Sport index was associated with slower and OPA with faster DNAm GrimAge Acc after adjusting the model for sex. Genetic factors and nonshared environmental factors in common with sport index explained 1.5%-2.7% and 1.9%-3.5%, respectively, of the variation in GrimAge Acc. The corresponding proportions considering OPA were 0.4%-1.8% and 0.7%-1.8%, respectively. However, these proportions were minor (<0.5%) after adjusting the model for smoking status. LTPA associates with slower and OPA with faster epigenetic aging. However, adjusting the models for smoking status, which may reflect the accumulation of unhealthy lifestyle habits, attenuated the associations.LTPA associates with slower and OPA with faster epigenetic aging. However, adjusting the models for smoking status, which may reflect the accumulation of unhealthy lifestyle habits, attenuated the associations. Exogenous ketones potentially provide an alternative, energetically advantageous fuel to power exercising skeletal muscle. However, there is limited evidence regarding their relative contribution to energy expenditure during exercise. Furthermore, the effect of blood ketone concentration and exercise intensity on exogenous ketone oxidation rates is unknown. Six athletes completed cycling ergometer exercise on three occasions within a single-blind, random-order controlled, crossover design study. Exercise duration was 60 min, consisting of 20-min intervals at 25%, 50%, and 75% maximal power output (WMax). Participants consumed (i) bitter flavored water (control), (ii) a low-dose β-hydroxybutyrate (βHB) ketone monoester (KME; 252 mg·kg BW-1, "low ketosis"), or (iii) a high-dose βHB KME (752 mg·kg BW-1, "high ketosis"). The KME contained a 13C isotope label, allowing for the determination of whole-body exogenous βHB oxidation rates through sampled respiratory gases. Despite an approximate doubling of bloodficiency was significantly improved when blood βHB concentration was raised to ~2 mM. Dorsal midbrain syndrome (DMS) consists of a constellation of clinical features, including reduced upgaze, pupillary light-near dissociation, lid retraction, convergence retraction, and eye misalignment. This syndrome results mostly from intrinsic or extrinsic mesodiencephalic tumors or strokes, obstructive hydrocephalus, failure of cerebrospinal fluid shunting to correct obstructive hydrocephalus, and head trauma. Published reports that include imaging corroboration are based on relatively small cohorts and have not included comprehensive patient self-reports on the impact of these abnormalities on quality of life. We conducted a retrospective review of cases of DMS identified between 1998 and 2019 at the University of Michigan using the Electronic Medical Record Search Engine. Patients were included only if they had been evaluated by a neuro-ophthalmologist and had a corroborative imaging abnormality. We collected data on symptoms and on neuro-ophthalmic and neurologic signs. We reviewed brain imaging rhone interviews with patients revealed that diplopia and upgaze deficit had less lasting impact on quality of life than did ataxia and concurrent nonneurologic problems.This large series expands on the clinical profile of DMS. Neoplasms and strokes were the most common causes. Obstructive hydrocephalus alone, identified as a major cause in the largest previously published series, was uncommon. At least 3 neuro-ophthalmic signs were present in nearly all patients, with upgaze deficit as predominant. Unlike an earlier report, this study found no correlation between brain imaging and clinical signs. Neuro-ophthalmic signs persisted even after neoplasms were successfully treated and improved only slightly after stroke. Telephone interviews with patients revealed that diplopia and upgaze deficit had less lasting impact on quality of life than did ataxia and concurrent nonneurologic problems. Given the widely distributed network of midbrain, pontine, cerebellar, and cortical areas involved in the neural control of vergence, one might expect various vergence deficits in stroke patients. In this article, we investigated the localizing value of bedside vergence testing with respect to different supratentorial and infratentorial infarction locations. Three hundred five stroke patients and 50 age-matched controls were examined prospectively by means of bedside tests to assess slow and fast binocular (i.e., symmetrical) as well as slow and fast monocular (i.e., asymmetrical) convergence. Infarction locations, as identified on MRI, were correlated with vergence performance using multinomial logistic regression. Vergence deteriorated with age in both stroke patients and healthy controls. Most infarction locations did not show significant associations with vergence parameters, apart from cases with parietal lobe lesions, which exhibited insufficient asymmetrical, slow and fast vergence for both the lrom our data is age. Older subjects show poor slow binocular as well as slow and fast monocular vergence. Extended white matter lesions are also correlated with deficient vergence ability suggesting a role for subcortical wide range connections in maintaining an intact vergence circuitry. Anti-acetylcholine receptor antibody (AChR-Abs) testing is a safe and simple ancillary method for confirming the diagnosis of myasthenia gravis. Despite the test's high sensitivity (85%-90%) for generalized myasthenia gravis, AChR-Abs testing has been reported to have a low sensitivity 44%-66% for ocular myasthenia gravis (OMG). The aim of the study is to assess the effectiveness of AChR binding Abs testing for diagnosing OMG by evaluating the test's sensitivity, specificity, positive predictive value, and negative predictive value. A retrospective chart review on 114 OMG suspects who presented to the emergency department of a tertiary eye center in Victoria, Australia, was completed. CP43 The patients presented with diplopia alone, ptosis alone, or the combination of diplopia and ptosis. All participants were followed up longitudinally in the neuro-ophthalmology outpatient clinics for the average of 2.8 months, where they have received AChR binding testing. The final diagnosis was only given to the patients who either were seropositive for AChR binding Abs and had a high clinical suspicion of OMG, or the patient who was seronegative for AChR binding Abs but was regarded as likely to have OMG clinically and responded to the diagnostic treatments (pyridostigmine bromide and immunosuppressant therapy).