Assessment of individuals at risk for falling entails comprehensive neurological and vestibular examinations. Chronic limitation in cervical mobility reduces gaze accuracy, potentially impairing navigation through complex visual environments. Additionally, humans with scoliosis have altered otolithic vestibular responses, causing imbalance. We sought to determine whether dynamic cervical mobility restrictions or static cervicothoracic impairments are also fall risk factors. We examined 435 patients referred for soft-tissue musculoskeletal complaints; 376 met criteria for inclusion (mean age 52; 266 women). Patients were divided into nonfallers, single fallers, and multiple fallers, less or greater than 65 years old. Subject characteristics, dynamic cervical rotations, and static cervicothoracic axial measurements were compared between groups. Fear of falling was evaluated using the Falls Efficacy Scale-International questionnaire. Long-standing cervicothoracic pain and stiffness conferred increased riskd mobility have increased fall frequency and fear of falling, independent of other fall risk factors and should undergo complete fall risk appraisal. During the outbreak of coronavirus disease 2019 (COVID-19), people are under the dual pressure of interpersonal isolation and concerns about infection. An evaluation of people's psychological status and risk factors is needed to conduct target interventions. This was a nationwide, multicenter, cross-sectional study using quota and snowball sampling methods during the COVID-19 epidemic in China. Participants' characteristics and experiences were obtained by an online questionnaire and telephone review. Psychological distress and sleep problems were measured by the Generalized Anxiety Disorder-7, the Patient Health Questionnaire-9, and the Insomnia Severity Index. A total of 23,500 participants were recruited, and 19,372 valid questionnaires were received from 11 centers. Overall, 11.0-13.3% of the participants had anxiety, depression, or insomnia symptoms, and 1.9-2.7% had severe symptoms. The prevalence of psychological and sleep problems has increased. Working as frontline medical staff (Odds Ratio OR=3.406), living in Hubei Province (OR=2.237), close contacts with COVID-19 (OR=1.808), and age 35-49years (OR=1.310) were risk factors for anxiety symptoms; no outside activity for 2weeks (OR=2.167) and age 35-49years (OR=1.198) were risk factors for depression symptoms; and living in Hubei Province (OR=2.376), no outside activity for 2weeks (OR=1.927), and age 35-49years (OR=1.262) were risk factors for insomnia symptoms. Only 1.9% of participants received counseling during the epidemic. Psychological and sleep problems increased during interpersonal isolation due to COVID-19. Current psychological interventions are far from sufficient.Psychological and sleep problems increased during interpersonal isolation due to COVID-19. Current psychological interventions are far from sufficient.Neutrophils are the first barriers for resisting the invasion, proliferation, and damage caused by Salmonella Typhimurium. However, the mechanisms that control this resistance are not completely understood. In this study, we established an in vitro Salmonella infection model in porcine neutrophils, and analyzed the cellular transcriptome by deep sequencing and flow cytometry. The results showed that ribosomal gene transcription was inhibited, and two of these genes, RPL39 and RPL9, were related to TRP53 activation. Furthermore, several important innate immunity genes were also inhibited. Knock-down of RPL39 and RPL9 by siRNA caused an approximate fourfold up-regulation of TRP53. Knock-down of RPL39 and RPL9 also resulted in a significant down-regulation of IFNG and TNF, indicating an inhibition of the innate immune response. Selleck Deferoxamine Silencing of RPL39 and RPL9 also resulted in the up-regulation of FAS, RB1, CASP6, and GADD45A, which play roles in cell cycle arrest and apoptosis. Neutrophils were either first treated with RPL39 siRNA, RPL9 siRNA, TRP53 activator, or TRP53 inhibitor, and then infected with Salmonella. Knock-down of RPL39 and RPL9, or treatment with TRP53 activator, can increase the intracellular proliferation of Salmonella in neutrophils. We speculate that much of the Salmonella virulence can be attributed to the enhancement of cell cycle arrest and the inhibition of the innate immune response, which allows the bacteria to successfully proliferate intracellularly.We describe an autopsied patient with familial parkinsonism and unclassified four repeat-tau (4R-tau) aggregation. She presented with bradykinesia, truncal dystonia, and mild amnesia at the age of 61 and then exhibited body weight loss (15 kg over 8 months), sleep disturbances, and progressive respiratory failure with CO2 narcosis. She died of respiratory failure at the age of 62, 14 months after disease onset. Her brother also showed parkinsonism at the age of 58 and suddenly died 6 months later. Postmortem examination revealed 4R-tau aggregation, which was characterized by neuronal globose-type tangles or pretangles, bush-like or miscellaneous astrocytic inclusions, and coiled bodies. The temporal tip, the striatum, the substantia nigra, the tegmentum of the midbrain, the medullary reticular formation, and the spinal cord were severely involved with tau aggregation. Argyrophilic grains and ballooned neurons were also found in the medial temporal structures, however, extensions of the 4R-aggregations in the case were clearly broader than those of the argyrophilic grains. Western blot analysis of sarkosyl-insoluble fractions from brain lysates revealed prominent bands of tau at both 33 kDa and 37 kDa. Genetic examinations did not reveal any known pathogenic mutations in MAPT, DCTN-1, PSEN-1, or familial or young-onset parkinsonism-related genes. The clinical manifestations, pathologic findings, and biochemical properties of aggregated tau in our patient cannot be explained by argyrophilic grain disease or other known 4R-tauopathies alone. Our results further extend the clinical and neuropathologic spectra of 4R-tauopathy. Alzheimer's disease (AD) is the most common type of dementia, and patients with advanced AD frequently lose the ability to identify family members. The fusiform gyrus (FUS) of the brain is critical in facial recognition. However, AD etiology in the FUS of AD patients is poorly understood. New analytical strategies are needed to reveal the genetic and epigenetic basis of AD in FUS. A complex of new analytical paradigms that integrates an array of transcriptomes and methylomes of normal controls, AD patients, and "AD-in-dish" models were used to identify genetic and epigenetic signatures of AD in FUS. Here we identified changes in gene expression that are specific to the FUS in brains of AD patients. These changes are closely linked to key genes in the AD network. Profiling of the methylome (5mC/5hmC/5fC/5caC) at base resolution identified 5 signature genes (COL2A1, CAPN3, COL14A1, STAT5A, SPOCK3) that exhibit perturbed expression, specifically in the FUS and display altered DNA methylome profiles that are common across AD-associated brain regions.