Recycling solar-grade silicon from end-of-life photovoltaic modules by Al-Si solvent refining.

The development of the solar market has been fast in the past decades, and the number of photovoltaic module installations is large. The photovoltaic modules have a lifetime of about 25 years and need recovery after that. The aluminium-back surface field (Al-BSF) module is the first kind of large-scale installed module and will come to its end of life in the next few years. The recycling of silicon material in the Al-BSF module is investigated in this work. The components of the module are separated, and the silicon material in the module is collected and then purified by (aluminium-silicon) Al-Si solvent refining for reuse. It is found that Al-Si solvent refining removed key impurity elements, namely boron and phosphorus, in the collected silicon. Kinetics has a great effect on boron and phosphorus removal, and boron and phosphorus contents in purified silicon decrease with decreasing cooling rate. The boron and phosphorus contents in silicon are lowered to 0.28 and 0.03 ppmw, respectively, after two times of Al-Si solvent refining with the cooling rate of 5.55 * 10-4 K second-1, and it meets the requirement of solar-grade silicon.

In vivo imaging reveals that pregabalin inhibits cortical spreading depression and propagation to subcortical brain structures.

Migraine is characterized by severe headaches that can be preceded by an aura likely caused by cortical spreading depression (SD). The antiepileptic pregabalin (Lyrica) shows clinical promise for migraine therapy, although its efficacy and mechanism of action are unclear. As detected by diffusion-weighted MRI (DW-MRI) in wild-type (WT) mice, the acute systemic administration of pregabalin increased the threshold for SD initiation in vivo. In familial hemiplegic migraine type 1 mutant mice expressing human mutations (R192Q and S218L) in the CaV2.1 (P/Q-type) calcium channel subunit, pregabalin slowed the speed of SD propagation in vivo. Acute systemic administration of pregabalin in vivo also selectively prevented the migration of SD into subcortical striatal and hippocampal regions in the R192Q strain that exhibits a milder phenotype and gain of CaV2.1 channel function. At the cellular level, pregabalin inhibited glutamatergic synaptic transmission differentially in WT, R192Q, and S218L mice. The study describes a DW-MRI analysis method for tracking the progression of SD and provides support and a mechanism of action for pregabalin as a possible effective therapy in the treatment of migraine.

Statistical properties of the rovibrational bound levels for Ar2Kr.

We calculate the rovibrational bound levels with total angular momentum J = 0, 1 of 40Ar284Kr trimer using the slow variable discretization method combined with the finite-element method-discrete variable representation basis. The statistical distributions of the rovibrational levels for JΠ=0e, 1e, and 1o symmetries are presented and the effects of the Axilrod-Teller potential term are considered. For the 0e and 1e symmetries, the Axilrod-Teller term makes the spectra become fully chaotic. However, for the 1o symmetry, statistical properties depend mainly on the coupling between K = 0 and K = 1 and the Axilrod-Teller term has a small effect.

Smart nanocomposite hydrogels based on azo crosslinked graphene oxide for oral colon-specific drug delivery.

A safe and efficient nanocomposite hydrogel for colon cancer drug delivery was synthesized using pH-sensitive and biocompatible graphene oxide (GO) containing azoaromatic crosslinks as well as poly (vinyl alcohol) (PVA) (GO-N=N-GO/PVA composite hydrogels). Curcumin (CUR), an anti-cancer drug, was encapsulated successfully into the hydrogel through a freezing and thawing process. Fourier transform infrared spectroscopy, scanning electron microscopy and Raman spectroscopy were performed to confirm the formation and morphological properties of the nanocomposite hydrogel. The hydrogels exhibited good swelling properties in a pH-sensitive manner. Drug release studies under conditions mimicking stomach to colon transit have shown that the drug was protected from being released completely into the physiological environment of the stomach and small intestine. In vivo imaging analysis, pharmacokinetics and a distribution of the gastrointestinal tract experiment were systematically studied and evaluated as colon-specific drug delivery systems. All the results demonstrated that GO-N=N-GO/PVA composite hydrogels could protect CUR well while passing through the stomach and small intestine to the proximal colon, and enhance the colon-targeting ability and residence time in the colon site. Therefore, CUR loaded GO-N=N-GO/PVA composite hydrogels might potentially provide a theoretical basis for the treatment of colon cancer with high efficiency and low toxicity.

Hyperspherical coupled channel calculations of energy and structure of (4)He-(4)He-Li(+) and its isotopic combinations.

The ground state vibrational energy and spatial features of (4)He-(4)He-Li(+) and its triatomic isotopic complexes are studied using the slow variable discretization (SVD) method in the hyperspherical coordinates for the zero total angular momentum. Our results show that the dominant structure of the system is an isosceles triangle with the shorter side associated with the two Li(+)-He distances using the sum-of-potential approximation. Corrections caused by the induced dipole-induced dipole interactions on the He atoms are also investigated. The effects are seen to be small and have a minor influence on the binding energy and the structure of present system. The results are also compared with the full ab initio calculations including all the three-body interactions and information of three-body corrections is obtained.

The weakly bound states and resonances of the BeHe2 triatomic system.

In the present study, we carry out a full search of the bound states and resonances of the He(2)Be triatomic system, with its isotopic variants (3)He(2)(9)Be, (3)He(4)He(9)Be, and (4)He(2)(9)Be using the hyperspherical method. Three-body long-range effects are also included in the computation by adding to the additive potential the Axilrod-Teller triple-dipole term. In addition, the possibility of the occurrence of Efimov-type states in these systems is discussed. We have found a bound state for each of the (3)He(2)(9)Be and (3)He(4)He(9)Be trimers, while one weakly bound excited state is also found to exist for the (4)He(2)(9)Be system.

Enhanced contextual fear memory in central serotonin-deficient mice.

Central serotonin (5-HT) dysregulation contributes to the susceptibility for mental disorders, including depression, anxiety, and posttraumatic stress disorder, and learning and memory deficits. We report that the formation of hippocampus-dependent spatial memory is compromised, but the acquisition and retrieval of contextual fear memory are enhanced, in central 5-HT-deficient mice. Genetic deletion of serotonin in the brain was achieved by inactivating Lmx1b selectively in the raphe nuclei of the brainstem, resulting in a near-complete loss of 5-HT throughout the brain. These 5-HT-deficient mice exhibited no gross abnormality in brain structures and had normal locomotor activity. Spatial learning in the Morris water maze was unaffected, but the retrieval of spatial memory was impaired. In contrast, contextual fear learning and memory induced by foot-shock conditioning was markedly enhanced, but this enhancement could be prevented by intracerebroventricular administration of 5-HT. Foot shock impaired long-term potentiation and facilitated long-term depression in hippocampal slices in WT mice but had no effect in 5-HT-deficient mice. Furthermore, bath application of 5-HT in 5-HT-deficient mice restored foot shock-induced alterations of hippocampal synaptic plasticity. Thus, central 5-HT regulates hippocampus-dependent contextual fear memory, and 5-HT modulation of hippocampal synaptic plasticity may be the underlying mechanism. The enhanced fear memory in 5-HT-deficient mice supports the notion that 5-HT deficiency confers susceptibility to posttraumatic stress disorder in humans.

Opioid withdrawal for 4 days prevents synaptic depression induced by low dose of morphine or naloxone in rat hippocampal CA1 area in vivo.

The formation of memory is believed to depend on experience- or activity-dependent synaptic plasticity, which is exquisitely sensitive to psychological stress since inescapable stress impairs long-term potentiation (LTP) but facilitates long-term depression (LTD). Our recent studies demonstrated that 4 days of opioid withdrawal enables maximal extents of both hippocampal LTP and drug-reinforced behavior; while elevated-platform stress enables these phenomena at 18 h of opioid withdrawal. Here, we examined the effects of low dose of morphine (0.5 mg kg(-1), i.p.) or the opioid receptor antagonist naloxone (1 mg kg(-1), i.p.) on synaptic efficacy in the hippocampal CA1 region of anesthetized rats. A form of synaptic depression was induced by low dose of morphine or naloxone in rats after 18 h but not 4 days of opioid withdrawal. This synaptic depression was dependent on both N-methyl-D-aspartate receptor and synaptic activity, similar to the hippocampal long-term depression induced by low frequency stimulation. Elevated-platform stress given 2 h before experiment prevented the synaptic depression at 18 h of opioid withdrawal; in contrast, the glucocorticoid receptor (GR) antagonist RU38486 treatment (20 mg kg(-1), s.c., twice per day for first 3 days of withdrawal), or a high dose of morphine reexposure (15 mg kg(-1), s.c., 12 h before experiment), enabled the synaptic depression on 4 days of opioid withdrawal. This temporal shift of synaptic depression by stress or GR blockade supplements our previous findings of potentially correlated temporal shifts of LTP induction and drug-reinforced behavior during opioid withdrawal. Our results therefore support the idea that stress experience during opioid withdrawal may modify hippocampal synaptic plasticity and play important roles in drug-associated memory. (c) 2009 Wiley-Liss, Inc.

Effects of prolonged exposure to context following contextual fear conditioning on synaptic properties in rat hippocampal slices.

Acute stressful events enhance plasma corticosterone release and profoundly affect synaptic functions, which are involved in the development of stress-related cognitive and mental disorders. However, how exposure to stressful context immediately after stress further modulates the physiological responses is not fully understood. Here, we found that acute stress inhibited paired-pulse facilitation in hippocampal slices of Wistar rats which were subjected to contextual fear conditioning. But such inhibition was reversed by subsequent prolonged exposure to foot-shock context or returning to home cage for 1 h. Interestingly, foot-shock stress-facilitated LTD induced by low frequency stimulation (LFS, 900 pulses at 1 Hz) was maintained by subsequent exposure to foot-shock context but was reversed by returning to home cage environment. Moreover, plasma corticosterone level was still kept higher in rats exposed to foot-shock context but not to home cage. Findings suggest that remaining in stressful environment immediately after stress maintains acute stress-facilitated LTD and higher level of neuroendocrine response. Our results also contribute to further understanding the critical role of timely intervention in mediating stress-related aversive changes in human.

Morphine withdrawal affects both delayed-escape behaviour in Morris water maze and hippocampal NR2A/2B expression ratio.

Repeated low-dose morphine treatment facilitates delayed-escape behaviour of hippocampus-dependent Morris water maze and morphine withdrawal influences hippocampal NMDA receptor-dependent synaptic plasticity. Here, we examined whether and how morphine withdrawal influenced delayed-escape behaviour and NR2A/2B expression ratio of hippocampal synaptosomes. We found that both delayed-escape behaviour and NR2A/2B expression ratio showed an inverted-U curve and peaked on 4-day withdrawal during a 20-day withdrawal period. Furthermore, treatment of the glucocorticoid receptor antagonist RU38486 for 3 days reduced delayed-escape behaviour and NR2A/2B ratio on 4-day withdrawal to a level similar to those of 18-h withdrawal. In contrast, elevated-platform stress enabled delayed-escape behaviour of 18-h withdrawal to a higher level similar to that of 4-day withdrawal, but had no significant effect on the NR2A/2B ratio. Similar behavioural effects were also found after intrahippocampal infusions of the NMDAR antagonist AP-5 or NR2B-containing NMDAR antagonist Ro25-6981 for 3 days. These findings suggest that delayed-escape behaviour enabled by repeated low-dose morphine treatment may be a useful and simple rat model for studying addictive memories to be retrieved by stress exposure.

Binding energy and geometry of e+ A (A=Li,Na) by the hyperspherical approach.

We calculate the binding energy and geometry of the weakly bound e(+)Li and e(+)Na systems within the framework of hyperspherical coordinates. The Schrodinger equation in hyperangular coordinates is solved at a series of fixed hyper-radii using B-splines and the resulting coupled hyper-radial equation is solved using the slow variable discretization method developed by Tolstikhin et al. [J. Phys. B 29, L389 (1996)]. Great efforts are made in optimizing the distribution of B-splines to overcome the slow convergence of the binding energy and geometrical quantities. This approach allows us to obtain the results with improved convergence that are in good agreement with the best values reported to date. In addition, an analysis of the structure of the two systems is also made and the e(+)Na system is seen to exhibit quantum halo features.

Inhibition of AMPAR endocytosis alleviates pentobarbital-induced spatial memory deficits and synaptic depression.

Our previous study has shown that pentobarbital causes memory deficits and impairs hippocampal synaptic plasticity. The Tat-GluA23Y peptide (GluA23Y) prevents activity-dependent α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) endocytosis. It enables early-phase long-term potentiation (LTP) to proceed to late-phase LTP allowing short-term memory to convert to long-term memory. The purpose of this study is to explore the potential effects of GluA23Y on pentobarbital-induced memory deficits through behavioral and electrophysiological paradigms. We found that in vivo intrahippocampal infusion of GluA23Y (100µM, 1µl per hippocampus) 30min prior to pentobarbital administration (8mM, 1µl per hippocampus) significantly rescued the pentobarbital-induced deficit of memory retrieval in rats during the Morris water maze test. Pre-incubation of GluA23Y (10µM) partially rescued bath application of pentobarbital-induced synaptic transmission of the CA3-CA1 pathway in hippocampal slices. More importantly, GluA23Y selectively upregulated the synaptic GluA2 expression that was suppressed by pentobarbital. Together, these results suggest that inhibition of GluA2-containing AMPAR endocytosis by GluA23Y increases the pentobarbital-suppressed basal synaptic transmission by upregulating the synaptic GluA2, and then subsequently alleviates spatial memory deficits. Therefore, inhibition of AMPAR endocytosis may be a potential therapeutic way to treat memory disorders caused by anesthetics.

Facilitated AMPAR endocytosis causally contributes to the maternal sleep deprivation-induced impairments of synaptic plasticity and cognition in the offspring rats.

Maternal sleep deprivation (MSD) has been suggested to be associated with increased frequency of neurodevelopmental disorders in offspring in both humans and animal models. However, the underlying cellular and molecular mechanism is still unclear. We have recently reported that MSD at different stages of pregnancy impairs the emotional and cognitive functions, and suppresses hippocampal CA1 long-term potentiation (LTP) in the offspring rats. Here, we report that the MSD induced LTP impairment at the CA1 hippocampus of the offspring rats is associated with increased long-term depression (LTD) and reduced expression of postsynaptic GluA2-containing α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs). Importantly, we found that inhibition of AMPAR endocytosis by a synthetic peptide Tat-GluA23Y (3 µmol/kg, i.p.) not only increased level of AMPARs and reduced LTD, but also restored LTP. Moreover, treatment with Tat-GluA23Y peptide markedly alleviated the MSD-induced impairments of spatial learning and memory; and decreased depressive- and anxiety-like behaviors in the offspring. Together, our findings suggest that the MSD-induced postsynaptic AMPAR endocytosis causally contributes to the impairments of hippocampal synaptic plasticity, thereby disrupting the emotional and cognitive functions in the offspring.

Exposure to chronic constant light impairs spatial memory and influences long-term depression in rats.

Exposure to chronic constant light (CCL) influences circadian rhythms and evokes stress. Since hippocampus is sensitive to stress, which facilitates long-term depression (LTD) in the hippocampal CA1 area, we examined whether CCL exposure influenced hippocampus-dependent spatial memory and synaptic plasticity in Wistar rats. Here we report that CCL exposure (3 weeks) disrupted 24-h cycle of locomotion activity in open field test. These rats showed shorter escape latency during initial phase of spatial learning but impaired hippocampus-dependent spatial memory without affecting the visual platform learning task in Morris water maze (MWM) compared with control rats. This effect may be due to stress adaptation as reflected by reduced thigmotaxis and anxiety-like behaviors in CCL rats. Moreover, in CA1 area of the hippocampal slices, CCL rats failed to show LTD by low frequency stimulation (LFS, 900 pulses, 1 Hz), while showed decreased short-term depression compared with control rats indicating the induction of LTD was influenced by CCL exposure. Furthermore, additional acute stress enabled LFS to induce LTD in control rats but not in CCL rats. Thus, these results suggested that CCL exposure impaired spatial memory and influenced hippocampal LTD, which may be due to stress adaptation.

[Influencing Factors on the Degradation of PFOS Through VUV-SO32].

The objective of this experiment was to investigate the influence of SO32-dosage, pH value, initial perfluorooctane sulfonate(PFOS)concentration as well as coexisting substances on the degradation and defluorination of PFOS by VUV-SO32- process. The results indicated that the increase of SO32- dosage could lead to rise in the concentration of active species hydrated electron(eaq-) and thus enhance the degradation and defluorination of PFOS. As the concentration of SO32- increased from 1 mmol·L-1 to 20 mmol·L-1, the degradation and defluorination rates of PFOS increased from 45% and 40% to 97% and 63%, respectively. The degradation and defluorination of PFOS were also enhanced with the increment of the solution pH values, and the defluorination was more sensitive to the pH values. In addition, more PFOS was degraded with the increase of initial PFOS mass concentration, although the degradation and defluorination rates of PFOS were reduced. When the initial PFOS mass concentration changed from 1 mg·L-1 to 50 mg·L-1, the degradation amount of PFOS after four hrs increased by about 50 times, probably due to the higher utilization proportion of eaq- at high pollutants concentration. Last but not least, the influence of co-existing substances, Cl- and HCO3-, on PFOS degradation could be neglected, whereas their effects on defluorination were observed. Defluorination of PFOS was enhanced with the increased Cl- concentration, however, increased first and then decreased with the increment of HCO3- concentration. It was also found that the presence of humic acid(HA) lowered degradation as well as defluorination of PFOS owing to the blockage of effective UV light and trapping of active species for photochemical reaction.

Hydrated electron based decomposition of perfluorooctane sulfonate (PFOS) in the VUV/sulfite system.

As one of the most reactive species, hydrated electron (eaq-) is promising for reductive decomposition of recalcitrant organic pollutants, such as perfluorooctane sulfonate (PFOS). In this study, PFOS decomposition using a vacuum ultraviolet (VUV)/sulfite system was systematically investigated in comparison with sole VUV and ultraviolet (UV)/sulfite systems. A fast and nearly complete (97.3%) PFOS decomposition was observed within 4h from its initial concentration of 37.2µM in the VUV/sulfite system. The observed rate constant (kobs) for PFOS decomposition in the studied system was 0.87±0.0060h-1, which was nearly 7.5 and 2 folds faster than that in sole VUV and UV/sulfite systems, respectively. Compared to previously studied UV/sulfite system, VUV/sulfite system enhanced PFOS decomposition in both weak acidic and alkaline pH conditions. In weak acidic condition (pH6.0), PFOS predominantly decomposed via direct VUV photolysis, whereas in alkaline condition (pH>9.0), PFOS decomposition was mainly induced by eaq- generated from both sulfite and VUV photolytic reactions. At a fixed initial solution pH (pH10.0), PFOS decomposition kinetics showed a positive linear dependence with sulfite dosage. The co-presence of humic acid (HA) and NO3- obviously suppressed PFOS decomposition, whereas HCO3- showed marginal inhibition. A few amount of short chain perfluorocarboxylic acids (PFCAs) were detected in PFOS decomposition process, and a high defluorination efficiency (75.4%) was achieved. These results suggested most fluorine atoms in PFOS molecule ultimately mineralized into fluoride ions, and the mechanisms for PFOS decomposition in the VUV/sulfite system were proposed.

Capsaicin Attenuates Amyloid-ß-Induced Synapse Loss and Cognitive Impairments in Mice.

Alzheimer's disease (AD) is the most common cause of progressive cognitive impairment in the aged. The aggregation of the amyloid ß-protein (Aß) is a hallmark of AD and is linked to synapse loss and cognitive impairment. Capsaicin, a specific agonist of the transient receptor potential vanilloid 1 (TRPV1), has been proven to ameliorate stress-induced AD-like pathological and cognitive impairments, but it is unclear whether TRPV1 activation can affect cognitive and synaptic functions in Aß-induced mouse model of AD. In this study, we investigated the effects of TRPV1 activation on spatial memory and synaptic plasticity in mice treated with Aß. To induce AD-like pathological and cognitive impairments, adult C57Bl/6 mice were microinjected with Aß42 (100 µM, 2.5 µl/mouse, i.c.v.). Two weeks after Aß42 microinjection, spatial learning and memory as well as hippocampal long-term potentiation (LTP) were examined. The results showed that Aß42 microinjection significantly impaired spatial learning and memory in the Morris water maze and novel object recognition tests compared with controls. These behavioral changes were accompanied by synapse loss and impaired LTP in the CA1 area of hippocampus. More importantly, daily capsaicin (1 mg/kg, i.p.) treatment throughout the experiment dramatically improved spatial learning and memory and synaptic function, as reflected by enhanced hippocampal LTP and reduced synapse loss, whereas the TRPV1 antagonist capsazepine (1 mg/kg, i.p.) treatment had no effects on cognitive and synaptic function in Aß42-treated mice. These results indicate that TRPV1 activation by capsaicin rescues cognitive deficit in the Aß42-induced mouse model of AD both structurely and functionally.

Acute behavioural stress facilitates long-term depression in temporoammonic-CA1 pathway.

Behavioural stress facilitates long-term depression in Schaffer collaterals-CA1 pathway, but it is unknown whether it influences long-term depression in temporoammonic fibres-CA1. Here, we report that low-frequency stimulation induced long-term depression and foot shock stress before slice preparation facilitated long-term depression in both pathways of young rat slices. When the field excitatory postsynaptic potentials were recorded by stimulating the two pathways alternately and low-frequency stimulation was given to the two pathways simultaneously, a reliable long-term depression was induced in Schaffer collaterals-CA1 but a reliable long-term potentiation took place in temporoammonic fibres-CA1. Interestingly, foot shock stress now enabled low-frequency stimulation to induce reliable long-term depressions in both pathways. These findings suggested that acute behavioural stress facilitated long-term depressions in both pathways and disrupted the interactions between pathways.

Enriched environment experience overcomes the memory deficits and depressive-like behavior induced by early life stress.

Stress in early life is believed to cause cognitive and affective disorders, and to disrupt hippocampal synaptic plasticity in adolescence into adult, but it is unclear whether exposure to enriched environment (EE) can overcome these effects. Here, we reported that housing rats in cages with limited nesting/bedding materials on postnatal days 2-21 reduced body weight gain, and this type of early life stress impaired spatial learning and memory of the Morris water maze and increased depressive-like behavior of the forced swim test in young adult rats (postnatal days 53-57). Early life stress also impaired long-term potentiation in hippocampal CA1 area of slices of young adult rats. Remarkably, EE experience on postnatal days 22-52 had no effect on spatial learning/memory and depressive-like behavior, but it significantly facilitated LTP in control rats, and completely overcame the effects of early life stress on young adult rats. These findings suggest that EE experience may be useful for clinical intervention in preventing cognitive and affective disorders during development.

GABA(A) Receptors in the Central Nucleus of the Amygdala Are Involved in Pain- and Itch-Related Responses.

UNLABELLED: Itch and pain are unpleasant sensations that distress many patients with disease. However, most studies have focused on the neural mechanisms of pain, and much less effort has been devoted to itch. It has been reported that itch and pain might share a common pathway, and γ-aminobutyric acid type A (GABA(A)) receptors in the central nucleus of the amygdala (CeA) are involved in pain modulation. However, the contribution of GABAA receptors in the CeA to the modulation of itch remains poorly understood. Herein, we report that bilateral intra-CeA microinjection of a selective GABAA receptor agonist muscimol hydrochloride (Mus; 50 ng per side), but not a selective GABAA receptor antagonist bicuculline (Bic; 20 ng per side) or vehicle, showed significant analgesic effects, reflected by an increase in tail-flick latency and a decrease in allyl isothiocyanate (mustard oil)-evoked ipsilateral forelimb wipes. More importantly, rats subjected to intra-CeA infusion of Bic showed a significantly greater number of scratching bouts and time in acute and chronic pruritus animal models than control rats. Conversely, intra-CeA infusion of Mus in animal models dramatically decreased the number of scratching bouts and time compared with control rats. In addition, intra-CeA infusion of Bic or Mus at the current dose had no obvious effects on other behaviors including locomotor activity and spontaneous facial grooming in rats subjected to cheek microinjection of 5-hydroxytryptamine. Taken together, these results indicate that the GABA(A) receptor-mediated inhibitory system in the CeA is involved in itch modulation as well as is known in pain control. PERSPECTIVE: Itch, especially chronic itch, remains a challenge in clinic. Results of this study showed that the GABAA receptors in the CeA play an important role in itch modulation, which might help us to better understand the mechanisms of itch and subsequently develop novel mechanisms-based strategies to treat chronic itch in clinic.