public health
surveillance, implementation of programs, and communications.
Dr. Thacker served as acting deputy director of CDC and deputy
administrator of the Agency for Toxic Substances and Disease Registry (ATSDR)
from February 1998 to October 1998. As acting deputy director of CDC, Dr.
Thacker assisted leading the agency of the U.S. Public Health Service in
promoting health and preventing disease, injury, and premature death. CDC’s 11
Centers, Institutes and Program Offices work closely with local, state, and
other federal agencies to protect public health. As deputy administrator of
ATSDR, Dr. Thacker assisted in administering the Public Health Service (PHS)
agency created by the Superfund law to prevent or mitigate adverse human health
effects and diminished quality of life resulting from exposure to hazardous
substances in the environment.
From January 1993 to December 1994, Dr. Thacker served as acting director
of CDC’s National Center for Environmental Health (NCEH). As acting director of
NCEH, he led the CDC program responsible for prevention of premature death,
illness, and disability due to environmental factors outside the workplace with
programs developed on the foundations of epidemiology, laboratory science, and
behavioral science.
He received his undergraduate degree in biochemistry at Princeton
University in 1969 and his M.D. from Mount Sinai School of Medicine in 1973. He
completed residency training in family medicine at the Duke University School of
Medicine in 1976, and was certified by the American Board of Family Practice in
1977. At Duke, Dr. Thacker was also a Robert Wood Johnson clinical scholar. From
July 1976 to June 1978, Dr. Thacker served as an Epidemic Intelligence Service
(EIS) Officer for CDC, stationed at the Washington, D.C. Health Department. In
1984, he was awarded an M.Sc. in epidemiology from the London School of Hygiene
and Tropical Medicine and received certification from the American Board of
Preventive Medicine. He currently holds appointments at both Emory University
School of Medicine and the Mount Sinai School of Medicine.
Dr. Thacker has published in a broad range of fields in public health,
including epidemiology, public health surveillance, meta-analysis, infectious
diseases, environmental public health, injury prevention, alcohol abuse, health
care delivery, and technology assessment.
Dr. Thacker is a retired Commissioned Officer in the U.S. Public Health
Service and is currently holding the grade of Assistant Surgeon General (Rear
Admiral, Upper Half).
Our Sincere condolences to the family and friends of Dr. Thacker.
...warmest regards, terry
please remember, all iatrogenic CJD is, is sporadic CJD before route and source of the CJD agent is verified AND documented. ...TSS
Saturday, February 12, 2011
Another Pathologists dies from CJD, another potential occupational death ?
another happenstance of bad luck, a spontaneous event from nothing, or
friendly fire ???
Sunday, February 10, 2013
Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection
report/CJD
Saturday, March 23, 2013
CJD Incidents Panel to be disbanded
Tuesday, March 5, 2013
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening
of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
FDA believes current regulation protects the public from BSE but reopens
comment period due to new studies
Tuesday, March 05, 2013
A closer look at prion strains Characterization and important implications
Prion
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
Wednesday, March 20, 2013
GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to
Expand Its Use of Reported Health Problems to Oversee Product
From: Terry S. Singeltary Sr.
Sent: Tuesday, March 19, 2013 2:46 PM
To: gomezj@gao.gov
Cc: siggerudk@gao.gov ; youngc1@gao.gov ; oighotline@gao.gov
Wednesday, February 20, 2013
World Organization for Animal Health Recommends United States' BSE Risk
Status Be Upgraded
Statement from Agriculture Secretary Tom Vilsack:
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and
TSE prion disease
Thursday, February 21, 2013
National Prion Disease Pathology Surveillance Center Cases Examined January
16, 2013
16 YEAR OLD SPORADIC FFI ?
Monday, January 14, 2013
Gambetti et al USA Prion Unit change another highly suspect USA mad cow
victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes
along with this BSe
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25,
2012
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Wednesday, June 13, 2012
MEXICO IS UNDER or MIS DIAGNOSING CREUTZFELDT JAKOB DISEASE AND OTHER PRION
DISEASE SOME WITH POSSIBLE nvCJD
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission
until now. Overall, 5 voles were positive with survival time between 281 and 596
d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like
PrPSc electrophoretic pattern, characterized by low molecular weight PrPres.
These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative
with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus
and the N-terminus. Second passages are in progress from these first successful
transmissions.
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
Sunday, March 31, 2013
Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years
old, shall we pray
TSS