Bone Bruises and Concomitant Meniscus and Cartilage Damage in Anterior Cruciate Ligament Injuries: A Systematic Review and Meta-Analysis.

(1) Background: Bone bruises in acute anterior cruciate ligament (ACL) injuries are closely linked to the occurrence of simultaneous meniscal and cartilage damage. Despite the frequent occurrence of associated injuries including bone bruises, meniscus, and cartilage damage in patients with ACL injuries, a systematic review of the relationships between the presence of bone bruises and the extent of meniscus and cartilage injuries has yet to be conducted. (2) Methods: Multiple comprehensive databases, including MEDLINE, EMBASE, and the Cochrane Library, were searched for studies that evaluated the relationship between bone bruises and meniscus or cartilage injuries following ACL injuries. Study selection, data extraction, and meta-analysis were performed. The Methodological Index for Non-Randomized Studies (MINORS) was used for quality assessments, and Review Manager 5.3 was used for data analysis. (3) Results: Data were extracted from 22 studies encompassing a total of 2891 patients with ACL injuries. Among the included studies, six studies investigated the relationships between bone bruises and medial meniscus (MM) or lateral meniscus (LM) injuries, while three studies investigated the relationships between bone bruises and cartilage injuries. There were no significant correlations between the presence of bone bruises and MM injuries (relative risk (RR) = 1.32; p = 0.61). A quantitative analysis indicated that individuals with bone bruises had a 2.71-fold higher likelihood of sustaining LM injuries than those without bone bruises (RR = 2.71; p = 0.0003). The analysis confirmed a significant relationship between bone bruises and cartilage injuries (RR = 6.18; p = 0.003). (4) Conclusions: Bone bruises occur most frequently in the lateral compartment. Bone bruises resulting from ACL injuries are related to accompanying LM injuries and cartilage injuries. Knowing these associations and the frequency of injuries may allow orthopedic surgeons to promptly address ACL-related meniscus and cartilage injuries on MRI results and in future clinical practice.

Demyelination and Na+ Channel Redistribution Underlie Auditory and Vestibular Dysfunction in PMP22-Null Mice.

Altered expression of peripheral myelin protein 22 (PMP22) results in demyelinating peripheral neuropathy. PMP22 exhibits a highly restricted tissue distribution with marked expression in the myelinating Schwann cells of peripheral nerves. Auditory and vestibular Schwann cells and the afferent neurons also express PMP22, suggesting a unique role in hearing and balancing. Indeed, neuropathic patients diagnosed with PMP22-linked hereditary neuropathies often present with auditory and balance deficits, an understudied clinical complication. To investigate the mechanism by which abnormal expression of PMP22 may cause auditory and vestibular deficits, we studied gene-targeted PMP22-null mice. PMP22-null mice exhibit an unsteady gait, have difficulty maintaining balance, and live for only ∼3-5 weeks relative to unaffected littermates. Histological analysis of the inner ear revealed reduced auditory and vestibular afferent nerve myelination and profound Na+ channel redistribution without PMP22. Yet, Na+ current density was unaltered, in stark contrast to increased K+ current density. Atypical postsynaptic densities and a range of neuronal abnormalities in the organ of Corti were also identified. Analyses of auditory brainstem responses (ABRs) and vestibular sensory-evoked potential (VsEP) revealed that PMP22-null mice had auditory and vestibular hypofunction. These results demonstrate that PMP22 is required for hearing and balance, and the protein is indispensable for the formation and maintenance of myelin in the peripheral arm of the eighth nerve. Our findings indicate that myelin abnormalities and altered signal propagation in the peripheral arm of the auditory nerve are likely causes of auditory deficits in patients with PMP22-linked neuropathies.

The Piezo channel is a mechano-sensitive complex component in the mammalian inner ear hair cell.

The inner ear is the hub where hair cells (HCs) transduce sound, gravity, and head acceleration stimuli to the brain. Hearing and balance rely on mechanosensation, the fastest sensory signals transmitted to the brain. The mechanoelectrical transducer (MET) channel is the entryway for the sound-balance-brain interface, but the channel-complex composition is not entirely known. Here, we report that the mouse utilizes Piezo1 (Pz1) and Piezo2 (Pz2) isoforms as MET-complex components. The Pz channels, expressed in HC stereocilia, and cell lines are co-localized and co-assembled with MET complex partners. Mice expressing non-functional Pz1 and Pz2 at the ROSA26 locus have impaired auditory and vestibular traits that can only be explained if the Pzs are integral to the MET complex. We suggest that Pz subunits constitute part of the MET complex and that interactions with other MET complex components yield functional MET units to generate HC MET currents.

Genetic and pharmacologic alterations of claudin9 levels suffice to induce functional and mature inner hair cells.

Hearing loss is the most common form of sensory deficit. It occurs predominantly due to hair cell (HC) loss. Mammalian HCs are terminally differentiated by birth, making HC loss incurable. Here, we show the pharmacogenetic downregulation of Cldn9, a tight junction protein, generates robust supernumerary inner HCs (IHCs) in mice. The putative ectopic IHCs have functional and synaptic features akin to typical IHCs and were surprisingly and remarkably preserved for at least fifteen months >50% of the mouse's life cycle. In vivo, Cldn9 knockdown using shRNA on postnatal days (P) P1-7 yielded analogous functional putative ectopic IHCs that were equally durably conserved. The findings suggest that Cldn9 levels coordinate embryonic and postnatal HC differentiation, making it a viable target for altering IHC development pre- and post-terminal differentiation.

The Piezo channel is central to the mechano-sensitive channel complex in the mammalian inner ear.

The inner ear is the hub where hair cells transduce sound, gravity, and head acceleration stimuli carried by neural codes to the brain. Of all the senses, hearing and balance, which rely on mechanosensation, are the fastest sensory signals transmitted to the central nervous system. The mechanoelectrical transducer (MET) channel in hair cells is the entryway for the sound-balance-brain interface, but the channel's composition has eluded biologists due to its complexity. Here, we report that the mouse utilizes Piezo1 (Pz1) and Piezo2 (Pz2) isoforms as central components of the MET complex. The Pz channel subunits are expressed in hair-cell stereocilia, are co-localized and co-assembled, and are essential components of the MET complex in vitro and in situ, including integration with the transmembrane channel (Tmc1/2) protein. Mice expressing non-functional Pz1 and Pz2, but not functional Pz1 at the ROSA26 locus under the control of hair-cell promoters, have impaired auditory and vestibular traits that can only be explained if Pz channel multimers are integral to the MET complex. We affirm that Pz protein subunits constitute MET channels and that functional interactions with components of the MET complex yield current properties resembling hair-cell MET currents. Our results demonstrate Pz is a MET channel component central to interacting with MET complex proteins. Results account for the MET channel pore and complex.

Predictive factors for conversion from conservatively to surgically treatment osteoporotic thoracolumbar compression fractures based on sagittal parameters and magnetic resonance imaging features.

PURPOSE: To investigate the relationship between sagittal plane characteristics of the spinal column and conservative treatment failure in acute osteoporotic spinal fractures (OSFs). METHODS: As a retrospective study of single-institute data, thoracolumbar OSF patients with similar propensities in terms of location of fractures and results of bone mineral density were analyzed. Among them, 43 patients (group I) who needed reconstructive surgical interventions and 39 patients (group II) who obtained successful treatment through conservative care were included. General demographic data, radiographic features of fractures, and magnetic resonance imaging (MRI) features of fractures were analyzed. To investigate the relationship between global sagittal alignment of the spine and occurrence of delayed complication following OSFs, radiological sagittal parameters were analyzed. RESULTS: The number of cases requiring reconstructive surgery was significantly higher when the index vertebra showed diffuse or mid-portion bone marrow changes in MRI. In terms of sagittal parameters, pelvic incidence (group I 59.1° ± 11.9°, group II 54.6° ± 9.8°) and thoracolumbar angle (group I 26.5° ± 14.1°, group II 17.4° ± 11.2°) were significantly higher in group I. Logistic regression analysis showed that higher pelvic incidence (OR 1.09, 95% CI 1.01-1.18, p value < 0.05) and higher thoracolumbar angle (OR 1.09, 95% CI 1.02-1.17, p value < 0.05) were significant risk factors for delayed complications requiring reconstructive surgery following OSFs. CONCLUSION: Delayed complications requiring reconstructive surgery following OSFs are related to sagittal plane parameters of the spine such as high pelvic incidences, in addition to previously known radiographic characteristics of fractures.

Detection of Prosthetic Loosening in Hip and Knee Arthroplasty Using Machine Learning: A Systematic Review and Meta-Analysis.

Background: prosthetic loosening after hip and knee arthroplasty is one of the most common causes of joint arthroplasty failure and revision surgery. Diagnosis of prosthetic loosening is a difficult problem and, in many cases, loosening is not clearly diagnosed until accurately confirmed during surgery. The purpose of this study is to conduct a systematic review and meta-analysis to demonstrate the analysis and performance of machine learning in diagnosing prosthetic loosening after total hip arthroplasty (THA) and total knee arthroplasty (TKA). Materials and Methods: three comprehensive databases, including MEDLINE, EMBASE, and the Cochrane Library, were searched for studies that evaluated the detection accuracy of loosening around arthroplasty implants using machine learning. Data extraction, risk of bias assessment, and meta-analysis were performed. Results: five studies were included in the meta-analysis. All studies were retrospective studies. In total, data from 2013 patients with 3236 images were assessed; these data involved 2442 cases (75.5%) with THAs and 794 cases (24.5%) with TKAs. The most common and best-performing machine learning algorithm was DenseNet. In one study, a novel stacking approach using a random forest showed similar performance to DenseNet. The pooled sensitivity across studies was 0.92 (95% CI 0.84-0.97), the pooled specificity was 0.95 (95% CI 0.93-0.96), and the pooled diagnostic odds ratio was 194.09 (95% CI 61.60-611.57). The I2 statistics for sensitivity and specificity were 96% and 62%, respectively, showing that there was significant heterogeneity. The summary receiver operating characteristics curve indicated the sensitivity and specificity, as did the prediction regions, with an AUC of 0.9853. Conclusions: the performance of machine learning using plain radiography showed promising results with good accuracy, sensitivity, and specificity in the detection of loosening around THAs and TKAs. Machine learning can be incorporated into prosthetic loosening screening programs.

Cisplatin Neurotoxicity Targets Specific Subpopulations and K+ Channels in Tyrosine-Hydroxylase Positive Dorsal Root Ganglia Neurons.

Among the features of cisplatin chemotherapy-induced peripheral neuropathy are chronic pain and innocuous mechanical hypersensitivity. The complete etiology of the latter remains unknown. Here, we show that cisplatin targets a heterogeneous population of tyrosine hydroxylase-positive (TH+) primary afferent dorsal root ganglion neurons (DRGNs) in mice, determined using single-cell transcriptome and electrophysiological analyses. TH+ DRGNs regulate innocuous mechanical sensation through C-low threshold mechanoreceptors. A differential assessment of wild-type and vitamin E deficient TH+ DRGNs revealed heterogeneity and specific functional phenotypes. The TH+ DRGNs comprise; fast-adapting eliciting one action potential (AP; 1-AP), moderately-adapting (≥2-APs), in responses to square-pulse current injection, and spontaneously active (SA). Cisplatin increased the input resistance and AP frequency but reduced the temporal coding feature of 1-AP and ≥2-APs neurons. By contrast, cisplatin has no measurable effect on the SA neurons. Vitamin E reduced the cisplatin-mediated increased excitability but did not improve the TH+ neuron temporal coding properties. Cisplatin mediates its effect by targeting outward K+ current, likely carried through K2P18.1 (Kcnk18), discovered through the differential transcriptome studies and heterologous expression. Studies show a potential new cellular target for chemotherapy-induced peripheral neuropathy and implicate the possible neuroprotective effects of vitamin E in cisplatin chemotherapy.

Intrinsic mechanical sensitivity of mammalian auditory neurons as a contributor to sound-driven neural activity.

Mechanosensation - by which mechanical stimuli are converted into a neuronal signal - is the basis for the sensory systems of hearing, balance, and touch. Mechanosensation is unmatched in speed and its diverse range of sensitivities, reaching its highest temporal limits with the sense of hearing; however, hair cells (HCs) and the auditory nerve (AN) serve as obligatory bottlenecks for sounds to engage the brain. Like other sensory neurons, auditory neurons use the canonical pathway for neurotransmission and millisecond-duration action potentials (APs). How the auditory system utilizes the relatively slow transmission mechanisms to achieve ultrafast speed, and high audio-frequency hearing remains an enigma. Here, we address this paradox and report that the mouse, and chinchilla, AN are mechanically sensitive, and minute mechanical displacement profoundly affects its response properties. Sound-mimicking sinusoidal mechanical and electrical current stimuli affect phase-locked responses. In a phase-dependent manner, the two stimuli can also evoke suppressive responses. We propose that mechanical sensitivity interacts with synaptic responses to shape responses in the AN, including frequency tuning and temporal phase locking. Combining neurotransmission and mechanical sensation to control spike patterns gives the mammalian AN a secondary receptor role, an emerging theme in primary neuronal functions.

Developmental Changes in Peripherin-eGFP Expression in Spiral Ganglion Neurons.

The two types of spiral ganglion neurons (SGNs), types I and II, innervate inner hair cells and outer hair cells, respectively, within the mammalian cochlea and send another process back to cochlear nuclei in the hindbrain. Studying these two neuronal types has been made easier with the identification of unique molecular markers. One of these markers, peripherin, was shown using antibodies to be present in all SGNs initially but becomes specific to type II SGNs during maturation. We used mice with fluorescently labeled peripherin (Prph-eGFP) to examine peripherin expression in SGNs during development and in aged mice. Using these mice, we confirm the initial expression of Prph-eGFP in both types I and II neurons and eventual restriction to only type II perikarya shortly after birth. However, while Prph-eGFP is uniquely expressed within type II cell bodies by P8, both types I and II peripheral and central processes continue to express Prph-eGFP for some time before becoming downregulated. Only at P30 was there selective type II Prph-eGFP expression in central but not peripheral processes. By 9 months, only the type II cell bodies and more distal central processes retain Prph-eGFP expression. Our results show that Prph-eGFP is a reliable marker for type II SGN cell bodies beyond P8; however, it is not generally a suitable marker for type II processes, except for central processes beyond P30. How the changes in Prph-eGFP expression relate to subsequent protein expression remains to be explored.

Prestin amplifies cardiac motor functions.

Cardiac cells generate and amplify force in the context of cardiac load, yet the membranous sheath enclosing the muscle fibers-the sarcolemma-does not experience displacement. That the sarcolemma sustains beat-to-beat pressure changes without experiencing significant distortion is a muscle-contraction paradox. Here, we report that an elastic element-the motor protein prestin (Slc26a5)-serves to amplify actin-myosin force generation in mouse and human cardiac myocytes, accounting partly for the nonlinear capacitance of cardiomyocytes. The functional significance of prestin is underpinned by significant alterations of cardiac contractility in Prestin-knockout mice. Prestin was previously considered exclusive to the inner ear's outer hair cells; however, our results show that prestin serves a broader cellular motor function.

Sustained Loss of Bdnf Affects Peripheral but Not Central Vestibular Targets.

The vestibular system is vital for proper balance perception, and its dysfunction contributes significantly to fall-related injuries, especially in the elderly. Vestibular ganglion neurons innervate vestibular hair cells at the periphery and vestibular nuclei and the uvula and nodule of the cerebellum centrally. During aging, these vestibular ganglion neurons degenerate, impairing vestibular function. A complete understanding of the molecular mechanisms involved in neurosensory cell survival in the vestibular system is unknown. Brain-derived neurotrophic factor (BDNF) is specifically required for the survival of vestibular ganglion neurons, as its loss leads to early neuronal death. Bdnf null mice die within 3 weeks of birth, preventing the study of the long-term effects on target cells. We use Pax2-cre to conditionally knock out Bdnf, allowing mice survival to approximately 6 months of age. We show that a long-term loss of Bdnf leads to a significant reduction in the number of vestibular ganglion neurons and a reduction in the number of vestibular hair cells. There was no significant decrease in the central targets lateral vestibular nucleus (LVN) or the cerebellum at 6 months. This suggests that the connectivity between central target cells and other neurons suffices to prevent their loss despite vestibular hair cell and ganglion neuron loss. Whether the central neurons would undergo eventual degeneration in the absence of Bdnf remains to be determined.

Altered Outer Hair Cell Mitochondrial and Subsurface Cisternae Connectomics Are Candidate Mechanisms for Hearing Loss in Mice.

Organelle crosstalk is vital for cellular functions. The propinquity of mitochondria, ER, and plasma membrane promote regulation of multiple functions, which include intracellular Ca2+ flux, and cellular biogenesis. Although the purposes of apposing mitochondria and ER have been described, an understanding of altered organelle connectomics related to disease states is emerging. Since inner ear outer hair cell (OHC) degeneration is a common trait of age-related hearing loss, the objective of this study was to investigate whether the structural and functional coupling of mitochondria with subsurface cisternae (SSC) was affected by aging. We applied functional and structural probes to equal numbers of male and female mice with a hearing phenotype akin to human aging. We discovered the polarization of cristae and crista junctions in mitochondria tethered to the SSC in OHCs. Aging was associated with SSC stress and decoupling of mitochondria with the SSC, mitochondrial fission/fusion imbalance, a remarkable reduction in mitochondrial and cytoplasmic Ca2+ levels, reduced K+-induced Ca2+ uptake, and marked plasticity of cristae membranes. A model of structure-based ATP production predicts profound energy stress in older OHCs. This report provides data suggesting that altered membrane organelle connectomics may result in progressive hearing loss.

Suppression of inflammation and fibrosis using soluble epoxide hydrolase inhibitors enhances cardiac stem cell-based therapy.

Stem cell replacement offers a great potential for cardiac regenerative therapy. However, one of the critical barriers to stem cell therapy is a significant loss of transplanted stem cells from ischemia and inflammation in the host environment. Here, we tested the hypothesis that inhibition of the soluble epoxide hydrolase (sEH) enzyme using sEH inhibitors (sEHIs) to decrease inflammation and fibrosis in the host myocardium may increase the survival of the transplanted human induced pluripotent stem cell derived-cardiomyocytes (hiPSC-CMs) in a murine postmyocardial infarction model. A specific sEHI (1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl)urea [TPPU]) and CRISPR/Cas9 gene editing were used to test the hypothesis. TPPU results in a significant increase in the retention of transplanted cells compared with cell treatment alone. The increase in the retention of hiPSC-CMs translates into an improvement in the fractional shortening and a decrease in adverse remodeling. Mechanistically, we demonstrate a significant decrease in oxidative stress and apoptosis not only in transplanted hiPSC-CMs but also in the host environment. CRISPR/Cas9-mediated gene silencing of the sEH enzyme reduces cleaved caspase-3 in hiPSC-CMs challenged with angiotensin II, suggesting that knockdown of the sEH enzyme protects the hiPSC-CMs from undergoing apoptosis. Our findings demonstrate that suppression of inflammation and fibrosis using an sEHI represents a promising adjuvant to cardiac stem cell-based therapy. Very little is known regarding the role of this class of compounds in stem cell-based therapy. There is consequently an enormous opportunity to uncover a potentially powerful class of compounds, which may be used effectively in the clinical setting.

Silver grass-derived activated carbon with coexisting micro-, meso- and macropores as excellent bioanodes for microbial colonization and power generation in sustainable microbial fuel cells.

In this study, highly biocompatible three-dimensional hierarchically porous activated carbon from the low-cost silver grass (Miscanthus sacchariflorus) has been fabricated through a facile carbonization approach and tested it as bioanode in microbial fuel cell (MFC) using Escherichia coli as biocatalyst. This silver grass-derived activated carbon (SGAC) exhibited an unprecedented specific surface area of 3027 m2 g-1 with the coexistence of several micro-, meso-, and macropores. The synergistic effect from pore structure (macropores - hosting E. coli to form biofilm and facilitates internal mass transfer; mesopores - favors fast electron transfer; and micropores - promotes nutrient transport to the biofilm) with very high surface area facilitates excellent extracellular electron transfer (EET) between the anode and biofilm which resulted in higher power output of 963 mW cm-2. Based on superior biocompatibility, low cost, environment-friendliness, and facile fabrication, the proposed SGAC bioanode could have a great potential for high-performance and cost-effective sustainable MFCs.

The local translation of KNa in dendritic projections of auditory neurons and the roles of KNa in the transition from hidden to overt hearing loss.

Local and privileged expression of dendritic proteins allows segregation of distinct functions in a single neuron but may represent one of the underlying mechanisms for early and insidious presentation of sensory neuropathy. Tangible characteristics of early hearing loss (HL) are defined in correlation with nascent hidden hearing loss (HHL) in humans and animal models. Despite the plethora of causes of HL, only two prevailing mechanisms for HHL have been identified, and in both cases, common structural deficits are implicated in inner hair cell synapses, and demyelination of the auditory nerve (AN). We uncovered that Na+-activated K+ (KNa) mRNA and channel proteins are distinctly and locally expressed in dendritic projections of primary ANs and genetic deletion of KNa channels (Kcnt1 and Kcnt2) results in the loss of proper AN synaptic function, characterized as HHL, without structural synaptic alterations. We further demonstrate that the local functional synaptic alterations transition from HHL to increased hearing-threshold, which entails changes in global Ca2+ homeostasis, activation of caspases 3/9, impaired regulation of inositol triphosphate receptor 1 (IP3R1), and apoptosis-mediated neurodegeneration. Thus, the present study demonstrates how local synaptic dysfunction results in an apparent latent pathological phenotype (HHL) and, if undetected, can lead to overt HL. It also highlights, for the first time, that HHL can precede structural synaptic dysfunction and AN demyelination. The stepwise cellular mechanisms from HHL to canonical HL are revealed, providing a platform for intervention to prevent lasting and irreversible age-related hearing loss (ARHL).

An ionic liquid incorporated in a quasi-solid-state electrolyte for high-temperature supercapacitor applications.

An ionic liquid (IL) incorporated in a quasi-solid-state electrolyte (ILQSE) is prepared using 1-ethyl-3-methylimidazolium tetrafluoroborate (EMIBF4) and poly (ethylene glycol dimethacrylayte) (PEGDMA) for high-temperature application of supercapacitors. The prepared ILQSE displays a thermal stability up to 150 °C and the supercapacitors exhibit a specific capacitance of 134 F g-1.

Early functional alterations in membrane properties and neuronal degeneration are hallmarks of progressive hearing loss in NOD mice.

Presbycusis or age-related hearing loss (ARHL) is the most common sensory deficit in the human population. A substantial component of the etiology stems from pathological changes in sensory and non-sensory cells in the cochlea. Using a non-obese diabetic (NOD) mouse model, we have characterized changes in both hair cells and spiral ganglion neurons that may be relevant for early signs of age-related hearing loss (ARHL). We demonstrate that hair cell loss is preceded by, or in parallel with altered primary auditory neuron functions, and latent neurite retraction at the hair cell-auditory neuron synapse. The results were observed first in afferent inner hair cell synapse of type I neurites, followed by type II neuronal cell-body degeneration. Reduced membrane excitability and loss of postsynaptic densities were some of the inaugural events before any outward manifestation of hair bundle disarray and hair cell loss. We have identified profound alterations in type I neuronal membrane properties, including a reduction in membrane input resistance, prolonged action potential latency, and a decrease in membrane excitability. The resting membrane potential of aging type I neurons in the NOD, ARHL model, was significantly hyperpolarized, and analyses of the underlying membrane conductance showed a significant increase in K+ currents. We propose that attempts to alleviate some forms of ARHL should include early targeted primary latent neural degeneration for effective positive outcomes.

Sodium-activated potassium channels shape peripheral auditory function and activity of the primary auditory neurons in mice.

Potassium (K+) channels shape the response properties of neurons. Although enormous progress has been made to characterize K+ channels in the primary auditory neurons, the molecular identities of many of these channels and their contributions to hearing in vivo remain unknown. Using a combination of RNA sequencing and single molecule fluorescent in situ hybridization, we localized expression of transcripts encoding the sodium-activated potassium channels KNa1.1 (SLO2.2/Slack) and KNa1.2 (SLO2.1/Slick) to the primary auditory neurons (spiral ganglion neurons, SGNs). To examine the contribution of these channels to function of the SGNs in vivo, we measured auditory brainstem responses in KNa1.1/1.2 double knockout (DKO) mice. Although auditory brainstem response (wave I) thresholds were not altered, the amplitudes of suprathreshold responses were reduced in DKO mice. This reduction in amplitude occurred despite normal numbers and molecular architecture of the SGNs and their synapses with the inner hair cells. Patch clamp electrophysiology of SGNs isolated from DKO mice displayed altered membrane properties, including reduced action potential thresholds and amplitudes. These findings show that KNa1 channel activity is essential for normal cochlear function and suggest that early forms of hearing loss may result from physiological changes in the activity of the primary auditory neurons.

Improved pseudocapacitive charge storage in highly ordered mesoporous TiO2/carbon nanocomposites as high-performance Li-ion hybrid supercapacitor anodes.

A Li-ion hybrid supercapacitor (Li-HSCs), an integrated system of a Li-ion battery and a supercapacitor, is an important energy-storage device because of its outstanding energy and power as well as long-term cycle life. In this work, we propose an attractive material (a mesoporous anatase titanium dioxide/carbon hybrid material, m-TiO2-C) as a rapid and stable Li+ storage anode material for Li-HSCs. m-TiO2-C exhibits high specific capacity (∼198 mA h g-1 at 0.05 A g-1) and promising rate performance (∼90 mA h g-1 at 5 A g-1) with stable cyclability, resulting from the well-designed porous structure with nanocrystalline anatase TiO2 and conductive carbon. Thereby, it is demonstrated that a Li-HSC system using a m-TiO2-C anode provides high energy and power (∼63 W h kg-1, and ∼4044 W kg-1).