Paracetamol degradation by photo-activated peroxydisulfate process (UV/PDS): kinetic study and optimization using central composite design.

In this study, peroxydisulfate (PDS) was successfully activated by UV-irradiation for the degradation of paracetamol (PCT) frequently detected in the environment. Results showed that increasing the initial PDS concentration from 5 to 20 mM promote the removal of PCT from 49.3% to 97.5% after 240 min of reaction time. As the initial PCT concentration increased from 0.066 to 0.132 mM, the degradation efficiency of PCT decreased from 98% to 73% after 240 min of reaction time, while the optimal pH was found to be 6. It is apparent that the degradation rate of PCT was favored by the lamp power regardless of the initial PCT concentration, for 0.132 mM of PCT, the degradation efficiency increased from 73% to 95% when the lamp power increased from 9 to 30 W, respectively. The kinetic of degradation of the PCT was described by a pseudo-second order kinetic model. The model obtained by central composite design led to the following optimal conditions for PCT degradation: 0.132 mM initial PCT concentration, 20 mM PDS dose, pH solution 6 and lamp power 30 W led to the removal of 92% of PCT at 25 °C within 240 min of reaction time.

Identification of a novel mutation in FOXL2 gene that leads to blepharophimosis ptosis epicanthus inversus and telecanthus syndrome in a Tunisian consanguineous family.

Mutations in FOXL2 gene are responsible for blepharophimosis ptosis epicanthus inversus and telecanthus syndrome (BPES). The BPES syndrome is a rare autosomal dominant genetic disease characterized by eyelid malformations associated with premature ovarian failure (BPES type I) or not (BPES type II). The human FOXL2 protein (376 aa) contains a 100 amino-acid DNA-binding forkhead domain (residues 52-152) and a polyalanine tract (residues 221-234). In the present study, we report the molecular investigation of four affected members with BPES syndrome in a Tunisian consanguineous family. To identify the causative mutation, we performed a direct sequencing of the FOXL2 gene. The sequence analysis of the coding exon revealed a novel frameshift mutation g.1113 dup C, c.876 dup C, p.P292 Fs. The mutation is located downstream of the polyalanine tract and causes the protein extension to 532 aa. This study reports for the first time a novel frameshift mutation in two-generation consanguineous Tunisian family with BPES. Our results expand the spectrum of FOXL2 mutations.