Aspects diagnostiques et thérapeutiques des malformations pulmonaires congénitales symptomatiques de l’enfant au Mali

Symptomatic congenital pulmonary malformations (CPM) in child are rare. The diagnosis is based on clinical, radiological and histopathological confrontation. The aim of this study is to derterminate the diagnostic, therapeutic and evolutionary profile of CPM in a poor ressources country. This was a retrospective study over a period of 8 years (from January 2012 to March 2020), including 13 cases treated for CPM in the thoracic surgery department of a teaching hospital in Mali. Among patients, we found 5 cases of congenital lobar emphysema (38.8%), 4 cases of pulmoary cyst (30.8%), 3 cases of cystic adenomatoid malformation of the lung (23%) and 1 case of pulmonary sequestration(7,7%). The sex ratio was 2,2. All patients were symptomatic with an average age of 8,5 months. The symptoms were dominated by respiratory infection (38,4%), dyspnea (30,8%), dyspnea with cyanosis(7,7), dyspnea with thoracic pain (7,7%), respiratory distress (7,7%) and hemoptysis (7,7%). The chest X-ray has allowed to orient the diagnosis in most cases and the thoracic scan set it in 100% of the cases. All the patients underwent surgery by thoracotomy. Lobectomy was done for 53,8 % followed by cystectomy in 30,8%, segmentectomy (7,7%) and pneumonectomy (7,7%) of patients. Histopathological examination confirmed the diagnosis of malformation in all cases. The postoperative outcome was uneventful for all the patients. Clinical manifestations evoks the diagnosis of symptomatic CPM, the chest X-ray allowed to orient it and the thoracic scan set it in all cases. The treatment is mainly surgical. Keywords: Pulmonary malformation, diagnosis, treatment, child, Mali

A previously undescribed pathway for pyrimidine catabolism

The b1012 operon of Escherichia coli K-12, which is composed of seven unidentified ORFs, is one of the most highly expressed operons under control of nitrogen regulatory protein C. Examination of strains with lesions in this operon on Biolog Phenotype MicroArray (PM3) plates and subsequent growth tests indicated that they failed to use uridine or uracil as the sole nitrogen source and that the parental strain could use them at room temperature but not at 37°C. A strain carrying an ntrB(Con) mutation, which elevates transcription of genes under nitrogen regulatory protein C control, could also grow on thymidine as the sole nitrogen source, whereas strains with lesions in the b1012 operon could not. Growth-yield experiments indicated that both nitrogens of uridine and thymidine were available. Studies with [(14)C]uridine indicated that a three-carbon waste product from the pyrimidine ring was excreted. After trimethylsilylation and gas chromatography, the waste product was identified by mass spectrometry as 3-hydroxypropionic acid. In agreement with this finding, 2-methyl-3-hydroxypropionic acid was released from thymidine. Both the number of available nitrogens and the waste products distinguished the pathway encoded by the b1012 operon from pyrimidine catabolic pathways described previously. We propose that the genes of this operon be named rutA–G for pyrimidine utilization. The product of the divergently transcribed gene, b1013, is a tetracycline repressor family regulator that controls transcription of the b1012 operon negatively