By adopting the differential age method, we utilize selected 17832 luminous red galaxies (LRGs) from Sloan Digital Sky Survey Data Release Seven (SDSS DR7) covering redshift 0 < z < 0.4 to measure Hubble parameters. Using a full spectrum fitting package UlySS, these spectra are reduced with single stellar population (SSP) models and optimal age information of our selected sample are derived. With the decreasing ageredshift relation, four new observational H(z) data (OHD) points are obtained, which are H(z) = 69.0 ± 19.6 km s −1 Mpc −1 at z = 0.07, H(z) = 68.6 ± 26.2 km s −1 Mpc −1 at z = 0.12, H(z)=72.9 ± 29.6 km s −1 Mpc −1 at z = 0.2 and H(z)=88.8 ± 36.6 km s −1 Mpc −1 at z = 0.28, respectively. Combined with other 21 available OHD data points, a performance of constraint on both flat and non-flat ΛCDM model is presented.
Abstract. This paper reviews progress on understanding biological carbon sequestration in the ocean with special reference to the microbial formation and transformation of recalcitrant dissolved organic carbon (RDOC), the microbial carbon pump (MCP). We propose that RDOC is a concept with a wide continuum of recalcitrance. Most RDOC compounds maintain their levels of recalcitrance only in a specific environmental context (RDOC t ). The ocean RDOC pool also contains compounds that may be inaccessible to microbes due to their extremely low concentration (RDOC c ). This differentiation allows us to appreciate the linkage between microbial source and RDOC composition on a range of temporal and spatial scales.Analyses of biomarkers and isotopic records show intensive MCP processes in the Proterozoic oceans when the MCP could have played a significant role in regulating climate. Understanding the dynamics of the MCP in conjunction with the better constrained biological pump (BP) over geological timescales could help to predict future climate trends. Integration of the MCP and the BP will require new research approaches and opportunities. Major goals include understanding the interactions between particulate organic carbon (POC) and RDOC that contribute to sequestration efficiency, and the concurrent determination of the chemical composition of organic carbon, microbial community composition and enzymatic activity. Molecular biomarkers and isotopic tracers should be employed to link water column processes Published by Copernicus Publications on behalf of the European Geosciences Union. N. Jiao et al.: Mechanisms of microbial carbon sequestration in the oceanto sediment records, as well as to link present-day observations to paleo-evolution. Ecosystem models need to be developed based on empirical relationships derived from bioassay experiments and field investigations in order to predict the dynamics of carbon cycling along the stability continuum of POC and RDOC under potential global change scenarios. We propose that inorganic nutrient input to coastal waters may reduce the capacity for carbon sequestration as RDOC. The nutrient regime enabling maximum carbon storage from combined POC flux and RDOC formation should therefore be sought.
Object Aneurysmal subarachnoid hemorrhage (SAH) causes devastating rates of mortality and morbidity. Accumulating studies indicate that early brain injury (EBI) greatly contributes to poor outcomes after SAH and that oxidative stress plays an important role in the development of EBI following SAH. Astaxanthin (ATX), one of the most common carotenoids, has a powerful antioxidative property. However, the potential role of ATX in protecting against EBI after SAH remains obscure. The goal of this study was to assess whether ATX can attenuate SAH-induced brain edema, blood-brain barrier permeability, neural cell death, and neurological deficits, and to elucidate whether the mechanisms of ATX against EBI are related to its powerful antioxidant property. Methods Two experimental SAH models were established, including a prechiasmatic cistern SAH model in rats and a one-hemorrhage SAH model in rabbits. Both intracerebroventricular injection and oral administration of ATX were evaluated in this experiment. Posttreatment assessments included neurological scores, body weight loss, brain edema, Evans blue extravasation, Western blot analysis, histopathological study, and biochemical estimation. Results It was observed that an ATX intracerebroventricular injection 30 minutes post-SAH could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, neural cell apoptosis, and neurological dysfunction) after SAH in rats. Meanwhile, delayed treatment with ATX 3 hours post-SAH by oral administration was also neuroprotective in both rats and rabbits. In addition, the authors found that ATX treatment could prevent oxidative damage and upregulate the endogenous antioxidant levels in the rat cerebral cortex following SAH. Conclusions These results suggest that ATX administration could alleviate EBI after SAH, potentially through its powerful antioxidant property. The authors conclude that ATX might be a promising therapeutic agent for EBI following SAH.
BackgroundGlioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioma stem cells (GSCs). Self-renewal is a complex biological process necessary for maintaining the glioma stem cells. Nuclear factor rythroid 2-related factor 2(Nrf2) plays a significant role in protecting cells from endogenous and exogenous stresses. Nrf2 is a key nuclear transcription factor that regulates antioxidant response element (ARE)-containing genes. Previous studies have demonstrated the significant role of Nrf2 in the proliferation of glioblastoma, and in their resistance to radioactive therapies. We examined the effect of knocking down Nrf2 in GSCs.MethodsNrf2 expression was down-regulated by shRNA transinfected with lentivirus. Expression levels of Nestin, Nrf2, BMI-1, Sox2 and Cyclin E were assessed by western blotting, quantitative polymerase chain reaction (qPCR) and immunohistochemistry analysis. The capacity for self-renewal in vitro was assessed by genesis of colonies. The capacity for self-renewal in vivo was analyzed by tumor genesis of xenografts in nude mice.ResultsKnockdown of Nrf2 inhibited the proliferation of GSCs, and significantly reduced the expression of BMI-1, Sox2 and CyclinE. Knocking down of Nrf2 changed the cell cycle distribution of GSCs by causing an uncharacteristic increase in the proportion of cells in the G2 phase and a decrease in the proportion of cells in the S phase of the cell cycle.ConclusionsNrf2 is required to maintain the self-renewal of GSCs, and its down-regulation can attenuate the self-renewal of GSCs significantly.
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