Person:
Ahmed, Hanan Hassan Fouad

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0000-0002-9939-1034
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57202277900
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Hanan Hassan Fouad Ahmed
Last Name
Ahmed
First Name
Hanan Hassan Fouad
Main Affiliation
Galala University
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Professor Medical Biochemistry & Molecular Biology

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2021 - 20237
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  • Publication
    Open Access
    Correction: Evaluation of CEP55, SERPINE1 and SMPD3 genes and proteins as diagnostic and prognostic biomarkers in gastric carcinoma in Egyptian patients
    (Springer Nature, 2023-02-09) Abdel-Tawab, Marwa Sayed; Ismaeel, Ahmed Yehia; Tammam, Ahmed Abd-Eltawab; Fahmy, Alzhraa M.; Shaaban, Saeed; Abdel-Salam, Soha Mahmoud; Abd Elazeem, Naglaa Adly; Ahmed, Hanan Hassan Fouad
    Background: Gastric carcinoma (GC) is a fatal disease. Detection of new biomarkers that can be utilized in the early diagnosis of GC is a pressing need. This present study assessed centrosomal protein-55 (CEP55)’ serpin family E member 1 (SERPINE1) and sphingomyelin phosphodiesterase 3 (SMPD3) genes and proteins in gastric adenocarcinoma with different tumor progression features. Thirty surgically resected gastric tissue samples from thirty patients suffered from gastric cancers were obtained. The gastric tissue samples were divided into tumorous (with different stages and grades) and adjacent non-tumorous samples. CEP55, SERPINE1 and SMPD3 genes were assessed by quantitative qRT-PCR, and their proteins were assessed by ELISA in the gastric tissue samples. Results: As regards SERPINE1, CEP55 genes and proteins, results revealed significant elevations in the GC samples (p < 0.0001). On the contrary, SMPD3 gene and protein revealed significant decreases as compared to non-tumorous samples. The studied genes and proteins showed highly significant specificity and sensitivity in the early detection of GC. SERPINE1 gene and protein revealed highly significant increases and positive correlations, while SMPD3 gene and protein revealed highly significant decreases and negative correlations as the tumor progresses. Conclusion: CEP55, SERPINE1 and SMPD3 genes and proteins could be used as useful biomarkers for the early detection of GC. SERPINE1 and SMPD3 genes and proteins might be used as risk and protective prognostic factors in GC, respectively.
  • Publication
    Metadata only
    The biomechanistic aspects of renal cortical injury induced by diesel exhaust particles in rats and the renoprotective contribution of quercetin pretreatment: Histological and biochemical study
    (Wiley, 2021) Morsi, Ahmed A.; Alasmari, Wardah Abdullah; Faruk, Eman Mohamed; Ahmed, Hanan Hassan Fouad
    Although several studies have reported a toxic effect of diesel exhaust particles (DEP) exposure on the kidney tissues, the involvement of autophagy/NF-kB signaling as encountered mechanisms and the protective effects of a natural flavonoid, quercetin on DEP remains unclear. Thirty-two albino rats were divided as control, quercetin-treated (60 mg/kg, oral), DEP-exposed (0.5 mg/kg, intra-tracheal), and quercetin/DEP-exposed groups. Specimens of the renal cortex were subjected to histo-biochemical study and immunohistochemical analysis using anti-NF-kB, and anti-LC3β antibodies followed by morphometric and statistical analyses. The expression level of autophagy genes was quantitatively evaluated using RT-PCR, as well. The DEP-exposed rats showed an elevation in the renal tissue levels of MDA and a decrease in the catalase and superoxide dismutase (p < .05). Histologically, there were cytoplasmic vacuolar changes in the lining cells of the renal tubules, glomerular atrophy, and vascular congestion. In addition, renal inflammation was evident as confirmed by the increased NF-kB immunoexpression. Moreover, the gene expression of Becn1, ATG5, and LC3β increased (p <. 0) due to DEP exposure. Conversely, quercetin pretreatment improved these renal histo-biochemical alterations (p < .05) and regulated autophagy/NF-kB pathways. Overall, the study proved the renal toxicity mediated by DEP exposure via precipitating renal inflammation, autophagy activation, and oxidative stress. Quercetin pretreatment could antagonize such machinery to protect the kidney against DEP.
  • Publication
    Open Access
    Do platelet rich plasma and folic acid reverse experimental induced ovarian failure: Emphasis on folliculogenesis, and ovarian steroidogenesis
    (2021-09-01) Alasmari, Wardah Abdullah; Faruk, Eman Mohamed; Nafea, Ola Elsayed; El-wafaey, Dalia Ibrahim; Manawy, Samia M.; Ahmed, Hanan Hassan Fouad
    Background: Valproic acid (VPA) is a commonly prescribed antiepileptic drug. VPA could mediate endocrinal reproductive dysfunction on a long-term use. This study was designed to evaluate the possible protective effects of platelet rich plasma (PRP) alone and PRP in combination with folic acid (FA) in a rat model of VPA induced ovarian failure. Materials and Methods: Thirty-five adult rats were randomly divided into five equal groups and 14 female rats were used for PRP preparation as control, VPA, co-treated VPA with FA, co-treated VPA with PRP and co-treated VPA with FA and PRP groups. All treatments were administered for 90 days. The effects of PRP and/or FA against VPA were evaluated through assessment of ovarian oxidant/antioxidant biomarkers, hormonal assay of reproductive hormones, quantification of mRNA gene expression for ovarian steroidogenesis pathway-encoding genes. Histopathological examination of the ovarian tissues was implemented. Results: Revealed that VPA exposure caused ovarian failure as documented by the decreased ovarian superoxide dismutase and catalase activities, increased ovarian malondialdehyde levels, diminished serum reproductive hormones concentrations and repressed the ovarian steroidogenesis pathway-encoding genes. In addition, VPA-induced marked ovarian histopathological alterations and impaired folliculogenesis. PRP and/or FA treatment improved ovarian function after VPA exposure. Adding FA to PRP produced more ovarian estrogen receptors immunoexpression than those produced by PRP alone. While other protective effects against VPA induced ovarian failure are equal between the two agents. Conclusion: PRP exhibited a protective role against VPA-induced ovarian failure in adult rats. A combined PRP and FA therapy is superior to PRP alone to some extent.
  • Publication
    Metadata only
    Evaluation of gene expression of PLEKHS1, AADAC, and CDKN3 as novel genomic markers in gastric carcinoma.
    (PLOS ONE, 2022-04-21) Abdel-Tawab, Marwa Sayed; Othman, Asmaa M; Eid, Ragaey A; Mohammed, Marwa Abdeltawab; Hassan, Ahmed; Reyad, Hoda Ramadan; Ahmed, Hanan Hassan Fouad
    Gastric cancer (GC) is considered lethal aggressive cancer. In Egypt, GC has a low incidence but unfortunately, it is mostly diagnosed at an advanced stage with a poor prognosis. Assessment of novel markers that can be used in the early detection of GC is an urgent need. The present study was performed to assess the association of the Pleckstrin homology domain-containing S1 (PLEKHS1)، arylacetamide deacetylase (AADAC, and Cyclin-dependent kinase inhibitor 3 (CDKN3) genes with GC and to correlate their gene expression levels with tumor stage, grade, and other clinicopathological features. The current work was performed on forty gastric tissue samples; twenty in Group 1 with GC tissues at different stages, and grades and twenty in Group 2 (control group) with non-tumorous tissue. PLEKHS1, AADAC, and CDKN3 gene expression were assessed by RT-qPCR. AADAC, CDKN3 genes were significantly (p<0.001) upregulated, while PLEKHS1 gene was significantly (p<0.001) downregulated in the GC group than the control group. AADAC gene expression exhibited a high significant (p<0.001) positive correlation with the tumor grades and the tumor stages. A high significant negative correlation between AADAC, and CDKN3 gene expression (r = -.760, p<0.001) was found. The three studied parameters showed high significant sensitivity and specificity in the prediction of the presence of GC. PLEKHS1, AADAC, and CDKN3 gene expressions were suggested to be used as diagnostic and predictive biomarkers of GC, additionally, AADAC may be used as a prognostic marker in these patients for further future confirming studies.
  • Publication
    Metadata only
    Inhibition of gene expression and production of iNOS and TNF-α in experimental model of neurodegenerative disorders stimulated microglia by Soy nano-isoflavone/stem cell-exosomes.
    (Elsevier, 2022-06-01) Faruk, Eman Mohamed; Hasan, Rehab Abd Allah; Taha, Neama Mahmoud; El-Shazly, Amal Mahmoud; Ahmed, Hanan Hassan Fouad
    The present study evaluated the therapeutic potential of soybean nano-isoflavone extract versus bone marrow mesenchymal stem cells derived extracellular exosomes (BMSCs-EXs) in experimentally induced neurodegenerative diseases in rats (ND). In this study, 36 albino male rats were divided into four groups: Group I (control rats); Group II (induced neurodegenerative disease in rats by intraperitoneal injection of d-galactose (120 mg/kg/day for 2 months); Group III (ND-induced rats treated with nano-isoflavone in doses of 10 mg/kg by oral gavage for 3 months); and Group IV (ND-induced rats treated with a single dose injection of BMSCs-EXs. The effect of BMSCs-EXs was evaluated by cerebral oxidant/antioxidant biomarkers, and mRNA gene expression quantitation for cerebral tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (i-NOS) and GAPDH pathway-encoding genes by real time reverse transcription polymerase chain reaction (RT-PCR) techniques. Then, histopathological examination of the cerebral cortical tissues. Our results showed that BMSC-EXs were successfully isolated and characterized. d-galactose produced a significant rise in the number of damaged neurons, decreased cerebral superoxide dismutase and catalase activities, increased cerebral malondialdehyde levels, downregulated the cerebral TNF-α, and i-NOS pathway-encoding genes. Furthermore, BMSC-EXs and nano-isoflavone treatments repaired damaged cerebral tissue and recovered its function greatly following induction of neurodegenerative disease. Treatment with either MSCs-EXs or nano-isoflavones led to significant improvement in the histological findings, reversed the degenerative effect of d-galactose, and had a favorable therapeutic utility against d- galactose-induced neurodegenerative disease.
  • Publication
    Metadata only
    Adipose-derived stem cell and their extracellular vesicles ameliorates immune function, and cardiac markers in experimental model of cardiorenal syndrome type III: TNF-α, IFN-γ and IL-10 cytokine production and their correlation with genotype
    (Elsevier, 2022-06) Alasmari, Wardah Abdullah; Faruk, Eman Mohamed; Radi, Rabab; El-wafaey, Dalia Ibrahim; Ahmed, Hanan Hassan Fouad
    Cardio-renal syndrome (CRS) denotes the convergence of heart-kidney interactions across several mechanisms. The current study is conducted to evaluate the anti-inflammatory role of adipose tissue-derived stem cells (ASCs) versus adipose stem cell-derived extracellular vesicles (ADSCs-EVs) in experimental model of cardiorenal syndrome type III. The study was conducted on 50 male rats that were equally divided to: group I (control group); Group II (experimental cardiorenal syndrome group) which induced by right renal artery ligation (ICRSIII); Group III (Sham-operated control group) which underwent surgical incision without renal artery ligation; Group IV (ICRSIII which received ADSCs-extracellular vesicles (ADSCs-EVs); Group V (ICRSIII which received adipose tissue stem cells (ASCs). Assessment of pro-inflammatory cytokines; IL-10, IL-1α, IL-6, IL-1 β, IFN-γ, NF-α and their mRNA gene expression quantitation, (NGAL), and brain natriuretic peptide (BNP) as markers of cardiac dysfunction, as well as histopathological examination of renal tissue was examined by H& E, Masson trichrome and periodic acid-Schiff stains (PAS). The ICRS group exhibited significant acute tubular injury with tubular dilation, loss of brush borders, epithelial flattening, and occasional sloughed cells in lumen. Use of either ADSCs-EVs or ASCs significantly ameliorated the histological findings of tubular injury. Proinflammatory cytokines, BNP and NGAL were significantly elevated in ICRSIII group as compared to all other studied groups. Administration of ADSCs-EVs or ASCs led to significant decrease in all proinflammatory cytokines as well as BNP and NGAL levels with no significant difference between them. In conclusion, ADSCs-EXs and ASCs exhibited significant repairing effects in experimental-induced cardiorenal syndrome type III as evidenced by amelioration of histological findings of tubular injury, anti-inflammatory effects, and the significant decrease in markers of cardiac dysfunction. ADSC-EVs reprogramed injured cardiac cells by activating regenerative processes.
  • Publication
    Metadata only
    Molecular and Cellular Mechanisms Involved in Adipose-derived stem cell and their extracellular vesicles in an Experimental Model of Cardio- renal Syndrome type 3: Histological and Biochemical Study.
    (Elsevier, 2022-06-07) Alasmari, Wardah Abdullah; Hosny, Somaya; Quthami, Khalid Al; Althobiany, Essa Abdulaziz Mohammed; Faruk, Eman Mohamed; Ahmed, Hanan Hassan Fouad
    A cardio-renal syndrome (CRS) is a medical condition in which kidney problems are accompanied by heart problems and diagnosed when acute kidney injury contributes to the development of acute cardiac injury. Regenerative medicine is becoming increasingly interested in adipose stem cells. We evaluated the effect of both adipose-derived stem cell extracellular vesicles (ADSCs-EVs) and adipose stem cells (ADSCs) on an experimental model of CRSIII. In this study, isolation, and further identification of ADSCs and ADSCs-EVs by transmission electron microscopy and flow cytometric analysis. Cardio-renal syndrome in rats was induced by renal artery ligation RAL followed by a single dose injection of both ADSCs and ADSCs-EVs in separate groups. The effects of ADSCs-EVs and ADSCs against induced CRSIII were evaluated by both renal and cardiac oxidant/antioxidant biomarkers, renal function, and mRNA gene expression quantitation for atrial natriuretic peptide (ANP), p300, and myocyte enhancer factor 2 (MEF2C and MEF2A), as well as myocardin (MYOCD), as molecules associated with cardiac hypertrophy. Additionally, histological and immunohistochemical studies of cardiac and renal tissues were done. ADSCs-EVs were effectively isolated and characterized. ADSCs-EVs and ADSCs reversed induced CRSIII, evidenced by considerably decreased serum urea and creatinine levels. Returned oxidant/antioxidant stability, and decreased caspase 3-mediated apoptotic programmed cell death in cardiac and renal tissues. Additionally, they led to successful down-regulation of hypertrophic cardiac genes levels and reversed histopathological cardiac and renal injures. ADSCs-derived extracellular vesicles and ADSCs injection restored damaged cardiac and renal tissue and improved its function greatly following induced CRSIII. They could therefore be useful as a means of protecting the heart from the deleterious effects of acute renal injury and reprogramed injured cardiac cells by activating regenerative processes. SIMPLE SUMMARY: Cardiorenal syndrome (CRS) type III is a subcategory of CRS whereby acute kidney injury (AKI) could contribute to the development of acute cardiac dysfunction. This study provided innovatory data regarding the role of adipose-derived stem cell extracellular vesicles ADSCs-EVs and adipose stem cells (ADSCs) in acute renal and cardiac dysfunction and renal biopsy specimens in the form of interstitial inflammation/tubular degeneration. The main cause of renal and cardiac dysfunction is identified to be the activation and accumulation of inflammatory cells and oxidants in the interstitium, surrounded by increased amounts of extracellular matrix, and ADSCs-EVs have been proposed as a contributor factor. The study has evidenced that both ADSCs-EVs and adipose stem cells display beneficial effects on renal and cardiac tissues survival in terms of the frequent occurrence of cardio-renal syndrome, ADSC-EVs treatment repaired damaged renal and cardiac tissues and recovered their function. ADSC-EVs reversed the effects of cardio-renal syndrome and reprogramed injured cells by activating regenerative processes. The clinical significance of the results presented in future studies needs to be investigated further.