bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protective Actions of Aspirin-Triggered (17R) Resolvin D1 and Its Analogue, 17R-Hydroxy-19-Para-Fluorophenoxy-Resolvin D1 Methyl Ester, in C5a-Dependent IgG Immune Complex–Induced Inflammation and Lung Injury
Authors: Tang Huifang , Liu Yanlan , Yan Chunguang , Petasis Nicos A. , Serhan Charles N. , Gao Hongwei 
Published: August 2014

Abstract
Increasing evidence suggests that the novel anti-inflammatory and proresolving mediators such as the resolvins play an important role during inflammation. However, the functions of these lipid mediators in immune complex–induced lung injury remain unknown. In this study, we determined the role of aspirin-triggered resolvin D1 (AT-RvD1) and its metabolically stable analog, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester (p-RvD1), in IgG immune complex–induced inflammatory responses in myeloid cells and injury in the lung. We show that lung vascular permeability in the AT-RvD1– or p-RvD1–treated mice was significantly reduced when compared with values in mice receiving control vesicle during the injury. Furthermore, i.v. administration of either AT-RvD1 or p-RvD1 caused significant decreases in the bronchoalveolar lavage fluid contents of neutrophils, inflammatory cytokines, and chemokines. Of interest, AT-RvD1 or p-RvD1 significantly reduced bronchoalveolar lavage fluid complement C5a level. By EMSA, we demonstrate that IgG immune complex–induced activation of NF-κB and C/EBPβ transcription factors in the lung was significantly inhibited by AT-RvD1 and p-RvD1. Moreover, AT-RvD1 dramatically mitigates IgG immune complex–induced NF-κB and C/EBP activity in alveolar macrophages. Also, secretion of TNF-α, IL-6, keratinocyte cell–derived chemokine, and MIP-1α from IgG immune complex–stimulated alveolar macrophages or neutrophils was significantly decreased by AT-RvD1. These results suggest a new approach to the blocking of immune complex–induced inflammation.
Adenosine Deaminase Acting on RNA 1 Limits RIG-I RNA Detection and Suppresses IFN Production Responding to Viral and Endogenous RNAs
Authors: Yang Shengyong , Deng Peng , Zhu Zhaowei , Zhu Jianzhong , Wang Guoliang , Zhang Liyong , Chen Alex F. , Wang Tony , Sarkar Saumendra N. , Billiar Timothy R. , Wang Qingde 
Published: August 2014

Abstract
Type I IFNs play central roles in innate immunity; however, overproduction of IFN can lead to immunopathology. In this study, we demonstrate that adenosine deaminase acting on RNA 1 (ADAR1), an RNA-editing enzyme induced by IFN, is essential for cells to avoid inappropriate sensing of cytosolic RNA in an inducible knockout cell model—the primary mouse embryo fibroblast derived from ADAR1 lox/lox and Cre-ER mice as well as in HEK293 cells. ADAR1 suppresses viral and cellular RNA detection by retinoic acid–inducible gene I (RIG-I) through its RNA binding rather than its RNA editing activity. dsRNA binds to both ADAR1 and RIG-I, but ADAR1 reduces RIG-I RNA binding. In the absence of ADAR1, cellular RNA stimulates type I IFN production without viral infection or exogenous RNA stimulation. Moreover, we showed in the ADAR1-inducible knockout mice that ADAR1 gene disruption results in high-level IFN production in neuronal tissues—the hallmark of Aicardi–Goutières syndrome, a heritable autoimmune disease recently found to be associated with ADAR1 gene mutations. In summary, this study found that ADAR1 limits cytosolic RNA sensing by RIG-I through its RNA binding activity; therefore, ADAR1 suppresses type I IFN production stimulated by viral and cellular RNAs. These results explain why loss of ADARA1 causes IFN induction and also indicates a mechanism for the involvement of ADAR1 in autoimmune diseases such as Aicardi–Goutières syndrome.
CXCL1 Contributes to Host Defense in Polymicrobial Sepsis via Modulating T Cell and Neutrophil Functions
Authors: Jin Liliang , Batra Sanjay , Douda David Nobuhiro , Palaniyar Nades , Jeyaseelan Samithamby 
Published: August 2014

Abstract
Severe bacterial sepsis leads to a proinflammatory condition that can manifest as septic shock, multiple organ failure, and death. Neutrophils are critical for the rapid elimination of bacteria; however, the role of neutrophil chemoattractant CXCL1 in bacterial clearance during sepsis remains elusive. To test the hypothesis that CXCL1 is critical to host defense during sepsis, we used CXCL1-deficient mice and bone marrow chimeras to demonstrate the importance of this molecule in sepsis. We demonstrate that CXCL1 plays a pivotal role in mediating host defense to polymicrobial sepsis after cecal ligation and puncture in gene-deficient mice. CXCL1 appears to be essential for restricting bacterial outgrowth and death in mice. CXCL1 derived from both hematopoietic and resident cells contributed to bacterial clearance. Moreover, CXCL1 is essential for neutrophil migration, expression of proinflammatory mediators, activation of NF-κB and MAPKs, and upregulation of adhesion molecule ICAM-1. rIL-17 rescued impaired host defenses in cxcl1−/− mice. CXCL1 is important for IL-17A production via Th17 differentiation. CXCL1 is essential for NADPH oxidase–mediated reactive oxygen species production and neutrophil extracellular trap formation. This study reveals a novel role for CXCL1 in neutrophil recruitment via modulating T cell function and neutrophil-related bactericidal functions. These studies suggest that modulation of CXCL1 levels in tissues and blood could reduce bacterial burden in sepsis.
T Cell–Derived IL-4/IL-13 Protects Mice against Fatal Schistosoma mansoni Infection Independently of Basophils
Authors: Schwartz Christian , Oeser Katharina , Prazeres da Costa Clarissa , Layland Laura E. , Voehringer David 
Published: August 2014

Abstract
Schistosomiasis is a severe and chronic disease caused by the parasitic trematode Schistosoma mansoni after deposition of eggs in the liver and intestines. The immune response to S. mansoni eggs is characterized by increased Th2 cells, eosinophilia, and high serum IgE levels. Granulomas are formed around the eggs to protect the organs against tissue damage caused by toxic products that are secreted from the eggs. Egg-derived components have further been shown to activate the IgE-mediated release of IL-4 and IL-13 from basophils, suggesting that basophils could be involved in protection against a fatal course of infection. Using T cell–specific IL-4/IL-13–deficient mice and basophil-deficient Mcpt8Cre mice, we determined the contribution of Th2 cells and basophils for protective immunity against S. mansoni egg–induced pathology during the patent stage of infection. Our results demonstrate that T cell–derived IL-4/IL-13 was essential for granuloma formation, IgE production, basophilia, differentiation of alternatively activated macrophages, and protection against fatal infection. Although basophils were recruited into liver granulomas, they appeared to be dispensable as a source of IL-4/IL-13 both for differentiation of Th2 cells and for prevention of weight loss and mortality.
TLR-Mediated Inflammatory Responses to Streptococcus pneumoniae Are Highly Dependent on Surface Expression of Bacterial Lipoproteins
Authors: Tomlinson Gillian , Chimalapati Suneeta , Pollard Tracey , Lapp Thabo , Cohen Jonathan , Camberlein Emilie , Stafford Sian , Periselneris Jimstan , Aldridge Christine , Vollmer Waldemar , Picard Capucine , Casanova Jean-Laurent , Noursadeghi Mahdad , Brown Jeremy 
Published: August 2014

Abstract
Streptococcus pneumoniae infections induce inflammatory responses that contribute toward both disease pathogenesis and immunity, but the host–pathogen interactions that mediate these effects are poorly defined. We used the surface lipoprotein-deficient ∆lgt pneumococcal mutant strain to test the hypothesis that lipoproteins are key determinants of TLR-mediated immune responses to S. pneumoniae. We show using reporter assays that TLR2 signaling is dependent on pneumococcal lipoproteins, and that macrophage NF-κB activation and TNF-α release were reduced in response to the ∆lgt strain. Differences in TNF-α responses between Δlgt and wild-type bacteria were abrogated for macrophages from TLR2- but not TLR4-deficient mice. Transcriptional profiling of human macrophages revealed attenuated TLR2-associated responses to ∆lgt S. pneumoniae, comprising many NF-κB–regulated proinflammatory cytokine and chemokine genes. Importantly, non-TLR2–associated responses were preserved. Experiments using leukocytes from IL-1R–associated kinase-4–deficient patients and a mouse pneumonia model confirmed that proinflammatory responses were lipoprotein dependent. Our data suggest that leukocyte responses to bacterial lipoproteins are required for TLR2- and IL-1R–associated kinase-4–mediated inflammatory responses to S. pneumoniae.
The E3 Ubiquitin Ligase Tripartite Motif 33 Is Essential for Cytosolic RNA–Induced NLRP3 Inflammasome Activation
Authors: Weng Leiyun , Mitoma Hiroki , Tricot Coline , Bao Musheng , Liu Ying , Zhang Zhiqiang , Liu Yong-Jun 
Published: August 2014

Abstract
NLRP3 is a key component of caspase-activating macromolecular protein complexes called inflammasomes. It has been found that DHX33 is a cytosolic dsRNA sensor for the NLRP3 inflammasome, which induces caspase-1–dependent production of IL-1β and IL-18 upon activation. However, how the cytosolic dsRNAs induce the interaction between DHX33 and the NLRP3 inflammasome remains unknown. In this study, we report that TRIM33, a member of the tripartite motif (TRIM) family, can bind DHX33 directly and induce DHX33 ubiquitination via the lysine 218 upon dsRNA stimulation. Knocking down of TRIM33 abolished the dsRNA-induced NLRP3 inflammasome activation in both THP-1–derived macrophages and human monocyte-derived macrophages. The ubiquitination of DHX33 by TRIM33 is lysine 63 specific and is required for the formation of the DHX33–NLRP3 inflammasome complex.
Cutting Edge: CD8+ Recent Thymic Emigrants Exhibit Increased Responses to Low-Affinity Ligands and Improved Access to Peripheral Sites of Inflammation
Authors: Berkley Amy M. , Fink Pamela J. 
Published: August 2014

Abstract
To explore the TCR sensitivity of recent thymic emigrants (RTEs), we triggered T cells with altered peptide ligands (APLs). Upon peptide stimulation in vitro, RTEs exhibited increased TCR signal transduction, and following infection in vivo with APL-expressing bacteria, CD8 RTEs expanded to a greater extent in response to low-affinity Ags than did their mature T cell counterparts. RTEs skewed to short-lived effector cells in response to all APLs but also were characterized by diminished cytokine production. RTEs responding to infection expressed increased levels of VLA-4, with consequent improved entry into inflamed tissue and pathogen clearance. These positive outcomes were offset by the capacity of RTEs to elicit autoimmunity. Overall, salient features of CD8 RTE biology should inform strategies to improve neonatal vaccination and therapies for cancer and HIV, because RTEs make up a large proportion of the T cells in lymphodepleted environments.
Acceptance of Low Vision Aids in Patients of ARMD, Myopic Degeneration and Diabetic Retinopathy
Authors: Singh Shilpa , Mithal Charu , Mithal Sandeep 
Published: August 2014

Purpose:
To compare and correlate the differences in acceptance of Low vision Aids in patients of ARMD, Myopic degeneration and Diabetic Retinopathy.

Materials and Methods:
Low Vision Aids were prescribed to each of the 15 patients in each group of Diabetic Retinopathy, Age Related Macular Degeneration and Myopic Degeneration with vision less that 6/18 in the better eye, with irreversible damage and their acceptance in each group was observed.

Results:
In patients of ARMD the mean scores pre LVA and post LVA were 25.33 and 32.47 and after applying Paired t test (two tailed t test) and taking P value as < .05 as statistically significant. And a p value <0.01 was found and this was considered to be statistically significant.
In patients of Myopic degeneration the mean scores pre LVA and post LVA were 26.00 and 37.27 and after applying Paired t test (two tailed t test) and taking P value as < .05 as statistically significant. And a p value <0.001 was found and this was considered to be extremely statistically significant.
In patients of DM the mean scores pre LVA and post LVA were 22.87 and 27.27 and after applying Paired t test (two tailed t test) and taking P value as < .05 as statistically significant. And a p value <0.2 was found and this was considered to be not statistically significant.

Conclusions:
Statistical methods concluded that low vision aids were of benefit in patients of Age Related Macular Degeneration and Myopic Degeneration, while they showed no benefit in patients of Diabetic Retinopathy.
Comparison of Corneal Endothelial Cell Loss between Torsional and Linear Phacoemulsification
Authors: Sawhney Amrita , Sridhar Uma , Tandon Charu 
Published: August 2014

Purpose:
To compare corneal endothelial cell loss between Torsional phacoemulsification and Linear phacoemulsification systems for cataract surgery.

Materials and Methods:
A prospective randomized study of 100 eyes of 100 patients, who underwent cataract surgery between September 2011 and September 2013, was done. They were divided into two groups, 50 patients underwent torsional phacoemulsification (phaco) and 50 patients underwent linear phacoemulsification. All patients were operated on same phaco machine by the same surgeon. Corneal endothelial cell loss comparison between the two groups was done using specular microscopy. Patients more than 40 years of age of either sex with senile cataract of nuclear sclerosis (NS) grade 2 -3 (according to LOCSII) were included in the study. Age <40, >70 years, corneal pathologies, poorly dilating pupil or posterior synechiae, pseudoexfoliation, subluxated lens, retinal pathology, glaucoma, diabetes mellitus, collagen vascular diseases, post refractive surgeries were excluded.

Results:
The mean percentage change of corneal endothelial cell density (ECD) from baseline was 3.5% in torsional group and 5.1% in linear group on postoperative day1 (p value= 0.026) 6.3% in torsional group and 9.8% in linear group on postoperative day 7 (p < 0.001) and 8.1% in torsional group and 10.78% in linear group on postoperative day 30 (p =0.001).

Conclusions:
There was statistically significant difference in corneal endothelial cell loss between torsional phacoemulsification and linear phacoemulsification systems for cataract surgery. The mean loss of corneal endothelial cells was statistically significantly less in torsional phacoemulsification than linear Phacoemulsification.
Diflunisal versus tafamidis on neuropathy and cardiomyopathy in hereditary transthyretin amyloidosis
Authors: Chao Chi‐Chao , Tzeng Shiou‐Ru , Chiang Ming‐Chang , Hsueh Hsueh‐Wen , Hsieh Wan‐Jen , Chao Yuan‐Chun , Cheng Mei‐Fang , Lin Yen‐Hung , Su Mao‐Yuan , Huang Chun‐Hsiang , Wang Yi‐Shiang , Hsieh Ming‐Fang , Tseng Ping‐Huei , Hsieh Sung‐Tsang 
Published: August 2024

AbstractObjectivesHereditary transthyretin (TTR) amyloidosis (ATTRv) is frequently complicated by polyneuropathy (ATTRv‐PN) and cardiomyopathy (ATTRv‐CM). The long‐term efficacy of diflunisal on both polyneuropathy and cardiomyopathy in ATTRv patients, especially those with non‐V30M genotypes, has not been fully investigated and compared with that of tafamidis.MethodsWe compared the structural and biochemical characteristics of A97S‐TTR complexed with tafamidis with those of diflunisal, and prospectively followed up and compared the progression of polyneuropathy and cardiomyopathy between ATTRv‐PN patients taking diflunisal and those taking tafamidis.ResultsBoth diflunisal and tafamidis effectively bind to the two thyroxine‐binding sites at the A97S‐TTR dimer–dimer interface and equally and almost sufficiently reduce amyloid fibril formation. Thirty‐five ATTRv‐PN patients receiving diflunisal and 22 patients receiving tafamidis were enrolled. Compared with no treatment, diflunisal treatment significantly delayed the transition of FAP Stage 1 to 2 and Stage 2 to 3 and decreased the deterioration in parameters of the ulnar nerve conduction study (NCS). The progression of FAP stage or NCS parameters did not differ between patients treated with diflunisal and those treated with tafamidis. Both diflunisal and tafamidis treatments significantly decreased radiotracer uptake on 99mTc‐PYP SPECT and stabilized cardiac wall thickness and blood pro‐B‐type natriuretic peptide levels. No significant adverse events occurred during diflunisal or tafamidis treatment.InterpretationsThe binding patterns of both tafamidis and diflunisal to A97S‐TTR closely resembled those observed in the wild type. Diflunisal can effectively delay the progression of polyneuropathy and cardiomyopathy with similar efficacy to tafamidis and may become a cost‐effective alternative treatment for late‐onset ATTRv‐PN.
Calcium Hexacyanoferrate (III) Nanocatalyst Enables Redox Homeostasis for Autism Spectrum Disorder Treatment
Authors: Feng Shini , Gong Yan , Xia Lili , Lang Yue , Shen Yizhe , Li Hui , Feng Wei , Chen Fuxue , Chen Yu 
Published: August 2024

AbstractAutism spectrum disorder (ASD) is a multifaced neurodevelopmental disorder with considerable heterogeneity, in which over‐generated reactive oxygen species (ROS) induce a cascade of pathological changes, including cellular apoptosis and inflammatory responses. Given the complex etiology of ASD, no effective treatment is available for ASD. In this work, a specific catalytic nanoenzyme, calcium hexacyanoferrate (III) nanocatalysts (CaH NCs), is designed and engineered for efficient ASD treatment. CaH NCs can mimic the activities of natural enzymes including superoxide dismutase, peroxidase, catalase, and glutathione peroxidase, which mitigates intracellular excessive ROS and regulates redox equilibrium. These CaH NCs modulate mitochondrial membrane potential, elevate B‐cell lymphoma‐2 levels, and suppress pro‐apoptotic proteins, including Caspase‐3 and B‐cell lymphoma‐2‐associated X, thus effectively reducing cellular apoptosis. Importantly, CaH NCs alleviate inflammation by upregulating anti‐inflammatory cytokine interleukin‐10 and downregulating pro‐inflammatory factors, resulting in attenuated activation of microglial and astrocytic and subsequent reduction in neuroinflammation. Subsequently, CaH NCs enhance social abilities, decrease anxiety levels, ameliorate repetitive behaviors, and improve learning and memory in ASD animal models through inflammation regulation and apoptosis inhibition. The CaH NCs in managing and preventing ASD represents a paradigm shift in autism treatment, paving the alternative but efficient way for clinical interventions in neurological conditions.
“Bowling Collision Effect” of CoMo6 Polyoxometalate Units Enables Wide Temperature Range from −20 to 60 °C and Dendrite Mitigation Li‐S Batteries
Authors: Li Yiding , Sun Kai , Fu Yujun , Wang Siqi , Zhuge Chenyu , Yin Xiaoqiang , Yang Zhibo , Li Zhenhua , Liu Dequan , Wang Xi , He Deyan 
Published: August 2024

AbstractTo improve the performance of Lithium‐Sulfur (Li‐S) batteries, the reaction catalysts of lithium polysulfides (LiPSs) reactions should have the characteristics of large surface area, efficient atomic utilization, high conductivity, small size, good stability, and strong adjustability. Herein, Anderson‐type polyoxometalate ([TMMo6O24]n−, TM = Co, Ni, Fe, represented by TMMo6 POMs) are used as the modified materials for Li‐S battery separator. By customizing the central metal atoms, this work gains insights into the layer‐by‐layer electron transfer mechanism between TMMo6 units and LiPSs, similar to the collision effect of a bowling ball. Theoretical analysis and in situ experimental characterization show that the changes of CoMo6 units with moderate binding energy and lowest Gibbs free energy result in the formation of robust polar bonds and prolonged S─S bonds after adsorption. Hence, the representative Li‐S battery with CoMo6 and graphene composite modified separator has a high initial capacity of 1588.6 mA h g−1 at 0.2 C, excellent cycle performance of more than 3000 cycles at 5 C, and uniform Li+ transport over 1900 h. More importantly, this work has revealed the inherent contradiction between the kinetics and thermodynamics, achieving a stable cycle in the temperature range of −20 to 60 °C.
Branched Oligomer‐Based Reversible Adhesives Enabled by Controllable Self‐Aggregation
Authors: Qin Chenxi , Yang Hao , Li Bin , Xing Zhencai , Yu Bo , Cai Meirong , Pei Xiaowei , Ma Yanfei , Zhou Feng , Liu Weimin 
Published: August 2024

AbstractSupramolecular adhesion material systems based on small molecules have shown great potential to unite the great contradiction between strong adhesion and reversibility. However, these material systems suffer from low adhesion strength/narrow adhesion span, limited designability, and single interaction due to fewer covalent bond content and action sites in small molecules. Herein, an ultrahigh‐strength and large‐span reversible adhesive enabled by a branched oligomer controllable self‐aggregation strategy is developed. The dense covalent bonds present in the branched oligomers greatly enhance adhesion strength without compromising reversibility. The resulting adhesive exhibits a large‐span reversible adhesion of ≈140 times, switching between ultra‐strong and tough adhesion strength (5.58 MPa and 5093.92 N m−1) and ultralow adhesion (0.04 MPa and 87.656 N m−1) with alternating temperature. Moreover, reversible dynamic double cross‐linking endows the adhesive with stable reversible adhesion transitions even after 100 cycles. This reversible adhesion property can also be remotely controlled via a voltage of 8 V, with a loading voltage duration of 45 s. This work paves the way for the design of reversible adhesives with long‐span outstanding properties using covalent polymers and offers a pathway for the rational design of high‐performance adhesives featuring both robust toughness and exceptional reversibility.
Grain Boundary Transport in the Argyrodite‐Type Li6PS5Br Solid Electrolyte: Influence of Misorientation and Anion Disorder on Li Ion Mobility
Authors: Sadowski Marcel , Albe Karsten 
Published: August 2024

AbstractTo realize efficient solid‐state batteries, many efforts are directed toward maximizing the bulk Li+ conductivity of sulfide superionic conductors, as demonstrated for the argyrodite‐type materials Li6PS5Cl and Li6PS5Br. Notably, in these archetype materials, the fast Li+ transport benefits from considerable anion disorder on the halide and sulfur sublattices. To further improve the Li+ conductivity, however, one must consider not only the bulk properties of the solid electrolyte (SE) but also microstructural aspects. It is, however, controversially discussed whether grain boundary (GB) transport is generally detrimental for the overall ion conductivity in agyrodite‐type SEs. Thus, by means of atomistic computer simulations, the Li+ ion transport is studied in twist and tilt GBs of Li6PS5Br, revealing that the Br/S site exchange determines whether the presence of GBs deteriorates the ionic conductivity: Whereas the material with 0% Br/S site exchange only shows locally limited bulk diffusion but enhanced GB conductivity, at higher degrees of site exchange, GBs deteriorate Li+ diffusion. These results show that the interplay of GB transport directly depends on the degree of site exchange in argyrodite‐type materials.