Publisher Correction: Enhanced ferroelectricity in ultrathin films grown directly on silicon.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Enhanced ferroelectricity in ultrathin films grown directly on silicon.

Ultrathin ferroelectric materials could potentially enable low-power perovskite ferroelectric tetragonality logic and nonvolatile memories1,2. As ferroelectric materials are made thinner, however, the ferroelectricity is usually suppressed. Size effects in ferroelectrics have been thoroughly investigated in perovskite oxides-the archetypal ferroelectric system3. Perovskites, however, have so far proved unsuitable for thickness scaling and integration with modern semiconductor processes4. Here we report ferroelectricity in ultrathin doped hafnium oxide (HfO2), a fluorite-structure oxide grown by atomic layer deposition on silicon. We demonstrate the persistence of inversion symmetry breaking and spontaneous, switchable polarization down to a thickness of one nanometre. Our results indicate not only the absence of a ferroelectric critical thickness but also enhanced polar distortions as film thickness is reduced, unlike in perovskite ferroelectrics. This approach to enhancing ferroelectricity in ultrathin layers could provide a route towards polarization-driven memories and ferroelectric-based advanced transistors. This work shifts the search for the fundamental limits of ferroelectricity to simpler transition-metal oxide systems-that is, from perovskite-derived complex oxides to fluorite-structure binary oxides-in which 'reverse' size effects counterintuitively stabilize polar symmetry in the ultrathin regime.

Identification of M2 Macrophage-Related Key Genes in Advanced Atherosclerotic Plaques by Network-Based Analysis.

ABSTRACT: Atherosclerotic plaque accounts for major adverse cardiovascular events because of its vulnerability. The classically activated macrophage (M1) and alternatively activated macrophage (M2) are implicated in the progression and regression of plaque, respectively. However, the therapeutic targets related to M2 macrophages still remain largely elusive. In this study, cell-type identification by estimating relative subsets of RNA transcripts and weighted gene coexpression network analysis algorithms were used to establish a weighted gene coexpression network for identifying M2 macrophage-related hub genes using GSE43292 data set. The results showed that genes were classified into 7 modules, with the blue module (Cor = 0.67, P = 3e-05) being the one that was most related to M2 macrophage infiltration in advanced plaques, and then 99 hub genes were identified from blue module. Meanwhile, 1289 differentially expressed genes were produced in GSE43292 data set. Subsequently, the intersection genes of hub genes and differentially expressed genes, including AKTIP , ASPN , FAM26E , RAB23 , PLS3 , and PLSCR4 , were obtained by Venn diagrams and named as key genes. Further validation using data sets GSE100927 and GSE41571 showed that 6 key genes all downregulated in advanced and vulnerable plaques compared with early and stable plaque samples (|Log2 (fold change)| > 0.5, P < 0.05 or 0.001), respectively. Receiver operator characteristic curve analysis indicated that the 6 key genes might have potential diagnostic value. The validation of key genes in the model in vitro and in vivo also demonstrated decreased mRNA expressions of AKTIP , ASPN , FAM26E , RAB23 , PLS3 , and PLSCR4 ( P < 0.05 or 0.001). Collectively, we identified AKTIP, ASPN, FAM26E, RAB23, PLS3, and PLSCR4 as M2 macrophage-related key genes during atherosclerotic progression, proposing potential intervention targets for advanced atherosclerotic plaques.

Association of Delirium with Long-Term Mortality in Critically Ill Patients with COPD Who Survived to Discharge: A Retrospective Cohort Study.

BACKGROUND: Critically ill patients with chronic obstructive pulmonary disease (COPD) face significant mortality after hospital discharge. Delirium is common in patients with COPD, but its impact on long-term mortality in critically ill COPD patients who survive to discharge remains uncertain. METHODS: Critically ill patients with COPD who survived to discharge were selected from the Medical Information Mart for Intensive Care IV database. Delirium was assessed using the Confusion Assessment Method for Intensive Care Unit. The primary outcome was 365- and 180-day mortality after discharge. The secondary outcomes included 90- and 30-day mortality following discharge, length of intensive care unit (ICU) and hospital stays, and nursing care needs after hospital discharge. RESULTS: Of the 2621 survivors of critically ill COPD patients, 982 had suffered delirium during their ICU stay and 709 died within 365 days after hospital discharge. Delirium was significantly associated with 365-day mortality after hospital discharge (adjusted hazard ratio [HR] 1.22; 95% confidence interval [CI] 1.02-1.47). The results were consistent for 180-, 90-, and 30-day post-discharge mortality (adjusted HR [95% CI]: 1.35 [1.09-1.66], 1.48 [1.16-1.89], and 1.68 [1.21-2.32], respectively). Additionally, patients with delirium had longer ICU and hospital stay (adjusted ß 2.75; 95% CI 2.35-3.16 and 4.25; 95% CI 3.51-4.98, respectively) and increased nursing care needs after hospital discharge (adjusted odds ratio, 1.56; 95% CI 1.13-2.14). CONCLUSION: ICU delirium was an independent risk factor for both long-term and short-term mortality in critically ill patients with COPD who survived to discharge.

Cucurbitacin E reduces IL-1ß-induced inflammation and cartilage degeneration by inhibiting the PI3K/Akt pathway in osteoarthritic chondrocytes.

BACKGROUND: Osteoarthritis is a degenerative joint disease. Cartilage degeneration is the earliest and most important pathological change in osteoarthritis, and persistent inflammation is one of the driving factors of cartilage degeneration. Cucurbitacin E, an isolated compound in the Cucurbitacin family, has been shown to have anti-inflammatory effects, but its role and mechanism in osteoarthritic chondrocytes are unclear. METHODS: For in vitro experiments, human chondrocytes were stimulated with IL-1ß, and the expression of inflammatory genes was measured by Western blotting and qPCR. The expression of extracellular matrix proteins was evaluated by immunofluorescence staining, Western blotting and saffron staining. Differences in gene expression between cartilage from osteoarthritis patients and normal cartilage were analysed by bioinformatics methods, and the relationship between Cucurbitacin E and its target was analysed by a cellular thermal shift assay, molecular docking analysis and molecular dynamics simulation. For in vivo experiments, knee osteoarthritis was induced by DMM in C57BL/6 mouse knee joints, and the effect of Cucurbitacin E on knee joint degeneration was evaluated. RESULTS: The in vitro experiments confirmed that Cucurbitacin E effectively inhibited the production of the inflammatory cytokine interleukin-1ß(IL-1ß) and cyclooxygenase-2 (COX-2) by IL-1ß-stimulated chondrocytes and alleviates extracellular matrix degradation. The in vivo experiments demonstrated that Cucurbitacin E had a protective effect on the knee cartilage of C57BL/6 mice with medial meniscal instability in the osteoarthritis model. Mechanistically, bioinformatic analysis of the GSE114007 and GSE117999 datasets showed that the PI3K/AKT pathway was highly activated in osteoarthritis. Immunohistochemical analysis of PI3K/Akt signalling pathway proteins in pathological slices of human cartilage showed that the level of p-PI3K in patients with osteoarthritis was higher than that in the normal group. PI3K/Akt were upregulated in IL-1ß-stimulated chondrocytes, and Cucurbitacin E intervention reversed this phenomenon. The cellular thermal shift assay, molecular docking analysis and molecular dynamics experiment showed that Cucurbitacin E had a strong binding affinity for the inhibitory target PI3K. SC79 activated Akt phosphorylation and reversed the effect of Cucurbitacin E on IL-1ß-induced chondrocyte degeneration, demonstrating that Cucurbitacin E inhibits IL-1ß-induced chondrocyte inflammation and degeneration by inhibiting the PI3K/AKT pathway. CONCLUSION: Cucurbitacin E inhibits the activation of the PI3K/AKT pathway, thereby alleviating the progression of OA. In summary, we believe that Cucurbitacin E is a potential drug for the treatment of OA.

The antimicrobial activity of cethromycin against Staphylococcus aureus and compared with erythromycin and telithromycin.

BACKGROUND: This study aims to explore the antibacterial activity of cethromycin against Staphylococcus aureus (S. aureus), and its relationship with multilocus sequence typing (MLST), erythromycin ribosomal methylase (erm) genes and macrolide-lincosamide-streptogramin B (MLSB) phenotypes of S. aureus. RESULTS: The minimum inhibitory concentrations (MICs) of cethromycin against 245 S. aureus clinical isolates ranged from 0.03125 to ≥ 8 mg/L, with the resistance of 38.8% in 121 methicillin-resistant S. aureus (MRSA). This study also found that cethromycin had strong antibacterial activity against S. aureus, with the MIC ≤ 0.5 mg/L in 55.4% of MRSA and 60.5% of methicillin-sensitive S. aureus (MSSA), respectively. The main MLSTs of 121 MRSA were ST239 and ST59, and the resistance of ST239 isolates to cethromycin was higher than that in ST59 isolates (P = 0.034). The top five MLSTs of 124 MSSA were ST7, ST59, ST398, ST88 and ST120, but there was no difference in the resistance of MSSA to cethromycin between these STs. The resistance of ermA isolates to cethromycin was higher than that of ermB or ermC isolates in MRSA (P = 0.016 and 0.041, respectively), but the resistance of ermB or ermC isolates to cethromycin was higher than that of ermA isolates in MSSA (P = 0.019 and 0.026, respectively). The resistance of constitutive MLSB (cMLSB) phenotype isolates to cethromycin was higher than that of inducible MLSB (iMLSB) phenotype isolates in MRSA (P < 0.001) or MSSA (P = 0.036). The ermA, ermB and ermC genes was mainly found in ST239, ST59 and ST1 isolates in MRSA, respectively. Among the MSSA, the ermC gene was more detected in ST7, ST88 and ST120 isolates, but more ermB genes were detected in ST59 and ST398 isolates. The cMLSB phenotype was more common in ST239 and ST59 isolates of MRSA, and was more frequently detected in ST59, ST398, and ST120 isolates of MSSA. CONCLUSION: Cethromycin had strong antibacterial activity against S. aureus. The resistance of MRSA to cethromycin may had some clonal aggregation in ST239. The resistance of S. aureus carrying various erm genes or MLSB phenotypes to cethromycin was different.

Tumor-Derived PD-L1+ Exosomes with Natural Inflammation Tropism for Psoriasis-Targeted Treatment.

Psoriasis is a chronic inflammatory disease whose etiology is directly related to the dysregulation of cutaneous immune homeostasis. However, how to finely modulate the skin immune microenvironment to restore homeostasis remains an important challenge. Inspired by the natural attribute of tumor exosomes in the immune escape, the tumor-derived exosomes as an active targeting nanoplatform for the effective treatment of inflammatory skin disorder were first reported. As keratinocytes and immune cells express high PD-1 during the onset of psoriasiform skin inflammation, the PD-L1-positive exosomes derived from melanoma cells carrying pristimerin with extremely anti-inflammatory potential were yielded to treat psoriasis. The PD-L1+ exosomes carrying pristimerin were characterized, and the cellular uptake was performed to evaluate the PD-1 target capability. The anti-inflammatory action of PD-L1+ exosomes carrying pristimerin was observed in both in vitro and in vivo models of psoriasis. Our exosomes substantially increased pristimerin uptake with CD4+ T cells and keratinocytes, significantly inhibited the proliferation of Th17 cells, and promoted Treg differentiation in a psoriasis-like model. Obviously, PD-L1+ exosomes carrying pristimerin significantly and safely reversed imiquimod (IMQ)-induced psoriasis in mice, indicated by reducing epidermal thickness, decreasing plaque formation, and suppressed excessive inflammatory response, due to its dual targeting of both CD4+ T cells and keratinocytes gathering around the lesion. The inflammatory cell infiltration and pro-inflammatory cytokine production in psoriasis were suppressed by our engineered exosomes. Besides, PD-L1+ exosomes carrying pristimerin treatment alleviated ferroptosis-related changes in psoriatic skin, thereby dampening excessive inflammation and, in turn, decreasing the abnormal proliferation of keratinocytes in psoriatic lesions. This study demonstrates that our engineered exosomes can not only act as a treat-to-target strategy for psoriasis treatment but also provide insight in clinical application of inflammatory disorders.

Association Between Endothelial Activation and Stress Index and 28-Day Mortality in Septic ICU patients: a Retrospective Cohort Study.

Background: Endothelial Activation and Stress Index (EASIX) is a reliable alternative biomarker of endothelial dysfunction. Because endothelial activation is involved in sepsis pathophysiology, we aimed to investigate the association between EASIX and prognosis in septic patients. Methods: Data were extracted from the Medical Information Mart for Intensive Care (MIMIC) IV database. EASIX scores were calculated using the formula: lactate dehydrogenase (U/L) × creatinine (mg/dL)/platelet count (109/L). Patients were grouped into tertiles according to log2 transformed EASIX. The primary and secondary outcomes were 28-day and 90-day mortality. Cox proportional hazards models, Kaplan-Meier curves, restricted cubic spline curves, and subgroup analyses were conducted to evaluate the association between EASIX and prognosis in septic patients. Results: A total of 7504 patients were included. Multivariable Cox proportional hazards analyses showed that higher log2-EASIX was associated with increased risk of 28-day mortality (HR, 1.10; 95% CI, 1.07-1.13; P < 0.001). Compared with tertile 1, the tertile 2 and 3 groups had higher risk of 28-day mortality [HR (95% CI) 1.24 (1.09-1.41); HR (95% CI) 1.51 (1.31-1.74)]; P for trend < 0.001). Similar results were found for 90-day mortality. Kaplan-Meier curves showed that patients with higher EASIX had lower 28-day and 90-day survival rates. A linear relationship was found between log2-EASIX and 28-day and 90-day mortality. Conclusion: High EASIX was significantly associated with an increased risk of 28-day and 90-day all-cause mortality in patients with sepsis.

Neobavaisoflavone Inhibits Biofilm Formation and α-Toxin Activity of Staphylococcus aureus.

Neobavaisoflavone had antimicrobial activities against Gram-positive multidrug-resistant (MDR) bacteria, but the effect of neobavaisoflavone on the virulence and biofilm formation of S. aureus has not been explored. The present study aimed to investigate the possible inhibitory effect of neobavaisoflavone on the biofilm formation and α-toxin activity of S. aureus. Neobavaisoflavone presented strong inhibitory effect on the biofilm formation and α-toxin activity of both methicillin-sensitive S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) strains at 25 µM, but did not affect the growth of S. aureus planktonic cells. Genetic mutations were identified in four coding genes, including cell wall metabolism sensor histidine kinase walK, RNA polymerase sigma factor rpoD, tetR family transcriptional regulator, and a hypothetical protein. The mutation of WalK (K570E) protein was identified and verified in all the neobavaisoflavone-induced mutant S. aureus isolates. The ASN501, LYS504, ILE544 and GLY565 of WalK protein act as hydrogen acceptors to form four hydrogen bonds with neobavaisoflavone by molecular docking analysis, and TRY505 of WalK protein contact with neobavaisoflavone to form a pi-H bond. In conclusion, neobavaisoflavone had excellent inhibitory effect on the biofilm formation and α-toxin activity of S. aureus. The WalK protein might be a potential target of neobavaisoflavone against S. aureus.

Training a deep operator network as a surrogate solver for two-dimensional parabolic-equation models.

Parabolic equations (PEs) are useful for modeling sound propagation in a range-dependent environment. However, this approach entails approximating a leading-order cross-derivative term in the PE square-root operators. Deep operator networks (DeepONets) are designed to approximate operators. In this paper, we train DeepONets to take complex sound pressure and speed of sound at any depth location of interest as inputs and approximate the PE square operator in modeling two-dimensional sound propagation. Once trained, a network can predict the far field for a wide variety of environmental conditions, without needing to approximate the operator or calculate the whole mode trajectory and at a lower computational cost. The original DeepONet learns the operator of a single function. By contrast, the modified version presented here learns multiple-input operators with Fourier features. Using computational and theoretical examples, we demonstrate that DeepONet is efficient for learning complex ocean acoustic physics with good accuracy.

Tubule-specific protein nanocages potentiate targeted renal fibrosis therapy.

BACKGROUND: Despite the dramatic advances in modern medicine, efficient therapeutic measures for renal fibrosis remain limited. Celastrol (CLT) is effective in treating renal fibrosis in rat models, while causing severe systemic toxicity. Thus, we designed a tubule-specific nanocage (K3-HBc NCs) that effectively deliver CLT to tubular epithelial cell in a virus-like manner. The targeting ligand (K3) to tubular epithelial cells was displayed on the surface of Hepatitis B core protein (HBc) NCs by genetic fusion to the major immunodominant loop region. Ultra-small CLT nanodots were subtly encapsulated into the cavity through electrostatic interaction with the disassembly and reassembly of K3-HBc NCs, to yield K3-HBc/CLT complex. The efficacy of K3-HBc/CLT NCs were demonstrated in Unilateral ureteral obstruction (UUO)-induced renal fibrosis. RESULTS: The self-assembled K3-HBc/CLT could specifically target tubular epithelial cells via affinity with K3 ligand binding to the megalin receptor, significantly attenuating renal fibrosis. Remarkably, K3-HBc/CLT NCs significantly increased therapeutic efficacy and reduced the systemic toxicity in comparison with free CLT in UUO-induced mouse renal fibrosis model. Importantly, analysis of RNA sequencing data suggested that the anti-fibrotic effect of K3-HBc/CLT could be attributed to suppression of premature senescence in tubular epithelial cells via p21Cip1 and p16Ink4a pathway. CONCLUSION: The tubule-specific K3-HBc/CLT represented a promising option to realize precise treatment for renal fibrosis.

A Particle Swarm Algorithm Based on a Multi-Stage Search Strategy.

Particle swarm optimization (PSO) has the disadvantages of easily getting trapped in local optima and a low search accuracy. Scores of approaches have been used to improve the diversity, search accuracy, and results of PSO, but the balance between exploration and exploitation remains sub-optimal. Many scholars have divided the population into multiple sub-populations with the aim of managing it in space. In this paper, a multi-stage search strategy that is dominated by mutual repulsion among particles and supplemented by attraction was proposed to control the traits of the population. From the angle of iteration time, the algorithm was able to adequately enhance the entropy of the population under the premise of satisfying the convergence, creating a more balanced search process. The study acquired satisfactory results from the CEC2017 test function by improving the standard PSO and improved PSO.

Particle Filtering for Localization of Broadband Sound Source Using an Ocean-Bottom Seismometer Sensor.

Passive source localization is a challenging task for one receiver, and the pressure sensor provides relatively simple information. An ocean-bottom seismometer (OBS) sensor placed on the seafloor surface can provide more information-not only pressure information, but also three-axis (x-, y-, and z-axis) velocity information at the seafloor interface. In this paper, an OBS sensor was used to estimate the position of the broadband sound source in a Pekeris shallow water waveguide with elastic bottom. As the dynamics that characterize ocean acoustic applications are inherently nonlinear, non-Gaussian, and non-stationary processes that quickly vary with space and time, sequential Bayesian filtering, such as particle filtering (PF), is able to adapt to these environmental changes. Simulation results show that the PF method with the vertical wave impedance (the ratio of the pressure and vertical particle velocity) in the frequency domain as a measurement vector is not affected by source depth and source spectrum information, making it more tolerant and more robust than that with pressure in positioning. Experimental data results verified the effectiveness of the PF method with the vertical wave impedance for the localization of the explosive source.

Novel Local Coding Algorithm for Finger Multimodal Feature Description and Recognition.

Recently, finger-based biometrics, including fingerprint (FP), finger-vein (FV) and finger-knuckle-print (FKP) with high convenience and user friendliness, have attracted much attention for personal identification. The features expression which is insensitive to illumination and pose variation are beneficial for finger trimodal recognition performance improvement. Therefore, exploring suitable method of reliable feature description is of great significance for developing finger-based biometric recognition system. In this paper, we first propose a correction approach for dealing with the pose inconsistency among the finger trimodal images, and then introduce a novel local coding-based feature expression method to further implement feature fusion of FP, FV, and FKP traits. First, for the coding scheme a bank of oriented Gabor filters is used for direction feature enhancement in finger images. Then, a generalized symmetric local graph structure (GSLGS) is developed to fully express the position and orientation relationships among neighborhood pixels. Experimental results on our own-built finger trimodal database show that the proposed coding-based approach achieves excellent performance in improving the matching accuracy and recognition efficiency.

Dual Role of Triptolide in Interrupting the NLRP3 Inflammasome Pathway to Attenuate Cardiac Fibrosis.

In a previous paper, we reported that triptolide (TP), a commonly used immunomodulator, could attenuate cardiac hypertrophy. This present study aimed to further explore the inhibition of cardiac fibrosis by TP and the possible mechanism from the perspective of the NOD-like receptor protein 3 (NLRP3) inflammasome. Hematoxylin-eosin and Masson's staining, immunohistochemistry, and immunofluorescence were performed to observe cardiac fibrotic changes in mice and mouse cardiac fibroblasts (CFs). The Western blot, colocalization, and immunoprecipitation were applied to detect protein expression and interactions. Results suggested that TP dose-dependently inhibited cardiac fibrosis induced by isoproterenol and collagen production of CFs induced by angiotensin II. TP exhibited an antifibrotic effect via inhibiting activation of the NLRP3 inflammasome, which sequentially decreased IL-1ß maturation, myeloid differentiation factor 88 (MyD88)-related phosphorylation of c-Jun N-terminal kinase (JNK), extracellular regulated protein kinase 1/2 (ERK1/2), and TGF-ß1/Smad signaling, and ultimately resulted in less collagen production. Moreover, TP showed no antifibrotic effect in Nlrp3-knockout CFs. Notably, TP inhibited the expression of NLRP3 and apoptosis-associated speck-like proteins containing a caspase recruitment domain (ASC) as well as inflammasome assembly, by interrupting the NLRP3-ASC interaction to inhibit inflammasome activation. Finally, TP indeed inhibited the NLRP3-TGFß1-Smad pathway in vivo. Conclusively, TP was found to play a dual role in interrupting the activation of the NLRP3 inflammasome to attenuate cardiac fibrosis.

Decreased Serum Brain-Derived Neurotrophic Factor May Indicate the Development of Poststroke Depression in Patients with Acute Ischemic Stroke: A Meta-Analysis.

BACKGROUND: Depression is a common complication after stroke and has been associated with poor outcome. Thus, it is of great importance to identify potential biomarkers that can aid in predicting and detecting patients with stroke at high risk of poststroke depression (PSD) development. Previous studies showed that brain-derived neurotrophic factor (BDNF) had potential use as a biomarker for discriminating patients with stroke at high risk of PSD. However, the results were inconsistent. METHODS: A meta-analysis was performed to evaluate the correlation between the peripheral BDNF levels and the development of PSD in the acute stage of stroke. RESULTS: Data were obtained from 4 studies including 499 patients with stroke. Among them, 171 patients were diagnosed with PSD at follow-ups. Our results showed that patients with stroke who were predisposed to developing PSD had significantly lower serum BDNF concentrations at the early stage of stroke. CONCLUSIONS: This study suggests a potential association between circulating BDNF concentrations at admission and subsequent PSD development, and provides additional support for the involvement of BDNF in the PSD development.

Cyclin-Dependent Kinase Inhibitor p21WAF1/CIP1 Facilitates the Development of Cardiac Hypertrophy.

BACKGROUND/AIMS: Adult cardiomyocytes can re-enter cell cycle as stimulated by prohypertrophic factors although they withdraw from cell cycle soon after birth. p21WAF1/CIP1, a cyclin-dependent kinase inhibitor, has been implicated in cardiac hypertrophy, however, its precise contribution to this process remains largely unclear. METHODS: The gene expression profile in left ventricle (LV) of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats was determined using quantitative PCR array and verified by real-time PCR and Western blotting. Hypertrophic response of H9c2 cells and neonatal rat ventricular myocytes (NRVM) were induced by angiotensin II (1 µmol/L). Cardiac hypertrophy of mice was elicited by isoproterenol (ISO) infusion (40 mg/kg per day for 14 days). p21-adenovirus and p21-siRNA were employed to transfect NRVM, and sterigmatocystin (STE, 3 mg/kg, ip, qd) was used to inhibit p21 activity. mRNA and protein expression levels of α- and ß-myosin heavy chain (MHC), p21WAF1/CIP1, calcineurin (CaN) and atrial natriuretic peptide (ANP) were assayed by realtime PCR and WB, respectively. RESULTS: Sixteen genes showed two-fold or greater changes between SHR and WKY rats, in which the expression of p21WAF1/CIP1 was upregulated by 4.15-fold (P=0.002) and reversed by losartan. Surface area, protein content, mRNA and protein expressions of ß-MHC, ANP and p21WAF1/CIP1 in H9c2 cells treated with AngII elevated significantly compared with control group. p21-Ad transfection markedly increased the surface area and ß-MHC mRNA expression of normal NRVMs, and p21-siRNA transfection decreased them in AngII-treated NRVMs. STE treatment decreased HW/BW and cross-sectional area, expression levels of ß-MHC, ANP and p21 significantly in ISO-treated mice. CONCLUSION: Our findings suggest that p21 facilitates the development of cardiac hypertrophy, and regulating the expression of p21 may be an approach to attenuate hypertrophic growth of cardiomyocytes.

Extracting the time domain Green's function from ocean ambient noise using acoustic vector sensors.

A function that closely resembles the two-point time-domain Green's function (TDGF) representing the time delays associated with multipath between the two sensors can be recovered by correlating the noise field measured by two sensors. Here, a technique for extracting the TDGF from ambient ocean noise using acoustic vector sensors is presented. Experimental results suggest that the averaging time to extract TDGF is greatly reduced if sound pressure sensors (hydrophones) are replaced by acoustic vector sensors. The direct arrival and bottom bounce arrival were extracted successfully with only 1 min of vertical velocity data, while the bottom bounce arrival was not extracted with even 10 min of sound pressure data.

Performance of micro-pressure double-cycle coupled membrane integrated bioreactor for the treatment of urban sewage.

Based on the theory of nitrogen and phosphorus removal and technical requirements, a micro-pressure double-cycle bioreactor coupled with membrane components was used to treat municipal wastewater. The method realized the simultaneous removal of organic matter, nitrogen, and phosphorus in the same reactor and had the characteristics of membrane bioreactor process. Results showed that the average removal efficiency of COD, NH+4-N, TN, and TP were 93.74%, 95.1%, 71.85%, and 81.03%, respectively. During operation, Proteobacteria and Bacteroidetes were the main dominant bacteria, and they had complete nitrogen and phosphorus metabolic pathways. Owing to the low protein content in the mixture, the design of film placement in the micro-precipitation zone was conducive to alleviating the membrane pollution caused by the accumulation of protein, thereby improving the effluent quality and extending the service life of the membrane components.