20 results on '"Hmida I"'
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2. Failures count too: effect of the application of commercial inoculum of arbuscular fungi in a vineyard during its plantation
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Baraza Elena, Hmida Islem, Borràs Joshua, and Bota Josefina
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rhizophagus irregularis ,funneliformis mosseae ,vine plantation ,ripening ,Plant culture ,SB1-1110 - Abstract
Symbiosis with arbuscular mycorrhizal fungi (AMF) has long been recognized for its positive impact on plant health. Today, various companies market AMF-based commercial inoculants as biofertilizers or biostimulants for sustainable agriculture. However, their consistent efficacy in real-world field settings remains uncertain. This study investigated the influence of a commercial AMF inoculant on a newly planted vineyard featuring a local grape cultivar grafted onto a common rootstock (‘Ritcher 110’). Over two years, the physiological well-being, growth, and productivity of 20 inoculated vines compared to 20 control counterparts were monitored. The impact of inoculation on soil bacterial diversity and the infectivity of soil was assessed. Notably, AMF-inoculated plants exhibited consistently lower values in photosynthesis, growth, and grape production, although statistical significance was not always reached. Additionally, the total production remained unaffected, but there was a significant decrease in °Brix and pH values, suggesting delayed grape ripening in mycorrhizal plants, potentially promoting secondary metabolites accumulation. Regarding soil effects, the inoculation's impact was slight, with no substantial changes in soil mycorrhizal infectivity and only slight shifts in the microbial community's metabolic profile. Numerous studies highlight the context-dependent nature of AMF inoculation's effects, making it challenging to predict outcomes in field conditions. Failures found in trials like the present one provides valuable scientific information, contributing to determine the prerequisites for effective biofertilizer use in commercial viticulture. Ultimately, the effectiveness of AMF-based biofertilizers remains contingent on specific conditions, exposing the need for additional research to ensure their consistent and reliable application.
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- 2024
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3. Élargissement du spectre phénotypique du syndrome meds (microcéphalie, épilepsie et diabète néonatal) lié au gène IER3IP1 : à propos d’un cas Tunisien présentant un hypogonadisme
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Rjiba, K., primary, Soyah, N., additional, Kammoun, M., additional, Hadj Hmida, I., additional, Saad, A., additional, Mcelreavey, K., additional, and Mougou-Zerelli, S., additional
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- 2020
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4. Qualité de vie et complications de la dérivation urinaire type Mifrofanoff
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Mseddi, M.A., primary, Rkhis, A., additional, Rebai, N., additional, Masmoudi, A., additional, Ben Hmida, I., additional, Hamza, M., additional, Fourati, M., additional, Smaoui, W., additional, Fakhfakh, S., additional, Hadjslimen, M., additional, and Mhiri, M.N., additional
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- 2018
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5. Les atteintes neurologiques inhabituelles révélatrices du syndrome de Gougerot-Sjögren : cinq cas
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Hmida, I., primary, Kchaou, M., additional, Ben Ali, N., additional, Fray, S., additional, Echebbi, S., additional, and Belal, S., additional
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- 2014
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6. Towards surgical treatment of status epilepticus complicating Lennox Gastaut syndrome: Place of the vagus nerve stimulation
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Mrabet, S., primary, Hmida, I., additional, Ali, N. Ben, additional, Kchaou, M., additional, Fradj, M., additional, and Belal, S., additional
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- 2013
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7. 736 Clinical and Cytogenetic Study in 116 Children Cohort with Sexual Ambiguity
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Hmida, I. B. H., primary, Dimassi, S., additional, Kammoun, M., additional, Helal, K. B., additional, Hannechi, H., additional, Seboui, H., additional, Gribaa, M., additional, Mougou-Zerelli, S., additional, and Saad, A., additional
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- 2012
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8. 732 Turner Syndrome: A Clinico-Cytogenetic Study of 37 Children
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Kammoun, M., primary, Mougou, S., additional, Brahem, R., additional, Ghali, N., additional, Hmida, I. B. H., additional, Dimassi, S., additional, Soyah, N., additional, Ghzel, H. E., additional, and Saad, A., additional
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- 2012
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9. Le profil épidémiologique, clinique et thérapeutique de l’angio-Behçet
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Ben Dhaou, B., primary, Boussema, F., additional, Hmida, I., additional, Aridhi, S., additional, Ketari, S., additional, Cherif, O., additional, and Rokbani, L., additional
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- 2010
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10. Summaries of the papers of the 4th National Congress of the Tunisian Society of Medical Oncology attached to the 4th Maghreb Congress of Oncology
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Abbes, I., Abdelhak, S., Abdelhedi, C., Abid, K., Abidi, R., Acacha, E., Achour, S., Achour, A., Adouni, O., Afrit, M., Ahlem, A., Akik, I., Akremi, M., Aloui, R., Aloulou, S., Ammar, N., Arem, S., Athimni, S., Attia, L., Attia, M., Ayadi, M., Ayadi, A., Ayadi, K., Ayadi, H., Ayadi, L., Ayadi, I., Ayari, J., Azzouz, H., Bacha, D., Bahloul, R., Bahri, I., Bahri, M., Bakir, D., Balti, M., Bargaoui, H., Batti, R., Bayar, R., Bdioui Thabet, A., Beji, M., Bel Hadj Hassen, S., Bel Haj Ali, A., Belaid, I., Belaid, A., Beldjiilali, Y., Belkacem, O., Bellamlih, O., Ben Abdallah, W., Ben Abdallah, M., Ben Abdellah, H., Ben Abderrahmen, S., Ben Ahmed, S., Ben Ahmed, K., Ben Ayache, M., Ben Ayoub, W., Ben Azaiz, M., Ben Azouz, M., Ben Daly, A., Ben Dhia, S., Ben Dhiab, M., Ben Dhiab, T., Ben Fatma, L., Ben Ghachem, D., Ben Hammadi, S., Ben Hassen, M., Ben Hassena, R., Ben Hassouna, J., Ben Kridis, W., Ben Leila, F., Ben Mahfoudh, K. H., Ben Mustapha, N., Ben Nasr, S., Ben Othman, F., Ben Rejeb, M., Ben Rekaya, M., Sami BenRhouma, Ben Safta, Z., Ben Safta, I., Ben Said, A., Ben Salah, M., Ben Salah, H., Ben Slama, S., Ben Temime, R., Ben Youssef, Y., Ben Zid, K., Benabdella, H., Benasr, S., Bengueddach, A., Benna, M., Benna, F., Bergaoui, H., Berrazaga, Y., Besbes, M., Bhiri, H., Bibi, M., Blel, A., Bohli, M., Bouali, S., Bouaouina, N., Bouassida, K., Bouaziz, H., Boubaker, J., Boudaouara, T., Boudaouara, Z., Boudaouara, O., Boughanmi, F., Boughattas, W., Boughizane, S., Bouguila, H., Bouhani, M., Bouhlel, B., Boujelbane, N., Boujemaa, M., Boulma, R., Bouraoui, S., Bouriga, R., Bourmech, M., Bousrih, C., Boussen, H., Boussen, N., Bouzaien, F., Bouzayene, F., Brahem, I., Briki, R., Chaabene, K., Chaabouni, M., Chaari, H., Chabchoub, I., Chachia, S., Chaker, K., Chamlali, M., Charfi, L., Charfi, M., Charfi, S., Charradi, H., Cheffai, I., Chelly, B., Chelly, I., Chenguel, A., Cherif, A., Cherif, O., Chiboub, A., Chouchene, A., Chraiet, N., Daghfous, A., Daldoul, A., Daoud, N., Daoud, J., Daoud, R., Daoud, E., Debaibi, M., Dhaouadi, S., Dhief, R., Dhouib, F., Dimassi, S., Djebbi, A., Doghri, R., Doghri, Y., Doudech, B., Dridi, M., El Amine, O., El Benna, H., El Khal, M. C., Eladeb, M., Elloumi, M., Elmeddeb, K., Enaceur, F., Ennouri, S., Essoussi, M., Ezzairi, F., Ezzine, A., Faleh, R., Fallah, S., Faouzi, N., Fathallah, K., Fehri, R., Feki, J., Fekih, M., Fendri, S., Fessi, Z., Fourati, N., Fourati, M., Frikha, I., Frikha, M., Gabsi, A., Gadria, S., Gamoudi, A., Gargoura, A., Gargouri, W., Ghariani, N., Ghazouani, E., Ghorbal, A., Ghorbel, L., Ghorbel, S., Ghozzi, A., Glili, A., Gmadh, K., Goucha, A., Gouiaa, N., Gritli, S., Guazzah, K., Guebsi, A., Guermazi, Z., Guermazi, F., Gueryani, N., Guezguez, M., Hacheni, F., Hachicha, M., Haddad, A., Haddaoui, A., Hadoussa, M., Haj Mansour, M., Hajjaji, A., Hajji, A., Hamdi, A., Hamdi, Y., Hammemi, R., Haouet, S., Hdiji, A., Hechiche, M., Hedfi, M., Helali, A. J., Henchiri, H., Heni, S., Hentati, A., Herbegue, K., Hidar, S., Hlaf, M., Hmida, W., Hmida, I., Hmida, L., Hmila Ben Salem, I., Hochlef, M., Hsairi, M., Jaffel, H., Jaidane, M., Jarraya, H., Jebsi, M., Jedidi, M., Jlassi, A., Jlassi, H., Jmal, H., Jmour, O., Jouini, M., Kabtni, W., Kacem, M., Kacem, S., Kacem, I., Kaid, M., Kairi, H., Kallel, M., Kallel, R., Kallel, F., Kammoun, H., Kamoun, S., Kanoun Belajouza, S., Karray, W., Karrit, S., Karrou, M., Kchir, N., Kdous, S., Kehili, H., Keskes, H., Khairi, H., Khalfallah, M. T., Khalifa, M. B., Khanfir, A., Khanfir, F., Khechine, W., Khemiri, S., Khiari, H., Khlif, A., Khouni, H., Khrouf, S., Kochbati, L., Korbi, I., Korbi, A., Krir, M. W., Ksaier, I., Ksantini, R., Ksantini, M., Ksantini, F., Ktari, K., Laabidi, S., Laamouri, B., Labidi, A., Lahmar, A., Lahouar, R., Lamine, O., Letaief, F., Limaiem, F., Limayem, I., Limem, S., Limem, F., Loghmari, A., M Ghirbi, F., Maamouri, F., Magherbi, H., Mahjoub, N., Mahjoub, M., Mahjoubi, K., Majdoub, S., Makhlouf, T., Makni, A., Makni, S., Mallat, N., Manai, M. H., Mansouri, H., Maoua, M., Marghli, I., Masmoudi, T., Mathlouthi, N., Meddeb, K., Medini, B., Mejri, N., Merdessi, A., Mesali, C., Mezlini, E., Mezlini, A., Mezni, E., Mghirbi, F., Mhiri, N., Mighri, N., Mlika, M., Mnejja, W., Mnif, H., Mokni, M., Mokrani, A., Mosbah, F., Moujahed, R., Mousli, A., Moussa, A., Mrad Dali, K., Mrizak, N., Msakni, I., Mzabi, S., Mzali, R., Mzoughi, Z., Naimi, Z., Najjar, S., Nakkouri, R., Nasr, C., Nasrallah, D., Nasri, M., Njim, L., Noubigh, G. E. F., Nouira, Y., Nouri, O., Omrani, S., Osmane, W., Ouanes, Y., Ouanna, N., Oubich, F., Oumelreit Belamlih, G., Rachdi, H., Rafraf, F., Rahal, K., Raies, H., Rammeh, S., Rebaii, N., Rekik, W., Rekik, H., Rhim, M. S., Rhim, S., Rihab, D., Rjiba, R., Rziga, T., Saad, H., Saad, A., Saadi, M., Said, N., Salah, R., Sallemi, N., Sassi, A., Sassi, K., Sassi Mahfoudh, A., Sbika, W., Sellami, A., Serghini, M., Sghaier, S., Sh Zidi, Y., Siala, W., Slimane, M., Slimani, O., Soltani, S., Souguir, M. K., Sridi, A., Tabet Zatla, A., Tajina, D., Talbi, G., Tbessi, S., Tebra Mrad, S., Temessek, H., Tlili, G., Toumi, N., Toumi, O., Toumia, N., Tounsi, H., Trigui, E., Triki, M., Triki, A., Turki, M., Werda, I., Yahyaoui, S., Yahyaoui, Y., Yaich, A., Yamouni, M., Yazid, D., Yousfi, A., Zaghouani, H., Zaied, S., Zairi, F., Zaraa, S., Zehani, A., Zenzri, Y., Zidi, A., Znaidi, N., Zouari, K., Zouari, S., Zoukar, O., and Zribi, A.
11. Towards surgical treatment of status epilepticus complicating Lennox Gastaut syndrome: Place of the vagus nerve stimulation.
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Anonymous, Hmida, I., Ali, N. Ben, Kchaou, M., Fradj, M., and Belal, S.
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- 2013
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12. Does Kidney Transplantation with Multiple Arteries Affect Graft Survival?
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Chabchoub, K., Mhiri, M.N., Bahloul, A., Fakhfakh, S., Ben Hmida, I., Hadj Slimen, M., Charfi, W., Abdennader, M., Frikha, I., and Hachicha, J.
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KIDNEY transplantation , *ARTERY transplantation , *GRAFT rejection , *HEALTH outcome assessment , *KIDNEY blood-vessels , *ORGAN donors , *COMPLICATIONS from organ transplantation - Abstract
Abstract: Introduction: We compared short- and long-term outcomes of renal transplants with single versus multiple arteries. Patients and methods: We retrospectively analyzed data from kidney transplants from 208 living donors performed between 1994 and 2010. Renal grafts were divided into two groups: single renal artery (n = 164) versus multiple renal arteries (n = 44). The groups were compared regarding early and late vascular and urological complications. Patient and graft survivals were compared using Kaplan-Meier survivorship curves with comparisons using the log-rank test. Results: Both groups were comparable regarding acute rejection episodes, posttransplant hypertension, postsurgery renal artery stenosis, and urologic complications. Only hemorrhagic complications and renal artery thrombosis were significantly higher in the multiple renal arteries group (P = .027 and .03, respectively). Warm ischemia time was significantly longer in the multiple renal arteries group without any influence on the incidence of acute tubular necrosis (P = .2). Mean creatinine clearance at 1 year was 65 versus 50 mL/min/1.73 m2 (P = .5) and at 5 years, 60 versus 55 mL/min/1.73 m2 (P = .1) for the single versus multiple renal arteries groups, respectively. Return to hemodialysis was necessary for 18.8% of the single and 16.1% of the multiple renal arteries group. Conclusion: The use of an allograft with multiple renal arteries is a safe, successful surgical procedure, that does not influence patient or graft survivals or increase surgical complication rates provided the surgical team is evolved with technical skill. [Copyright &y& Elsevier]
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- 2011
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13. Ipsilateral blooming of microbleeds after Hyperintense Acute Reperfusion Marker sign in an ischemic Stroke patient, a case report.
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Saccaro LF, Bekri I, De Malherbe M, Hmida I, and Pico F
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- Aged, Cerebral Hemorrhage complications, Cerebral Hemorrhage etiology, Gadolinium, Humans, Magnetic Resonance Imaging methods, Male, Reperfusion, Brain Ischemia complications, Brain Ischemia diagnostic imaging, Ischemic Stroke, Stroke complications, Stroke diagnosis, Subarachnoid Hemorrhage complications
- Abstract
Background: Hyperintense Acute Reperfusion Marker (HARM) is a hyperintense subarachnoid signal on FLAIR MRI sequence caused by gadolinium contrast leakage into the subpial space. While, on FLAIR, HARM may mimic subarachnoid hemorrhage, it is differentiated from it on computed tomography (CT) and SWAN MRI sequences. Cerebral microbleeds are black, rounded spots on SWAN caused by blood-products deposition following red blood cell leakage from small cerebral vessels brain. Both microbleeds and HARM carry important prognostic implication as they are associated with blood-brain barrier disruption and an increased risk of intracerebral hemorrhage., Case Presentation: A 79-year-old man presented with aphasia and right hemiparesis due to ischemic stroke with left middle cerebral artery occlusion. Admission NIHSS score was 7, and he was successfully treated by intravenous thrombolysis and mechanical thrombectomy. On day 1, his clinical condition worsened, and he had an urgent gadolinium-enhanced MRI. There was no evidence of early recurrence, nor of hemorrhage on SWAN or on FLAIR. Left middle cerebral artery was permeable. The patient was anticoagulated for newly diagnosed atrial fibrillation, and a second MRI following a generalized tonic-clonic seizure showed multiple left hemispheric diffusion-weighted imaging (DWI) hyperintense spots and a left hemispheric sub-arachnoid hyperintensity on FLAIR, compatible with a subarachnoid hemorrhage. This diagnosis was excluded by SWAN MRI sequence and a normal cerebral CT the same day. The diagnosis of HARM was retained. At day 9, patient's condition improved, and a control MRI did not show evidence of HARM. However, numerous microbleeds were detected in the left hemisphere only (ipsilateral with HARM and stroke)., Conclusions: This case highlights first of all the importance of differentiating HARM and subarachnoid hemorrhage, especially in an anticoagulated patient with clinical aggravation. Secondly, it is crucial to identify microbleeds and understand their pathophysiology, as they are associated with higher risk of hemorrhage and stroke recurrence in ischemic stroke patients. Finally, the mono-hemispheric appearance of microbleeds in this case suggests for the first time that, in some acute ischemic stroke patients, a relationship between HARM and cerebral microbleeds may exist., (© 2022. The Author(s).)
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- 2022
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14. Further report of MEDS syndrome: Clinical and molecular delineation of a new Tunisian case.
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Rjiba K, Soyah N, Kammoun M, Hadj Hmida I, Saad A, Mcelreavey K, and Mougou-Zerelli S
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- Carrier Proteins chemistry, Cryptorchidism genetics, Diabetes Mellitus genetics, Epilepsy genetics, Humans, Infant, Newborn, Infant, Newborn, Diseases genetics, Karyotype, Male, Membrane Proteins chemistry, Mutation, Missense, Protein Domains, Psychomotor Disorders genetics, Syndrome, Carrier Proteins genetics, Cryptorchidism pathology, Diabetes Mellitus pathology, Epilepsy pathology, Infant, Newborn, Diseases pathology, Membrane Proteins genetics, Psychomotor Disorders pathology
- Abstract
Recently, an autosomal recessive disorder including the triad of microcephaly, infantile epileptic encephalopathy, and permanent neonatal diabetes syndrome (MEDS, OMIM#614231) has emerged as a new distinguishing syndrome. Eight cases of whom seven from Arab countries, have been reported in association with biallelic variants in the IER3IP1 gene (Immediate early response-3 interacting protein-1). Here, we describe a Tunisian boy who presented with permanent neonatal diabetes, microcephaly, generalized seizures and hypovirilized external genitalia consisting of a small genitalia and unilateral cryptorchidism. Chromosomal analysis indicated a 46, XY karyotype in all metaphases. Exome sequencing identified a homozygous missense variant (c.62 T > G; p. Val21Gly) in the IER3IP1 gene, that is predicted to alter the protein structure within the hydrophobic/transmembrane. This variant was previously reported in two cases associated with MEDS. This is the first reported case of MEDS in Tunisia. Our report focuses on the IER3IP1 related phenotypic spectrum and assumes abnormal genitalia as part of the syndrome. Consequently, we recommend to perform hormonal testing on this topic to understand the effect of the IER3IP1 variant on the male genital pathway., (Copyright © 2021. Published by Elsevier Masson SAS.)
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- 2021
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15. Disorders of sex development in Wolf-Hirschhorn syndrome: a genotype-phenotype correlation and MSX1 as candidate gene.
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Rjiba K, Ayech H, Kraiem O, Slimani W, Jelloul A, Ben Hadj Hmida I, Mahdhaoui N, Saad A, and Mougou-Zerelli S
- Abstract
Background: Wolf-Hirschhorn (WHS) is a set of congenital physical anomalies and mental retardation associated with a partial deletion of the short arm of chromosome 4. To establish a genotype-phenotype correlation; we carried out a molecular cytogenetic analysis on two Tunisian WHS patients. Patient 1 was a boy of 1-year-old, presented a typical WHS phenotype while patient 2, is a boy of 2 days presented an hypospadias, a micropenis and a cryptorchidie in addition to the typical WHS phenotype. Both the array comparative genomic hybridization and fluorescence in situ hybridization techniques were used., Results: Results of the analysis showed that patient 2 had a greater deletion size (4.8 Mb) of chromosome 4 than patient 1 (3.4 Mb). Here, we notice that the larger the deletion, the more genes are likely to be involved, and the more severe the phenotype is likely to be. If we analyze the uncommon deleted region between patient1 and patient 2 we found that the Muscle Segment Homeobox (MSX1) gene is included in this region. MSX1 is a critical transcriptional repressor factor, expressed in the ventral side of the developing anterior pituitary and implicated in gonadotrope differentiation. Msx1 acts as a negative regulatory pituitary development by repressing the gonadotropin releasing hormone (GnRH) genes during embryogenesis. We hypothesized that the deletion of MSX1 in our patient may deregulate the androgen synthesis., Conclusion: Based on the MSX1 gene function, its absence might be indirectly responsible for the hypospadias phenotype by contributing to the spatiotemporal regulation of GnRH transcription during development.
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- 2021
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16. Summaries of the papers of the 4th National Congress of the Tunisian Society of Medical Oncology attached to the 4th Maghreb Congress of Oncology.
- Author
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Abbes I, Abdelhak S, Abdelhedi C, Abid K, Abidi R, Acacha E, Achour S, Achour A, Adouni O, Afrit M, Ahlem A, Akik I, Akremi M, Aloui R, Aloulou S, Ammar N, Arem S, Athimni S, Attia L, Attia M, Ayadi M, Ayadi A, Ayadi K, Ayadi H, Ayadi L, Ayadi I, Ayari J, Azzouz H, Bacha D, Bahloul R, Bahri I, Bahri M, Bakir D, Balti M, Bargaoui H, Batti R, Bayar R, Bdioui Thabet A, Beji M, Bel Hadj Hassen S, Bel Haj Ali A, Belaid I, Belaid A, Beldjiilali Y, Belkacem O, Bellamlih O, Ben Abdallah W, Ben Abdallah M, Ben Abdellah H, Ben Abderrahmen S, Ben Ahmed S, Ben Ahmed K, Ben Ayache M, Ben Ayoub W, Ben Azaiz M, Ben Azouz M, Ben Daly A, Ben Dhia S, Ben Dhiab M, Ben Dhiab T, Ben Fatma L, Ben Ghachem D, Ben Hammadi S, Ben Hassen M, Ben Hassena R, Ben Hassouna J, Ben Kridis W, Ben Leila F, Ben Mahfoudh KH, Ben Mustapha N, Ben Nasr S, Ben Othman F, Ben Rejeb M, Ben Rekaya M, Ben Rhouma S, Ben Safta Z, Ben Safta I, Ben Said A, Ben Salah M, Ben Salah H, Ben Slama S, Ben Temime R, Ben Youssef Y, Ben Zid K, Benabdella H, Benasr S, Bengueddach A, Benna M, Benna F, Bergaoui H, Berrazaga Y, Besbes M, Bhiri H, Bibi M, Blel A, Bohli M, Bouali S, Bouaouina N, Bouassida K, Bouaziz H, Boubaker J, Boudaouara T, Boudaouara Z, Boudaouara O, Boughanmi F, Boughattas W, Boughizane S, Bouguila H, Bouhani M, Bouhlel B, Boujelbane N, Boujemaa M, Boulma R, Bouraoui S, Bouriga R, Bourmech M, Bousrih C, Boussen H, Boussen N, Bouzaien F, Bouzayene F, Brahem I, Briki R, Chaabene K, Chaabouni M, Chaari H, Chabchoub I, Chachia S, Chaker K, Chamlali M, Charfi L, Charfi M, Charfi S, Charradi H, Cheffai I, Chelly B, Chelly I, Chenguel A, Cherif A, Cherif O, Chiboub A, Chouchene A, Chraiet N, Daghfous A, Daldoul A, Daoud N, Daoud J, Daoud R, Daoud E, Debaibi M, Dhaouadi S, Dhief R, Dhouib F, Dimassi S, Djebbi A, Doghri R, Doghri Y, Doudech B, Dridi M, El Amine O, El Benna H, El Khal MC, Eladeb M, Elloumi M, Elmeddeb K, Enaceur F, Ennouri S, Essoussi M, Ezzairi F, Ezzine A, Faleh R, Fallah S, Faouzi N, Fathallah K, Fehri R, Feki J, Fekih M, Fendri S, Fessi Z, Fourati N, Fourati M, Frikha I, Frikha M, Gabsi A, Gadria S, Gamoudi A, Gargoura A, Gargouri W, Ghariani N, Ghazouani E, Ghorbal A, Ghorbel L, Ghorbel S, Ghozzi A, Glili A, Gmadh K, Goucha A, Gouiaa N, Gritli S, Guazzah K, Guebsi A, Guermazi Z, Guermazi F, Gueryani N, Guezguez M, Hacheni F, Hachicha M, Haddad A, Haddaoui A, Hadoussa M, Haj Mansour M, Hajjaji A, Hajji A, Hamdi A, Hamdi Y, Hammemi R, Haouet S, Hdiji A, Hechiche M, Hedfi M, Helali AJ, Henchiri H, Heni S, Hentati A, Herbegue K, Hidar S, Hlaf M, Hmida W, Hmida I, Hmida L, Hmila Ben Salem I, Hochlef M, Hsairi M, Jaffel H, Jaidane M, Jarraya H, Jebsi M, Jedidi M, Jlassi A, Jlassi H, Jmal H, Jmour O, Jouini M, Kabtni W, Kacem M, Kacem S, Kacem I, Kaid M, Kairi H, Kallel M, Kallel R, Kallel F, Kammoun H, Kamoun S, Kanoun Belajouza S, Karray W, Karrit S, Karrou M, Kchir N, Kdous S, Kehili H, Keskes H, Khairi H, Khalfallah MT, Khalifa MB, Khanfir A, Khanfir F, Khechine W, Khemiri S, Khiari H, Khlif A, Khouni H, Khrouf S, Kochbati L, Korbi I, Korbi A, Krir MW, Ksaier I, Ksantini R, Ksantini M, Ksantini F, Ktari K, Laabidi S, Laamouri B, Labidi A, Lahmar A, Lahouar R, Lamine O, Letaief F, Limaiem F, Limayem I, Limem S, Limem F, Loghmari A, M'ghirbi F, Maamouri F, Magherbi H, Mahjoub N, Mahjoub M, Mahjoubi K, Majdoub S, Makhlouf T, Makni A, Makni S, Mallat N, Manai MH, Mansouri H, Maoua M, Marghli I, Masmoudi T, Mathlouthi N, Meddeb K, Medini B, Mejri N, Merdessi A, Mesali C, Mezlini E, Mezlini A, Mezni E, Mghirbi F, Mhiri N, Mighri N, Mlika M, Mnejja W, Mnif H, Mokni M, Mokrani A, Mosbah F, Moujahed R, Mousli A, Moussa A, Mrad Dali K, Mrizak N, Msakni I, Mzabi S, Mzali R, Mzoughi Z, Naimi Z, Najjar S, Nakkouri R, Nasr C, Nasrallah D, Nasri M, Njim L, Noubigh GEF, Nouira Y, Nouri O, Omrani S, Osmane W, Ouanes Y, Ouanna N, Oubich F, Oumelreit Belamlih G, Rachdi H, Rafraf F, Rahal K, Raies H, Rammeh S, Rebaii N, Rekik W, Rekik H, Rhim MS, Rhim S, Rihab D, Rjiba R, Rziga T, Saad H, Saad A, Saadi M, Said N, Salah R, Sallemi N, Sassi A, Sassi K, Sassi Mahfoudh A, Sbika W, Sellami A, Serghini M, Sghaier S, Sh Zidi Y, Siala W, Slimane M, Slimani O, Soltani S, Souguir MK, Sridi A, Tabet Zatla A, Tajina D, Talbi G, Tbessi S, Tebra Mrad S, Temessek H, Tlili G, Toumi N, Toumi O, Toumia N, Tounsi H, Trigui E, Triki M, Triki A, Turki M, Werda I, Yahyaoui S, Yahyaoui Y, Yaich A, Yamouni M, Yazid D, Yousfi A, Zaghouani H, Zaied S, Zairi F, Zaraa S, Zehani A, Zenzri Y, Zidi A, Znaidi N, Zouari K, Zouari S, Zoukar O, and Zribi A
- Published
- 2017
17. Novel homozygous nonsense mutations in the luteinizing hormone receptor (LHCGR) gene associated with 46,XY primary amenorrhea.
- Author
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Ben Hadj Hmida I, Mougou-Zerelli S, Hadded A, Dimassi S, Kammoun M, Bignon-Topalovic J, Bibi M, Saad A, Bashamboo A, and McElreavey K
- Subjects
- Adult, Amenorrhea diagnosis, Amenorrhea physiopathology, DNA Mutational Analysis, Disorder of Sex Development, 46,XY diagnosis, Disorder of Sex Development, 46,XY physiopathology, Exome, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Phenotype, Young Adult, Amenorrhea etiology, Codon, Nonsense, Disorder of Sex Development, 46,XY genetics, Homozygote, Receptors, LH genetics
- Abstract
Objective: To determine the genetic cause of 46,XY primary amenorrhea in three 46,XY girls., Design: Whole exome sequencing., Setting: University cytogenetics center., Patient(s): Three patients with unexplained 46,XY primary amenorrhea were included in the study., Intervention(s): Potentially pathogenic variants were confirmed by Sanger sequencing, and familial segregation was determined where parents' DNA was available., Main Outcome Measure(s): Exome sequencing was performed in the three patients, and the data were analyzed for potentially pathogenic mutations. The functional consequences of mutations were predicted., Result(s): Three novel homozygous nonsense mutations in the luteinizing hormone receptor (LHCGR) gene were identified:c.1573 C→T, p.Gln525Ter, c.1435 C→T p.Arg479Ter, and c.508 C→T, p.Gln170Ter., Conclusion(s): Inactivating mutations of the LHCGR gene may be a more common cause of 46,XY primary amenorrhea than previously considered., (Copyright © 2016 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.)
- Published
- 2016
- Full Text
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18. Parkinsonism and Sjögren's Syndrome: A Fortuitous Association or a Shared Immunopathogenesis?
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Kchaou M, Ben Ali N, Hmida I, Fray S, Jamoussi H, Jalleli M, Echebbi S, Achouri A, and Belal S
- Abstract
Background. The Sjögren Syndrome (SS) can include various manifestations of central nervous system impairment. Extrapyramidal signs are known to be very rare and unusually discovered on early onset in this pathology. Observation. A 46-year-old woman with a history of progressive Parkinsonism for 6 years and a normal brain magnetic resonance imaging was partially improved with levodopa therapy. The later discovery of a sicca syndrome led to performing of further investigations, which revealed the presence of anti-SSA antibodies and a sialoadenitis of grade 4 according to Chisholm's classification on labial salivary gland biopsy. The diagnosis of primary SS was established and the adjunction of corticotherapy has remarkably improved Parkinson's signs without use of other immunosuppressive agents. Conclusion. Based on these findings, we discuss the hypothesis of either a causal link between SS and Parkinsonism or a fortuitous association of two distinct pathologies with or without a shared immunopathogenesis.
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- 2015
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19. [Retroperitoneal schwanoma associated to renal oncocytoma].
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Zakhama W, Binous MY, Ben Hmida I, Chraiti H, Boudokhane M, and Fodha M
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- Aged, Female, Humans, Incidental Findings, Adenoma, Oxyphilic diagnosis, Kidney Neoplasms diagnosis, Neoplasms, Multiple Primary diagnosis, Neurilemmoma diagnosis, Retroperitoneal Neoplasms diagnosis
- Published
- 2011
20. Evolution of impaired renal function after external continent urinary diversion (Mitrofanoff principle).
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Mhiri MN, Chabchoub K, Fakhfakh S, Hmida IB, Slimen MH, Bahloul A, Yaiche S, Charfeddine K, and Hachicha J
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- Adolescent, Adult, Aged, Child, Child, Preschool, Digestive System Surgical Procedures methods, Female, Humans, Male, Middle Aged, Quality of Life, Urinary Bladder Diseases therapy, Urinary Tract pathology, Ileum surgery, Kidney physiology, Urinary Bladder Diseases surgery, Urinary Diversion methods
- Abstract
Objective: To study the evolution of impaired renal function after external continent urinary diversion (Mitrofanoff principle) (ECUD-M) associated with ileocystoplasty., Patients and Methods: Over 18 years from 1992 to 2009, ECUD-M with ileocystoplasty was performed in 120 patients with mean age of 25.5 years. Renal impairment was evident in 43 patients (17 children and 26 adults)., Results: Ninety percent of patients demonstrated a neurologic bladder and mild to moderate renal failure. Initially, all patients underwent continuous bladder drainage for a mean of 3 weeks. Renal function improved in 35 patients, although with persistent mild renal insufficiency. The other patients demonstrated moderate persistent residual renal insufficiency. During a mean follow-up of 10 years (range, 1-18 years), renal function returned to normal in 13 patients, stabilized at lower values in 15, and remained moderate in 5. After a mean follow-up of 8 years (range, 6-12 years), renal failure gradually worsened, increasing to higher values in 6 patients and leading to hemodialysis in 4. One patient underwent living-donor kidney transplantation, with good evolution., Conclusion: ECUD-M with ileocystoplasty can lead to normalization unless stabilizationof impaired residual renal function by eliminating the obstructive factor provides self-adequate management of the diversion. The procedure delays for the need forhemodialysis therapy, and enables patients to prepare for kidney transplantation into a previously reconstructed lower urinary tract., (Copyright © 2011 Elsevier Inc. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
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