Fu Der Mai

Fabrication of porous TiO2 film on Ti foil by hydrothermal process and its photocatalytic efficiency and mechanisms with ethyl violet dye

Most of commercial dyes and pigments have rather complicated polyaromatic chemical structures with prolonged lifetime surviving in the Mother Nature. However, TiO(2) has been reported as one of the best photocatalytic candidates for degrading dye pollutants. In this report, TiO(2) film/Ti foil was prepared by hydrothermal reaction in alkali solution, the porous TiO(2) film with microcrystalline structure has been obtained. The porous structure of TiO(2) film was analyzed and characterized by XRD, FE-SEM and XPS. This is the first report that demonstrates that TiO(2) film/Ti foil has an excellent commercial application potential for photocatalytic degradation of Ethyl Violet (EV). Especially, because of refluxing at 100 degrees C, the porous TiO(2) film structure remained undisturbed, and EV decomposed in the period of 20 h. In addition, porous TiO(2)-mediated EV photo degradation mechanism has been proposed, as intermediates are isolated and clearly identified by GC-MS and HPLC-PDA-ESI-MS.

Sleep deprivation predisposes liver to oxidative stress and phospholipid damage: a quantitative molecular imaging study

Sleep disorders are associated with an increased rate of various metabolic disturbances, which may be related to oxidative stress and consequent lipid peroxidation. Since hepatic phosphatidylcholine plays an important role in metabolic regulation, the aim of the present study was to determine phosphatidylcholine expression in the liver following total sleep deprivation. To determine the effects of total sleep deprivation, we used adult rats implanted for polygraphic recording. Phosphatidylcholine expression was examined molecularly by the use of time‐of‐flight secondary ion mass spectrometry, along with biochemical solid‐phase extraction. The parameters of oxidative stress were investigated by evaluating the hepatic malondialdehyde levels as well as heat shock protein 25 immunoblotting and immunohistochemistry. In normal rats, the time‐of‐flight secondary ion mass spectrometry spectra revealed specific peaks (m/z 184 and 224) that could be identified as molecular ions for phosphatidylcholine. However, following total sleep deprivation, the signals for phosphatidylcholine were significantly reduced to nearly one‐third of the normal values. The results of solid‐phase extraction also revealed that the phosphatidylcholine concentration was noticeably decreased, from 15.7 µmol g–1 to 9.4 µmol g–1, after total sleep deprivation. By contrast, the biomarkers for oxidative stress were drastically up‐regulated in the total sleep deprivation‐treated rats as compared with the normal ones (4.03 vs. 1.58 nmol mg–1 for malondialdehyde levels, and 17.1 vs. 6.7 as well as 1.8 vs. 0.7 for heat shock protein 25 immunoblotting and immunoreactivity, respectively). Given that phosphatidylcholine is the most prominent component of all plasma lipoproteins, decreased expression of hepatic phosphatidylcholine following total sleep deprivation may be attributed to the enhanced oxidative stress and the subsequent lipid peroxidation, which would play an important role in the formation or progression of total sleep deprivation‐induced metabolic diseases.

Sleep deprivation impairs Ca2+ expression in the hippocampus: ionic imaging analysis for cognitive deficiency with TOF-SIMS.

Sleep deprivation causes cognitive dysfunction in which impaired neuronal plasticity in hippocampus may underlie the molecular mechanisms of this deficiency. Considering calcium-mediated NMDA receptor subunit 1 (NMDAR1) and neuronal nitric oxide synthase (nNOS) activation plays an important role in the regulation of neuronal plasticity, the present study is aimed to determine whether total sleep deprivation (TSD) would impair calcium expression, together with injury of the neuronal plasticity in hippocampus. Adult rats subjected to TSD were processed for time-of-flight secondary ion mass spectrometry, NMDAR1 immunohistochemistry, nNOS biochemical assay, cytochrome oxidase histochemistry, and the Morris water maze learning test to detect ionic, neurochemical, bioenergetic as well as behavioral changes of neuronal plasticity, respectively. Results indicated that in normal rats, strong calcium signaling along with intense NMDAR1/nNOS expression were observed in hippocampal regions. Enhanced calcium imaging and neurochemical expressions corresponded well with strong bioenergetic activity and good performance of behavioral testing. However, following TSD, both calcium intensity and NMDAR1/nNOS expressions were significantly decreased. Behavioral testing also showed poor responses after TSD. As proper calcium expression is essential for maintaining hippocampal neuronal plasticity, impaired calcium expression would depress downstream NMDAR1-mediated nNOS activation, which might contribute to the initiation or development of TSD-related cognitive deficiency.

Impaired sodium levels in the suprachiasmatic nucleus are associated with the formation of cardiovascular deficiency in sleep-deprived rats

Biological rhythms are a ubiquitous feature of all higher organisms. The rhythmic center of mammals is located in the suprachiasmatic nucleus (SCN), which projects to a number of brainstem centers to exert diurnal control over many physiological processes, including cardiovascular regulation. Total sleep deprivation (TSD) is a harmful condition known to impair cardiovascular activity, but the molecular mechanisms are unknown. As the inward sodium current has long been suggested as playing an important role in driving the spontaneous firing of the SCN, the present study aimed to determine if changes in sodium expression, together with its molecular machinery (Na‐K ATPase) and rhythmic activity within the SCN, would occur during TSD. Adult rats subjected to different periods of TSD were processed for time‐of‐flight secondary ion mass spectrometry, Na‐K ATPase assay, and cytochrome oxidase (COX) (an endogenous bioenergetic marker for neuronal activity) histochemistry. Cardiovascular dysfunction was determined through analysis of heart rate and changes in mean arterial pressure. Results indicated that, in normal rats, strong sodium signals were expressed throughout the entire SCN. Enzymatic data corresponded well with spectrometric findings in which high levels of Na‐K ATPase and COX were observed in this nucleus. However, following TSD, all parameters including sodium imaging, sodium intensity as well as COX activities were drastically decreased. Na‐K ATPase showed an increase in responsiveness following TSD. Both heart rate and mean arterial pressure measurements indicated an exaggerated pressor effect following TSD treatment. As proper sodium levels are essential for SCN activation, reduced SCN sodium levels may interrupt the oscillatory control, which could serve as the underlying mechanism for the initiation or development of TSD‐related cardiovascular deficiency.

Comprehensive Application of Time-of-flight Secondary Ion Mass Spectrometry (TOF-SIMS) for Ionic Imaging and Bio-energetic Analysis of Club Drug-induced Cognitive Deficiency

Excessive exposure to club drug (GHB) would cause cognitive dysfunction in which impaired hippocampal Ca2+-mediated neuroplasticity may correlate with this deficiency. However, the potential changes of in vivo Ca2+ together with molecular machinery engaged in GHB-induced cognitive dysfunction has never been reported. This study aims to determine these changes in bio-energetic level through ionic imaging, spectrometric, biochemical, morphological, as well as behavioral approaches. Adolescent rats subjected to GHB were processed for TOF-SIMS, immunohistochemistry, biochemical assay, together with Morris water maze to detect the ionic, molecular, neurochemical, and behavioral changes of GHB-induced cognitive dysfunction, respectively. Extent of oxidative stress and bio-energetics were assessed by levels of lipid peroxidation, Na+/K+ ATPase, cytochrome oxidase, and [14C]-2-deoxyglucose activity. Results indicated that in GHB intoxicated rats, decreased Ca2+ imaging and reduced NMDAR1, nNOS, and p-CREB reactivities were detected in hippocampus. Depressed Ca2+-mediated signaling corresponded well with intense oxidative stress, diminished Na+/K+ ATPase, reduced COX, and decreased 2-DG activity, which all contributes to the development of cognitive deficiency. As impaired Ca2+-mediated signaling and oxidative stress significantly contribute to GHB-induced cognitive dysfunction, delivering agent(s) that improves hippocampal bio-energetics may thus serve as a promising strategy to counteract the club drug-induced cognitive dysfunction emerging in our society nowadays.

Melatonin Successfully Rescues Hippocampal Bioenergetics and Improves Cognitive Function following Drug Intoxication by Promoting Nrf2-ARE Signaling Activity

Prolonged exposure to gamma‐hydroxybutyric acid (GHB) would cause drug intoxication in which impaired cognitive function results from enhanced hippocampal oxidative stress may serve as a major symptom in this deficiency. Considering melatonin possesses significant anti‐oxidative efficacy, this study aimed to determine whether melatonin would successfully promote the nuclear factor erythroid 2‐related factor 2 and antioxidant responsive element (Nrf2‐ARE) signaling, depress oxidative stress, and rescue hippocampal bioenergetics and cognitive function following drug intoxication injury. Adolescent rats subjected to 10 days of GHB were received melatonin at doses of either 10 or 100 mg/kg. Time‐of‐flight secondary ion mass spectrometry, biochemical assay, quantitative histochemistry, [14C]‐2‐deoxyglucose analysis, together with Morris water maze were employed to detect the molecular signaling, oxidative status, bioenergetic level, as well as the cognitive performances, respectively. Results indicated that in GHB‐intoxicated rats, enhanced oxidative stress, increased cholesterol level, and decreased anti‐oxidative enzymes activities were detected in hippocampal regions. Intense oxidative stress paralleled well with reduced bioenergetics and poor performance in behavioral testing. However, in rats treated with melatonin following GHB intoxication, all above parameters and cognitive function were gradually returned to nearly normal levels. Melatonin also remarkably promoted the translocation of Nrf2 from cytoplasm to nucleus in a dose‐dependent manner, thereby increased the Nrf2‐ARE signaling‐related downstream anti‐oxidative enzymes activities. As melatonin effectively rescues hippocampal bioenergetics through depressing the oxidative stress by promoting Nrf2‐ARE molecular machinery, this study thus highlights for the first time that clinical use of melatonin may serve as a therapeutic strategy to improve the cognitive function in unsuspecting victims suffered from GHB intoxication injury.

Redistribution of Cav2.1 channels and calcium ions in nerve terminals following end-to-side neurorrhaphy: ionic imaging analysis by TOF–SIMS

The P/Q-type voltage-dependent calcium channel (Cav2.1) in the presynaptic membranes of motor nerve terminals plays an important role in regulating Ca2+ transport, resulting in transmitter release within the nervous system. The recovery of Ca2+-dependent signal transduction on motor end plates (MEPs) and innervated muscle may directly reflect nerve regeneration following peripheral nerve injury. Although the functional significance of calcium channels and the levels of Ca2+ signalling in nerve regeneration are well documented, little is known about calcium channel expression and its relation with the dynamic Ca2+ ion distribution at regenerating MEPs. In the present study, end-to-side neurorrhaphy (ESN) was performed as an in vivo model of peripheral nerve injury. The distribution of Ca2+ at regenerating MEPs following ESN was first detected by time-of-flight secondary ion mass spectrometry, and the specific localization and expression of Cav2.1 channels were examined by confocal microscopy and western blotting. Compared with other fundamental ions, such as Na+ and K+, dramatic changes in the Ca2+ distribution were detected along with the progression of MEP regeneration. The re-establishment of Ca2+ distribution and intensity were correlated with the functional recovery of muscle in ESN rats. Furthermore, the re-clustering of Cav2.1 channels after ESN at the nerve terminals corresponded with changes in the Ca2+ distribution. These results indicated that renewal of the Cav2.1 distribution within the presynaptic nerve terminals may be necessary for initiating a proper Ca2+ influx and shortening the latency of muscle contraction during nerve regeneration.