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High myopia is a leading cause of blindness worldwide. It may lead to emotional defects that rely closely on the link between visual sensation and the central nervous system. However, the extent of the defects and its underlying mechanism remain unknown. Here, we report that highly myopic patients exhibit greater anxiety, accompanied by higher CC chemokine ligand 2 (CCL2) and monocyte levels in the blood. Similar findings are found in the mouse model of high myopia. Mechanistic evaluations using GFP-positive bone marrow chimeric mice, parabiotic mouse model, enhanced magnetic resonance imaging, etc., show that highly myopic visual stimulation increases CCL2 expression in eyes, aggravates monocyte/macrophage infiltration into eyes and brains, and disrupts blood–ocular barrier and blood–brain barrier of mice. Conversely, Ccl2-deficient highly myopic mice exhibit attenuated ocular and brain infiltration of monocytes/macrophages, reduced disruption of the blood–ocular barrier and blood–brain barrier, and less anxiety. Substantial alleviation of high myopia-related anxiety can also be achieved with the administration of CCL2-neutralizing antibodies. Our results establish the association between high myopia and anxiety, and implicate the CCL2-mediated inflammatory pathogenesis as an underlying mechanism. [ABSTRACT FROM AUTHOR]

Introduction: To evaluate the characteristics of optic nerve head (ONH) in highly myopic eyes and its role in predicting intraocular pressure (IOP) spikes after cataract surgery. Methods: Patients who are highly myopic and were scheduled for cataract surgery were enrolled in this prospective case series study. IOP was measured preoperatively and at 1 day and 3 days postoperatively. ONH characteristics including area, tilt ratio, lamina cribrosa (LC) thickness, and depth, and the presence of LC defects were evaluated with enhanced depth imaging optical coherence tomography. Factors influencing LC defects and early IOP spike were investigated using multivariate stepwise logistic regression. Results: In total, 200 highly myopic eyes of 200 patients were analyzed: 35.00% had small ONH, 53.00% had ONH tilt, and 14.00% had LC defects. Multivariate analysis demonstrated female patients with larger ONH area and deeper LC tended to have LC defects (all P < 0.05). As to postoperative IOP, IOP change, and incidence of IOP spikes, eyes with small ONH, ONH tilt, and LC defects had similar (all P > 0.05), higher (all P < 0.05), and lower (all P < 0.05) outcomes compared with those without the corresponding characteristic, respectively. Multivariate analysis showed that presence of LC defects and thicker LC were protective factors for early IOP spikes, and axial length > 28 mm was a risk factor (all P < 0.05). Conclusion: Female patients with larger ONH area and deeper LC tend to have LC defects, which, together with thicker LC, was correlated with less IOP spikes in highly myopic eyes. Trial Registration: This study was conducted as part of a larger project, the Shanghai High Myopia Study, registered at www.clinicaltrials.gov (accession number NCT03062085). [ABSTRACT FROM AUTHOR]

The therapeutic efficacy of whole tumor cell vaccines (TCVs) is modest, which has delayed their translation into personalized immunotherapies in the clinic. Here, we develop a TCV platform based on photothermal nanoparticle-loaded tumor cells, which can be rationally applied to diverse tumor types to achieve on-demand boost of anti-tumor immune responses for inhibiting tumor growth. During the fabrication process, mild photothermal heating by near-infrared (NIR) laser irradiation induces the nanoparticle-bearing tumor cells to express heat shock proteins as endogenous adjuvants. After a single vaccination at the back of tumor-bearing mice, non-invasive NIR laser irradiation further induces mild hyperthermia at vaccination site, which promotes the recruitment, activation, and antigen presentation by dendritic cells. Using an indicator we term fluctuation of tumor growth rate, we determine appropriate irradiation regimens (including optimized irradiation intervals and times). This TCV platform enables on-demand NIR manipulation of immune responses, and we demonstrate potent therapeutic efficacy against six murine models that mimick a range of clinical scenarios, including a model based on humanized mice and patient-derived tumor xenografts. Whole autologous tumor cell vaccine (TCV) has been proposed as a tool for cancer immunotherapy. Here the authors describe the design of a TCV platform based on photothermal nanoparticle-loaded tumor cells, triggering NIR laser irradiation induced anti-tumor immune responses at the vaccination site. [ABSTRACT FROM AUTHOR]

The outcomes of toric intraocular lens (IOL) implantation in correcting asymmetric bowtie corneal astigmatism remain uncertain. The accurate measurement of corneal astigmatism is essential for surgical planning. In this prospective cohort study, patients with asymmetric or symmetric bowtie corneal astigmatism who underwent toric IOL implantation were recruited. Preoperative corneal astigmatism was measured with an IOLMaster and Pentacam (including the simulated keratometry (SimK), total corneal refractive power (TCRP), and wavefront aberration (WFA) modes). At 3 months after surgery, the refractive outcomes and residual astigmatic refractive errors were compared with patients with symmetric bowtie astigmatism. The prediction errors (the differences between the calculated actual corneal astigmatism and the measured corneal astigmatism) were compared among the different measurement modes in the asymmetric group. There were no differences in residual astigmatism between the asymmetric and symmetric groups. However, the mean absolute residual astigmatic refractive error was greater in the asymmetric group than in the symmetric group (0.72 ± 0.42 D vs. 0.53 ± 0.24 D, p = 0.043). In the asymmetric group, the mean absolute prediction errors for the IOLMaster, SimK, TCRP and WFA modes were 0.53 ± 0.40, 0.56 ± 0.47, 0.68 ± 0.52, and 0.43 ± 0.40 D, respectively. The Pentacam WFA mode was the most accurate mode (p < 0.05). The absolute prediction error of the WFA mode was positively correlated with the total corneal irregular astigmatism higher-order aberrations and coma (r = 0.416 and r = 0.473, respectively; both p < 0.05). Our study suggests toric IOL implantation effectively corrected asymmetric bowtie corneal astigmatism. The Pentacam WFA mode may be the most accurate measurement mode, although its accuracy decreased as asymmetry increased. [ABSTRACT FROM AUTHOR]

These authors contributed equally: Xiangjia Zhu, Yu Du, Dan Li, Jie Xu Correction to: I Nature Communications i https://doi.org/10.1038/s41467-021-22041-2, published online 08 April 2021 In this article, the grant numbers 81790643 and 82121003 relating to the National Natural Science Foundation of the People's Republic of China were omitted. In addition, the affiliation details for Zhenglin Yang were incorrectly given as 'Sichuan Provincial Key Laboratory for Human Disease Gene Study, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China' but should have been 'Sichuan Provincial Key Laboratory for Human Disease Gene Study and the Center for Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, University of Electronic Science and Technology, Chengdu, China'. and 'Research Unit for Blindness Prevention of Chinese Academy of Medical Sciences (2019RU026), Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, Sichuan, China'. Author Correction: Aberrant TGF- 1 signaling activation by MAF underlies pathological lens growth in high myopia. [Extracted from the article]

For the first time, β-Ga2O3 were prepared on 4H-SiC (0001) substrates using a low-pressure chemical vapor deposition (LPCVD) technique. The obtained β-Ga2O3/4H-SiC heterostructures display strongly preferential growth orientation along the < 2 01> of β-Ga2O3. Combining the experimental results, interfacial properties, such as the work of adhesion (Wad), electronic properties and bonding characteristics of β-Ga2O3(2 01)/4H-SiC(0001) heterointerface were systemically studied using first principles. Four different β-Ga2O3(2 01)/4H-SiC(0001) interface models composed of different atom stacking sequences were established. It was found that the interface consisting of silicon terminated of 4H-SiC (0001), and oxygen terminated of β-Ga2O3(2 01) (Si-O) has the lowest relaxation energy and the highest stability. Results indicated that the binding of interface Si and C to the O atoms is stronger than that to the Ga atoms. The results of the difference charge density and electron localization function reveals that the Si and C atoms at interface are bonded with O atoms of β-Ga2O3 by covalent bonds, in which Si-O and C-O covalent bonds play a favorable role in the final stable configurations formation. This work will provide a further understanding of the various electronic behaviors of the β-Ga2O3(2 01)/4H-SiC(0001) heterointerface. [ABSTRACT FROM AUTHOR]

High-myopic cataract (HMC) is a complex cataract with earlier onset and more rapid progress than age-related cataract (ARC). Circular RNAs (circRNAs) have been implicated in many diseases. However, their involvement in HMC remain largely unexplored. To investigate the role of dysregulated circRNAs in HMC, lens epithelium samples from 24 HMC and 24 ARC patients were used for whole transcriptome sequencing. Compared with ARC, HMC had 3687 uniquely expressed circRNAs and 1163 significantly differentially expressed circRNAs (DEcRs) (|log2FC| > 1, p < 0.05). A putative circRNA-miRNA-mRNA network was constructed based on correlation analysis. We validated the differential expression of 3 DEcRs by quantitative polymerase chain reaction (qPCR) using different sets of samples. We further investigated the role of circAFF1 in cultured lens epithelial cells (LECs) and found that the overexpression of circAFF1 promoted cell proliferation, migration and inhibited apoptosis. We also showed that circAFF1 upregulated Tropomyosin 1 (TPM1) expression by sponging miR-760, which was consistent with the network prediction. Collectively, our study suggested the involvement of circRNAs in the pathogenesis of HMC and provide a resource for further study on this topic. [ABSTRACT FROM AUTHOR]

On the basis of an external and static perspective on the topological structure of collaborative innovation networks, it is extremely difficult to answer the two most important concerns, namely, which structure is ideal and how to develop it in practice. By contrast, this study transfers to internal and dynamic perspectives, and then proposes that the essence of developing the ideal network lies in choosing the best partners. Therefore, we firstly propose the basic decision-making rules for selecting partners. In order of priority: knowledge distance, knowledge complementarity and barter exchange. Secondly, a model is constructed to describe this process of selecting partners and exchanging knowledge. Thirdly, the simulation results show that a small-world network is ideal in the initial stage of collaborative innovation. However, a random network is ideal in the mature periods. This result shows that the ideal network structure is not fixed, but affected by the life cycle of collaborative innovation alliance. Furthermore, this supports the notion that a small world is spontaneously generated in the real world, and also confirms that the formation of a small-world network will be driven intrinsically by a firm's demand for external knowledge, and not necessarily by the external driving force of social capital. Finally, these findings solve the above two most important questions. [ABSTRACT FROM AUTHOR]

Tumor immune microenvironment exerts a profound effect on the population of infiltrating immune cells. Tissue inhibitor of matrix metalloproteinase 1 (TIMP1) is frequently overexpressed in a variety of cells, particularly during inflammation and tissue injury. However, its function in cancer and immunity remains enigmatic. In this study, we find that TIMP1 is substantially up-regulated during tumorigenesis through analyzing cancer bioinformatics databases, which is further confirmed by IHC tissue microarrays of clinical samples. The TIMP1 level is significantly increased in lymphocytes infiltrating the tumors and correlated with cancer progression, particularly in GBM. Notably, we find that the transcriptional factor Sp1 binds to the promoter of TIMP1 and triggers its expression in GBM. Together, our findings suggest that the Sp1-TIMP1 axis can be a potent biomarker for evaluating immune cell infiltration at the tumor sites and therefore, the malignant progression of GBM. [ABSTRACT FROM AUTHOR]

In this work, a desired Cu2O catalyst supported on graphitic carbon nitride and reduced graphene oxide hybrid (Cu2O/g-C3N4–rGO) with excellent catalytic performance in the reduction of 4-nitrophenol (4-NP) by NaBH4 has been fabricated. X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), electrochemical impedance spectroscopy (EIS), N2 adsorption/desorption and Fourier-transform infrared (FTIR) techniques as well as catalytic test using the reduction of 4-NP by NaBH4 as probe reaction have been used to investigate the structure–properties relationship of the as-prepared Cu2O/g-C3N4–rGO composites. The results demonstrate that ultrafine Cu2O nanoparticles can be stably anchored on g-C3N4–rGO hybrid by tuning the initial ratio of rGO (reduced graphene oxide) to g-C3N4, where homogeneous dispersion of g-C3N4 on sheet-like rGO plays a very important role in confining the ultrafine Cu2O nanoparticles and excellent catalytic performance is noticed on Cu2O/g-C3N4–rGO composite for the reduction of 4-NP by NaBH4 with an activity parameter up to 6330 s-1g-1. [ABSTRACT FROM AUTHOR]

Targeting subcellular organelle with multilevel damage has shown great promise for antitumor therapy. Here, we report a core-shell type of nanoagent with iron (III) carboxylate metal-organic frameworks (MOFs) as shell while upconversion nanoparticles (UCNPs) as core, which enables near-infrared (NIR) light-triggered synergistically reinforced oxidative stress and calcium overload to mitochondria. The folate decoration on MOFs shells enables efficient cellular uptake of nanoagents. Based on the upconversion ability of UCNPs, NIR light mediates Fe3+-to-Fe2+ reduction and simultaneously activates the photoacid generator (pHP) encapsulated in MOFs cavities, which enables release of free Fe2+ and acidification of intracellular microenvironment, respectively. The overexpressed H2O2 in mitochondria, highly reactive Fe2+ and acidic milieu synergistically reinforce Fenton reactions for producing lethal hydroxyl radicals (•OH) while plasma photoacidification inducing calcium influx, leading to mitochondria calcium overload. The dual-mitochondria-damage-based therapeutic potency of the nanoagent has been unequivocally confirmed in cell- and patient-derived tumor xenograft models in vivo. Targeting damage to mitochondria has become an effective strategy antitumor therapies. Here, the authors report on nanoagents with upconversion nanoparticles as cores and photoacid-loaded MOFs as shells for NIR triggered Fenton reaction, acidification and calcium overload to provide synergistic mitochondrial damage. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) typically plays biphasic biological roles in living organisms with subnormal H2S exerting cytoprotective effects such as participating in cardioprotective signaling pathways while H2S with higher-than-normal concentrations in localized tissues acting the opposite way such as inhibiting mitochondrial respiration. Such concentration-dependent biological and pathological roles of H2S with the wide involvement of mitochondria and the elusive feature of H2S definitely highlight the vital significance of fast and precise estimation of the physiological level of H2S in specific microenvironments, particularly within cellular mitochondria. In this work, we developed a new type of fluorescent probe (QcyCHO) featured with H2S-triggered off-to-on near-infrared (NIR) fluorescence conversion within ~ 10 min, limit of detection (LOD) down to 8.3 nM, and high recognition specificity over other similarly interfering species. The ideal mitochondrion-targeting ability, high recognition specificity over typical interfering substances and other physiologically relevant species, and the ability for mapping intracellular H2S in living cells of QcyCHO probe were also unequivocally confirmed, which imply its potential for shedding light on the biology of H2S and therapeutic development in H2S-associated diseases by identifying the specific physiological stimuli inducing H2S production and determining the levels of H2S at the location and time of stimulation. [ABSTRACT FROM AUTHOR]

Previous studies show that mortalin, a HSP70 family member, contributes to the development and progression of ovarian cancer. However, details of the transcriptional regulation of mortalin remain unknown. We aimed to determine whether NF‐κB p65 participates in the regulation of mortalin expression in ovarian cancer cells and to elucidate the underlying mechanism. Chromatin immunoprecipitation and luciferase reporter assay were used to identify mortalin gene sequences, to which NF‐κB p65 binds. Results indicated that NF‐κB p65 binds to the mortalin promoter at a site with the sequence 'CGGGGTTTCA'. Using lentiviral pLVX‐NF‐κB‐puro and Lentivirus‐delivered NF‐κB short hairpin RNA (shRNA), we created ovarian cancer cell lines in which NF‐κB p65 was stably up‐regulated and down‐regulated. Using these cells, we found that downregulation of NF‐κB p65 inhibits the growth and migration of ovarian cancer cells. Further experimental evidence indicated that downregulation of NF‐κB p65 reduced mortalin, and upregulation of mortalin rescued the proliferation and migration of ovarian cancer cells reduced by NF‐κB p65 knockdown. In conclusion, NF‐κB p65 binds to the mortalin promoter and promotes ovarian cancer cells proliferation and migration via regulating mortalin. [ABSTRACT FROM AUTHOR]