Amani Mankai

Prof. Amani Mankai

Higher School of Sciences and Health Techniques, University of Tunis El Manar, Tunis,

Research Focus & Metrics

Academic Career Length

22Years (2005-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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25 July 2024 in Nutrients
Verified
Journal Article
Open access
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CBChiara Biggi
Chiara Biggi
Beatrice BiasiniBeatrice Biasini
Beatrice Biasini
NONives Ogrinc
Nives Ogrinc
LSLidija Strojnik
Lidija Strojnik
IEIsabella Endrizzi
Isabella Endrizzi
DMDavide Menozzi
Davide Menozzi
Given the global decline in adherence to the Mediterranean Diet (MD), even within its native region, it is key to identify the factors influencing this trend to mitigate the negative health outcomes associated with westernized diets. To this end, 4025 individuals (49.6% women, 42.6 ± 14.2 y/o) from Greece, Italy, Morocco, Slovenia, and Tunisia remotely completed a series of measures assessing motives, attitudes, and psychosocial factors related to MD adherence, which was evaluated using the MEDAS questionnaire. The results suggested medium-to-low adherence across all countries, with the highest adherence in Italy and Morocco and the lowest in Slovenia. Structural equation modeling revealed that positive attitudes toward the healthiness of food were the strongest predictors of adherence, whereas picky eating was a significant negative predictor in all countries except Greece. Adherence to the MD was positively influenced by health motivations in Morocco and weight control in Slovenia and Greece, while sensory appeal negatively influenced adherence in Italy. Additionally, price and convenience were significant barriers in Tunisia and Greece, whereas a preference for local and seasonal foods promoted adherence in Morocco and Greece. Overall, our findings underscore the need for country-specific interventions and policies that address distinct local factors and motivations to ease favorable shifts in dietary patterns toward MD principles.

1 February 2006 in Pathologie Biologie
Verified
Journal Article
Closed access
AMAmani Mankai
Amani Mankai
HLH. Landolsi
H. Landolsi
ACA. Chahed
A. Chahed
LGL. Gueddah
L. Gueddah
MLM. Limem
M. Limem
IGI. Ghedira
I. Ghedira

14 September 2008 in Cancer Research
Verified
Journal Article
Open access
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AMAmani Mankai
Amani Mankai
ABAnne Bordron
Anne Bordron
YRYves Renaudineau
Yves Renaudineau
CMChristine Martins-Carvalho
Christine Martins-Carvalho
Shinichiro TakahashiShinichiro Takahashi
Shinichiro Takahashi
PYPierre Youinou
Pierre Youinou
The anti-CD20 monoclonal antibody rituximab has been less successful in treating chronic lymphocytic leukemia (CLL) than lymphoma, possibly due to the lower density of CD20 on B lymphocytes from CLL patients than on those from lymphoma patients. This lowering may result from insufficiency of one of the transcription factors of cd20. Of these, purine-rich box-1 (PU.1) is poorly expressed in CLL. To estimate its weight in CD20 expression, pu.1 cDNA was transfected into CLL B cells and shown to raise the membrane expression of CD20 and to improve the rituximab-induced lysis of transfected cells. Granulocyte macrophage colony-stimulating factor and all-trans-retinoic acids were not involved in the defective expression of PU.1 or the excessive methylation of the pu.1 gene, because 6 of 14 CLL samples tested were normally methylated. This was confirmed by the failure of DNA methyltransferase inhibitors to restore pu.1 transcription in hypermethylated CLL, and, in fact, the expression of PU.1 was down-regulated by excessive expression of the FMS proto-oncogene–like tyrosine kinase 3 (Flt3) receptor. This abnormality is consistent with our finding of elevated levels of Flt3 ligand (FL) in 20 of 23 CLL sera tested. We propose that FL-dependent increased Flt3 signaling prevents the expression of PU.1, which down-regulates that of CD20, and accounts for resistance of leukemic B cells to rituximab-induced lysis. [Cancer Res 2008;68(18):7512–9]

10 April 2012 in Rheumatology International
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Journal Article
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AMAmani Mankai
Amani Mankai
WSWahiba Sakly
Wahiba Sakly
YTYosra Thabet
Yosra Thabet
AAAchouak Achour
Achouak Achour
WMWiem Manoubi
Wiem Manoubi
IGIbtissem Ghedira
Ibtissem Ghedira

1 January 2007 in Scandinavian Journal of Gastroenterology
Verified
Journal Article
Closed access
DTDorsaf Toumi
Dorsaf Toumi
AMAmani Mankai
Amani Mankai
RBRamla Belhadj
Ramla Belhadj
LGLeila Ghedira-Besbes
Leila Ghedira-Besbes
MJMoncef Jeddi
Moncef Jeddi
IGIbtissem Ghedira
Ibtissem Ghedira
To evaluate, retrospectively, the frequency of anti-Saccharomyces cerevisiae antibodies (ASCA) in patients with coeliac disease. ASCA, IgG and IgA were determined by ELISA in sera of 238 coeliac patients. The patients were divided into three groups: group I - 125 untreated patients; group II - 42 patients under a strict gluten-free diet (GFD); and group III - 71 patients who did not comply with a GFD. Sera of 80 healthy blood donors served as controls. The frequency of ASCA (IgG or IgA) was significantly higher in untreated coeliac patients than in the control group (27.2% versus 3.7%, p=10(-5)). In 238 coeliac patients, the frequency of ASCA was significantly higher in adults than in children (35.4% versus 21.1%, p=0.01). In group III, the frequency of ASCA was significantly higher in adults than in children (60% versus 26.1%, p=0.004). In 238 coeliac patients, ASCA IgG were significantly more frequent than ASCA IgA in both children (19% versus 6.3%, p=0.001) and adults (33.3% versus 12.5%, p=5.10(-4)). In children, ASCA IgG were negative in group II and positive in 20% of group I (p=0.01). In adults, the frequency of ASCA IgG was also significantly lower in group II than in group I (9.5% versus 34%, p=0.03). A high frequency of ASCA has been found in coeliac patients. The frequency of ASCA was not statistically different between patients with successful adherence to GFD and healthy controls.

13 April 2010 in Endocrine Pathology
Verified
Journal Article
Closed access
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WSWahiba Sakly
Wahiba Sakly
AMAmani Mankai
Amani Mankai
NSNabil Sakly
Nabil Sakly
YTYosra Thabet
Yosra Thabet
AAAchouak Achour
Achouak Achour
IGIbtissem Ghedira
Ibtissem Ghedira