Role Of Different Layers Research Articles

Identifying dominant recombination mechanisms in spiro-based conventional perovskite solar cells: Roles of interface and bulk recombination

Perovskite solar cells (PSCs) have been popular in the photovoltaic (PV) community, owing to their ease of processing and high efficiency. In order to improve their device performance, the interfaces are believed to play a vital role. In this regard, the interfacial energies and the associated physical processes such as charge transport, accumulation and recombination have been the focus of the research community. Despite the rise in power conversion efficiency (PCE) and all development, PSCs still suffer from the charge carrier recombination. As a result, highly efficient PSCs cannot meet the theoretical values of fill factor (FF) and open-circuit voltage ( VOC). Therefore, to reach out to the theoretical limit of performance for PSCs, carrier recombination needs to be controlled both in the bulk and at the corresponding interfaces. Herein, we have systematically studied the recombination in PSCs by establishing the role of different layers of PSCs using electrochemical impedance spectroscopy (EIS). To get insights into the role of different layers in recombination we fabricated PSCs with n-i-p configuration and changed the thickness of TiO 2 electron transport layer (ETL), absorber layer, and spiro-OMeTAD hole transport layer (HTL). Our results suggest that the recombination is reduced in case of devices with thicker HTL and is trap-assisted recombination. These results are in good agreement with impedance spectroscopy analysis. The value of recombination resistance (extracted by fitting of Nyquist response) is higher at VOC, which is consistent with higher VOC in these two cases. In case of the increased ETL thickness, the performance of the device is dropped since the increased interfacial resistance encourages the recombination. Our study presents a simple and effective approach to elucidate the dominating recombination sites in PSCs and improve the device performance.

Pb biosorption by Leclercia adecarboxylata: Protective and immobilized mechanisms of extracellular polymeric substances

Immobilization of lead by phosphate solubilizing bacteria (PSBs) has much advantages compared to conventional bioremediation methods due to the high efficiencies of immobilization particularly in the formation of insoluble Pb-phosphate compounds. The growth characteristics of Leclercia adecarboxylata, a lead resistance PSB, with the presence of Pb(NO3)2 was observed, and the role of different layers of extracellular polymeric substance (EPS) in Pb2+ adsorption were also explored. Results showed that high concentration of Pb2+ could inhibit the growth and metabolism of PSBs, especially in inhibiting the formation of intermediate products of the tricarboxylic acid cycle, such as succinic acid and citric acid. As the first reactive barrier to resist lead stress, soluble EPS (S-EPS) showed maximum adsorption ability of Pb2+, reached to 0.59 mmol·g−1, while the maximum sorption capacities of loosely bound EPS (LB-EPS) and tightly bound EPS (TB-EPS) were 0.011 mmol·g−1 and 0.004 mmol·g−1 for Pb2+, respectively. Three-dimensional fluorescence spectrum demonstrated that tyrosine protein-like substances and tryptophan protein-like substances were likely to play a significant role in resistance of lead stress in three layers of EPS, while carboxyl (COOH), hydroxyl (OH) and amino functional groups on EPS provided the bounding sites for immobilizing Pb2+. X-ray diffraction (XRD) investigation revealed that Pb2+ loaded on EPS did not form new crystalline phases, indicated that complexation was the dominant mechanism to remove lead ions in EPS. In addition, both with hydrophobic and hydrophilic groups in EPS were found, which could also capture Pb2+ through electrostatic attraction and ion-exchange. All the results obtained shown that the secretion of EPS by Leclercia adecarboxylata was one of the mechanisms to resist heavy metal stress and also could reduce the bioavailability of lead.

The role of epigenetics in osteoarthritis: current perspective.

The purpose of this review is to provide an update of recent advances in the established role of different layers of epigenetic control mechanism that are used by joint cells to ensure tissue homeostasis and cope with changing microenvironment (e.g. ageing or disease). New studies have further strengthened the evidence that joint tissue cells highly dependent on epigenetic control mechanisms, such as methylation at CpG-sites, noncoding RNAs and histone modifications to assure phenotypic plasticity and respective tissue homeostasis. Advancements towards high-dimensional molecular profiles and functional follow-up studies have started to uncover the complexity of these interacting networks of control. These studies highlight that in time loosening of epigenetic control increase the propensity of joint tissues to engage an osteoarthritis disease phenotype. Identification of changes in epigenetically regulated control mechanisms in joint tissues has provided novel insight into underlying mechanism of ongoing osteoarthritis disease pathophysiology. Such insight is crucial to enable development of evidence-based therapeutic options.

Simulating the spread of activation in neocortical circuits

Dynamics in the brain are shaped by the connectivity of neocortical circuits and by incoming sensory information. The neocortical columnar architecture has been hypothesized to be a module for shaping dynamics to perform information processing. However, the dynamics and routing of information flow between elements of neocortical columns and amongst neocortical columns remains poorly understood. Using NEURON[1] , we simulated a set of 11 horizontally connected layered neocortical columns which consisted of event-driven rule-based neurons wired according to known anatomical data and driven with random white-noise synaptic inputs [2]. We simulated afferent sensory inputs via the thalamus by strong stimulation of layer 4 pyramidal neuron AMPA/NMDA synapses in selected columns. To trace the role of different neocortical layers in information flow within and between columns, we simulated the focal application of the sodium channel blocker, tetrodotoxin (TTX), by inactivating selected layers of selected columns. We tuned the network in order to achieve realistic cell firing rates and to avoid a high frequency of spontaneous population spikes. During baseline, a physiological frequency spectrum appeared as an emergent property, displaying dominant frequencies that were not present in either the inputs, or in the intrinsic or activated frequencies of any of the cell groups. Thalamic stimuli evoked a brief population spike within layer 4. This population spike recruited recurrent activation within the column, evoking a set of 4-8 population spike discharges lasting from 500 - 1000 ms. The activity within the stimulated column spread in the classical neocortical column pathway: layer 4 -> layer 2/3 -> layer 5. After excitation reached layer 5, it spread to the neighboring columns by activating horizontal connections between layer 5 pyramidal cells. This activity then spread within the neighboring column from L5 to L2/3 pyramidal cells. After recurrent activation within L2/3, downward activation from L2/3 to L5 pyramidal cells initiated activity propagation from L5 to the next neighboring column. This activation sequence led to waves of population spikes gradually spreading outward from the initially stimulated column(s). We found that selective blockage of layer 2/3 neurons via TTX simulation attenuated, but did not block the flow of activity between columns. Instead, activity was able to propagate from the stimulated L4 -> L5 pyramidal cells and then to neighboring columns via the L5 horizontal projections. When we blocked layer 5 neurons of stimulated columns, we found that activity was no longer able to flow from the stimulated to neighboring columns. Our simulations demonstrate physiologically realistic spread of activation both within and between columns. Verifying the role of different layers in intra- and inter-columnar activation spread may be clinically relevant for containing seizures, where runaway excitation may be prevented by selective micro-ablation.

Cuts in Spain fall heavily on the brain: the CIBERNED plight

Cuts in Spain fall heavily on the brain: the CIBERNED plight

A functional study of the skin barrier to evaporative water loss by means of repeated cellophane-tape stripping

The functional role of different layers of the horny layer in preventing evaporative water loss was studied by an adhesive cellophane-tape stripping technique. The increase in transepidermal water loss, as described by a mathematical equation based on curve-fitting analysis, was shown to be proportional to the decrease in thickness of the horny layer. In the second half of the curve the experimental data showed slightly higher transepidermal-water-loss values than would be expected on the basis of proportionality with thickness of the stratum corneum. The data suggest that the outer layers of the horny layer are also important in forming a barrier to evaporative water loss.

Role of different layers of the dorsal lateral geniculate body in genesis of cortical association responses in cats

1. In response to electrical stimulation of the upper two layers (A and A1) of the dorsal lateral geniculate body by a single pulse of threshold strength a response arises only (or predominantly) in the visual cortex. A response to similar stimulation of the lower layer (B) of the lateral geniculate body arises only (or predominantly) in the association cortex. 2. During suprathreshold stimulation of the upper two layers of the dorsal lateral geniculate body the primary response is accompanied by an association response, and if the lower layer is stimulated in the same way the association response is accompanied by a primary response. The effect of this stimulation is evidently due to spread of the stimulating current to neighboring layers. 3. After electrolytic destruction of the central part of the lower layer of the dorsal lateral geniculate body, the association response to suprathreshold stimulation of neighboring layers no longer arises. 4. After injury to the lower layer of the dorsal lateral geniculate body, only the cortical association response to flashes disappears, while responses to stimuli of other modalities are completely unaffected. 5. A response in the association cortex arises only to stimulation of the contralateral optic nerve. 6. During stimulation of different layers of the dorsal lateral geniculate body by paired stimuli, the association component of the test response (when separated by a definite interval) is blocked only if the lower layer (B) is stimulated by a conditioning stimulus. 7. It is concluded from these findings that visual impulses responsible for the association response, in contrast to impulses responsible for the primary response, relay in the lower (B) layer of the dorsal lateral geniculate body.