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A El Meziane

Publications and source records attributed to A El Meziane.

9 recordsLinked to original sources

[Cardiac hydatidosis with dissemination to the pulmonary parenchyma and the pulmonary artery].

Multiple thoracic hydatic disease involving a cardiac and pulmonary localization is exceptional and prognosis is poor. We report a case in a 21-year-old male who presented repeated episodes of hemoptysis. The chest x-ray showed multiple opacities. The thoracic computed tomography and echocardiography visualized cystic formations in the heart and the pulmonary arteries. Hydatic serology was strongly positive. Medical treatment with albendazole was given but the patient died from massive hemoptysis before the cardiac and pulmonary artery cysts could be removed surgically (a procedure which requires extracorporeal circulation). A hydatic cyst of the pulmonary artery is usually secondary to a cardiac localization. The risk is dissemination into the pulmonary and eventually systemic circulation. An arterial localization must be carefully ruled out in all patients with multiple or cardiac hydatidosis. Treatment is surgical to avoid dissemination.

Adult↗

[Mediastinal paraganglioma with pleural metastasis. A case report].

Paraganglioma is rare tumor arising from chromaffine cells. We report a 39-year-old man who was diagnosed with anterior mediastinal paraganglioma. Computed tomography (CT) revealed a solid mass in the anterior mediastinum. Surgical biopsies obtained by sternotomy confirmed histologic and immunohistochemical features of paraganglioma. Surgical removal of this vascularized and invasive tumor was not possible to. External radiotherapy was performed. Three years later, the patient developed chest pain. CT findings showed right nodular pleural masses. Transparietal biopsy confirmed the same pathological aspect of paraganglioma. Chemotherapy was proposed without significant response. This observation confirmed the rare course of paraganglioma to pleural metastases. Treatment of paraganglioma is mainly surgery if the mass is resectable.

Adult↗

[Devic's optic neuromyelitis and pulmonary tuberculosis].

INTRODUCTION: Optic neuromyelitis or Devic's syndrome is a very rare disease affecting the optic tracts and the spinal cord. Its association with evolving pulmonary tuberculosis has been noted in a handful of case reports. CASE REPORT: The authors reportthe case of a 40 year old patient with evolving pulmonary tuberculosis who experienced bilateral blindness followed by paraplegia and sphincter disturbance. Clinical examination and investigations excluded direct tuberculous involvement of the nervous system or a reaction to antituberculous therapy and Devic's syndrome was diagnosed, based on Wingerchurk's criteria. Following treatment with corticosteroids and antituberculous chemotherapy, the patient recovered normal mobility and sphincter control but remained completely blind. CONCLUSIONS: Throughout this case report, the authors emphasise the rarity of this association and discuss the pathophysiological mechanism, which appears to be an immune dysfunction triggered by mycobacterial infection.

Adult↗

[Amoebic infections of the lung and pleura].

INTRODUCTION: Pleuropulmonary involvement is the second most common extra-intestinal manifestation of entamoeba histolytica infection after liver abscess. CASE REPORT: We report 2 cases of pleuropulmonary disease occurring in two men aged 32 and 48 years following an episode of dysentery. Purulent pleural infection was noted in one case. In the other both lung and liver abscesses occurred. CONCLUSION: The diagnosis was confirmed by strongly positive serology in both cases. Treatment with metronidazole (1.5 g per day) for 15 days combined with pleural drainage led to a satisfactory outcome in both cases.

Adult↗

[Pulmonary actinomycosis. Two cases].

We report two cases of pulmonary actinomycosis in two young men. These observations are an opportunity to review the usual difficulties of diagnosis and the clinical, radiological and therapeutic characteristics in patients with this rare disease. Pulmonary actinomycosis often appears in a debilitated patient with significant disease of the teeth and gingival margins. High-dose penicillin G which is the standard treatment generally provides cure.

Actinomycosis↗

Air pollution: a new respiratory risk for cities in low-income countries.

Since the major accidents that occurred in the 1960s, air pollution has commonly been considered as a respiratory risk factor whose effects are most often studied in industrialised countries. Our aim is to show that it is now the turn of low- and middle-income countries to take this risk factor into account. After a discussion of the characteristics of air pollution, how it is diffused and the main known health effects (short- and long-term effects), we describe the specific differences between the cities in the North and the South. As a result of late industrialisation, cities in the South are now faced with pollution from industrial sources and urban traffic with polluting vehicles. The case of Algeria and Morocco illustrates this situation and its potential health risks. In order to prevent the health risks of air pollution in the cities of the South, systems for measuring pollution levels and epidemiological surveillance need to be put in place rapidly. This strategy can only work if it is supported by a strong partnership from industrialised countries.

Africa↗

Genotypic stability, segregation and selection in heteroplasmic human cell lines containing np 3243 mutant mtDNA.

The mitochondrial genotype of heteroplasmic human cell lines containing the pathological np 3243 mtDNA mutation, plus or minus its suppressor at np 12300, has been followed over long periods in culture. Cell lines containing various different proportions of mutant mtDNA remained generally at a consistent, average heteroplasmy value over at least 30 wk of culture in nonselective media and exhibited minimal mitotic segregation, with a segregation number comparable with mtDNA copy number (>/=1000). Growth in selective medium of cells at 99% np 3243 mutant mtDNA did, however, allow the isolation of clones with lower levels of the mutation, against a background of massive cell death. As a rare event, cell lines exhibited a sudden and dramatic diversification of heteroplasmy levels, accompanied by a shift in the average heteroplasmy level over a short period (<8 wk), indicating selection. One such episode was associated with a gain of chromosome 9. Analysis of respiratory phenotype and mitochondrial genotype of cell clones from such cultures revealed that stable heteroplasmy values were generally reestablished within a few weeks, in a reproducible but clone-specific fashion. This occurred independently of any straightforward phenotypic selection at the individual cell-clone level. Our findings are consistent with several alternate views of mtDNA organization in mammalian cells. One model that is supported by our data is that mtDNA is found in nucleoids containing many copies of the genome, which can themselves be heteroplasmic, and which are faithfully replicated. We interpret diversification and shifts of heteroplasmy level as resulting from a reorganization of such nucleoids, under nuclear genetic control. Abrupt remodeling of nucleoids in vivo would have major implications for understanding the developmental consequences of heteroplasmy, including mitochondrial disease phenotype and progression.

Base Sequence↗

A tRNA suppressor mutation in human mitochondria.

Mitochondrial mutations are associated with a wide spectrum of human diseases. A common class of point mutations affects tRNA genes, and mutations in the tRNA-leu(UUR) gene (MTTL1) are the most frequently detected. In earlier studies, we showed that lung carcinoma cybrid cells containing high levels (greater than 95%) of mutated mtDNA from a patient with the pathological nucleotide pair (np) 3243 tRNA-leu(UUR) mutation can remain genotypically stable over time, and exhibit severe defects in mitochondrial respiratory metabolism. From such a cybrid containing 99% mutated mtDNA, we have isolated a spontaneous derivative that retains mutant mtDNA at this level but which has nevertheless reverted to the wild-type phenotype, based on studies of respiration, growth in selective media, mitochondrial protein synthesis and biogenesis of mitochondrial membrane complexes. The cells are heteroplasmic for a novel anticodon mutation in tRNA-leu(CUN) at np 12300, predicted to generate a suppressor tRNA capable of decoding UUR leucine codons. The suppressor mutation represents approximately 10% of the total mtDNA, but was undetectable in a muscle biopsy sample taken from the original patient or in the parental cybrid. These results indicate that the primary biochemical defect in cells with high levels of np 3243 mutated mtDNA is the inability to translate UUR leucine codons.

Anticodon↗

Mitochondrial tRNALeu isoforms in lung carcinoma cybrid cells containing the np 3243 mtDNA mutation.

We have investigated the representation of structural isoforms of the two mitochondrial leucyl tRNAs in lung carcinoma cybrid cell lines containing the np 3243 (MELAS) mtDNA mutation, alone or in combination with the np 12300 suppressor mutation. The mutant tRNALeu(UUR) is aminoacylated very poorly or not at all, whereas the suppressor tRNALeu(CUN) is efficiently aminoacylated. Deacylated mitochondrial tRNALeu(CUN) is present, in all human cells tested, in two structural isoforms that are separable on denaturing gels, indicating a difference in primary structure. The ratio of the two isoforms differs between cell types and is strongly biased towards one isoform in lung carcinoma cybrids containing high levels of the np 3243 mutation, compared with control cybrids. We propose that structural modification of tRNALeu(CUN) could be a natural suppression mechanism for the np 3243 and other mitochondrial tRNALeu(UUR) mutations and could underlie some of the phenotypic variability of np 3243 disease.

Acylation↗