Epidemiological characteristics of Pandemic Influenza A (H1N1-2009) in Zhanjiang, China

Background: A novel influenza A virus strain (H1N1-2009) spread first in Mexico and the United Stated in late April 2009, leading to the first influenza pandemic of the 21st century. The objective of this study was to determine the epidemiological and virological characteristics of the pandemic influenza A (H1N1-2009) in Zhanjiang, China. Methods: The case and outbreak reports of influenza-like illness (ILI) were collected from the Chinese information system of disease control and prevention and the influenza surveillance system of Zhanjiang city. Real-time RT-PCR was conducted, and epidemic and virological characteristics of the virus were analyzed using descriptive epidemiological methods and Chi-square trend tests. Results: A total of 276 reported cases were confirmed from July 16, 2009 to June 30, 2010. The attack rate of outbreak was from 1.1% to 6.0%. The disease peak occurred in December 2009, after which the outbreak subsided gradually. The last case was confirmed in April 2010. Conclusion: The main population struck by the H1N1-2009 virus was young adults, youths and children. The outbreaks most frequently occurred in schools, and most cases were acquired locally

Production of mobile invertebrate communities on shallow reefs from temperate to tropical seas

Primary productivity of marine ecosystems is largely driven by broad gradients in environmental and ecological properties. By contrast, secondary productivity tends to be more variable, influenced by bottom-up (resource-driven) and top-down (predatory) processes, other environmental drivers, and mediation by the physical structure of habitats. Here, we use a continental-scale dataset on small mobile invertebrates (epifauna), common on surfaces in all marine ecosystems, to test influences of potential drivers of temperature-standardized secondary production across a large biogeographic range. We found epifaunal production to be remarkably consistent along a temperate to tropical Australian latitudinal gradient of 28.6°, spanning kelp forests to coral reefs (approx. 3500 km). Using a model selection procedure, epifaunal production was primarily related to biogenic habitat group, which explained up to 45% of total variability. Production was otherwise invariant to predictors capturing primary productivity, the local biomass of fishes (proxy for predation pressure), and environmental, geographical, and human impacts. Highly predictable levels of epifaunal productivity associated with distinct habitat groups across continental scales should allow accurate modelling of the contributions of these ubiquitous invertebrates to coastal food webs, thus improving understanding of likely changes to food web structure with ocean warming and other anthropogenic impacts on marine ecosystems

Structure and mechanism of human DNA polymerase η

The variant form of the human syndrome xeroderma pigmentosum (XPV) is caused by a deficiency in DNA polymerase eta (Pol eta), a DNA polymerase that enables replication through ultraviolet-induced pyrimidine dimers. Here we report high-resolution crystal structures of human Pol eta at four consecutive steps during DNA synthesis through cis-syn cyclobutane thymine dimers. Pol eta acts like a 'molecular splint' to stabilize damaged DNA in a normal B-form conformation. An enlarged active site accommodates the thymine dimer with excellent stereochemistry for two-metal ion catalysis. Two residues conserved among Pol eta orthologues form specific hydrogen bonds with the lesion and the incoming nucleotide to assist translesion synthesis. On the basis of the structures, eight Pol eta missense mutations causing XPV can be rationalized as undermining the molecular splint or perturbing the active-site alignment. The structures also provide an insight into the role of Pol eta in replicating through D loop and DNA fragile sites

Accountable Tracing Signatures from Lattices

Group signatures allow users of a group to sign messages anonymously in the name of the group, while incorporating a tracing mechanism to revoke anonymity and identify the signer of any message. Since its introduction by Chaum and van Heyst (EUROCRYPT 1991), numerous proposals have been put forward, yielding various improvements on security, efficiency and functionality. However, a drawback of traditional group signatures is that the opening authority is given too much power, i.e., he can indiscriminately revoke anonymity and there is no mechanism to keep him accountable. To overcome this problem, Kohlweiss and Miers (PoPET 2015) introduced the notion of accountable tracing signatures (ATS) - an enhanced group signature variant in which the opening authority is kept accountable for his actions. Kohlweiss and Miers demonstrated a generic construction of ATS and put forward a concrete instantiation based on number-theoretic assumptions. To the best of our knowledge, no other ATS scheme has been known, and the problem of instantiating ATS under post-quantum assumptions, e.g., lattices, remains open to date. In this work, we provide the first lattice-based accountable tracing signature scheme. The scheme satisfies the security requirements suggested by Kohlweiss and Miers, assuming the hardness of the Ring Short Integer Solution (RSIS) and the Ring Learning With Errors (RLWE) problems. At the heart of our construction are a lattice-based key-oblivious encryption scheme and a zero-knowledge argument system allowing to prove that a given ciphertext is a valid RLWE encryption under some hidden yet certified key. These technical building blocks may be of independent interest, e.g., they can be useful for the design of other lattice-based privacy-preserving protocols.Comment: CT-RSA 201

Next-to-leading order QCD predictions for Z0H0+jetZ^0 H^0 + {\rm jet} production at LHC

We calculate the complete next-to-leading order (NLO) QCD corrections to the $Z^0H^0$ production in association with a jet at the LHC. We study the impacts of the NLO QCD radiative corrections to the integrated and differential cross sections and the dependence of the cross section on the factorization/renormalization scale. We present the transverse momentum distributions of the final $Z^0$-, Higgs-boson and leading-jet. We find that the NLO QCD corrections significantly modify the physical observables, and obviously reduce the scale uncertainty of the LO cross section. The QCD K-factors can be 1.183 and 1.180 at the $\sqrt{s}=14 TeV$ and $\sqrt{s}=7 TeV$ LHC respectively, when we adopt the inclusive event selection scheme with $p_{T,j}^{cut}=50 GeV$, $m_H=120 GeV$ and $\mu=\mu_r=\mu_f=\mu_0 \equiv 1/2(m_Z+m_H)$. Furthermore, we make the comparison between the two scale choices, $\mu=\mu_0$ and $\mu=\mu_1=1/2(E_{T}^{Z}+E_{T}^{H}+ \sum_{j}E_{T}^{jet})$, and find the scale choice $\mu=\mu_1$ seems to be more appropriate than the fixed scale $\mu=\mu_0$.Comment: 18 pages, 7 figure

Preconditioning of mesenchymal stromal cells with low-intensity ultrasound: influence on chondrogenesis and directed SOX9 signaling pathways

Background: Continuous low-intensity ultrasound (cLIUS) facilitates the chondrogenic differentiation of human mesenchymal stromal cells (MSCs) in the absence of exogenously added transforming growth factor-beta (TGFβ) by upregulating the expression of transcription factor SOX9, a master regulator of chondrogenesis. The present study evaluated the molecular events associated with the signaling pathways impacting SOX9 gene and protein expression under cLIUS. Methods: Human bone marrow-derived MSCs were exposed to cLIUS stimulation at 14 kPa (5 MHz, 2.5 Vpp) for 5 min. The gene and protein expression of SOX9 was evaluated. The specificity of SOX9 upregulation under cLIUS was determined by treating the MSCs with small molecule inhibitors of select signaling molecules, followed by cLIUS treatment. Signaling events regulating SOX9 expression under cLIUS were analyzed by gene expression, immunofluorescence staining, and western blotting. Results: cLIUS upregulated the gene expression of SOX9 and enhanced the nuclear localization of SOX9 protein when compared to non-cLIUS-stimulated control. cLIUS was noted to enhance the phosphorylation of the signaling molecule ERK1/2. Inhibition of MEK/ERK1/2 by PD98059 resulted in the effective abrogation of cLIUS-induced SOX9 expression, indicating that cLIUS-induced SOX9 upregulation was dependent on the phosphorylation of ERK1/2. Inhibition of integrin and TRPV4, the upstream cell-surface effectors of ERK1/2, did not inhibit the phosphorylation of ERK1/2 and therefore did not abrogate cLIUS-induced SOX9 expression, thereby suggesting the involvement of other mechanoreceptors. Consequently, the effect of cLIUS on the actin cytoskeleton, a mechanosensitive receptor regulating SOX9, was evaluated. Diffused and disrupted actin fibers observed in MSCs under cLIUS closely resembled actin disruption by treatment with cytoskeletal drug Y27632, which is known to increase the gene expression of SOX9. The upregulation of SOX9 under cLIUS was, therefore, related to cLIUS-induced actin reorganization. SOX9 upregulation induced by actin reorganization was also found to be dependent on the phosphorylation of ERK1/2. Conclusions: Collectively, preconditioning of MSCs by cLIUS resulted in the nuclear localization of SOX9, phosphorylation of ERK1/2 and disruption of actin filaments, and the expression of SOX9 was dependent on the phosphorylation of ERK1/2 under cLIUS

Id-1 stimulates cell proliferation through activation of EGFR in ovarian cancer cells

Increased EGFR (epidermal growth factor receptor) expression has been reported in many types of human cancer and its levels are positively associated with advanced cancers. Recently, upregulation of Id-1 (inhibitor of differentiation or DNA binding) protein was found in over 70% of ovarian cancer samples and correlated with poor survival of ovarian cancer patients. However, the molecular mechanisms responsible for the role of Id-1 in ovarian cancer are not clear. The aim of this study was to investigate the effect of Id-1 on ovarian cancer proliferation and its association with the EGFR pathway. To achieve this, we transfected an Id-1 expression vector into three ovarian cancer cell lines and examined cell proliferation rate by flow cytometry and bromodeoxyuridine staining. We found that ectopic Id-1 expression led to increased cell proliferation demonstrated by increased BrdU incorporation rate and S-phase fraction. The Id-1-induced cell growth was associated with upregulation of EGFR at both transcriptional and protein levels. In contrast, inactivation of Id-1 through transfection of an Id-1 antisense vector resulted in downregulation of EGFR. Our results indicate that increased Id-1 in ovarian cancer cells may promote cancer cell proliferation through upregulation of EGFR. Our findings also implicate that Id-1 may be a potential target for the development of novel strategies in the treatment of ovarian cancer. © 2004 Cancer Research UK.link_to_OA_fulltex