Table of Contents
1
UI - 11547357
AU - Menssen HD; Brandt N; Leben R; Muller F; Thiel E; Melber K
TI -
Measurement of hematological, clinical chemistry, and infection
parameters from hirudinized blood collected in universal blood sampling
tubes.
SO - Semin Thromb Hemost 2001 Aug;27(4):349-56
AD - Dept. III Hematology, Oncology and Transfusion Medicine, Benjamin
Franklin Hospital, Freien Universitat, Hindenburgdamm 30, 12203 Berlin,
Germany. hmenssen@zedat.fu-berlin.de
Hirudin, the anticoagulatory polypeptide of the leech Hirudo
medicinalis, strongly inhibits thrombus formation by specifically
interacting with thrombin. For diagnostic purposes, hirudin should be
superior to other anticlotting compounds because it only minimally
alters the mineral, protein, and cellular blood constituents. To test
this hypothesis, hirudinized and routinely processed venous blood from
80 healthy volunteers and patients was subjected to a variety of
automated blood tests. A strong correlation was found between the
results of automated complete blood counts obtained from
K(2)-ethylenediaminetetraacetic acid (EDTA) anticoagulated and
hirudinized blood (1000 antithrombin units [ATU] hirudin/ml). In
addition, clinical chemistry and serological infection parameters
(asparlat amintransferase [ASAT], lactate dehydrogenase [LDH], sodium,
and so on, and antibodies against hepatitis B and C and human
immunodeficiency virus [HIV]1/2, respectively) correlated well when
measured in serum as compared with hirudinized plasma. Contrary to
single clotting factors, global coagulation parameters (activated
partial thromboplastin time [aPTT], prothrombin time [PT]) could not be
measured in hirudinized blood. Recombinant hirudin neither interfered
with immunophenotyping of mononuclear cells using FACScan analysis, nor
did it alter the detection of Wilms' tumor gene expression by RT-PCR
technology even at high doses (5000 ATU hirudin). Thus, a
hirudin-containing blood sampling tube can be designed as a universal
blood sampling tube (UBT) for testing the majority of diagnostic blood
parameters.
2
UI - 11880727
AU - Dome JS; Coppes MJ
TI -
Recent advances in Wilms tumor genetics.
SO - Curr Opin Pediatr 2002 Feb;14(1):5-11
AD - Department of Hematology and Oncology, St. Jude Children's Research
Hospital, Tennessee 38105-2794, USA. jeff.dome@stjude.org
The past decade has witnessed substantial growth in our knowledge of the
genes and loci that are altered in Wilms tumor. Although Wilms tumor was
one of the original paradigms of Knudson's two-hit model of cancer
formation, it has become apparent that several genetic events contribute
to Wilms tumorigenesis. Recent research has identified targets and
regulators of the first Wilms tumor gene, WT1, has uncovered several
candidate genes at the second Wilms tumor locus, WT2, and has identified
two familial Wilms tumor loci, FWT1 and FWT2. The recent discovery of
activating beta-catenin mutations in some Wilms tumors has also
implicated the Wnt signaling pathway in this neoplasm. Recurrent
abnormalities of other loci, including 16q, 1p, and 7p, have indicated
that these sites may harbor Wilms tumor genes. An enhanced understanding
of these and other genetic lesions will provide the foundation for novel
targeted Wilms tumor therapies.
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