RESUMEN
Recent progress in wettability-patterned microchips has facilitated the development of ultra-trace detection in multiple biomedical and food safety fields. The existence of a superhydrophilic trap can realize targeted deposition of the analyte. However, the wetting transition from the Cassie-Baxter state to the Wenzel state usually occurs during evaporation and leads to a larger deposition footprint, which has a strong impact on the detection sensitivity and uniformity. In this paper, we report an integrated design, fabrication, and evaporation strategy to avoid the transition for high-performance attomolar surface-enhanced Raman scattering (SERS) detection. An improved force balance model was proposed to design the microstructures of wettability-patterned microchips, which were fabricated by nanosecond laser direct writing and surface fluorination. The microchips were composed of superhydrophobic micro-grooves and superhydrophilic traps, by which the targeted deposition of Au nanoparticles and rhodamine 6G (R6G) onto a minimal area of â¼70 × 70 µm2 was realized after a two-step heated evaporation. Accordingly, the detection limit was down to the attomolar level (5 × 10-18 M) with SERS enhancement factors (EFs) exceeding 1010. More importantly, the Raman signals showed good uniformity (RSD of 11.5%) for the concentration of 2 × 10-17 M. A good linear relationship was obtained in the quantitative concentration range of 10-12 M to 5 × 10-18 M with a high correlation coefficient (R2) of 0.996. These wettability-patterned microchips exhibit high performance (that is, both good sensitivity and good uniformity) in the detection of ultra-trace molecules in aqueous solutions, avoiding the need for expensive equipment and considerable skill in operations. The proposed strategy could also be applied to other microfluidic devices for rapid and simple analyte pre-concentration.
RESUMEN
BACKGROUND: Acute postoperative pain plays an important role in the perioperative neurocognitive disorders (PND). The pathogenesis of PND is still unknown, but it is generally believed that peripheral and central nervous system inflammation play an important role, and acute postoperative pain is also thought to aggravate postoperative inflammatory response. The aim of the present study is to explore the effect of acute postoperative pain on peripheral and central nervous system inflammation and related cognitive impairment behaviour in elderly rats after surgery. METHODS: Rats were assigned into four groups: control, surgery for internal fixation for tibial fracture, surgery with analgesia using intraperitoneal morphine, and morphine without surgery. Pain was assessed by the Subjective Pain Scale. The spatial memory of rats was assessed by the Morris water maze (delayed matching task) from the second day to the seventh day after surgery (POD2-POD7). In part of the rats, the pro-inflammatory cytokines TNF-α in plasma, the medial prefrontal cortex (mPFC), and the hippocampus were determined by ELISA on the POD2. The activation of microglia and the expression of c-Fos in the hippocampal CA1 regions and mPFC were detected by the immunohistochemical method on the POD2. RESULTS: Acute postoperative pain and spatial memory impairment occurred after operation, and postoperative analgesia could significantly improve the both parameters. Additionally, on the POD2, the levels of TNF-α in plasma, hippocampus and mPFC were significantly increased, while the activation of microglia cells and the expression c-Fos in the hippocampal CA1 regions and mPFC were significantly increased. And postoperative analgesia with morphine significantly inhibited the above reactions. CONCLUSION: Our data suggest that acute postoperative pain increases the incidence of perioperative neurocognitive disorders. Peripheral and central nervous system inflammation may be involved in this cognitive impairment. And reducing the intensity of acute postoperative pain may be one of the main preventive strategies for PND.
