Efficient removal of phosphorus and nitrogen from aquatic environment using sepiolite-MgO nanocomposites: preparation, characterization, removal performance, and mechanism.

Excessive phosphorus will lead to eutrophication in aquatic environment; the efficient removal of phosphorus is crucial for wastewater engineering and surface water management. This study aimed to fabricate a nanorod-like sepiolite-supported MgO (S-MgO) nanocomposite with high specific surface area for efficient phosphate removal using a facile microwave-assisted method and calcining processes. The impact of solution pH, adsorbent dosage, contact time, initial phosphate concentrations, Ca2+ addition, and N/P ratio on the phosphate removal was extensively examined by the batch experiments. The findings demonstrated that the S-MgO nanocomposite exhibited effective removal performance for low-level phosphate (0 ~ 2.0 mM) within the pH range of 3.0 ~ 10.0. Additionally, the nanocomposite can synchronously remove phosphate and ammonium in high-level nutrient conditions (> 2.0 mM), with the maximum removal capacities of 188.49 mg P/g and 89.78 mg N/g. Quantitative and qualitative analyses confirmed the successful harvesting of struvite in effluent with high-phosphate concentrations, with the mechanisms involved attributed to a synergistic combination of sorption and struvite crystallization. Due to its proficient phosphate removal efficiency, cost-effectiveness, and substantial removal capacity, the developed S-MgO nanocomposite exhibits promising potential for application in phosphorus removal from aquatic environments.

Vitamin D3 Supplementation Attenuates Surgery-Induced Neuroinflammation and Cognitive Impairment by Regulating NLRP3 Inflammasome in Mice.

Neuroinflammation plays a dominant role in the progression of postoperative cognitive dysfunction (POCD). Vitamin D has been known to have important regulatory functions in inflammation and immune response. The NOD-like receptor protein 3 (NLRP3) is an essential inflammasome in the inflammatory response and could be activated by anesthesia and surgery. In this study, male C57BL/6 mice aged 14-16 months were given VD3 for 14 days straight before having an open tibial fracture surgery. The animals were either sacrificed to obtain the hippocampus or tested in a Morris water maze test. Western blot was employed to estimate the levels of NLRP3, ASC, and caspase-1, immunohistochemistry was used to identify microglial activation, and an enzyme-linked immunosorbent assay was used to measure the expression of IL-18 and IL-1ß, while using the corresponding assay kits to assess ROS and MDA levels to reflect the oxidative stress status. We showed that VD3 pretreatment significantly improved surgery-induced memory and cognitive dysfunctions in aged mice, which was linked to the inactivation of the NLRP3 inflammasome and the inhibition of neuroinflammation. This finding provided a novel preventative strategy for clinically reducing postoperative cognitive impairment in elderly surgical patients. This study has some limitations. Gender differences in the effects of VD3 were not considered, and only male mice were used. Additionally, VD3 was given as a preventative measure; however, it is unknown whether it has any therapeutic benefits for POCD mice. This trial is registered with ChiCTR-ROC-17010610.

Supplement of Lipid Emulsion to Epinephrine Improves Resuscitation Outcomes of Asphyxia-Induced Cardiac Arrest in Aged Rats.

OBJECTIVE: The goal of the study was to investigate the efficacy of lipid supplement to epinephrine-based therapy in resuscitation of asphyxia-induced cardiac arrest in aged rats. METHODS: The study included two parts: in experiment A, rats underwent asphyxial cardiac arrest and cardiopulmonary resuscitation, randomized to receive epinephrine and normal saline (control group, n=22), epinephrine and intralipid 20% (long-chain triglycerides (LCT) group, n=22) or epinephrine and lipovenoes 20% (LCT/medium-chain triglcerides (MCT) group, n=22). Return of spontaneous circulation, recurrence of asystole after resuscitation, hemodynamic metrics, arterial blood gas values, neurological assessment score and indexes of pulmonary transudation were recorded. In experiment B, rats using the same model and resuscitation protocol were randomly divided into 21 groups: Control 0, Control 20, Control 40, Control 60, Control 80, Control 100, Control 120, LCT 0, LCT 20, LCT 40, LCT 60, LCT 80, LCT 100, LCT 120, LCT/MCT 0, LCT/MCT 20, LCT/MCT 40, LCT/MCT 60, LCT/MCT 80, LCT/MCT 100 and LCT 120 (n=10, the subscripts represent respective endpoint of observation in minutes). Myocardial bioenergetics were determined. RESULTS: In experiment A, the LCT and LCT/MCT groups had a shorter time to return of spontaneous circulation (ROSC) (P=0.001and P<0.001, respectively) and higher survival rate (P=0.033 and P=0.014, respectively) compared with the Control group. The LCT/MCT group had higher MAP (P<0.001 and P=0.001, respectively), HR (P<0.001 and P=0.004, respectively) and RPP (P<0.001 and P<0.001, respectively) compared with the Control and LCT groups, respectively. In experiment B, the LCT/MCT group had a higher energy charge compared with the control group at 20 (P<0.001) and 40 (P<0.001) minutes. The LCT group had higher energy charge compared with the Control group at 40 (P<0.001) and 60 (P<0.001) minutes. CONCLUSION: The supplement of lipid emulsion to epinephrine improves resuscitation outcomes of asphyxia-induced cardiac arrest than epinephrine alone in our in vivo model of aged rat. LCT/MCT emulsion may be superior to LCT emulsion in epinephrine-based resuscitation.

Effects of mild and moderate hypothemia therapy on expression of cerebral neuron apoptosis related proteins and glial fiber acidic protein after rat cardio-pulmonary resuscitation.

To explore the effects of different degrees of hypothermia on brain tissue apoptosis after cardio-pulmonary resuscitation (CPR). Cardiac arrest for 5 min induced by asphyxia method was used to create CPR model. 30 SD rats were randomly divided into control group (normothermia), 33 °C hypothermia group and 30 °C hypothermia group with ten rats in each. Rats in control group received routine treatment at 25 °C room temperature after CPR; Rats in mild hypothermia and moderate hypothermia groups were given hypothermia treatment 0.5 h after CPR. Brain tissue in all groups was taken 24 h after CPR, and immunohistochemistry was used to detect the caspase-3 in cerebral cortex and glial fiber acidic protein (GFAP) expression in astrocyte. Western blotting was used to detect Bcl-2 and Bax protein expression, and histopathological change was observed in brain tissue. Compare to the control group, caspase-3 expression in cerebral neurons in hypothermia group was significantly decreased (p<0.01), which was significantly lower in 30 °C group than that in 33 °C group (p > 0.05); GFAP level in hypothermia groups was significantly increased (p < 0.01), which was higher in 30 °C hypothermia group than that in 33 °C hypothermia group (p < 0.05); Bcl-2 expression level in hypothermia group was significantly increased (p < 0.01), which was higher in 30 °C hypothermia group than that in 33 °C hypothermia group (p < 0.05); The level of Bax had no significant difference among the three groups. Hypothermia-regulated GFAP expression by decreasing caspase-3 expression and increasing Bcl-2 expression to promote brain cell signaling transduction, and further inhibited cell apoptosis and reduced brain injury. Moderate hypothermia therapy is more effective than mild hypothermia in preventing brain injure.