Multiple Strategies to Fabricate a Highly Stable 2D CuIICuI-Organic Framework with High Proton Conductivity.

Using multifunctional organic ligands with multiple acidic groups (carboxylate and sulfonate groups) to synthesize metal-organic frameworks (MOFs) bearing effective H-bond networks is a promising strategy to obtain highly proton conductive materials. In this work, a highly stable two-dimensional MOF, [CuII5CuI2(µ3-OH)4(H2O)6(L)2(H2L)2]·3H2O (denoted as YCu161; H3L = 6-sulfonaphthalene-1,4-dicarboxylic acid) containing mixed-valence [CuII5CuI2(µ3-OH)4]8+ subunits, was successfully prepared. It exhibited excellent stability and temperature- and humidity-dependent proton conduction properties. Its optimal proton conductivity reached 1.84 × 10-3 S cm-1 at 90 °C and 98% relative humidity. On the basis of a crystal structure analysis, water vapor adsorption test results, and activation energy calculations, we deduced the proton conduction pathway and mechanism. Apparently, uncoordinated sulfonic and carboxyl groups and a network of abundant H-bonds inside the framework were responsible for the efficient proton transfer. Therefore, the strategy of selecting suitable bifunctional ligands to construct two-dimensional Cu-cluster-based MOFs with excellent proton conductivity is feasible.

Notch1 protects against myocardial ischaemia-reperfusion injury via regulating mitochondrial fusion and function.

Mitochondrial fusion and fission dynamic are critical to the myocardial protection against ischaemia-reperfusion injury. Notch1 signalling plays an important role in heart development, maturation and repair. However, the role of Notch1 in the myocardial mitochondrial fusion and fission dynamic remains elusive. Here, we isolated myocardial cells from rats and established myocardial ischaemia-reperfusion injury (IRI) model. We modulated Notch1, MFN1 and DRP1 expression levels in myocardial cells via infection with recombinant adenoviruses. The results showed that Notch1 improves the cell viability and mitochondrial fusion in myocardiocytes exposed to IRI. These improvements were dependent on the regulation of MFN1 and DRP1. On the mechanism, we found that MNF1 is transcriptionally activated by RBP-Jk in myocardiocytes. Notch1 also improves the mitochondrial membrane potential in myocardiocytes exposed to IRI. Moreover, we further confirmed the protection of the Notch1-MFN1/Drp1 axis on the post-ischaemic recovery of myocardial performance is associated with the preservation of the mitochondrial structure. In conclusion, this study presented a detailed mechanism by which Notch1 signalling improves mitochondrial fusion during myocardial protection.

Inhibition of the Notch1 pathway induces peripartum cardiomyopathy.

Increased expression and activity of cardiac and circulating cathepsin D and soluble fms-like tyrosine kinase-1 (sFlt-1) have been demonstrated to induce and promote peripartum cardiomyopathy (PPCM) via promoting cleavage of 23-kD prolactin (PRL) to 16-kD PRL and neutralizing vascular endothelial growth factor (VEGF), respectively. We hypothesized that activation of Hes1 is proposed to suppress cathepsin D via activating Stat3, leading to alleviated development of PPCM. In the present study, we aimed to investigate the role of Notch1/Hes1 pathway in PPCM. Pregnant mice between prenatal 3 days and postpartum 3 weeks were fed with LY-411575 (a notch inhibitor, 10 mg/kg/d). Ventricular function and pathology were evaluated by echocardiography and histological analysis. Western blotting analysis was used to examine the expression at the protein level. The results found that inhibition of Notch1 significantly promoted postpartum ventricular dilatation, myocardial hypertrophy and myocardial interstitial fibrosis and suppressed myocardial angiogenesis. Western blotting analysis showed that inhibition of Notch1 markedly increased cathepsin D and sFlt-1, reduced Hes1, phosphorylated Stat3 (p-Stat3), VEGFA and PDGFB, and promoted cleavage of 23k-D PRL to 16-kD PRL. Collectively, inhibition of Notch1/Hes1 pathway induced and promoted PPCM via increasing the expressions of cathepsin D and sFlt-1. Notch1/Hes1 was a promising target for prevention and therapeutic regimen of PPCM.

Notch1-Nrf2 signaling crosstalk provides myocardial protection by reducing ROS formation.

Both the Notch1 and Keap1-Nrf2 signaling pathways have cardioprotective effects, but the role of Notch1-Nrf2 crosstalk in myocardial ischemia-reperfusion injury is unclear. In this study, we established hypoxia-reoxygenation in neonate rat myocardial cells and employed γ-secretase inhibitor and curcumin to inhibit and activate the Notch1 and Keap1-Nrf2 signaling pathways, respectively. We found that the combined action of the Notch1 and Keap1-Nrf2 signaling pathways significantly increased cardiomyocyte viability, inhibited cardiomyocyte apoptosis, reduced the formation of reactive oxygen species, and increased antioxidant activities. In conclusion, these findings suggest that Notch1-Nrf2 crosstalk exerts myocardial protection by reducing the formation of reactive oxygen species.

NSD2 promotes ventricular remodelling mediated by the regulation of H3K36me2.

Histone lysine methylation plays an important role in the regulation of ventricular remodelling. NSD2 is involved in many types of tumours through enhancing H3K36me2 expression. However, the role of NSD2 in the regulation of histone lysine methylation during ventricular remodelling remains unclear. In this study, we established cardiac hypertrophy model in C57BL/6 mice by transverse aortic constriction and found that histone lysine methylation participated in ventricular remodelling regulation via the up-regulation of H3K27me2 and H3K36me2 expression. In addition, we constructed transgenic C57BL/6 mice with conditional knockout of NSD2 (NSD2-/- ) in the myocardium. NSD2-/- C57BL/6 mice had milder ventricular remodelling and significantly improved cardiac function compared with wild-type mice, and the expression of H3K36me2 but not H3K27me2 was down-regulated. In conclusion, NSD2 promotes ventricular remodelling mediated by the regulation of H3K36me2.

Notch1 provides myocardial protection by improving mitochondrial quality control.

Mitochondrial quality control is a new target for myocardial protection. Notch signaling plays an important role in heart development, maturation, and repair. However, the role of Notch in the myocardial mitochondrial quality control remains elusive. In this study, we isolated myocardial cells from rats and established myocardial ischemia reperfusion injury (IRI) model. We modulated Notch1 expression level in myocardial cells via infection with recombinant adenoviruses Ad-N1ICD and Ad-shN1ICD. We found that IR reduced myocardial cells viability, but Notch1 overexpression increased the viability of myocardial cells exposed to IRI. In addition, Notch1 overexpression improved ATP production, increased mitochondrial fusion and decreased mitochondrial fission, and inhibited mitophagy in myocardial cells exposed to IRI. However, N1ICD knockdown led to opposite effects. The myocardial protection role of Notch1 was related to the inhibition of Pink1 expression and Mfn2 and Parkin phosphorylation. In conclusion, Notch1 exerts myocardial protection and this is correlated with the maintenance of mitochondrial quality control and the inhibition of Pink1/Mfn2/Parkin signaling.

Notch signaling inhibits cardiac fibroblast to myofibroblast transformation by antagonizing TGF-ß1/Smad3 signaling.

PURPOSE: During myocardial infarction (MI), cardiac fibroblasts (CFs) transform into myofibroblast (CMT). This study aimed to investigate the crosstalk of Notch1 and transforming growth factor-ß1 (TGF-ß1)/Smad3 signaling in the regulation of CMT and myocardial fibrosis. METHODS: Primary CFs were isolated from young rats and treated with TGF-ß1 or adenovirus to overexpress or knockdown Notch1 intracellular domain (N1ICD) or Smad3. RESULTS: TGF-ß1 decreased the expression of fibroblast markers but increased the expression of myofibroblast markers in rat CFs. TGF-ß1 increased the proliferation, invasion, and adhesion, and the secretion of collagen I of CFs, and these effects were inhibited by N1ICD overexpression. Moreover, endogenous Smad3 phosphorylation in CFs was enhanced by N1ICD knockdown, whereas TGF-ß1 induced Smad3 phosphorylation was antagonized by the N1ICD overexpression. Conversely, endogenous N1ICD activation in CFs was antagonized by Smad3, whereas TGF-ß1 induced N1ICD inactivation was antagonized by Smad3 knockdown. Coimmunoprecipitation showed that N1ICD interacted with Smad3 and immunostaining revealed the colocalization of N1ICD and Smad3 in the nuclei of CFs. Moreover, we demonstrated the functional antagonism of N1ICD and Smad3 on the phenotypes of CFs. Finally, TGF-ß1/Smad3 signaling promoted whereas Notch signaling inhibited myocardial fibrosis in rat MI model. CONCLUSION: Notch signaling inhibits CMT by antagonizing TGF-ß1/Smad3 signaling. Notch signaling activators and TGF-ß1/Smad3 signaling inhibitors could be exploited for therapeutic intervention to inhibit myocardial fibrosis after MI.

NSD2 silencing alleviates pulmonary arterial hypertension by inhibiting trehalose metabolism and autophagy.

Nuclear receptor binding SET domain 2 (NSD2)-mediated metabolic reprogramming has been demonstrated to regulate oncogenesis via catalyzing the methylation of histones. The present study aimed to investigate the role of NSD2-mediated metabolic abnormality in pulmonary arterial hypertension (PAH). Monocrotaline (MCT)-induced PAH rat model was established and infected with adeno-associated virus carrying short hairpin RNA (shRNA) targeting NSD2. Hemodynamic parameters, ventricular function, and pathology were evaluated by microcatheter, echocardiography, and histological analysis. Metabolomics changes in lung tissue were analyzed by LC-MS. The results showed that silencing of NSD2 effectively ameliorated MCT-induced PAH and right ventricle dysfunction, and partially reversed pathological remodeling of pulmonary artery and right ventricular hypertrophy. In addition, the silencing of NSD2 markedly reduced the di-methylation level of H3K36 (H3K36me2 level) and inhibited autophagy in pulmonary artery. Non-targeted LC-MS based metabolomics analysis indicated that trehalose showed the most significant change in lung tissue. NSD2-regulated trehalose mainly affected ABC transporters, mineral absorption, protein digestion and absorption, metabolic pathways, and aminoacyl-tRNA biosynthesis. In conclusion, we reveal a new role of NSD2 in the pathogenesis of PAH related to the regulation of trehalose metabolism and autophagy via increasing the H3K36me2 level. NSD2 is a promising target for PAH therapy.

Two-Dimensional Excitonic Metal-Organic Framework: Design, Synthesis, Regulation, and Properties.

A family of two-dimensional (2D) Zn-based metal-organic frameworks (MOFs) with exitonic emission have been successfully synthesized under hydrothermal conditions. When isophthalic acid ligands with different substitutions are introduced, the crystal structures and fluorescence properties are significantly changed. Hirshfeld surface calculation is used to study the nuances of diverse substitutions during the construction of all of the crystals. The solid fluorescence results indicate that there are obvious two-channel emissions, including intralayer excimers and interlayer trapped excitons, both in 1 and 2 with a double-layer structure and in 3 with a single-layer structure, mainly exhibiting intralayer emission. Furthermore, the fluorescence changes on morphology transformations are explored after mechanical exfoliation consisting of grinding and ultrasonicaation of MOFs 1-3. The regulation and control of crystal structure and morphology can suppress emission based on interlayer excitons, achieving adjustment of the overall emitting color. To the best of our knowledge, this is the first report of 2D bilayer MOFs with dual-channel emissions, which provides a new structural model for synthesizing new exciton materials.

miR-21 promotes cardiac fibroblast-to-myofibroblast transformation and myocardial fibrosis by targeting Jagged1.

Myocardial fibrosis after myocardial infarction (MI) is a leading cause of heart diseases. MI activates cardiac fibroblasts (CFs) and promotes CF to myofibroblast transformation (CMT). This study aimed to investigate the role of miR-21 in the regulation of CMT and myocardial fibrosis. Primary rat CFs were isolated from young SD rats and treated with TGF-ß1, miR-21 sponge or Jagged1 siRNA. Cell proliferation, invasion and adhesion were detected. MI model was established in male SD rats using LAD ligation method and infected with recombinant adenovirus. The heart function and morphology was evaluated by ultrasonic and histological analysis. We found that TGF-ß1 induced the up-regulation of miR-21 and down-regulation of Jagged1 in rat CFs. Luciferase assay showed that miR-21 targeted 3'-UTR of Jagged1 in rat CFs. miR-21 sponge inhibited the transformation of rat CFs into myofibroblasts, and abolished the inhibition of Jagged1 mRNA and protein expression by TGF-ß1. Furthermore, these effects of miR-21 sponge on rat CFS were reversed by siRNA mediated knockdown of Jagged1. In vivo, heart dysfunction and myocardial fibrosis in MI model rats were partly improved by miR-21 sponge but were aggravated by Jagged1 knockdown. Taken together, these results suggest that miR-21 promotes cardiac fibroblast-to-myofibroblast transformation and myocardial fibrosis by targeting Jagged1. miR-21 and Jagged1 are potential therapeutic targets for myocardial fibrosis.

Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction.

Currently, the role of Notch signaling during myocardial infarction (MI) remains controversy. In this study we used in vitro and in vivo approaches to investigate the role of Notch signaling in MI. Using cultured human umbilical vein endothelial cells exposed to hypoxia/reoxygenation (H/R), we demonstrated that H/R inhibited the proliferation, VEGF secretion, and tube formation of HUVECs, and these effects were correlated with the inhibition of Notch signaling. Furthermore, these effects were antagonized by overexpression of NICD but aggravated by knockdown of NICD. In addition, in MI model rats we found that heart dysfunction and angiogenesis in model rats was partly improved by NICD overexpression but was aggravated by knockdown of NICD. In conclusion, these data demonstrate that Notch signaling is downregulated in H/R injury in the hearts. Artificial activation of Notch signaling could promote myocardial survival and angiogenesis and improve cardiac function following H/R injury.

Selective Adsorption of Dyes and Fe3+ Sensing via Tb3+ Incorporation in an Anionic Cadmium-Organic Framework.

A three-dimensional (3D) anionic cadmium-organic framework, namely [(CH3)2NH2][Cd1.5(DMTDC)2] ⋅ 2DMA ⋅ 0.5H2O (Cd-MOF; DMA=N,N-dimethylacetamide), was successfully synthesized under solvothermal conditions by using a linear thienothiophene-containing dicarboxylate ligand, 3,4-dimethylthieno [2,3-b]-thiophene-2,5-dicar-boxylic acid (H2DMTDC). Single-crystal X-ray diffraction analysis reveals that Cd-MOF exhibits a 3D anionic framework with pcu α-Po topology, featuring rectangle and rhombus-shaped channels along b- and c- axis direction. Cd-MOF demonstrates selective adsorption of cationic dyes over anionic and neutral dyes. Additionally, Tb3+-loaded Cd-MOF serves as a fast-response fluorescence sensor for the sensitive detection of Fe3+ ions with a low limit of detection (8.90×10-7 M) through fluorescence quenching.

[Cataract surgery rate and its impacting factors in Jiangsu Province in 2012].

OBJECTIVE: To survey the cataract surgery rate (CSR) according to the report data and its influencing factors of Jiangsu Province in 2012 so as to further improve CSR in China. METHODS: Through government websites in 2012, gross domestic product (GDP) and GDP per capital of 13 cities in Jiangsu Province and 7 counties of Nantong City reported to the Ministry of Health in China were collected to calculate CSR. The relationship between GDP and CSR of Jiangsu Province and Nantong City were analyzed with Spearman's rank correlation, and the differences in the proportion of cataract surgery between government and private hospitals were analyzed by Chi-square test. RESULTS: CSR in Jiangsu Province in 2012 was 939 cases per million population per year. Nantong City had the highest CSR (1362 cases per million population per year) and Suqian City the lowest (129 cases per million population per year). The GDP of 13 cities in Jiangsu Province had a positive correlation with CSR (spearman r = 0.59, P = 0.03), but there was no significant correlation with GDP per capital (spearman r = 0.50, P = 0.08). No significant correlation existed between GDP, GDP per capital and CSR of 7 counties of Nantong City (spearman r = -0.04, P = 0.94; spearman r = -0.29, P = 0.53). The proportion of private hospitals of Nantong was 33.3% and surgery cases were 4557 (45.9%). The CSR of Rugao County in 2012 was 3317 cases per million population per year. CONCLUSION: Socioeconomic level may be related with CSR. Providing village cataract screening services and lowering surgical costs help to boost CSR in China.

[Prevalence and surgical status of cataract among adults aged 50 years or above in rural Jiangsu Province].

OBJECTIVE: To survey the prevalence, operative status, surgical coverage rate and social burden rate of cataract blindness among older adults aged 50 years or above in 2 typical counties (district) of Jiangsu Province, China in 2010. METHODS: Cluster sampling was used in randomly selected 12 867 individuals aged 50 years or above in 58 clusters in Funing County of Northern Jiangsu and Binhu District of Southern Jiangsu. Among them, 12 053 individuals received visual acuity and eye examinations (response rate 93.8%). Lens and cataract operative status were evaluated by slit-lamp biomicroscope. Data bank was established by Epidata3.0 Software. Statistical analyses were performed with Stata/SE Statistical Software, version 10.0. Confidence intervals and P values (significant at P < 0.05) for prevalence of cataract, surgical coverage rate of cataract, social burden rate and surgical outcomes of cataract blindness were calculated with adjustment for clustering effects and stratification associated with the sampling design. RESULTS: Among 12 503 individuals, there were 2208 cases of cataract with a prevalence of 18.3%. The prevalence of cataract was higher in the aged, female and lower-income persons (P < 0.05). Among 2208 cataract patients, cataract surgery was performed in 263 cases (11.9%). The surgical coverage rate of cataract was 59.7% and the social burden rate of cataract blindness 1.93%. The social burden rate of cataract blindness was higher in the aged persons (P < 0.01). In 357 eyes with cataract surgery, the rate of intraocular lens implantation was 85.7%. At Binhu, 71.0% of eyes with cataract surgery underwent phacoemulsification. At Funing, 73.6% of eyes underwent modern extra-capsular surgery respectively. Post-operative presenting and best corrected visual acuity over 0.7 was 11.2% and 19.6% of operated eyes respectively. The main causes of post-operative eyes with worse visual acuity (< 0.3) were post-capsular opacity and retinal disorders. CONCLUSION: Cataract is the most common and important eye disease that may lead into blindness and severe visual impairment among older adults aged 50 years or above. The coverage rate of cataract surgery is higher in Jiangsu province than in other provinces. The visual outcomes of surgery is less than ideal. An important task in blindness prevention of Jiangsu province still is the elimination of cataract blindness and the improvement of visual outcomes for cataract surgery in the future.

[Research on common laws during membrane enrichment of six herbal volatile oils--physicochemical property and fingerprint similarity].

Membrane enrichment process of Chinese medicine volatile oil is green, practical and has a good application prospects. Schizonepetae Herba et al. six chinese medicine oily water were filtrated with polyvinylidene fluoride (PVDF) membrane with MWCO 70 000, at 40 degrees C, 0.1 MPa and 150 r x min(-1), common laws of physicochemical property of six oily water and fingerprint similarity between original and preserved oil were studied during membrane enrichment. Results were as follows: pH was gradually reduced to the minimum; conductivity firstly became larger, then smaller until 0; viscosity gradually increased to a maximum; surface tension gradually decreased to a minimum; turbidity firstly gradually increased, then reduced to a minimum; density gradually decreased to a minimum, but the change trend was opposite for Acori Tatarinowii Rhizoma with heavy oil; salinity was 0. In the end, pH reached a maximum and density reached a maximum (contrary for Acori Tatarinowii Rhizoma) and the other physicochemical property values reached a minimum for the last permeate. Fingerprint similarity between original and enriched volatile oil was above 90%. The above results provided data support and theoretical basis for the industrialization of membrane enrichment volatile oil technology.

NSD2 promotes pressure overload-induced cardiac hypertrophy via activating circCmiss1/TfR1/ferroptosis signaling.

Heart failure typically occurs early in the clinical course of sustained cardiac hypertrophy that is accompanied by maladaptive remodeling of the heart. It is critical to discover new mechanisms and effective therapeutic targets to prevent and cure pathological cardiac hypertrophy. The objective of the study was to evaluate the effects of circRNAs on NSD2-induced ventricular remodeling. We screened the dysregulated circRNAs in normal or NSD2-/- C57BL/6 mice with or without transverse aortic constriction (TAC), and found that circCmss1 significantly increased in normal TAC mice, but decreased in NSD2-/- TAC mice. Angiotensin II(Ang II)induced neonatal cardiomyocyte hypertrophy in vitro and the pressure overload-induced cardiac hypertrophy in vivo can be reduced by Knocking down circCmss1. We further investigated the downstream signaling of circCmss1 in the progression of NSD2-promoted ventricular remodeling and discovered that circCmss1 could interact with a transcription factor EIF4A3 and induce the expression of transferrin receptor 1 (TfR1), thus activating the ferroptosis in cardiomyocytes. This study highlights the significance of NSD2 activation of circCmss1/EIF4A3/TfR1 as therapeutic targets for treating pathological myocardial hypertrophy.

The origins and dynamic changes of C3- and S100A10-positive reactive astrocytes after spinal cord injury.

Accaumulating studies focus on the effects of C3-positive A1-like phenotypes and S100A10-positive A2-like phenotypes of reactive astrocytes on spinal cord injury (SCI), however the origins and dynamic changes of C3- and S100A10-positive reactive astrocytes after SCI remain poorly understood. Through transgenic mice and lineage tracing, we aimed to determine the origins of C3- and S100A10-positive reactive astrocytes. Meanwhile, the distribution and dynamic changes in C3- and S100A10-positive reactive astrocytes were also detected in juvenile and adult SCI mice models and cultured astrocytes. Combing with bulk RNA sequencing (RNA-seq), single-cell RNA sequencing (scRNA-seq) and bioinformatic analysis, we further explored the dynamic transcripts changes of C3- and S100A10-positive reactive astrocytes after SCI. We confirmed that resident astrocytes produced both C3- and S100A10-positive reactive astrocytes, whereas ependymal cells regenerated only S100A10-positive reactive astrocytes in lesion area. Importantly, C3-positive reactive astrocytes were predominantly activated in adult SCI mice, while S100A10-positive reactive astrocytes were hyperactivated in juvenile mice. Furthermore, we observed that C3- and S100A10-positive reactive astrocytes had a dynamic transformation process at different time in vitro and vivo, and a majority of intermediate states of C3- and S100A10-positive reactive astrocytes were found during transformation. RNA-seq and scRNA-seq results further confirmed that the transcripts of C3-positive reactive astrocytes and their lipid toxicity were gradually increased with time and age. In contrast, S100A10-positive reactive astrocytes transcripts increased at early time and then gradually decreased after SCI. Our results provide insight into the origins and dynamic changes of C3- and S100A10-positive reactive astrocytes after SCI, which would be valuable resources to further target C3- and S100A10-positive reactive astrocytes after SCI.

Corrigendum: Non-alcoholic fatty liver disease is associated with aortic calcification: a cohort study with propensity score matching.

[This corrects the article DOI: 10.3389/fendo.2022.880683.].

Highly efficient and selective capture Pb(II) through a novel metal-organic framework containing bifunctional groups.

The design and development of materials with a selective adsorption capacity for Pb(II) are very important for environmental governance and ecological safety. In this work, a novel 3D metal-organic framework ([Cd2H4L4Cl2SO4]·4H2O, Cd-MOF) is constructed using a multiple pyrazole heterocycles tetraphenylethylene-based ligand (H4L4) and CdSO4 which containing Pb(II) adsorption sites (SO42-). Studies have shown that the Cd-MOF has outstanding stability, and its maximum adsorption value of Pb(II) can be as high as 845.55 mg/g, which is higher than that of most MOFs or MOFs modified materials. It is worth emphasizing that the Cd-MOF have excellent recyclability due to the unique adsorption mechanism of the Cd-MOF. Thermodynamic studies have shown that Pb(II) adsorption of the Cd-MOF is a spontaneous endothermic process. Specific selective adsorption, exceptional stability and remarkable recyclability make the Cd-MOF a potential material for industrial capture and recovery of Pb(II) from water.

The relationship between cognitive impairment and superoxide dismutase activity in untreated first-episode patients with schizophrenia.

Objectives: Cognitive decline is an essential characteristic of schizophrenia and may be due to the disturbance between reactive oxygen species generation and antioxidant capacity. The study aimed to explore the association between cognitive deficits and antioxidant defence parameters in untreated first-episode patients with schizophrenia.Methods: We determined important antioxidant enzymes, total superoxide dismutase (SOD) and manganese SOD (MnSOD), and their relationship with cognitive impairment in 168 untreated patients with first-episode schizophrenia and 168 age- and sex-matched healthy controls. The evaluation of psychopathological symptoms of all patients was based on the Positive and Negative Syndrome Scale (PANSS). We measured cognitive function by the Repeated Battery for the Assessment of Neuropsychological Status (RBANS) and activities of total SOD and MnSOD in all participants.Results: The results showed that untreated patients with first-episode schizophrenia had deficient cognitive functioning in four RBANS indices and total scores, except for the visuospatial/constructional index, as well as higher plasma total SOD activity compared with the control subjects. In addition, significant negative correlations were identified between MnSOD activity and attention index or RBANS total score in patients.Conclusions: Our results suggest that oxidative stress may be partly responsible for cognitive dysfunction in the early course of schizophrenia.