A nine-redox-related lncRNA signature consisted of 
  , 
  , 
  , 
  , 
  , 
  , 
  , 
  , and 
  was significantly associated with overall survival in ccRCC patients. The signature proved efficient, and thus, a nomogram was successfully assembled. In addition, the GSEA results demonstrated that two major redox-related functions were enhanced in the high-risk group ccRCC patients.
 
  Our findings robustly demonstrate that the nine-redox-related lncRNA signature could serve as an efficient prognostic indicator for ccRCC.
 Our findings robustly demonstrate that the nine-redox-related lncRNA signature could serve as an efficient prognostic indicator for ccRCC.A wide range of clinical applications in regenerative medicine were opened decades ago with the discovery of adult stem cells. Highly promising adult stem cells are mesenchymal stem/stromal cells derived from adipose tissue (ADSCs), primarily because of their abundance and accessibility. These cells have multipotent properties and have been used extensively to carry out autologous transplants. However, the biology of these cells is not entirely understood. Among other factors, the regeneration capacity of these cells will depend on both their capacity of proliferation/differentiation and the robustness of the biochemical pathways that allow them to survive under adverse conditions like those found in damaged tissues. The transcription factors, such as Nanog and Sox2, have been described as playing an important role in stem cell proliferation and differentiation. Also, the so-called longevity pathways, in which AMPK and SIRT1 proteins play a crucial role, are essential for cell homeostasis under stressful situations. These pathways act by inhibiting the translation through downregulation of elongation factor-2 (eEF2). In order to deepen knowledge of mesenchymal stem cell biology and which factors are determinant in the final therapeutic output, we evaluate in the present study the levels of all of these proteins in the ADSCs from humans and rats and how these levels are affected by aging and the oxidative environment. Due to the effect of aging and oxidative stress, our results suggest that before performing a cell therapy with ADSCs, several aspects reported in this study such as oxidative stress status and proliferation and differentiation capacity should be assessed on these cells. This would allow us to know the robustness of the transplanted cells and to predict the therapeutic result, especially in elder patients, where probably ADSCs do not carry out their biological functions in an optimal way.Recent reports indicate that oxidative stress is involved in the pathobiology of acute spinal cord injury or compression myelopathy. We conducted an observational study to determine levels of oxidative stress markers in serum from 80 patients who underwent spinal surgery to treat neurological symptoms related to lumbar degenerative disorders. Serum samples were collected before surgery and at 3 months, 6 months, and 1 year after surgery. Derivatives of reactive oxygen metabolites (ROM) in the serum samples were measured to gauge the level of oxidative stress. For preoperative neurological evaluation, patients were assessed for motor weakness in the lower extremities. We divided the patient samples into two groups ROM decreasing at 1 year after surgery (G group) and ROM increasing at 1 year after surgery (W group). Then, we evaluated clinical outcomes using the visual analog scale and Oswestry disability index (ODI). Among the samples from the 80 enrolled patients, mean ROM levels before surgery increased to 388.5 ± 92.0, indicating the presence of moderate oxidative stress. The level of ROM gradually decreased after surgery and 1 year after surgery the levels had significantly decreased to 367.6 ± 83.3 (p less then 0.05). In patients who exhibited motor weakness, ROM values were significantly increased compared to those patients who had no motor weakness (p less then 0.05). In analyses of clinical outcomes, ODI values for the W group 1 year after surgery were significantly higher than those for the G group (p less then 0.05). Moderate oxidative stress was present in patients who had lumbar degenerative disorders and the degree of oxidative stress gradually improved within 1 year after surgery. The clinical results suggest that neurogenic oxidative stress can be mitigated by surgery for patients with lumbar degenerative disorders, and residual oxidative stress reflects poor surgical outcomes.NLRC3 inhibits inflammatory responses.  https://www.selleckchem.com/products/ex229-compound-991.html  Neuroinflammation induces and accelerates the onset of Alzheimer's disease (AD). This study is aimed at investigating whether NLRC3 plays a role in neuroinflammation, Aβ accumulation, and neuroprotection in AD mice. 12-month-old APP/PS1 transgenic and C57 mice were used for studies in vivo. In vitro, organotypic hippocampal slices were cultured. We found that the expression of NLRC3 was downregulated in the brain tissues of APP/PS1 mice. Mice in the APP/PS1 group had a significant attenuation of learning and memory ability compared to the control group, and the ability was improved in APP/PS1 + LV-NLRC3 mice. The expressions of 6E10, GFAP, Iba1, and PI3K in the hippocampus and brains of APP/PS1 mice were significantly higher than those of the control group, while the expressions of NeuN were lower than that of the control group. With the overexpression of NLRC3 in the APP/PS1 + LV-NLRC3 group, the expressions of 6e10, GFAP, Iba1, and PI3K were significantly lower, while the expression of NeuN was significantly higher compared to the APP/PS1 group. NLRC3 colocalized with NeuN. PI3K activation with 740YP increased the expression of GFAP and Iba-1 in the hippocampus with the exogenous NLRC3 protein. We conclude that NLRC3 may play an important role in the development and progression of AD. Downregulation of NLRC3 can lead to the activation of PI3K, resulting in abnormal plaque deposition, glial cell activation, and neuron loss during AD. NLRC3 delays the progression of AD in APP/PS1 mice via inhibiting PI3K activation.Amyloid-beta (Aβ) is a critical etiological factor for late-onset familial Alzheimer's disease (AD). However, an early-onset AD has been found to be related with an Aβ mutation in glutamic acid 22-to-lysine (Italian type E22K). Why only one single point mutation at E22 residue induces AD remains unclear. Here, we report that a Chinese familial AD pedigree with E22K mutation was associated with higher levels of serum hydrogen peroxide (H2O2) and lower activity of catalase (a H2O2 degrading enzyme) than controls. Further, we found that E22K binding with catalase caused more severe H2O2 accumulation in the brains of E22K-injected rats than Aβ-injected rats. Unexpectedly, H2O2 bound with the mutation site 22K residue of E22K and elicited more rapid aggregation of E22K than Aβ in vitro. Moreover, H2O2 acted with E22K synergistically to induce higher cellular toxicity than with Aβ. Notably, intrahippocampal infusion of E22K led to more severe plaque deposition, neuron death, and more rapid memory decline than Aβ-injected rats.