LPS-induced monocarboxylate transporter-1 inhibition facilitates lactate accumulation triggering epithelial-mesenchymal transformation and pulmonary fibrosis.

The epithelial-mesenchymal transformation (EMT) process of alveolar epithelial cells is recognized as involved in the development of pulmonary fibrosis. Recent evidence has shown that lipopolysaccharide (LPS)-induced aerobic glycolysis of lung tissue and elevated lactate concentration are associated with the pathogenesis of sepsis-associated pulmonary fibrosis. However, it is uncertain whether LPS promotes the development of sepsis-associated pulmonary fibrosis by promoting lactate accumulation in lung tissue, thereby initiating EMT process. We hypothesized that monocarboxylate transporter-1 (MCT1), as the main protein for lactate transport, may be crucial in the pathogenic process of sepsis-associated pulmonary fibrosis. We found that high concentrations of lactate induced EMT while moderate concentrations did not. Besides, we demonstrated that MCT1 inhibition enhanced EMT process in MLE-12 cells, while MCT1 upregulation could reverse lactate-induced EMT. LPS could promote EMT in MLE-12 cells through MCT1 inhibition and lactate accumulation, while this could be alleviated by upregulating the expression of MCT1. In addition, the overexpression of MCT1 prevented LPS-induced EMT and pulmonary fibrosis in vivo. Altogether, this study revealed that LPS could inhibit the expression of MCT1 in mouse alveolar epithelial cells and cause lactate transport disorder, which leads to lactate accumulation, and ultimately promotes the process of EMT and lung fibrosis.

The Polo-Like Kinase 1-Mammalian Target of Rapamycin Axis Regulates Autophagy to Prevent Intestinal Barrier Dysfunction During Sepsis.

The intestines play a crucial role in the development of sepsis. The balance between autophagy and apoptosis in intestinal epithelial cells is dynamic and determines intestinal permeability. The present study focused on the potential role of autophagy in sepsis-induced intestinal barrier dysfunction and explored the mechanisms in vivo and in vitro. Excessive apoptosis in intestinal epithelia and a disrupted intestinal barrier were observed in septic mice. Promoting autophagy with rapamycin reduced intestinal epithelial apoptosis and restored intestinal barrier function, presenting as decreased serum diamine oxidase (DAO) and fluorescein isothiocyanate-dextran 40 (FD40) levels and increased expression of zonula occludens-1 (ZO-1) and Occludin. Polo-like kinase 1 (PLK1) knockdown in mice ameliorated intestinal epithelial apoptosis and the intestinal barrier during sepsis, whereas these effects were reduced with chloroquine and enhanced with rapamycin. PLK1 also promoted cell autophagy and improved lipopolysaccharide-induced apoptosis and high permeability in vitro. Moreover, PLK1 physically interacted with mammalian target of rapamycin (mTOR) and participated in reciprocal regulatory crosstalk in intestinal epithelial cells during sepsis. This study provides novel insight into the role of autophagy in sepsis-induced intestinal barrier dysfunction and indicates that the PLK1-mTOR axis may be a promising therapeutic target for sepsis.

Asymmetric Organocatalytic 1,3-Dipolar Cycloaddition of Azomethine Ylides with ß-Substituted Cyclic Enones.

The enantioselective and diastereoselective control of 1,3-dipolar cycloaddition reactions to ß-substituted cyclic enones has been developed. The 1,3-dipolar cycloaddition of phthalazinium dicyanomethanides with cyclic dienones affords chiral tetrahydropyrrolo[2,1-a]phthalazine derivatives 3 through vinylogous iminium ion activation by combining a cinchona-based primary amine C3 and a chiral camphorsulfonic acid additive. Conversely, with a weaker 3,5-bis(trifluoromethyl)benzoic acid additive, the 1,3-dipolar cycloaddition of phthalazinium dicyanomethanides with ß-substituted cyclic enones leads to chiral hexahydroisoindolo[1,2-a]phthalazin-10(8H)-one derivatives 4 with excellent stereocontrol via endo-dienamine activation.

Vascular smooth muscle-specific LRRC8A knockout ameliorates angiotensin II-induced cerebrovascular remodeling by inhibiting the WNK1/FOXO3a/MMP signaling pathway.

Hypertensive cerebrovascular remodeling involves the enlargement of vascular smooth muscle cells (VSMCs), which activates volume-regulated Cl- channels (VRCCs). The leucine-rich repeat-containing family 8 A (LRRC8A) has been shown to be the molecular identity of VRCCs. However, its role in vascular remodeling during hypertension is unclear. In this study, we used vascular smooth muscle-specific LRRC8A knockout (CKO) mice and an angiotensin II (Ang II)-induced hypertension model. The results showed that cerebrovascular remodeling during hypertension was ameliorated in CKO mice, and extracellular matrix (ECM) deposition was reduced. Based on the RNA-sequencing analysis of aortic tissues, the level of matrix metalloproteinases (MMPs), such as MMP-9 and MMP-14, were reduced in CKO mice with hypertension, which was further verified in vivo by qPCR and immunofluorescence analysis. Knockdown of LRRC8A in VSMCs inhibited the Ang II-induced upregulation of collagen I, fibronectin, and matrix metalloproteinases (MMPs), and overexpression of LRRC8A had the opposite effect. Further experiments revealed an interaction between with-no-lysine (K)-1 (WNK1), which is a "Cl--sensitive kinase", and Forkhead transcription factor O3a (FOXO3a), which is a transcription factor that regulates MMP expression. Ang II induced the phosphorylation of WNK1 and downstream FOXO3a, which then increased the expression of MMP-2 and MMP-9. This process was inhibited or potentiated when LRRC8A was knocked down or overexpressed, respectively. Overall, these results demonstrate that LRRC8A knockout in vascular smooth muscle protects against cerebrovascular remodeling during hypertension by reducing ECM deposition and inhibiting the WNK1/FOXO3a/MMP signaling pathway, demonstrating that LRRC8A is a potential therapeutic target for vascular remodeling-associated diseases such as stroke.

Quantum teleportation of physical qubits into logical code spaces.

Quantum error correction is an essential tool for reliably performing tasks for processing quantum information on a large scale. However, integration into quantum circuits to achieve these tasks is problematic when one realizes that nontransverse operations, which are essential for universal quantum computation, lead to the spread of errors. Quantum gate teleportation has been proposed as an elegant solution for this. Here, one replaces these fragile, nontransverse inline gates with the generation of specific, highly entangled offline resource states that can be teleported into the circuit to implement the nontransverse gate. As the first important step, we create a maximally entangled state between a physical and an error-correctable logical qubit and use it as a teleportation resource. We then demonstrate the teleportation of quantum information encoded on the physical qubit into the error-corrected logical qubit with fidelities up to 0.786. Our scheme can be designed to be fully fault tolerant so that it can be used in future large-scale quantum technologies.

A perovskite solar cell-photothermal-thermoelectric tandem system for enhanced solar energy utilization.

Photovoltaic-thermoelectric (PV-TE) tandem system has been considered as an effective way to fully utilize the solar spectrum, and has been demonstrated in a perovskite solar cell (PSC)-thermoelectric (TE) configuration. However, the conventional PSC-TE tandem architecture cannot convert infrared light transmitted through the upper PSC into heat effectively, impeding the heat-electricity conversion of TE devices. Herein, a semi-transparent PSC-photothermal-TE tandem system is designed for improved photothermal utilization. Through optimizing the buffer layer of the back transparent electrode, semi-transparent PSC with a power conversion efficiency (PCE) of 13% and an average transmittance of 53% in the range of 800-1500 nm was obtained. On this basis, a photothermal thin film was introduced between the semi-transparent PSC and the TE device, which increased the efficiency contribution ratio of the TE device from 14% to 19%, showing enhanced utilization of AM 1.5 G solar spectrum and improved photo-thermal-electric conversion efficiency.

We have constructed a semi-transparent perovskite solar cell-photothermal-thermoelectric tandem system through the optimization of transparent back electrode and the introduction of photothermal thin-film, realizing enhanced utilization of solar energy.

Integrin ß3 Mediates Sepsis and Mechanical Ventilation-Associated Pulmonary Fibrosis Through Glycometabolic Reprogramming.

Mechanical ventilation (MV) has become a clinical first-line treatment option for patients with respiratory failure. However, it was unclear whether MV further aggravates the process of sepsis-associated pulmonary fibrosis and eventually leads to sepsis and mechanical ventilation-associated pulmonary fibrosis (S-MVPF). This study aimed to explore the mechanism of S-MVPF concerning integrin ß3 activation in glycometabolic reprogramming of lung fibroblasts. We found that MV exacerbated sepsis-associated pulmonary fibrosis induced by lipopolysaccharide, which was accompanied by proliferation of lung fibroblasts, increased deposition of collagen in lung tissue, and increased procollagen type I carboxy-terminal propeptide in the bronchoalveolar lavage fluid. A large number of integrin ß3- and pyruvate kinase M2-positive fibroblasts were detected in lung tissue after stimulation with lipopolysaccharide and MV, with an increase in lactate dehydrogenase A expression and lactate levels. S-MVPF was primarily attenuated in integrin ß3-knockout mice, which also resulted in a decrease in the levels of pyruvate kinase M2, lactate dehydrogenase A, and lactate. In conclusion, MV aggravated sepsis-associated pulmonary fibrosis, with glycometabolic reprogramming mediated by integrin ß3 activation. Thus, integrin ß3-mediated glycometabolic reprogramming might be a potential therapeutic target for S-MVPF.

Unconditional and Robust Quantum Metrological Advantage beyond N00N States.

Quantum metrology employs quantum resources to enhance the measurement sensitivity beyond that can be achieved classically. While multiphoton entangled N00N states can in principle beat the shot-noise limit and reach the Heisenberg limit, high N00N states are difficult to prepare and fragile to photon loss which hinders them from reaching unconditional quantum metrological advantages. Here, we combine the idea of unconventional nonlinear interferometers and stimulated emission of squeezed light, previously developed for the photonic quantum computer Jiuzhang, to propose and realize a new scheme that achieves a scalable, unconditional, and robust quantum metrological advantage. We observe a 5.8(1)-fold enhancement above the shot-noise limit in the Fisher information extracted per photon, without discounting for photon loss and imperfections, which outperforms ideal 5-N00N states. The Heisenberg-limited scaling, the robustness to external photon loss, and the ease-of-use of our method make it applicable in practical quantum metrology at a low photon flux regime.

Solving Graph Problems Using Gaussian Boson Sampling.

Gaussian boson sampling (GBS) is not only a feasible protocol for demonstrating quantum computational advantage, but also mathematically associated with certain graph-related and quantum chemistry problems. In particular, it is proposed that the generated samples from the GBS could be harnessed to enhance the classical stochastic algorithms in searching some graph features. Here, we use Jiǔzhang, a noisy intermediate-scale quantum computer, to solve graph problems. The samples are generated from a 144-mode fully connected photonic processor, with photon click up to 80 in the quantum computational advantage regime. We investigate the open question of whether the GBS enhancement over the classical stochastic algorithms persists-and how it scales-with an increasing system size on noisy quantum devices in the computationally interesting regime. We experimentally observe the presence of GBS enhancement with a large photon-click number and a robustness of the enhancement under certain noise. Our work is a step toward testing real-world problems using the existing noisy intermediate-scale quantum computers and hopes to stimulate the development of more efficient classical and quantum-inspired algorithms.

Gaussian Boson Sampling with Pseudo-Photon-Number-Resolving Detectors and Quantum Computational Advantage.

We report new Gaussian boson sampling experiments with pseudo-photon-number-resolving detection, which register up to 255 photon-click events. We consider partial photon distinguishability and develop a more complete model for the characterization of the noisy Gaussian boson sampling. In the quantum computational advantage regime, we use Bayesian tests and correlation function analysis to validate the samples against all current classical spoofing mockups. Estimating with the best classical algorithms to date, generating a single ideal sample from the same distribution on the supercomputer Frontier would take ∼600 yr using exact methods, whereas our quantum computer, Jiǔzhang 3.0, takes only 1.27 µs to produce a sample. Generating the hardest sample from the experiment using an exact algorithm would take Frontier∼3.1×10^{10} yr.

Robot-assisted versus navigation-assisted screw placement in spinal vertebrae.

PURPOSE: Both robots and navigation are effective strategies for optimizing screw placement, as compared to freehand placement. However, few studies have compared the accuracy and efficiency of these two techniques. Thus, the purpose of this study is to compare the accuracy and efficiency of robotic and navigation-assisted screw placement in the spinal vertebrae. METHODS: The 24 spine models were divided into a robot- and navigation-assisted groups according to the left and right sides of the pedicle. The C-arm transmits image data simultaneously to the robot and navigates using only one scan. After screw placement, the accuracy of the two techniques were compared using "angular deviation" and "Gertzbein and Robbins scale" in different segments (C1-7, T1-4, T5-8, T9-12, and L1-S1). In addition, operation times were compared between robot- and navigation-assisted groups. RESULTS: Robots and navigation systems can simultaneously assist in screw placement. The robot-assisted group had significantly less angular deviation than the navigation-assisted group from C1 to S1 (p < 0.001). At the C1-7 and T1-4 segments, the robot-assisted group had a higher rate of acceptable screws than the robot-assisted group. However, at the T5-8, T9-12, and L1-S1 segments, no significant difference was found in the incidence of acceptable screws between the two groups. Moreover, robot-assisted screw placement required less operative time than navigation (p < 0.05). CONCLUSION: The robot is more accurate and efficient than navigation in aiding screw placement. In addition, robots and navigation can be combined without increasing the number of fluoroscopic views.

Experimental Refutation of Real-Valued Quantum Mechanics under Strict Locality Conditions.

Quantum mechanics is commonly formulated in a complex, rather than real, Hilbert space. However, whether quantum theory really needs the participation of complex numbers has been debated ever since its birth. Recently, a Bell-like test in an entanglement-swapping scenario has been proposed to distinguish standard quantum mechanics from its real-valued analog. Previous experiments have conceptually demonstrated, yet not satisfied, the central requirement of independent state preparation and measurements and leave several loopholes. Here, we implement such a Bell-like test with two separated independent sources delivering entangled photons to three separated parties under strict locality conditions that are enforced by spacelike separation of the relevant events, rapid random setting generation, and fast measurement. With the fair-sampling assumption and closed loopholes of independent source, locality, and measurement independence simultaneously, we violate the constraints of real-valued quantum mechanics by 5.30 standard deviations. Our results disprove the real-valued quantum theory to describe nature and ensure the indispensable role of complex numbers in quantum mechanics.

Differential roles of NMDAR subunits 2A and 2B in mediating peripheral and central sensitization contributing to orofacial neuropathic pain.

The spinal N-methyl-d-aspartate receptor (NMDAR), particularly their subtypes NR2A and NR2B, plays pivotal roles in neuropathic and inflammatory pain. However, the roles of NR2A and NR2B in orofacial pain and the exact molecular and cellular mechanisms mediating nervous system sensitization are still poorly understood. Here, we exhaustively assessed the regulatory effect of NMDAR in mediating peripheral and central sensitization in orofacial neuropathic pain. Von-Frey filament tests showed that the inferior alveolar nerve transection (IANX) induced ectopic allodynia behavior in the whisker pad of mice. Interestingly, mechanical allodynia was reversed in mice lacking NR2A and NR2B. IANX also promoted the production of peripheral sensitization-related molecules, such as interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, brain-derived neurotrophic factor (BDNF), and chemokine upregulation (CC motif) ligand 2 (CCL2), and decreased the inward potassium channel (Kir) 4.1 on glial cells in the trigeminal ganglion, but NR2A conditional knockout (CKO) mice prevented these alterations. In contrast, NR2B CKO only blocked the changes of Kir4.1, IL-1ß, and TNF-α and further promoted the production of CCL2. Central sensitization-related c-fos, glial fibrillary acidic protein (GFAP), and ionized calcium-binding adaptor molecule 1 (Iba-1) were promoted and Kir4.1 was reduced in the spinal trigeminal caudate nucleus by IANX. Differential actions of NR2A and NR2B in mediating central sensitization were also observed. Silencing of NR2B was effective in reducing c-fos, GFAP, and Iba-1 but did not affect Kir4.1. In contrast, NR2A CKO only altered Iba-1 and Kir4.1 and further increased c-fos and GFAP. Gain-of-function and loss-of-function approaches provided insight into the differential roles of NR2A and NR2B in mediating peripheral and central nociceptive sensitization induced by IANX, which may be a fundamental basis for advancing knowledge of the neural mechanisms' reaction to nerve injury.

WiFi Energy-Harvesting Antenna Inspired by the Resonant Magnetic Dipole Metamaterial.

WiFi energy harvesting is a promising solution for powering microsensors and microsystems through collecting electromagnetic (EM) energies that exist everywhere in modern daily lives. In order to harvest EM energy, we proposed a metamaterial-inspired antenna (MIA) based on the resonant magnetic dipole operating in the WiFi bands. The MIA consists of two metallic split-ring resonators (SRRs), separated by an FR4 dielectric layer, in the broadside coupled configuration. The incident EM waves excite surface currents in the coupled SRRs, and the energy is oscillating between them due to near-field coupling. By varying the vertical distance of the two SRRs, we may achieve impedance matching without complicated matching networks. Collected EM energy can be converted to DC voltages via a rectifier circuit at the output of the coupling coil. Measured results demonstrate that the designed MIA may resonate at 2.4 GHz with a deep-subwavelength form factor (14 mm×14 mm×1.6 mm). The WiFi energy-harvesting capability of the proposed MIA with an embedded one-stage Dickson voltage multiplier has also been evaluated. A rectified DC voltage is approximately 500 mV when the MIA is placed at a distance of 2 cm from the WiFi transmit antenna with a 9 dBm transmitting power. The proposed compact MIA in this paper is of great importance for powering future distributed microsystems.

Direct and Simultaneous Identification of Multiple Mitochondrial Reactive Oxygen Species in Living Cells Using a SERS Borrowing Strategy.

Identification of different mitochondrial reactive oxygen species (ROS) simultaneously in living cells is vital for understanding the critical roles of different ROS in biological processes. To date, it remains a great challenge to develop ROS probes for direct and simultaneous identification of multiple ROS with high specificity. Herein, we report a SERS-borrowing-strategy-based nanoprobe (Au@Pt core-shell nanoparticles) for simultaneous and direct identification of different ROS by their distinct Raman fingerprints. Isotope substitution experiments and DFT calculations confirmed the ability of Au@Pt nanoprobe to capture and identify different mitochondrial ROS (i.e. ⋅OOH, H2 O2 , and ⋅OH). When functionalized with triphenylphosphine (TPP), the Au@Pt-TPP nanoprobe located to mitochondria and detected multiple ROS simultaneously in living cells under oxidative stimulation. Our method offers a new tool for the study of the functions of various ROS in biological processes.

Sepsis induces muscle atrophy by inhibiting proliferation and promoting apoptosis via PLK1-AKT signalling.

Sepsis and sepsis-induced skeletal muscle atrophy are common in patients in intensive care units with high mortality, while the mechanisms are controversial and complicated. In the present study, the atrophy of skeletal muscle was evaluated in sepsis mouse model as well as the apoptosis of muscle fibres. Sepsis induced atrophy of skeletal muscle and apoptosis of myofibres in vivo and in vitro. In cell-based in vitro experiments, lipopolysaccharide (LPS) stimulation also inhibited the proliferation of myoblasts. At the molecular level, the expression of polo-like kinase 1 (PLK1) and phosphorylated protein kinase B (p-AKT) was decreased. Overexpression of PLK1 partly rescued LPS-induced apoptosis, proliferation suppression and atrophy in C2C12 cells. Furthermore, inhibiting the AKT pathway deteriorated LPS-induced atrophy in PLK1-overexpressing C2C12 myotubes. PLK1 was found to participate in regulating apoptosis and E3 ubiquitin ligase activity in C2C12 cells. Taken together, these results indicate that sepsis induces skeletal muscle atrophy by promoting apoptosis of muscle fibres and inhibiting proliferation of myoblasts via regulation of the PLK1-AKT pathway. These findings enhance understanding of the mechanism of sepsis-induced skeletal muscle atrophy.

Robust Self-Testing of Multiparticle Entanglement.

Quantum self-testing is a device-independent way to certify quantum states and measurements using only the input-output statistics, with minimal assumptions about the quantum devices. Because of the high demand on tolerable noise, however, experimental self-testing was limited to two-photon systems. Here, we demonstrate the first robust self-testing for multiphoton genuinely entangled quantum states. We prepare two examples of four-photon graph states, the Greenberger-Horne-Zeilinger states with a fidelity of 0.957(2) and the linear cluster states with a fidelity of 0.945(2). Based on the observed input-output statistics, we certify the genuine four-photon entanglement and further estimate their qualities with respect to realistic noise in a device-independent manner.

Phase-Programmable Gaussian Boson Sampling Using Stimulated Squeezed Light.

We report phase-programmable Gaussian boson sampling (GBS) which produces up to 113 photon detection events out of a 144-mode photonic circuit. A new high-brightness and scalable quantum light source is developed, exploring the idea of stimulated emission of squeezed photons, which has simultaneously near-unity purity and efficiency. This GBS is programmable by tuning the phase of the input squeezed states. The obtained samples are efficiently validated by inferring from computationally friendly subsystems, which rules out hypotheses including distinguishable photons and thermal states. We show that our GBS experiment passes a nonclassicality test based on inequality constraints, and we reveal nontrivial genuine high-order correlations in the GBS samples, which are evidence of robustness against possible classical simulation schemes. This photonic quantum computer, Jiuzhang 2.0, yields a Hilbert space dimension up to ∼10^{43}, and a sampling rate ∼10^{24} faster than using brute-force simulation on classical supercomputers.

Predictive value of a reduction in the level of high-density lipoprotein-cholesterol in patients with non-small-cell lung cancer undergoing radical resection and adjuvant chemotherapy: a retrospective observational study.

BACKGROUND: Cancer patients often exhibit chemotherapy-associated changes in serum lipid profiles, however, their prognostic value before and after adjuvant chemotherapy on survival among non-small-cell lung cancer (NSCLC) patients is unknown. METHODS: NSCLC patients undergoing radical resection and subsequent adjuvant chemotherapy from 2013 to 2017 at Sun Yat-sen University Cancer Center were retrospectively reviewed. Fasted serum lipid levels were measured before and after chemotherapy. The optimal lipid cut-off values at baseline and fluctuation were determined using X-tile™. The fluctuations in serum lipid levels and disease-free survival (DFS) were assessed. RESULTS: Serum cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), triglyceride, apolipoprotein (Apo) A-I, and ApoB all significantly increased after adjuvant chemotherapy. X-tile determined 1.52 mmol/L of HDL-C and 0.74 g/L of ApoB as the optimal cut-off values before chemotherapy. Patients with HDL-C ≥ 1.52 mmol/L (median DFS: not reached vs. 26.30 months, P = 0.0005) and a decreased HDL-C level after adjuvant chemotherapy (median DFS: 80.43 vs. 26.12 months, P = 0.0204) had a longer DFS. An HDL-C level that increased by ≥ 0.32 mmol/L after chemotherapy indicated a worse DFS. A high baseline ApoB level were associated with a superior DFS. In the univariate analysis and the multivariate Cox analyses, a high baseline HDL-C level and a HDL-C reduction after adjuvant chemotherapy were independent indicators for superior DFS. High baseline HDL-C was related to N0-1 stage (χ2 = 6.413, P = 0.011), and HDL-C fluctuation was significantly correlated with specific chemotherapy regimens (χ2 = 5.002, P = 0.025). CONCLUSIONS: Adjuvant chemotherapy increased various lipid levels in resected NSCLC patients. A higher HDL-C level before chemotherapy and a reduced HDL-C level after adjuvant chemotherapy were independent predictors of longer DFS in patients with curable NSCLC.

Sepsis induces variation of intestinal barrier function in different phase through nuclear factor kappa B signaling.

The intestinal barrier function disrupted in sepsis, while little is known about the variation in different phases of sepsis. In this study, mouse models of sepsis were established by caecal ligation and puncture (CLP). The H&E staining of sections and serum diamine oxidase concentration were evaluated at different timepoint after CLP. TUNEL assay and EdU staining were performed to evaluate the apoptosis and proliferation of intestinal epithelium. Relative protein expression was assessed by Western blotting and serum concentrations of pro-inflammatory cytokines was measured by ELISA. The disruption of intestinal barrier worsened in the first 24 h after the onset of sepsis and gradually recovered over the next 24 h. The percentage of apoptotic cell increased in the first 24 h and dropped at 48 h, accompanied with the proliferative rate of intestinal epithelium inhibited in the first 6 h and regained in the later period. Furthermore, the activity of nuclear factor kappa B (NF-κB) presented similar trend with the intestinal barrier function, shared positive correction with apoptosis of intestinal epithelium. These findings reveal the conversion process of intestinal barrier function in sepsis and this process is closely correlated with the activity of NF-κB signaling.