Decellularized extracellular matrix (dECM) is widely used in regenerative medicine as a scaffold material due to its unique biological activity and good biocompatibility. Hydrogel is a three-dimensional network structure polymer with high water content and high swelling that can simulate the water environment of human tissues, has good biocompatibility, and can exchange nutrients, oxygen, and waste with cells. At present, hydrogel is the ideal biological material for tissue engineering. In recent years, rapid development of the hydrogel theory and technology and progress in the use of dECM to form hydrogels have attracted considerable attention to dECM hydrogels as an innovative method for tissue engineering and regenerative medicine. This article introduces the classification of hydrogels, and focuses on the history and formation of dECM hydrogels, the source of dECM, the application of dECM hydrogels in tissue engineering and the commercial application of dECM materials.When an individual is under stress, the undesired effect on the brain often exceeds expectations. Additionally, when stress persists for a long time, it can trigger serious health problems, particularly depression. Recent studies have revealed that depressed patients have a higher rate of brain aging than healthy subjects and that depression increases dementia risk later in life. However, it remains unknown which factors are involved in brain aging triggered by chronic stress. The most critical change during brain aging is the decline in cognitive function. In addition, cellular senescence is a stable state of cell cycle arrest that occurs because of damage and/or stress and is considered a sign of aging. We used the chronic unpredictable stress (CUS) model to mimic stressful life situations and found that, compared with nonstressed control mice, CUS-treated C57BL/6 mice exhibited depression-like behaviors and cognitive decline. Additionally, the protein expression of the senescence marker p16INK4a was increased in the hippocampus, and senescence-associated β-galactosidase (SA-β-gal)-positive cells were found in the hippocampal dentate gyrus (DG) in CUS-treated mice. Furthermore, the levels of SA-β-gal or p16INK4a were strongly correlated with the severity of memory impairment in CUS-treated mice, whereas clearing senescent cells using the pharmacological senolytic cocktail dasatinib plus quercetin (D + Q) alleviated CUS-induced cognitive deficits, suggesting that targeting senescent cells may be a promising candidate approach to study chronic stress-induced cognitive decline. Our findings open new avenues for stress-related research and provide new insight into the association of chronic stress-induced cellular senescence with cognitive deficits.The precise mechanisms underlying the detrimental effects of early life adversity (ELA) on adult mental health remain still elusive. To date, most studies have exclusively targeted neuronal populations and not considered neuron-glia crosstalk as a crucially important element for the integrity of stress-related brain function. Here, we have investigated the impact of ELA, in the form of a limited bedding and nesting material (LBN) paradigm, on a glial subpopulation with unique properties in brain homeostasis, the NG2+ cells. First, we have established a link between maternal behavior, activation of the offspring's stress response and heterogeneity in the outcome to LBN manipulation. We further showed that LBN targets the hippocampal NG2+ transcriptome with glucocorticoids being an important mediator of the LBN-induced molecular changes. LBN altered the NG2+ transcriptome and these transcriptional effects were correlated with glucocorticoids levels. The functional relevance of one LBN-induced candidate gene, Scn7a, could be confirmed by an increase in the density of voltage-gated sodium (Nav) channel activated currents in hippocampal NG2+ cells. Scn7a remained upregulated until adulthood in LBN animals, which displayed impaired cognitive performance. Considering that Nav channels are important for NG2+ cell-to-neuron communication, our findings provide novel insights into the disruption of this process in LBN mice.Childhood maltreatment (CM) is an established major risk factor for a number of negative health outcomes later in life.  https://www.selleckchem.com/products/td139.html  While epigenetic mechanisms, such as DNA methylation (DNAm), have been proposed as a means of embedding this environmental risk factor, little is known about its timing and trajectory, especially in very young children. It is also not clear whether additional environmental adversities, often experienced by these children, converge on similar DNAm changes. Here, we calculated a cumulative adversity score, which additionally to CM includes socioeconomic status (SES), other life events, parental psychopathology and epigenetic biomarkers of prenatal smoking and alcohol consumption. We investigated the effects of CM alone as well as the adversity score on longitudinal DNAm trajectories in the Berlin Longitudinal Child Study. This is a cohort of 173 children aged 3-5 years at baseline of whom 86 were exposed to CM. These children were followed-up for 2 years with extensive psychometric and biologi within long non-coding RNAs, the majority of associations were found with the adversity score with convergent association with indicators of adverse prenatal exposures. This study highlights the importance of mapping not only of the epigenome but also the exposome and extending the observational timeframe to well before birth.Patients with gastroesophageal reflux disease (GERD) are routinely treated with proton pump inhibitors (PPIs), despite many reports of increased fracture risk associated with PPI use. Notably, the skeletal properties in patients with GERD prior to PPI therapy have not been addressed. We hypothesized that PPI-naïve GERD patients have bone impairment, and that short-term treatment with PPI has minimal skeletal effects. To test this, 17 (12 men/5 women) GERD patients age 32-73 years, not previously exposed to PPI, and 17 age- and sex-matched controls were enrolled from September 2010 to December 2012. Bone mineral density (BMD) at lumbar spine, femoral neck, total hip, and trabecular bone score (TBS) at the lumbar spine, a marker of bone microarchitecture, were measured by dual X-ray absorptiometry. Markers of bone turnover and calcium homeostasis, and gastric hormones were analyzed. The same parameters were measured after three months of treatment with the PPI pantoprazole. The GERD patients displayed a significantly lower TBS at baseline than controls (1.