Blocking OLFM4/galectin-3 axis in placental polymorphonuclear myeloid-derived suppressor cells triggers intestinal inflammation in newborns.

Fetal growth restriction (FGR) is a major cause of premature and low-weight births, which increases the risk of necrotizing enterocolitis (NEC); however, the association remains unclear. We report a close correlation between placental polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) and NEC. Newborns with previous FGR exhibited intestinal inflammation and more severe NEC symptoms than healthy newborns. Placental PMN-MDSCs are vital regulators of fetal development and neonatal gut inflammation. Placental single-cell transcriptomics revealed that PMN-MDSCs populations and olfactomedin-4 gene (Olfm4) expression levels were significantly increased in PMN-MDSCs in later pregnancy compared to those in early pregnancy and non-pregnant females. Female mice lacking Olfm4 in myeloid cells mated with wild-type males showed FGR during pregnancy, with a decreased placental PMN-MDSCs population and expression of growth-promoting factors (GPFs) from placental PMN-MDSCs. Galectin-3 (Gal-3) stimulated the OLFM4-mediated secretion of GPFs by placental PMN-MDSCs. Moreover, GPF regulation via OLFM4 in placental PMN-MDSCs was mediated via hypoxia inducible factor-1α (HIF-1α). Notably, the offspring of mothers lacking Olfm4 exhibited intestinal inflammation and were susceptible to NEC. Additionally, OLFM4 expression decreased in placental PMN-MDSCs from pregnancies with FGR and was negatively correlated with neonatal morbidity. These results revealed that placental PMN-MDSCs contributed to fetal development and ameliorate newborn intestinal inflammation.

Exceptionally high proton conductivity in Eu2O3 by proton-coupled electron transfer mechanism.

Proton conductors are typically developed by doping to introduce structural defects such as oxygen vacancies to facilitate ionic transport through structural bulk conduction mechanism. In this study, we present a novel electrochemical proton injection method via an in situ fuel cell process, demonstrating proton conduction in europium oxide (Eu2O3) through a surficial conduction mechanism for the first time. By tuning Eu2O3 into a protonated form, H-Eu2O3, we achieved an exceptionally high proton conductivity of 0.16 S cm-1. Distribution of relaxation time (DRT) analysis was employed to investigate the proton transport behavior and reveal the significant contribution of surface proton transport to the overall conductivity of Eu2O3. Remarkably, H-Eu2O3 exhibited a low activation energy for ionic transport, comparable to the best ceramic electrolytes available. The proton-coupled electron transfer (PCET) mechanism describes this novel surficial proton conduction mechanism. These findings provide new possibilities for developing advanced proton conductors with improved performance.

DNAJ heat shock protein family member C1 can regulate proliferation and migration in hepatocellular carcinoma.

Background: DNAJ heat shock protein family (Hsp40) member C1(DNAJC1) is a member of the DNAJ family. Some members of the DNAJ gene family had oncogenic properties in many cancers. However, the role of DNAJC1 in hepatocellular carcinoma (HCC) was unclear. Methods: In this study, expression and prognostic value of DNAJC1 in HCC were analyzed by bioinformatics. Quantitative real-time PCR and Western blotting were used to verify DNAJC1 expression in liver cancer cell lines. Furthermore, immunohistochemical (IHC) was used to detect DNAJC1 expression in liver cancer tissues. Subsequently, the effect of DNAJC1 on the proliferation, migration, invasion and apoptosis of HCC cells was detected by knocking down DNAJC1. Finally, gene set enrichment analysis (GSEA) was used to investigate the potential mechanism of DNAJC1 and was verified by Western blotting. Results: DNAJC1 was highly expressed in HCC and was significantly associated with the prognosis of patients with HCC. Importantly, the proliferation, migration and invasion of Huh7 and MHCC97H cells were inhibited by the knockdown of DNAJC1 and the knockdown of DNAJC1 promoted Huh7 and MHCC97H cell apoptosis. Furthermore, compared to the negative control group, DNAJC1 knockdown in Huh7 and MHCC97H cells promoted the expression of p21, p53, p-p53(Ser20), Bax and E-cadherin proteins, while inhibiting the expression of PARP, MMP9, Vimentin, Snai1, Bcl-2 and N-cadherin proteins. Conclusions: DNAJC1 had a predictive value for the prognosis of HCC. Knockdown of DNAJC1 may inhibit HCC cell proliferation, migration and invasion and promote the HCC cell apoptosis through p53 and EMT signaling pathways.

METTL3-dependent m6A methylation facilitates uterine receptivity and female fertility via balancing estrogen and progesterone signaling.

Infertility is a worldwide reproductive health problem and there are still many unknown etiologies of infertility. In recent years, increasing evidence emerged and confirmed that epigenetic regulation played a leading role in reproduction. However, the function of m6A modification in infertility remains unknown. Here we report that METTL3-dependent m6A methylation plays an essential role in female fertility via balancing the estrogen and progesterone signaling. Analysis of GEO datasets reveal a significant downregulation of METTL3 expression in the uterus of infertile women with endometriosis or recurrent implantation failure. Conditional deletion of Mettl3 in female reproductive tract by using a Pgr-Cre driver results in infertility due to compromised uterine endometrium receptivity and decidualization. m6A-seq analysis of the uterus identifies the 3'UTR of several estrogen-responsive genes with METTL3-dependent m6A modification, like Elf3 and Celsr2, whose mRNAs become more stable upon Mettl3 depletion. However, the decreased expression levels of PR and its target genes, including Myc, in the endometrium of Mettl3 cKO mice indicate a deficiency in progesterone responsiveness. In vitro, Myc overexpression could partially compensate for uterine decidualization failure caused by Mettl3 deficiency. Collectively, this study reveals the role of METTL3-dependent m6A modification in female fertility and provides insight into the pathology of infertility and pregnancy management.

Synthetic Biology Pathway to Nucleoside Triphosphates for Expanded Genetic Alphabets.

One horizon in synthetic biology seeks alternative forms of DNA that store, transcribe, and support the evolution of biological information. Here, hydrogen bond donor and acceptor groups are rearranged within a Watson-Crick geometry to get 12 nucleotides that form 6 independently replicating pairs. Such artificially expanded genetic information systems (AEGIS) support Darwinian evolution in vitro. To move AEGIS into living cells, metabolic pathways are next required to make AEGIS triphosphates economically from their nucleosides, eliminating the need to feed these expensive compounds in growth media. We report that "polyphosphate kinases" can be recruited for such pathways, working with natural diphosphate kinases and engineered nucleoside kinases. This pathway in vitro makes AEGIS triphosphates, including third-generation triphosphates having improved ability to survive in living bacterial cells. In α-32P-labeled forms, produced here for the first time, they were used to study DNA polymerases, finding cases where third-generation AEGIS triphosphates perform better with natural enzymes than second-generation AEGIS triphosphates.

mTORC1 signaling pathway integrates estrogen and growth factor to coordinate vaginal epithelial cells proliferation and differentiation.

The mouse vaginal epithelium cyclically exhibits cell proliferation and differentiation in response to estrogen. Estrogen acts as an activator of mTOR signaling but its role in vaginal epithelial homeostasis is unknown. We analyzed reproductive tract-specific Rptor or Rictor conditional knockout mice to reveal the role of mTOR signaling in estrogen-dependent vaginal epithelial cell proliferation and differentiation. Loss of Rptor but not Rictor in the vagina resulted in an aberrant proliferation of epithelial cells and failure of keratinized differentiation. As gene expression analysis indicated, several estrogen-mediated genes, including Pgr and Ereg (EGF-like growth factor) were not induced by estrogen in Rptor cKO mouse vagina. Moreover, supplementation of EREG could activate the proliferation and survival of vaginal epithelial cells through YAP1 in the absence of Rptor. Thus, mTORC1 signaling integrates estrogen and growth factor signaling to mediate vaginal epithelial cell proliferation and differentiation, providing new insights into vaginal atrophy treatment for post-menopausal women.

Effects of a polysaccharide extract from Amomum villosum Lour. on gastric mucosal injury and its potential underlying mechanism.

AVLP-2, a novel acidic polysaccharide, was isolated and purified from Amomum villosum Lour. The structural characteristics of the polysaccharides were characterized using monosaccharide composition, methylation, FT-IR, and NMR techniques. Results showed that AVLP-2 comprises galactose and glucose monomers, has a molecular weight of 10.488 kDa, and has backbone structures →4)-α-d-GalAp-(1→3,4)-α-d-GalAp-(1→, →4)-α-d-GalAp-(1→6)-α-d-Galp-(1→, and n→6)-α-d-Galp-(1→4)-ß-d-Glcp-(1→, with α-d-Galp-(1→ branches. Furthermore, AVLP-2 had a significant protective effect against oxidative stress in alcohol-induced injury and LPS inflammation models GES-1 cells by regulating the levels of ROS and inflammatory factors. In the animal experiments, AVLP-2 improved the oxidative stress status of the gastric mucosa by increasing SOD activity and GSH levels and inhibiting the excessive generation of malondialdehyde in tissues. The levels of MPO, IL-1ß, IL-10, and NF-κB p65 were downregulated, while that of TNF-α was upregulated by AVLP-2 treatment, thereby reducing the alcohol-induced inflammation.

The kinase PDK1 regulates regulatory T cell survival via controlling redox homeostasis.

Rationale: Regulatory T cells (Treg cells) play an important role in maintaining peripheral tolerance by suppressing over-activation of effector T cells. The kinase PDK1 plays a pivotal role in conventional T cell development. However, whether PDK1 signaling affects the homeostasis and function of Treg cells remains elusive. Methods: In order to evaluate the role of PDK1 in Treg cells from a genetic perspective, mice carrying the floxed PDK1 allele were crossbred with Foxp3Cre mice to efficiently deleted PDK1 in Foxp3+ Treg cells. Flow cytometry was used to detect the immune cell homeostasis of WT and PDK1fl/flFoxp3Cre mice. RNA-seq was used to assess the differences in transcriptional expression profile of WT and PDK1-deficient Treg cells. The metabolic profiles of WT and PDK1-deficient Treg cells were tested using the Glycolysis Stress Test and Mito Stress Test Kits by the Seahorse XFe96 Analyser. Results: PDK1 was essential for the establishment and maintenance of Treg cell homeostasis and function. Disruption of PDK1 in Treg cells led to a spontaneous fatal systemic autoimmune disorder and multi-tissue inflammatory damage, accompanied by a reduction in the number and function of Treg cells. The deletion of PDK1 in Treg cells destroyed the iron ion balance through regulating MEK-ERK signaling and CD71 expression, resulting in excessive production of intracellular ROS, which did not depend on the down-regulation of mTORC1 signaling. Inhibition of excessive ROS, activated MEK-Erk signaling or overload Fe2+ could partially rescue the survival of PDK1-deficient Treg cells. Conclusion: Our results defined a key finding on the mechanism by which PDK1 regulates Treg cell survival via controlling redox homeostasis.

Exosome-Depleted Excretory-Secretory Products of the Fourth-Stage Larval Angiostrongylus cantonensis Promotes Alternative Activation of Macrophages Through Metabolic Reprogramming by the PI3K-Akt Pathway.

Angiostrongylus cantonensis (AC), which parasitizes in the brain of the non-permissive host, such as mouse and human, is an etiologic agent of eosinophilic meningitis. Excretory-secretory (ES) products play an important role in the interaction between parasites and hosts' immune responses. Inflammatory macrophages are responsible for eosinophilic meningitis induced by AC, and the soluble antigens of Angiostrongylus cantonensis fourth stage larva (AC L4), a mimic of dead AC L4, aggravate eosinophilic meningitis in AC-infected mice model via promoting alternative activation of macrophages. In this study, we investigated the key molecules in the ES products of AC L4 on macrophages and observed the relationship between metabolic reprogramming and the PI3K-Akt pathway. First, a co-culture system of macrophage and AC L4 was established to define the role of AC L4 ES products on macrophage polarization. Then, AC L4 exosome and exosome-depleted excretory-secretory products (exofree) were separated from AC L4 ES products using differential centrifugation, and their distinct roles on macrophage polarization were confirmed using qPCR and ELISA experiments. Moreover, AC L4 exofree induced alternative activation of macrophages, which is partially associated with metabolic reprogramming by the PI3K-Akt pathway. Next, lectin blot and deglycosylation assay were done, suggesting the key role of N-linked glycoproteins in exofree. Then, glycoproteomic analysis of exofree and RNA-seq analysis of exofree-treated macrophage were performed. Bi-layer PPI network analysis based on these results identified macrophage-related protein Hexa as a key molecule in inducing alternative activation of macrophages. Our results indicate a great value for research of helminth-derived immunoregulatory molecules, which might contribute to drug development for immune-related diseases.

Spontaneous mainstream anammox in a full-scale wastewater treatment plant with hybrid sludge retention time in a temperate zone of China.

Spontaneous anammox bacteria enrichment at mainstream conditions was reported in a full-scale Wastewater Treatment Plant (WWTP) in a temperate zone of China. The mainstream anammox was observed after WWTP process retrofit, which constructed a hybrid sludge retention time (SRT) system by providing moving carriers in the anaerobic/anoxic tank and was initially designed to enhance the denitrification process in a conventional anaerobic/anoxic/oxic process. The hybrid SRT system achieved 86.0 ± 4.6% total nitrogen (TN) removal via combined mainstream anammox and conventional denitrification. Autotrophic denitrification via mainstream anammox was confirmed by various shreds of evidence including high-throughput sequencing, specific anammox activity test, and 15 N isotopic tracing. Long-term anammox bacteria existence in the biofilm of the carrier in anoxic zones was detected in a much higher relative abundance compared with other spots. The contribution of anammox activity to TN removal was estimated at around 20%-30%. The reasons leading to spontaneous anammox enrichment were mainly attributed to the carriers for slow-growing bacteria growth and dissolved oxygen gradient in the anoxic tank (caused by intermittent aeration) for nitrite production. The insights of this full-scale case study provide important perspectives for future mainstream anammox application, and also the design of an energy-neutral WWTP process. PRACTITIONER POINTS: Spontaneous mainstream anammox in a full-scale WWTP after its retrofit in a temperate zone of China was reported. Anammox bacteria enrichment and long-term stability on moving carriers at mainstream conditions was achieved by modified hybrid SRT system. The hybrid SRT system achieve stable nitrogen removal even in cold winter and high BOD/N situation by combining mainstream anammox with conventional denitrification. Long term full-scale operation demonstrated excellent nitrogen removal with about 20%-30% contribution of mainstream anammox. This full-scale case study provided perspectives for future optimizing mainstream anammox application, and also energy-neutral WWTP process design.

Ladder-Type Heteroheptacenes with Different Heterocycles for Nonfullerene Acceptors.

The design, synthesis, and characterization of two novel nonfullerene acceptors (M8 and M34) based on ladder-type heteroheptacenes with different heterocycles are reported. Replacing the furan heterocycles with the thiophene heterocycles in the heteroheptacene backbone leads to a hypsochromically shifted absorption band and greatly improved carrier transport for the resulting nonfullerene acceptor (M34) although the π-π-stacking distances are barely affected. Bulk-heterojunction polymer solar cells fabricated from M34 and a wide band gap polymer (PM6) as the donor showed a best power conversion efficiency (PCE) of 15.24 % with an open circuit voltage (VOC ) of 0.91 V, much higher than a PCE of 4.21 % and a VOC of 0.83 V for the counterparts based on M8:PM6. These results highlight the importance of key atoms in the construction of high-performance nonfullerene acceptors.

The potential risk of Schistosoma mansoni transmission by the invasive freshwater snail Biomphalaria straminea in South China.

Schistosomes infect more than 200 million people worldwide, and globally, over 700 million people are at risk of infection. The snail Biomphalaria straminea, as one of the intermediate hosts of Schistosoma mansoni, consecutively invaded Hong Kong in 1973, raising great concern in China. In this study, a malacological survey was conducted over a period of four years, and investigations were performed on the mechanism of susceptibility of B. straminea to S. mansoni. B. straminea was investigated in China from 2014 to 2018. Out of 185 investigated sites, 61 were positive for stages of black B. straminea (BBS), which shows pigmented spots. Twenty of the 61 sites were positive for red B. straminea (RBS), which is partially albino and red colored. Phylogenetic analyses based on cox1 and 18S rRNA sequences demonstrated that both phenotypes were clustered with Brazilian strains. No S. mansoni infections were detected in field-collected snail. However, in laboratory experiments, 4.17% of RBS were susceptible to a Puerto Rican strain of S. mansoni, while BBS was not susceptible. The highest susceptibility rate (70.83%) was observed in the F2 generation of RBS in lab. The density of RBS has increased from south to north and from west to east in Guangdong since 2014. Five tyrosinase tyrosine metabolism genes were upregulated in BBS. Transcriptome comparisons of RBS and BBS showed that ficolin, C1q, MASP-like, and membrane attack complex (MAC)/perforin models of the complement system were significantly upregulated in BBS. Our study demonstrated that B. straminea is widely distributed in Hong Kong and Guangdong Province, which is expanding northwards very rapidly as a consequence of its adaptation to local environments. Our results suggest that B. straminea from South China is susceptible to S. mansoni, implying the high potential for S. mansoni transmission and increased S. mansoni infection risk in China.

Control over π-π stacking of heteroheptacene-based nonfullerene acceptors for 16% efficiency polymer solar cells.

Nonfullerene acceptors are being investigated for use in polymer solar cells (PSCs), with their advantages of extending the absorption range, reducing the energy loss and therefore enhancing the power conversion efficiency (PCE). However, to further boost the PCE, mobilities of these nonfullerene acceptors should be improved. For nonfullerene acceptors, the π-π stacking distance between cofacially stacked molecules significantly affects their mobility. Here, we demonstrate a strategy to increase the mobility of heteroheptacene-based nonfullerene acceptors by reducing their π-π stacking distances via control over the bulkiness of lateral side chains. Incorporation of 2-butyloctyl substituents into the nonfullerene acceptor (M36) leads to an increased mobility with a reduced π-π stacking distance of 3.45 Å. Consequently, M36 affords an enhanced PCE of 16%, which is the highest among all acceptor-donor-acceptor-type nonfullerene acceptors to date. This strategy of control over the bulkiness of side chains on nonfullerene acceptors should aid the development of more efficient PSCs.

An Aptamer-Nanotrain Assembled from Six-Letter DNA Delivers Doxorubicin Selectively to Liver Cancer Cells.

Expanding the number of nucleotides in DNA increases the information density of functional DNA molecules, creating nanoassemblies that cannot be invaded by natural DNA/RNA in complex biological systems. Here, we show how six-letter GACTZP DNA contributes this property in two parts of a nanoassembly: 1) in an aptamer evolved from a six-letter DNA library to selectively bind liver cancer cells; and 2) in a six-letter self-assembling GACTZP nanotrain that carries the drug doxorubicin. The aptamer-nanotrain assembly, charged with doxorubicin, selectively kills liver cancer cells in culture, as the selectivity of the aptamer binding directs doxorubicin into the aptamer-targeted cells. The assembly does not kill untransformed cells that the aptamer does not bind. This architecture, built with an expanded genetic alphabet, is reminiscent of antibodies conjugated to drugs, which presumably act by this mechanism as well, but with the antibody replaced by an aptamer.

TCF1 and LEF1 Control Treg Competitive Survival and Tfr Development to Prevent Autoimmune Diseases.

CD4+ Foxp3+ T regulatory (Treg) cells are key players in preventing lethal autoimmunity. Tregs undertake differentiation processes and acquire diverse functional properties. However, how Treg's differentiation and functional specification are regulated remains incompletely understood. Here, we report that gradient expression of TCF1 and LEF1 distinguishes Tregs into three distinct subpopulations, particularly highlighting a subset of activated Treg (aTreg) cells. Treg-specific ablation of TCF1 and LEF1 renders the mice susceptible to systemic autoimmunity. TCF1 and LEF1 are dispensable for Treg's suppressive capacity but essential for maintaining a normal aTreg pool and promoting Treg's competitive survival. As a consequence, the development of T follicular regulatory (Tfr) cells, which are a subset of aTreg, is abolished in TCF1/LEF1-conditional knockout mice, leading to unrestrained T follicular helper (Tfh) and germinal center B cell responses. Thus, TCF1 and LEF1 act redundantly to control the maintenance and functional specification of Treg subsets to prevent autoimmunity.

Visible Light-Driven Self-Powered Device Based on a Straddling Nano-Heterojunction and Bio-Application for the Quantitation of Exosomal RNA.

This paper reports the design and fabrication of a self-powered biosensing device based on TiO2 nanosilks (NSs)@MoS2 quantum dots (QDs) and demonstrates a bioapplication for the quantitative detection of exosomal RNA ( Homo sapiens HOXA distal transcript antisense RNA, HOTTIP). This self-powered device features enhanced power output compared to TiO2 NSs alone. This is attributed to the formation of a heterojunction structure with suitable band offset derived from the hybridization between TiO2 NSs and MoS2 QDs, i.e., the straddling (Type I) band alignment. The sensitization effect and excellent visible light absorption provided by MoS2 QDs can prolong interfacial carrier lifetime and improve energy conversion efficiency. This self-powered biosensing device has been successfully applied in quantitative HOTTIP detection through effective hybridization between a capture probe and HOTTIP. The successful capture of HOTTIP leads to a sequential decrease in power output, which is utilized for ultrasensitive quantitative HOTTIP detection, with a linear relationship of power output change versus the logarithm of HOTTIP concentration ranging from 5 fg/mL to 50 000 ng/mL and a detection limit as low as 5 fg/mL. This TiO2 NSs@MoS2 QDs-based nanomaterial has excellent potential for a superior self-powered device characterized by economical and portable self-powered biosensing. Moreover, this self-powered, visible-light-driven device shows promising applications for cancer biomarker quantitative detection.

Facile approach to prepare HSA-templated MnO2 nanosheets as oxidase mimic for colorimetric detection of glutathione.

In this work, a simple, rapid, and highly sensitive colorimetric assay for the determination of glutathione (GSH) was developed. It employs human serum albumin (HSA)-templated MnO2 nanosheets as an artificial oxidase. HSA-templated MnO2 nanosheets can oxidize 3,3',5,5'-tetramethylbenzidine (TMB) to a blue oxTMB product with a significant increase in absorbance at 652 nm in the absence of H2O2. When GSH is introduced, the MnO2 nanosheets are reduced to Mn2+ ions, thereby inhibiting the formation of oxTMB. Based on these findings, a simple colorimetric assay was developed for the detection GSH in the range of 10 nM to 5 µM with a low detection limit of 5.6 nM. Importantly, the proposed method was successfully used for quantitative determination of GSH in biological fluids, such as human serum samples.

Matching Users' Preference under Target Revenue Constraints in Data Recommendation Systems.

This paper focuses on the problem of finding a particular data recommendation strategy based on the user preference and a system expected revenue. To this end, we formulate this problem as an optimization by designing the recommendation mechanism as close to the user behavior as possible with a certain revenue constraint. In fact, the optimal recommendation distribution is the one that is the closest to the utility distribution in the sense of relative entropy and satisfies expected revenue. We show that the optimal recommendation distribution follows the same form as the message importance measure (MIM) if the target revenue is reasonable, i.e., neither too small nor too large. Therefore, the optimal recommendation distribution can be regarded as the normalized MIM, where the parameter, called importance coefficient, presents the concern of the system and switches the attention of the system over data sets with different occurring probability. By adjusting the importance coefficient, our MIM based framework of data recommendation can then be applied to systems with various system requirements and data distributions. Therefore, the obtained results illustrate the physical meaning of MIM from the data recommendation perspective and validate the rationality of MIM in one aspect.

ZrMOF nanoparticles as quenchers to conjugate DNA aptamers for target-induced bioimaging and photodynamic therapy.

Porphyrinic metal-organic framework (MOF) nanoparticles for photodynamic therapy solve the photosensitizer problems of poor solubility, self-quenching and aggregation. However, their low selectivity towards malignant tissues is an obstacle for bioimaging and a bottle-neck to cellular uptake for highly efficient photodynamic therapy of cancer. Here, ZrMOF nanoparticles as quenchers to conjugate DNA aptamers were developed for target-induced bioimaging and photodynamic therapy. A phosphate-terminal aptamer prepared by solid-phase DNA synthesis was anchored on the surface of ZrMOF nanoparticles through strong coordination between phosphate and zirconium. Based on π-π stacking-induced quenching of TAMRA by ZrMOF nanoparticles, target-induced imaging is achieved due to the structural change of the aptamer upon binding with the target. Aptamer-conjugated ZrMOF nanoparticles with target binding ability significantly enhanced the photodynamic therapy effect. Furthermore, phosphate-terminal aptamer conjugation method can be generalized to other types of MOF nanomaterials, such as UiO-66 and HfMOF nanoparticles, which can be potentially used in biochemistry.

Corrigendum to "Inhibiting Interleukin 17 Can Ameliorate the Demyelination Caused by A. cantonensis via iNOS Inhibition".

[This corrects the article DOI: 10.1155/2017/3513651.].