Intensive carbon combustion in sintering packed bed via steam spraying: An experimental study on carbon monoxide emission reduction.

Improving the combustion efficiency of solid fuels is important for reducing carbon monoxide emissions in the iron ore sintering process. In this paper, the surface steam spraying technology is introduced in the sintering process based on the auxiliary combustion effect of steam on coke, and its potential to reduce carbon monoxide emissions is demonstrated. Thermogravimetric analysis experiments of coke breeze in air and air-steam mixed atmosphere are carried out, and the results show that the introduction of steam can reduce the concentration of carbon monoxide in the exhaust gas from 183×10-6 to 78×10-6. At the same time, the mechanisms of carbon monoxide emission reduction by surface steam spraying technology are analyzed from the thermodynamic and kinetic perspectives. Then, a series of laboratory-scale sintering pot tests are carried out under no spraying operation, interval spraying operation, and continuous spraying operation. The results indicate that both interval and continuous spraying operations can reduce carbon monoxide emissions. The optimal mode of steam spraying under the present experimental conditions is continuously spraying for 13 min at a volume rate of 0.053 m3/min. Compared with no spraying, the average carbon monoxide concentration in the exhaust gas is reduced from 7565×10-6 to 6231×10-6, and total carbon monoxide emissions for per ton sinter are reduced from 13.46 m3/t to 9.51 m3/t.

Inhibition of Notch 1 signaling in the subacute stage after stroke promotes striatal astrocyte-derived neurogenesis.

Inhibition of Notch1 signaling has been shown to promote astrocyte-derived neurogenesis after stroke. To investigate the regulatory role of Notch1 signaling in this process, in this study, we used a rat model of stroke based on middle cerebral artery occlusion and assessed the behavior of reactive astrocytes post-stroke. We used the γ-secretase inhibitor N-[N-(3,5-diuorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester (DAPT) to block Notch1 signaling at 1, 4, and 7 days after injury. Our results showed that only administration of DAPT at 4 days after stroke promoted astrocyte-derived neurogenesis, as manifested by recovery of white matter fiber bundle integrity on magnetic resonance imaging, which is consistent with recovery of neurologic function. These findings suggest that inhibition of Notch1 signaling at the subacute stage post-stroke mediates neural repair by promoting astrocyte-derived neurogenesis.

Serum sulfonylurea receptor-1 as a biomarker of clinical severity and prognosis in patients with traumatic brain injury.

BACKGROUND: Sulfonylurea receptor-1 (Sur1) plays an important role in acute brain injury. We determine whether serum Sur1 concentrations are associated with traumatic severity and clinical outcome after traumatic brain injury (TBI). METHODS: Serum Sur1 concentrations were measured in 100 healthy controls and 138 patients with moderate to severe TBI. Glasgow coma scale (GCS) and Rotterdam computed tomography (CT) classification were recorded to assess traumatic severity. Glasgow outcome scale (GOS) score of 1-3 at posttraumatic 3 months was defined as an unfavorable outcome. RESULTS: Serum Sur1 concentrations were markedly higher in patients than in controls. Serum Sur1 concentrations of patients were highly correlated with GCS score, Rotterdam CT classification and GOS score. Patients with unfavorable outcome displayed markedly higher serum Sur1 concentrations than those presenting with favorable outcome. Under receiver operating characteristic curve, serum Sur1 concentrations significantly distinguished patients at risk of unfavorable outcome. Serum Sur1 emerged as an independent predictor for unfavorable outcome. CONCLUSIONS: Rising serum Sur1 concentrations are highly correlated with traumatic severity and are independently associated with poor prognosis after TBI, indicating that serum Sur1 may have the potential to be a useful prognostic biomarker of TBI.

Comparative Study on Foaming Properties of Egg White with Yolk Fractions and Their Hydrolysates.

As an excellent foaming agent, egg white protein (EWP) is always contaminated by egg yolk in the industrial processing, therefore, decreasing its foaming properties. The aim of this study was to simulate the industrial EWP (egg white protein with 0.5% w/w of egg yolk) and characterize their foaming and structural properties when hydrolyzed by two types of esterase (lipase and phospholipase A2). Results showed that egg yolk plasma might have been the main fraction, which led to the poor foaming properties of the contaminated egg white protein compared with egg yolk granules. After hydrolyzation, both foamability and foam stability of investigated systems thereof (egg white protein with egg yolk, egg white protein with egg yolk plasma, and egg white protein with egg yolk granules) increased significantly compared with unhydrolyzed ones. However, phospholipids A2 (PLP) seemed to be more effective on increasing their foaming properties as compared to those systems hydrolyzed by lipase (LP). The schematic diagrams of yolk fractions were proposed to explain the aggregation and dispersed behavior exposed in their changes of structures after hydrolysis, suggesting the aggregated effects of LP on yolk plasma and destructive effects of PLP on yolk granules, which may directly influence their foaming properties.

Neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury.

The aim of the present study was to assess the neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury (DAI). DAI rats were orally gavaged with berberine at a dose of 200 mg/kg of body weight for 4 weeks. Behavioral tests were used to analyze the neuroprotective effect of berberine against DAI-induced learning and memory deficits. In the present study, treatment with berberine significantly protected against DAI-induced inhibition of learning and memory in rats. Notably, berberine significantly suppressed the levels of tumor necrosis factor, interleukin-1ß and monocyte chemoattractant protein-1, as well as reduced the protein expression levels of nuclear factor-κB, Bcl-2-associated X protein and cytochrome c in DAI rats. In addition, berberine significantly suppressed the protein expression of p38 mitogen-activated protein kinase, activating transcription factor 2 and vascular endothelial growth factor in DAI rats. These results suggested that berberine exhibited a neuroprotective effect against learning and memory deficits in severe DAI through the suppression of inflammation, angiogenesis and apoptosis in a rat model.

The value of ESWAN in diagnosis and differential diagnosis of prostate cancer: Preliminary study.

OBJECTIVE: To evaluate the value of enhanced T2 star-weighted angiography (ESWAN) in diagnosis and differential diagnosis of prostate cancer by comparing the multiple indices of ESWAN in benign prostatic hyperplasia (BPH), prostate cancer (PCa) and the normal peripheral zone (PZ). METHODS: Traditional MRI and ESWAN were performed on forty-nine clinically-diagnosed PCa patients, sixty BPH patients, and forty-six normal adult males. The ESWAN indices (magnitude value, phase value, R2* value and T2* value) measured on different regions of interest (ROIs) were analyzed. Additionally, receiver operating characteristic (ROC) analysis was performed to obtain the area under the curve (AUC), sensitivity, specificity, and optimal cut-off points of PCa and BPH, PCa and PZ respectively. RESULTS: The magnitude value, phase value, R2* value and T2* value of PZ were 1529.43±254.43, 0.0689±0.1619, 16.57±8.11, 82.75±53.87, respectively; the magnitude value, phase value, R2* value, and T2* value of PCa were 1540.18±338.62, -0.0176±0.0919, 26.93±11.31, and 45.99±17.43, respectively; the magnitude value, phase value, R2* value, and T2* value of BPH were 1579.49±285.28, 0.0209±0.0839, 20.69±3.95, and 51.56±8.90, respectively. Compared with normal PZ, phase value of PCa was lower (t=-3.302, P=0.001), R2* value higher (t=5.326, P=0.000), and T2* value lower (t=-4.570, P=0.000); compared with BPH, phase value of PCa was lower (t=-2.261, P=0.026), R2* value higher (t=3.988, P=0.000), and T2* value lower (t=-2.155, P=0.033). When PCa and PZ were distinguished, the AUC of magnitude value, phase value, R2* value, and T2* value were respectively 0.539 (P=0.510), 0.679 (P=0.0007), 0.811 (P<0.0001), and 0.762 (P<0.0001); the diagnosis efficiency of R2* value was higher than that of T2* value (P=0.037), while the diagnosis efficiency of T2* value was equivalent to phase value (P=0.256). When PCa was differentiated from BPH, the AUC of magnitude value, phase value, R2* value, and T2* value were 0.518 (P=0.752), 0.612 (P=0.039), 0.705 (P=0.0001), and 0.685 (P=0.0006), respectively; there was no statistical difference in the diagnostic efficiency of phase value, R2* value, and T2* value. CONCLUSIONS: The phase value, R2* value and T2* value can distinguish PCa and normal PZ, PCa and BPH, so they are valuable for the diagnosis and differential diagnosis of PCa, moreover, the diagnostic efficiency of R2* value is better than other indices.

Microwave exposure impairs synaptic plasticity in the rat hippocampus and PC12 cells through over-activation of the NMDA receptor signaling pathway.

OBJECTIVE: The aim of this study is to investigate whether microwave exposure would affect the N-methyl-D-aspartate receptor (NMDAR) signaling pathway to establish whether this plays a role in synaptic plasticity impairment. METHODS: 48 male Wistar rats were exposed to 30 mW/cm2 microwave for 10 min every other day for three times. Hippocampal structure was observed through H&E staining and transmission electron microscope. PC12 cells were exposed to 30 mW/cm2 microwave for 5 min and the synapse morphology was visualized with scanning electron microscope and atomic force microscope. The release of amino acid neurotransmitters and calcium influx were detected. The expressions of several key NMDAR signaling molecules were evaluated. RESULTS: Microwave exposure caused injury in rat hippocampal structure and PC12 cells, especially the structure and quantity of synapses. The ratio of glutamic acid and gamma-aminobutyric acid neurotransmitters was increased and the intracellular calcium level was elevated in PC12 cells. A significant change in NMDAR subunits (NR1, NR2A, and NR2B) and related signaling molecules (Ca2+/calmodulin-dependent kinase II gamma and phosphorylated cAMP-response element binding protein) were examined. CONCLUSION: 30 mW/cm2 microwave exposure resulted in alterations of synaptic structure, amino acid neurotransmitter release and calcium influx. NMDAR signaling molecules were closely associated with impaired synaptic plasticity.

Where are we in the modelling of traumatic brain injury? Models complicated by secondary brain insults.

BACKGROUND: Traumatic brain injury (TBI) contributes to a substantial number of deaths and cases of disability. Despite well-established experimental models and years of carefully conducted research, a clinical therapeutic breakthrough in TBI has lagged. This may be due, in part, to the discrepancies between commonly used experimental models and clinical scenarios. METHOD: Secondary insults, such as hypotension and hypoxemia, have been well demonstrated as powerful determinants of outcomes from TBI. Despite the frequency of secondary insults in patients with TBI, they are rarely incorporated into most existing models of TBI. This review focuses on the combined injury models, especially coupled with systemic secondary insults, and aims to provide a new view to guiding future research endeavors in this field. RESULTS: A growing number of experimental models of TBI complicated by certain secondary insult have been gradually introduced and characterized. Correspondingly, the pathophysiological changes following combined injuries and the interactive effects of primary injury with secondary insults can be studied more in-depth. CONCLUSION: A more complete understanding of the interactions between the injured brain and secondary insults represents a potentially fruitful avenue that may increase the likelihood of developing effective therapies. Experimental models of TBI should not only attempt to model the focal or diffuse changes resulting from external forces, but also integrate, when appropriate, secondary insults reminiscent of human situations.