Estimation of electrical muscle activity during gait using inertial measurement units with convolution attention neural network and small-scale dataset.

In general, muscle activity can be directly measured using Electromyography (EMG) or calculated with musculoskeletal models. However, both methods are not suitable for non-technical users and unstructured environments. It is desired to establish more portable and easy-to-use muscle activity estimation methods. Deep learning (DL) models combined with inertial measurement units (IMUs) have shown great potential to estimate muscle activity. However, it frequently occurs in clinical scenarios that a very small amount of data is available and leads to limited performance of the DL models, while the augmentation techniques to efficiently expand a small sample size for DL model training are rarely used. The primary aim of the present study was to develop a novel DL model to estimate the EMG envelope during gait using IMUs with high accuracy. A secondary aim was to develop a novel model-based data augmentation method to improve the performance of the estimation model with small-scale dataset. Therefore, in the present study, a time convolutional network-based generative adversarial network, namely MuscleGAN, was proposed for data augmentation. Moreover, a subject-independent regression DL model was developed to estimate EMG envelope. Results suggested that the proposed two-stage method has better generalization and estimation performance than the commonly used existing methods. Pearson correlation coefficient and normalized root-mean-square errors derived from the proposed method reached up to 0.72 and 0.13, respectively. It was indicated that the MuscleGAN indeed improved the estimation accuracy of lower limb EMG envelope from 70% to 72%. Thus, even using only two IMUs and a very small-scale dataset, the proposed model is still capable of accurately estimating lower limb EMG envelope, demonstrating considerable potential for its application in clinical and daily life scenarios.

ROS-induced oxidative stress and mitochondrial dysfunction: a possible mechanism responsible for noise-induced ribbon synaptic damage.

Evidence suggests that damage to the ribbon synapses (RS) may be the main cause of auditory dysfunction in noise-induced hearing loss (NIHL). Oxidative stress is implicated in the pathophysiology of synaptic damage. However, the relationship between oxidative stress and RS damage in NIHL remains unclear. To investigate the hypothesis that noise-induced oxidative stress is a key factor in synaptic damage within the inner ear, we conducted a study using mice subjected to single or repeated noise exposure (NE). We assessed auditory function using auditory brainstem response (ABR) test and examined cochlear morphology by immunofluorescence staining. The results showed that mice that experienced a single NE exhibited a threshold shift and recovered within two weeks. The ABR wave I latencies were prolonged, and the amplitudes decreased, suggesting RS dysfunction. These changes were also demonstrated by the loss of RS as evidenced by immunofluorescence staining. However, we observed threshold shifts that did not return to baseline levels following secondary NE. Additionally, ABR wave I latencies and amplitudes exhibited notable changes. Immunofluorescence staining indicated not only severe damage to RS but also loss of outer hair cells. We also noted decreased T-AOC, ATP, and mitochondrial membrane potential levels, alongside increased hydrogen peroxide concentrations post-NE. Furthermore, the expression levels of 4-HNE and 8-OHdG in the cochlea were notably elevated. Collectively, our findings suggest that the production of reactive oxygen species leads to oxidative damage in the cochlea. This mitochondrial dysfunction consequently contributes to the loss of RS, precipitating an early onset of NIHL.

A meta-analysis on the impact of resistance training on phase angle in middle-aged and older individuals.

PURPOSE: To determine the impact of resistance training (RT) on phase angle (PhA) in middle-aged and older individuals via meta-analysis, explore effects in subgroups, and identify optimal RT protocol. MATERIALS AND METHODS: We searched five databases using predefined criteria, assessed literature quality per Cochrane 5.1 Handbook, and used Revman 5.3 for effect size aggregation, bias assessment, sensitivity analysis, and subgroup analysis. RESULTS: RT improved PhA in middle-aged and older individuals (d = 0.34, 95 % CI: 0.27-0.40, P < 0.05). Effective subgroups included Suspension (d = 0.62, 95 % CI: 0.33-0.90, P < 0.05), free-weights and machine (d = 0.36, 95 % CI: 0.28-0.45, P < 0.05), equipment training (d = 0.24, 95 % CI: 0.13-0.36, P < 0.05), and moderate-intensity RT (d = 0.34, 95 % CI: 0.27-0.42, P < 0.05). RT was conducted 2-3 times/week (d = 0.20, 95 % CI: 0.01-0.38, P < 0.05) or (d = 0.38, 95 % CI: 0.30-0.47, P < 0.05). PhA improved after 8 weeks (d = 0.37, 95 % CI: 0.23-0.51, P < 0.05), 12 weeks (d = 0.35, 95 % CI: 0.26-0.44, P < 0.05), and ≥ 24 weeks (d = 0.26, 95 % CI: 0.11-0.41, P < 0.05) of RT in aged and older individuals. Low- and high-intensity RT, elastic band training, and weekly exercises did not significantly improve PhA. CONCLUSIONS: RT enhances PhA in middle-aged and older adults. For optimal results, we recommend 2-3 weekly sessions of free weights and machine training lasting at least 8 weeks.

Analysis of Immune and Prognostic-Related lncRNA PRKCQ-AS1 for Predicting Prognosis and Regulating Effect in Sepsis.

Background: Sepsis was a high mortality and great harm systemic inflammatory response syndrome caused by infection. lncRNAs were potential prognostic marker and therapeutic target. Therefore, we expect to screen and analyze lncRNAs with potential prognostic markers in sepsis. Methods: Transcriptome sequencing and limma was used to screen dysregulated RNAs. Key RNAs were screened by correlation analysis, lncRNA-mRNA co-expression and weighted gene co-expression network analysis. Immune infiltration, gene set enrichment analysis and gene set variation analysis were used to analyze the immune correlation. Kaplan-Meier curve, receiver operator characteristic curve, Cox regression analysis and nomogram were used to analyze the correlation between key RNAs and prognosis. Sepsis model was established by lipopolysaccharide-induced HUVECs injury, and then cell viability and migration ability were detected by cell counting kit-8 and wound healing assay. The levels of apoptosis-related proteins and inflammatory cytokines were detected by RT-qPCR and Western blot. Reactive Oxygen Species and superoxide dismutase were detected by commercial kit. Results: Fourteen key differentially expressed lncRNAs and 663 key differentially expressed genes were obtained. And these lncRNAs were closely related to immune cells, especially T cell activation, immune response and inflammation. Subsequently, Subsequently, lncRNA PRKCQ-AS1 was identified as the regulator for further investigation in sepsis. RT-qPCR results showed that PRKCQ-AS1 expression was up-regulated in clinical samples and sepsis model cells, which was an independent prognostic factor in sepsis patients. Immune correlation analysis showed that PRKCQ-AS1 was involved in the immune response and inflammatory process of sepsis. Cell function tests confirmed that PRKCQ-AS1 could inhibit sepsis model cells viability and promote cell apoptosis, inflammatory damage and oxidative stress. Conclusion: We constructed immune-related lncRNA-mRNA regulatory networks in the progression of sepsis and confirmed that PRKCQ-AS1 is an important prognostic factor affecting the progression of sepsis and is involved in immune response.

Estimation of Lower Limb Joint Angles and Joint Moments during Different Locomotive Activities Using the Inertial Measurement Units and a Hybrid Deep Learning Model.

Using inertial measurement units (IMUs) to estimate lower limb joint kinematics and kinetics can provide valuable information for disease diagnosis and rehabilitation assessment. To estimate gait parameters using IMUs, model-based filtering approaches have been proposed, such as the Kalman filter and complementary filter. However, these methods require special calibration and alignment of IMUs. The development of deep learning algorithms has facilitated the application of IMUs in biomechanics as it does not require particular calibration and alignment procedures of IMUs in use. To estimate hip/knee/ankle joint angles and moments in the sagittal plane, a subject-independent temporal convolutional neural network-bidirectional long short-term memory network (TCN-BiLSTM) model was proposed using three IMUs. A public benchmark dataset containing the most representative locomotive activities in daily life was used to train and evaluate the TCN-BiLSTM model. The mean Pearson correlation coefficient of joint angles and moments estimated by the proposed model reached 0.92 and 0.87, respectively. This indicates that the TCN-BiLSTM model can effectively estimate joint angles and moments in multiple scenarios, demonstrating its potential for application in clinical and daily life scenarios.

Decoding the deactivation mechanism of R192W mutation of ZAP-70 using molecular dynamics simulations and binding free energy calculations.

CONTEXT: ZAP-70 (zeta-chain-associated protein of 70 kDa), serving as a critical regulator for T cell antigen receptor signaling, represents an attractive therapeutic target for autoimmunity disease. How the mechanistical mechanism of ZAP-70 to a human autoimmune syndrome-associated R192W mutation remains unclear. The results indicated that the R192W mutation of ZAP-70 clearly affected the conformational flexibility of the N-terminal ITAM-Y2P. Structural analysis unveiled that the R192W mutation of ZAP-70 caused the exposure of the N-terminal ITAM-Y2P to the solvent. MM-GBSA binding free energy calculations exhibited that the R192W mutation decreased the binding affinity of ITAM-Y2P to the ZAP-70 mutant. Residue-based free energy decomposition further revealed that the protein-peptide interaction networks involving electrostatic interactions provide significant contributions for complex formation. The energy unfavorable residues include Arg43, Arg192, Tyr240, and Lys244 from ZAP-70 and Asn301, Leu303, pY304, and pY315 from ITAM-Y2P in the R192W mutant. Our obtained results may help the understanding of the deactivation mechanism of ZAP-70 induced by the R192W mutation. METHODS: In the work, multiple replica molecular dynamics simulations and molecular mechanics-generalized Born surface area (MM-GBSA) method were performed to reveal the doubly phosphorylated ITAMs (ITAM-Y2P)-mediated deactivation mechanism of ZAP-70 induced by the R192W mutation.

Notch mediates the glycolytic switch via PI3K/Akt signaling to support embryonic development.

BACKGROUND: Energy metabolism disorder or insufficient energy supply during incubation will affect the development and survival of avian embryos. Especially, ß-oxidation could not provide the continuous necessary energy for avian embryonic development due to the increasing energy demand under hypoxic conditions during the mid-late embryonic stages. The role and mechanism of hypoxic glycolysis replacing ß-oxidation as the main source of energy supply for avian embryonic development in the mid-late stages is unclear. RESULTS: Here, we found that in ovo injection with glycolysis inhibitor or γ-secretase inhibitor both decreased the hepatic glycolysis level and impaired goose embryonic development. Intriguingly, the blockade of Notch signaling is also accompanied by the inhibition of PI3K/Akt signaling in the embryonic primary hepatocytes and embryonic liver. Notably, the decreased glycolysis and impaired embryonic growth induced by the blockade of Notch signaling were restored by activation of PI3K/Akt signaling. CONCLUSIONS: Notch signaling regulates a key glycolytic switch in a PI3K/Akt-dependent manner to supply energy for avian embryonic growth. Our study is the first to demonstrate the role of Notch signaling-induced glycolytic switching in embryonic development, and presents new insight into the energy supply patterns in embryogenesis under hypoxic conditions. In addition, it may also provide a natural hypoxia model for developmental biology studies such as immunology, genetics, virology, cancer, etc.

Extended Application of Inertial Measurement Units in Biomechanics: From Activity Recognition to Force Estimation.

Abnormal posture or movement is generally the indicator of musculoskeletal injuries or diseases. Mechanical forces dominate the injury and recovery processes of musculoskeletal tissue. Using kinematic data collected from wearable sensors (notably IMUs) as input, activity recognition and musculoskeletal force (typically represented by ground reaction force, joint force/torque, and muscle activity/force) estimation approaches based on machine learning models have demonstrated their superior accuracy. The purpose of the present study is to summarize recent achievements in the application of IMUs in biomechanics, with an emphasis on activity recognition and mechanical force estimation. The methodology adopted in such applications, including data pre-processing, noise suppression, classification models, force/torque estimation models, and the corresponding application effects, are reviewed. The extent of the applications of IMUs in daily activity assessment, posture assessment, disease diagnosis, rehabilitation, and exoskeleton control strategy development are illustrated and discussed. More importantly, the technical feasibility and application opportunities of musculoskeletal force prediction using IMU-based wearable devices are indicated and highlighted. With the development and application of novel adaptive networks and deep learning models, the accurate estimation of musculoskeletal forces can become a research field worthy of further attention.

Identification of a novel porcine Teschovirus 2 strain as causative agent of encephalomyelitis in suckling piglets with high mortality in China.

BACKGROUND: Porcine Teschovirus (PTV), also named Teschovirus A, is prevalent in pig populations, mainly causing neurological symptoms, diarrhea, pneumonia, and reproductive failure, however the morbidity and mortality are usually low in pig farms. CASE PRESENTATION: In this study, we reported a PTV outbreak investigation in one large-scale pig farm in China with severe symptoms including diarrhea, lethargy, locomotor ataxia, nystagmus, paralysis of the hind limbs, and coma in piglets. More importantly, the mortality reached 38% in suckling pigs, which is remarkably high in PTV history. A novel PTV strain, named HeNZ1, was isolated from cerebral samples of one suckling pig and the genome sequence was obtained by NGS sequencing. Phylogenetic and evolutionary divergence analyses revealed that HeNZ1 belongs to PTV genotype 2. Surprisingly, the VP1 coding region of HeNZ1 shares the highest sequence similarity with European PTV-2 strains, instead of China domestic PTV-2 strains, implying it may not derive from China local PTV-2 strains. Multiple sequence alignment and B cell epitope prediction of PTV VP1 and VP2 protein revealed 10 B cell epitopes, 5 mutant clusters and 36 unique mutation sites, of which 19 unique mutation sites are located in B cell epitopes and exposed on the surface of VP1 or VP2, implying significant antigenic drift potential of HeNZ1. CONCLUSION: These results indicate that HeNZ1 is a highly virulent PTV-2 strain, which capable of causing severe neurological symptoms and high mortality in piglets. Bioinformatic analysis suggest that HeNZ1 is genetically and antigenically different from other Chinese PTV-2 strains. Overall, current case expanded our understanding of PTV-2 clinical spectrum and revealed the emergence of a highly virulent PTV-2 strain with substantial genetic diversity and antigenic drift potential in VP1 and VP2.

AAV-ie-mediated UCP2 overexpression accelerates inner hair cell loss during aging in vivo.

BACKGROUND: Uncoupling protein 2 (UCP2), activated by excessive reactive oxygen species (ROS) in vivo, has the dual effect of reducing ROS to protect against oxidative stress and reducing ATP production to regulate cellular metabolism. Both the UCP2 and ROS are increased in cochleae in age-related hearing loss (ARHL). However, the role of UCP2 in sensory hair cells in ARHL remains unclear. METHODS: Male C57BL/6 J mice were randomly assigned to an 8-week-old group (Group 1), a 16-week-old group (Group 2), a 16-week-old + adeno-associated virus-inner ear (AAV-ie) group (Group 3), and a 16-week-old + AAV-ie-UCP2 group (Group 4). Mice aged 8 weeks were administrated with AAV-ie-GFP or AAV-ie-UCP2 via posterior semicircular canal injection. Eight weeks after this viral intervention, hearing thresholds and wave-I amplitudes were tested by auditory brainstem response (ABR). Subsequently, the cochlear basilar membrane was dissected for investigation. The number of hair cells and inner hair cell (IHC) synapses, the level of ROS, and the expression of AMP-activated protein kinase α (AMPKα), were assessed by immunofluorescence staining. In addition, mitochondrial function was determined, and the expression of AMPKα and UCP2 proteins was further evaluated using western blotting. RESULTS: Mice with early-onset ARHL exhibited enhanced oxidative stress and loss of outer hair cells and IHC synapses, while UCP2 overexpression aggravated hearing loss and cochlear pathophysiological changes in mice. UCP2 overexpression resulted in a notable decrease in the number of IHCs and IHC synapses, caused ATP depletion and excessive ROS generation, increased AMPKα protein levels, and promoted IHC apoptosis, especially in the apical and middle turns of the cochlea. CONCLUSION: Collectively, our data suggest that UCP2 overexpression may cause mitochondrial dysfunction via energy metabolism, which activates mitochondrion-dependent cellular apoptosis and leads to IHC loss, ultimately exacerbating ARHL.

Heterozygous MYH9 Mutations in 2 Children With Cochlear Nerve Canal Stenosis.

MYH9 is a gene that encodes for a subunit of the myosin heavy chain IIA protein. Mutations in MYH9 are associated with hematologic abnormalities, renal dysfunction, and hearing loss. Bony cochlear nerve canal stenosis (CNCS), which is diagnosed on computed tomography (CT) imaging, has been associated with congenital deafness, cochlear nerve aplasia/hypoplasia, and inner ear malformations. We report two cases of CNCS presenting with profound congenital hearing loss whom we diagnosed with mutations in MYH9 and discuss the genotype-phenotype association and implications for management.

SIRT3-mediated deacetylation protects inner hair cell synapses in a H2O2-induced oxidative stress model in vitro.

Oxidative stress is considered a driving event in the damage to inner hair cell (IHC) synapses. Mitochondrial deacetylase sirtuin 3 (SIRT3) is an important regulator of reactive oxygen species (ROS) production. However, the effect of SIRT3 on IHC synapses remains elusive. In this study, we treated cochlear basilar membrane (CBM) with hydrogen peroxide (H2O2) to establish an oxidative stress model in vitro. The H2O2-induced CBM exhibited decreased the number of IHC synapses with low levels of ATP and mitochondrial membrane potential. Additionally, H2O2-induced CBM showed markedly reduced levels of forkhead box protein O 3a (FOXO3a), superoxide dismutase 2 (SOD2), and isocitrate dehydrogenase 2 (IDH2), thereby increasing ROS generation. SIRT3 overexpression via administrating nicotinamide riboside in the H2O2-induced CBM protected IHC synapses against oxidative stress and inhibited hair cell apoptosis. We further demonstrated that SIRT3 overexpression led to upregulation of IDH2, and hypoacetylation of several proteins, such as FOXO3a and SOD2, which in turn reduced the levels of ROS and improved mitochondrial function. Collectively, these findings reveal that overexpressing SIRT3 may be a potential therapeutic approach for damaged IHC synapses induced by oxidative stress.

Clinical characteristics in unilateral cochlear nerve canal stenosis.

OBJECTIVE: To characterize the clinical features of patients with congenital hearing loss and unilateral cochlear nerve canal stenosis (CNCS). METHODS: A retrospective review of 12 patients with unilateral CNCS diagnosed between January 2018 and December 2019 at a tertiary referral hospital was performed. RESULTS: Of the 12 patients identified, there were 6 males and 6 females. All patients presented with hearing loss, with no other chief complaints. Two patients had accessory auricles. Eleven patients had a severe to profound sensorineural hearing loss on the affected side, while 1 patient had an isolated high-frequency hearing loss. Nine patients demonstrated atresia of the cochlear nerve canal (CNC), while three patients had a stenotic, but patent, CNC. CONCLUSION: Prompt radiologic diagnosis of patients with unilateral CNCS is important for patient counseling and appropriate rehabilitation.

Late career participation of late retirees in the age of the silver tsunami: understanding the influencing mechanism of health status and employment-based health insurance participation.

BACKGROUND: The delayed retirement initiative and population aging have led to a growing group of late retirees. However, it remains unclear whether the existing employment-based health insurance system can effectively match the recently proposed initiative and support late retirees, especially those with pre-existing function limitations. Thus, this study aims to investigate the influencing mechanism of China's Urban Employee Basic Medical Insurance (UEBMI), physical functioning limitation (PFL) and difficulty in instrumental activities of daily living (IADLs) on labour participation of late retirees in China. METHODS: This study uses data from the China Health and Retirement Longitudinal Study (CHARLS) survey, which tracks the quality of life among older adults in China (valid sample size = 5560). RESULTS: Empirical results show that China's employment-based health insurance (i.e. UEBMI) and health conditions (i.e. PFL and difficulty in IADLs) are positively associated with late retirees' withdrawal from late career participation. In addition, a higher level of difficulty in IADLs could strengthen the effect of PFL on late retirees' withdrawal from late career participation, which could be further buffered by UEBMI beneficiary status. CONCLUSION: In the formulation of delayed retirement policies, it is necessary to consider the influencing mechanism of the social health insurance system and health conditions on late career participation of older workers to ensure policy effectiveness.

Delineating the activation mechanism and conformational landscape of a class B G protein-coupled receptor glucagon receptor.

Class B G protein-coupled receptors (GPCRs) are important targets in the treatment of metabolic syndrome and diabetes. Although multiple structures of class B GPCRs-G protein complexes have been elucidated, the detailed activation mechanism of the receptors remains unclear. Here, we combine Gaussian accelerated molecular dynamics simulations and Markov state models (MSM) to investigate the activation mechanism of a canonical class B GPCR, human glucagon receptor-GCGR, including the negative allosteric modulator-bound inactive state, the agonist glucagon-bound active state, and both glucagon- and Gs-bound fully active state. The free-energy landscapes of GCGR show the conformational ensemble consisting of three activation-associated states: inactive, active, and fully active. The structural analysis indicates the high dynamics of GCGR upon glucagon binding with both active and inactive conformations in the ensemble. Significantly, the H8 and TM6 exhibits distinct features from the inactive to the active states. The additional simulations demonstrate the role of H8 in the recruitment of Gs. Gs binding presents a crucial function of stabilizing the glucagon binding site and MSM highlights the absolute requirement of Gs to help the GCGR reach the fully active state. Together, our results reveal the detailed activation mechanism of GCGR from the view of conformational dynamics.

ROS-Induced Oxidative Damage and Mitochondrial Dysfunction Mediated by Inhibition of SIRT3 in Cultured Cochlear Cells.

Sensorineural hearing loss (SNHL) is one of the most common causes of disability worldwide. Previous evidence suggests that reactive oxygen species (ROS) may play an important role in the occurrence and development of SNHL, while its mechanism remains unclear. We cultured dissected organs of Corti in medium containing different concentrations (0, 0.25, 0.5, 0.75, 1, and 1.25 mM) of hydrogen peroxide (H2O2) and established a four-concentration model of 0, 0.5, 0.75, and 1 mM to study different degrees of damage. We examined ROS-induced mitochondrial damage and the role of sirtuin 3 (SIRT3). Our results revealed that the number of ribbon synapses and hair cells appeared significantly concentration-dependent decrease with exposure to H2O2. Outer hair cells (OHCs) and inner hair cells (IHCs) began to be lost, and activation of apoptosis of hair cells (HCs) was observed at 0.75 mM and 1 mM H2O2, respectively. In contrast with the control group, the accumulation of ROS was significantly higher, and the mitochondrial membrane potential (MMP) was lower in the H2O2-treated groups. Furthermore, the expression of SIRT3, FOXO3A, and SOD2 proteins declined, except for an initial elevation of SIRT3 between 0 and 0.75 mM H2O2. Administration of the selective SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine resulted in increased damage to the cochlea, including loss of ribbon synapses and hair cells, apoptosis of hair cells, more production of ROS, and reduced mitochondrial membrane potential. Thoroughly, our results highlight that ROS-induced mitochondrial oxidative damage drives hair cell degeneration and apoptosis. Furthermore, SIRT3 is crucial for preserving mitochondrial function and protecting the cochlea from oxidative damage and may represent a possible therapeutic target for SNHL.

The interaction of delayed retirement initiative and the multilevel social health insurance system on physical health of older people in China.

With many social challenges posed by an ageing population, the delayed retirement initiative has received wide attention from policymakers. However, China's current multi-level social health insurance system seems not perfect and not ready for the delayed retirement initiative. The public are generally concerned that the benefits of late retirees cannot be well guaranteed. Using data from China Health and Retirement Longitudinal Study (CHARLS) and the chorological design (CHARLS-2015 and -2018 waves), this study finds that (1) late retirement could be beneficial for physical health among older adults; (2) there have disparities between the effects of different social health insurances on physical health among older adults; (3) social health insurances could weaken the benefits of late retirement to physical health among older adults. Results imply that China's current multi-level social medical insurance system may lag behind the proposed delayed retirement initiative and have policy limitations for late retirees.

Sirtuin-3 Protects Cochlear Hair Cells Against Noise-Induced Damage via the Superoxide Dismutase 2/Reactive Oxygen Species Signaling Pathway.

Mitochondrial oxidative stress is involved in hair cell damage caused by noise-induced hearing loss (NIHL). Sirtuin-3 (SIRT3) plays an important role in hair cell survival by regulating mitochondrial function; however, the role of SIRT3 in NIHL is unknown. In this study, we used 3-TYP to inhibit SIRT3 and found that this inhibition aggravated oxidative damage in the hair cells of mice with NIHL. Moreover, 3-TYP reduced the enzymatic activity and deacetylation levels of superoxide dismutase 2 (SOD2). Subsequently, we administered adeno-associated virus-SIRT3 to the posterior semicircular canals and found that SIRT3 overexpression significantly attenuated hair cell injury and that this protective effect of SIRT3 could be blocked by 2-methoxyestradiol, a SOD2 inhibitor. These findings suggest that insufficient SIRT3/SOD2 signaling leads to mitochondrial oxidative damage resulting in hair cell injury in NIHL. Thus, ameliorating noise-induced mitochondrial redox imbalance by intervening in the SIRT3/SOD2 signaling pathway may be a new therapeutic target for hair cell injury.

Homogeneous-to-Heterogeneous: Unsupervised Learning for RGB-Infrared Person Re-Identification.

RGB-Infrared (RGB-IR) cross-modality person re-identification (re-ID) is attracting more and more attention due to requirements for 24-h scene surveillance. However, the high cost of labeling person identities of an RGB-IR dataset largely limits the scalability of supervised models in real-world scenarios. In this paper, we study the unsupervised RGB-IR person re-ID problem (or briefly uRGB-IR re-ID) in which no identity annotations are available in RGB-IR cross-modality datasets. Considering that intra-modality (i.e., RGB-RGB or IR-IR) re-ID is much easier than cross-modality re-ID and can provide shared knowledge for RGB-IR re-ID, we propose a two-stage method to solve the uRGB-IR re-ID, namely homogeneous-to-heterogeneous learning. In the first stage, the unsupervised self-learning method is conducted to learn the intra-modality feature representation and to generate the pseudo-labeled identities of person images separately for each modality. In the second stage, heterogeneous learning is used to learn a shared discriminative feature representation by distilling the knowledge from intra-modality pseudo-labels, to align two modalities via a modality-based consistent learning module, and finally to target modality-invariant learning via a pseudo-labeled positive instance selection module. With the use of homogeneous-to-heterogeneous learning, the proposed unsupervised framework greatly reduces the modality gap and thus learns a robust feature representation against RGB and infrared modalities, leading to promising accuracy. We also propose a novel cross-modality re-ranking approach that includes a self-modality search and a cycle-modality search to tailor the uRGB-IR re-ID. Unlike conventional re-ranking, the proposed re-ranking method takes a modality-based constraint into re-ranking and thus can select more reliable nearest neighbors, which greatly improves uRGB-IR re-ID. The experimental results demonstrate the superiority of our approach on the SYSU-MM01 and RegDB datasets.

Cochlear Nerve Canal Stenosis: Association With MYH14 and MYH9 Genes.

The bony cochlear nerve canal transmits the cochlear nerve as it passes from the fundus of the internal auditory canal to the cochlea. Stenosis of the cochlear nerve canal, defined as a diameter less than 1.0 mm in transverse diameter, is associated with inner ear anomalies and severe to profound congenital hearing loss. We describe an 11-month-old infant with nonsyndromic congenital sensorineural hearing loss with cochlear nerve canal stenosis. Next-generation sequencing revealed heterozygous mutations in MYH9 and MYH14, encoding for the inner ear proteins myosin heavy chain IIA and IIC. The patient's hearing was rehabilitated with bilateral cochlear implantation.