Insights into an Amorphous NiCoB Nanoparticle-Catalyzed MgH2 System for Hydrogen Storage.

In the paper, we synthesized amorphous NiCoB nanoparticles by a simple chemical reduction method and employed them as high-activity catalysts to considerably improve the hydrogen storage properties of MgH2. The MgH2-NiCoB composite quickly absorbed 3.6 wt % H2 at a low temperature of 85 °C and released 5.5 wt % H2 below 270 °C within 600 s. It is worth noting that the hydrogenation activation energy was reduced to 33.0 kJ·mol-1. Detailed microstructure analysis reveals that MgB2, Mg2Ni/Mg2NiH4, and Mg2Co/Mg2CoH5 were in situ generated during the first de/absorption cycle and dispersed at the surface of NiCoB. These active ingredients created lots of boundary interfaces to facilitate the hydrogen diffusion and destabilize the Mg-H bonds, thus decreasing the kinetic barriers. This work provides support for a promising catalytic effect of amorphous NiCoB on de/absorption reactions of MgH2, showing new ways for designing Mg-based hydrogen storage systems toward practical application.

Enhanced hydrogen storage kinetics of MgH2 by the synergistic effect of Mn3O4/ZrO2 nanoparticles.

As an ideal material for solid-state hydrogen storage, magnesium hydride (MgH2) has attracted enormous attention due to its cost-effectiveness, abundant resources, and outstanding reversibility. However, the high thermodynamics and poor kinetics of MgH2 still hinder its practical application. In this work, a simple stirring-hydrothermal method was used to successfully prepare bimetallic Mn3O4/ZrO2 nanoparticles, which were subsequently doped into MgH2 by mechanical ball milling to improve its hydrogen sorption performance. The MgH2 + 10 wt% Mn3O4/ZrO2 composite began discharging hydrogen at 219 °C, which was 111 °C lower compared to the as-synthesized MgH2. At 250 °C, the MgH2 + 10 wt% Mn3O4/ZrO2 composite released 6.4 wt% hydrogen within 10 min, whereas the as-synthesized MgH2 reluctantly released 1.4 wt% hydrogen even at 335 °C. Moreover, the dehydrogenated MgH2 + 10 wt% Mn3O4/ZrO2 sample started to charge hydrogen at room temperature. 6.0 wt% hydrogen was absorbed when heated to 250 °C under 3 MPa H2 pressure, and 4.1 wt% hydrogen was taken up within 30 min at 100 °C at the same hydrogen pressure. In addition, compared with the as-synthesized MgH2, the de/rehydrogenation activation energy values of the MgH2 + 10 wt% Mn3O4/ZrO2 composite were decreased to 64.52 ± 13.14 kJ mol-1 and 16.79 ± 4.57 kJ mol-1, respectively, which incredibly contributed to the enhanced hydrogen de/absorption properties of MgH2.

Constructing Mg2Co-Mg2CoH5 nano hydrogen pumps from LiCoO2 nanosheets for boosting the hydrogen storage property of MgH2.

Herein, an active positive electrode material, LiCoO2 nanosheets, was synthesized via a two-step method, which demonstrated a remarkable catalytic effect for the hydrogen storage property of MgH2. Incorporated with LiCoO2 nanosheets, MgH2 started to release hydrogen at 180 °C and a desorption content as high as 5.5 wt% H2 was attained within 60 min at 250 °C. The dehydrogenation activation energy was significantly decreased to 48.5 ± 0.4 kJ mol-1, achieving a 68.9% reduction compared to MgH2. It was verified by microstructural studies that Li+ served as an "anchor" to facilitate a uniform distribution of LiCoO2 "boat" among the MgH2 "ocean", benefitting the self-assembly of numerous Mg2Co-Mg2CoH5 couples on the surface of MgH2 during the cycling process. Meanwhile, the in situ formed Mg2Co-Mg2CoH5 couples were not restricted to offering multiple channels for fast hydrogen diffusion but also worked as "nano hydrogen pumps" to accelerate Mg/MgH2 hydrogen charging and discharging. This study provides an interesting example of effective cooperation between Li+ and Co3+ on improving the catalytic action toward MgH2. It shall shed light on efficient designing of high-efficient catalysts in hydrogen storage areas or other energy-related fields.

Potential of D-cycloserine in the treatment of behavioral and neuroinflammatory disorders in Parkinson's disease and studies that need to be performed before clinical trials.

Hyperactivation of glutamatergic N-methyl-D-aspartate (NMDA) receptors has been implicated in the excitotoxicity and pathophysiology of Parkinson's disease (PD). NMDA receptor blockers have been used clinically to treat dementia, but their efficacy is controversial. Modulation of NMDA receptors might improve neuroinflammation and cognitive deficits in PD. D-cycloserine (DCS), a partial agonist binding to the glycine binding site of NMDA receptors, has been demonstrated to improve cognitive function in primates and rodents. Our previous study showed that DCS can reduce motor, emotional, and cognitive dysfunctions, as well as neuroinflammation and neurodegeneration in a PD animal model and may therefore have potential for the treatment of neuroinflammation and cognitive dysfunction in patients with PD. In addition, increased expression of cyclooxygenase type-2 (COX-2) has been observed in dopaminergic neurons and activated microglia in the brain of both PD patients and PD animal models. COX-2 inhibitors can suppress activation of microglia and protect dopaminergic neurons from degeneration. Thus, a combination of DCS and COX-2 inhibitors might prove useful in suppressing neuroinflammation and cognitive deficits in PD.

Effects of MK-801 on recognition and neurodegeneration in an MPTP-induced Parkinson's rat model.

Several years after the diagnosis of Parkinson's disease (PD), 20-30% of PD patients develop dementia, known as Parkinson's disease dementia (PDD), the features of which include impairment of short-term memory and recognition function. Hyperactivation of the glutamatergic system is implicated in the neurodegeneration seen in PD. The aim of this study was to determine the effects of MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist, on short-term memory and object recognition in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD rat animal model. MPTP was injected stereotaxically into the substantia nigra pars compacta (SNc) of male Wistar rats, then, starting 1 day later (day 1), the rats were injected daily with MK-801 (0.2 mg/kg/day, i.p.) and rats underwent a bar test on days 1-7, a T-maze test on days 8-10, and object recognition test on days 12-14. On day 1, the animals showed motor dysfunction, which recovered to control levels on day 7. MPTP-lesioned rats showed impairment of working memory in the T-maze test and of recognition in the object recognition test, both of which were prevented by MK-801 treatment. Furthermore, MPTP lesion-induced dopaminergic degeneration in the nigrostriatal system, microglial activation in the SNc, and cell loss in the hippocampal CA1 area were all improved by MK-801 treatment. These results suggest that NMDA receptors are involved in PD-related neuronal and behavioral dysfunction.

Blockade of metabotropic glutamate receptors inhibits cognition and neurodegeneration in an MPTP-induced Parkinson's disease rat model.

Hyperactivity of the glutamatergic system is involved in excitotoxicity and neurodegeneration in Parkinson's disease (PD). Metabotropic glutamate receptor subtype 5 (mGluR5) modulates glutamatergic transmission and thus has been proposed as a potential target for neuroprotective drugs. The aim of this study was to determine the effects of 2-methyl-6-(phenylethynyl)-pyridine (MPEP), an mGluR5 antagonist, on working memory, object recognition, and neurodegeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD rat model. Male Wistar rats were stereotaxically injected with MPTP into the substantia nigra pars compacta (SNc). Starting 1 day after lesioning (day 1), the rats were treated daily with MPEP (2mg/kg/day, i.p.) for 14 days and rats underwent a T-maze test on days 8-10 and an object recognition test on days 12-14. MPTP-lesioned rats showed impairments of working memory in the T-maze test and of recognition function in the object recognition test and both effects were prevented by MPEP treatment. Furthermore, MPTP lesion-induced dopaminergic degeneration in the nigrostriatal system, microglial activation in the SNc, and cell loss in the hippocampal CA1 area were all inhibited by MPEP treatment. These data provide support for a role of mGluR5s in the pathophysiology of PD and suggest that MPEP is a promising pharmacological tool for the development of new treatments for dementia associated with PD.