Disease relevance of MAEA

• PURPOSE: We studied the establishment of a transplantable tumor, EMP-K1, derived from extramammary Paget's disease and the morphology and unique hormone dependence of this tumor [1].
• PATIENTS AND METHODS: A total of 31 patients with hormone-refractory prostate cancer received IV EMP as a 30- to 90-minute infusion weekly (n = 28) or for 3 consecutive days followed by a single weekly dose (n = 3) [2].
• PURPOSE: To determine the dose-limiting toxicities, maximum-tolerated dose, and pharmacokinetics of intravenous estramustine phosphate (IV EMP) [2].
• During acute graft versus host disease (aGVHD), significantly higher levels of EMP were detected than in patients without aGVHD (18.5/microl s=10.1 vs. 14.6/microl SD = 11.5; P = 0.004) while infectious complications did not alter EMP levels significantly [3].
• We assessed several thrombophilia markers as well as circulating total and endothelial microparticles (TMP/EMP) and soluble CD40 ligand (CD40L) [4].

Psychiatry related information on MAEA

• Two one-hour educational sessions reviewed with EMP (but not CON) the physician's role in requesting donation, donor criteria, required-request legislation, and services available from organ procurement professionals [5].

High impact information on MAEA

• We performed microarray analysis to identify genes involved in EMP release by the endothelial cell line HMEC-1 in response to thrombin [6].
• The involvement of caspase-2 in ROCK-II activation independently of cell death points out a novel signaling pathway that emphasizes the proteolytic activity of caspase in EMP generation in response to cell activation [6].
• Pharmacokinetics of EMP and the metabolites estramustine (EaM), estromustine (EoM), estradiol, and estrone were assessed after weeks 1 and 4 of treatment [2].
• Compared with age-matched control subjects, type 1 diabetic patients presented significantly higher numbers of platelet and endothelial microparticles (PMP and EMP), total annexin V-positive blood cell microparticles (TMP), and increased levels of TMP-associated procoagulant activity [7].
• Notably, plasma CD144-EMP identified a subpopulation of established CAD patients in DM subjects without typical anginal symptoms (OR 10.6, 95% CI 3.9 to 29.5, p < 0.001) [8].

Chemical compound and disease context of MAEA

• Stimulation of growth by both androgen and estrogen of the EMP-K1 transplantable tumor with androgen and estrogen receptors from human extramammary Paget's disease in nude mice [1].
• Estracyt (EMP) has been used for the treatment of hormone refractory prostate cancer for many years [9].
• We have, therefore, examined the level of the four metabolites, estromustine (EoM), estramustine (EaM), estrone, and estradiol in the tumor and serum of 14 patients with T2 and T3 prostate cancer receiving a single i.v. dose of 600 mg of EMP, about 12 h before radical prostatectomy [9].
• Twenty-two orchiectomized men with progressive stage D2 prostate cancer were treated with a 3-week cycle of estramustine phosphate (EMP: from day 3 to day 21) and androgen priming (from day 1 to day 4) [10].
• METHODS: The subjects were 15 patients with HRPC who displayed disease progression while receiving PTX/EMP/carboplatin combination chemotherapy [11].

Biological context of MAEA

• The levels of CD144-EMP reflected the degree of in vitro hydrogen-peroxide-induced EC injury and impairment of in vivo endothelium-dependent coronary vasodilation (p < 0.01) [8].
• Endothelial cells release microparticles < approximately 1.5 microm (EMP) during activation or apoptosis [12].
• Since PMP22 has been implicated in the regulation of cell proliferation and apoptosis, it appears likely that these novel members of the PMP22/EMP/MP20 protein family are also involved in similar regulatory processes in a variety of tissues [13].
• The tissue distribution of estramustine and estromustine, two cytotoxic lipophilic metabolites of estramustine phosphate (Estracyt, EMP) was studied in rats and humans [14].
• Hexose-monophosphate shunt (HMPS), glycolytic pathway (EMP) and antioxidant enzyme activities were determined by standard methods [15].

Anatomical context of MAEA

• This SPA uses the specific interactions of [3H]R(+)-methanandamide (MAEA) and FAAH expressing microsomes to evaluate the displacement activity of FAAH inhibitors [16].
• This suggests that CD31+ EMP is a marker of acute injury, whereas CD51+ EMP reflects chronic injury of endothelium [12].
• RESULTS: Annexin V-positive MP in the patients originated predominantly from platelets (PMP), and to a lesser extent from erythrocytes, endothelial cells (EMP) and granulocytes (GMP) [17].
• The use of DD2 is illustrated in a series of EMP vs. IgC curves, calculated for selected examples of negatively charged lipid membranes [18].
• Thus, our results demonstrate that estramustine and estromustine are stored in adipose tissue after the administration of EMP; this is important for the pharmacokinetics and, consequently for the therapeutic effects of Estracyt [14].

Associations of MAEA with chemical compounds

• METHODS: We characterized EMP using anti-CD144 (VE-Cadherin) antibody in various atherosclerosis-related cells and investigated the association between the levels of CD144-positive microparticles and hydrogen-peroxide-induced EC injury and acetylcholine-induced coronary vasomotion [8].
• Measurement of Se-EMP may provide an additional and sensitive approach for assessing Se nutriture in human subjects [19].
• Limiting dietary ascorbic acid to about 20 mg/d appeared to reduce the time-related retention of absorbed selenite and the size of Se-EMP [20].
• The CD31+ EMP concentration showed a positive association with gadolinium enhancement in patients with MS [12].
• A total of 82 patients with HRPC were evaluated during 751 treatment cycles, either with estramustine (EMP)/vinorelbine or with EMP/docetaxel [21].

Analytical, diagnostic and therapeutic context of MAEA

• METHODS: Platelet-poor plasma (PPP) from 50 patients with MS (30 in exacerbation and 20 in remission) and 48 controls were labeled with fluorescein isothiocyanate (FITC)-conjugated anti-CD31 and anti-CD51 (vitronectin receptor) antibodies, and two classes of EMP (CD31+ and CD51+) were assayed by flow cytometry [12].
• RESULTS: EMP were not significantly influenced by conditioning regimens with non-myeloablative chemotherapy and 4 Gy total body irradiation (TBI) or by myeloablative regimens containing 12 Gy TBI [3].
• CONCLUSIONS: Elevation of EMP during aGVHD might express severe endothelial cell injury within this complication after hematopoietic stem cell transplantation and might serve as a diagnostic test for early differentiation of aGVHD from other transplanted related complications [3].
• A treatment regimen was designed to improve systemic control by neoadjuvant targeting of hormone-sensitive and -insensitive micrometastatic disease and to improve local control by escalating the biologic effective dose to the prostate using estramustine (EMP) concurrently with radiotherapy [22].
• Observations include: three consistent X-ray diffraction patterns; no resolution of cellular EMP by electron microscopy; increasing Ca/Mg, Ca/P during calcification [23].

References