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Afef Nahdi Imen Hammami Wided Kouidhi Abderrahman Chargui Awatef Ben Ammar Mohamed Hédi Hamdaoui Ahmed El May Michèle El May 《Journal of molecular histology》2010,41(4-5):233-245
The impact of garlic, known for its antioxidant activities, on iron metabolism has been poorly investigated. The aim of this work was to study the effect of crude garlic pre-treatment on iron-mediated lipid peroxidation, proliferation and autophagy for 5 weeks. Rats were fed distilled water or garlic solution (1 g/kg body weight) by gavage for the first 3 weeks as pre-treatment and received a basal diet supplemented or not with ferrous sulfate (650 mg Fe/kg diet) for the last 2 weeks of treatment. Immunohistochemistry labeling and ultrastuctural observations were used to evaluate the iron deleterious effects in the liver. Iron supplementation induced cell proliferation predominantly in non parenchymal cells comparing to hepatocytes, but not apoptosis. In addition, iron was accumulated within the hepatic lysosomes where it triggers autophagy as evidenced by the formation of autophagic vesicles detected by LC3-II staining. It also induced morphologic alterations of the mitochondrial membranes due to increased lipid peroxidation as shown by elevated iron and malondialdehyde concentrations in serum and tissues. Garlic pre-treatment reduced iron-catalyzed lipid peroxidation by decreasing the malondialdehyde level in the liver and colon and by enhancing the status of antioxidants. In addition, garlic reduced the iron-mediated cell proliferation and autophagy by lowering iron storage in the liver and protected mitochondrial membrane. Based on these results, garlic treatment significantly prevented iron-induced oxidative stress, proliferation and autophagy at both biochemical and histological levels due to its potent free radical scavenging and antioxidant properties. 相似文献
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D. M. Fathallah Mohamed Bejaoui Denis Lepaslier Khelifa Chater William S. Sly Koussay Dellagi 《Human genetics》1997,99(5):634-637
A splice junction mutation at the exon 2 – intron 2 boundary of the carbonic anhydrase II (CA II) gene was previously shown
to be the unique mutation underlying the CA II deficiency syndrome in patients of Arab descent. Fourteen Tunisian (Maghrebian)
families with a history of osteopetrosis, renal tubular acidosis, mental retardation, and CA II deficiency were studied to
test the hypothesis that the mutation, found in all 24 patients, derived from a common ancestor originating in the Arabic
Peninsula. A filiation study permitted us to trace these families back to a common Arabic tribe that settled in the Maghreb
in the tenth century, indicating a common ethnic origin for these families. Segregation of the mutation with a TaqI biallelic restriction site polymorphism upstream of the CA II gene was studied by sequence-tagged site analysis in all the
family members. These studies showed cosegregation of the Taq (-) allele with the mutation in 12 families out of 14. This observation supports a founder effect to explain the common CA
II deficiency allele in this population. In the remaining two families, a genomic recombination or gene conversion occurred
between the TaqI restriction marker and the mutation causing the disease. The relatively high recombination frequency suggests the presence
of a hot spot for recombination or gene conversion at the CA II locus.
Received: 5 July 1996 / Revised: 25 October 1996 相似文献
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Jamal T Barbouche MR Ben Hariz M Bejaoui M Fathallah MD Dellagi K 《Archives de l'Institut Pasteur de Tunis》1998,75(3-4):177-183
Leukocyte adhesion deficiency (LAD) was suspected in a three weeks old girl from a family with an established history of LAD with a lack (less then 1%) of the beta 2 integrins CD 11a, b/CD 18 expression at the leukocytes surface, was engrafted with her mother HLA identical bone marrow at the age of 14 months. Repeated post transplantation (up to 22 months). Immunological assessments showed a good engraftment with 97% of the lymphocytes expressing CD11a/CD18. Cells proliferated normally in response to PHA and to Tetanus toxo?d after revaccination. The level of serum immunoglobulins was normal. Investigation of the CD18 intragenic polymorphic marker Avall before and after bone marrow transplantation (BMT) showed a transition from the Avall +/+ genotype to the mother's Avall +/- genotype. Similarly DNA fingerprints obtained with the patient genomic DNA, prepared from PBMC, prior and after transplantation, showed that the patient's DNA fingerprints pattern matched the mother's one. These findings are consistent with the good engraftment observed clinically. This study emphasizes the usefulness of the molecular techniques to evaluate the degree of chimerism in monitoring the outcome of bon marrow transplantation. 相似文献
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Zinc mitigates renal ischemia‐reperfusion injury in rats by modulating oxidative stress,endoplasmic reticulum stress,and autophagy 下载免费PDF全文
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Ochratoxin A (OTA) is a very dangerous mycotoxin, the presence of which is often reported in different foods, as well as in beverages such as grapes, grape juices and wines. Detoxifying these products is therefore of prime importance in protecting consumer health, and biological approaches have been the most promising methods. In this report, 40 isolates representing the black apergilli species Aspergillus carbonarius, A. niger aggregate and A. japonicus, isolated on French grapes, were assessed for OTA degradation capacities in CZAPEK yeast extract broth (CYB) and in a synthetic grape juice medium (SGM) contaminated with OTA at 2 mg L(-1) (5 microM). It was clearly observed that in both media these fungi had the ability to degrade OTA to OTalpha (ochratoxinalpha). However, there were differences between the media used and species tested during OTA degradation. In SGM and CYB, 77% and 45% of the isolates, respectively were able to degrade more than 80% of the OTA. Despite a better growth on SGM, specific OTA degradation was higher on CYB for most of the isolates. Kinetic studies carried out on SGM with three black Aspergillus isolates all showed different OTA degradation rates. After 9 days of incubation, OTalpha had decreased, whereas an unknown compound appeared. A. niger could be the first interesting species for OTA detoxification processes, followed by A. japonicus. 相似文献
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Awatef Jelassi Mohamed Najah Afef Slimani Imen Jguirim Mohamed Naceur Slimane Mathilde Varret 《Current Genomics》2013,14(1):25-32
Autosomal dominant hypercholesterolemia (ADH) is characterized by an isolated elevation of plasmatic low-density lipoprotein (LDL), which predisposes to premature coronary artery disease (CAD) and early death. ADH is largely due to mutations in the low-density lipoprotein receptor gene (LDLR), the apolipoprotein B-100 gene (APOB), or the proprotein convertase subtilisin/kexin type 9 (PCSK9). Early diagnosis and initiation of treatment can modify the disease progression and its outcomes. Therefore, cascade screening protocol with a combination of plasmatic lipid measurements and DNA testing is used to identify relatives of index cases with a clinical diagnosis of ADH. In Tunisia, an attenuated phenotypic expression of ADH was previously reported, indicating that the establishment of a special screening protocol is necessary for this population. 相似文献
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Awatef Allouch Cristina Di Primio Audrey Paoletti Gabrielle Lê-Bury Frdric Subra Valentina Quercioli Roberta Nardacci Annie David Hla Saïdi Anna Cereseto David M. Ojcius Guillaume Montagnac Florence Niedergang Gianfranco Pancino Asier Saez-Cirion Mauro Piacentini Marie-Lise Gougeon Guido Kroemer Jean-Luc Perfettini 《Cell death and differentiation》2020,27(12):3243
Understanding the viral–host cell interface during HIV-1 infection is a prerequisite for the development of innovative antiviral therapies. Here we show that the suppressor of G2 allele of skp1 (SUGT1) is a permissive factor for human immunodeficiency virus (HIV)-1 infection. Expression of SUGT1 increases in infected cells on human brain sections and in permissive host cells. We found that SUGT1 determines the permissiveness to infection of lymphocytes and macrophages by modulating the nuclear import of the viral genome. More importantly, SUGT1 stabilizes the microtubule plus-ends (+MTs) of host cells (through the modulation of microtubule acetylation and the formation of end-binding protein 1 (EB1) comets). This effect on microtubules favors HIV-1 retrograde trafficking and replication. SUGT1 depletion impairs the replication of HIV-1 patient primary isolates and mutant virus that is resistant to raltegravir antiretroviral agent. Altogether our results identify SUGT1 as a cellular factor involved in the post-entry steps of HIV-1 infection that may be targeted for new therapeutic approaches.Subject terms: Infectious diseases, Immunopathogenesis 相似文献