O objetivo deste trabalho é demonstrar a confecção de um obturador de feixe óptico a partir de um disco rígido de computador. O controle de corrente do dispositivo é feito por modulação de largura de pulso (Pulse width modulation - PWM), uma técnica que permite variar níveis de tensão/corrente por meio do ajuste da largura de pulso de um sinal digital. Este controle é feito de forma a minimizar a potência dissipada no dispositivo, aumentando assim sua vida útil. O núcleo do circuito de controle de corrente é o Arduino Uno, uma placa de microcontrolador de baixo custo e de fácil programação, amplamente utilizado como plataforma para prototipagem eletrônica. Por fim, a título de ilustração, apresentamos o uso do obturador de feixe óptico desenvolvido em um sistema de microfabricação via fotopolimerização por absorção de dois fótons, no qual ele tem papel fundamental.

This work demonstrates the development of an optical shutter from a computer hard disk. The electrical current control of the device is made by pulse width modulation, a technique that allows varying current/voltage levels by adjusting the pulse width of a digital signal. This control is made in order to minimize the power dissipated into the device, thus raising its lifetime. The main unit of the control circuit is Arduino Uno, a low cost and ease of programming microcontroller board, extensively used as a platform for electronic prototyping. As an example, we present the use of an optical shutter developed in a microfabrication setup via two-photon polymerization, in which it plays an important role.

SUMMARY P450 oxidoreductase deficiency (PORD) is a variant of congenital adrenal hyperplasia that is caused by POR gene mutations. The POR gene encodes a flavor protein that transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to all microsomal cytochrome P450 type II (including 21-hydroxylase, 17α-hydroxylase 17,20 lyase and aromatase), which is fundamental for their enzymatic activity. POR mutations cause variable impairments in steroidogenic enzyme activities that result in wide phenotypic variability ranging from 46,XX or 46,XY disorders of sexual differentiation, glucocorticoid deficiency, with or without skeletal malformations similar to Antley-Bixler syndrome to asymptomatic newborns diagnosed during neonatal screening test. Little is known about the PORD long-term evolution. We described a 46,XX patient with mild atypical genitalia associated with severe bone malformation, who was diagnosed after 13 years due to sexual infantilism. She developed large ovarian cysts and late onset adrenal insufficiency during follow-up, both of each regressed after hormone replacement therapies. We also described a late surgical approach for the correction of facial hypoplasia in a POR patient.

OBJECTIVE: The expression of transcription factors involved in early pituitary development, such as PROP1 and POU1F1, has been detected in pituitary adenoma tissues. In this study, we sought to characterize the transcriptional profiles of PROP1, POU1F1, and TBX19 in functioning and nonfunctioning pituitary adenomas in an attempt to identify their roles in tumorigenesis and hormone hypersecretion. METHODS: RT-qPCR analyses were performed to assess the transcriptional pattern of PROP1, POU1F1, TBX19, and hormone-producing genes in tissue samples of corticotrophinomas (n = 10), somatotrophinomas (n = 8), and nonfunctioning adenomas (n = 6). RESULTS: Compared with normal pituitary tissue, POU1F1 was overexpressed in somatotrophinomas by 3-fold. PROP1 expression was 18-fold higher in corticotrophinomas, 10-fold higher in somatotrophinomas, and 3-fold higher in nonfunctioning adenomas. TBX19 expression was 27-fold higher in corticotrophinomas. Additionally, the level of TBX19 mRNA positively correlated with that of pro-opiomelanocortin (r = 0.49, p = 0.014). CONCLUSIONS: Our data demonstrate that PROP1 is overexpressed in pituitary adenomas, mainly in corticotrophinomas. Together with previously published data showing that patients who harbor PROP1 loss-of-function mutations present a progressive decline in corticotrope function, our results support a role for PROP1 in pituitary tumor development and in the maintenance of cell lineages committed to corticotrophic differentiation.