Hybridized Nanogenerators for Multifunctional Self-Powered Sensing: Principles, Prototypes, and Perspectives.

Sensors are a key component of the Internet of Things (IoTs) to collect information of environments or objects. Considering the tremendous number and complex working conditions of sensors, multifunction and self-powered feathers are two basic requirements. Nanogenerators are a kind of devices based on the triboelectric, piezoelectric, or pyroelectric effects to harvest ambient energy and then converting to electricity. The hybridized nanogenerators that combined multiple effects in one device have great potential in multifunctional self-powered sensors because of the unique superiority such as generating electrical signals directly, responding to diverse stimuli, etc. This review aims at introducing the latest advancements of hybridized nanogenerators for multifunctional self-powered sensing. Firstly, the principles and sensor prototypes based on TENG are summarized. To avoid signal interference and energy insufficiently, the multifunctional self-powered sensors based on hybridized nanogenerators are reviewed. At last, the challenges and future development of multifunctional self-powered sensors have prospected.

Developmental changes of BKCa channels depend on differentiation status in cultured podocytes.

The podocyte is a remarkable cell type, which encases the capillaries of the kidney glomerulus. Podocytes are of keen interests because of their key roles in kidney development and disease. Large-conductance Ca(2+)-activated K(+) channels (BKCa channels) are important ion channels located in podocytes and play the essential role in regulating calcium homeostasis cell signaling. In this research, we studied the undergoing developmental changes of BKCa channels and their contribution to functional maturation of podocytes. Our results showed that the distribution of BKCa channels changed with the maturity of differentiation in a conditionally immortalized mouse podocyte cell line. Additionally, the increase of BKCa channel protein expression was detected by immunofluorescence staining with confocal microscopy in podocytes, which was consistent with the increase in the current density of BKCa channels examined by whole-cell patch-clamp technique. Our results suggested that the developmental changes of BKCa channels may help podocytes adapt to changes in pressure gradients occurring in physiological conditions. Those findings may have implications for understanding the physiology and development of kidney and will also serve as a baseline for future studies designed to investigate developmental changes of ion channel expression in podocytes.

Peroxynitrite alters GABAergic synaptic transmission in immature rat hippocampal slices.

Increasing of peroxynitrite (ONOO(-)) production during ischemia in the immature brain was considered to be associated with impaired cognitive function. GABAergic synapses played an important role in memory formation including the induction of long-term potentiation (LTP) and long-term depression (LTD) in hippocampus. In the present study, we examined the effects of acute exposure of the ONOO(-) donor, SIN-1 on GABAergic synaptic transmission in immature rat hippocampal slices with whole-cell patch-clamp recordings. The results showed that SIN-1 increased the peak amplitude of evoked inhibitory postsynaptic currents (eIPSCs) and decreased paired pulse ratio via the formation of ONOO(-). In addition, it also increased the frequency of spontaneous (but not miniature) IPSCs in a dose-dependent manner without altering amplitudes or rise and decay times of both (sIPSCs and mIPSCs). It further demonstrated that the presynaptic action of SIN-1 was external calcium dependent and was not related to the changes of interneuron excitability. This study provides electrophysiological evidences from developing hippocampal slices to support that SIN-1 enhances action potential-dependent GABA release. It suggests that the potentiation effect of ONOO(-) may contribute to hyperexcitability and seizures and may underlie one of the mechanisms by which ischemia increases seizure susceptibility in the immature brain.

Attenuated effect of tungsten carbide nanoparticles on voltage-gated sodium current of hippocampal CA1 pyramidal neurons.

Nanomaterials and relevant products are now being widely used in the world, and their safety becomes a great concern for the general public. Tungsten carbide nanoparticles (nano-WC) are widely used in metallurgy, aeronautics and astronautics, however our knowledge regarding the influence of nano-WC on neurons is still lacking. The aim of this study was to investigate the impact of nano-WC on tetrodotoxin (TTX)-sensitive voltage-activated sodium current (I(Na)) of hippocampal CA1 pyramidal neurons. Results showed that acute exposure of nano-WC attenuated the peak amplitudes of I(Na) in a concentration-dependent manner. The minimal effective concentration was 10(-5)g/ml. The exposure of nano-WC significantly decreased current amplitudes of the current-voltage curves of I(Na) from -50 to+50 mV, shifted the steady-state activation and inactivation curves of I(Na) negatively and delayed the recovery of I(Na) from inactivation state. After exposure to nano-WC, the peak amplitudes, overshoots and the V-thresholds of action potentials (APs) were markedly reduced. These results suggested that exposure of nano-WC could influence some characteristics of APs evoked from the hippocampal CA1 neurons by modifying the kinetics of voltage-gated sodium channels (VGSCs).

Effects of nanoparticle zinc oxide on spatial cognition and synaptic plasticity in mice with depressive-like behaviors.

BACKGROUND: Nanomaterials, as a new kind of materials, have been greatly applied in different fields due to their special properties. With the industrialization of nanostructured materials and increasing public exposure, the biosafety and potential influences on central nervous system (CNS) have received more attention. Nanosized zinc oxide (nanoZnO) was suggested to up-regulate neuronal excitability and to induce glutamate release in vitro. Therefore, we hypothesized nanoparticles of nanoZnO may lead to changes in balance of neurotransmitter or neuronal excitability of CNS. This study was to investigate if there were effects of nanoZnO on animal model of depression. METHODS: Male Swiss mice were given lipopolysaccharides (LPS, 100 µg/kg, 100 µg/ml, every other day, 8 times, i.p.) from weaning to induce depressive-like behaviors. NanoZnO (5.6 mg/kg, 5.6 mg/ml, every other day, 8 times, i.p.) was given as the interaction. The mouse model was characterized using the methods of open field test, tail suspension test and forced swim test. Furthermore, the spatial memory was evaluated using Morris water maze (MWM) and the synaptic plasticity was assessed by measuring the long-term potentiation (LTP) in the perforant pathway (PP) to dentate gyrus (DG) in vivo. RESULTS: Results indicated that model mice showed disrupted spatial memory and LTP after LPS injections and the behavioral and electrophysiological improvements after nanoZnO treatment. CONCLUSION: Data suggested that nanoZnO may play some roles in CNS of mental disorders, which could provide some useful direction on the new drug exploring and clinical researches.

Inhibitory effect of tungsten carbide nanoparticles on voltage-gated potassium currents of hippocampal CA1 neurons.

The effects of tungsten carbide nanoparticles (nano-WC) on the properties of voltage-dependent potassium currents and evoked action potentials were studied in the hippocampal CA1 pyramidal neurons of rats at the ages of postnatal days 10-14 using the whole-cell patch-clamp technique. The results indicated that: (1) the amplitudes of transient outward potassium current (I(A)) and delayed rectifier potassium current (I(K)) were significantly decreased by 10(-7) g/ml nano-WC, while the current-voltage curves of I(A) and I(K) were significantly decreased by nano-WC from +10 to +90 mV. (2) Nano-WC produced a depolarizing shift in the steady-state activation curve of I(A) and I(K) with increased slope factors, and delayed the recovery of I(A) from inactivation, but no significant effects were found on the inactivation of I(A). (3) Nano-WC prolonged the evoked action potential duration and lowered the firing rate. These results suggest that 10(-7) g/ml nano-WC can decrease the amplitudes of I(A) and I(K) currents by reducing the opening number of voltage-gated potassium channels and delaying the recovery of I(A) from inactivation, which indicate that nano-WC has the potential neurotoxicity.

Protective effects of exogenous hydrogen sulfide on neurons of hippocampus in a rat model of brain ischemia.

Many studies have demonstrated the cytoprotective effects of hydrogen sulfide (H(2)S) in vitro and/or in vivo ischemic injury. The aim of the current study was to investigate whether exogenous H(2)S attenuates the neuronal injury induced by brain ischemia. As an H(2)S donor, sodium hydrosulfide (NaHS) was administered intraperitoneally (5.6 mg/kg/day, i.p.). The effects of exogenous H(2)S on neurons of ischemic hippocampus were examined by using measurement of behavior, electrophysiology, morphology and immunohistochemical staining, respectively. Our results showed that exogenous H(2)S significantly improved spatial learning and memory deficits induced by brain ischemia (P < 0.01). Exogenous H(2)S enhanced synaptic plasticity in the hippocampus of brain-ischemic rats, inhibited the edema around pyramidal neurons and the nuclear shrink induced by ischemia, and promoted the expression of growth-associated protein-43 (GAP-43) in the CA1 region of hippocampus post ischemia. The results suggest a protective effect and therapeutic potential of H(2)S in the treatment of brain ischemia.

[Chronic toxicity of 97% isopropyl thioxanthone in rat by oral administration for 2 years].

OBJECTIVE: To study the oral chronic toxicity of 97% isopropyl thioxanthone (97% ITX) in rats, determine the no-observed adverse effect levels (NOAEL). METHODS: Four groups of rats were fed with foodstuff containing 97% ITX in the dosage of 1000.0, 250.0, 62.5 mg/kg respectively for 2 years. The general behavior, body weight, food availability ect. were observed during the experiment. At the end of the experiment, blood and urine samples were collected for routine and biochemical assays. The internal organs were taken for calculating their organ coefficients and histopathological examinations. RESULTS: During the experimental period, no obvious abnormality were found in the experimental animals. The body weight and the total food availability rate in the high dosage group of male were lower than that of control (P < 0.05). Hematology examination showed that the quantity of Hb and RBC in high dosage groups of both the male and female and Hb in the male middle group were all lower than the control group (P < 0.01 or P < 0.05). Analysis of correlation indicated that r = -0.433, P < 0.01 in male, r = -0.337, P < 0.01 in female of Hb; r = -0.266, P < 0.05 in male, r = -0.317, P < 0.01 in female of RBC. There were obviously negative correlation. Serum biochemistry examination showed the concentration of CHO in the high and middle dosage treated rats of male and female were higher than that of the control (P < 0.01 or P < 0.05). Analysis of correlation indicated that r = 0.497, P < 0.01 in male, r = 0.417, P < 0.01 in female. No abnormality were found in urine examination. The organ weight and organ coefficient such as liver, were higher than control group (P < 0.01). The result of histopathological examinations displayed that the renal tubule Cast and the tubulointerstitial nephritis in the treated groups were higher than that of control group (P < 0.01). CONCLUSION: 97% ITX could obviously interfere with the animals' physical condition, and reduce the number of RBC and the concentration of Hb in the blood, interact metabolism of lipoid and induce the concentration of CHO in the serum. The livers of the treated rats are compensatory enlarged. And kidneys of the poisoning animals are damaged. The 2 years oral NOAEL of 97% ITX in rats are more than 4.63 mg/kg for female rats, and larger than 4.06 mg/kg for male rats.