Double-Enzyme Active Vanadium Nanospheres-Mediated Ratiometric Multicolor Immunosensors for Sensitive Detection of the T-2 Toxin.

Owing to its high throughput, simplicity, and rapidity, enzyme-linked immunosorbent assay (ELISA) has attracted much attention in the field of immunoassays. However, the traditional ELISA usually affords a single signal readout and the labeling ability of the enzyme used is poor, resulting in low accuracy and a limited detection range. Herein, a vanadium nanospheres (VNSs)-mediated competitive ratio nanozymes-linked immunosorbent assay (VNSs-RNLISA) was created for the sensitive detection of the T-2 toxin (T-2). As the key to the biosensor, the VNSs with superoxide dismutase-like and peroxidase-like dual-enzyme mimetic activities were synthesized by a one-step hydrothermal method, which oxidized 1,1-diphenyl-2-picryl-hydrazyl fading and catalyzed 3,3',5,5'-tetramethylbenzidine (TMB) color development. Therefore, T-2 could not only be qualitatively measured with the naked eye but also be quantitatively evaluated by monitoring the ratio of absorbance at 450 and 517 nm wavelengths. Moreover, the characterization of a VNSs-labeled antibody probe showed strong dual-enzymatic activity, excellent stability, and high affinity with T-2 [the affinity constant (ka) was approximately 1.36 × 108 M-1], which can significantly improve the detection sensitivity. The limit of detection of VNSs-RNLISA was 0.021 ng/mL, which was approximately 27-fold more sensitive than the single signal nanozymes-linked immunosorbent assay (0.561 ng/mL). Besides, the change in the ratio of absorbance (Δ450/Δ517) decreased linearly in a range of 0.22-13.17 ng/mL, outperforming the detection range of a single-mode nano-enzyme-linked immunosorbent assay using TMB by a factor of 1.6 times. Furthermore, the VNSs-RNLISA was successfully used to identify T-2 in maize and oat samples, with recoveries ranging from 84.216 to 125.371%. Overall, this tactic offered a promising platform for the quick detection of T-2 in food and might broaden the application range of the enzyme-linked immunosorbent assay.

Accelerated Oxygen Evolution Kinetics by Engineering Heterojunction Coupling of Amorphous NiFe Hydr(oxy)oxide Nanosheet Arrays on Self-Supporting Ni-MOFs.

Designing definite transition metal heterointerfaces is considered an effective strategy for the construction of efficient and robust oxygen evolution reaction (OER) electrocatalysts, but rather challenging. Herein, amorphous NiFe hydr(oxy)oxide nanosheet arrays (A-NiFe HNSAs) are grown in situ on the surface of a self-supporting Ni metal-organic frameworks (SNMs) electrode via a combination strategy of ion exchange and hydrolytic co-deposition for efficient and stable large-current-density water oxidation. The existence of the abundant metal-oxygen bonds on the heterointerfaces can not only be of great significance to alter the electronic structure and accelerate the reaction kinetics, but also enable the redistribution of Ni/Fe charge density to effectively control the adsorption behavior of important intermediates with a close to the optimal d-band center, dramatically narrowing the energy barriers of the OER rate-limiting steps. By optimizing the electrode structure, the A-NiFe HNSAs/SNMs-NF exhibits outstanding OER performance with small overpotentials of 223 and 251 mV at 100 and 500 mA cm-2 , a low Tafel slope of 36.3 mV dec-1 , and excellent durability during 120 h at 10 mA cm-2 . This work significantly provides an avenue to understand and realize rationally designed heterointerface structures toward effective oxygen evolution in water-splitting applications.

Causal relationships between potential risk factors and chronic rhinosinusitis: a bidirectional two-sample Mendelian randomization study.

PURPOSE: Smoking, alcohol consumption, allergic rhinitis (AR), asthma, and obesity are associated with chronic rhinosinusitis (CRS), albeit the causal relationships between them remain elusive. Therefore, we conducted a bidirectional two-sample Mendelian randomization (MR) study to investigate the bidirectional causal effects between these potential risk factors and CRS. METHODS: The data for daily cigarette consumption, age of smoking initiation, weekly alcohol consumption, AR, asthma, body mass index (BMI), and CRS were drawn from large sample size genome-wide association studies. Single-nucleotide polymorphisms associated with each exposure were considered instrumental variables in this study. We investigated causal effects by using the inverse-variance weighted (IVW) method with random effects, and weighted median and MR-Egger methods were used for sensitivity analyses. Pleiotropic effects were detected and corrected by the MR pleiotropy residual sum and outlier test and MR-Egger model. RESULTS: We found the causal effects of daily cigarette consumption (IVW, OR = 1.15, 95% CI 1.00-1.32, p = 0.046), AR (IVW, OR = 4.77, 95% CI 1.61-14.13, p = 0.005), asthma (IVW, OR = 1.45, 95% CI 1.31 - 1.60, p < 0.001), and BMI (IVW, OR = 1.05, 95% CI 1.00-1.09, p = 0.028) on CRS. Furthermore, we found a causal effect of CRS on asthma (IVW OR = 1.08, 95% CI 1.05-1.12, p < 0.001). CONCLUSIONS: We confirmed the causal effects of daily cigarette consumption, AR, asthma, and BMI on CRS, and the causal effect of CRS on asthma, while no causal relationship between age of smoking initiation, weekly alcohol consumption, and CRS was found. These findings are expected to provide high-quality causal evidence for clinical practice and the pathogenesis of CRS and asthma.

Single-cell sequencing analysis and transcriptome analysis constructed the macrophage related gene-related signature in lung adenocarcinoma and verified by an independent cohort.

BACKGROUND: Recent studies have emphasized the close relationship between macrophages and tumor immunity, and the prognosis of lung adenocarcinoma (LUAD) patients is intimately linked to this. Nonetheless, the prognostic signature and classification of different immune patterns in LUAD patients based on the macrophages is largely unexplored. METHODS: Two sc-RNAseq datasets of LUAD patients were collected and reprocessed. The differentially expressed genes (DEGs) related to macrophages between LUAD tissues and normal lung tissues were then identified. Based upon the above genes, three distinct immune patterns in the TCGA-LUAD cohort were identified. The ssGSEA and CIBERSORT were applied for immune profiling and characterization of different subtypes. A four-gene prognostic signature for LUAD patients was established based on the DEGs between the subtypes using stepwise multi-Cox regression. TCGA-LUAD cohort was used as training set. Five GEO-LUAD datasets and an independent cohort containing 112 LUAD samples were used for validation. TIDE (tumor immune dysfunction and exclusion) and drug sensitivity analyses were also performed. RESULTS: Macrophage-related differentially expressed genes were found out using the publicly available scRNA-seq data of LUAD. Three different immune patterns which were proved to have distinct immune infiltration characteristics in the TCGA-LUAD cohort were recognized based on the above macrophage-related genes. Thereafter, 174 DEGs among the above three different immune patterns were figured out; on the basis of this, a four-gene prognostic signature was constructed. This signature distinguished the prognosis of LUAD patients well in various GSE datasets as well as our independent cohort. Further analyses revealed that patients which had a higher risk score also accompanied with a lower immune infiltration level and a worse response to several immunotherapy biomarkers. CONCLUSION: This study highlighted that macrophage were significantly associated with TME diversity and complexity. The four-gene prognostic signature could be used for predicting outcomes and immune landscapes for patients with LUAD.

Designing Heteroatom-Codoped Iron Metal-Organic Framework for Promotional Photoreduction of Carbon Dioxide to Ethylene.

Rational engineering active sites and vantage defects of catalysts are promising but grand challenging task to enhance photoreduction CO2 to high value-added C2 products. In this study, we designed an N,S-codoped Fe-based MIL-88B catalyst with well-defined bipyramidal hexagonal prism morphology via a facile and effective process, which was synthesized by addition of appropriate 1,2-benzisothiazolin-3-one (BIT) and acetic acid to the reaction solution. Under simulated solar irradiation, the designed catalyst exhibits high C2 H4 evolution yield of 17.7 µmol g-1 ⋅h, which has been rarely achieved in photocatalytic CO2 reduction process. The synergistic effect of Fe-N coordinated sites and reasonable defects in the N,S-codoped photocatalyst can accelerate the migration of photogenerated carriers, resulting in high electron density, and this in turn helps to facilitate the formation and dimerization of C-C coupling intermediates for C2 H4 effectively.

Perm1 promotes cardiomyocyte mitochondrial biogenesis and protects against hypoxia/reoxygenation-induced damage in mice.

Normal contractile function of the heart depends on a constant and reliable production of ATP by cardiomyocytes. Dysregulation of cardiac energy metabolism can result in immature heart development and disrupt the ability of the adult myocardium to adapt to stress, potentially leading to heart failure. Further, restoration of abnormal mitochondrial function can have beneficial effects on cardiac dysfunction. Previously, we identified a novel protein termed Perm1 (PGC-1 and estrogen-related receptor (ERR)-induced regulator, muscle 1) that is enriched in skeletal and cardiac-muscle mitochondria and transcriptionally regulated by PGC-1 (peroxisome proliferator-activated receptor gamma coactivator 1) and ERR. The role of Perm1 in the heart is poorly understood and is studied here. We utilized cell culture, mouse models, and human tissue, to study its expression and transcriptional control, as well as its role in transcription of other factors. Critically, we tested Perm1's role in cardiomyocyte mitochondrial function and its ability to protect myocytes from stress-induced damage. Our studies show that Perm1 expression increases throughout mouse cardiogenesis, demonstrate that Perm1 interacts with PGC-1α and enhances activation of PGC-1 and ERR, increases mitochondrial DNA copy number, and augments oxidative capacity in cultured neonatal mouse cardiomyocytes. Moreover, we found that Perm1 reduced cellular damage produced as a result of hypoxia and reoxygenation-induced stress and mitigated cell death of cardiomyocytes. Taken together, our results show that Perm1 promotes mitochondrial biogenesis in mouse cardiomyocytes. Future studies can assess the potential of Perm1 to be used as a novel therapeutic to restore cardiac dysfunction induced by ischemic injury.

Cardiomyocyte Expression of ZO-1 Is Essential for Normal Atrioventricular Conduction but Does Not Alter Ventricular Function.

RATIONALE: ZO-1 (Zonula occludens-1), a plasma membrane-associated scaffolding protein regulates signal transduction, transcription, and cellular communication. Global deletion of ZO-1 in the mouse is lethal by embryonic day 11.5. The function of ZO-1 in cardiac myocytes (CM) is largely unknown. OBJECTIVE: To determine the function of CM ZO-1 in the intact heart, given its binding to other CM proteins that have been shown instrumental in normal cardiac conduction and function. METHODS AND RESULTS: We generated ZO-1 CM-specific knockout (KO) mice using α-Myosin Heavy Chain-nuclear Cre (ZO-1cKO) and investigated physiological and electrophysiological function by echocardiography, surface ECG and conscious telemetry, intracardiac electrograms and pacing, and optical mapping studies. ZO-1cKO mice were viable, had normal Mendelian ratios, and had a normal lifespan. Ventricular morphometry and function were not significantly different between the ZO-1cKO versus control (CTL) mice, basally in young or aged mice, or even when hearts were subjected to hemodynamic loading. Atrial mass was increased in ZO-1cKO. Electrophysiological and optical mapping studies indicated high-grade atrioventricular (A-V) block in ZO-1cKO comparing to CTL hearts. While ZO-1-associated proteins such as vinculin, connexin 43, N-cadherin, and α-catenin showed no significant change with the loss of ZO-1, Connexin-45 and Coxsackie-adenovirus (CAR) proteins were reduced in atria of ZO-1cKO. Further, with loss of ZO-1, ZO-2 protein was increased significantly in ventricular CM in a presumed compensatory manner but was still not detected in the AV nodal myocytes. Importantly, the expression of the sodium channel protein NaV1.5 was altered in AV nodal cells of the ZO-1cKO versus CTL. CONCLUSIONS: ZO-1 protein has a unique physiological role in cardiac nodal tissue. This is in alignment with its known interaction with CAR and Cx45, and a new function in regulating the expression of NaV1.5 in AV node. Uniquely, ZO-1 is dispensable for function of the working myocardium.

Prognosis of patients with hepatocellular carcinoma and portal vein tumor thrombus treated with combination of transarterial chemoembolization and palliative thermal ablation.

PURPOSE: Transarterial chemoembolization (TACE) was obtained acceptable benefit for advanced hepatocellular carcinoma (HCC). Here in this study, we compared the benefit of TACE combined palliative thermal ablation with TACE alone for HCC with portal vein tumor thrombus (PVTT). METHODS: Patients with HCC and PVTT were retrospectively analyzed from January 2012 to December 2017, who accepted treatment of TACE alone (TACE group) or TACE plus palliative thermal ablation (TACE + P-ablation group). Propensity score matching (PSM) was applied to balance differences between the two groups. Overall survival (OS) and progression-free survival (PFS) rates were compared between groups. RESULTS: Median follow-up time was 7.4 (3.0-60.0) months. In the cohort, 142 patients were enrolled in TACE group and 86 patients were enrolled in TACE + P-ablation group. The pre-PSM estimated 6-, 12-, and 18-month OS rates for the TACE + P-ablation group were 70.9, 46.5, and 31%, respectively, whereas rates for the TACE group were 57, 23.1, and 10%, respectively. After PSM, OS and PFS rates remained coincident with the pre-PSM. Risk factors for poor OS included PVTT type III and type II relative to type I (HR = 1.76; 95% CI, 1.13-2.74; p = .01) and (HR = 1.86; 95% CI, 1.2-2.88; p = .006), TACE alone (HR = 1.40; 95% CI, 1.01-1.96; p = .04), a single TACE treatment (HR = 2.69; 95% CI, 1.79-4.03; p < .001), 2 or 3 TACE treatments (HR = 2.02; 95% CI, 1.32-3.09; p = .001). CONCLUSIONS: The combination of TACE and palliative thermal ablation for HCC with PVTT could obtain delayed progression and longer survival.

Successive Phase Transitions and Dual Dielectric Switching in an Organic-Inorganic Hybrid Perovskite.

Molecular phase transition compounds have become a hot research area in recent years because of their potential as functional materials, such as ferroelectrics, ferroelastics, dielectric switches, etc. However, materials combining switchable dielectric properties and ferroelasticity are still rare. Here, we reported an organic-inorganic hybrid perovskite, [CPtmp][Cd(SCN)3] (1) ([CPtmp]+ is a cyclopentyltrimethylphosphonium cation), with a potential ferroelastic property. This material undergoes three structural phase transitions at 247/226, 335/312, and 349/341 K (upon heating/cooling). The successive phase transitions are mainly caused by the stepwise ordering of [CPtmp]+ cations and the concomitant deformation of [Cd(SCN)3]- anionic chains revealed by structural analyses, which triggers the double-step dielectric switching in 1 as well. These results would inspire further exploration on molecular dielectric switches with ferroelastic properties.

The Role of MIF-173G/C Gene Polymorphism in the Susceptibility of Autoimmune Diseases.

Some certain genetic polymorphisms have been considered to implicate in the pathogenesis and progression of autoimmune diseases and may predispose to an early stage of general autoimmune susceptibility. Recent studies have been conducted to investigate the association between macrophage migration inhibitory factor- (MIF-) 173G/C gene polymorphism and autoimmune diseases; however, the results were not exactly identical. In the present study, a systematic review and meta-analysis of case-control studies was performed to estimate the relationship. A comprehensive search of PubMed, Ebsco, EMbase, WanFang databases and CNKI was done. Odds ratio (ORs) and corresponding 95% confidence intervals (CIs) were combined to pool the effect size. The publication bias was examined by Begg's funnel plots and Egger's test. RevMan 5.3 and STATA 12.0 software were used for statistical processing. 23 papers were included, and the results revealed that MIF-173G/C was significantly associated with an increased risk of autoimmune diseases in five genetic models (recessive genetic model: OR = 1.95, 95% CI: 1.52-2.50; dominant genetic model: OR = 1.35, 95% CI: 1.24-1.46; allele model: OR = 1.32, 95% CI: 1.23-1.41; homozygote model: OR = 1.92, 95% CI: 1.57-2.35; heterozygote model: OR = 4.92, 95% CI: 4.03-6.02), whether in Asia, Europe, or North America. Furthermore, subgroup analysis showed an increasing risk in rheumatoid arthritis (RA), ulcerative colitis (UC), Crohn's disease (CD), atopic dermatitis (AD), Henoch-Schonlein purpura (HSP), and Henoch-Schonlein purpura nephritis (HSPN), but it was not related to the susceptibility of autoimmune hepatitis (AIH). Therefore, it could be considered that MIF-173G/C polymorphism could increase the susceptibility of autoimmune diseases, while there may be the discrepancy of disease entity.

Loss of mouse cardiomyocyte talin-1 and talin-2 leads to ß-1 integrin reduction, costameric instability, and dilated cardiomyopathy.

Continuous contraction-relaxation cycles of the heart require strong and stable connections of cardiac myocytes (CMs) with the extracellular matrix (ECM) to preserve sarcolemmal integrity. CM attachment to the ECM is mediated by integrin complexes localized at the muscle adhesion sites termed costameres. The ubiquitously expressed cytoskeletal protein talin (Tln) is a component of muscle costameres that links integrins ultimately to the sarcomere. There are two talin genes, Tln1 and Tln2. Here, we tested the function of these two Tln forms in myocardium where Tln2 is the dominant isoform in postnatal CMs. Surprisingly, global deletion of Tln2 in mice caused no structural or functional changes in heart, presumably because CM Tln1 became up-regulated. Tln2 loss increased integrin activation, although levels of the muscle-specific ß1D-integrin isoform were reduced by 50%. With this result, we produced mice that had simultaneous loss of both CM Tln1 and Tln2 and found that cardiac dysfunction occurred by 4 wk with 100% mortality by 6 mo. ß1D integrin and other costameric proteins were lost from the CMs, and membrane integrity was compromised. Given that integrin protein reduction occurred with Tln loss, rescue of the phenotype was attempted through transgenic integrin overexpression, but this could not restore WT CM integrin levels nor improve heart function. Our results show that CM Tln2 is essential for proper ß1D-integrin expression and that Tln1 can substitute for Tln2 in preserving heart function, but that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dilated cardiomyopathy.

Half-Sandwich Iridium and Ruthenium Complexes: Effective Tracking in Cells and Anticancer Studies.

Half-sandwich metal-based anticancer complexes suffer from uncertain targets and mechanisms of action. Herein we report the observation of the images of half-sandwich iridium and ruthenium complexes in cells detected by confocal microscopy. The confocal microscopy images showed that the cyclopentadienyl iridium complex 1 mainly accumulated in nuclei in A549 lung cancer cells, whereas the arene ruthenium complex 3 is located in mitochondria and lysosomes, mostly in mitochondria, although both complexes entered A549 cells mainly through energy-dependent active transport. The nuclear morphological changes caused by Ir complex 1 were also detected by confocal microscopy. Ir complex 1 is more potent than cisplatin toward A549 and HeLa cells. DNA binding studies involved interaction with the nucleobases 9-ethylguanine, 9-methyladenine, ctDNA, and plasmid DNA. The determination of bovine serum albumin binding was also performed. Hydrolysis, stability, nucleobase binding, and catalytic NAD+/NADH hydride transfer tests for complexes 1 and 3 were also carried out. Both complexes activated depolarization of mitochondrial membrane potential and intracellular ROS overproduction and induced cell apoptosis. Complex 3 arrested the cell cycle at the G0/G1 phase by inactivation of CDK 4/cyclin D1. This work paves the way to track and monitor half-sandwich metal complexes in cells, shines a light on understanding their mechanism of action, and indicates their potential application as theranostic agents.

Nicotine promotes vascular endothelial growth factor secretion by human trophoblast cells under hypoxic conditions and improves the proliferation and tube formation capacity of human umbilical endothelial cells.

Pre-eclampsia, characterized as defective uteroplacental vascularization, remains the major cause of maternal and fetal mortality and morbidity. Previous epidemiological studies demonstrated that cigarette smoking reduced the risk of pre-eclampsia. However, the molecular mechanism remains elusive. In the present study, it is demonstrated that a low dose of nicotine decreased soluble vascular endothelial growth factor receptor 1 (sFlt1) secretion in human trophoblast cells under hypoxic conditions. Nicotine was then observed to promote vascular endothelial growth factor (VEGF) secretion by reducing sFlt1 secretion and increasing VEGF mRNA transcription. Further data showed that nicotine enhanced hypoxia-mediated hypoxia-inducible factor-1α (HIF-1α) expression and HIF-1α small interfering RNA abrogated nicotine-induced VEGF secretion, indicating that HIF-1α may be responsible for nicotine-mediated VEGF transcription under hypoxic conditions. Moreover, conditioned medium from human trophoblast cells treated with nicotine under hypoxic conditions promoted the proliferation and tube formation capacity of human umbilical endothelial cells (HUVEC) by promoting VEGF secretion. These findings indicate that nicotine may promote VEGF secretion in human trophoblast cells under hypoxic conditions by reducing sFlt1 secretion and up-regulating VEGF transcription and improve the proliferation and tube formation of HUVEC cells, which may contribute to elucidate the protective effect of cigarette smoking against pre-eclampsia.

Integrins and integrin-related proteins in cardiac fibrosis.

Cardiac fibrosis is one of the major components of the healing mechanism following any injury of the heart and as such may contribute to both systolic and diastolic dysfunction in a range of pathophysiologic conditions. Canonically, it can occur as part of the remodeling process that occurs following myocardial infarction or that follows as a response to pressure overload. Integrins are cell surface receptors which act in both cellular adhesion and signaling. Most importantly, in the context of the continuously contracting myocardium, they are recognized as mechanotransducers. They have been implicated in the development of fibrosis in several organs, including the heart. This review will focus on the involvement of integrins and integrin-related proteins, in cardiac fibrosis, outlining the roles of these proteins in the fibrotic responses in specific cardiac pathologies, discuss some of the common end effectors (angiotensin II, transforming growth factor beta 1 and mechanical stress) through which integrins function and finally discuss how manipulation of this set of proteins may lead to new treatments which could prove useful to alter the deleterious effects of cardiac fibrosis.

Caveolin modulates integrin function and mechanical activation in the cardiomyocyte.

ß1 integrins (ß1) transduce mechanical signals in many cells, including cardiac myocytes (CM). Given their close localization, as well as their role in mechanotransduction and signaling, we hypothesized that caveolin (Cav) proteins might regulate integrins in the CM. ß1 localization, complex formation, activation state, and signaling were analyzed using wild-type, Cav3 knockout, and Cav3 CM-specific transgenic heart and myocyte samples. Studies were performed under basal and mechanically loaded conditions. We found that: (1) ß1 and Cav3 colocalize in CM and coimmunoprecipitate from CM protein lysates; (2) ß1 is detected in a subset of caveolae; (3) loss of Cav3 caused reduction of ß1D integrin isoform and active ß1 integrin from the buoyant domains in the heart; (4) increased expression of myocyte Cav3 correlates with increased active ß1 integrin in adult CM; (5) in vivo pressure overload of the wild-type heart results in increased activated integrin in buoyant membrane domains along with increased association between active integrin and Cav3; and (6) Cav3-deficient myocytes have perturbed basal and stretch mediated signaling responses. Thus, Cav3 protein can modify integrin function and mechanotransduction in the CM and intact heart.

Talin1 has unique expression versus talin 2 in the heart and modifies the hypertrophic response to pressure overload.

Integrins are adhesive, signaling, and mechanotransduction proteins. Talin (Tln) activates integrins and links it to the actin cytoskeleton. Vertebrates contain two talin genes, tln1 and tln2. How Tln1 and Tln2 function in cardiac myocytes (CMs) is unknown. Tln1 and Tln2 expression were evaluated in the normal embryonic and adult mouse heart as well as in control and failing human adult myocardium. Tln1 function was then tested in the basal and mechanically stressed myocardium after cardiomyocyte-specific excision of the Tln1 gene. During embryogenesis, both Tln forms are highly expressed in CMs, but in the mature heart Tln2 becomes the main Tln isoform, localizing to the costameres. Tln1 expression is minimal in the adult CM. With pharmacological and mechanical stress causing hypertrophy, Tln1 is up-regulated in CMs and is specifically detected at costameres, suggesting its importance in the compensatory response to CM stress. In human failing heart, CM Tln1 also increases compared with control samples from normal functioning myocardium. To directly test Tln1 function in CMs, we generated CM-specific Tln1 knock-out mice (Tln1cKO). Tln1cKO mice showed normal basal cardiac structure and function but when subjected to pressure overload showed blunted hypertrophy, less fibrosis, and improved cardiac function versus controls. Acute responses of ERK1/2, p38, Akt, and glycogen synthase kinase 3 after mechanical stress were strongly blunted in Tln1cKO mice. Given these results, we conclude that Tln1 and Tln2 have distinct functions in the myocardium. Our data show that reduction of CM Tln1 expression can lead to improved cardiac remodeling following pressure overload.

A combined evaluation of the characteristics and acute toxicity of antibiotic wastewater.

The conventional parameters and acute toxicities of antibiotic wastewater collected from each treatment unit of an antibiotic wastewater treatment plant have been investigated. The investigation of the conventional parameters indicated that the antibiotic wastewater treatment plant performed well under the significant fluctuation in influent water quality. The results of acute toxicity indicated that the toxicity of antibiotic wastewater could be reduced by 94.3 percent on average after treatment. However, treated antibiotic effluents were still toxic to Vibrio fischeri. The toxicity of antibiotic production wastewater could be attributed to the joint effects of toxic compound mixtures in wastewater. Moreover, aerobic biological treatment processes, including sequencing batch reactor (SBR) and aerobic biofilm reactor, played the most important role in reducing toxicity by 92.4 percent. Pearson׳s correlation coefficients revealed that toxicity had a strong and positive linear correlation with organic substances, nitrogenous compounds, S(2-), volatile phenol, cyanide, As, Zn, Cd, Ni and Fe. Ammonia nitrogen (NH4(+)) was the greatest contributor to toxicity according to the stepwise regression method. The multiple regression model was a good fit for [TU50-15 min] as a function of [NH4(+)] with the determination coefficient of 0.981.