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16. Traumatisme sur rein pathologique : y a-t-il une sur-morbidité ?

Author

Maatougui, J., primary, Saadi, A., additional, Chakroun, M., additional, Bellali, M., additional, Allouche, M., additional, Jrad, M., additional, Derouiche, A., additional, Bouzouita, A., additional, Ben Slama, M., additional, Hamdoun, M., additional, Ayed, H., additional, and Chebil, M., additional

Published
2021
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18. Geotrichum capitatum fungemia in patients treated for acute leukemia

Author

Kallel A, Balkis Meddeb, Bahri O, Ben Neji H, M. Bchir, Kalthoum Kallel, and Hamdoun M

Subjects
Geotrichum capitatum, medicine.medical_specialty, Acute leukemia, business.industry, medicine.disease, Gastroenterology, Amphotéricine B, Infectious Diseases, Internal medicine, Amphotericin B, medicine, In patient, business, Fungemia, medicine.drug
Published
2019
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20. Impact de la leucospermie sur les résultats d'ICSI.

Author

Boughzala, I., Kacem Berjeb, K., Hamdoun, M., Hermi, A., Chtourou, S., Sammouda, I., Chebly, D., Rokbani, S., Saadi, A., Aouini, H., Mahjoubi, M., Bouzouita, A., Chakroun, N., Braham, M., and Chakroun, M.

Abstract

Copyright of Proges en Urologie is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2024
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28. Two cases of sudden death due to pulmonary tumor thrombotic microangiopathy caused by occult gastric carcinoma

Author

Mehdi Ben Khelil, Chkirbene, Y., Azzouz, H., Haouet, S., and Hamdoun, M.

Subjects
Adult, Male, Death, Sudden, Young Adult, Fatal Outcome, Lung Neoplasms, Stomach Neoplasms, Thrombotic Microangiopathies, Hypertension, Pulmonary, Humans, Female, Autopsy, Carcinoma, Signet Ring Cell
Abstract

We present two cases of occult gastric carcinoma associated to a large pulmonary tumors thrombosis microangiopathy (PTTM). The first case is a 28 years-old man. He was dead due to a respiratory failure. Autopsy showed a whitish indurated mass invading the stomach wall. Histological findings showed a primary "signet ring" gastric adenocarcinoma with pulmonary carcinomatosis and multiple PTTM and a heart metastasis. The second case is a 24 years-old pregnant woman. The main symptoms were nausea and stomach discomfort and they were seen as pregnancy signs. She was dead because of respiratory failure, 10 hours after a vaginal delivery. Autopsy showed the absence of any cause of death related to the delivery and the presence of a whitish indurated mass in the stomach. Histological findings showed a primary "signet ring" gastric adenocarcinoma, with pulmonary carcinomatosis and multiple PTTM.

Published
2017

30. Emerging contaminants - pesticides, PPCPs, microbial degradation products and natural substances as inhibitors of multixenobiotic defense in aquatic organisms

Author

Smital, Tvrtko, Luckenbach, Till, Sauerborn, Roberta, Hamdoun, M. Amro, Vega, L. Rebecca, and Epel, David

Subjects
multixenobiotic reistance (MXR), MXR inhibitors, environmental pollutants, PPCPs, pesticides, synthetic musk fragrances
Abstract

The environmental presence of so-called chemosensitizers or inhibitors of the multixenobiotic resistance (MXR) defense system in aquatic organisms could cause an increase in intracellular accumulation and toxic effects of other xenobiotics normally effluxed by MXR transport proteins (P-gps, MRPs). MXR inhibition with concomitant detrimental effects has been shown in several studies with aquatic organisms exposed to both model MXR inhibitors and environmental pollutants. The presence of MXR inhibitors has been demonstrated in environmental samples from polluted locations at concentrations that could abolish P-gp transport activity. However, it is not clear whether the inhibition observed after exposure to environmental samples is a result of saturation of MXR transport proteins by numerous substrates present in polluted waters or results from the presence of powerful MXR inhibitors. And are potent environmental MXR inhibitors natural or man-made chemicals? As a consequence of these uncertainties, no official action has been taken to monitor and control the release and presence of MXR inhibitors into aquatic environments. In this paper we present our new results addressing these critical questions. Ecotoxicological significance of MXR inhibition was supported in in vivo studies that demonstrated an increase in the production of mutagenic metabolites by mussels and an increase in the number of sea urchin embryos with apoptotic cells after exposure to model MXR inhibitors. We also demonstrated that MXR inhibitors are present among both conventional and emerging man-made pollutants: some pesticides and synthetic musk fragrances show extremely high MXR inhibitory potential at environmentally relevant concentrations. In addition, the biological transformation of crude oil hydrocarbons into MXR inhibitors by oil-degrading bacteria and the risk potentially caused by powerful natural MXR inhibitors produced by invasive species were emphasized.

Published
2004

41. Wnt signaling is involved in human articular chondrocyte de-differentiation in vitro.

Author

Sassi, N, Laadhar, L, Allouche, M, Zandieh-Doulabi, B, Hamdoun, M, Klein-Nulend, J, Makni, S, and Sellami, S

Subjects
OSTEOARTHRITIS, CARTILAGE cells, MATRIX metalloproteinases, PHYSIOLOGICAL effects of nitric oxide, BIOMARKERS, GENE expression, MICROSCOPY, PHYSIOLOGY
Abstract

Osteoarthritis is the most prevalent form of arthritis in the world. Certain signaling pathways, such as the wnt pathway, are involved in cartilage pathology. Osteoarthritic chondrocytes undergo morphological and biochemical changes that lead to chondrocyte de-differentiation. We investigated whether the Wnt pathway is involved in de-differentiation of human articular chondrocytes in vitro. Human articular chondrocytes were cultured for four passages in the presence or absence of IL-1 in monolayer or micromass culture. Changes in cell morphology were monitored by light microscopy. Protein and gene expression of chondrocyte markers and Wnt pathway components were determined by Western blotting and qPCR after culture. After culturing for four passages, chondrocytes exhibited a fibroblast-like morphology. Collagen type II and aggrecan protein and gene expression decreased, while collagen type I, matrix metalloproteinase 13, and nitric oxide synthase expressions increased. Wnt molecule expression profiles changed; Wnt5a protein expression, the Wnt target gene, c-jun, and in Wnt pathway regulator, sFRP4 increased. Treatment with IL-1 caused chondrocyte morphology to become more filament-like. This change in morphology was accompanied by extinction of col II expression and increased col I, MMP13 and eNOS expression. Changes in expression of the Wnt pathway components also were observed. Wnt7a decreased significantly, while Wnt5a, LRP5, β-catenin and c-jun expressions increased. Culture of human articular chondrocytes with or without IL-1 not only induced chondrocyte de-differentiation, but also changed the expression profiles of Wnt components, which suggests that the Wnt pathway is involved in chondrocyte de-differentiation in vitro. [ABSTRACT FROM AUTHOR]

Published
2014
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42. The roles of canonical and non-canonical Wnt signaling in human de-differentiated articular chondrocytes.

Author

Sassi, N, Laadhar, L, Allouche, M, Zandieh-Doulabi, B, Hamdoun, M, Klein-Nulend, J, Makni, S, and Sellami, S

Subjects
OSTEOARTHRITIS, CARTILAGE cells, CELL differentiation, WNT genes, CELL culture, PHYSIOLOGY, DISEASE risk factors
Abstract

Osteoarthritis is the most prevalent form of arthritis in the world and it is becoming a major public health problem. Osteoarthritic chondrocytes undergo morphological and biochemical changes that lead to de-differentiation. The involvement of signaling pathways, such as the Wnt pathway, during cartilage pathology has been reported. Wnt signaling regulates critical biological processes. Wnt signals are transduced through at least three intracellular signaling pathways including the canonical Wnt/β-catenin pathway, the Wnt/Ca2 + pathway and the Wnt/planar cell polarity pathway. We investigated the involvement of the Wnt canonical and non-canonical pathways in human articular chondrocyte de-differentiation in vitro. Human articular chondrocytes were cultured through four passages with no treatment, or with sFRP3 treatment, an inhibitor of Wnt pathways, or with DKK1 treatment, an inhibitor of the canonical pathway. Chondrocyte-secreted markers and Wnt pathway components were analyzed using western blotting and qPCR. Inhibition of the Wnt pathway showed that the canonical Wnt signaling probably is responsible for inhibition of collagen II expression, activation of metalloproteinase 13 expression and regulation of Wnt7a and c-jun expression during chondrocyte de-differentiation in vitro. Our results also suggest that expressions of eNOS, Wnt5a and cyclinE1 are regulated by non-canonical Wnt signaling. [ABSTRACT FROM AUTHOR]

Published
2014
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45. 46th Medical Maghrebian Congress. November 9-10, 2018. Tunis

Author

Alami Aroussi, A., Fouad, A., Omrane, A., Razzak, A., Aissa, A., Akkad, A., Amraoui, A., Aouam, A., Arfaoui, A., Belkouchi, A., Ben Chaaben, A., Ben Cheikh, A., Ben Khélifa, A., Ben Mabrouk, A., Benhima, A., Bezza, A., Bezzine, A., Bourrahouat, A., Chaieb, A., Chakib, A., Chetoui, A., Daoudi, A., Ech-Chenbouli, A., Gaaliche, A., Hassani, A., Kassimi, A., Khachane, A., Labidi, A., Lalaoui, A., Masrar, A., Mchachi, A., Nakhli, A., Ouakaa, A., Siati, A., Toumi, A., Zaouali, A., Condé, A. Y., Haggui, A., Belaguid, A., abdelkader jalil el hangouche, Gharbi, A., Mahfoudh, A., Bouzouita, A., Aissaoui, A., Ben Hamouda, A., Hedhli, A., Ammous, A., Bahlous, A., Ben Halima, A., Belhadj, A., Blel, A., Brahem, A., Banasr, A., Meherzi, A., Saadi, A., Sellami, A., Turki, A., Ben Miled, A., Ben Slama, A., Daib, A., Zommiti, A., Chadly, A., Jmaa, A., Mtiraoui, A., Ksentini, A., Methnani, A., Zehani, A., Kessantini, A., Farah, A., Mankai, A., Mellouli, A., Touil, A., Hssine, A., Ben Safta, A., Derouiche, A., Jmal, A., Ferjani, A., Djobbi, A., Dridi, A., Aridhi, A., Bahdoudi, A., Ben Amara, A., Benzarti, A., Ben Slama, A. Y., Oueslati, A., Soltani, A., Chadli, A., Aloui, A., Belghuith Sriha, A., Bouden, A., Laabidi, A., Mensi, A., Sabbek, A., Zribi, A., Green, A., Ben Nasr, A., Azaiez, A., Yeades, A., Belhaj, A., Mediouni, A., Sammoud, A., Slim, A., Amine, B., Chelly, B., Jatik, B., Lmimouni, B., Daouahi, B., Ben Khelifa, B., Louzir, B., Dorra, A., Dhahri, B., Ben Nasrallah, C., Chefchaouni, C., Konzi, C., Loussaief, C., Makni, C., Dziri, C., Bouguerra, C., Kays, C., Zedini, C., Dhouha, C., Mohamed, C., Aichaouia, C., Dhieb, C., Fofana, D., Gargouri, D., Chebil, D., Issaoui, D., Gouiaa, D., Brahim, D., Essid, D., Jarraya, D., Trad, D., Ben Hmida, E., Sboui, E., Ben Brahim, E., Baati, E., Talbi, E., Chaari, E., Hammami, E., Ghazouani, E., Ayari, F., Ben Hariz, F., Bennaoui, F., Chebbi, F., Chigr, F., Guemira, F., Harrar, F., Benmoula, F. Z., Ouali, F. Z., Maoulainine, F. M. R., Bouden, F., Fdhila, F., Améziani, F., Bouhaouala, F., Charfi, F., Chermiti Ben Abdallah, F., Hammemi, F., Jarraya, F., Khanchel, F., Ourda, F., Sellami, F., Trabelsi, F., Yangui, F., Fekih Romdhane, F., Mellouli, F., Nacef Jomli, F., Mghaieth, F., Draiss, G., Elamine, G., Kablouti, G., Touzani, G., Manzeki, G. B., Garali, G., Drissi, G., Besbes, G., Abaza, H., Azzouz, H., Said Latiri, H., Rejeb, H., Ben Ammar, H., Ben Brahim, H., Ben Jeddi, H., Ben Mahjouba, H., Besbes, H., Dabbebi, H., Douik, H., El Haoury, H., Elannaz, H., Elloumi, H., Hachim, H., Iraqi, H., Kalboussi, H., Khadhraoui, H., Khouni, H., Mamad, H., Metjaouel, H., Naoui, H., Zargouni, H., Elmalki, H. O., Feki, H., Haouala, H., Jaafoura, H., Drissa, H., Mizouni, H., Kamoun, H., Ouerda, H., Zaibi, H., Chiha, H., Saibi, H., Skhiri, H., Boussaffa, H., Majed, H., Blibech, H., Daami, H., Harzallah, H., Rkain, H., Ben Massoud, H., Jaziri, H., Ben Said, H., Ayed, H., Harrabi, H., Chaabouni, H., Ladida Debbache, H., Harbi, H., Yacoub, H., Abroug, H., Ghali, H., Kchir, H., Msaad, H., Manai, H., Riahi, H., Bousselmi, H., Limem, H., Aouina, H., Jerraya, H., Ben Ayed, H., Chahed, H., Snéne, H., Lahlou Amine, I., Nouiser, I., Ait Sab, I., Chelly, I., Elboukhani, I., Ghanmi, I., Kallala, I., Kooli, I., Bouasker, I., Fetni, I., Bachouch, I., Bouguecha, I., Chaabani, I., Gazzeh, I., Samaali, I., Youssef, I., Zemni, I., Bachouche, I., Bouannene, I., Kasraoui, I., Laouini, I., Mahjoubi, I., Maoudoud, I., Riahi, I., Selmi, I., Tka, I., Hadj Khalifa, I., Mejri, I., Béjia, I., Bellagha, J., Boubaker, J., Daghfous, J., Dammak, J., Hleli, J., Ben Amar, J., Jedidi, J., Marrakchi, J., Kaoutar, K., Arjouni, K., Ben Helel, K., Benouhoud, K., Rjeb, K., Imene, K., Samoud, K., El Jeri, K., Abid, K., Chaker, K., Bouzghaîa, K., Kamoun, K., Zitouna, K., Oughlani, K., Lassoued, K., Letaif, K., Hakim, K., Cherif Alami, L., Benhmidoune, L., Boumhil, L., Bouzgarrou, L., Dhidah, L., Ifrine, L., Kallel, L., Merzougui, L., Errguig, L., Mouelhi, L., Sahli, L., Maoua, M., Rejeb, M., Ben Rejeb, M., Bouchrik, M., Bouhoula, M., Bourrous, M., Bouskraoui, M., El Belhadji, M., Essakhi, M., Essid, M., Gharbaoui, M., Haboub, M., Iken, M., Krifa, M., Lagrine, M., Leboyer, M., Najimi, M., Rahoui, M., Sabbah, M., Sbihi, M., Zouine, M., Chefchaouni, M. C., Gharbi, M. H., El Fakiri, M. M., Tagajdid, M. R., Shimi, M., Touaibia, M., Jguirim, M., Barsaoui, M., Belghith, M., Ben Jmaa, M., Koubaa, M., Tbini, M., Boughdir, M., Ben Salah, M., Ben Fraj, M., Ben Halima, M., Ben Khalifa, M., Bousleh, M., Limam, M., Mabrouk, M., Mallouli, M., Rebeii, M., Ayari, M., Belhadj, M., Ben Hmida, M., Boughattas, M., Drissa, M., El Ghardallou, M., Fejjeri, M., Hamza, M., Jaidane, M., Jrad, M., Kacem, M., Mersni, M., Mjid, M., Serghini, M., Triki, M., Ben Abbes, M., Boussaid, M., Gharbi, M., Hafi, M., Slama, M., Trigui, M., Taoueb, M., Chakroun, M., Ben Cheikh, M., Chebbi, M., Hadj Taieb, M., Ben Khelil, M., Hammami, M., Khalfallah, M., Ksiaa, M., Mechri, M., Mrad, M., Sboui, M., Bani, M., Hajri, M., Mellouli, M., Allouche, M., Mesrati, M. A., Mseddi, M. A., Amri, M., Bejaoui, M., Bellali, M., Ben Amor, M., Ben Dhieb, M., Ben Moussa, M., Chebil, M., Cherif, M., Fourati, M., Kahloul, M., Khaled, M., Machghoul, M., Mansour, M., Abdesslem, M. M., Ben Chehida, M. A., Chaouch, M. A., Essid, M. A., Meddeb, M. A., Gharbi, M. C., Elleuch, M. H., Loueslati, M. H., Sboui, M. M., Mhiri, M. N., Kilani, M. O., Ben Slama, M. R., Charfi, M. R., Nakhli, M. S., Mourali, M. S., El Asli, M. S., Lamouchi, M. T., Cherti, M., Khadhraoui, M., Bibi, M., Hamdoun, M., Kassis, M., Touzi, M., Ben Khaled, M., Fekih, M., Khemiri, M., Ouederni, M., Hchicha, M., Ben Attia, M., Yahyaoui, M., Ben Azaiez, M., Bousnina, M., Ben Jemaa, M., Ben Yahia, M., Daghfous, M., Haj Slimen, M., Assidi, M., Belhadj, N., Ben Mustapha, N., El Idrissislitine, N., Hikki, N., Kchir, N., Mars, N., Meddeb, N., Ouni, N., Rada, N., Rezg, N., Trabelsi, N., Bouafia, N., Haloui, N., Benfenatki, N., Bergaoui, N., Yomn, N., Maamouri, N., Mehiri, N., Siala, N., Beltaief, N., Aridhi, N., Sidaoui, N., Walid, N., Mechergui, N., Mnif, N., Ben Chekaya, N., Bellil, N., Dhouib, N., Achour, N., Kaabar, N., Mrizak, N., Chaouech, N., Hasni, N., Issaoui, N., Ati, N., Balloumi, N., Haj Salem, N., Ladhari, N., Akif, N., Liani, N., Hajji, N., Trad, N., Elleuch, N., Marzouki, N. E. H., Larbi, N., M Barek, N., Rebai, N., Bibani, N., Ben Salah, N., Belmaachi, O., Elmaalel, O., Jlassi, O., Mihoub, O., Ben Zaid, O., Bouallègue, O., Bousnina, O., Bouyahia, O., El Maalel, O., Fendri, O., Azzabi, O., Borgi, O., Ghdes, O., Ben Rejeb, O., Rachid, R., Abi, R., Bahiri, R., Boulma, R., Elkhayat, R., Habbal, R., Tamouza, R., Jomli, R., Ben Abdallah, R., Smaoui, R., Debbeche, R., Fakhfakh, R., El Kamel, R., Gargouri, R., Jouini, R., Nouira, R., Fessi, R., Bannour, R., Ben Rabeh, R., Kacem, R., Khmakhem, R., Ben Younes, R., Karray, R., Cheikh, R., Ben Malek, R., Ben Slama, R., Kouki, R., Baati, R., Bechraoui, R., Fradi, R., Lahiani, R., Ridha, R., Zainine, R., Kallel, R., Rostom, S., Ben Abdallah, S., Ben Hammamia, S., Benchérifa, S., Benkirane, S., Chatti, S., El Guedri, S., El Oussaoui, S., Elkochri, S., Elmoussaoui, S., Enbili, S., Gara, S., Haouet, S., Khammeri, S., Khefecha, S., Khtrouche, S., Macheghoul, S., Mallouli, S., Rharrit, S., Skouri, S., Helali, S., Boulehmi, S., Abid, S., Naouar, S., Zelfani, S., Ben Amar, S., Ajmi, S., Braiek, S., Yahiaoui, S., Ghezaiel, S., Ben Toumia, S., Thabeti, S., Daboussi, S., Ben Abderahman, S., Rhaiem, S., Ben Rhouma, S., Rekaya, S., Haddad, S., Kammoun, S., Merai, S., Mhamdi, S., Ben Ali, R., Gaaloul, S., Ouali, S., Taleb, S., Zrour, S., Hamdi, S., Zaghdoudi, S., Ammari, S., Ben Abderrahim, S., Karaa, S., Maazaoui, S., Saidani, S., Stambouli, S., Mokadem, S., Boudiche, S., Zaghbib, S., Ayedi, S., Jardek, S., Bouselmi, S., Chtourou, S., Manoubi, S., Bahri, S., Halioui, S., Jrad, S., Mazigh, S., Ouerghi, S., Toujani, S., Fenniche, S., Aboudrar, S., Meriem Amari, S., Karouia, S., Bourgou, S., Halayem, S., Rammeh, S., Yaïch, S., Ben Nasrallah, S., Chouchane, S., Ftini, S., Makni, S., Miri, S., Saadi, S., Manoubi, S. A., Khalfallah, T., Mechergui, T., Dakka, T., Barhoumi, T., M Rad, T. E. B., Ajmi, T., Dorra, T., Ouali, U., Hannachi, W., Ferjaoui, W., Aissi, W., Dahmani, W., Dhouib, W., Koubaa, W., Zhir, W., Gheriani, W., Arfa, W., Dougaz, W., Sahnoun, W., Naija, W., Sami, Y., Bouteraa, Y., Elhamdaoui, Y., Hama, Y., Ouahchi, Y., Guebsi, Y., Nouira, Y., Daly, Y., Mahjoubi, Y., Mejdoub, Y., Mosbahi, Y., Said, Y., Zaimi, Y., Zgueb, Y., Dridi, Y., Mesbahi, Y., Gharbi, Y., Hellal, Y., Hechmi, Z., Zid, Z., Elmouatassim, Z., Ghorbel, Z., Habbadi, Z., Marrakchi, Z., Hidouri, Z., Abbes, Z., Ouhachi, Z., Khessairi, Z., Khlayfia, Z., Mahjoubi, Z., and Moatemri, Z.

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