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BACKGROUND In china, the grade of phosphate ores has decreased fiercely in recent years. Existing solvents are low-efficient for the extraction of wet-process phosphoric acid produced by low-grade phosphate ores. Organic solvent dibutyl sulfoxide was developed to improve the extraction capacity of wet-process phosphoric acid, especially for the low-acid concentration. RESULTS The effects of extraction time, temperature, phosphoric acid concentration and impurities concentration on the extraction were investigated. The extraction process is exothermic and the enthalpy change is −5.86 kJ/mol. Dibutyl sulfoxide is relatively selective for Mg2+ and Al3+ while the selectivities of Fe3+, F− and SO42− are moderate. The liquid-liquid equilibrium of water-dibutyl sulfoxide-phosphoric acid system was determined at 298.15 K. The stability of dibutyl sulfoxide and the process flows of extraction, scrubbing and stripping were investigated. The extraction mechanism of dibutyl sulfoxide for phosphoric acid was proposed and the extracted complex H3PO4·0.3DBSO was obtained. CONCLUSION Dibutyl sulfoxide is demonstrated as powerful solvent for the extraction of wet-process phosphoric acid even at low-concentration. Dibutyl sulfoxide can be potential supplemental organic solvent for the extraction of wet-process phosphoric acid produced by low-grade phosphate ores.

Excessive extracellular glutamate leads to neuronal death in central nervous system. Excitatory glutamate transporter subtype 2 (GLT-1) carries bulk of glutamate reuptake in cerebral ischemia. Although GLT-1 expression fluctuates during the period of ischemia, little is known about its regulatory mechanism. Here we show an up-regulation of GLT-1 via mammalian target of rapamycin (mTOR)-Akt-nuclear factor-кB (NF-кB) signaling cascade in oxygen glucose deprivation (OGD). We found that brief rapamycin treatment significantly increased GLT-1 expression in cultured astrocytes. Rapamycin increased phosphorylation of raptor at Ser792 and decreased phosphorylation of rictor at Thr1135, suggesting that both mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) are involved in GLT-1 expression. This conclusion was further confirmed by raptor and rictor disruption experiments. Akt was activated by mTORC1 inhibition and required for GLT-1 expression because triciribine, a specific inhibitor of Akt, blocked the increase of GLT-1 expression. mTOR-Akt cascade then activated NF-кB and increased кB-motif-binding phosphoprotein (KBBP) expression and GLT-1 transcription. We next demonstrated that mTOR-Akt-NF-кB cascade was activated in OGD and subsequently caused the upregulation of GLT-1. Supporting evidence included: (1) inhibition of Akt or NF-кB occluded OGD-induced GLT-1 upregulation; (2) Raptor knock-down plus OGD did not add to the increase of GLT-1 expression; (3) Intact mTORC2 was required for GLT-1 enhancement. In summary, our data first showed that mTOR-Akt-NF-кB cascade played critical roles to up-regulate GLT-1 in OGD. This signaling cascade may work to promote glutamate uptake in brain ischemia and neurodegenerative diseases.

In order to purify phosphoric acid hemihydrate (H3PO4·0.5H2O) crystal further, the effects of sweating time and sweating temperature on purification are investigated in a dry-sweating process. Experimental results indicate the content of Mg, As, Sb and Pb in the H3PO4·0.5H2O crystal decreases with increasing sweating time and sweating temperature during sweating process and show the same tendency to decrease with time at different sweating temperatures. The purification rate coefficients of H3PO4·0.5H2O crystals for Mg, As, Sb and Pb are determined. They increase with an increase in sweating temperature. The Arrhenius equation can be successfully used to describe the relationship between the purification rate coefficient and the absolute sweating temperature. The activation energy of sweating for Mg, As, Sb and Pb in the H3PO4·0.5H2O crystal are calculated using these experimental data. These values for Mg, As, Sb and Pb are 130.13, 193.59, 98.51 and 102.29 kJ mol−1, respectively.

In order to purify phosphoric acid, the suspension melt crystallization process was studied. The suspension crystallization experiments were carried out with 80, 84 and 88 wt% phosphoric acid melt at the cooling rates of 0.05, 0.1 and 0.2 K/min, respectively. Sweating experiments were executed for various crystals obtained in suspension crystallization step. The purification effects of the sweating parameters including sweating time, initial inclusion amount and initial impurity content were studied. The inclusion fraction increases with the increase in cooling rate. The inclusion fraction of the crystals which were formed with feed concentration of 84 wt% phosphoric acid melt is lowest among the three feed concentrations. Different impurities have different purification performances during sweating. High inclusion amount and low impurity concentration favor the purification of H3PO4·0.5H2O crystals during sweating.

Niemann-Pick disease type C (NPC) is a progressive neurodegenerative disorder characterized by accumulation of free cholesterol in lysosomes, mainly due to a mutation in the NPC1 gene. The pathophysiological basis of the neural disorders in NPC, however, is not well understood. We found that the hippocampal field excitatory postsynaptic potential (fEPSP) was enhanced in NPC1 mutant mice. A1-receptor antagonist or adenosine degrading enzyme enhanced the fEPSP in both types of mice, but had a much weaker effect in the mutant mice, suggesting less tonic inhibition of synaptic transmission by endogenous adenosine in the mutant. Further evidence showed impaired hippocampal long term potentiation (LTP) in mutant mice. Supplement of A1 agonist N6-Cyclopentyladenosine (CPA) partially rescued the impaired LTP in mutant mice. Moreover, adenosine release from hippocampal slices was significantly decreased in the mutant. The enhanced excitatory synaptic transmission and the decreased synaptic plasticity due to the decreased adenosine release in NPC brain may partially contribute to the neural disorders of NPC disease, such as seizures, neurodegeneration, and dementia.

In this study, we investigated the effects of interleukin-2 (IL-2) on dendritic filopodia, dendritic arborization, and spine maturation during the development of cultured rat hippocampal neurons. The cultured hippocampal neurons were transfected with F-GFP (farnesylated enhanced green fluorescent protein) at DIV5 to display the subtle structure of dendrites, and were then treated with IL-2 at various concentrations for different time before living cell image observation. We found that both the dendritic arborization and the length of dendrites per neuron at DIV7, DIV10, and DIV14 were increased under IL-2 treatment in a dose-dependent manner, and the strongest IL-2 effects on both dendritic number and length were observed at DIV7. Also, there was a significant increase in the mobility of dendritic filopodia in neurons at DIV7 treated with 10 ng/mL IL-2 for 48 hr from DIV5. In addition, IL-2 caused an increase in spine density of neurons at DIV14 either treated with IL-2 from DIV5 to DIV7 or from DIV5 to DIV14, but did not affect neurons treated from DIV12 to DIV14. These results indicate that IL-2 affects the dendritic development and spinogenesis of cultured hippocampal neurons, especially during the early developmental stage. Anat Rec, 2010. © 2010 Wiley-Liss, Inc.

Using histamine and the H3 receptor antagonist thioperamide, the roles of histamine receptors in NMDA-induced necrosis were investigated in rat cultured cortical neurons. Within 3 h of intense NMDA insult, most neurons died by necrosis. Histamine reversed the neurotoxicity in a concentration-dependent manner and showed peak protection at a concentration of 10(-7) m. This protection was antagonized by the H2 receptor antagonists cimetidine and zolantidine but not by the H1 receptor antagonists pyrilamine and diphenhydramine. In addition, the selective H2 receptor agonist amthamine mimicked the protection by histamine. This action was prevented by cimetidine but not by pyrilamine. 8-Bromo-cAMP also mimicked the effect of histamine. In contrast, both the adenylyl cyclase inhibitor 9-(tetrahydro-2-furanyl)-9H-purine-6-amine and the cAMP-dependent protein kinase inhibitor N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinolinesulfonamide reversed the protection by histamine. Thioperamide also attenuated NMDA-induced excitotoxicity, which was reversed by the H3 receptor agonist (R)-alpha-methylhistamine but not by pyrilamine and cimetidine. In addition, the protection by thioperamide was inhibited by the GABA(A) receptor antagonists picrotoxin and bicuculline. Further study demonstrated that the protection by thioperamide was due to increased GABA release in NMDA-stimulated samples. These results indicate that not only the H2 receptor/cAMP/cAMP-dependent protein kinase pathway but also the H3 receptor/GABA release pathway can attenuate NMDA-induced neurotoxicity.

Stress impairs hippocampal long-term potentiation (LTP), but it is unknown whether the stress evoked by opiate withdrawal has the same effect. Here the authors report that opiate withdrawal for 4 days does not influence basal synaptic transmission, but results in a greatly increased LTP in hippocampal CA1 area in anesthetized rats. Elevated-platform stress enabled a large LTP in rats withdrawn for only 18 h, but the glucocorticoid receptor antagonist RU38486 (twice per day for 3 days) prevented the large LTP on 4 days withdrawal. Moreover, 4 days withdrawal enhanced the NMDAR-mediated EPSCs, in which the NR2A-containing NMDAR-mediated EPSC was increased but the NR2B-containing NMDAR-mediated EPSC was decreased. These results suggest that adaptive changes of the NMDAR and glucocorticoid receptor functions during 4 days of opiate withdrawal may enable stress to facilitate hippocampal LTP, potentially contributing to the opiate withdrawal experience-dependent modifications of hippocampal functions. (c) 2006 Wiley-Liss, Inc.

A polyclonal antibody for the NMDA receptor subunit NR2D has been developed that identifies an approximately 160-kDa band on immunoblots from NR2D transfected cells and CNS tissues. No cross-reactivity is seen with other NMDA receptor subunits. The NR2D receptor subunit is N-glycosylated in both brain and transfected cells. Transfected cells expressing NR2D are immunofluorescently labeled, whereas untransfected cells or cells transfected with other NMDA receptor subunit cDNAs are not. Similarly, the NR2D subunit is selectively and quantitatively immunoprecipitated, whereas the NR1, NR2A, or NR2B subunit is not. The relative densities of the NR2D subunit in nine areas of postnatal day 7 and adult rat brains have been determined by quantitative immunoblotting. NR2D was expressed at highest levels in the thalamus, midbrain, medulla, and spinal cord, whereas intermediate levels of this subunit were found in the cortex and hippocampus. Low or undetectable levels were seen in the olfactory bulb, striatum, and cerebellum. Following a peak after the first week of birth, NR2D protein levels decreased by about twofold in adulthood in all rat brain regions examined. More complete ontogenic profiles were determined for the diencephalon, telencephalon, and spinal cord where similar ontogenic patterns were seen. NR2D protein is present at high levels at embryonic stages of development, rises to a peak at postnatal day 7, and decreases but remains measurable during late postnatal life. This study demonstrates the generation and characterization of an antibody selective for the NR2D NMDA receptor subunit as well as a determination of the distribution and ontogenic profile of this subunit in rat brain. The results suggest that native NMDA receptors containing the NR2D subunit may have functional roles not only in the young brain but also in adult brain.