Determination of phthalate esters in physiological saline solution by monolithic silica spin column extraction method

Monolithic silica spin column extraction （MonoSpin-SPE） was developed as a simple, sensitive, and eco-friendly pretreatment method which combined with ultra-fast liquid chromatography-mass spectrometry （UFLC-MS） to determine the levels of six phthalate esters, dimethyl- （DMP）, diethyl- （DEP）, dipropyl- [ DPrP], butyl-benzyl- （BBP）, dicyclohexyl- （DcHP）, and di-n-octyl-（DOP） phthalate in physiological saline samples. Under optimized experimental conditions, the method was linear in the following ranges： 0.2- 50 μg/L for DMP, DEP, DPrP, DcHP and DOP; 5- 100 μg/L for BBP. The correlation coefficients （R2 ） were in the range of 0. 9951 - 0. 9995 for all the analytes and the limits of detection （LODs） and limits of quantification （LOQs） were in the ranges of 0.02 - 0.9 μg/L and 0.08 - 2.7μg/L, respectively. The pretreatment process showed good reproducibility with inter-day and intra-day relative standard deviations （RSDs） below 8.5% and 11.2%, respectively. This method was used to determine the levels of six phthalate esters in physiological saline samples and the recoveries ranged from 71.2% to 107.3%. DMP and DEP were found in actual physical saline samples （brand A and brand B）.

Friction and Wear Behavior of Fine-grained Alumina Ceramic under Physiological Saline Conditions

Sliding friction and wear behavior of two different grain-size aluminas （average grain size = 0.6 and 2 μm） was studied in physiological saline environment. Relationship between time and wear loss was observed. The wear loss volume increased with increased sliding time and fine-grained alumina exhibits a lower value. In the initial wear-in period, grains pull-out caused by grain-boundary microcracking is the dominant wear mechanism of submicron grained alumina. In the case of alumina of large grain size, intergranular and transgranular fracture is the basic wear mechanism. As the sliding time increases, compaction of wear debris on sliding surface of fine and coarsen alumina determines the wear characteristics.

Hydrogen-rich saline injection into the subarachnoid cavity within 2 weeks promotes recovery after acute spinal cord injury

Hydrogen can relieve tissue-damaging oxidative stress, inflammation and apoptosis. Injection of hydrogen-rich saline is an effective method for transporting molecular hydrogen. We hypothesized that hydrogen-rich saline would promote the repair of spinal cord injury induced by Allen＇s method in rats. At 0.5, 1, 2, 4, 8, 12 and 24 hours after injury, then once daily for 2 weeks, 0.25 mL/kg hydrogen-rich saline was infused into the subarachnoid space through a catheter. Results at 24 hours, 48 hours, 1 week and 2 weeks after injury showed that hydrogen-rich saline markedly reduced cell death, inflammatory cell infiltration, serum malondialdehyde content, and caspa se-3 immunoreactivity, elevated serum superoxide dismutase activity and calcitonin gene-related peptide immunoreactivity, and improved motor function in the hindlimb. The present study confirms that hydrogen-rich saline injected within 2 weeks of injury effectively contributes to the repair of spinal cord injury in the acute stage.

Neuroprotective effect of angiotensin Ⅱ type 2 receptor during cerebral ischemia/reperfusion

Angiotensin Ⅱ type 2 receptor（AT2R） activation has been shown to protect against stroke,but its precise mechanism remains poorly understood.We investigated whether the protective effect of AT2 R against ischemia/reperfusion injury is mediated by the suppression of immune and inflammatory responses.Rat models of middle cerebral artery occlusion were intraperitoneally injected with physiological saline,the AT2 R agonist CGP42112（1 mg/kg per day） or antagonist PD123319（1 mg/kg per day）.In the CGP42112 group,AT2 R expression increased,the infarct area decreased,interleukin-1β and tumor necrosis factor-α expression decreased,and interleukin-10 expression increased compared with the saline group.Antagonisin AT2 R using PD123319 produced the opposite effects.These results indicate that AT2 R activation suppresses immune and inflammatory responses,and protects against cerebral ischemia/reperfusion injury.