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OBJECTIVE: Given the complex and unclear etiology of neck pain, it is important to understand the differences in central sensitization as well as psychosocial factors in individuals with chronic neck pain and healthy controls. The purpose of this study was to benchmark differences in central sensitization, psychosocial factors, and range of motion between people with nonspecific chronic neck pain and healthy controls and to analyze the correlation between pain intensity, neck disability, and psychosocial factors in people with chronic neck pain. METHODS: Thirty individuals with chronic neck pain and 30 healthy controls were included in this case-control study. Outcome measures were as follows: central sensitization (pressure pain threshold, temporal summation, and conditioned pain modulation), psychosocial factors (depressive symptoms, pain catastrophizing, and quality of life), and active cervical range of motion. RESULTS: People with neck pain had lower local pressure pain threshold, a decrease in conditioned pain modulation, more depressive symptoms, greater pain catastrophizing, lower quality of life, and reduced range of motion for neck rotation when compared with healthy controls. In people with neck pain, moderate correlations were observed between pain intensity and quality of life (ρ = -0.479), disability and pain catastrophizing (ρ = 0.379), and disability and quality of life (ρ = -0.456). CONCLUSIONS: People with neck pain have local hyperalgesia, impaired conditioning pain modulation, depressive symptoms, pain catastrophizing, low quality of life, and reduced active range of motion during neck rotation, which should be taken into account during assessment and treatment. IMPACT: This study shows that important outcomes, such as central sensitization and psychosocial factors, should be considered during assessment and treatment of individuals with nonspecific chronic neck pain. In addition, pain intensity and neck disability are correlated with psychosocial factors.

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The liver contains a mixture of hepatocytes with diploid or polyploid (tetraploid, octaploid, etc.) nuclear content. Polyploid hepatocytes are commonly found in adult mammals, representing ~90% of the entire hepatic pool in rodents. The cellular and molecular mechanisms that regulate polyploidization have been well characterized; however, it is unclear whether diploid and polyploid hepatocytes function similarly in multiple contexts. Answering this question has been challenging because proliferating hepatocytes can increase or decrease ploidy, and animal models with healthy diploid-only livers have not been available. Mice lacking E2f7 and E2f8 in the liver (liver-specific E2f7/E2f8 knockout; LKO) were recently reported to have a polyploidization defect, but were otherwise healthy. Herein, livers from LKO mice were rigorously characterized, demonstrating a 20-fold increase in diploid hepatocytes and maintenance of the diploid state even after extensive proliferation. Livers from LKO mice maintained normal function, but became highly tumorigenic when challenged with tumor-promoting stimuli, suggesting that tumors in LKO mice were driven, at least in part, by diploid hepatocytes capable of rapid proliferation. Indeed, hepatocytes from LKO mice proliferate faster and out-compete control hepatocytes, especially in competitive repopulation studies. In addition, diploid or polyploid hepatocytes from wild-type (WT) mice were examined to eliminate potentially confounding effects associated with E2f7/E2f8 deficiency. WT diploid cells also showed a proliferative advantage, entering and progressing through the cell cycle faster than polyploid cells, both in vitro and during liver regeneration (LR). Diploid and polyploid hepatocytes responded similarly to hepatic mitogens, indicating that proliferation kinetics are unrelated to differential response to growth stimuli. Conclusion: Diploid hepatocytes proliferate faster than polyploids, suggesting that the polyploid state functions as a growth suppressor to restrict proliferation by the majority of hepatocytes.

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BACKGROUND: This study evaluated the structure and amount of variability of surface electromyography (sEMG) patterns and ankle force data during low-level isometric contractions in diabetic subjects with different degrees of neuropathy. METHODS: We assessed 10 control subjects and 38 diabetic patients, classified as absent, mild, moderate, or severe neuropathy, by a fuzzy system based on clinical variables. Multichannel sEMG (64-electrode matrix) of tibialis anterior and gastrocnemius medialis muscles were acquired during isometric contractions at 10%, 20%, and 30% of the maximum voluntary contraction, and force levels during dorsi- and plantarflexion were recorded. Standard deviation and sample entropy of force signals were calculated and root mean square and sample entropy were calculated from sEMG signals. Differences among groups of force and sEMG variables were verified using a multivariate analysis of variance. FINDINGS: Overall, during dorsiflexion contractions, moderate and severe subjects had higher force standard deviation and moderate subjects had lower force sample entropy. During plantarflexion, moderate subjects had higher force standard deviation and all diabetic subjects had lower entropy. Tibialis anterior presented higher root mean square in absent group and lower entropy in mild subjects. For gastrocnemius medialis, entropy was higher in severe and lower in moderate subjects. INTERPRETATION: Diabetic neuropathy affects the complexity of the neuromuscular system during low-level isometric contractions, reducing the system's capacity to adapt to challenging mechanical demands. The observed patterns of neuromuscular complexity were not associated with disease severity, with the majority of alterations recorded in moderate subject.

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