The purpose of this study was to evaluate the usefulness of the sonographic characteristics of papillary thyroid carcinoma (PTC) with Hashimoto’s thyroiditis (HT) for predicting central lymph node metastasis (CLNM). One hundred thirty-three patients who underwent thyroidectomy and central cervical lymph node dissection for PTC with coexistent HT were retrospectively analyzed. All PTCs with HT were preoperatively evaluated by ultrasound (US) regarding their nodular number, size, component, shape, margin, echogenicity, calcification, capsule contact with protrusion, vascularity and contrast enhanced ultrasound (CEUS) parameters. Univariate analysis demonstrated that patients with PTCs with HT and CLNM more frequently had age ≤ 45 years, size > 10 mm, a wider than tall shape, microcalcification, hypo-enhancement and peak intensity index 10 mm and CEUS hypo-enhancement were independent characteristics for the presence of CLNM. Our study indicated that preoperative US characteristics could offer help in predicting CLNM in PTCs with coexistent HT.Objectives Magnetization transfer (MT) imaging exploits the interaction between bulk water protons and protons contained in macromolecules to induce signal changes through a special radiofrequency pulse. MT detects muscle damage in patients with neuromuscular conditions, such as limb-girdle muscular dystrophies or Charcot-Marie-Tooth disease, which are characterized by progressive fiber loss and replacement by fatty tissue. In Pompe disease, in which there is, in addition, an accumulation of glycogen inside the muscle fibers, MT has not been tested yet. Our aim is to estimate MT ratio (MTR) in the skeletal muscle of these patients and correlate it with intramuscular fat fraction (FF) and results of muscle function tests. Methods We obtained two-point axial Dixon and Dixon-MT sequences of the right thigh on a 1.5 Teslas MRI scanner in 60 individuals, including 29 late onset Pompe disease patients, 2 patients with McArdle disease, and 29 age and sex matched healthy controls. FF and MTR were estimated. Muscle fue tool to identify muscle loss in patients with Pompe disease and shows a good correlation with muscle function tests. Therefore, the MT technique can be useful in monitoring muscle degeneration in Pompe disease in clinical trials or natural history studies.Background The population-based studies conducted thus far do not provide conclusive evidence of the link between diabetic retinopathy (DR) and stroke. The aim of the present systematic review was to determine whether DR is specifically associated with stroke. Methods MEDLINE, Embase, and Web of Science were systematically searched from their inception to July 31, 2020. All cohort studies that reported associations between the presence of DR and incident stroke were included. The pooled hazard ratios (HRs), pooled risk ratios (RRs), and 95% confidence intervals (CIs) were calculated. Results The meta-analysis included 19 cohort studies involving 81,452 diabetic patients. The pooled effect size of any DR related to stroke was 1.25 for HR (95% CI 1.12-1.39; P less then 0.0001) and 1.96 for RR (95% CI 1.60-2.39; P less then 0.0001). Subgroup analysis for the type of diabetes yielded pooled HR of 1.29 (95% CI 1.10-1.50; P = 0.001) in patients with type 2 diabetes mellitus (T2DM). The pooled RR was 2.29 (95% CI 1.77-2.96; P less then 0.0001) in patients with T2DM. Two studies addressed the DR-related stroke among type 1 diabetes mellitus (T1DM) patients. One study found a significant association between DR and stroke (OR 1.6; 95% CI 1.1-2.3; P less then 0.01), while the other did not identify an association between these two conditions (RR 1.40; 95% CI 0.62-2.18; P = 0.178). Conclusions The presence of DR is associated with an increased risk of stroke in diabetic patients. buy CRCD2 This correlation is robust in T2DM patients but uncertain in T1DM patients. Our findings indicate that DR is an important biomarker for the prediction of stroke. To further validate the role of DR in stroke-risk stratification, additional research is required on the association between the stage of DR and stroke risk, and more studies including T1DM patients are necessary.Glaucoma is the second leading cause of blindness worldwide, affecting ~80 million people by 2020 (1, 2). The condition is characterized by a progressive loss of retinal ganglion cells (RGCs) and their axons accompanied by visual field loss. The underlying pathophysiology of glaucoma remains elusive. Glaucoma is recognized as a multifactorial disease, and lowering intraocular pressure (IOP) is the only treatment that has been shown to slow the progression of the condition. However, a significant number of glaucoma patients continue to go blind despite intraocular pressure-lowering treatment (2). Thus, the need for alternative treatment strategies is indisputable. Accumulating evidence suggests that glial cells play a significant role in supporting RGC function and that glial dysfunction may contribute to optic nerve disease. Here, we review recent advances in understanding the role of glial cells in the pathophysiology of glaucoma. A particular focus is on the dynamic and essential interactions between glial cells and RGCs and potential therapeutic approaches to glaucoma by targeting glial cells.The late neuropathological effects of traumatic brain injury have yet to be fully elucidated, particularly with respect to community-based cohorts. To contribute to this critical gap in knowledge, we designed a multimodal neuropathological study, integrating traditional and quantitative approaches to detect pathologic changes in 532 consecutive brain autopsies from participants in the Adult Changes in Thought (ACT) study. Diagnostic evaluation including assessment for chronic traumatic encephalopathy (CTE) and quantitative immunoassay-based methods were deployed to examine levels of pathological (hyperphosphorylated) tau (pTau) and amyloid (A) β in brains from ACT participants with (n = 107) and without (n = 425) history of remote TBI with loss of consciousness (w/LOC). Further neuropathological assessments included immunohistochemistry for α-synuclein and phospho-TDP-43 pathology and astro- (GFAP) and micro- (Iba1) gliosis, mass spectrometry analysis of free radical injury, and gene expression evaluation (RNA sequencing) in a smaller sub-cohort of matched samples (49 cases with TBI and 49 non-exposed matched controls).