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R-spondins are a family of secreted Wnt agonists. One of the family members, R-spondin 2 (RSPO2), has an important role in embryonic development, bone formation and myogenic differentiation; however, its role in human cancers remains largely unknown. Here we show that RSPO2 expression is downregulated in human colorectal cancers (CRCs) due to promoter hypermethylation, and that the RSPO2 reduction correlates with tumour differentiation, size and metastasis. Overexpression of RSPO2 suppresses CRC cell proliferation and tumorigenicity, whereas the depletion of RSPO2 enhances tumour cell growth. RSPO2 has an inhibitory effect on Wnt/β-catenin signaling in the CRC cells that show suppressed cell proliferation. In human CRC cells, the RSPO2-induced inhibition of Wnt signaling depends on leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5); RSPO2 interacts with LGR5 to stabilize the membrane-associated zinc and ring finger 3 (ZNRF3). Our data suggest that RSPO2 functions as a tumour suppressor in human CRCs, and these data reveal a RSPO2-induced, LGR5-dependent Wnt signaling-negative feedback loop that exerts a net growth-suppressive effect on CRC cells.

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Summary The security of space information network (SIN) is getting more and more important now. Because of the special features of SIN (e.g., the dynamic and unstable topology, the highly exposed links, the restricted computation power, the flexible networking methods, and so on), the security protocol for SIN should have a balance between security properties and computation/storage overhead. Although a lot of security protocols have been proposed recently, few can provide overall attacks resistance power with low computation and storage cost. To solve this problem, in this paper we propose a lightweight authentication scheme for space information network. It is mainly based on the self‐updating strategy for user's temporary identity. The scheme consists of two phases, namely, the registration phase and the authentication phase. All the computing operations involved are just hash function (h), the bit‐wise exclusive‐or operation (⊕), and the string concatenation operation (||), which are of low computation cost. The security properties discussion and the attacks–resistance power analysis show that the proposed authentication scheme can defend against various typical attacks, especially denial of service attacks. It is sufficiently secure with the lowest computation and storage costs. Furthermore, the formal security proof in SVO logic also demonstrates that the scheme can satisfy the security goals very well. Copyright © 2016 John Wiley & Sons, Ltd.

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This study tested the Escape Theory prediction that individuals blaming themselves for failure experience increased accessibility to implicit suicidal mind. One hundred and thirty-eight undergraduate medical students were randomly assigned to three groups: failure-related priming, success-related priming, and control. Following experimental conditions, participants completed a death/suicide Implicit Association Test. Results revealed significant differences between groups in accessibility to implicit suicidal mind. Furthermore, priming manipulation interacted with individual differences in locus of control (LOC). Significant differences in accessibility to implicit suicidal mind were observed in individuals with internal LOC, while effects of priming manipulation were eliminated in individuals with external LOC.

To avoid the abuse and misuse of antibiotics, procalcitonin (PCT) and C-reactive protein (CRP) have been used as new approaches to identify different types of infection. Multiple databases were adopted to search relevant studies, and the articles that satisfied the inclusion criteria were included. Meta-analyses were conducted with Review Manager 5.0, and to estimate the quality of each article, risk of bias was assessed. Eight articles satisfied the inclusion criteria. The concentrations of both PCT and CRP in patients with bacterial infection were higher than those with non-bacterial infection. Both PCT and CRP levels in patients with G− bacterial infection were higher than in those with G+ bacterial infection and fungus infection. In the G+ bacterial infection group, a higher concentration of CRP was observed compared with fungus infection group, while the difference of PCT between G+ bacterial infection and fungus infection was not significant. Our study suggested that both PCT and CRP are helpful to a certain extent in detecting pneumonia caused by different types of infection.

Human cytomegalovirus (HCMV), like many other DNA viruses, can cause genome instability and activate a DNA damage response (DDR). Activation of ataxia-telangiectasia mutated (ATM), a kinase activated by DNA breaks, is a hallmark of the HCMV-induced DDR. Here we investigated the activation of caspase-2, an initiator caspase activated in response to DNA damage and supernumerary centrosomes. Of 7 HCMV strains tested, only strain AD169 activated caspase-2 in infected fibroblasts. Treatment with an ATM inhibitor or inactivation of PIDD or RAIDD inhibited caspase-2 activation, indicating that caspase-2 was activated by the PIDDosome. A set of chimeric HCMV strains was used to identify the genetic basis of this phenotype. Surprisingly, we found a single nucleotide polymorphism within the AD169 UL55 ORF, resulting in a D275Y amino acid exchange within glycoprotein B (gB), to be responsible for caspase-2 activation. As gB is an envelope glycoprotein required for fusion with host cell membranes, we tested whether gB(275Y) altered viral entry into fibroblasts. While entry of AD169 expressing gB(275D) proceeded slowly and could be blocked by a macropinocytosis inhibitor, entry of wild-type AD169 expressing gB(275Y) proceeded more rapidly, presumably by envelope fusion with the plasma membrane. Moreover, gB(275Y) caused the formation of syncytia with numerous centrosomes, suggesting that cell fusion triggered caspase-2 activation. These results suggest that gB variants with increased fusogenicity accelerate viral entry, cause cell fusion, and thereby compromise genome stability. They further suggest the ATM-PIDDosome-caspase-2 signaling axis alerts the cell of potentially dangerous cell fusion.