Strenuous expression of porcine epidemic diarrhea virus ORF3 protein suggests host resistance.

Porcine epidemic diarrhea virus is attenuated upon adaptation to cell culture. Exclusively genomic mutations have been traced to the ORF3 gene of the laboratory strains. Previous attempts to express the protein were unsuccessful. We sought to express the ORF3 protein in both mammalian and bacteria cells as a prerequisite for investigation of the protein's role. For prokaryotic expression, two vector systems, pET28-a(+) and pGEX-4T-1 were constructed and expressed in Escherichia coli cells. For eukaryotic analyses, ORF3/pEGFP-C1 vector constructs were expressed in human embryonic, green monkey kidney and mouse fibrous cells. Intriguingly, there was minimal expression of the ORF3 gene. Following a documented hint that truncated ORF3 revealed higher expression, ORF3 gene was truncated. The simple modular architecture research tool analysis predicted two transmembrane domains between amino acid (aa) 41-63 and aa 76-98. Consequently, we generated two fragments; ORF-N (aa 1-98) inclusive of transmembrane domains and ORF3-C (aa 99-224). These truncated sequences were constructed as the whole gene here referred to as ORF3 wild type (wt). Coomassie blue stained gels revealed bands of ORF3-C expressed as a fusion protein of 17.5 and 39 kDa in pET28-a(+) and pGEX-4T-1 vectors, respectively. In contrast, ORF3-N was not. Additionally, ORF3-N induction decreased total cellular proteins suggesting inhibition of protein synthesis or metabolism. Solubility tests carried out at 30 °C, 25 °C and 18 °C showed that ORF3 formed inclusion bodies. Similar findings were observed in mammalian cells. Noteworthy, morphological distortions appeared in mammalian cells expressing ORF3 protein or its truncated mutants suggesting significance in host viability.

MLPH is a novel adipogenic factor controlling redox homeostasis to inhibit lipid peroxidation in adipocytes.

Abnormal adipose tissue formation is associated with metabolic disorders such as obesity, diabetes, and liver and cardiovascular diseases. Thus, identifying the novel factors that control adipogenesis is crucial for understanding these conditions and developing targeted treatments. In this study, we identified the melanosome-related factor MLPH as a novel adipogenic factor. MLPH was induced during the adipogenesis of 3T3-L1 cells and human mesenchymal stem cells. Although MLPH did not affect lipid metabolism, such as lipogenesis or lipolysis, adipogenesis was severely impaired by MLPH depletion. We observed that MLPH prevented excess reactive oxygen species (ROS) accumulation and lipid peroxidation during adipogenesis and in mature adipocytes. In addition, increased MLPH expression was observed under cirrhotic conditions in liver cancer cells and its overexpression also reduced ROS and lipid peroxidation. Our findings demonstrate that MLPH is a novel adipogenic factor that maintains redox homeostasis by preventing lipid peroxidation and ROS accumulation, which could lead to metabolic diseases.

Imaging the optic nerve with optical coherence tomography.

Optical coherence tomography (OCT) is a non-invasive imaging technology, which may be used to generate in vivo quantitative and qualitative measures of retinal structure. In terms of quantitative metrics, peripapillary retinal nerve fiber layer (pRNFL) thickness provides an indirect evaluation of axonal integrity within the optic nerve. Ganglion layer measures derived from macular scans indirectly reflect retinal ganglion cell status. Notably, ganglion layer indices are platform dependent and may include macular ganglion cell inner plexiform layer (mGCIPL), ganglion cell layer (GCL), and ganglion cell complex (GCC) analyses of thickness or volume. Interpreted together, pRNFL thickness and ganglion layer values can be used to diagnose optic neuropathies, monitor disease progression, and gauge response to therapeutic interventions for neuro-ophthalmic conditions. Qualitative assessments of the optic nerve head, using cross-sectional transverse axial, en face, and circular OCT imaging, may help distinguish papilledema from pseudopapilloedema, and identify outer retinal pathology. Innovations in OCT protocols and approaches including enhanced depth imaging (EDI), swept source (SS) techniques, and angiography (OCTA) may offer future insights regarding the potential pathogenesis of different optic neuropathies. Finally, recent developments in artificial intelligence (AI) utilizing OCT images may overcome longstanding challenges, which have plagued non-vision specialists who often struggle to perform reliable ophthalmoscopy. In this review, we aim to discuss the benefits and pitfalls of OCT, consider the practical applications of this technology in the assessment of optic neuropathies, and highlight scientific discoveries in the realm of optic nerve imaging that will ultimately change how neuro-ophthalmologists care for patients.

Treatment Outcome of Conjunctival Cyst Ablation by Pattern Scan Laser.

PURPOSE: To evaluate the effectiveness of conjunctival cyst ablation using pattern scan laser photoablation. METHODS: Ninety-four cases of symptomatic conjunctival cysts were included. After staining the surface of a conjunctival cyst with a dark-purple marker pen, an incision was made into the conjunctival cyst using a 26-gauge needle. Low-energy photoablation using 3 × 3 grids of spots was then applied around the incision site for a mean of 50 times. The laser spots were 400 µm in size, the power delivered ranged from 400 to 450 mW, and the duration of each laser pulse was 80 ms. RESULTS: During a mean follow-up period of 6.5 months (range 6-16 months), 84 cases of conjunctival cysts (89.4%) were successfully corrected by conducting either 1 or 2 laser sessions. The cyst was completely resolved after a single laser session in 74 cases (78.7%). There were 20 cases of recurrence, which involved fixed, thick, and large cysts. The conjunctival cyst recurred again after the second laser session in 2 of the 12 eyes in which the procedure was repeated. The remaining 8 cases were observed without additional treatment. No postoperative complications such as conjunctival scarring or persistent ocular irritation were observed. CONCLUSIONS: Pattern scan laser photoablation of a conjunctival cyst with the adjunctive use of cyst surface staining to increase the amount of thermal laser energy absorption is a simple and effective method for treating conjunctival cysts in an outpatient clinic.

Insights into the Pathogenesis and Development of Recombinant Japanese Encephalitis Virus Genotype 3 as a Vaccine.

Japanese encephalitis virus (JEV), a flavivirus transmitted by mosquitoes, has caused epidemics and severe neurological diseases in Asian countries. In this study, we developed a cDNA infectious clone, pBAC JYJEV3, of the JEV genotype 3 strain (EF571853.1) using a bacterial artificial chromosome (BAC) vector. The constructed infectious clone was transfected into Vero cells, where it exhibited infectivity and induced cytopathic effects akin to those of the parent virus. Confocal microscopy confirmed the expression of the JEV envelope protein. Comparative analysis of growth kinetics revealed similar replication dynamics between the parental and recombinant viruses, with peak titers observed 72 h post-infection (hpi). Furthermore, plaque assays demonstrated comparable plaque sizes and morphologies between the viruses. Cryo-electron microscopy confirmed the production of recombinant virus particles with a morphology identical to that of the parent virus. Immunization studies in mice using inactivated parental and recombinant viruses revealed robust IgG responses, with neutralizing antibody production increasing over time. These results showcase the successful generation and characterization of a recombinant JEV3 virus and provide a platform for further investigations into JEV pathogenesis and vaccine development.

Depletion of proteasome subunit PSMD1 induces cancer cell death via protein ubiquitination and DNA damage, irrespective of p53 status.

Hepatocellular carcinoma (HCC) is characterized by high incidence and fatality rates worldwide. In our exploration of prognostic factors in HCC, the 26s proteasome subunit, non-ATPase 1 (PSMD1) protein emerged as a significant contributor, demonstrating its potential as a therapeutic target in this aggressive cancer. PSMD1 is a subunit of the 19S regulatory particle in the 26S proteasome complex; the 19S particle controls the deubiquitination of ubiquitinated proteins, which are then degraded by the proteolytic activity of the complex. Proteasome-targeting in cancer therapy has received significant attention because of its practical application as an established anticancer agent. We investigated whether PSMD1 plays a critical role in cancer owing to its prognostic significance. PSMD1 depletion induced cell cycle arrest in G2/M phase, DNA damage and apoptosis of cancer cells, irrespective of the p53 status. PSMD1 depletion-mediated cell death was accompanied by an increase in overall protein ubiquitination. These phenotypes occurred exclusively in cancer cells, with no effects observed in normal cells. These findings indicate that PSMD1 depletion-mediated ubiquitination of cellular proteins induces cell cycle arrest and eventual death in cancer cells, emphasizing PSMD1 as a potential therapeutic target in HCC.

A one-step immunoassay based on switching peptides for diagnosis of porcine epidemic diarrhea virus (PEDV) using screened Fv-antibodies.

In this study, a one-step immunoassay for porcine epidemic diarrhea virus (PEDV) based on Fv-antibodies and switching peptides was developed, and the assay results of PEDV were obtained by just mixing samples without any further reaction or washing steps. The Fv-antibodies with binding affinity to the spike protein of PEDV were screened from the Fv-antibody library using the receptor-binding domain (RBD) of the spike protein as a screening probe. Screened Fv-antibodies with binding affinities to the RBD antigen were expressed, and the binding constants (KD) were calculated to be 83-142 nM. The one-step immunoassay for the detection of PEDV was configured as a displacement immunoassay using a fluorescence-labeled switching peptide. The one-step immunoassay based on switching peptides was performed using PEDV, and the limit of detection (LOD) values for PEDV detection were estimated to be Ct = 39.7-36.4. Compared with the LOD value for a conventional lateral flow immunoassay (Ct = 33.0), the one-step immunoassay showed a remarkably improved LOD for the detection of PEDV. Finally, the interaction between the screened Fv-antibodies and the PEDV RBD was investigated using docking simulations and compared with the amino acid sequences of the receptors on host cells, such as aminopeptidase N (APN) and angiotensin-converting enzyme-2 (ACE-2).

Anatomical Relationship between the Inferior Temporal Septum and the Temporal Branch of the Facial Nerve for Clinical Applications.

BACKGROUND: The inferior temporal septum (ITS) is a fibrous adhesion between the superficial temporal fascia and the superficial layer of the deep temporal fascia. This study identified detailed the anatomical relationship between the ITS and the temporal branch of the facial nerve (TBFN) for facial nerve preservation during temple interventions. METHODS: Among 33 Korean cadavers, 43 sides of TBFNs in temporal regions were dissected after identifying the ITS between the superficial temporal fascia and superficial layer of the deep temporal fascia through blunt dissection. The topography of the ITS and TBFN were investigated with reference to several facial landmarks. Regional relationships with the ITS and TBFN within the temporal fascial layers were histologically defined from five specimens. RESULTS: At the level of the inferior orbital margin by the tragion, the mean distances from the lateral canthus to the anterior and posterior branches of the TBFN were 5 and 6.2 cm, respectively. At the lateral canthus level, the mean distance from the lateral canthus to the posterior branch of the TBFN was similar to that to the ITS, at 5.5 cm. At the superior orbital margin level, the posterior branch of the TBFN ran cranial to the ITS adjacent to the frontotemporal region. The TBFN ran through the subsuperficial temporal fascia layer and the nerve fibers located cranially, and within the ITS meshwork in the upper temporal compartment. CONCLUSION: The area of caution during superficial temporal fascia interventions related to the TBFN was clearly identified in the upper temporal compartment, which is known to lack important structures.

Superimposition Study to Determine the Angular Arterial Distribution and Its Clinical Application.

BACKGROUND: The purpose of this study was to determine the distribution of the angular artery (AA) in the medial canthal area with the aim of defining an arterial course to prevent AA injury during facial surgery in this region. METHODS: The authors dissected 36 hemifaces of 18 cadavers. The horizontal distance from the vertical level through the medial canthus to the AAs was measured. The AA course of each specimen was then recorded, and all of them were then superimposed to determine the AA course. The diameter and depth of the AA around the medial canthal area were also investigated using ultrasonography on living subjects. RESULTS: The horizontal distances from the medial canthus level and 2 cm below the medial canthus were 9.0 ± 2.0 mm (mean ± SD) and 1.9 ± 2.4 mm, respectively. The superimposed image demonstrated that most of the AAs were present inside the vertical line through the medial canthus. Ultrasonography indicated that the AA was 2.3 ± 0.9 mm below the skin and 1.7 ± 0.3 mm in diameter. CONCLUSIONS: The AA course was relatively constant along the nasojugal fold. The AAs were most often present between the middle of the medial canthus and the facial midline, but were very scarce in both the medial and lateral thirds. Knowledge of the detailed course of the AA may help surgeons to avoid arterial injury and decrease the risk of surgical morbidities around the nasal root and medial canthal area.

HDAC-Specific Inhibitors Induce the Release of Porcine Epidemic Diarrhea Virus via the COPII-Coated Vesicles.

Porcine epidemic diarrhea virus (PEDV) is an alpha-coronavirus causing acute diarrhea and high mortality in neonatal suckling piglets, resulting in huge economic losses for the global swine industry. The replication, assembly and cell egression of PEDV, an enveloped RNA virus, are mediated via altered intracellular trafficking. The underlying mechanisms of PEDV secretion are poorly understood. In this study, we found that the histone deacetylase (HDAC)-specific inhibitors, trichostatin A (TSA) and sodium butyrate (NaB), facilitate the secretion of infectious PEDV particles without interfering with its assembly. We found that PEDV N protein and its replicative intermediate dsRNA colocalize with coat protein complex II (COPII)-coated vesicles. We also showed that the colocalization of PEDV and COPII is enhanced by the HDAC-specific inhibitors. In addition, ultrastructural analysis revealed that the HDAC-specific inhibitors promote COPII-coated vesicles carrying PEDV virions and the secretion of COPII-coated vesicles. Consistently, HDAC-specific inhibitors-induced PEDV particle secretion was abolished by Sec24B knockdown, implying that the HDAC-specific inhibitors-mediated COPII-coated vesicles are required for PEDV secretion. Taken together, our findings provide initial evidence suggesting that PEDV virions can assemble in the endoplasmic reticulum (ER) and bud off from the ER in the COPII-coated vesicles. HDAC-specific inhibitors promote PEDV release by hijacking the COPII-coated vesicles.

NADH elevation during chronic hypoxia leads to VHL-mediated HIF-1α degradation via SIRT1 inhibition.

BACKGROUND: Under conditions of hypoxia, cancer cells with hypoxia inducible factor-1α (HIF-1α) from heterogeneous tumor cells show greater aggression and progression in an effort to compensate for harsh environmental conditions. Extensive study on the stability of HIF-1α under conditions of acute hypoxia in cancer progression has been conducted, however, understanding of its involvement during the chronic phase is limited. METHODS: In this study, we investigated the effect of SIRT1 on HIF1 stability in a typical chronic hypoxic conditon that maintains cells for 24 h under hypoxia using Western blotting, co-IP, measurement of intracellular NAD + and NADH levels, semi-quantitative RT-PCR analysis, invasion assay, gene knockdown. RESULTS: Here we demonstrated that the high concentration of pyruvate in the medium, which can be easily overlooked, has an effect on the stability of HIF-1α. We also demonstrated that NADH functions as a signal for conveyance of HIF-1α degradation via the SIRT1 and VHL signaling pathway under conditions of chronic hypoxia, which in turn leads to attenuation of hypoxically strengthened invasion and angiogenic activities. A steep increase in the level of NADH occurs during chronic hypoxia, leading to upregulation of acetylation and degradation of HIF-1α via inactivation of SIRT1. Of particular interest, p300-mediated acetylation at lysine 709 of HIF-1α is recogonized by VHL, which leads to degradation of HIF-1α via ubiquitin/proteasome machinary under conditions of chronic hypoxia. In addition, we demonstrated that NADH-elevation-induced acetylation and subsequent degradation of HIF-1α was independent of proline hydroxylation. CONCLUSIONS: Our findings suggest a critical role of SIRT1 as a metabolic sensor in coordination of hypoxic status via regulation of HIF-1α stability. These results also demonstrate the involvement of VHL in degradation of HIF-1α through recognition of PHD-mediated hydroxylation in normoxia and p300-mediated HIF-1α acetylation in hypoxia.

Topography of the frontal branch of the facial nerve and its clinical implication for temporal direct browplasty.

Due to anatomic proximity to the surgical site, iatrogenic trauma to the frontal branch of the facial nerve (FbFN) with resultant brow paralysis is a recognized major complication of temporal direct browplasty. This study was aimed to elucidate the course of the FbFN in the area superolateral to the brow in order to facilitate safer temporal direct browplasty by preventing facial nerve injury. Forty-five hemifaces from 32 embalmed Korean cadavers were dissected. A horizontal line connecting the tragion to lateral canthus was established. Then, an oblique line passing through the lateral canthus and 45° to the horizontal line was used as reference line. The mean distance from the lateral canthus to the points where the FbFN cross the reference line was measured. The angle between the FbFN and reference line at the crossing points were also recorded. After crossing the zygomatic arch, FbFN continues in an anteriorly inclining curve across the temporal region, passing near the lateral end of the brow as it heads toward frontalis muscles. During the course, the FbFN laying in the innominate fascial layer was divided into 3 branches. The anterior and posterior branch of FbFN crossed the reference line superiorly and laterally at 3 and 4 cm from the lateral canthus, respectively. In conclusion, the oculofacial surgeon must bring the dissection plane of the forehead tissue more superficially around the 3 cm superolaterally to the lateral canthus in the direction of 45° from the horizontal line in order to avoid nerve injury.

Recent advances in understanding DNA methylation of prostate cancer.

Epigenetic modifications, such as DNA methylation, is widely studied in cancer. DNA methylation patterns have been shown to distinguish between benign and malignant tumors in various cancers, including prostate cancer. It may also contribute to oncogenesis, as it is frequently associated with downregulation of tumor suppressor genes. Aberrant patterns of DNA methylation, in particular the CpG island hypermethylator phenotype (CIMP), have shown associative evidence with distinct clinical features and outcomes, such as aggressive subtypes, higher Gleason score, prostate-specific antigen (PSA), and overall tumor stage, overall worse prognosis, as well as reduced survival. In prostate cancer, hypermethylation of specific genes is significantly different between tumor and normal tissues. Methylation patterns could distinguish between aggressive subtypes of prostate cancer, including neuroendocrine prostate cancer (NEPC) and castration resistant prostate adenocarcinoma. Further, DNA methylation is detectable in cell-free DNA (cfDNA) and is reflective of clinical outcome, making it a potential biomarker for prostate cancer. This review summarizes recent advances in understanding DNA methylation alterations in cancers with the focus on prostate cancer. We discuss the advanced methodology used for evaluating DNA methylation changes and the molecular regulators behind these changes. We also explore the clinical potential of DNA methylation as prostate cancer biomarkers and its potential for developing targeted treatment of CIMP subtype of prostate cancer.

Ubiquitination Links DNA Damage and Repair Signaling to Cancer Metabolism.

Changes in the DNA damage response (DDR) and cellular metabolism are two important factors that allow cancer cells to proliferate. DDR is a set of events in which DNA damage is recognized, DNA repair factors are recruited to the site of damage, the lesion is repaired, and cellular responses associated with the damage are processed. In cancer, DDR is commonly dysregulated, and the enzymes associated with DDR are prone to changes in ubiquitination. Additionally, cellular metabolism, especially glycolysis, is upregulated in cancer cells, and enzymes in this metabolic pathway are modulated by ubiquitination. The ubiquitin-proteasome system (UPS), particularly E3 ligases, act as a bridge between cellular metabolism and DDR since they regulate the enzymes associated with the two processes. Hence, the E3 ligases with high substrate specificity are considered potential therapeutic targets for treating cancer. A number of small molecule inhibitors designed to target different components of the UPS have been developed, and several have been tested in clinical trials for human use. In this review, we discuss the role of ubiquitination on overall cellular metabolism and DDR and confirm the link between them through the E3 ligases NEDD4, APC/CCDH1, FBXW7, and Pellino1. In addition, we present an overview of the clinically important small molecule inhibitors and implications for their practical use.

Hepatic progesterone receptor membrane component 1 attenuates ethanol-induced liver injury by reducing acetaldehyde production and oxidative stress.

Alcohol-associated liver disease (ALD) is caused by excessive abuse of alcohol. One of the most representative causes of ALD is the action of acetaldehyde. Acetaldehyde is a toxic material produced when alcohol is metabolized through some enzymes, and it causes endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and tissue injury. In this study, we assessed the relationship between Progesterone receptor membrane component 1 (PGRMC1) and ALD because PGRMC1 is expressed in the ER and mitochondria in the liver. Using the chronic and binge alcohol feeding models, we assessed acetaldehyde level, liver damage, alcohol-degrading enzymes, and ER stress. Compared with wild-type (WT) mice ethanol-fed Pgrmc1 knockout (KO) mice had higher levels of alanine aminotransferase (ALT) and alcohol-degrading enzymes, and Pgrmc1 KO mice had high serum acetaldehyde and ER stress levels compared with WT mice with control and ethanol feeding. Loss of Pgrmc1 increased acetaldehyde production through increased expression of alcohol dehydrogenase and catalase, which led to increased ER stress and suggested that cell death was promoted. In conclusion, it has been proposed that the loss of PGRMC1 could promote ALD and cause liver damage in alcohol-abusing humans.NEW & NOTEWORTHY Loss of Pgrmc1 increased acetaldehyde production, and excess acetaldehyde consequently increased ER stress, which activates apoptosis. Since low expression of PGRMC1 is vulnerable to alcoholic liver damage, the loss of PGRMC1 expression may increase susceptibility to ALD.

Inhibition of angiotensin converting enzyme increases PKCßI isoform expression via activation of substance P and bradykinin receptors in cultured astrocytes of mice.

BACKGROUND: Angiotensin-converting enzyme inhibitor (ACEi) inhibits the catalysis of angiotensin I to angiotensin II and the degradation of substance P (SP) and bradykinin (BK). While the possible relationship between ACEi and SP in nociceptive mice was recently suggested, the effect of ACEi on signal transduction in astrocytes remains unclear. OBJECTIVES: This study examined whether ACE inhibition with captopril or enalapril modulates the levels of SP and BK in primary cultured astrocytes and whether this change modulates PKC isoforms (PKCα, PKCßI, and PKCε) expression in cultured astrocytes. METHODS: Immunocytochemistry and Western blot analysis were performed to examine the changes in the levels of SP and BK and the expression of the PKC isoforms in primary cultured astrocytes, respectively. RESULTS: The treatment of captopril or enalapril increased the immunoreactivity of SP and BK significantly in glial fibrillary acidic protein-positive cultured astrocytes. These increases were suppressed by a pretreatment with an angiotensin-converting enzyme. In addition, treatment with captopril increased the expression of the PKCßI isoform in cultured astrocytes, while there were no changes in the expression of the PKCα and PKCε isoforms after the captopril treatment. The captopril-induced increased expression of the PKCßI isoform was inhibited by a pretreatment with the neurokinin-1 receptor antagonist, L-733,060, the BK B1 receptor antagonist, R 715, or the BK B2 receptor antagonist, HOE 140. CONCLUSIONS: These results suggest that ACE inhibition with captopril or enalapril increases the levels of SP and BK in cultured astrocytes and that the activation of SP and BK receptors mediates the captopril-induced increase in the expression of the PKCßI isoform.

Quality of life in intermittent exotropia for Korean children and their parents.

BACKGROUND: Patients with strabismus are more likely to have mental health problems, including high rates of depressive symptoms and social phobia. Intermittent exotropia (IXT) typically occurs in early childhood and is more common in Asian populations. We aim to assess the health-related quality of life (HRQOL) concerns in children with intermittent exotropia (IXT) using the Intermittent Exotropia Questionaire (IXTQ), and their associations with the clinical severity of IXT and the parents' HRQOL concerns. METHODS: IXT, defined as both distance and near exodeviation ≥ 10 prism diopters were eligible for inclusion. The final IXTQ score is calculated using the mean score for all items, and ranges from 0 (worst HRQOL) to 100 (best HRQOL). The correlations of child IXTQ scores with their deviation angle and stereoacuity were measured, as were those with their parent's IXTQ scores. RESULTS: One hundred twenty-two children with IXT (aged 5-17 years) and one parent for each child completed the child and parent IXTQ, respectively. The greatest HRQOL concern for each child with IXT and their parent was "Worry about eyes" (frequency 88%, score 35.0 ± 27.8). Lower child IXTQ scores were associated with a larger distance (r = 0.24, p = 0.007) and near deviation angle (r = 0.2, p = 0.026). "It bothers me because I have to wait for my eyes to clear up" and "Waiting for their eyes to clear up" were more common in children with a larger deviation angle (both p < 0.05). The parent IXTQ scores (52.1 ± 25.3) were lower than the child ones (79.7 ± 15.8) and showed a positive correlation with child IXTQ scores (r = 0.26, p = 0.004). Lower parent IXTQ scores were associated with poor distance stereoacuity (r = 0.23, p = 0.01). CONCLUSION: The HRQOL of IXT children was positively related to that of their parents. A larger deviation angle and worse distance stereoacuity function may predict more-negative impacts on children and their parents, respectively.

Non-Arteritic Ischemic Optic Neuropathy Following COVID-19 Vaccination in Korea: A Case Series.

BACKGROUND: To report the clinical manifestations of non-arteritic anterior ischemic optic neuropathy (NAION) cases after coronavirus disease 2019 (COVID-19) vaccination in Korea. METHODS: This multicenter retrospective study included patients diagnosed with NAION within 42 days of COVID-19 vaccination. We collected data on vaccinations, demographic features, presence of vascular risk factors, ocular findings, and visual outcomes of patients with NAION. RESULTS: The study included 16 eyes of 14 patients (6 men, 8 women) with a mean age of 63.5 ± 9.1 (range, 43-77) years. The most common underlying disease was hypertension, accounting for 28.6% of patients with NAION. Seven patients (50.0%) had no vascular risk factors for NAION. The mean time from vaccination to onset was 13.8 ± 14.2 (range, 1-41) days. All 16 eyes had disc swelling at initial presentation, and 3 of them (18.8%) had peripapillary intraretinal and/or subretinal fluid with severe disc swelling. Peripapillary hemorrhage was found in 50% of the patients, and one (6.3%) patient had peripapillary cotton-wool spots. In eight fellow eyes for which we were able to review the fundus photographs, the horizontal cup/disc ratio was less than 0.25 in four eyes (50.0%). The mean visual acuity was logMAR 0.6 ± 0.7 at the initial presentation and logMAR 0.7 ± 0.8 at the final visit. CONCLUSION: Only 64% of patients with NAION after COVID-19 vaccination have known vascular and ocular risk factors relevant to ischemic optic neuropathy. This suggests that COVID-19 vaccination may increase the risk of NAION. However, overall clinical features and visual outcomes of the NAION patients after COVID-19 vaccination were similar to those of typical NAION.

Risk of consecutive esotropia after surgery for intermittent exotropia according to passive duction force.

PURPOSE: To determine the relationship between consecutive esotropia (ET) and passive duction force (PDF) in patients with intermittent exotropia (XT). METHODS: The study enrolled 70 patients in whom PDF was measured under general anesthesia prior to XT surgery. The preferred eye for fixation (PE) and the nonpreferred eye for fixation (NPE) were determined using a cover-uncover test. The patients were subdivided into two groups according to the angle of deviation at 1 month postoperation: (1) consecutive ET (CET group), >10 prism diopters (PD) of ET; and (2) non-CET (NCET group), ≤10 ET or residual exodeviation. The relative PDF of the medial rectus muscle (MRM) was obtained by subtracting the ipsilateral PDF of the lateral rectus muscle (LRM) from the PDF of the MRM. RESULTS: The PDFs for the LRM in the PE in the CET and NCET groups were 47.28 g and 58.59 g, respectively (p = 0.147), and 56.18 g and 46.59 g for the MRM (p = 0.11), and in the NPE were 59.84 g and 55.25 g, respectively, for the LRM (p = 0.993), and 49.12 g and 50.53 g, respectively, for the MRM (p = 0.81). However, in the PE, the PDF in the MRM was larger in the CET group than in the NCET group (p = 0.045), which was positively associated with the postoperatively overcorrected angle of deviation (p = 0.017). CONCLUSIONS: An increased relative PDF in the MRM in the PE was a risk factor for consecutive ET after XT surgery. Quantitative evaluation of the PDF could be considered when planning strabismus surgery to achieve the desired surgical outcome.