|1.||Zhu, Daling: 25 articles (05/2015 - 05/2003)|
|2.||Zhang, Lei: 12 articles (08/2014 - 02/2009)|
|3.||Ma, Jun: 7 articles (09/2013 - 01/2010)|
|4.||Ma, Cui: 6 articles (09/2013 - 11/2010)|
|5.||Guo, Lei: 6 articles (11/2010 - 06/2008)|
|6.||Shen, Tingting: 5 articles (01/2015 - 10/2012)|
|7.||Ran, Yajuan: 4 articles (08/2014 - 08/2010)|
|8.||Liu, Yun: 4 articles (05/2013 - 10/2011)|
|9.||Qiu, Zhaoping: 4 articles (01/2012 - 02/2009)|
|10.||Wang, Zhigang: 4 articles (09/2010 - 06/2008)|
|1.||Kidney Diseases (Kidney Disease)
12/01/2012 - "Hence, in this study, we wanted (1) to analyze 5-, 12- and 15-HETE levels in non-diabetic chronic kidney disease (CKD) patients, already undergoing regular hemodialysis treatment, and determine factors that may influence these eicosanoids' generation, as well as, (2) to verify whether application of glucose-containing, instead of glucose-free, dialyzing fluids may be beneficial for the limitation of 5-, 12- and 15-HETE synthesis during a single hemodialysis session. "
01/01/2015 - "Our study indicates that hypoxia-induced pulmonary vascular remodeling is associated with increased levels of 15-LO-2 and 15-HETE. "
05/01/2006 - "In the present study, ring of rabbit PA with specific Kv channel blockers were employed to functionally identify certain channel subtypes that took part in the process of 15-HETE induced pulmonary vasoconstriction; RT-PCR and Western blotting analysis were also used to measure the expression of subtypes of Kv in PASMCs exposed to 15-HETE,chronic hypoxia. "
01/01/2015 - "By silencing PGC-1α, the action against cell viability suppression induced by 15-HETE was blocked, not only in normoxic condition but also in hypoxia-stimulated condition. "
09/01/2013 - "The interaction in hypoxia between 15-HETE and PlGF created a PlGF-15-LO-15-HETE loop, leading to endothelial dysfunction. "
01/01/2013 - "In addition, the proliferation, migration and cell-cycle transition from G0/G1 phase to S phase induced by hypoxia were inhibited by TERT knockdown, which were rescued by 15-HETE addition. "
09/01/1990 - "Regulation of tumor cell adhesion by intracellular 13-HODE: 15-HETE ratio."
09/01/1990 - "We performed studies to determine whether tumor cells (TCs) produce 13-hydroxyoctadecadienoic acid (13-HODE) and 15-hydroxyeicosatetraenoic acid (15-HETE), and to determine the relationship between TC and endothelial cell (EC) 13-HODE and 15-HETE synthesis, and TC adhesion to ECs and their underlying extracellular matrix (ECM). "
07/22/1988 - "In this study, we have measured (1) the relative binding of 5-, 12- and 15-HETE, and 13-HODE to endothelial cell monolayers, and (2) their effects on endothelial cell adhesivity with platelets, PMNs and tumor cells. "
07/22/1988 - "Binding of 13-HODE and 5-, 12- and 15-HETE to endothelial cells and subsequent platelet, neutrophil and tumor cell adhesion."
10/01/2007 - "Neither 15-HETE nor 13-HODE showed a significant opposite trend toward levels found in BP. (b) Tissue specimens representing common EOC histotypes showed strong coexpressions of cyclooxygenases (COX-1) and prostaglandin E synthases (PGES-1) on tumor cells, whereas intratumoral or peritumoral MO/MA coexpressed COX-1 and COX-2 and PGES-1 and PGES-2, respectively. "
|4.||Nasal Polyps (Nasal Polyp)
01/01/2011 - "Our study demonstrated that aspirin-induced 15-HETE generation in nasal polyps from aspirin-sensitive patients is not associated with activation of mast cells and eosinophils. "
02/01/1987 - "The predominant arachidonic acid metabolite in both nasal polyps and mucosa with 15-HETE. "
02/01/1987 - "The HPLC analysis showed that the predominant metabolite in nasal polyp was 15-HETE, especially in polyps from aspirin sensitive patients. "
|5.||Hypertension (High Blood Pressure)
08/14/2010 - "This study establishes the factor involved in 15-HETE-protecting PASMC from apoptosis and the regulation of HSP90 by 15-HETE may be an important mechanism underlying the treatment of pulmonary artery hypertension and provide a novel therapeutic target in future."
01/01/2012 - "Taken together, our data indicates that iNOS is a novel signaling transduction pathway, which is necessary for the effects of 15-HETE in protection PASMCs from apoptosis and may be an important mechanism underlying the treatment of pulmonary artery hypertension and also provides a novel therapeutic insight in future."
|3.||Aligeron (AS 2)
|5.||Arachidonic Acid (Vitamin F)
|7.||Aspirin (Acetylsalicylic Acid)
|1.||Renal Dialysis (Hemodialysis)
|2.||Prostatectomy (Retropubic Prostatectomy)