RESUMEN
Undoped and Dy-doped CdSe nanoparticles are synthesized and then characterized by the SEM, XRD, FT-IR, XPS and BET methods, which verify successful preparation of the doped catalyst. The sonocatalytic degradation of anazolene sodium as a model azo dye is higher than sonolysis process and the 2% Dy-doped CdSe with band gap of 1.42eV exhibits the greatest sonocatalytic performance. The decolorization efficiency (DE%) of sonocatalysis with 2% Dy-doped CdSe, undoped CdSe and sonolysis after 90min of the process is 91.32%, 56.13% and 39.14%, respectively. In addition, the sonocatalytic degradation of anazolene sodium increases with enhancement of the dopant, catalyst dosage, ultrasonic power, dissolved gasses and decreasing of initial anazolene sodium concentration. Furthermore, with addition of chloroform, sulfate, chloride and ethanol as the radical scavengers, the DE% decreases indicating the controlling mechanism of free radicals for the dye degradation. Besides, the results reveal the appropriate reusability of the catalyst and various degradation by-products are identified using the GC-MS technique. Eventually, the empirical kinetic model is expanded by nonlinear regression analysis for prediction of pseudo first-order constants in various operational conditions.
RESUMEN
OBJECTIVE: To present an Iranian patient with a nonclassic form of multiple endocrine neoplasia type 1 (MEN 1) who presented with ectopic Cushing syndrome (CS) secondary to a corticotropin (ACTH)-producing thymic neuroendocrine tumor (NET), recurrent renal stones, and a giant cell granuloma of the jaw due to primary hyperparathyroidism (PHPT) without involvement of the pituitary or pancreas. METHODS: Relevant imaging and hormonal evaluations were performed. The patient was operated on 2 occasions for a thymic NET and on 3 occasions for PHPT. DNA from a peripheral blood sample was extracted for sequencing of the MEN1 gene. RESULT: Histopathologic evaluation of the thymic tumor removed during the first surgery showed an atypical carcinoid tumor with a Ki-67 labeling index of 5%. Evaluation after the second surgery revealed an invasive carcinoid tumor with a Ki-67 labeling index of 30%. Parathyroid pathology was suggestive of glandular hyperplasia. Menin gene sequencing revealed a novel frameshift mutation c.1642_1648dup in exon 10. CONCLUSION: This case of MEN 1 is unusual because most thymic NETs in MEN 1 are nonfunctional, and secretion of ACTH or other ectopic hormones rarely occurs. In patients presenting with thymic NETs, the possibility of MEN 1 should be considered, especially in the presence of hyperparathyroidism. This case also demonstrates that the behavior of thymic NETs can change over time from slow-growing tumors to highly invasive neoplasia, and that ectopic ACTH can be produced by these tumors in the context of MEN 1.