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PADGEM (GMP140) is a component of Weibel-Palade bodies of human endothelial cells 总被引:65,自引:10,他引:55
PADGEM protein (PADGEM), also known as GMP140, is a platelet alpha- granule membrane protein that is translocated to the external membrane after platelet activation. Although the biosynthesis of this protein was originally thought to be confined to megakaryocytes, the synthesis of PADGEM in endothelial cells was recently demonstrated (McEver et al: Blood 70:1974a, 1987). We now describe the subcellular localization of this protein in endothelial cells. Immunofluorescence staining of permeabilized human umbilical vein endothelial cells with KC4, a well characterized monoclonal antibody to PADGEM, showed positively stained elongated structures similar in distribution and shape to Weibel-Palade bodies. Their identity as Weibel-Palade bodies was confirmed by double label immunofluorescence using KC4 and a polyclonal antiserum to von Willebrand factor (vWf), a protein known to be specifically stored in these organelles. All Weibel-Palade bodies were found to contain PADGEM. In contrast to strong perinuclear staining produced with anti- vWf antibodies, no significant perinuclear staining was obtained with KC4, indicating that relatively little PADGEM is present in the endoplasmic reticulum and in the Golgi apparatus. In endothelial cells treated with secretagogues that stimulate vWf release the elongated structures positive for PADGEM disappeared, further identifying these structures as Weibel-Palade bodies. This observation extends the parallels between Weibel-Palade bodies and alpha-granules and suggests a possible functional association between vWf and PADGEM. 相似文献
3.
This column contains the presidential address presented during the Third Annual Meeting of the American Association of Heart Failure Nurses on June 28, 2007, in San Diego, California, titled "Building the Foundation of Excellence in Heart Failure Nursing." 相似文献
4.
Prospective computerized simulation of breast cancer: comparison of computer predictions with nine sets of biological and clinical data 总被引:1,自引:0,他引:1
A computer program which accepts clinically relevant information can be used to predict breast cancer growth, response to chemotherapy, and disease-free survival. The computer output is patient individualized because the program is highly iterative and simulates up to 2500 patients with exactly the same clinical presentation. Computer predictions have been compared to a broad spectrum of breast cancer data, and a high degree of correlation has been established. There are numerous significant clinical implications which can be derived from the computer model. Among these are the following. (a) Breast cancer tumors do not grow continuously but may have up to five growth plateaus each lasting from a small fraction of a year up to approximately 8 yr. (b) Adjuvant chemotherapy, such as 6-mo treatment with cyclophosphamide-methotrexate-5-fluorouracil, does not eradicate tumors but just reduces the number of viable cells by a factor of 10 to 100 and sets the eventual growth back by several years. This may partially explain why the age-adjusted death rate from breast cancer has not changed in the past 50 yr. (c) The computer model challenges the underlying principles in support of short-term intensive adjuvant chemotherapy, namely Gompertzian kinetics and genetically acquired tumor resistance to drugs. (d) The computer model questions the evidence opposing long-term maintenance chemotherapy protocols and suggests that maintenance protocols should be reexamined. 相似文献
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Did you ever think, “If we just had a little money we could…”? The current health care environment is wrought with financial stressors that can be overwhelming and take up most of our time. Such stress can limit the development of a professional practice environment if you let it. How do you not only survive but thrive in this financial climate? 相似文献
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Martin C. Robson MD ; Diane M. Cooper PhD RN ; Rummana Aslam MD ; Lisa J. Gould MD PhD ; Keith G. Harding MBChB MRCGP FRCS ; David J. Margolis MD MSCE PhD ; Diane E. Ochs RN ; Thomas E. Serena MD ; Robert J. Snyder DPM ; David L. Steed MD ; David R. Thomas MD ; Laurel Wiersema-Bryant RN BC ANP 《Wound repair and regeneration》2008,16(2):147-150
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Dibenzo[a,l]pyrene-induced DNA adduction, tumorigenicity, and Ki-ras oncogene mutations in strain A/J mouse lung 总被引:1,自引:0,他引:1
Prahalad AK; Ross JA; Nelson GB; Roop BC; King LC; Nesnow S; Mass MJ 《Carcinogenesis》1997,18(10):1955-1963
Dibenzo[a,l]pyrene (DB[a,l]P), an environmental polycyclic aromatic
hydrocarbon, is the most potent carcinogen ever tested in mouse skin and
rat mammary gland. In this study, DB[a,l]P was examined for DNA adduction,
tumorigenicity, and induction of Ki-ras oncogene mutations in tumor DNA in
strain A/J mouse lung. Groups of mice received a single i.p. injection of
0.3, 1.5, 3.0, or 6.0 mg/kg DB[a,l]P in tricaprylin. Following treatment,
DNA adducts were measured at times between 1 and 28 days, while tumors were
counted at 250 days and analyzed for the occurrence of point mutations in
codons 12 and 61 of the Ki-ras oncogene. DB[a,l]P in strain A/J mouse lung
induced six major and four minor DNA adducts. Maximal levels of adduction
occurred between 5 and 10 days after injection followed by a gradual
decrease. DB[a,l]P-DNA adducts in lung tissue were derived from both anti-
and syn-11,12- dihydroxy-13,14-epoxy-
11,12,13,14-tetrahydrodibenzo[a,l]pyrene (DB[a,l]PDE) and both
deoxyadenosine (dAdo) and deoxyguanosine (dGuo) residues in DNA as revealed
by cochromatography. The major adduct was identified as a product of the
reaction of an anti-DB[a,l]PDE with dAdo in DNA. DB[a,l]P induced
significant numbers of lung adenomas in a dose- dependent manner, with the
highest dose (6.0 mg/kg) yielding 16.1 adenomas/mouse. In
tricaprylin-treated control animals, there were 0.67 adenomas/mouse. Based
on the administered dose, DB[a,l]P was more active than other environmental
carcinogens including benzo[a]pyrene. As a function of time-integrated DNA
adduct levels, DB[a,l]P induced lung adenomas with about the same potency
as other PAHs, suggesting that the adducts formed by DB[a,l]P are similar
in carcinogenic potency to other PAHs in the strain A/J mouse lung model.
Analysis of the Ki- ras mutation spectrum in DB[a,l]P-induced lung tumors
revealed the predominant mutations to be G-->T transversions in the
first base of codon 12, A-->G transitions in the second base of codon
12, and A-->T transversions in the second or third base of codon 61,
concordant with the DNA adduct profile.
相似文献