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In response to the current problems of high startup wind speed, complex design schemes, and inability to accurately measure the average wind speed of the entire section of the roadway using wind speed sensors, based on the principle of ultrasonic opposed wind measurement, a mine opposed wind speed and direction sensor with STM32 as the core is designed. The overall structure of the sensor, the design of the transmitting and receiving circuit, the filtering algorithm, and the software process are introduced. This sensor has changed the wind measurement method from point to surface, using a single ARM core and measuring the wind speed at the centerline of the roadway through long-distance (5-12 m) ultrasonic wind measurement technology. This wind speed represents the average wind speed of the entire roadway. It greatly improves the accuracy and real-time performance of roadway wind speed measurement. A test prototype is developed based on the design scheme, and the test results in a circular wind tunnel show that the measured values of the sensor has good consistency with the standard wind speed values in the range of 0.1-15 m/s, with a measurement error of less than 0.1 m/s. It can meet the precision requirements of intelligent mines for roadway wind speed measurement.

Methanol is a promising alternative fuel due to its wide availability of raw materials, mature production processes, and low production cost. However, because of the low cetane number, methanol must include a more reactive fuel to assist with combustion when used in compression ignition (CI) engines. In this study, based on the optical CI engine platform, methanol is injected into the intake port, and diesel is directly injected into the cylinder to achieve dual-fuel combustion. The effects of the methanol energy ratios and diesel split injection strategies on combustion are investigated. The results show that the premixed blue flame was mainly concentrated in the near wall region, whereas the yellow flame produced by diesel combustion tended to concentrate in the central region as the methanol energy ratio increased. When the methanol energy ratio exceeded 50%, the ignition delay was significantly prolonged, while the flame area was greatly reduced. Meanwhile, the peak values for the cylinder pressure and heat release rate decreased significantly, indicating a significant deterioration in combustion. At the earlier diesel pre-injection timing at −58°, the overall dual-fuel combustion at each main injection timing exhibited low-temperature premixed combustion characteristics, with a lower peak exothermic rate and flame brightness. At the later pre-injection timing at −33°, the spray flame at all main injection timings could be observed, with higher peak heat release rates and indications of thermal efficiency. Combustion at later main injection timings was characterized by diffusion combustion, and the main injection timing could effectively regulate the combustion process through phase adjustment. [ABSTRACT FROM AUTHOR]

It was to investigate the neuroprotective mechanism of tanshinone after cerebral infarction via the Kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant reaction element (ARE) signaling pathway. Forty specific pathogen-free (SPF) Sprague Dawley (SD) rats were selected, all of which were male, approximately seven weeks old, weighing 250 ± 25 g. They were randomly divided into a model group, a non-model operation group, a positive control group, and an experimental group with ten SD rats in each group. The model of cerebral infarction in rats was established by the wire occlusion method. The model group and non-model operation group (control group) were injected with normal saline daily, the negative control group was injected with Keap1 gene inhibitor daily, and the experimental group was injected with tanshinone IIA (10 mg·kg−1·d−1) daily. Animal behavior analysis was performed on the 7th day after the operation, and pathology and the neuroprotective effects of tanshinone IIA on cells were assessed, including cell proliferation, autophagy, oxidative damage, and mitochondrial membrane permeability. The neuroprotective mechanism based on the Keap1-Nrf2/ARE pathway was explored and analyzed. Compared with the model group, the number of Keap1 proteins in the experimental group and the control group was substantially reduced (P < 0.05), and the experimental group was substantially different from the model group (P < 0.01). The protein expression of Nrf2, HO-1, and NQO1 increased substantially (P < 0.05), and the experimental group was substantially different from the model group (P < 0.01). In summary, tanshinone IIA promoted the proliferation of nerve cells, inhibited the production of cellular reactive oxygen species, inhibited the change in mitochondrial membrane potential, and activated the Keap1-Nrf2/ARE signaling pathway. It also induced and regulated the upregulation of downstream NQO1, HO-1, etc. and protected cells from cerebral infarction. [ABSTRACT FROM AUTHOR]