Yanfei Zhang

The application of oxygen sensors based on Tunable Diode Laser Absorption Spectroscopy (TDLAS) in the industrial field has received extensive attention. However, most of the existing studies construct detection systems using discrete devices, making it difficult to apply them in the industrial field. In this work, through the optimization of the sensor circuit, the size of the core components of the sensor is reduced to 7.8 × 7.8 × 11.8 cm³, integrating the laser, photodetector, and system control circuit. A novel integrated optical path design is proposed for the optical mechanical structure, which enhances the structural integration and long-term optical path stability while reducing the system assembly complexity. The interlocking design of the laser-driven digital-to-analog converter (DAC) and photocurrent acquisition analog-to-digital converter (ADC) reduces the requirements of the harmonic signal extraction for the system hardware. By adopting a high-precision ADC and a high-resolution pulse-width modulation (PWM), the peak-to-peak value of the laser temperature control noise is reduced to 2 m°C, thereby reducing the detection noise of the sensor. This oxygen detection system has a minimum response time of 0.1 s. Under the condition of a 0.5 m detection optical path, the Allan variance shows that when the integration time is 5.6 s, the detection limit reaches 53.4 ppm, which is ahead of the detection accuracy of similar equipment under the very small system size.

Summary: Previous investigations have found that ebselen is able to treat neurodegenerative diseases caused by radical and acute total cerebral ischaemia. The aim of the present study was to investigate the neuroprotective effects of ebselen in a traumatic brain injury (TBI) model. Ninety Sprague‐Dawley rats were randomly divided into five groups (n = 18 in each): (i) sham operation; (ii) an injury model group; (iii) low‐dose (3 mg/kg) ebselen‐treated group; (iv) a moderate‐dose (10 mg/kg) ebselen‐treated group; and (v) a high‐dose (30 mg/kg) ebselen‐treated group. The TBI model was created according using a modified weight‐drop model. Neurological severity score (NSS), brain water content and histopathological deficits were assessed as parameters of injury severity. Expression of nitric oxide (NO), inducible NO synthase (iNOS) mRNA, Toll‐like receptor (TLR) and phosphorylated (p‐) p38 mitogen‐activated protein kinase (MAPK) were examined by chemical colorimetry, quantitative polymerase chain reaction and western blotting 24 h after intragastric ebselen administration. Rats in the TBI model group exhibited markedly more severe neurological injury (higher NSS, more brain water content and more histopathological deficits) than those in the sham‐operated group. Ebselen treatment significantly ameliorated the neurological injury of TBI rats in a dose‐dependent manner. Moreover, ebselen significantly reduced the NO and iNOS mRNA levels and inhibited TLR4 and p‐p38 MAPK expression, indicating the involvement of NO and p38 MAPK signalling pathways in the neuroprotection afforded by ebselen. In conclusion, ebselen ameliorated neurological injury, possibly by reducing NO levels and modulating the TLR4‐mediated p38 MAPK signalling pathway. Therefore, ebselen may have potential to treat secondary injuries of TBI.