Newly observed low-lying Ω = 1 state of PbO.

High-resolution spectroscopy of lead monoxide was performed in a range of 22 400-25 300 cm-1. A new Ω = 1 state located between the a1 and A0+ states was observed, and it is labeled c1. Spectroscopic constants, including the hyperfine interaction coefficient, were determined for the a1 and c1 states. The vibrational levels of these two electronic states are located closely to each other, and the interaction between them causes gradual exchange of electronic state properties in our observation wave number range. Our observation poses a question for the band assignment for the b0- state, which has some resemblance with this c1 state.

Genetically Modified Rice Is Associated with Hunger, Health, and Climate Resilience.

While nearly one in nine people in the world deals with hunger, one in eight has obesity, and all face the threat of climate change. The production of rice, an important cereal crop and staple food for most of the world's population, faces challenges due to climate change, the increasing global population, and the simultaneous prevalence of hunger and obesity worldwide. These issues could be addressed at least in part by genetically modified rice. Genetic engineering has greatly developed over the century. Genetically modified rice has been approved by the ISAAA's GM approval database as safe for human consumption. The aim behind the development of this rice is to improve the crop yield, nutritional value, and food safety of rice grains. This review article provides a summary of the research data on genetically modified rice and its potential role in improving the double burden of malnutrition, primarily through increasing nutritional quality as well as grain size and yield. It also reviews the potential health benefits of certain bioactive components generated in genetically modified rice. Furthermore, this article discusses potential solutions to these challenges, including the use of genetically modified crops and the identification of quantitative trait loci involved in grain weight and nutritional quality. Specifically, a quantitative trait locus called grain weight on chromosome 6 has been identified, which was amplified by the Kasa allele, resulting in a substantial increase in grain weight and brown grain. An overexpressing a specific gene in rice, Oryza sativa plasma membrane H+-ATPase1, was observed to improve the absorption and assimilation of ammonium in the roots, as well as enhance stomatal opening and photosynthesis rate in the leaves under light exposure. Cloning research has also enabled the identification of several underlying quantitative trait loci involved in grain weight and nutritional quality. Finally, this article discusses the increasing threats of climate change such as methane-nitrous oxide emissions and global warming, and how they may be significantly improved by genetically modified rice through modifying a water-management technique. Taken together, this comprehensive review will be of particular importance to the field of bioactive components of cereal grains and food industries trying to produce high-quality functional cereal foods through genetic engineering.

Identification of mild cognitive impairment subtypes predicting conversion to Alzheimer's disease using multimodal data.

Mild cognitive impairment (MCI) is a high-risk condition for conversion to Alzheimer's disease (AD) dementia. However, individuals with MCI show heterogeneous patterns of pathology and conversion to AD dementia. Thus, detailed subtyping of MCI subjects and accurate prediction of the patients in whom MCI will convert to AD dementia is critical for identifying at-risk populations and the underlying biological features. To this end, we developed a model that simultaneously subtypes MCI subjects and predicts conversion to AD and performed an analysis of the underlying biological characteristics of each subtype. In particular, a heterogeneous mixture learning (HML) method was used to build a decision tree-based model based on multimodal data, including cerebrospinal fluid (CSF) biomarker data, structural magnetic resonance imaging (MRI) data, APOE genotype data, and age at examination. The HML model showed an average F1 score of 0.721, which was comparable to the random forest method and had significantly more predictive accuracy than the CART method. The HML-generated decision tree was also used to classify-five subtypes of MCI. Each MCI subtype was characterized in terms of the degree of abnormality in CSF biomarkers, brain atrophy, and cognitive decline. The five subtypes of MCI were further categorized into three groups: one subtype with low conversion rates (similar to cognitively normal subjects); three subtypes with moderate conversion rates; and one subtype with high conversion rates (similar to AD dementia patients). The subtypes with moderate conversion rates were subsequently separated into a group with CSF biomarker abnormalities and a group with brain atrophy. The subtypes identified in this study exhibited varying MCI-to-AD conversion rates and differing biological profiles.

Rapid and sensitive SARS-CoV-2 detection using a homogeneous fluorescent immunosensor Quenchbody with crowding agents.

Antigen tests for SARS-CoV-2 are widely used by the public during the ongoing COVID-19 pandemic, which demonstrates the societal impact of homogeneous immunosensor-related technologies. In this study, we used the PM Q-probe and Quenchbody technologies to develop a SARS-CoV-2 nucleocapsid protein (N protein) homogeneous immunosensor based on a human anti-N protein antibody. For the first time, we uncovered the crowding agent's role in improving the performance of the double-labeled Quenchbody, and the possible mechanisms behind this improvement are discussed. The 5% polyethylene glycol 6000 significantly improved both the response speed and sensitivity of SARS-CoV-2 Quenchbodies. The calculated limit of detection for recombinant N protein was 191 pM (9 ng mL-1) within 15 min of incubation, which was 9- to 10-fold lower than the assay without adding crowding agent. We also validated the developed immunosensor in a point-of-care test by measuring specimens from COVID-19-positive patients using a compact tube fluorometer. In brief, this work shows the feasibility of Quenchbody homogeneous immunosensors as rapid and cost-efficient tools for the diagnosis and high-throughput analysis of swab samples in large-scale monitoring and epidemiological studies of COVID-19 or other emerging infectious diseases.

A heterozygous LAMA5 variant may contribute to slowly progressive, vinculin-enhanced familial FSGS and pulmonary defects.

The LAMA5 gene encodes laminin α5, an indispensable component of glomerular basement membrane and other types of basement membrane. A homozygous pathological variant in LAMA5 is known to cause a systemic developmental syndrome including glomerulopathy. However, the roles of heterozygous LAMA5 gene variants in human renal and systemic diseases have remained unclear. We performed whole-exome sequencing analyses of a family with slowly progressive nephropathy associated with hereditary focal segmental glomerulosclerosis, and we identified what we believe to be a novel probable pathogenic variant of LAMA5, NP_005551.3:p.Val3687Met. In vitro analyses revealed cell type-dependent changes in secretion of variant laminin α5 laminin globular 4-5 (LG4-5) domain. Heterozygous and homozygous knockin mice with a corresponding variant of human LAMA5, p.Val3687Met, developed focal segmental glomerulosclerosis-like pathology with reduced laminin α5 and increased glomerular vinculin levels, which suggested that impaired cell adhesion may underlie this glomerulopathy. We also identified pulmonary defects such as bronchial deformity and alveolar dilation. Reexaminations of the family revealed phenotypes compatible with reduced laminin α5 and increased vinculin levels in affected tissues. Thus, the heterozygous p.Val3687Met variant may cause a new syndromic nephropathy with focal segmental glomerulosclerosis through possibly defective secretion of laminin α5. Enhanced vinculin may be a useful disease marker.

Protein-bound sialic acid in saliva contributes directly to salivary anti-influenza virus activity.

The oral cavity is an entrance for respiratory viruses, such as influenza. Recently, saliva has been shown to exert both antimicrobial and antiviral activities. Thus, saliva may be a biological factor that contributes to the prevention of influenza infection. However, the actual salivary anti-influenza A virus (IAV) activity in individuals and its determinant factors are unknown. By assessing individual variations in salivary anti-IAV activity in 92 people using an established new high-throughput system in this study, we found that the anti-IAV activity varied widely between individuals and showed a significant positive correlation with protein-bound sialic acid (BSA) level (ρ = 0.473; p < 0.001). Furthermore, the anti-IAV activity of saliva with enzymatically reduced BSA content was significantly lower. These results indicate that BSA is a direct regulator of salivary anti-IAV activity and is a determinant of individual differences. Additionally, after comparing the anti-IAV activity across the groups by age, anti-IAV activity in young people (aged 5-19 years) were lower than in adults aged 20-59 years and elderly people aged 60-79 years. Our study suggests that BSA levels in saliva may be important in preventing influenza infection.

Precise equilibrium structure determination of thiophene (c-C4H4S) by rotational spectroscopy-Structure of a five-membered heterocycle containing a third-row atom.

The rotational spectrum of thiophene (c-C4H4S) has been collected between 8 and 360 GHz. Samples of varying deuterium-enrichment were synthesized to yield all possible deuterium-substituted isotopologues of thiophene. A total of 26 isotopologues have been measured and least-squares fit using A- and S-reduced distorted-rotor Hamiltonians in the Ir representation. The resultant rotational constants (A0, B0, and C0) from each reduction were converted to determinable constants (A″, B″, and C″) to remove the impact of centrifugal distortion. The computed vibrational and electron mass corrections [CCSD(T)/cc-pCVTZ] were applied to the determinable constants to obtain semi-experimental equilibrium rotational constants (Ae, Be, and Ce) for 24 isotopologues. A precise semi-experimental equilibrium (re SE) structure has been achieved from a least-squares fit of the equilibrium moments of inertia. The combination of the expanded isotopologue rotational data with high-level computational work establishes a precise re SE structure for this sulfur-containing heterocycle. The CCSD(T)/cc-pCV5Z structure has been obtained and corrected for the extrapolation to the complete basis set, electron correlation beyond CCSD(T), relativistic effects, and the diagonal Born-Oppenheimer correction. The precise re SE structure is compared to the resulting "best theoretical estimate" structure. Several of the best theoretical re structural parameters fall within the narrow statistical limits (2σ) of the re SE results. The possible origin of the discrepancies for the computed parameters that fall outside the statistical uncertainties is discussed.

Genome-wide copy number variation analysis of hepatitis B infection in a Japanese population.

Genome-wide association studies have been performed to identify common genetic variants associated with hepatitis B (HB). However, little is known about copy number variations (CNVs) in HB. In this study, we performed a genome-wide CNV analysis between 1830 healthy controls and 1031 patients with HB infection after quality control. Using signal calling by the Axiom Analysis Suite and CNV detection by PennCNV software, we obtained a total of 4494 CNVs across all individuals. The genes with CNVs that were found only in the HB patients were associated with the immune system, such as antigen processing. A gene-level CNV association test revealed statistically significant CNVs in the contactin 6 (CNTN6) gene. Moreover, we also performed gene-level CNV association tests in disease subgroups, including hepatocellular carcinoma patients, liver cirrhosis patients, and HBV carriers, including asymptomatic carriers and patients with HBV-derived chronic hepatitis. Our findings from germline cells suggested that patient-specific CNVs may be inherent genetic risk factors for HB.

Cyclosporine A Treatment of Proteinuria in a New Case of MAFB-Associated Glomerulopathy without Extrarenal Involvement: A Case Report.

The MAFB gene encodes an important basic leucine zipper transcription factor that functions in glomerular podocytes, macrophages, and osteoclasts. Recently, MAFB was identified as the gene that was responsible for causing nephropathy with focal segmental glomerulosclerosis (FSGS) with multicentric carpotarsal osteolysis (MCTO) or Duane retraction syndrome (DRS). Here, we describe a patient with nephropathy associated with FSGS who exhibited a novel stop-gain variant in the MAFB gene (NM_005461:c.590C>A (p.Ser197Ter)). The patient's father exhibited proteinuria with FSGS with possible DRS, whereas the patient exhibited nephropathy with FSGS and nearly normal eye movement and hearing function, as well as intact bone structure in the extremities. Conventional oral steroids or immunosuppressive drugs have not demonstrated effectiveness for patients with nephropathy who exhibit pathogenic variants in MAFB, except for a patient with nephropathy with FSGS and MCTO who experienced attenuated proteinuria within the subnephrotic range in response to cyclosporine A (CyA) treatment for at least 4 years. Thus, we attempted administration of CyA in our patient. Unexpectedly, the patient demonstrated good and rapid responses to CyA, including a partial reduction in proteinuria from approximately 2.0 g/g Cr to proteinuria within the subnephrotic range (0.27 g/g Cr) after 13 months of observation. Our findings suggest that CyA may be a suitable treatment option for patients with nephropathy with FSGS who exhibit pathogenic MAFB variants.

Development of a mugineic acid family phytosiderophore analog as an iron fertilizer.

Iron (Fe) is an essential nutrient, but is poorly bioavailable because of its low solubility in alkaline soils; this leads to reduced agricultural productivity. To overcome this problem, we first showed that the soil application of synthetic 2'-deoxymugineic acid, a natural phytosiderophore from the Poaceae, can recover Fe deficiency in rice grown in calcareous soil. However, the high cost and poor stability of synthetic 2'-deoxymugineic acid preclude its agricultural use. In this work, we develop a more stable and less expensive analog, proline-2'-deoxymugineic acid, and demonstrate its practical synthesis and transport of its Fe-chelated form across the plasma membrane by Fe(III)•2'-deoxymugineic acid transporters. Possibility of its use as an iron fertilizer on alkaline soils is supported by promotion of rice growth in a calcareous soil by soil application of metal free proline-2'-deoxymugineic acid.

A quantum thermometric sensing and analysis system using fluorescent nanodiamonds for the evaluation of living stem cell functions according to intracellular temperature.

Intracellular thermometry techniques play an important role in elucidating the relationship between the intracellular temperature and stem cell functions. However, there have been few reports on thermometry techniques that can detect the intracellular temperature of cells during several days of incubation. In this study, we developed a novel quantum thermometric sensing and analysis system (QTAS) using fluorescent nanodiamonds (FNDs). FNDs could label adipose tissue-derived stem cells (ASCs) at high efficiency with 24 h of incubation, and no cytotoxicity was observed in ASCs labeled with less than 500 µg mL-1 of FNDs. The peak of FNDs was confirmed at approximately 2.87 GHz with the characteristic fluorescence spectra of NV centers that could be optically detected (optically detected magnetic resonance [ODMR]). The ODMR peak clearly shifted to the high-frequency side as the temperature decreased and gave a mean temperature dependence of -(77.6 ± 11.0) kHz °C-1, thus the intracellular temperature of living ASCs during several days of culturing could be precisely measured using the QTAS. Moreover, the intracellular temperature was found to influence the production of growth factors and the degree of differentiation into adipocytes and osteocytes. These data suggest that the QTAS can be used to investigate the relationship between intracellular temperature and cellular functions.

Family history of diabetes in both parents is strongly associated with impaired residual ß-cell function in Japanese type 2 diabetes patients.

AIMS/INTRODUCTION: The objective of the present study was to clarify the association of the type and number of first-degree family history of diabetes (FHD) with the clinical characteristics, especially with residual ß-cell function, in type 2 diabetes patients. MATERIALS AND METHODS: A total of 1,131 type 2 diabetes patients were recruited and divided into four groups according to FHD information as follows: (i) patients without FHD (FHD-); (ii) those with at least one sibling who had diabetes without parental diabetes (FHD+); (iii) those with one parent (FHD++); or (iv) those with both parents (FHD+++) who had diabetes with or without a sibling with diabetes. RESULTS: The percentages of the FHD-, FHD+, FHD++ and FHD+++ groups were 49.4%, 13.4%, 34.0% and 3.2%, respectively. Patients in the FHD++ and FHD+++ groups were significantly younger at the time of diabetes diagnosis (P < 0.001) than those in the FHD- and FHD+ groups, even after adjusting for confounding factors. In addition, the levels of insulin secretion were significantly lower in the patients in the FHD+, FHD++ and FHD+++ groups than those in the FHD- group (P < 0.05) after adjusting for confounding factors, and the patients in the FHD+++ group presented with the lowest levels of insulin secretion among the four groups. CONCLUSIONS: Our results showed that in type 2 diabetes patients, the degree of the associations between FHD and clinical characteristics differs according to the number and the type of FHD. In particular, FHD in both parents is most strongly associated with impaired residual ß-cell function.

PDIP38/PolDIP2 controls the DNA damage tolerance pathways by increasing the relative usage of translesion DNA synthesis over template switching.

Replicative DNA polymerases are frequently stalled at damaged template strands. Stalled replication forks are restored by the DNA damage tolerance (DDT) pathways, error-prone translesion DNA synthesis (TLS) to cope with excessive DNA damage, and error-free template switching (TS) by homologous DNA recombination. PDIP38 (Pol-delta interacting protein of 38 kDa), also called Pol δ-interacting protein 2 (PolDIP2), physically associates with TLS DNA polymerases, polymerase η (Polη), Polλ, and PrimPol, and activates them in vitro. It remains unclear whether PDIP38 promotes TLS in vivo, since no method allows for measuring individual TLS events in mammalian cells. We disrupted the PDIP38 gene, generating PDIP38-/- cells from the chicken DT40 and human TK6 B cell lines. These PDIP38-/- cells did not show a significant sensitivity to either UV or H2O2, a phenotype not seen in any TLS-polymerase-deficient DT40 or TK6 mutants. DT40 provides a unique opportunity of examining individual TLS and TS events by the nucleotide sequence analysis of the immunoglobulin variable (Ig V) gene as the cells continuously diversify Ig V by TLS (non-templated Ig V hypermutation) and TS (Ig gene conversion) during in vitro culture. PDIP38-/- cells showed a shift in Ig V diversification from TLS to TS. We measured the relative usage of TLS and TS in TK6 cells at a chemically synthesized UV damage (CPD) integrated into genomic DNA. The loss of PDIP38 also caused an increase in the relative usage of TS. The number of UV-induced sister chromatid exchanges, TS events associated with crossover, was increased a few times in PDIP38-/- human and chicken cells. Collectively, the loss of PDIP38 consistently causes a shift in DDT from TLS to TS without enhancing cellular sensitivity to DNA damage. We propose that PDIP38 controls the relative usage of TLS and TS increasing usage of TLS without changing the overall capability of DDT.

Subjective Household Economic Status and Obesity in Toddlers: A Cross-Sectional Study of Daycare Centers in Japan.

BACKGROUND: Although lower household economic status is known to be a risk factor for obesity among school-age children, such an association among toddlers remains unclear. The present study investigated the association between household economic status and obesity in toddlers. DESIGN: We conducted a cross-sectional study of children aged 4 years attending daycare centers in Japan. Information on subjective household economic status ["affluent", "neither", "less affluent", or "non-affluent"] was collected via questionnaire from the children's guardians in 2015. Based on measured values of height and weight, obesity was defined using the International Obesity Task Force cut-offs of overweight (BMI ≥17.47 for boys and ≥17.19 for girls). We used the logistic regression model to investigate the association between household economic status and obesity. RESULTS: Among 1,848 respondents, the prevalence of obesity was 6.8%. Non-affluent household economic status was associated with a significantly higher probability of obesity in toddlers; the multivariate adjusted odds ratio for "non-affluent" households was 2.31 (95% confidence interval, 1.23-4.33) compared with "affluent" households. CONCLUSION: Perception of non-affluent economic status by the guardian was associated with a higher probability of toddler obesity. This result suggests that non-affluent household economic status is associated with obesity in toddlers.

Identification of genetic risk factors of aggressive periodontitis using genomewide association studies in association with those of chronic periodontitis.

To identify the genetic risk factors for aggressive periodontitis (AgP), it is important to understand the progression and pathogenesis of AgP. The purpose of this review was to summarize the genetic risk factors for AgP identified through a case-control genomewide association study (GWAS) and replication study. The initial studies to identify novel AgP risk factors were potentially biased because they relied on previous studies. To overcome this kind of issue, an unbiased GWAS strategy was introduced to identify genetic risk factors for various diseases. Currently, three genes glycosyltransferase 6 domain containing 1 (GLT6D1), defensin α1 and α3 (DEFA1A3), and sialic acid-binding Ig-like lectin 5 (SIGLEC5) that reach the threshold for genomewide significance have been identified as genetic risk factors for AgP through a case-control GWAS.

Analysis of an ADTKD family with a novel frameshift mutation in MUC1 reveals characteristic features of mutant MUC1 protein.

BACKGROUND: Medullary cystic kidney disease Type 1 is an autosomal dominant tubulointerstitial kidney disease (ADTKD). Recently, mucin 1 (MUC1) was identified as a causal gene of medullary cystic kidney disease (ADTKD-MUC1). However, the MUC1 mutation was found to be a single cytosine insertion in a single copy of the GC-rich variable number of tandem repeats (VNTRs), which are very difficult to analyze by next-generation sequencing. To date, other mutations have not been detected in ADTKD-MUC1, and the mutant MUC1 protein has not been analyzed because of the difficulty of genetically modifying the VNTR sequence. METHODS: We conducted whole-exome analyses of an ADTKD family by next-generation sequencing. We also performed histopathological analyses of a renal biopsy from a pedigree family member. We constructed a mutant protein expression vector based on the patient genome sequence and characterized the nature of the mutant protein. RESULTS: We found a novel frameshift mutation before the VNTR in the MUC1 gene. The resulting mutant MUC1 protein had a very similar amino acid sequence and predicted 3D structure to the previously reported mutant protein. Notably, the recombinant mutant MUC1 protein was trapped in the cytoplasm and appeared to self-aggregate. The patient native mutant protein was also found in urine exosomes. CONCLUSIONS: This novel frameshift mutation in the MUC1 gene and consequent mutant protein may contribute to the future discovery of the pathophysiology of ADTKD-MUC1. The mutant MUC1 protein in urine exosomes may be used for non-DNA-related diagnosis.

HDR-del: A tool based on Hamming distance for prioritizing pathogenic chromosomal deletions in exome sequencing.

High-density oligonucleotide arrays have widely been used to detect pathogenic chromosomal deletions. In addition to high-density oligonucleotide arrays, programs using whole-exome sequencing have become available for estimating copy-number variations using depth of coverage. Here, we propose a new statistical method, HDR-del, to prioritize pathogenic chromosomal deletions based on Hamming distance in exome sequencing. In vcf (variant call format) files generated from exome sequencing, hemizygous chromosomal deletion regions lack heterozygous variants and lead to apparent long runs of homozygosity (ROH). In our Hamming distance ratio (HDR)-del approach, we calculate the "difference" in heterozygous status between an affected individual and control individuals using the HDR over all candidate chromosomal deletion regions defined as ROH longer than 1Mbp. Using a suitable test statistic, which is expected to be large for a true pathogenic deletion region, we prioritize candidate chromosomal deletion regions based on this statistic. In our approach, we were able to considerably narrow down true pathogenic chromosomal deletion regions, which were confirmed by high-density oligonucleotide arrays in four mitochondrial disease patients. Our HDR-del approach represents an easy method for detecting chromosomal deletions.

Identification of core gene networks and hub genes associated with progression of non-alcoholic fatty liver disease by RNA sequencing.

AIM: Non-alcoholic fatty liver disease (NAFLD) progresses because of the interaction between numerous genes. Thus, we carried out a weighted gene coexpression network analysis to identify core gene networks and key genes associated with NAFLD progression. METHODS: We enrolled 39 patients with mild NAFLD (fibrosis stages 0-2) and 21 with advanced NAFLD (fibrosis stages 3-4). Total RNA was extracted from frozen liver biopsies, and sequenced to capture a large dynamic range of expression levels. RESULTS: A total of 1777 genes differentially expressed between mild and advanced NAFLD (q-value <0.05) clustered into four modules. One module was enriched for genes that encode cell surface or extracellular matrix proteins, and are involved in cell adhesion, proliferation, and signaling. This module formed a scale-free network containing four hub genes (PAPLN, LBH, DPYSL3, and JAG1) overexpressed in advanced NAFLD. PAPLN is a component of the extracellular matrix, LBH and DPYSL3 are reported to be tumor suppressors, and JAG1 is tumorigenic. Another module formed a random network, and was enriched for genes that accumulate in the mitochondria. These genes were downregulated in advanced NAFLD, reflecting impaired mitochondrial function. However, the other two modules did not form unambiguous networks. KEGG analysis indicated that 71 differentially expressed genes were involved in "pathways in cancer". Strikingly, expression of half of all differentially expressed genes was inversely correlated with methylation of CpG sites (q-value <0.05). Among clinical parameters, serum type IV collagen 7 s was most strongly associated with the epigenetic status in NAFLD. CONCLUSIONS: Newly identified core gene networks suggest that the NAFLD liver undergoes mitochondrial dysfunction and fibrosis, and acquires tumorigenic potential epigenetically. Our data provide novel insights into the pathology and etiology of NAFLD progression, and identify potential targets for diagnosis and treatment.

Spinal cord infarction following epidural and general anesthesia: a case report.

BACKGROUND: Epidural anesthesia is widely used for postoperative analgesia and rarely causes permanent neurological complications. We report a case of paraplegia following abdominal surgery under combined epidural/general anesthesia. CASE PRESENTATION: A 75-year-old woman underwent a scheduled abdominal total hysterectomy and bilateral salpingo-oophorectomy for suspected endometrial cancer. In the operating room, an epidural catheter was inserted at T11/12 while the patient was conscious. The needle entered smoothly, with no observed bleeding, paresthesia, or pain, and general anesthesia was induced. During surgery, 4 mL of 0.25% levobupivacaine and 0.1 mg of fentanyl were administered via the epidural catheter, and a solution of 2.5 µg/mL fentanyl and 0.2% levobupivacaine was continuously infused at 4 mL/h for postoperative analgesia. The patient promptly regained consciousness and could move her bilateral lower extremities without difficulty upon leaving the operating room. During the first postoperative night, she complained of an absence of sensation and weakness in the lower extremities. By the morning of the second postoperative day, she had developed paralysis and sensory losses associated with touch, temperature, pinprick, and vibration below T5. The epidural infusion was stopped. Magnetic resonance imaging (MRI) revealed a hyperintense area of the thoracic cord from T8 to T11, and spinal cord infarction was suspected. Ossification of the yellow spinal ligaments between T11 and T12, resulting in thoracic canal stenosis and thoracic spinal cord compression, were observed. Notably, the epidural catheter was inserted at the same site where the thoracic canal stenosis was present. CONCLUSIONS: Permanent neurological complications of epidural anesthesia are rare. Studies of neurological complications after epidural/spinal anesthesia have noted the possibility of spinal anomalies, such as lumbar stenosis, in relation to neurological complications after epidural/spinal anesthesia. In this case, the onset of spinal cord infarction may have occurred coincidentally with catheter insertion into the site of existing spinal stenosis. Therefore, it is important to evaluate lower extremity symptoms and consider spinal disease before administering epidural anesthesia. Spinal cord infarction may be prevented by preoperatively identifying spinal lesions using computed tomography or MRI in cases of suspected spinal disease.