Selenium effectively inhibits ROS-mediated apoptotic neural precursor cell death in vitro and in vivo in traumatic brain injury

AbstractThis study was designed to investigate possible prevention of apoptotic cell death by selenium, an antioxidant, using cultured brain-derived neural progenitor cells (NPCs) and an experimental mouse brain trauma (BT) model. We tested some of the neuroprotective effects of sodium selenite in NPC cells by monitoring thioredoxin reductase (TR) expression, optimum H2O2 removal, and consequent inhibition of pro-apoptotic events including cytochrome c release and caspase 3 and 9 activation. Analysis of key apoptotic regulators during H2O2-induced apoptosis of NPCs showed that selenite blocks the activation of c-jun N-terminal protein kinase (JNK)/P38 mitogen-activated protein kinase (MAPK), and Akt survival protein. Moreover, selenite activates p44/42 MAPK and inhibits the downregulation of Bcl2 in selenite-treated NPC cells. For in vivo experiments, the effects of selenite on H2O2 neurotoxicity were tested using several biochemical and morphologic markers. Here we show that selenite potentially inhibits H2O2-induced apoptosis of NPCs and in traumatic brain injury. This in vivo protective function was also associated with inhibition of H2O2-induced reactive oxygen species (ROS) generation, cytochrome c release and caspase 3 and 9 activation. Our data show that the protective function of selenite through attenuation of secondary pathological events most likely results from its comprehensive effects that block apoptotic cell death, resulting in the maintenance of functional neurons and in inhibition of astrogliosis. The finding that selenite administration prevents secondary pathological events in an animal model of traumatic brain injury, as well as its efficacy, may provide novel drug targets for treating brain trauma

Exploring Satisfaction with and Trust in Social Networking Sites through the Lens of Fan Pages: Uncertainty Reduction and General Systems Theory Perspective

The purpose of this study is to examine social networking sites (SNS) users’ overall satisfaction with and trust in SNS, as related to their activities of visiting fan pages. We employ two theories—uncertainty reduction theory (URT) and general systems theory (GST)—to examine antecedents affecting overall satisfaction with and trust in SNS. Using a web-based survey, we analyzed 200 SNS users who follow at least one company’s fan page, and utilized seemingly unrelated regression (SUR) models to empirically test our hypotheses. Our findings indicate that uncertainty reduction strategies supported by URT are significantly associated with perceived usefulness of companies’ posts in their fan pages. In turn, perceived usefulness of those posts promotes more visits to the fan page. Finally, users’ perceived usefulness of fan page posts eventually accounts for the overall satisfaction with and trust in SNS. The implications and limitations are discussed at the end of this study

REX-1 Expression and p38 MAPK Activation Status Can Determine Proliferation/Differentiation Fates in Human Mesenchymal Stem Cells

BACKGROUND: REX1/ZFP42 is a well-known embryonic stem cell (ESC) marker. However, the role of REX1, itself, is relatively unknown because the function of REX1 has only been reported in the differentiation of ESCs via STAT signaling pathways. Human mesenchymal stem cells (hMSCs) isolated from young tissues and cancer cells express REX1. METHODOLOGY/PRINCIPAL FINDING: Human umbilical cord blood-derived MSCs (hUCB-MSCs) and adipose tissue-derived MSCs (hAD-MSCs) strongly express REX1 and have a lower activation status of p38 MAPK, but bone marrow-derived MSCs (hBM-MSCs) have weak REX1 expression and higher activation of p38 MAPK. These results indicated that REX1 expression in hMSCs was positively correlated with proliferation rates but inversely correlated with the phosphorylation of p38 MAPK. In hUCB-MSCs, the roles of REX1 and p38 MAPK were investigated, and a knockdown study was performed using a lentiviral vector-based small hairpin RNA (shRNA). After REX1 knockdown, decreased cell proliferation was observed. In REX1 knocked-down hUCB-MSCs, the osteogenic differentiation ability deteriorated, but the adipogenic potential increased or was similar to that observed in the controls. The phosphorylation of p38 MAPK in hUCB-MSCs significantly increased after REX1 knockdown. After p38 MAPK inhibitor treatment, the cell growth in REX1 knocked-down hUCB-MSCs almost recovered, and the suppressed expression levels of CDK2 and CCND1 were also restored. The expression of MKK3, an upstream regulator of p38 MAPK, significantly increased in REX1 knocked-down hUCB-MSCs. The direct binding of REX1 to the MKK3 gene was confirmed by a chromatin immunoprecipitation (ChIP) assay. CONCLUSIONS/SIGNIFICANCE: These findings showed that REX1 regulates the proliferation/differentiation of hMSCs through the suppression of p38 MAPK signaling via the direct suppression of MKK3. Therefore, p38 MAPK and REX-1 status can determine the cell fate of adult stem cells (ASCs). These results were the first to show the role of REX1 in the proliferation/differentiation of ASCs

The diameter of the world wide web

Despite its increasing role in communication, the world wide web remains the least controlled medium: any individual or institution can create websites with unrestricted number of documents and links. While great efforts are made to map and characterize the Internet's infrastructure, little is known about the topology of the web. Here we take a first step to fill this gap: we use local connectivity measurements to construct a topological model of the world wide web, allowing us to explore and characterize its large scale properties.Comment: 5 pages, 1 figure, updated with most recent results on the size of the ww

DHP-Derivative and Low Oxygen Tension Effectively Induces Human Adipose Stromal Cell Reprogramming

BACKGROUND AND METHODS: In this study, we utilized a combination of low oxygen tension and a novel anti-oxidant, 4-(3,4-dihydroxy-phenyl)-derivative (DHP-d) to directly induce adipose tissue stromal cells (ATSC) to de-differentiate into more primitive stem cells. De-differentiated ATSCs was overexpress stemness genes, Rex-1, Oct-4, Sox-2, and Nanog. Additionally, demethylation of the regulatory regions of Rex-1, stemnesses, and HIF1alpha and scavenging of reactive oxygen species were finally resulted in an improved stem cell behavior of de-differentiate ATSC (de-ATSC). Proliferation activity of ATSCs after dedifferentiation was induced by REX1, Oct4, and JAK/STAT3 directly or indirectly. De-ATSCs showed increased migration activity that mediated by P38/JUNK and ERK phosphorylation. Moreover, regenerative efficacy of de-ATSC engrafted spinal cord-injured rats and chemical-induced diabetes animals were significantly restored their functions. CONCLUSIONS/SIGNIFICANCE: Our stem cell remodeling system may provide a good model which would provide insight into the molecular mechanisms underlying ATSC proliferation and transdifferentiation. Also, these multipotent stem cells can be harvested may provide us with a valuable reservoir of primitive and autologous stem cells for use in a broad spectrum of regenerative cell-based disease therapy

Quantum Optical Induced-Coherence Tomography by a Hybrid Interferometer

Quantum interferometry based on induced-coherence phenomena has demonstrated the possibility of undetected-photon measurements. Perturbation in the optical path of probe photons can be detected by interference signals generated by quantum mechanically correlated twin photons propagating through a different path, possibly at a different wavelength. To the best of our knowledge, this work demonstrates for the first time a hybrid-type induced-coherence interferometer that incorporates a Mach-Zehnder-type interferometer for visible photons and a Michelson-type interferometer for infrared photons, based on double-pass pumped spontaneous parametric down-conversion. This configuration enables infrared optical measurements via the detection of near-visible photons and provides methods for characterizing the quality of measurements by identifying photon pairs of different origins. The results verify that the induced-coherence interference visibility is approximately the same as the heralding efficiencies between twin photons along the relevant spatial modes. Applications to both time-domain and frequency-domain quantum-optical induced-coherence tomography for three-dimensional test structures are demonstrated. The results prove the feasibility of practical undetected-photon sensing and imaging techniques based on the presented structure