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141.
Rehab H. Abd El‐Aleam Riham F. George Kevin J. Lee Adam B. Keeton Gary A. Piazza Amr A. Kamel Mahmoud E. El‐Daly Ghaneya S. Hassan Hamdy M. Abdel‐Rahman 《Archiv der Pharmazie》2019,352(8)
A series of 1,2,4‐triazolo[1,5‐a]pyrimidine derivatives was designed, synthesized, and screened for their phosphodiesterase (PDE 4B) inhibitory activity and bronchodilation ability. Compound 7e showed 41.80% PDE 4B inhibition at 10 µM. Eight compounds were screened for their bronchodilator activity, where compounds 7f and 7e elicited promising bronchodilator activity with EC50 values of 18.6 and 57.1 µM, respectively, compared to theophylline (EC50 = 425 µM). Molecular docking at the PDE 4B active site revealed a binding mode and docking scores comparable to those of a reference ligand, consistent with their PDE 4B inhibition activity. 相似文献
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Complete or partial thrombosis of the inferior vena cava is usually due to pre-existing malformation of the vessel, malignant tumors, ascending thrombosis, or thrombophilic disorders. We report the case of an 81-year-old woman, in whom a partial thrombosis of the vena cava was observed in the CT scan when re-staging was performed after six cycles of R-CHOP because of high-grade malignant non-Hodgkin lymphoma. Before chemotherapy was started, the patient had undergone an operation of the lumbar spine using cement augmentation. Retrospective analysis showed that cement had penetrated a segmental vein and spilled into the vena cava leading to formation of an adhering blood thrombus. The patient was free of symptoms and anticoagulation was started. Spillage of cement frequently occurs in the process of vertebroplasty and kyphoplasty and may result in serious sequelae. As these procedures are increasingly being used, physicians should be aware of these complications if a patient presents with thrombosis of the caval vein or signs of pulmonary embolism. 相似文献
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Gamliel-Lazarovich A Abassi Z Khatib S Tavori H Vaya J Aviram M Keidar S 《Atherosclerosis》2012,222(1):92-98
AimSerum paraoxonase 1 (PON1) is an HDL-associated lipolactonase and its association with hypertension is controversial. We studied the possible role of PON1 in blood pressure (BP) regulation, by using PON1 knockout (PON1KO) mice.Methods and resultsBoth, systolic and diastolic BPs were lower in PON1KO compared to WT mice. Hypotension detected in PON1KO is probably neither related to nitric oxide/guanylate cyclase-mediated vasodilation nor to angiotensin II or aldosterone-mediated vasoconstriction. Surprisingly, when challenged by high-salt diet, BP was further reduced in PON1KO mice. The later, pointed to a possible involvement of transient receptor potential vanilloid 4 (TRPV4), and indeed, administration of ruthenium red, a TRPV4 blocker, resulted in a sharp rise in BP. The protein levels of TRPV4 in kidneys of PON1KO were not higher than in WT. However, the renal level of 5,6-epoxyeicosatrienoic acid (5,6-EET), a TRPV4 specific agonist, was significantly higher in PON1KO compared with WT mice. 5,6-EET levels were further elevated under high-salt diet or administration of arachidonic acid. Injection of inhibitor of CYP450 epoxygenase resulted in increased BP in PON1KO mice. Injection of recombinant human PON1 resulted in elevation of BP and a concomitant reduction in renal content of 5,6-EET. PON1, in vitro, metabolized 5,6-EET, but not other EETs, to its corresponding diol. Vasodilation, blocked by excess of dietary K+ but not reversed by depletion of cellular Ca2+ stores, point to endothelial-derived hyperpolarization-like response.ConclusionThe present study shows causal, direct relationship between PON1 and blood pressure which is mediated, at least in part, by the regulation of 5,6-EET. 相似文献
147.
Zaman T Agarwal S Anabtawi AG Patel NS Ellis SG Tuzcu EM Kapadia SR 《The American journal of cardiology》2012,110(2):167-172
We sought to determine the angiographic severity of coronary lesions leading to ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) with a focus on determining the impact of interval from initial angiogram to subsequent clinical event. In the late 1980s angiographic data on lesion characteristics that culminated in STEMI and NSTEMI were obtained from angiograms obtained several months before MI. It is not clear whether the conclusions on lesion severity would be different if elapsed interval from baseline angiogram to clinical event was factored in the analysis. From 2003 through 2010, we identified 84 patients with NSTEMI and 41 patients with STEMI in vessels without previous intervention. These patients had ≥1 previous angiographic study at our center. Angiograms were reanalyzed with quantitative coronary angiography, and relevant clinical data were obtained from medical records. Similar to previous studies, 71% of patients with STEMI and 63% of patients with NSTEMI had <50% baseline stenosis at the culprit site when the interval from initial angiogram to MI was >3 months. Interestingly, lesions that led to STEMI ≤3 months after evaluation were more severe than those leading to STEMI in >3 months (59 ± 31% vs 36 ± 21%, p = 0.02) with 57% of lesions having >50% stenosis. Although most MIs occurred at sites that did not have significant obstruction when examined >3 months before MI, most baseline lesions showed significant luminal narrowing when examined ≤3 months before STEMI. In conclusion, high-grade coronary stenosis may be an important predictor of STEMI in subsequent months. 相似文献
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Hassan T Rage A Kanna S Hassan ZU 《The American journal of medicine》2012,125(1):e13; author reply e15-e13; author reply e16
150.
Li Z Huang H Li Y Jiang X Chen P Arnovitz S Radmacher MD Maharry K Elkahloun A Yang X He C He M Zhang Z Dohner K Neilly MB Price C Lussier YA Zhang Y Larson RA Le Beau MM Caligiuri MA Bullinger L Valk PJ Delwel R Lowenberg B Liu PP Marcucci G Bloomfield CD Rowley JD Chen J 《Blood》2012,119(10):2314-2324
Increased expression levels of miR-181 family members have been shown to be associated with favorable outcome in patients with cytogenetically normal acute myeloid leukemia. Here we show that increased expression of miR-181a and miR-181b is also significantly (P < .05; Cox regression) associated with favorable overall survival in cytogenetically abnormal AML (CA-AML) patients. We further show that up-regulation of a gene signature composed of 4 potential miR-181 targets (including HOXA7, HOXA9, HOXA11, and PBX3), associated with down-regulation of miR-181 family members, is an independent predictor of adverse overall survival on multivariable testing in analysis of 183 CA-AML patients. The independent prognostic impact of this 4-homeobox-gene signature was confirmed in a validation set of 271 CA-AML patients. Furthermore, our in vitro and in vivo studies indicated that ectopic expression of miR-181b significantly promoted apoptosis and inhibited viability/proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced expression of PBX3. Thus, the up-regulation of the 4 homeobox genes resulting from the down-regulation of miR-181 family members probably contribute to the poor prognosis of patients with nonfavorable CA-AML. Restoring expression of miR-181b and/or targeting the HOXA/PBX3 pathways may provide new strategies to improve survival substantially. 相似文献