Highly efficient nanostructured CoFe2 O4 thin film electrodes for electrochemical degradation of rhodamine B.

In this work, we report the application of highly efficient electrodeposited cobalt ferrite (CoFe2 O4 ) thin films in electrochemical degradation of rhodamine B. XRD, FTIR and Raman spectroscopic studies confirmed the formation of single phase CoFe2 O4 . SEM analysis revealed a very fine nanorods dispersed uniformly with average size around 30 nm. UV-Vis spectrophotometry emphasized that the optical band gap value is 1.6 eV. Moreover, the elaborated CoFe2 O4 thin films showed a good efficiency for the electrochemical degradation of an aqueous solution of rhodamine B (RhB) attaining 99% during the first 3 min of reaction time. The trapping experiments revealed that the hydroxyl radicals were the main active species leading to the removal of RhB initial concentration of 10 mg/L in a very short time. PRACTITIONER POINTS: A simple electrodeposition technique was used to fabricate CoFe2 O4 thin. XRD and FTIR studies revealed the formation of pure cubic spinel phase. Nano-rod like morphology has been successfully synthesized. The rhodamine B aqueous solution has been completely decolorized using the obtained CoFe2 O4 thin films.

LRSAM1 variants and founder effect in French families with ataxic form of Charcot-Marie-Tooth type 2.

Currently only 25-30% of patients with axonal forms of Charcot-Marie-Tooth disease (CMT) receive a genetic diagnosis. We aimed to identify the causative gene of CMT type 2 in 8 non-related French families with a distinct clinical phenotype. We collected clinical, electrophysiological, and laboratory findings and performed genetic analyses in four different French laboratories. Seventy-two patients with autosomal dominant inheritance were identified. The disease usually started in the fourth decade and the clinical picture was dominated by sensory ataxia (80%), neuropathic pain (38%), and length-dependent sensory loss to all modalities. Electrophysiological studies showed a primarily axonal neuropathy, with possible isolated sensory involvement in milder phenotypes. Disease severity varied greatly but the clinical course was generally mild. We identified 2 novel variants in LRSAM1 gene: a deletion of 4 amino acids, p.(Gln698_Gln701del), was found in 7 families and a duplication of a neighboring region of 10 amino acids, p.(Pro702_Gln711dup), in the remaining family. A common haplotype of ~450 kb suggesting a founder effect was noted around LRSAM1 in 4 families carrying the first variant. LRSAM1 gene encodes for an E3 ubiquitin ligase important for neural functioning. Our results confirm the localization of variants in its catalytic C-terminal RING domain and broaden the phenotypic spectrum of LRSAM1-related neuropathies, including painful and predominantly sensory ataxic forms.