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American Journal of Medical and Biological Research

ISSN (Print): 2328-4080

ISSN (Online): 2328-4099

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Monitoring of Thoracic Aortic Aneurysm in Blood by Fluorescence Spectroscopy

1Department of Medical and Clinical Biochemistry, Pavol Jozef Šafárik University, Faculty of Medicine, Košice, Slovakia

2Department of Cardiovascular Surgery, Pavol Jozef Šafárik University, Faculty of Medicine and VUSCH, Košice, Slovakia

3Institute of Physics, Pavol Jozef Šafárik University, Faculty of Science, Košice, Slovakia

American Journal of Medical and Biological Research. 2015, 3(5), 128-132
doi: 10.12691/ajmbr-3-5-2
Copyright © 2015 Science and Education Publishing

Cite this paper:
Zuzana Guľašová, Vladimíra Tomečková, Miroslava Bilecová-Rabajdová, Beáta Veliká, Panayotis Artemiou, Vladimír Komanický, Mária Mareková. Monitoring of Thoracic Aortic Aneurysm in Blood by Fluorescence Spectroscopy. American Journal of Medical and Biological Research. 2015; 3(5):128-132. doi: 10.12691/ajmbr-3-5-2.

Correspondence to: Zuzana  Guľašová, Department of Medical and Clinical Biochemistry, Pavol Jozef Šafárik University, Faculty of Medicine, Košice, Slovakia. Email:


Components of the blood plasma and serum represent a mixture of various endogenous substances with fluorescence properties. The aim of this work was a detection of pathological changes in blood of patients with thoracic aortic aneurysm by fluorescence spectroscopy and atomic force microscopy. The resulting autofluorescence of fluorophores in blood of patients with thoracic aortic aneurysm decreased in comparison with healthy subjects. The structure of the thoracic aorta was changed during the thoracic aortic aneurysm, what was manifested as the structural modifications in blood of patients observed by using atomic force microscopy. The fluorescence analysis and atomic force microscopy present new experimental ways in the study of the thoracic aortic aneurysm.



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The Irreversible Inhibition of the MAPKp38 Pathway Downregulates LPS-augmented Release of Interleukin-Related Inflammatory Cytokines (IL-1β, IL-6): Immune Surveillance Unraveling IκB-α/NF-κB Phosphorylation State-independent Mechanism in vitro

1Department of Medical Laboratory Sciences, Faculty of Health Sciences, Beirut Arab University, Beirut, Lebanon

American Journal of Medical and Biological Research. 2015, 3(5), 133-138
doi: 10.12691/ajmbr-3-5-3
Copyright © 2015 Science and Education Publishing

Cite this paper:
John J Haddad. The Irreversible Inhibition of the MAPKp38 Pathway Downregulates LPS-augmented Release of Interleukin-Related Inflammatory Cytokines (IL-1β, IL-6): Immune Surveillance Unraveling IκB-α/NF-κB Phosphorylation State-independent Mechanism in vitro. American Journal of Medical and Biological Research. 2015; 3(5):133-138. doi: 10.12691/ajmbr-3-5-3.

Correspondence to: John  J Haddad, Department of Medical Laboratory Sciences, Faculty of Health Sciences, Beirut Arab University, Beirut, Lebanon. Email:


Background: The participation of signaling pathways involving the mitogen-activated protein kinases (MAPKs) in regulating the inflammatory response characterized by the release of cytokines is not well established in the alveolar epithelium. We have previously examined the effect of MAPKp38 blockade on the in vitro release of TNF-α, indicating the likely involvement of other pro-inflammatory cytokines. Methods: This study investigated the selective inhibition of MAPKp38 in modulating the release of interleukin-related inflammatory cytokines, including IL-1β and IL-6. LPS-mediated release of cytokines is closely associated with the blockade of MAPK by the compound SB203580, an irreversible and selective inhibitor of MAPKp38, independent of MAPKERK (p42/p44) and MAPKJNK. Results: Pre-treatment with ascending concentrations of SB203580 (0.1 – 100 μM) prior to LPS administration downregulated/attenuated the release of IL-1β, IL-6 and TNF-α in a dose-dependent and dose-independent manners. Furthermore, unraveling the immune molecular pathways likely involved with MAPKp38-mediated secretion of cytokines revealed that SB203580 increased IκB-α phosphorylation, where IκB-α is considered the main cytosolic inhibitor of the transcription factor involved with regulating the processes of cellular inflammation, NF-κB. This upregulation of the phosphorylation status of IκB-α was accompanied by downregulating the cytosolic accumulation of the non-phosphorylated form of IκB-α, indicating normal nuclear translocation of the associated transcription factor. Conclusions: These results show that MAPKp38 is required, at least in part, for the release of inflammatory cytokines induced by LPS, a mechanism that is independent of the phosphorylation of IκB-α. In addition, the MAPKp38-dependent release of cytokines seemingly does not require the activation of the NF-κB pathway.



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Impact of Nigella Sativa, Omega-3 Fatty Acids and Chromium Picolinate on NF-κB /leptin-insulin Axis in Obese Subjects with Non-alcoholic Fatty Liver Disease

1Departments of Medical Biochemistry, Faculty of Medicine, Tanta University, Egypt

2Department of Clinical Biochemistry and Molecular Medicine, Taibah Faculty of Medicine, Taibah University, Al-Madinah Al-Munawwarah, Saudi Arabia

3Ph.D in Medical Biochemistry, Faculty of Medicine, Tanta University, Egypt

4Department of Internal Medicine, Faculty of Medicine, Tanta University, Egypt

5Department of Medical Biochemistry, Sohag Faculty of Medicine, Sohag University, Egypt

American Journal of Medical and Biological Research. 2015, 3(6), 139-145
doi: 10.12691/ajmbr-3-6-1
Copyright © 2015 Science and Education Publishing

Cite this paper:
Noha M. Shafik, Reham A. Mariah, Sherine Ragab Shafik, Loai Mohammed El-Ahwal, Salah Mohamed El Sayed. Impact of Nigella Sativa, Omega-3 Fatty Acids and Chromium Picolinate on NF-κB /leptin-insulin Axis in Obese Subjects with Non-alcoholic Fatty Liver Disease. American Journal of Medical and Biological Research. 2015; 3(6):139-145. doi: 10.12691/ajmbr-3-6-1.

Correspondence to: Salah  Mohamed El Sayed, Department of Clinical Biochemistry and Molecular Medicine, Taibah Faculty of Medicine, Taibah University, Al-Madinah Al-Munawwarah, Saudi Arabia. Email:,


Background: The global problem of obesity epidemic involves an increased risk of non-alcoholic fatty liver disease (NAFLD) whereby oxidative stress induces fibrogenesis. Objectives: to assess the coordinated impact of obesity management strategy on nuclear factor kappa beta/p65 mRNA expression and biochemical parameters of oxidative stress, glycemic status and adipokines. Subjects and methods: This study was carried out on 60 subjects classified into, 15 normal healthy controls (group І) and 45 obese subjects who were divided equally into three groups: obese subjects with NAFLD (group ІІ), obese subjects who received natural product supplements (nigella sativa, green tea andchromium picolinate) (groupІІІ),obese subjects who received omega-3 fatty acids (group ІV) andthose who received caloric restricted diet (CRD) and exercise for 6 months. All groups were subjected to measurement of body mass index, waist to hip ratio (WHR), spectrophotometric measurement of serum levels of glucose, malondialdehyde (MDA) and total antioxidant capacity (AOC%), NF-κB /P65 subunit expression levels by real time-PCR in peripheral bloodmononuclear cells, estimation of levels of insulin, insulin like growth factor-1, leptin, adiponectin, fibronectin and oxidized LDL by enzyme linked immunosorbent assays. Results: There was a significant decrease inNF-κB/p65 mRNA expression in peripheral blood mononuclear cells, reduction in the levels of oxLDL, decreased insulin resistance and decreased leptin resistance which might be linked to hypoadiponectinemia. Levels of (AOC %) were significantly elevated after treatment. This was evident alongside reduction of BMI, WHR and fibrogenic potential in NAFLD. Conclusion: natural product supplements, CRD and exercise ameliorated the fibrogenic and atherogenic consequences of immune-inflammatory and oxidative stress-induced pathological mechanisms associated with obesity.



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