Horner's Syndrome with Abducens Nerve Palsy

A 68-year-old male patient presented with a week of sudden diplopia. He had been diagnosed with nasopharyngeal cancer 8 months prior and had undergone chemotherapy with radiotherapy. Eight-prism diopter right esotropia in the primary position and a remarkable limitation in abduction in his right eye were observed. Other pupillary disorders and lid drooping were not found. After three weeks, the marginal reflex distance 1 was 3 mm in the right eye and 5 mm in the left eye. The pupil diameter was 2.5 mm in the right eye, and 3 mm in the left eye under room illumination. Under darkened conditions, the pupil diameter was 3.5 mm in the right eye, and 5 mm in the left eye. After topical application of 0.5% apraclonidine, improvement in the right ptosis and reversal pupillary dilatation were observed. On brain magnetic resonance imaging, enhanced lesions on the right cavernous sinus, both sphenoidal sinuses, and skull base suggested the invasion of nasopharyngeal cancer. Lesions on the cavernous sinus need to be considered in cases of abducens nerve palsy and ipsilateral Horner's syndrome

Vision Improvement with Refractive Correction Does Not Completely Exclude Major Eye Diseases: Analyses of Visually Impaired South Korean Population in the Korea National Health and Nutrition Examination Survey 2009–2011

Purpose. To investigate the association between vision improvement with refractive correction in the visually impaired eyes and the prevalence of ocular comorbidities in the South Korean population. Materials and Methods. The data of 24,620 individuals in the Korea National Health and Nutrition Examination Survey (KNHANES 2009–2011) were reviewed. Visual impairment was defined as a presenting visual acuity < 20/60. The participants with visual impairment in at least one eye were divided into 3 groups according to the best-corrected visual acuity (group 1: <20/30, group 2: ≥20/30 but <20/25, and group 3: ≥20/25). The prevalence of ocular comorbidities was estimated and compared between the three groups. Results. Visual impairment in at least one eye was found in 3031 individuals. Groups 1, 2, and 3 comprised 23.5%, 22.2%, and 54.3% of these visually impaired eyes, respectively. The prevalence of cataract, diabetic retinopathy, age-related macular degeneration, corneal opacity, blepharoptosis, and pterygium was similar to or even higher in group 2 compared to group 1. The prevalence of glaucoma and age-related macular degeneration was 5.40% and 11.39%, respectively, in group 2 and 3.31% and 3.76%, respectively, in group 3. Conclusions. Appropriate ophthalmologic examination is necessary even if people exhibit vision improvement after optical correction

Hyaluronan Binding Motifs of USP17 and SDS3 Exhibit Anti-Tumor Activity

BACKGROUND: We previously reported that the USP17 deubiquitinating enzyme having hyaluronan binding motifs (HABMs) interacts with human SDS3 (suppressor of defective silencing 3) and specifically deubiquitinates Lys-63 branched polyubiquitination of SDS3 resulting in negative regulation of histone deacetylase (HDAC) activity in cancer cells. Furthermore, USP17 and SDS3 mutually interact with each other to block cell proliferation in HeLa cells but the mechanism for this inhibition in cell proliferation is not known. We wished to investigate whether the HABMs of USP17 were responsible for tumor suppression activity. METHODOLOGY/PRINCIPAL FINDINGS: Similarly to USP17, we have identified that SDS3 also has three consecutive HABMs and shows direct binding with hyaluronan (HA) using cetylpyridinium chloride (CPC) assay. Additionally, HA oligosaccharides (6-18 sugar units) competitively block binding of endogenous HA polymer to HA binding proteins. Thus, administration of HA oligosaccharides antagonizes the interaction between HA and USP17 or SDS3. Interestingly, HABMs deleted USP17 showed lesser interaction with SDS3 but retain its deubiquitinating activity towards SDS3. The deletion of HABMs of USP17 could not alter its functional regulation on SDS3-associated HDAC activity. Furthermore, to explore whether HABMs in USP17 and SDS3 are responsible for the inhibition of cell proliferation, we investigated the effect of USP17 and SDS3-lacking HABMs on cell proliferation by soft agar, apoptosis, cell migration and cell proliferation assays. CONCLUSIONS: Our results have demonstrated that these HABMs in USP17 and its substrate SDS3 are mainly involved in the inhibition of anchorage-independent tumor growth

Predictive Potential of Circulating Ube2h mRNA as an E2 Ubiquitin-Conjugating Enzyme for Diagnosis or Treatment of Alzheimer’s Disease

Neurodegenerative disorders are caused by neuronal cell death, miscommunications between synapse, and abnormal accumulations of proteins in the brain. Alzheimer&rsquo;s disease (AD) is one of the age-related disorders, which are the most common degenerative disorders today, and strongly affects memory consolidation and cognitive function in the brain. Amyloid-&beta; and tau proteins are triggers for AD pathogenesis, and usually used as AD candidate biomarkers in the clinical research. Especially, clinical exam, brain imaging and molecular biological methods are being used to diagnosis for AD. Genome-wide association study (GWAS) is a new biomedical method, and its use contributes to understanding many human diseases, including brain diseases. Here, we identified ubiquitin conjugating enzyme E2 (Ube2) gene expression in neurons through GWAS. The subfamilies of Ube2&rsquo;s genetic expression and inborn errors affect the ubiquitin proteasome system (UPS), leading to protein degradation in the brain. We found that only Ube2h mRNA transcription was significantly increased in the blood from AD, however we did not find any change of Ube2 subfamily genes&rsquo; expression in the blood and brain tissue. These data may provide information for diagnosis or clinical approach, and suggest that cell-free circulating Ube2h mRNA is a novel potential biomarker for AD

Discoveries for Long Non-Coding RNA Dynamics in Traumatic Brain Injury

In recent years, our understanding of long non-coding RNAs (lncRNAs) has been challenged with advances in genome sequencing and the widespread use of high-throughput analysis for identifying novel lncRNAs. Since then, the characterization of lncRNAs has contributed to the establishment of their molecular roles and functions in transcriptional regulation. Although genetic studies have so far explored the sequence-based primary function of lncRNAs that guides the expression of target genes, recent insights have shed light on the potential of lncRNAs for widening the identification of biomarkers from non-degenerative to neurodegenerative diseases. Therefore, further advances in the genetic characteristics of lncRNAs are expected to lead to diagnostic accuracy during disease progression. In this review, we summarized the latest studies of lncRNAs in TBI as a non-degenerative disease and discussed their potential limitations for clinical treatment

A flowchart showing study participants for final analysis.

<p>A flowchart showing study participants for final analysis.</p

Review of population-based studies of risk factors associated with esodeviation and exodeviation in children.

<p>Review of population-based studies of risk factors associated with esodeviation and exodeviation in children.</p