Objective:To do the research on the layout and construction preparation for 3.0T high-field nuclear magnetic resonance equipment room, greatly shorten the construction time and save money for hospital by the safe and convenient usage. Methods: According to the specific characteristics of hospital sitting in full consideration of transportation and distribution, ventilation, bearing, electromagnetic interference and so on, we implement gradually, were ready to work in the construction. Results: Computer room location requirements bearing within 10 tons, magnets, center of 3 m in ferromagnetic material to do assessment, and moving around the car and the transformer must be beyond 3G line, required a special transformer and the capacity of more than 150 kVA. Equipment grounding resistance is less than 2 ohms, shielding room of insulation is greater than 1000 ohms. Super tube is higher than 3.8 m above the ground, there be no air conditioning air inlet. Water-cooled machine well ventilated, northern region need to get the winter outdoor antifreeze. Exhaust air change per hour between magnet design of not less than 12 times. Conclusion: Hospital construction for large equipment and ancillary equipment is installed in the process of each link to match reasonably, pay attention to the collaboration between different units and at the same time. Reasonable equipment layout and construction preparation is the guarantee of equipment installation smoothly.

Increased microglial activation and neuroinflammation within autonomic brain regions such as the rostral ventrolateral medulla (RVLM) have been implicated in stress-induced hypertension (SIH). Prorenin, a member of the brain renin-angiotensin system (RAS), can directly activate microglia. The present study aimed to investigate the effects of prorenin on microglial activation in the RVLM of SIH rats. Rats were subjected to intermittent electric foot-shocks plus noise, this stress was administered for 2 h twice daily for 15 consecutive days, and mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were monitored. The results showed that MAP and RSNA were augmented, and this paralleled increased pro-inflammatory phenotype (M1) switching. Prorenin and its receptor (PRR) expression and the NLR family pyrin domain containing 3 (NLRP3) activation were increased in RVLM of SIH rats. In addition, PLX5622 (a microglial depletion agent), MCC950 (a NLRP3 inhibitor), and/or PRO20 (a (Pro)renin receptor antagonist) had antihypertensive effects in the rats. The NLRP3 expression in the RVLM was decreased in SIH rats treated with PLX5622. Mito-tracker staining showed translocation of NLRP3 from mitochondria to the cytoplasm in prorenin-stimulated microglia. Prorenin increased the ROS-triggering M1 phenotype-switching and NLRP3 activation, while MCC950 decreased the M1 polarization. In conclusion, upregulated prorenin in the RVLM may be involved in the pathogenesis of SIH, mediated by activation of the microglia-derived NLRP3 inflammasome. The link between prorenin and NLRP3 in microglia provides insights for the treatment of stress-related hypertension.