Pyroptosis inhibition alleviates acute lung injury via E-twenty-six variant gene 5-mediated downregulation of gasdermin D.

BACKGROUND: Acute lung injury (ALI) is a life-threatening condition characterized by excessive pulmonary inflammation, yet its precise pathophysiology remains elusive. Pyroptosis, a programmed cell death mechanism controlled by gasdermin D (GSDMD), has been linked to the etiology of ALI. This study investigated the regulatory functions of the transcription factor E-twenty-six variant gene 5 (ETV5) and GSDMD in ALI. METHODS: Lipopolysaccharide (LPS) was used to treat BEAS-2B cells (50 mmol/mL) and establish an LPS-induced mouse model of ALI (by intratracheal administration, 3 mg/kg). Protein-protein docking, immunofluorescence analysis, western blotting, real-time quantitative polymerase chain reaction, and dual-luciferase reporter gene assay were used to examine ETV5-mediated negative feedback regulation of GSDMD and its effects on pyroptosis and ALI. RESULTS: Our results showed that the physiological function of ETV5 was reduced by its downregulated expression, which impeded its nuclear translocation in ALI mice. Increased pyroptosis and enhanced production of inflammatory cytokines were associated with LPS-induced ALI. ETV5 overexpression in LPS-treated BEAS-2B cells decreased the expression of total and membrane-bound GSDMD, negatively regulated GSDMD, and prevented pyroptosis. The expression of inflammatory cytokines was subsequently reduced due to this inhibition, which, in turn, reduced ALI. Molecular docking analysis and dual-luciferase reporter gene assay results indicated a direct interaction between ETV5 and GSDMD, which inhibited GSDMD production. CONCLUSION: Our results indicate that ETV5 inhibits pyroptosis, decreases the expression of inflammatory cytokines, and negatively regulates GSDMD expression to ameliorate ALI symptoms.

Partial Rhombencephalosynapsis Presenting in an Adult with Cerebello-Trigeminal-Dermal Dysplasia.

Gomez-Lopez-Hernandez syndrome (GLHS), also known as cerebello-trigeminal-dermal dysplasia, is a neurocutaneous disorder typically presenting in childhood. GLHS is characterized by rhombencephalosynapsis (RES) and partial alopecia, with or without trigeminal anesthesia. We describe a rare case of GLHS in a paucisymptomatic adult who presented with new-onset seizure-like activity. Magnetic resonance imaging revealed partial midline fusion of the cerebellar hemispheres, incomplete development of vermis, and slight medialization of the dentate nuclei: all consistent with the diagnosis of RES. Radiographic evidence combined with partial alopecia, truncal ataxia, and muscular hypotonia are suggestive GLHS diagnosis. Our report not only highlights the importance of maintaining GLHS on the differential for new-onset seizure-like activity, but also demonstrates how patients with GLHS may be minimally symptomatic and diagnosed in adulthood. Lay Summary: The Gomez-Lopez-Hernandez syndrome (GLHS), or cerebellotrigeminal-dermal dysplasia, is a rare condition that affects both the nervous system and the skin. It involves abnormal development of the brain, partial alopecia [thinning of hair], and loss of sensation in the face. One specific brain malformation, called rhombencephalosynapsis (RES), results from abnormal formation of the cerebellum and is seen in GHLS.Both RES and GLHS present early in childhood, and cases presenting later in life are exceptionally rare. Here we describe a young adult with RES and GLHS whose normal development and mild clumsiness eluded recognition by doctors until early adulthood when she presented with a single seizure.

An Observational Study: Association Between Atopic Dermatitis and Bacterial Colony of the Skin Based on 16S rRNA Gene Sequencing.

Aim: Atopic dermatitis (AD) often accompanies skin infections, and bacterial skin infections often cause persistent and worsening symptoms. In this study, we explored the key changes in the microbiota of AD patients, as well as the effects of different ages and the severity of rash on changes in the microbiota. Patients and Methods: A total of 95 AD patients and 77 healthy volunteers were recruited. The AD patients were divided into three groups based age and three groups according to the EASI score. Microorganisms collected from the skin were analyzed through 16S rRNA gene sequencing, revealing species diversity via α and ß diversity analyses. Species compositions were compared at the phylum and genus levels. The significance of skin microbiota at the genus level was assessed using the random forest algorithm. Finally, the impact of relationships between different microbial communities on the microbial community composition and the pathogenesis of AD was explored using Pearson correlation coefficients. Results: The species diversity of the skin microbiota in the AD group significantly decreased. Compared with that in the healthy volunteers (HV) group, the bacterial diversity in the two groups of samples significantly differed. Staphylococcus dominated the bacterial communities, and as AD symptoms gradually worsened, the abundance of Staphylococcus gradually increased. Among all bacterial genera with a relative abundance greater than 1%, Staphylococcus showed a negative correlation with other genera, and showed significant consistency in specimens from different age groups. Conclusion: Changes in the abundance of Staphylococcus in the skin bacterial colonies are the main cause of AD. Brevundimonas, Paracoccus, Corynebacterium, and Veillonella may serve as characteristic biomarkers for AD. These results indicate that altering the microbiota composition of the skin may aid in the treatment of AD.

Fabrication of Multiple-Channel Electrochemical Microneedle Electrode Array via Separated Functionalization and Assembly Method.

Real-time monitoring of physiological indicators inside the body is pivotal for contemporary diagnostics and treatments. Implantable electrodes can not only track specific biomarkers but also facilitate therapeutic interventions. By modifying biometric components, implantable electrodes enable in situ metabolite detection in living tissues, notably beneficial in invasive glucose monitoring, which effectively alleviates the self-blood-glucose-managing burden for patients. However, the development of implantable electrochemical electrodes, especially multi-channel sensing devices, still faces challenges: (1) The complexity of direct preparation hinders functionalized or multi-parameter sensing on a small scale. (2) The fine structure of individual electrodes results in low spatial resolution for sensor functionalization. (3) There is limited conductivity due to simple device structures and weakly conductive electrode materials (such as silicon or polymers). To address these challenges, we developed multiple-channel electrochemical microneedle electrode arrays (MCEMEAs) via a separated functionalization and assembly process. Two-dimensional microneedle (2dMN)-based and one-dimensional microneedle (1dMN)-based electrodes were prepared by laser patterning, which were then modified as sensing electrodes by electrochemical deposition and glucose oxidase decoration to achieve separated functionalization and reduce mutual interference. The electrodes were then assembled into 2dMN- and 1dMN-based multi-channel electrochemical arrays (MCEAs), respectively, to avoid damaging functionalized coatings. In vitro and in vivo results demonstrated that the as-prepared MCEAs exhibit excellent transdermal capability, detection sensitivity, selectivity, and reproducibility, which was capable of real-time, in situ glucose concentration monitoring.

Genome-wide DNA methylation analysis identifies potent CpG signature for temzolomide response in non-G-CIMP glioblastomas with unmethylated MGMT promoter: MGMT-dependent roles of GPR81.

PURPOSES: To identify potent DNA methylation candidates that could predict response to temozolomide (TMZ) in glioblastomas (GBMs) that do not have glioma-CpGs island methylator phenotype (G-CIMP) but have an unmethylated promoter of O-6-methylguanine-DNA methyltransferase (unMGMT). METHODS: The discovery-validation approach was planned incorporating a series of G-CIMP-/unMGMT GBM cohorts with DNA methylation microarray data and clinical information, to construct multi-CpG prediction models. Different bioinformatic and experimental analyses were performed for biological exploration. RESULTS: By analyzing discovery sets with radiotherapy (RT) plus TMZ versus RT alone, we identified a panel of 64 TMZ efficacy-related CpGs, from which a 10-CpG risk signature was further constructed. Both the 64-CpG panel and the 10-CpG risk signature were validated showing significant correlations with overall survival of G-CIMP-/unMGMT GBMs when treated with RT/TMZ, rather than RT alone. The 10-CpG risk signature was further observed for aiding TMZ choice by distinguishing differential outcomes to RT/TMZ versus RT within each risk subgroup. Functional studies on GPR81, the gene harboring one of the 10 CpGs, indicated its distinct impacts on TMZ resistance in GBM cells, which may be dependent on the status of MGMT expression. CONCLUSIONS: The 64 TMZ efficacy-related CpGs and in particular the 10-CpG risk signature may serve as promising predictive biomarker candidates for guiding optimal usage of TMZ in G-CIMP-/unMGMT GBMs.

The Gomez-Lopez-Hernandez Syndrome: The Contribution of 2 Hispanic Giants of Pediatric Neurology.

The specialty of Pediatric Neurology emerged during the 20th century, a period in which many neurologists played significant roles in revolutionizing this field. Two acclaimed pediatric neurologists of Hispanic origin, Drs Manual Gomez and Arturo Lopez-Hernandez, made substantial contributions to the literature on pediatric neurology. One of their remarkable contributions was their discovery of a new, rare neurocutaneous syndrome with variable phenotype, the Gomez-Lopez-Hernandez syndrome (GLHS). Here, we describe the current understanding of GLHS and the historical background of how 2 celebrated Hispanic pediatric neurologists discovered this rare, sporadic syndrome during a time when there was a limited representation of minorities in the medical profession.

Helicity-resolved Raman scattering of MoS2 bulk crystal.

Helicity-resolved Raman spectroscopy (HRRS) can effectively distinguish the Raman modes of two-dimensional (2D) layered materials by phonon symmetry. In this paper, we systematically investigated the phonon helicity selection of basal and edge planes of MoS2 bulk by HRRS. We find that the symmetry of the crystal structure changes the helicity selection of the E1g, E1 2g, and A1g modes in the edge plane. The theoretical calculation results confirm that the E1 2g and A1g modes of the basal plane exhibit a perfect helicity exchange, and the helicity selections of the E1 2g and A1g modes of the edge plane are eliminated or weakened. Our study provides references for phonon helicity selection of 2D layered materials represented by MoS2.

Preparation, characteristics and cytotoxicity of green synthesized selenium nanoparticles using Paenibacillus motobuensis LY5201 isolated from the local specialty food of longevity area.

Selenium is an essential micronutrient element. For the extremely biotoxic of selenite, Selenium nanoparticles (SeNPs) is gaining increasing interest. In this work, a selenium-enriched strain with highly selenite-resistant (up to 173 mmol/L) was isolated from the local specialty food of longevity area and identified as Paenibacillus motobuensis (P. motobuensis) LY5201. Most of the SeNPs were accumulated extracellular. SeNPs were around spherical with a diameter of approximately 100 nm. The X-ray photoelectron spectroscopy and Fourier transform infrared spectroscopy showed that the purified SeNPs consisted of selenium and proteins. Our results suggested that P. motobuensis LY5201could be a suitable and robust biocatalyst for SeNPs synthesis. In addition, the cytotoxicity effect and the anti-invasive activity of SeNPs on the HepG2 showed an inhibitory effect on HepG2, indicating that SeNPs could be used as a potential anticancer drug.

A ROS/Akt/NF-κB Signaling Cascade Mediates Epidermal Growth Factor-Induced Epithelial-Mesenchymal Transition and Invasion in Human Breast Cancer Cells.

Background: As one of the most widely used anti-diabetic drugs for type II diabetes, metformin has been shown to exhibit anti-cancer activity in recent years. Epidermal growth factor (EGF) and its receptor, EGFR, play important roles in cancer metastasis in various tumors, including breast cancer. Epithelial-mesenchymal transition (EMT) is a critical process for cancer invasion and metastasis. In this study, we use EGF as a metastatic inducer to investigate the effect of metformin on cancer cell migration, invasion and EMT. Methods: Human breast cancer MCF-7 cells were exposed to EGF with or without metformin or N-acetyl cysteine (NAC). The effects of metformin on breast cancer cell proliferation were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The production of reactive oxygen species (ROS) was tested using 2,7-dichlorodihydrofluorecein diacetate (DCFH-DA). The migratory and invasive abilities of tumor cells were analyzed using wound healing assay and transwell invasion assay, respectively. The expressions of E-cadherin, N-cadherin and Snail were tested using real-time quantitative polymerase chain reaction (qRT-PCR) and western blotting at mRNA and protein levels. The activation of protein kinase B (Akt) and nuclear factor kappa B (NF-κB) were measured by western blotting. Results: Our results showed that metformin inhibited breast cancer cell proliferation in a dose-dependent manner with or without EGF. EGF-induced alterations in cell morphology that are characteristic of EMT were reversed by metformin. Metformin also inhibited the EGF-modulated expression of E-cadherin, N-cadherin and Snail and further suppressed cell invasion and migration. In addition, metformin suppressed EGF-induced phosphorylation of Akt and NF-κB. ROS is involved in EGF-induced cancer invasion and activation of phosphatidylinositol 3-kinase (PI3K)/Akt/NF-κB pathway. Conclusion: Taken together, these data indicate that metformin suppresses EGF-induced breast cancer cell migration, invasion and EMT through the inhibition of the PI3K/Akt/NF-κB pathway. These results provide a novel mechanism to explain the role of metformin as a potent anti-metastatic agent in breast cancer cells.

Optical characteristics of bilayer decoupling MoS2 grown by the CVD method.

Study of exciton recombination process is of great significance for the optoelectronic device applications of two-dimensional transition metal chalcogenides (TMDCs). This research investigated the decoupling MoS2 structures by photoluminescence (PL) measurements. First, PL intensity of the bilayer MoS2 (BLM) is about twice of that of the single layer MoS2 (SLM) at low temperature, indicating no transition from direct bandgap to indirect bandgap for BLM due to the decrease of interlayer coupling which can be shown by Raman spectra. Then, the localized exciton emission appears for SLM at 7 K but none for BLM, showing different exciton localization characteristics. The PL evolution with respect to the excitation intensity and the temperature further reveal the filling, interaction, and the redistribution among free exciton states and localized exciton states. These results provide very useful information for understanding the localized states and carrier dynamics in BLM and SLM.

Combination therapy (toripalimab and lenvatinib)-associated toxic epidermal necrolysis in a patient with metastatic liver cancer: A case report.

BACKGROUND: Both programmed cell death-1 (PD-1) inhibitors and lenvatinib, which have a synergistic effect, are promising drugs for tumor treatment. It is generally believed that combination therapy with a PD-1 inhibitor and lenvatinib is safe and effective. However, we report a case of toxic epidermal necrolysis (TEN), a grade 4 toxicity, after this combination therapy. CASE SUMMARY: A 39-year-old male presented with erythema, blisters and erosions on the face, neck, trunk and limbs 1 wk after receiving combination therapy with lenvatinib and toripalimab, a PD-1 inhibitor. The skin injury covered more than 70% of the body surface area. He was previously diagnosed with liver cancer with cervical vertebra metastasis. Histologically, prominent necrotic keratinocytes, hyperkeratosis, liquefaction of basal cells and acantholytic bullae were observed in the epidermis. Blood vessels in the dermis were infiltrated by lymphocytes and eosinophils. Direct immunofluorescence staining was negative. Thus, the diagnosis was confirmed to be TEN (associated with combination therapy with toripalimab and lenvatinib). Full-dose and long-term corticosteroids, high-dose intravenous immunoglobulin and targeted antibiotic drugs were administered. The rashes gradually faded; however, as expected, the tumor progressed. Therefore, sorafenib and regorafenib were given in succession, and the patient was still alive at the 10-mo follow-up. CONCLUSION: Cautious attention should be given to rashes that develop after combination therapy with PD-1 inhibitors and lenvatinib. Large-dose and long-course glucocorticoids may be crucial for the treatment of TEN associated with this combination treatment.

Machine learning predicts cancer-associated deep vein thrombosis using clinically available variables.

PURPOSE: To develop and validate machine learning (ML) models for cancer-associated deep vein thrombosis (DVT) and to compare the performance of these models with the Khorana score (KS). METHODS: We randomly extracted data of 2100 patients with cancer between Jan. 1, 2017, and Oct. 31, 2019, and 1035 patients who underwent Doppler ultrasonography were enrolled. Univariate analysis and Lasso regression were applied to select important predictors. Model training and hyperparameter tuning were implemented on 70% of the data using a ten-fold cross-validation method. The remaining 30% of the data were used to compare the performance with seven indicators (area under the receiver operating characteristic curve [AUC], sensitivity, specificity, accuracy, balanced accuracy, Brier score, and calibration curve), among all five ML models (linear discriminant analysis [LDA], logistic regression [LR], classification tree [CT], random forest [RF], and support vector machine [SVM]), and the KS. RESULTS: The incidence of cancer-associated DVT was 22.3%. The top five predictors were D-dimer level, age, Charlson Comorbidity Index (CCI), length of stay (LOS), and previous VTE (venous thromboembolism) history according to RF. Only LDA (AUC = 0.773) and LR (AUC = 0.772) outperformed KS (AUC = 0.642), and combination with D-dimer showed improved performance in all models. A nomogram and web calculator https://webcalculatorofcancerassociateddvt.shinyapps.io/dynnomapp/ were used to visualize the best recommended LR model. CONCLUSION: This study developed and validated cancer-associated DVT predictive models using five ML algorithms and visualized the best recommended model using a nomogram and web calculator. The nomogram and web calculator developed in this study may assist doctors and nurses in evaluating individualized cancer-associated DVT risk and making decisions. However, other prospective cohort studies should be conducted to externally validate the recommended model.

Factors Influencing Residents' Psychological Status During Standardized Training in COVID-19.

Objectives: To explore the influencing factors of residents' psychological status during standardized training in COVID-19 for finding ways to promote their mental health. Methods: A total of 760 residents were surveyed with a structured questionnaire. Correlation analysis was used to analyze the influencing factors of psychological status of the residents, and a mediation model was constructed to verify the mediating role of satisfaction. Results: Age, willingness to study medicine, and satisfaction were positively correlated with negative psychological status (P < 0.05). And gender, only child or not, and annual household income (RMB) were negatively correlated with negative psychological status (P < 0.01). Residents' satisfaction with standardized training mode plays a complete mediating role between annual household income and negative psychological status. Conclusions: Our findings emphasize the importance of concentrating on resident's psychological status and family economic situation. And relative departments should take action to optimize the standardized training mode to improve the satisfaction.

Full-color photon-counting single-pixel imaging.

We propose and experimentally demonstrate a high-efficiency single-pixel imaging (SPI) scheme by integrating time-correlated single-photon counting (TCSPC) with time-division multiplexing to acquire full-color images at an extremely low light level. This SPI scheme uses a digital micromirror device to modulate a sequence of laser pulses with preset delays to achieve three-color structured illumination, then employs a photomultiplier tube into the TCSPC module to achieve photon-counting detection. By exploiting the time-resolved capabilities of TCSPC, we demodulate the spectrum-image-encoded signals, and then reconstruct high-quality full-color images in a single round of measurement. Based on this scheme, strategies such as single-step measurement, high-speed projection, and undersampling can further improve imaging efficiency.

Experience of comprehensive interventions in reducing occupational exposure to COVID-19.

IMPORTANCE: The infection of medical personnel with COVID-19 was a disaster for both patients and doctors. However, some effective measures can prevent medical staff from becoming infected. This article introduces those measures and thus provides a reference for other hospitals. OBJECTIVE: In order to reduce the risk of occupational exposure and of the infection of medical staff, this article analyzed the factors, causes and experience of medical personnel on their occupational exposure to COVID-19. Some effective and targeted intervention measures can be implemented in order to avoid the occupational exposure of medical staff to COVID-19. EVIDENCE REVIEW: In this single-center case series involving 196 medical personnel, occupational exposure to COVID-19 was present. Nursing staff accounted for 67.35% of those cases. The relationships with an exposure source were found to be as follows: doctors and patients (87.24%), colleagues (10.20%), and roommates (2.55%). Occupational exposure was found to be present in the clinical department, radiology department, central sterile supply department, as well as in the outpatient clinics and operating rooms. The non-surgical departments accounted for 72.96% and direct contact accounted for 84.69% while failure to wear surgical masks (84.18%) and operating on the patient without wearing goggles/face shield (8.16%) were the main causes of occupational exposure. The occurrence of occupational exposure to COVID-19 declined to 0.19% after an extensive and comprehensive intervention program. CONCLUSIONS AND RELEVANCE: Some effective measures such as hand hygiene, wearing surgical masks in and around the hospital, reasonable use of goggles/face screens, raising awareness of protective measures, minimizing the number of elective operations, strengthening training as well as many other control measures were instrumental in reducing occupational exposure. For any medical institution there is room for improvement in terms of personal protection to reduce occupational exposure.

Activation of silent information regulator 1 exerts a neuroprotective effect after intracerebral hemorrhage by deacetylating NF-κB/p65.

Nuclear factor (NF)-κB-mediated neuroinflammation is an important mechanism of intracerebral hemorrhage (ICH)-induced neurotoxicity. Silent information regulator 1 (SIRT1) plays a multi-protective effect in a variety of diseases by deacetylating and inhibiting NF-κB/p65. However, the role of SIRT1 in brain damage following ICH remains unclear. We hypothesized that SIRT1 can protect against ICH-induced brain damage by inhibiting neuroinflammation through deacetylating NF-κB/p65. The ICH model was induced in vivo (with collagenase) and in vitro (with hemoglobin). Resveratrol and Ex527 were administered to activate or inhibit SIRT1, respectively. Western blot, immunohistochemistry, and immunofluorescence assays were performed to detect the expression of SIRT1 and p65. Enzyme-linked immunosorbent assays (ELISAs) were used to explore tumor necrosis factor (TNF)-α and interleukin (IL)-1ß release. The neurological score, brain water content, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and brain hemoglobin content were determined to evaluate the neuroprotective effect of SIRT1. SIRT1 expression was decreased, whereas the level of acetylated p65 (Ac-p65) was elevated after ICH in vivo. Moreover, hemoglobin treatment decreased the expression of SIRT1 in vitro. Activation of SIRT1 by resveratrol had a neuroprotective effect, along with decreased levels of Ac-p65, IL-1ß, TNF-α, and apoptosis after ICH. The effect of resveratrol was abolished by the SIRT1 inhibitor Ex527. Our results are consistent with the hypothesis that SIRT1 exerts a neuroprotective effect after ICH by deacetylating p65 to inhibit the NF-κB-dependent inflammatory response.

Predicting disease risks by matching quantiles estimation for censored data.

In time to event data analysis, it is often of interest to predict quantities such as t-year survival rate or the survival function over a continuum of time. A commonly used approach is to relate the survival time to the covariates by a semiparametric regression model and then use the fitted model for prediction, which usually results in direct estimation of the conditional hazard function or the conditional estimating equation. Its prediction accuracy, however, relies on the correct specification of the covariate-survival association which is often difficult in practice, especially when patient populations are heterogeneous or the underlying model is complex. In this paper, from a prediction perspective, we propose a disease-risk prediction approach by matching an optimal combination of covariates with the survival time in terms of distribution quantiles. The proposed method is easy to implement and works flexibly without assuming a priori model. The redistribution-of-mass technique is adopted to accommodate censoring. We establish theoretical properties of the proposed method. Simulation studies and a real data example are also provided to further illustrate its practical utilities.

Cx43 silencing inhibits mechanical stress-induced apoptosis in mouse articular chondrocyte / 中南大学学报(医学版)

To explore the effect of connexin 43 (Cx43) silence on the apoptosis in mouse chondrocyte under mechanical stress.
 Methods: Mouse chondrocyte ATDC5 cells were divided into a control group, a mechanical stress group, a Cx43 siRNA transfection group, a scramble siRNA transfection group, a mechanical stress+scramble group, and a mechanical stress+siCx43 group. Flexcell FX-5000 system was used to produce mechanical stress on ATDC5 cells cultured in vitro. The mRNA and protein level of Cx43 was detected by quantitative RT-PCR (RT-qPCR) and Western blot. The cell activity and cell apoptosis was detected by cell counting kit-8 (CCK-8) method and flow cytometry, respectively. Caspase-3 activity was detected by colorimetric assay. The protein expression of Bcl-2, Bax, p-JNK and JNK was detected by Western blot.
 Results: Mechanical stress upregulated the mRNA and protein expression of Cx43 (both P<0.05). Transfection of Cx43 siRNA significantly decreased Cx43 mRNA and protein level (both P<0.05). After stimulation with mechanical stress, chondrocyte viability was significantly decreased, whereas cell apoptosis and caspase-3 activity were increased (both P<0.05). Mechanical stress obviously upregulated Bax protein level, and downregulated Bcl-2 protein expression and Bcl-2/Bax (both P<0.05). Cx43 siRNA transfection significantly increased cell viability, inhibited cell apoptosis and caspase-3 activity (both P<0.05). Cx43 siRNA also inhibited Bax expression, and increased the Bcl-2 protein expression and Bcl-2/Bax (both P<0.05). Furthermore, Cx43 siRNA significantly suppressed the p-JNK expression induced by mechanical stress (P<0.05).
 Conclusion: Cx43 silence inhibits mechanical stress-induced apoptosis in chondrocyte, which might be mediated by JNK signaling pathway.