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Seddik Hammad

About Seddik Hammad:
No description specified

SEEK ID: https://seek.lisym.org/people/36

Location: Germany

Expertise: Omics, Animal experimentalist, Imaging and image analysis

Tools: confocal microscopy, Animal facility, Metabolomics, Microarray analysis

ORCID: Not specified

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LiSyM network

This comprises the whole LiSyM network

Public web page: http://www.lisym.org

Chronic Liver Disease Progression (LiSyM-DP - Pillar II)

Chronic liver diseases (CLD) progression leads to cirrhosis, often cancer, and ultimately to organ failure and death. Because of the complexity of this scenario, a Systems Medicine approach is chosen to develop strategies to better characterize progression and resolution of fibrosis. Pillar II aims to define key molecular mechanisms and structural changes in tissue architecture during the progression of CLD by visualizing and quantifying at a cellular level, tissue and organ scale.

Public web page: Not specified

Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF - Pillar III)

The incidence of this life-threatening acute-on-chronic liver failure (ACLF) is increasing, and early detection and cure are urgent clinical needs. Pillar III applies a Systems Medicine approach to identify the critical mechanisms of acute-on-chronic liver failure (ACLF) and to foster liver regeneration and repair.

Public web page: Not specified

Julia/Yan
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)

Pillar II dooley

Snapshots: No snapshots

1 hidden item
CCl4 Treatment in mice
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
No description specified

Person responsible: Seddik Hammad

Snapshots: No snapshots

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Metabolic CCl4
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
No description specified

Contributor: Seddik Hammad

Assay type: Proteomics

Technology type: FACS

Snapshots: No snapshots

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Movies for quantification
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
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Creator: Seddik Hammad

Contributor: Seddik Hammad

TextBookData
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
No description specified

Creators: None

Contributor: Seddik Hammad

F4-80
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
No description specified

Creators: None

Contributor: Seddik Hammad

F4/80 staining after acute damage by CCl4
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
No description specified

Creators: None

Contributor: Seddik Hammad

Voids in CCl4
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)

Voids in CCl4

Creators: None

Contributor: Seddik Hammad

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TGF-β2 silencing to target biliary-derived liver diseases
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)

Abstract

Not specified

Authors: Anne Dropmann, Steven Dooley, Bedair Dewidar, Seddik Hammad, Tatjana Dediulia, Julia Werle, Vanessa Hartwig, Shahrouz Ghafoory, Stefan Woelfl, Hanna Korhonen, Michel Janicot, Katja Wosikowski, Timo Itzel, Andreas Teufel, Detlef Schuppan, Ana Stojanovic, Adelheid Cerwenka, Stefanie Nittka, Albrecht Piiper, Timo Gaiser, Naiara Beraza, Malgorzata Milkiewicz, Piotr Milkiewicz, John G Brain, David E J Jones, Thomas S Weiss, Ulrich M Zanger, Matthias Ebert, Nadja M Meindl-Beinker

Date Published: 28th Jan 2020

Journal: Gut

Assessment of Chemotherapy-Induced Organ Damage with Ga-68 Labeled Duramycin.
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)

Abstract (Expand)

PURPOSE: Evaluation of [(68)Ga]NODAGA-duramycin as a positron emission tomography (PET) tracer of cell death for whole-body detection of chemotherapy-induced organ toxicity. PROCEDURES: Tracer specificity … of Ga-68 labeled NODAGA-duramycin was determined in vitro using competitive binding experiments. Organ uptake was analyzed in untreated and doxorubicin, busulfan, and cisplatin-treated mice 2 h after intravenous injection of [(68)Ga]NODAGA-duramycin. In vivo data were validated by immunohistology and blood parameters. RESULTS: In vitro experiments confirmed specific binding of [(68)Ga]NODAGA-duramycin. Organ toxicities were detected successfully using [(68)Ga]NODAGA-duramycin PET/X-ray computed tomography (CT) and confirmed by immunohistochemistry and blood parameter analysis. Organ toxicities in livers and kidneys showed similar trends in PET/CT and immunohistology. Busulfan and cisplatin-related organ toxicities in heart, liver, and lungs were detected earlier by PET/CT than by blood parameters and immunohistology. CONCLUSION: [(68)Ga]NODAGA-duramycin PET/CT was successfully applied to non-invasively detect chemotherapy-induced organ toxicity with high sensitivity in mice. It, therefore, represents a promising alternative to standard toxicological analyses with a high translational potential.

Authors: A. Rix, N. I. Drude, Anna Mrugalla, F. Baskaya, K. Y. Pak, B. Gray, H. J. Kaiser, R. H. Tolba, E. Fiegle, Wiltrud Lederle, F. M. Mottaghy, F. Kiessling

Date Published: 8th Aug 2019

Journal: Mol Imaging Biol

Adenovirusmediated overexpression of bone morphogenetic protein9 promotes methionine choline deficiencyinduced nonalcoholic steatohepatitis in nonobese mice.
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)

Abstract (Expand)

Liver inflammation and macrophage infiltration are critical steps in the progression of nonalcoholic fatty liver to the development of nonalcoholic steatohepatitis. Bone morphogenetic protein9 is a … cytokine involved in the regulation of chemokines and lipogenesis. However, the function of bone morphogenetic protein9 in nonalcoholic steatohepatitis is still unknown. The present study hypothesized that bone morphogenetic protein9 may contribute to steatohepatitis in mice fed a methionine choline deficiency diet (MCD). C57BL/6 mice overexpressing bone morphogenetic protein9 and control mice were fed the MCD diet for 4 weeks. Liver tissue and serum samples were obtained for subsequent measurements. Bone morphogenetic protein9 overexpression exacerbated steatohepatitis in mice on the MCD diet, as indicated by liver histopathology, increased serum alanine aminotransferase activity, aspartate transaminase activity, hepatic inflammatory gene expression and M1 macrophage recruitment. Although bone morphogenetic protein9 overexpression did not affect the expression of profibrogenic genes, including Collagen I (alpha)1 or matrix metalloproteinase (MMP) 9, it did upregulate the expression of transforming growth factorbeta and plasminogen activator inhibitor 1, and downregulated the expression of MMP2. The above results indicate that bone morphogenetic protein9 exerts a proinflammatory role in MCD dietinduced nonalcoholic steatohepatitis.

Authors: Q. Li, B. Liu, K. Breitkopf-Heinlein, H. Weng, Yixin Jiang, P. Dong, Steven Dooley, K. Xu, H. Ding

Date Published: 20th Jul 2019

Journal: Mol Med Rep

TGF-beta in Hepatic Stellate Cell Activation and Liver Fibrogenesis-Updated 2019.
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)

Abstract (Expand)

Liver fibrosis is an advanced liver disease condition, which could progress to cirrhosis and hepatocellular carcinoma. To date, there is no direct approved antifibrotic therapy, and current treatment … is mainly the removal of the causative factor. Transforming growth factor (TGF)-beta is a master profibrogenic cytokine and a promising target to treat fibrosis. However, TGF-beta has broad biological functions and its inhibition induces non-desirable side effects, which override therapeutic benefits. Therefore, understanding the pleiotropic effects of TGF-beta and its upstream and downstream regulatory mechanisms will help to design better TGF-beta based therapeutics. Here, we summarize recent discoveries and milestones on the TGF-beta signaling pathway related to liver fibrosis and hepatic stellate cell (HSC) activation, emphasizing research of the last five years. This comprises impact of TGF-beta on liver fibrogenesis related biological processes, such as senescence, metabolism, reactive oxygen species generation, epigenetics, circadian rhythm, epithelial mesenchymal transition, and endothelial-mesenchymal transition. We also describe the influence of the microenvironment on the response of HSC to TGF-beta. Finally, we discuss new approaches to target the TGF-beta pathway, name current clinical trials, and explain promises and drawbacks that deserve to be adequately addressed.

Authors: B. Dewidar, C. Meyer, Steven Dooley, A. N. Meindl-Beinker

Date Published: 11th Nov 2019

Journal: Cells

Editorial: Systems Biology and Bioinformatics in Gastroenterology and Hepatology
LiSyM network

Abstract

Not specified

Authors: Peter Jansen, Kai Breuhahn, Andreas Teufel, Steven Dooley

Date Published: 22nd Nov 2019

Journal: Front. Physiol.

Pillar II presentations (one file) - Jamboree, Leipzig2019
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
No description specified

Creator: Seddik Hammad

Contributor: Seddik Hammad

Pillar II: Outline poster-Jamboree2019-Leipzig
Chronic Liver Disease Progression (LiSyM-DP - Pillar II), LiSyM network
No description specified

Creator: Seddik Hammad

Contributor: Seddik Hammad

Pillar III: AG Dooley Poster-Jamboree2019-Leipzig
Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF - Pillar III), LiSyM network
No description specified

Creator: Seddik Hammad

Contributor: Seddik Hammad

AG Dooley Poster- Jamboree2019-Leipzig
Chronic Liver Disease Progression (LiSyM-DP - Pillar II), LiSyM network
No description specified

Creator: Seddik Hammad

Contributor: Seddik Hammad

07052019-V1-Pillar 2: TissueScale Presentation (Seddik/Dirk)
Chronic Liver Disease Progression (LiSyM-DP - Pillar II)
No description specified

Creator: Seddik Hammad

Contributor: Seddik Hammad

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