| 1. |
|
|
| 2. |
- Adam, Lina N., et al.
(author)
-
Exploring nitric oxide as a crucial prognostic biomarker of coronary artery disease
- 2023
-
In: Prostaglandins & other lipid mediators. - : Elsevier. - 1098-8823 .- 2212-196X. ; 165
-
Journal article (peer-reviewed)abstract
- Purpose: The study aimed to examine if the polymorphism of the endothelial nitric oxide synthase (eNOS) gene variable number of tandem repeats (VNTR) and the serum NO levels are associated with CAD.Materials/methods: Case-control study, 70 CAD and 30 control subjects were enrolled. The eNOS gene poly-morphism was measured by polymerase chain reaction-agarose gel electrophoresis and the serum NO was assessed by using an ELISA plate and reader covering 540 nm.Results: Uncovering the area under curve (AUC) for serum NO, which was (0.6821), indicating that NO seemed to be a critical prognostic biomarker of CAD; also, glucose, serum creatinine and total bilirubin proved to be sig-nificant predictors of CAD with AUC (0.6793, 0.6717 and 0.6662) respectively. Furthermore, higher serum NO levels were associated with the eNOS (ab) genotype. Revealing the intron (a) allele was protective against CAD. Moreover, diminished levels of serum NO in CAD groups compared to controls (P < 0.05). Additionally, Multiple logistic regression analysis shows a significantly high Odds ratio associated with CAD in the Duhok population.Conclusions: The eNOS (ab) variant seems to be a protective CAD factor for patients. Low serum NO levels are another risk factor for the advancement of CAD, suggesting their involvement in atherosclerosis. The (a) allele's protective effect is mediated through changes in eNOS promoter activity and higher NO levels.
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Arend, Andres, et al.
(author)
-
Electron microscope immunocytochemical localization of cyclooxygenase-1 and-2 in pseudopregnant rat corpus luteum during luteolysis
- 2004
-
In: Prostaglandins & other lipid mediators. - New York : Elsevier. - 1098-8823 .- 2212-196X. ; 74:1-4, s. 1-10
-
Journal article (peer-reviewed)abstract
- Prostaglandins converted from arachidonic acid by cyclooxygenases play an important regulatory role in regression of the corpus luteum. To reveal luteal distribution of cyclooxygenase isoforms during luteolysis, an electron microscope immunocytochemical study was performed. Cyclooxygenase-1 and -2 were found both in luteal steroid-producing and interstitial cells on days 13, 15 and 18 of the adult pseudopregnant rat. Cyclooxygenase-2 immunolabelling was predominantly seen in non-luteal cells. The two enzymes were localized in similar fashion to the plasma membrane, rough and smooth endoplasmic reticulum, lipid bodies and mitochondria, but differently in the nuclear compartment. Cyclooxygenase-1 labelling was found only in the perinuclear region, while cyclooxygenase-2 was localized to the nuclear envelope, region of condensed heterochromatin as well as at the perimeter of the heterochromatin. Nuclear residence may indicate additional roles for cyclooxygenase-2 in regulating gene expression. Identification of both enzymes on lipid bodies suggests that these inclusions may be involved in luteal prostanoid production.
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Bengtsson, Astrid, et al.
(author)
-
Leukotriene D(4) induces AP-1 but not NFkappaB signaling in intestinal epithelial cells.
- 2008
-
In: Prostaglandins & other Lipid Mediators. - : Elsevier BV. - 1098-8823. ; 85:3-4, s. 100-106
-
Journal article (peer-reviewed)abstract
- We have previously shown that leukotriene D(4) (LTD(4)), a known pro-inflammatory mediator, induces increased survival and proliferation of intestinal epithelial cells. In this study we examined whether LTD(4) functions via activation of the transcription factors NFkappaB and AP-1, which are potent inducers of mitogenesis. We found that the NFkappaB inhibitory protein IkappaBalpha was not degraded upon LTD(4) stimulation. Furthermore, nuclear translocation of the classical p65 or alternative p52 subunits of NFkappaB was not observed. Accordingly, LTD(4) stimulation failed to induce NFkappaB transcriptional activity. Instead we found that LTD(4) induced phosphorylation of c-Jun-N-terminal kinase (JNK) and transcriptional activity of AP-1, which could be reduced by a JNK inhibitor. Moreover, LTD(4) induced cell proliferation, and this effect was also blocked upon addition of a JNK inhibitor. Our findings show for the first time that JNK/AP-1 but not NFkappaB is a downstream target of LTD(4) in intestinal epithelial cells, suggesting that AP-1 is an important mediator of LTD(4)-induced mitogenic effects.
|
|
