ABSTRACT
This corrects the article DOI: 10.1038/cddis.2014.82.
ABSTRACT
Aging refers to the physical and functional decline of the tissues over time that often leads to age-related degenerative diseases. Accumulating evidence implicates that the senescence of neural stem cells (NSCs) is of paramount importance to the aging of central neural system (CNS). However, exploration of the underlying molecular mechanisms has been hindered by the lack of proper aging models to allow the mechanistic examination within a reasonable time window. In the present study, we have utilized a hydroxyurea (HU) treatment protocol and effectively induced postnatal subventricle NSCs to undergo cellular senescence as determined by augmented senescence-associated-ß-galactosidase (SA-ß-gal) staining, decreased proliferation and differentiation capacity, increased G0/G1 cell cycle arrest, elevated reactive oxygen species (ROS) level and diminished apoptosis. These phenotypic changes were accompanied by a significant increase in p16, p21 and p53 expression, as well as a decreased expression of key proteins in various DNA repair pathways such as xrcc2, xrcc3 and ku70. Further proteomic analysis suggests that multiple pathways are involved in the HU-induced NSC senescence, including genes related to DNA damage and repair, mitochondrial dysfunction and the increase of ROS level. Intriguingly, compensatory mechanisms may have also been initiated to interfere with apoptotic signaling pathways and to minimize the cell death by downregulating Bcl2-associated X protein (BAX) expression. Taken together, we have successfully established a cellular model that will be of broad utilities to the molecular exploration of NSC senescence and aging.
Subject(s)
Cellular Senescence , Neural Stem Cells/metabolism , Stress, Physiological , Animals , Animals, Newborn , Apoptosis , Cell Cycle Checkpoints , Cell Differentiation , Cell Proliferation , Cells, Cultured , Cellular Senescence/drug effects , Cyclin-Dependent Kinase Inhibitor p16/metabolism , Cyclin-Dependent Kinase Inhibitor p21/metabolism , DNA Damage , DNA Repair Enzymes/metabolism , Hydroxyurea/pharmacology , Mice , Neural Stem Cells/drug effects , Neural Stem Cells/pathology , Protein Interaction Mapping , Proteomics/methods , Reactive Oxygen Species/metabolism , Signal Transduction , Spheroids, Cellular , Stress, Physiological/drug effects , Time Factors , Tumor Suppressor Protein p53/metabolismABSTRACT
Cognitive-behavioural therapy (CBT) and its effects on temporomandibular disorders (TMD) have been examined in several studies. We are trying to combine results of these studies and to explore the effectiveness. MEDLINE, EMBASE, Cochrane Central Register of Controlled Trial, Pubmed and the Chinese Biomedical Literature Data were searched to collect randomised and semi-randomised controlled trials (RCTs), comparing CBT with any control group receiving other dental treatments. Two authors independently retrieved, extracted and assessed the quality of included studies. The search strategy resulted in 323 studies, of which five met the inclusion criteria, including three RCTs and two semi-RCTs. The quality of the included studies was diverse. Meta-analysis was not performed owing to five studies involving different comparison groups and follow-up periods. The effect of CBT on patients with TMD is inconsistent among the studies, so no firm conclusion could be drawn in this systematic review. There is insufficient evidence to make firm recommendations for the use of CBT over other intervention for the treatment of TMD. Further high-quality RCTs are clearly needed for this theme.
Subject(s)
Cognitive Behavioral Therapy , Temporomandibular Joint Disorders/therapy , Adolescent , Adult , Aged , Female , Follow-Up Studies , Humans , Male , Middle Aged , Randomized Controlled Trials as Topic , Temporomandibular Joint Disorders/psychology , Treatment Outcome , Young AdultABSTRACT
Perinatal asphyxia is one of the major causes of cerebral injury in neonates. It may be due to the increased endogenous opioid-like substances (OLS) in the body. The levels of three OLS, namely leucine-enkephalin (LEK), beta-endorphin (beta-EP) and dynorphin A1-13 (DynoA1-13) of 44 cases with neonatal asphyxia were studied by radioimmunoassay. The OLS level in plasma and cerebral spinal fluid (CSF) were higher in asphyxiated group than those in the control group, especially in asphyxiated cases with fetal distress. The OLS levels of CSF were also higher in cases with cerebral injury than in those without cerebral injury, while the levels of OLS in plasma had no difference in these two groups. The relationship between OLS levels and asphyxia and cerebral injury is also discussed.