BRD9-SMAD2/3 Orchestrates Stemness and Tumorigenesis in Pancreatic Ductal Adenocarcinoma.

BACKGROUND & AIMS: The dismal prognosis of pancreatic ductal adenocarcinoma (PDAC) is linked to the presence of pancreatic cancer stem-like cells (CSCs) that respond poorly to current chemotherapy regimens. The epigenetic mechanisms regulating CSCs are currently insufficiently understood, which hampers the development of novel strategies for eliminating CSCs. METHODS: By small molecule compound screening targeting 142 epigenetic enzymes, we identified that bromodomain-containing protein BRD9, a component of the BAF histone remodeling complex, is a key chromatin regulator to orchestrate the stemness of pancreatic CSCs via cooperating with the TGFß/Activin-SMAD2/3 signaling pathway. RESULTS: Inhibition and genetic ablation of BRD9 block the self-renewal, cell cycle entry into G0 phase and invasiveness of CSCs, and improve the sensitivity of CSCs to gemcitabine treatment. In addition, pharmacological inhibition of BRD9 significantly reduced the tumorigenesis in patient-derived xenografts mouse models and eliminated CSCs in tumors from pancreatic cancer patients. Mechanistically, inhibition of BRD9 disrupts enhancer-promoter looping and transcription of stemness genes in CSCs. CONCLUSIONS: Collectively, the data suggest BRD9 as a novel therapeutic target for PDAC treatment via modulation of CSC stemness.

A novel murine model of mania.

Neuropathological mechanisms of manic syndrome or manic episodes in bipolar disorder remain poorly characterised, as the research progress is severely limited by the paucity of appropriate animal models. Here we developed a novel mania mice model by combining a series of chronic unpredictable rhythm disturbances (CURD), which include disruption of circadian rhythm, sleep deprivation, exposure to cone light, with subsequent interference of followed spotlight, stroboscopic illumination, high-temperature stress, noise disturbance and foot shock. Multiple behavioural and cell biology tests comparing the CURD-model with healthy controls and depressed mice were deployed to validate the model. The manic mice were also tested for the pharmacological effects of various medicinal agents used for treating mania. Finally, we compared plasma indicators of the CURD-model mice and the patients with the manic syndrome. The CURD protocol produced a phenotype replicating manic syndrome. Mice exposed to CURD presented manic behaviours similar to that observed in the amphetamine manic model. These behaviours were distinct from depressive-like behaviours recorded in mice treated with a depression-inducing protocol of chronic unpredictable mild restraint (CUMR). Functional and molecular indicators in the CURD mania model showed multiple similarities with patients with manic syndrome. Treatment with LiCl and valproic acid resulted in behavioural improvements and recovery of molecular indicators. A novel manic mice model induced by environmental stressors and free from genetic or pharmacological interventions is a valuable tool for research into pathological mechanisms of mania.

Rewiring of 3D Chromatin Topology Orchestrates Transcriptional Reprogramming and the Development of Human Dilated Cardiomyopathy.

BACKGROUND: Transcriptional reconfiguration is central to heart failure, the most common cause of which is dilated cardiomyopathy (DCM). The effect of 3-dimensional chromatin topology on transcriptional dysregulation and pathogenesis in human DCM remains elusive. METHODS: We generated a compendium of 3-dimensional epigenome and transcriptome maps from 101 biobanked human DCM and nonfailing heart tissues through highly integrative chromatin immunoprecipitation (H3K27ac [acetylation of lysine 27 on histone H3]), in situ high-throughput chromosome conformation capture, chromatin immunoprecipitation sequencing, assay for transposase-accessible chromatin using sequencing, and RNA sequencing. We used human induced pluripotent stem cell-derived cardiomyocytes and mouse models to interrogate the key transcription factor implicated in 3-dimensional chromatin organization and transcriptional regulation in DCM pathogenesis. RESULTS: We discovered that the active regulatory elements (H3K27ac peaks) and their connectome (H3K27ac loops) were extensively reprogrammed in DCM hearts and contributed to transcriptional dysregulation implicated in DCM development. For example, we identified that nontranscribing NPPA-AS1 (natriuretic peptide A antisense RNA 1) promoter functions as an enhancer and physically interacts with the NPPA (natriuretic peptide A) and NPPB (natriuretic peptide B) promoters, leading to the cotranscription of NPPA and NPPB in DCM hearts. We revealed that DCM-enriched H3K27ac loops largely resided in conserved high-order chromatin architectures (compartments, topologically associating domains) and their anchors unexpectedly had equivalent chromatin accessibility. We discovered that the DCM-enriched H3K27ac loop anchors exhibited a strong enrichment for HAND1 (heart and neural crest derivatives expressed 1), a key transcription factor involved in early cardiogenesis. In line with this, its protein expression was upregulated in human DCM and mouse failing hearts. To further validate whether HAND1 is a causal driver for the reprogramming of enhancer-promoter connectome in DCM hearts, we performed comprehensive 3-dimensional epigenome mappings in human induced pluripotent stem cell-derived cardiomyocytes. We found that forced overexpression of HAND1 in human induced pluripotent stem cell-derived cardiomyocytes induced a distinct gain of enhancer-promoter connectivity and correspondingly increased the expression of their connected genes implicated in DCM pathogenesis, thus recapitulating the transcriptional signature in human DCM hearts. Electrophysiology analysis demonstrated that forced overexpression of HAND1 in human induced pluripotent stem cell-derived cardiomyocytes induced abnormal calcium handling. Furthermore, cardiomyocyte-specific overexpression of Hand1 in the mouse hearts resulted in dilated cardiac remodeling with impaired contractility/Ca2+ handling in cardiomyocytes, increased ratio of heart weight/body weight, and compromised cardiac function, which were ascribed to recapitulation of transcriptional reprogramming in DCM. CONCLUSIONS: This study provided novel chromatin topology insights into DCM pathogenesis and illustrated a model whereby a single transcription factor (HAND1) reprograms the genome-wide enhancer-promoter connectome to drive DCM pathogenesis.

Demystifying Cancer Etiology via 3D Genome Mapping.

Ramanand et al. perform the first high-resolution 3D genome mapping via ChIA-PET to capture RNAPII-associated chromatin interactions in normal prostate epithelial and prostate cancer cells. They describe how genetics, epigenetics, and the 3D genome architecture are coordinated in the aberrant gene expression that drives prostate cancer development.

Associations of habitual glucosamine use with SARS-CoV-2 infection and hospital admission and death with COVID-19: Evidence from a large population based cohort study.

The coronavirus disease 2019 (COVID-19) pandemic has led to a fundamental number of morbidity and mortality worldwide. Glucosamine was indicated to help prevent and control RNA virus infection preclinically, while its potential therapeutic effects on COVID-19-related outcomes are largely unknown. To assess the association of habitual glucosamine use with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, hospital admission, and mortality with COVID-19 in a large population based cohort. Participants from UK Biobank were reinvited between June and September 2021 to have SARS-CoV-2 antibody testing. The associations between glucosamine use and the risk of SARS-CoV-2 infection were estimated by logistic regression. Hazard ratios (HRs) and 95% confidence intervals (CIs) for COVID-19-related outcomes were calculated using COX proportional hazards model. Furthermore, we carried out propensity-score matching (PSM) and stratified analyses. At baseline, 42 673 (20.7%) of the 205 704 participants reported as habitual glucosamine users. During median follow-up of 1.67 years, there were 15 299 cases of SARS-CoV-2 infection, 4214 cases of COVID-19 hospital admission, and 1141 cases of COVID-19 mortality. The fully adjusted odds ratio of SARS-CoV-2 infection with glucosamine use was 0.96 (95% CI: 0.92-1.01). The fully adjusted HR were 0.80 (95% CI: 0.74-0.87) for hospital admission, and 0.81 (95% CI: 0.69-0.95) for mortality. The logistic regression and Cox proportional hazard analyses after PSM yielded consistent results. Our study demonstrated that habitual glucosamine use is associated with reduced risks of hospital admission and death with COVID-19, but not the incidence of SARS-CoV-2 infection.

Leptin Attenuates Fear Memory by Inhibiting Astrocytic NLRP3 Inflammasome in Post-traumatic Stress Disorder Model.

Accumulating evidence suggests that the activation of nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome contributes to the pathophysiology of post-traumatic stress disorder (PTSD). Astrocytes, the homeostatic cells of the central nervous system are intimately involved into pathophysiology of various mental disorders including PTSD. We demonstrated previously that leptin exerts neuroprotection and ameliorates chronic sleep deprivation-induced depressive-like behaviours. Here, we extended the study of therapeutic effects of leptin to PTSD model mice. We discovered that PTSD is associated with significant activation of NLRP3 inflammasome in astrocytes sorted from GFAP-GFP transgenic mice, while administration of leptin markedly suppressed the activation of astrocytic NLRP3 inflammasome. Leptin effectively improved PTSD-associated behavioural alterations including fear memory, cognitive impairments, and depressive-like behaviours. Therapeutic effects of leptin were mediated by the signal transducer and activator of transcription 3 (STAT3) in astrocytes. In addition, the PTSD-related activation of NLRP3 inflammasome impairs astrocytic mitochondria suppressing ATP synthesis and leading to an increased ROS production. Leptin reversed mitochondrial inhibition by stimulating STAT3 in astrocytes. We propose leptin as a novel candidate for the pharmacological treatment of PTSD.

A DFT study on methanol decomposition over single atom Pt/CeO2 catalysts: the effect of the position of Pt.

Pt/CeO2 catalysts exhibit excellent catalytic performance for the methanol dehydrogenation (MD) reaction. In this work, MD reactions on three systems of Pt1/CeO2(110)), Pt7/CeO2(110), and Pt1/Ce1-xO2(110) are investigated via density functional theory (DFT) calculations. The CH3OH adsorption, electronic structure of the catalyst, and mechanism of methanol decomposition (MD) are systematically calculated. The results reveal that the d-band center of the Pt atom moves away from the Fermi level in the order of Pt1/CeO2(110) < Pt7/CeO2(110) < Pt1/Ce1-xO2(110), and the order of the activity of the MD reaction is Pt1/CeO2(110) < Pt7/CeO2(110) < Pt1/Ce1-xO2(110). The results of the microkinetic dynamics simulation verify that only Pt1/Ce1-xO2(110) is conducive to the decomposition of methanol at low temperatures (373 K), and the products CO and H2 are easily dissociated from the catalyst surface. This work uncovers that both the small size and the Ce vacancy substituted sites of Pt favor the performance of the Pt/CeO2 catalyst, and provides theoretical guidance for the construction and design of efficient metal-support catalysts for the MD reaction.

Integrative epigenomic profiling reveal AP-1 is a key regulator in intrahepatich cholangiocarcinoma.

Intrahepatic cholangiocarcinoma (ICC) is a malignant tumor with poor prognosis while its mechanisms of pathogenesis remain elusive. In this study, we performed systemic epigenomic and transcriptomic profiling via MNase-seq, ChIP-seq and RNA-seq in normal cholangiocyte and ICC cell lines. We showed that active histone modifications (H3K4me3, H3K4me1 and H3K27ac) were less enriched on cancer-related genes in ICC cell lines compared to control. The region of different histone modification patterns is enrichment in sites of AP-1 motif. Subsequent analysis showed that ICC had different nucleosome occupancy in differentially expressed genes compared to a normal cell line. Furthermore, we found that AP-1 plays a key role in ICC and regulates ICC-related genes through its AP-1 binding site. This study is the first report showing the global features of histone modification, transcript, and nucleosome profiles in ICC; we also show that the transcription factor AP-1 might be a key target gene in ICC.

Revisiting 3D chromatin architecture in cancer development and progression.

Cancer development and progression are demarcated by transcriptional dysregulation, which is largely attributed to aberrant chromatin architecture. Recent transformative technologies have enabled researchers to examine the genome organization at an unprecedented dimension and precision. In particular, increasing evidence supports the essential roles of 3D chromatin architecture in transcriptional homeostasis and proposes its alterations as prominent causes of human cancer. In this article, we will discuss the recent findings on enhancers, enhancer-promoter interaction, chromatin topology, phase separation and explore their potential mechanisms in shaping transcriptional dysregulation in cancer progression. In addition, we will propose our views on how to employ state-of-the-art technologies to decode the unanswered questions in this field. Overall, this article motivates the study of 3D chromatin architecture in cancer, which allows for a better understanding of its pathogenesis and develop novel approaches for diagnosis and treatment of cancer.

An Accurate and Convenient Method of Vehicle Spatiotemporal Distribution Recognition Based on Computer Vision.

The Convenient and accurate identification of the traffic load of passing vehicles is of great significance to bridge health monitoring. The existing identification approaches often require prior environment knowledge to determine the location of the vehicle load, i.e., prior information of the road, which is inconvenient in practice and therefore limits its application. Moreover, camera disturbance usually reduces the measurement accuracy in case of long-term monitoring. In this study, a novel approach to identify the spatiotemporal information of passing vehicles is proposed based on computer vision. The position relationship between the camera and the passing vehicle is established, and then the location of the passing vehicle can be calculated by setting the camera shooting point as the origin. Since the angle information of the camera is pre-determined, the identification result is robust to camera disturbance. Lab-scale test and field measurement have been conducted to validate the reliability and accuracy of the proposed method.

On-Site Detection of SARS-CoV-2 Antigen by Deep Learning-Based Surface-Enhanced Raman Spectroscopy and Its Biochemical Foundations.

A rapid, on-site, and accurate SARS-CoV-2 detection method is crucial for the prevention and control of the COVID-19 epidemic. However, such an ideal screening technology has not yet been developed for the diagnosis of SARS-CoV-2. Here, we have developed a deep learning-based surface-enhanced Raman spectroscopy technique for the sensitive, rapid, and on-site detection of the SARS-CoV-2 antigen in the throat swabs or sputum from 30 confirmed COVID-19 patients. A Raman database based on the spike protein of SARS-CoV-2 was established from experiments and theoretical calculations. The corresponding biochemical foundation for this method is also discussed. The deep learning model could predict the SARS-CoV-2 antigen with an identification accuracy of 87.7%. These results suggested that this method has great potential for the diagnosis, monitoring, and control of SARS-CoV-2 worldwide.

Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases.

Metabolic function and energy production in eukaryotic cells are regulated by mitochondria, which have been recognized as the intracellular 'powerhouses' of eukaryotic cells for their regulation of cellular homeostasis. Mitochondrial function is important not only in normal developmental and physiological processes, but also in a variety of human pathologies, including cardiac diseases. An emerging topic in the field of cardiovascular medicine is the implication of mitochondrial nucleoid for metabolic reprogramming. This review describes the linear/3D architecture of the mitochondrial nucleoid (e.g., highly organized protein-DNA structure of nucleoid) and how it is regulated by a variety of factors, such as noncoding RNA and its associated R-loop, for metabolic reprogramming in cardiac diseases. In addition, we highlight many of the presently unsolved questions regarding cardiac metabolism in terms of bidirectional signaling of mitochondrial nucleoid and 3D chromatin structure in the nucleus. In particular, we explore novel techniques to dissect the 3D structure of mitochondrial nucleoid and propose new insights into the mitochondrial retrograde signaling, and how it regulates the nuclear (3D) chromatin structures in mitochondrial diseases.

Multimodal imaging and electroretinography highlights the role of VEGF in the laser-induced subretinal fibrosis of monkey.

Age-related macular degeneration (AMD) is a leading cause of blindness. Laser-induced nonhuman primate choroidal neovascularization (CNV) is a widely used animal model of neovascular AMD. Subretinal fibrosis (SFb) is the major limiting factor of effective anti-VEGF therapy for neovascular AMD, yet SFb has never been systematically analyzed in the primate CNV model and if VEGF directly affect SFb is unknown. We recruited a large cohort of rhesus macaques to study the occurrence, multimodal imaging and electroretinography (ERG) features, and related cytokines of SFb. Here we show that among 33 rhesus macaques, 88% CNV eyes developed SFb. Spectral domain optical coherence tomography (SD-OCT) identified four types of subretinal hyper-reflective material (SHRM) of SFb in primate. Multimodal imaging is reliable for monitoring SFb and matches the histological results well. Reduced amplitude of oscillatory potentials correlates with the thinning of inner retina layers and is a possible SFb indicator. Iba1+ microglia/macrophage cells infiltrated in the fibrotic lesions, and aqueous cytokine analysis identified four fibrosis-related factors (GM-CSF, IL-10, TGFß2 and VEGF). Unexpectedly, we found sustained expression of VEGF may be an important inducer of SFb, and anti-VEGF therapy actually partially suppresses SFb. Taken together, our data suggest the laser-induced primate SFb model, coupled with multimodal imaging and ERG recording, is a useful system to dissect the pathogenesis and explore the rationale of treatment for SFb; and combined therapy with anti-VEGF and anti-fibrosis agents is necessary for AMD treatment.

Noble-metal nanoparticle labelling multiplex miRNAs by ICP-MS readout with internal standard isotopes of 115In and 209Bi.

Inductively coupled plasma-mass spectrometry (ICP-MS) is one of the most powerful techniques for multiplex nucleotide assay owing to the virtue of the high resolution of multiple-elements' mass to charge ratio, in a mass spectrum. Here, a small sized (less than 20 nm) noble-metal nanoparticle labelled ICP-MS (NP-ICP-MS) is proposed for high-throughput microRNA (miRNA) determination. Three miRNA targets - miR-486-5p, miR-221, and miR-21 - in serum, were distinguished by single-stranded DNA (ssDNA) probes labelled with a small sized noble-metal nanoparticle - silver nanoparticles (AgNPs), platinum nanoparticles (PtNPs), and gold nanoparticles (AuNPs). The counting isotopes ion intensity per second (CPS) of the noble-metal label versus internal standard isotope intensity of 115In and 209Bi, exhibited good linearity in the range 0.25 pM to 100 pM with correlation coefficients (R2) of 0.9680, 0.9305, and 0.9418. The specific sandwich-type miRNA assay using the sensitive NP-ICP-MS readout pushed the detection limits down to 0.18 pM for miR-221, 0.23 pM for miR-486-5p, and 0.22 pM for miR-21. And the relative standard deviations (RSDs) for 10 pM target miRNA were less than 3.7%. This work promises a potential ultrasensitive ICP-MS bioassay of multiplex miRNA biomarkers for clinical serum diagnosis.

Effect of point defects on acetylene hydrogenation reaction over Ni(111) surface: a density functional theory study.

Density functional theory (DFT) calculations are carried out to investigate the effect of point defects on acetylene hydrogenation reaction over Ni(111) surface with three different defect concentrations (DC = 0.0500, 0.0625, and 0.0833), compared with the perfect Ni(111) surface. The adsorptions of C2 species and H atoms and the mechanism of acetylene hydrogenation via the ethylene pathway are systematically analyzed. The results indicate that the existence of defects will make C2 species and H atoms more inclined to adsorb near the defects. Introducing an appropriate amount of point defect concentration can enhance the catalytic activity and ethylene selectivity of Ni. In this work, DC = 0.0625 Ni(111) surface has the highest catalytic activity and selectivity of ethylene. This work provides useful theoretical information on the effect of defects on acetylene hydrogenation and is helpful for the design of Ni and related metal catalysts with defects.

Anion exchange behavior of MIIAl layered double hydroxides: a molecular dynamics and DFT study.

The ion exchange reaction has been extensively used in the field of synthesis of functionalized supramolecular materials such as layered double hydroxides (LDHs), ion-embedded batteries, sewage disposal and so on. In this work, the factors influencing the anion exchange behavior in the LDH gallery, such as the exchange domain, the exchange order, the driving force, and the diffusion of the anions, are investigated systematically using molecular dynamics (MD) simulations and density functional theory (DFT) methods in view of both thermodynamics and dynamics. 159 models of MIIRAl-A-LDHs (MII = Mg, Ni, Zn; R = 1.4-8, A = OH-, Cl-, Br-, NO3-, HCOO-, C6H5SO3-, CO32-, SO42-, and PO43-, respectively) are calculated. The results reveal that the anion exchange domain (interlayer distance) in LDHs is determined not only by the size and their arrangement modes of the guest anions, but also by the charges the anions carry. The relative binding energies of different anions and the Gibbs free energy changes of the anion exchange reactions in LDHs decrease in the order of PO43- > CO32- > SO42- > OH- > Cl- > Br- > HCOO- > NO3- > C6H5SO3-, which is in accordance with the experimental anion exchange order. The stronger the hydrogen bonding between the anion and the host, the larger the charge transfer, and the smaller the electronegativity of the anion, the more difficult it is for the anion to be exchanged out from LDH interlayer. In addition, for the anions with the same charges, the relative binding energy is linearly well correlated with the interlayer spacing. By analyzing the contribution of each energetic item comprising the total potential energy, it is found that the major driving force of anion exchange is the electrostatic force. The diffusion coefficient (D) along the c direction is nearly equal to zero, suggesting that the diffusion of anions occurs mainly in the ab plane of the LDH cell. It also can be inferred that when the cell parameter c < 24.0 Å, the anion exchange order is mainly determined by the thermodynamic factors, whereas when c > 24.0 Å, both the thermodynamic and the dynamic factors cast the same effect on the anion exchange behavior. This work provides an in-depth understanding of the anion exchange behavior, and is helpful guidance for the design and synthesis of functionalized guest anion intercalated LDHs and related materials using the anion-exchange method.

Heterogeneity of adult masseter muscle satellite cells with cardiomyocyte differentiation potential.

Although resident cardiac stem cells have been reported, regeneration of functional cardiomyocytes (CMs) remains a challenge. The present study identifies an alternative progenitor source for CM regeneration without the need for genetic manipulation or invasive heart biopsy procedures. Unlike limb skeletal muscles, masseter muscles (MM) in the mouse head are developed from Nkx2-5 mesodermal progenitors. Adult masseter muscle satellite cells (MMSCs) display heterogeneity in developmental origin and cell phenotypes. The heterogeneous MMSCs that can be characterized by cell sorting based on stem cell antigen-1 (Sca1) show different lineage potential. While cardiogenic potential is preserved in Sca1+ MMSCs as shown by expression of cardiac progenitor genes (including Nkx2-5), skeletal myogenic capacity is maintained in Sca1- MMSCs with Pax7 expression. Sca1+ MMSC-derived beating cells express cardiac genes and exhibit CM-like morphology. Electrophysiological properties of MMSC-derived CMs are demonstrated by calcium transients and action potentials. These findings show that MMSCs could serve as a novel cell source for cardiomyocyte replacement.

Association of Fucosyltransferase 2 Gene Variant with Inflammatory Bowel Diseases: A Meta-Analysis.

BACKGROUND Ulcerative colitis (UC) and Crohn's disease (CD) are the 2 main type of inflammatory bowel diseases (IBDs). Several studies have been conducted to investigate the association of fucosyltransferase 2 gene (rs601338) variant with UC and CD, but the results were inconsistent. Here, we performed a meta-analysis to clarify this issue based on a relatively larger sample size. MATERIAL AND METHODS A systematic literature search was conducted in PubMed, Embase, CNKI, and Chinese Wangfang databases up to 31 May 2018. Meta results were synthesized by using crude odds ratio with 95% confidence interval. Heterogeneity, sensitivity analysis, subgroup analysis, and publication bias were assessed using STATA 11.0 software. RESULTS A total of 8 relevant studies including 3874 IBDs patients (1872 UC cases, 2002 CD cases) and 5445 controls were included for meta-analysis. We found a significant association between rs601338 A allele and risk of IBDs in the Chinese population (OR=2.35, 95%CI=1.66~3.34, P=0.001), but not in whites. Stratified by disease type, we found a significant association between rs601338 polymorphism with CD and UC in the Chinese population, but not in the white population. In addition, funnel plot and Egger's linear regression test suggests no publication bias in all genetic models. CONCLUSIONS Fucosyltransferase 2 gene (rs601338) polymorphism is associated with susceptibility to IBD, UC, and CD in the Chinese population, but these results might not be generalizable to other ethnic populations. Further well-designed studies are needed to confirm these findings.

Unilateral visual impairment in a patient undergoing chemotherapy: a case report and clinical findings.

BACKGROUND: Visual impairment occurred as an infrequent form of chemotherapeutic toxicity and was often underestimated despite of several reports. We described a case of acute unilateral visual impairment after one cycle of intravenous chemotherapy of a normal dose, aiming at raising attention to chemotherapy-induced ocular toxicity. CASE PRESENTATION: The patient developed a progressive vision loss in the right eye during the chemotherapy. After one cycle of intravenous chemotherapy, her visual acuity decreased by 0.6 in the right eye (VOD = 0.4) compared to the previous value of 1.0 (VOD = 1.0). No evidence of ocular infiltration was observed from the cerebral magnetic resonance imaging (MRI). During her follow-up period, we documented the ophthalmologic examinations including visual acuity, visual field (VF), visual evoked potential (VEP), electroretinogram (ERG), fundus photograph (FP), fundus fluorescein angiography (FFA) and optical coherence tomography (OCT). Ophthalmoscope examination and fundus photograph showed optic disc edema, fuzzy boundary and linear hemorrhages in her right eye. Fundus fluorescein angiography (FFA) revealed capillary underdevelopment at the nasal and superior temporal area of the optic disc in the early phase and capillary fluorescein leakage in the late phase. The result of VEP test suggested the impaired function of the optic nerve. Thus, a diagnosis of nonarteritic anterior ischemic optic neuropathy (NAION) was made by the ophthalmologist according to these results. The patient was prescribed prednisone combined with neuroprotective drugs, which did not work. After the cessation of chemotherapy, her impaired vision gradually recovered. CONCLUSIONS: This is the first reported case of acute visual impairment in a patient who underwent chemotherapy of a normal dose. It is indicated that while receiving benefits from chemotherapy, cancer patients simultaneously suffer from the risk of vision loss.