Stacking-Engineered Heterostructures in Transition Metal Dichalcogenides.

The layer-by-layer assembly of 2D transition metal dichalcogenide monolayer blocks to form a 3D stack, with a precisely chosen sequence/angle, is the newest development for these materials. In this way, one can create "van der Waals heterostructures (HSs)," opening up a new realm of materials engineering and novel devices with designed functionalities. Herein, a detailed systematic review of transition metal dichalcogenide stacking-engineered heterostructures, from controllable fabrication to typical characterization, and stacking-correlated physical behaviors is presented. Furthermore, recent advances in stacking design, such as stacking sequence, twist angles, and moiré superlattice heterojunctions, are also comprehensively summarized. Finally, the remaining challenges and possible strategies for using stacking engineering to tune the properties of 2D materials are also outlined.

Recent advances of small molecule fluorescent probes for distinguishing monoamine oxidase-A and monoamine oxidase-B in vitro and in vivo.

Monoamine oxidases (MAO-A and MAO-B) are the two flavin adenine dinucleotide (FAD) enzymes that play an important role in neurotransmitter homeostasis and in protection against biogenic amines. The two MAO enzymes are related to various diseases such as neurological disorders, cancer or other systemic diseases. It is crucial to distinguish these two subtypes in order to explore the pathogenesis and pathophysiology of different diseases. In this review, the relationship between MAOs and related diseases is briefly introduced. Additionally, we summarize the recent advances in small molecule fluorescent probes for specific detection of MAO-A and MAO-B.

Superior effect of hypertonic saline over mannitol to attenuate cerebral edema in a rabbit bacterial meningitis model.

OBJECTIVE: Adjunctive therapies that reduce the cerebral edema in bacterial meningitis include osmotic agents. There is a lack of information comparing mannitol vs. hypertonic saline as an osmotic agent for adjunctive therapy of bacterial meningitis. We attempted to elucidate the impact of hypertonic saline in cerebral edema in the setting of bacterial meningitis as well as to explore potential mechanisms of action. DESIGN: Randomized controlled in vivo study. SETTING: University research laboratory. SUBJECTS: Rabbits. INTERVENTIONS: A rabbit model of bacterial meningitis was used comparing 3% hypertonic saline with 20% mannitol as adjunctive therapy. MEASUREMENTS AND MAIN RESULTS: Adjunctive 3% hypertonic saline treatment persistently elevated mean arterial pressure as compared with the model or ampicillin group (p < .01). Although both 20% mannitol and 3% hypertonic saline efficiently elevated serum osmolality for almost 5 hrs (p < .01), 20% mannitol lowered intracranial pressure for only a short time (<2 hrs) and did not elevate cerebral perfusion pressure. Three percent hypertonic saline treatment efficiently lowered intracranial pressure and elevated cerebral perfusion pressure for almost 5 hrs (p < .01). Furthermore, 3% hypertonic saline treatment efficiently elevated serum Na+ concentration for >5 hrs (p < .01). Three percent hypertonic saline treatment was superior to 20% mannitol in lowering leukocyte number and protein content in cerebrospinal fluid (p < .01). Three percent hypertonic saline treatment reduced water content and Evans blue incorporation in the brain (p < .01). Three percent hypertonic saline treatment inhibited aquaporin 4 expression (p < .01) and attenuated pathologic brain damage more efficiently compared with adjuvant 20% mannitol treatment (p < .01). CONCLUSIONS: Adjunctive 3% hypertonic saline treatment significantly elevated mean arterial pressure, reduced intracranial pressure, greatly improved cerebral perfusion pressure, inhibited brain aquaporin 4 expression, reduced cerebral edema, and attenuated brain damage with a superior effect over 20% mannitol in a rabbit bacterial meningitis model.

Glutamate mediates hyperoxia-induced newborn rat lung injury through N-methyl-D-aspartate receptors.

Our laboratory found that the N-methyl-D-aspartate receptor (NMDAR) antagonist, MK-801, was able to decrease hyperoxia-induced lung damage. To further search for direct evidence of glutamate and its NMDARs participating in hyperoxia-induced lung injury, the amount of glutamate in the bronchoalveolar lavage fluid and the expression of NMDAR 2D in lung tissue were tracked in newborn rats that were exposed to 95% oxygen for 1, 3, and 7 days. The protective effect of MK-801 was then observed at different hyperoxia exposure times. As demonstrated by RT-PCR, NMDAR 2D expression was much higher in hyperoxia exposure on the third and the seventh days than in the air control group. The levels of glutamate in the bronchoalveolar lavage fluid on the first and third days of hyperoxia exposure were significantly higher than in the air control group. MK-801 alleviated lung injury and inflammatory reaction induced by 95% O(2) for 3 and 7 days. These results indicate that large amounts of endogenous glutamate from the lungs were released, and its NMDAR were expressed strongly under conditions of high oxygen concentration. We conclude that the endogenous glutamate mediated newborn rat lung damage induced by hyperoxia through NMDARs.