Raskelgaard9934

Background and Aims YKL-40, an inflammatory biomarker, has been reported to be involved in the process and progression of atherosclerosis. Several studies have investigated the association between YKL-40 and plaque and suggested YKL-40 might be a potential biomarker for plaque instability. This study aimed to investigate the association between YKL-40 and carotid plaque instability. Methods Based on a community-based study in Beijing from February 2014 to May 2016, 1,132 participants with carotid plaques were enrolled in this study. Data on demographics and medical history were collected through face-to-face interviews, and fasting blood samples were collected and stored. We used ultrasound to evaluate the presence of carotid plaque and its instability. The level of YKL-40 was measured by enzyme-linked immunosorbent assay (ELISA). Multivariate logistic regression analysis was performed to investigate the association between YKL-40 level and carotid atherosclerotic plaque instability. Results The mean age of the 1,132 participants was 58.0 (52.0-64.0) years, and 560 (49.5%) were male. Unstable plaques were detected in 855 (75.53%) participants. YKL-40 level was classified into four groups according to its quartile quartile 1 less then 25.47 ng/mL, quartile 2 25.47-39.53 ng/mL, quartile 3 39.53-70.55 ng/mL, quartile 4 ≥70.55 ng/mL. After adjusting for age, sex, smoking, alcohol drinking, medical history, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, homocysteine, high-sensitivity C-reactive protein, and plaque thickness, the top quartiles of YKL-40 level were significantly associated with unstable plaque (quartile 3 OR 2.10, 95% CI 1.29-3.40; quartile 4 OR 1.70, 95% CI 1.04-2.80). Conclusion This study found that YKL-40 was associated with carotid plaque instability determined by ultrasound. Individuals with high YKL-40 may have a higher risk of unstable carotid plaque.This review will provide a comprehensive, up-to-date review of the current knowledge regarding the pathophysiology of muscle contractures in cerebral palsy. Although much has been known about the clinical manifestations of both dynamic and static muscle contractures, until recently, little was known about the underlying mechanisms for the development of such contractures. In particular, recent basic science and imaging studies have reported an upregulation of collagen content associated with muscle stiffness. Paradoxically, contractile elements such as myofibrils have been found to be highly elastic, possibly an adaptation to a muscle that is under significant in vivo tension. Sarcomeres have also been reported to be excessively long, likely responsible for the poor force generating capacity and underlying weakness seen in children with cerebral palsy (CP). Overall muscle volume and length have been found to be decreased in CP, likely secondary to abnormalities in sarcomerogenesis. Recent animal and clinical work has suggested that the use of botulinum toxin for spasticity management has been shown to increase muscle atrophy and fibrofatty content in the CP muscle. Given that the CP muscle is short and small already, this calls into question the use of such agents for spasticity management given the functional and histological cost of such interventions. Recent theories involving muscle homeostasis, epigenetic mechanisms, and inflammatory mediators of regulation have added to our emerging understanding of this complicated area.Background Neuronal intranuclear inclusion disease (NIID) is a rare neurodegenerative disease. Because of variable clinical manifestations, NIID was often misdiagnosed. According to published case reports, the common clinical manifestations of NIID include dementia, muscle weakness, autonomic impairment, sensory disturbance, rigidity, ataxia convulsions, etc. this website However, no cases of oromandibular dystonia were mentioned. Case Presentation We describe a case of a 58-year-old woman presenting with mouth involuntary chewing initially. She started to show hand tremors, ataxia, and walking instability until 2 years later. Diffusion-weighted imaging showed high intensity signal along the corticomedullary junction. Fluid-attenuated inversion recovery imaging showed white matter hyperintensity. Electromyography (EMG) indicated peripheral nerve degeneration. Neuropsychological testing showed memory loss. Finally, skin biopsy and GGC repeat expansions in the NOTCH2NLC (Notch 2 N-terminal like C) gene confirmed the diagnosis of NIID. Conclusion This case demonstrated that oromandibular dystonia could be the first symptom of NIID. This case report provides new characteristics of NIID and broadens its clinical spectrum.Growing evidence implicates a distinct role of disturbed slow-wave sleep in neurodegenerative diseases. Reduced non-rapid eye movement (NREM) sleep slow-wave activity (SWA), a marker of slow-wave sleep intensity, has been linked with age-related cognitive impairment and Alzheimer disease pathology. However, it remains debated if SWA is associated with cognition in Parkinson disease (PD). Here, we investigated the relationship of regional SWA with cognitive performance in PD. In the present study, 140 non-demented PD patients underwent polysomnography and were administered the Montréal Cognitive Assessment (MoCA) to screen for cognitive impairment. We performed spectral analysis of frontal, central, and occipital sleep electroencephalography (EEG) derivations to measure SWA, and spectral power in other frequency bands, which we compared to cognition using linear mixed models. We found that worse MoCA performance was associated with reduced 1-4 Hz SWA in a region-dependent manner (F2, 687 =11.67, p less then 0.001). This effect was driven by reduced regional SWA in the lower delta frequencies, with a strong association of worse MoCA performance with reduced 1-2 Hz SWA (F2, 687 =18.0, p less then 0.001). The association of MoCA with 1-2 Hz SWA (and 1-4 Hz SWA) followed an antero-posterior gradient, with strongest, weaker, and absent associations over frontal (rho = 0.33, p less then 0.001), central (rho = 0.28, p less then 0.001), and occipital derivations, respectively. Our study shows that cognitive impairment in PD is associated with reduced NREM sleep SWA, predominantly in lower delta frequencies (1-2 Hz) and over frontal regions. This finding suggests a potential role of reduced frontal slow-wave sleep intensity in cognitive impairment in PD.