L-type Ca2+ channels mediate regulation of glutamate release by subthreshold potential changes.

Subthreshold depolarization enhances neurotransmitter release evoked by action potentials and plays a key role in modulating synaptic transmission by combining analog and digital signals. This process is known to be Ca2+ dependent. However, the underlying mechanism of how small changes in basal Ca2+ caused by subthreshold depolarization can regulate transmitter release triggered by a large increase in local Ca2+ is not well understood. This study aimed to investigate the source and signaling mechanisms of Ca2+ that couple subthreshold depolarization with the enhancement of glutamate release in hippocampal cultures and CA3 pyramidal neurons. Subthreshold depolarization increased presynaptic Ca2+ levels, the frequency of spontaneous release, and the amplitude of evoked release, all of which were abolished by blocking L-type Ca2+ channels. A high concentration of intracellular Ca2+ buffer or blockade of calmodulin abolished depolarization-induced increases in transmitter release. Estimation of the readily releasable pool size using hypertonic sucrose showed depolarization-induced increases in readily releasable pool size, and this increase was abolished by the blockade of calmodulin. Our results provide mechanistic insights into the modulation of transmitter release by subthreshold potential change and highlight the role of L-type Ca2+ channels in coupling subthreshold depolarization to the activation of Ca2+-dependent signaling molecules that regulate transmitter release.

Differential involvement of mitochondria in post-tetanic potentiation at intracortical excitatory synapses of the medial prefrontal cortex.

Post-tetanic Ca2+ release from mitochondria produces presynaptic residual calcium, which contributes to post-tetanic potentiation. The loss of mitochondria-dependent post-tetanic potentiation is one of the earliest signs of Alzheimer's model mice. Post-tetanic potentiation at intracortical synapses of medial prefrontal cortex has been implicated in working memory. Although mitochondrial contribution to post-tetanic potentiation differs depending on synapse types, it is unknown which synapse types express mitochondria-dependent post-tetanic potentiation in the medial prefrontal cortex. We studied expression of mitochondria-dependent post-tetanic potentiation at different intracortical synapses of the rat medial prefrontal cortex. Post-tetanic potentiation occurred only at intracortical synapses onto layer 5 corticopontine cells from commissural cells and L2/3 pyramidal neurons. Among post-tetanic potentiation-expressing synapses, L2/3-corticopontine synapses in the prelimbic cortex were unique in that post-tetanic potentiation depends on mitochondria because post-tetanic potentiation at corresponding synapse types in other cortical areas was independent of mitochondria. Supporting mitochondria-dependent post-tetanic potentiation at L2/3-to-corticopontine synapses, mitochondria-dependent residual calcium at the axon terminals of L2/3 pyramidal neurons was significantly larger than that at commissural and corticopontine cells. Moreover, post-tetanic potentiation at L2/3-corticopontine synapses, but not at commissural-corticopontine synapses, was impaired in the young adult Alzheimer's model mice. These results would provide a knowledge base for comprehending synaptic mechanisms that underlies the initial clinical signs of neurodegenerative disorders.

The downregulation of Kv1 channels in Lgi1-/-mice is accompanied by a profound modification of its interactome and a parallel decrease in Kv2 channels.

In animal models of LGI1-dependent autosomal dominant lateral temporal lobe epilepsy, Kv1 channels are downregulated, suggesting their crucial involvement in epileptogenesis. The molecular basis of Kv1 channel-downregulation in LGI1 knock-out mice has not been elucidated and how the absence of this extracellular protein induces an important modification in the expression of Kv1 remains unknown. In this study we analyse by immunofluorescence the modifications in neuronal Kv1.1 and Kv1.2 distribution throughout the hippocampal formation of LGI1 knock-out mice. We show that Kv1 downregulation is not restricted to the axonal compartment, but also takes place in the somatodendritic region and is accompanied by a drastic decrease in Kv2 expression levels. Moreover, we find that the downregulation of these Kv channels is associated with a marked increase in bursting patterns. Finally, mass spectrometry uncovered key modifications in the Kv1 interactome that highlight the epileptogenic implication of Kv1 downregulation in LGI1 knock-out animals.

Impact of supra-maximal interval training vs. high-intensity interval training on cardiac auto-regulation response in physically active adults.

PURPOSE: This study aimed to examine the impact of supra-maximal interval training (SMIT) and high-intensity interval training (HIIT) on cardiac auto-regulation response. METHODS: Physically active young adults volunteered to participate in the study with a randomized cross-over counterbalanced design (N = 12). HIIT sessions consisted of 20 bouts of 10 s of exercise followed by 50 s of recovery, totaling 20 min at two different intensities; "all-out (SMIT)" vs. "115-130% Wmax (HIIT)". The cardiac auto-regulation included heart rate variability (HRV) and vascular function. HRV and vascular function were measured at baseline and five different time points after acute exercise. RESULTS: The SMIT was higher in workload (31%), peak heart rate (28%), and rate of perceived exertion (40%) compared with HIIT (all p < 0.001). The R-R interval, NN50, and pNN50 measured until 60 min after acute exercise was higher in the HIIT compared with SMIT (all p < 0.05). The SMIT elicited a greater shift in ln LF/HF ratio immediately after acute exercise (3802%, p < 0.01) and induced a decrease in bilateral ba-PWV at the time point 5 min after acute exercise, persisting until 65 min after (p < 0.05). Yet, HIIT showed no change over time in the frequency domain of HRV and blood vascular tone after cessation of acute exercise. CONCLUSION: Our findings confirmed that SMIT is a more potent modulator of the autonomic nervous system compared with HIIT. Further study is needed to monitor through complete recovery to baseline, to understand acute cardiac auto-regulation response after cessation of various exercise intensities identical interval training protocol.

Gradual decorrelation of CA3 ensembles associated with contextual discrimination learning is impaired by Kv1.2 insufficiency.

The associative network of hippocampal CA3 is thought to contribute to rapid formation of contextual memory from one-trial learning, but the network mechanisms underlying decorrelation of neuronal ensembles in CA3 is largely unknown. Kv1.2 expressions in rodent CA3 pyramidal cells (CA3-PCs) are polarized to distal apical dendrites, and its downregulation specifically enhances dendritic responses to perforant pathway (PP) synaptic inputs. We found that haploinsufficiency of Kv1.2 (Kcna2+/-) in CA3-PCs, but not Kv1.1 (Kcna1+/-), lowers the threshold for long-term potentiation (LTP) at PP-CA3 synapses, and that the Kcna2+/- mice are normal in discrimination of distinct contexts but impaired in discrimination of similar but slightly distinct contexts. We further examined the neuronal ensembles in CA3 and dentate gyrus (DG), which represent the two similar contexts using in situ hybridization of immediate early genes, Homer1a and Arc. The size and overlap of CA3 ensembles activated by the first visit to the similar contexts were not different between wild type and Kcna2+/- mice, but these ensemble parameters diverged over training days between genotypes, suggesting that abnormal plastic changes at PP-CA3 synapses of Kcna2+/- mice is responsible for the impaired pattern separation. Unlike CA3, DG ensembles were not different between two genotype mice. The DG ensembles were already separated on the first day, and their overlap did not further evolve. Eventually, the Kcna2+/- mice exhibited larger CA3 ensemble size and overlap upon retrieval of two contexts, compared to wild type or Kcna1+/- mice. These results suggest that sparse LTP at PP-CA3 synapse probably supervised by mossy fiber inputs is essential for gradual decorrelation of CA3 ensembles.

Expeditious Electrochemical Synthesis of Mesoporous Chalcogenide Flakes: Mesoporous Cu2 Se as a Potential High-Rate Anode for Sodium-Ion Battery.

Nanostructured copper selenide (Cu2 Se) attracts much interest as it shows outstanding performance as thermoelectric, photo-thermal, and optical material. The mesoporous structure is also a promising morphology to obtain better performance for electrochemical and catalytic applications, thanks to its high surface area. A simple one-step electrochemical method is proposed for mesoporous chalcogenides synthesis. The synthesized Cu2 Se material has two types of mesopores (9 and 18 nm in diameter), which are uniformly distributed inside the flakes. These materials are also implemented for sodium (Na) ion battery (NIB) anode as a proof of concept. The electrode employing the mesoporous Cu2 Se exhibits superior and more stable specific capacity as a NIB anode compared to the non-porous samples. The electrode also exhibits excellent rate tolerance at each current density, from 100 to 1000 mA g-1 . It is suggested that the mesoporous structure is advantageous for the insertion of Na ions inside the flakes. Electrochemical analysis indicates that the mesoporous electrode possesses more prominent diffusion-controlled kinetics during the sodiation-desodiation process, which contributes to the improvement of Na-ion storage performance.

Noise-Resistant Demosaicing with Deep Image Prior Network and Random RGBW Color Filter Array.

In this paper, we propose a deep-image-prior-based demosaicing method for a random RGBW color filter array (CFA). The color reconstruction from the random RGBW CFA is performed by the deep image prior network, which uses only the RGBW CFA image as the training data. To our knowledge, this work is a first attempt to reconstruct the color image with a neural network using only a single RGBW CFA in the training. Due to the White pixels in the RGBW CFA, more light is transmitted through the CFA than in the case with the conventional RGB CFA. As the image sensor can detect more light, the signal-to-noise-ratio (SNR) increases and the proposed demosaicing method can reconstruct the color image with a higher visual quality than other existing demosaicking methods, especially in the presence of noise. We propose a loss function that can train the deep image prior (DIP) network to reconstruct the colors from the White pixels as well as from the red, green, and blue pixels in the RGBW CFA. Apart from using the DIP network, no additional complex reconstruction algorithms are required for the demosaicing. The proposed demosaicing method becomes useful in situations when the noise becomes a major problem, for example, in low light conditions. Experimental results show the validity of the proposed method for joint demosaicing and denoising.

Identification of Point Defects in Atomically Thin Transition-Metal Dichalcogenide Semiconductors as Active Dopants.

Selective doping in semiconductors is essential not only for monolithic integrated circuity fabrications but also for tailoring their properties including electronic, optical, and catalytic activities. Such active dopants are essentially point defects in the host lattice. In atomically thin two-dimensional (2D) transition-metal dichalcogenides (TMDCs), the roles of such point defects are particularly critical in addition to their large surface-to-volume ratio, because their bond dissociation energy is relatively weaker, compared to elemental semiconductors. In this Mini Review, we review recent advances in the identifications of diverse point defects in 2D TMDC semiconductors, as active dopants, toward the tunable doping processes, along with the doping methods and mechanisms in literature. In particular, we discuss key issues in identifying such dopants both at the atomic scales and the device scales with selective examples. Fundamental understanding of these point defects can hold promise for tunability doping of atomically thin 2D semiconductor platforms.

Kv4.1, a Key Ion Channel For Low Frequency Firing of Dentate Granule Cells, Is Crucial for Pattern Separation.

The dentate gyrus (DG) in the hippocampus may play key roles in remembering distinct episodes through pattern separation, which may be subserved by the sparse firing properties of granule cells (GCs) in the DG. Low intrinsic excitability is characteristic of mature GCs, but ion channel mechanisms are not fully understood. Here, we investigated ionic channel mechanisms for firing frequency regulation in hippocampal GCs using male and female mice, and identified Kv4.1 as a key player. Immunofluorescence analysis showed that Kv4.1 was preferentially expressed in the DG, and its expression level determined by Western blot analysis was higher at 8-week than 3-week-old mice, suggesting a developmental regulation of Kv4.1 expression. With respect to firing frequency, GCs are categorized into two distinctive groups: low-frequency (LF) and high-frequency (HF) firing GCs. Input resistance (Rin) of most LF-GCs is lower than 200 MΩ, suggesting that LF-GCs are fully mature GCs. Kv4.1 channel inhibition by intracellular perfusion of Kv4.1 antibody increased firing rates and gain of the input-output relationship selectively in LF-GCs with no significant effect on resting membrane potential and Rin, but had no effect in HF-GCs. Importantly, mature GCs from mice depleted of Kv4.1 transcripts in the DG showed increased firing frequency, and these mice showed an impairment in contextual discrimination task. Our findings suggest that Kv4.1 expression occurring at late stage of GC maturation is essential for low excitability of DG networks and thereby contributes to pattern separation.SIGNIFICANCE STATEMENT The sparse activity of dentate granule cells (GCs), which is essential for pattern separation, is supported by high inhibitory inputs and low intrinsic excitability of GCs. Low excitability of GCs is thought to be attributable to a high K+ conductance at resting membrane potentials, but this study identifies Kv4.1, a depolarization-activated K+ channel, as a key ion channel that regulates firing of GCs without affecting resting membrane potentials. Kv4.1 expression is developmentally regulated and Kv4.1 currents are detected only in mature GCs that show low-frequency firing, but not in less mature high-frequency firing GCs. Furthermore, mice depleted of Kv4.1 transcripts in the dentate gyrus show impaired pattern separation, suggesting that Kv4.1 is crucial for sparse coding and pattern separation.

Inter-spike mitochondrial Ca2+ release enhances high frequency synaptic transmission.

KEY POINTS: Presynaptic mitochondria not only absorb but also release Ca2+ during high frequency stimulation (HFS) when presynaptic [Ca2+ ] is kept low (<500 nm) by high cytosolic Ca2+ buffer or strong plasma membrane calcium clearance mechanisms under physiological external [Ca2+ ]. Mitochondrial Ca2+ release (MCR) does not alter the global presynaptic Ca2+ transients. MCR during HFS enhances short-term facilitation and steady state excitatory postsynaptic currents by increasing vesicular release probability. The intra-train MCR may provide residual calcium at interspike intervals, and thus support high frequency neurotransmission at central glutamatergic synapses. ABSTRACT: Emerging evidence indicates that mitochondrial Ca2+ buffering contributes to local regulation of synaptic transmission. It is unknown, however, whether mitochondrial Ca2+ release (MCR) occurs during high frequency synaptic transmission. Confirming the previous notion that 2 µm tetraphenylphosphonium (TPP+ ) is a specific inhibitor of the mitochondrial Na+ /Ca2+ exchanger (mNCX), we studied the role of MCR via mNCX in short-term plasticity during high frequency stimulation (HFS) at the calyx of Held synapse of the rat. TPP+ reduced short-term facilitation (STF) and steady state excitatory postsynaptic currents during HFS at mature calyx synapses under physiological extracellular [Ca2+ ] ([Ca2+ ]o  = 1.2 mm), but not at immature calyx or at 2 mm [Ca2+ ]o . The inhibitory effects of TPP+ were stronger at synapses with morphologically complex calyces harbouring many swellings and at 32°C than at simple calyx synapses and at room temperature. These effects of TPP+ on STF were well correlated with those on the presynaptic mitochondrial [Ca2+ ] build-up during HFS. Mitochondrial [Ca2+ ] during HFS was increased by TPP+ at mature calyces under 1.2 mm [Ca2+ ]o , and further enhanced at 32°C, but not under 2 mm [Ca2+ ]o or at immature calyces. The close correlation of the effects of TPP+ on mitochondrial [Ca2+ ] with those on STF suggests that mNCX contributes to STF at the calyx of Held synapses. The intra-train MCR enhanced vesicular release probability without altering global presynaptic [Ca2+ ]. Our results suggest that MCR during HFS elevates local [Ca2+ ] near synaptic sites at interspike intervals to enhance STF and to support stable synaptic transmission under physiological [Ca2+ ]o .

Postnatal maturation of glutamate clearance and release kinetics at the rat and mouse calyx of Held synapses.

Although calyx of Held synapses undergo dramatic changes around the hearing onset, previous in vivo studies suggest that the calyx synapses undergo further post-hearing maturation process. While developmental changes over the hearing onset have been extensively studied, this post-hearing maturation process remained relatively little investigated. Because of post-hearing maturation, previous results from studies around hearing onset and studies of post-hearing calyx synapses are somewhat inconsistent. Here, we characterized the post-hearing maturation of calyx synapses with regard to in vitro electrophysiological properties in rats and mice. We found that parameters for residual glutamate in the cleft during a train, EPSC kinetics, and vesicle pool size became close to a full mature level by P14, but they further matured until P16 in the rats. Consistently, the phasic and slow EPSCs evoked by action potential trains at P16 calyx synapses were not different from those at P18 or P25 under physiological extracellular [Ca2+ ]o (1.2 mM). In contrast, the parameters for residual current and EPSC kinetics displayed drastic changes until P16 in mice, and slow EPSCs during the train further decreased between P16 and P18, suggesting that maturation of calyx synapses progresses at least up to P16 in rats and P18 in mice.

Disparities in Short-Term Depression Among Prefrontal Cortex Synapses Sustain Persistent Activity in a Balanced Network.

Persistent activity of cue-representing neurons in the prefrontal cortex (PFC) is regarded as a neural basis for working memory. The contribution of short-term synaptic plasticity (STP) at different types of synapses comprising the cortical network to persistent activity, however, remains unclear. Characterizing STP at synapses of the rat PFC layer 5 network, we found that PFC synapses exhibit distinct STP patterns according to presynaptic and postsynaptic identities. Excitatory postsynaptic currents (EPSCs) from corticopontine (Cpn) neurons were well sustained throughout continued activity, with stronger depression at synapses onto fast-spiking interneurons than those onto pyramidal cells. Inhibitory postsynaptic currents (IPSCs) were sustained at a weaker level compared with EPSC from Cpn synapses. Computational modeling of a balanced network incorporating empirically observed STP revealed that little depression at recurrent excitatory synapses, combined with stronger depression at other synapses, could provide the PFC with a unique synaptic mechanism for the generation and maintenance of persistent activity.

Deep Learning-Based Optimal Smart Shoes Sensor Selection for Energy Expenditure and Heart Rate Estimation.

Wearable technologies are known to improve our quality of life. Among the various wearable devices, shoes are non-intrusive, lightweight, and can be used for outdoor activities. In this study, we estimated the energy consumption and heart rate in an environment (i.e., running on a treadmill) using smart shoes equipped with triaxial acceleration, triaxial gyroscope, and four-point pressure sensors. The proposed model uses the latest deep learning architecture which does not require any separate preprocessing. Moreover, it is possible to select the optimal sensor using a channel-wise attention mechanism to weigh the sensors depending on their contributions to the estimation of energy expenditure (EE) and heart rate (HR). The performance of the proposed model was evaluated using the root mean squared error (RMSE), mean absolute error (MAE), and coefficient of determination (R2). Moreover, the RMSE was 1.05 ± 0.15, MAE 0.83 ± 0.12 and R2 0.922 ± 0.005 in EE estimation. On the other hand, and RMSE was 7.87 ± 1.12, MAE 6.21 ± 0.86, and R2 0.897 ± 0.017 in HR estimation. In both estimations, the most effective sensor was the z axis of the accelerometer and gyroscope sensors. Through these results, it is demonstrated that the proposed model could contribute to the improvement of the performance of both EE and HR estimations by effectively selecting the optimal sensors during the active movements of participants.

Association of mGluR-Dependent LTD of Excitatory Synapses with Endocannabinoid-Dependent LTD of Inhibitory Synapses Leads to EPSP to Spike Potentiation in CA1 Pyramidal Neurons.

The input-output relationships in neural circuits are determined not only by synaptic efficacy but also by neuronal excitability. Activity-dependent alterations of synaptic efficacy have been extensively investigated, but relatively less is known about how the neuronal output is modulated when synaptic efficacy changes are associated with neuronal excitability changes. In this study, we demonstrate that paired pulses of low-frequency stimulation (PP-LFS) induced metabotropic glutamate receptor (mGluR)-dependent LTD at Schaffer collateral (SC)-CA1 synapses in Sprague Dawley rats (both sexes), and this LTD was associated with EPSP to spike (E-S) potentiation, leading to the increase in action potential (AP) outputs. Threshold voltage (Vth) for APs evoked by synaptic stimulation and that by somatic current injection were hyperpolarized significantly after PP-LFS. Blockers of GABA receptors mimicked and occluded PP-LFS effects on E-S potentiation and Vth hyperpolarization, suggesting that suppression of GABAergic mechanisms is involved in E-S potentiation after PP-LFS. Indeed, IPSCs and tonic inhibitory currents were reduced after PP-LFS. The IPSC reduction was accompanied by increased paired-pulse ratio, and abolished by AM251, a blocker for Type 1 cannabinoid receptors, suggesting that PP-LFS suppresses presynaptic GABA release by mGluR-dependent endocannabinoids signaling. By contrast, a Group 1 mGluR agonist, 3, 5-dihydroxyphenylglycine, induced LTD at SC-CA1 synapses but failed to induce significant IPSC reduction and AP output increase. We propose that mGluR signaling that induces LTD coexpression at excitatory and inhibitory synapses regulates an excitation-inhibition balance to increase neuronal output in CA1 neurons.SIGNIFICANCE STATEMENT Long-lasting forms of synaptic plasticity are usually associated with excitability changes, the ability to fire action potentials. However, excitability changes have been regarded to play subsidiary roles to synaptic plasticity in modifying neuronal output. We demonstrate that, when metabotropic glutamate receptor-dependent LTD is induced by paired pulses of low-frequency stimulation, the action potential output in response to a given input paradoxically increases, indicating that increased excitability is more powerful than synaptic depression. This increase is mediated by the suppression of a presynaptic GABA release via metabotropic glutamate receptor-dependent endocannabinoid signaling. Our study shows that neuronal output changes do not always follow the direction of synaptic plasticity at excitatory synapses, highlighting the importance of regulating inhibitory tone via endocannabinoid signaling.

Intracellular Zn2+ Signaling Facilitates Mossy Fiber Input-Induced Heterosynaptic Potentiation of Direct Cortical Inputs in Hippocampal CA3 Pyramidal Cells.

Repetitive action potentials (APs) in hippocampal CA3 pyramidal cells (CA3-PCs) backpropagate to distal apical dendrites, and induce calcium and protein tyrosine kinase (PTK)-dependent downregulation of Kv1.2, resulting in long-term potentiation of direct cortical inputs and intrinsic excitability (LTP-IE). When APs were elicited by direct somatic stimulation of CA3-PCs from rodents of either sex, only a narrow window of distal dendritic [Ca2+] allowed LTP-IE because of Ca2+-dependent coactivation of PTK and protein tyrosine phosphatase (PTP), which renders non-mossy fiber (MF) inputs incompetent in LTP-IE induction. High-frequency MF inputs, however, could induce LTP-IE at high dendritic [Ca2+] of the window. We show that MF input-induced Zn2+ signaling inhibits postsynaptic PTP, and thus enables MF inputs to induce LTP-IE at a wide range of [Ca2+]i values. Extracellular chelation of Zn2+ or genetic deletion of vesicular zinc transporter abrogated the privilege of MF inputs for LTP-IE induction. Moreover, the incompetence of somatic stimulation was rescued by the inhibition of PTP or a supplement of extracellular zinc, indicating that MF input-induced increase in dendritic [Zn2+] facilitates the induction of LTP-IE by inhibiting PTP. Consistently, high-frequency MF stimulation induced immediate and delayed elevations of [Zn2+] at proximal and distal dendrites, respectively. These results indicate that MF inputs are uniquely linked to the regulation of direct cortical inputs owing to synaptic Zn2+ signaling.SIGNIFICANCE STATEMENT Zn2+ has been mostly implicated in pathological processes, and the physiological roles of synaptically released Zn2+ in intracellular signaling are little known. We show here that Zn2+ released from hippocampal mossy fiber (MF) terminals enters postsynaptic CA3 pyramidal cells, and plays a facilitating role in MF input-induced heterosynaptic potentiation of perforant path (PP) synaptic inputs through long-term potentiation of intrinsic excitability (LTP-IE). We show that the window of cytosolic [Ca2+] that induces LTP-IE is normally very narrow because of the Ca2+-dependent coactivation of antagonistic signaling pairs, whereby non-MF inputs become ineffective in inducing excitability change. The MF-induced Zn2+ signaling, however, biases toward facilitating the induction of LTP-IE. The present study elucidates why MF inputs are more privileged for the regulation of PP synapses.

Demosaicing of RGBW Color Filter Array Based on Rank Minimization with Colorization Constraint.

Recently, the white (w) channel has been incorporated in various forms into color filter arrays (CFAs). The advantage of using the W channel is that W pixels have less noise than RGB pixels; therefore, under low-light conditions, pixels with high fidelity can be obtained. However, RGBW CFAs normally suffer from spatial resolution degradation due to a smaller number of color pixels than in RGB CFAs. Therefore, even though the reconstructed colors have higher sensitivity, which results in larger CPSNR values, there are some color aliasing artifacts due to a low resolution. In this paper, we propose a rank minimization-based color interpolation method with a colorization constraint for the RGBW format with a large number of W pixels. The rank minimization can achieve a broad interpolation and preserve the structure in the image, and it thereby eliminates the color artifacts. However, the colors fade from this global process. Therefore, we further incorporate a colorization constraint into the rank minimization process for better reproduction of the colors. Experimental results show that the images can be reconstructed well even from noisy pattern images obtained under low-light conditions.

Joint Demosaicing and Denoising Based on a Variational Deep Image Prior Neural Network.

A joint demosaicing and denoising task refers to the task of simultaneously reconstructing and denoising a color image from a patterned image obtained by a monochrome image sensor with a color filter array. Recently, inspired by the success of deep learning in many image processing tasks, there has been research to apply convolutional neural networks (CNNs) to the task of joint demosaicing and denoising. However, such CNNs need many training data to be trained, and work well only for patterned images which have the same amount of noise they have been trained on. In this paper, we propose a variational deep image prior network for joint demosaicing and denoising which can be trained on a single patterned image and works for patterned images with different levels of noise. We also propose a new RGB color filter array (CFA) which works better with the proposed network than the conventional Bayer CFA. Mathematical justifications of why the variational deep image prior network suits the task of joint demosaicing and denoising are also given, and experimental results verify the performance of the proposed method.

Prediction of maximal oxygen consumption using the Young Men's Christian Association-step test in Korean adults.

PURPOSE: To develop accurate and practical prediction models of maximal oxygen consumption (VO2max) using the Young Men's Christian Association (YMCA)-step test in South Korean adults. METHODS: In total, 568 adults (20-66 years) were included in this study. To develop and cross-validate prediction models of VO2max, the total sample was divided into 80% training and 20% testing using a simple random sampling method. VO2max was measured using the maximal-graded exercise treadmill test. Sex, age, 1-min recovery heart rate, body weight, and height were measured as potential predictors. Each test was conducted within a 2- to 3-day interval, ensuring sufficient rest. Preliminary prediction models were developed from training datasets, which were cross-validated using regression analyses and/or repeated-measures analysis of variance. The accuracy of prediction models was evaluated using R2, standard error of estimate (SEE), and mean difference (MD) against a criterion-measured VO2max. RESULTS: The average age and VO2max were 43.5 ± 12.9 years and 39.1 ± 7.5 ml/kg/min, respectively. For model development, three practical models with acceptable accuracy were developed (R2 = 0.56-0.61; SEE = 4.74-5.01). For model cross-validation, significant relationships between the criterion-measured and predicted VO2max were observed in all three models (R2 = 0.56-0.61; SEE = 4.62-4.88). The difference between criterion-measured and predicted VO2max was not significant in the models (MD =- 0.03 to - 0.14). CONCLUSIONS: The prediction models included 3-5 variables as significant predictors of VO2max and had acceptable accuracy in a large sample of South Korean adults. The selected models provide a simple and practical method to estimate VO2max using the YMCA-step test for South Korean adults.

The elevation training mask induces modest hypoxaemia but does not affect heart rate variability during cycling in healthy adults.

This study examined the acute effects of the elevation training mask (ETM) on haemodynamics and heart rate variability (HRV) at rest, during cycling, and during recovery in healthy adults. Fifteen healthy male (N=9) and female (N=6) adults (27.0 ± 1.14 years) completed two trials with the mask (MASK) and without the mask (CON). The 40-minute cycling exercise protocol included 10-minute phases of (1) rest, (2) 50% of VO2peak cycling, (3) 70% of VO2peak cycling, and (4) recovery. Blood pressure and pulse oximetry saturation (SPO2) were measured at each phase. An Actiwave-Cardio ECG monitor (CamNtech, UK) was used to measure HRV variables including time and frequency domains. A greater response in systolic blood pressure (p=.035) was observed at rest while SPO2 (p=.033) was lower during high-intensity cycling (70% of VO2peak) in the MASK trial. The HRV indices were not different between trials during cycling. However, heart rate (p=.047) was greater while inter-beat interval and sympathovagal balance (the ratio between low-frequency and high-frequency components; ln LF/HF, p=.01) were lower in the MASK than the CON trials during recovery. Wearing an ETM during high-intensity cycling (70% of VO2peak) induces modest hypoxaemia. Although this device did not affect HRV changes during cycling, it seems to delay the cardiac-autonomic recovery from exercise. Healthy adults may be required to perform high-intensity exercise with an ETM to simulate a hypoxic environment, but future studies are needed to determine whether repeated exposure to this condition provides similar benefits as altitude training.

A cellular mechanism of muscle memory facilitates mitochondrial remodelling following resistance training.

KEY POINTS: Referring to the muscle memory theory, previously trained muscles acquire strength and volume much faster than naive muscles. Using extreme experimental models such as synergist ablation or steroid administration, previous studies have demonstrated that the number of nuclei increases when a muscle becomes enlarged, which serves as a cellular muscle memory mechanism for the muscle. In the present study, we found that, when rats were subjected to physiologically relevant resistance training, the number of myonuclei increased and was retained during a long-term detraining period. The acquired myonuclei were related to a greater degree of muscle hypertrophic and mitochondrial biogenesis processes following subsequent hypertrophic conditions. Our data suggest a cellular mechanism supporting the notion that exposing young muscles to resistance training would help to restore age-related muscle loss coupled with mitochondrial dysfunction in later life. ABSTRACT: Muscle hypertrophy induced by resistance training is accompanied by an increase in the number of myonuclei. The acquired myonuclei are viewed as a cellular component of muscle memory by which muscle enlargement is promoted during a re-training period. In the present study, we investigated the effect of exercise preconditioning on mitochondrial remodelling induced by resistance training. Sprague-Dawley rats were divided into four groups: untrained control, training, pre-training or re-training. The training groups were subjected to weight loaded-ladder climbing exercise training. Myonuclear numbers were significantly greater (up to 20%) in all trained muscles compared to untrained controls. Muscle mass was significantly higher in the re-training group compared to the training group (∼2-fold increase). Mitochondrial content, mitochondrial biogenesis gene expression levels and mitochondrial DNA copy numbers were significantly higher in re-trained muscles compared to the others. Oxidative myofibres (type I) were significantly increased only in the re-trained muscles. Furthermore, in vitro studies using insulin-like growth factor-1-treated L6 rat myotubes demonstrated that myotubes with a higher myonuclear number confer greater expression levels of both mitochondrial and nuclear genes encoding for constitutive and regulatory mitochondrial proteins, which also showed a greater mitochondrial respiratory function. These data suggest that myonuclei acquired from previous training facilitate mitochondrial biogenesis in response to subsequent retraining by (at least in part) enhancing cross-talk between mitochondria and myonuclei in the pre-conditioned myofibres.