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1.  Quasi-two-dimensional superconductivity from dimerization of atomically ordered AuTe2Se4/3 cubes 
Nature Communications  2017;8:871.
The emergent phenomena such as superconductivity and topological phase transitions can be observed in strict two-dimensional (2D) crystalline matters. Artificial interfaces and one atomic thickness layers are typical 2D materials of this kind. Although having 2D characters, most bulky layered compounds, however, do not possess these striking properties. Here, we report quasi-2D superconductivity in bulky AuTe2Se4/3, where the reduction in dimensionality is achieved through inducing the elongated covalent Te–Te bonds. The atomic-resolution images reveal that the Au, Te, and Se are atomically ordered in a cube, among which are Te–Te bonds of 3.18 and 3.28 Å. The superconductivity at 2.85 K is discovered, which is unraveled to be the quasi-2D nature owing to the Berezinsky–Kosterlitz–Thouless topological transition. The nesting of nearly parallel Fermi sheets could give rise to strong electron–phonon coupling. It is proposed that further depleting the thickness could result in more topologically-related phenomena.
Emergent phenomena often appear in crystals in the two-dimensional limit but are rare in bulky compounds. Here, Guo et al. report a quasi-two-dimensional superconductivity in a bulk material AuTe2Se4/3 at 2.85 K, potentially owing to a topological transition.
doi:10.1038/s41467-017-00947-0
PMCID: PMC5636790  PMID: 29021625
2.  Adiposity and blood pressure among 55 000 relatively lean rural adults in southwest of China 
Chen, X | Du, H | Zhang, J | Chen, X | Luo, G | Que, X | Zhang, N | Bian, Z | Guo, Y | Li, L | Chen, Z | Wu, X
doi:10.1038/jhh.2017.13
PMCID: PMC5508804  PMID: 28589951
3.  Adenosine A2A receptor inactivation alleviates early-onset cognitive dysfunction after traumatic brain injury involving an inhibition of tau hyperphosphorylation 
Translational Psychiatry  2017;7(5):e1123-.
Tau is a microtubule-associated protein, and the oligomeric and hyperphosphorylated forms of tau are increased significantly after neurotrauma and considered important factors in mediating cognitive dysfunction. Blockade of adenosine A2A receptors, either by caffeine or gene knockout (KO), alleviates cognitive dysfunction after traumatic brain injury (TBI). We postulated that A2AR activation exacerbates cognitive impairment via promoting tau hyperphosphorylation. Using a mouse model of moderate controlled cortical impact, we showed that TBI induced hyperphosphorylated tau (p-tau) in the hippocampal dentate gyrus and spatial memory deficiency in the Morris water maze test at 7 days and 4 weeks after TBI. Importantly, pharmacological blockade (A2AR antagonist ZM241385 or non-selective adenosine receptor antagonist caffeine) or genetic inactivation of A2ARs reduced the level of tau phosphorylation at Ser404 and alleviated spatial memory dysfunction. The A2AR control of p-tau is further supported by the observations that a KO of A2AR decreased the activity of the tau phosphorylation kinases, glycogen synthase kinase-3β (GSK-3β) and protein kinase A (PKA) after TBI, and by that CGS21680 (A2AR agonist) exacerbated okadaic acid-induced tau hyperphosphorylation in cultured primary hippocampal neurons. Lastly, CGS21680-induced neuronal tau hyperphosphorylation and axonal injury were effectively alleviated by individual treatments with ZM241385 (A2AR antagonist), H89 (PKA antagonist) and SB216763 (GSK-3β antagonist), or by the combined treatment with H89 and SB216763. Our findings suggest a novel mechanism whereby A2AR activation triggers cognitive dysfunction by increasing the phosphorylation level of tau protein after TBI and suggest a promising therapeutic and prophylactic strategy by targeting aberrant A2AR signaling via tau phosphorylation.
doi:10.1038/tp.2017.98
PMCID: PMC5534966  PMID: 28485728
4.  HPV16 DNA and integration in normal and malignant epithelium: implications for the etiology of laryngeal squamous cell carcinoma 
Annals of Oncology  2017;28(5):1105-1110.
Background
Molecular evidence suggests that human papillomavirus (HPV) has a role in the etiology of oropharyngeal squamous cell carcinoma. However, the role of HPV in laryngeal squamous cell carcinoma (LSCC) is unclear.
Patients and methods
We conducted a case–control study using tumor tissue specimens from 300 LSCC patients and vocal cord polyp specimens from 300 cancer-free controls. HPV genotype, HPV16 viral load and viral integration status, and p16 expression were determined.
Results
The prevalence of HPV (all types) was higher in cases than controls [21 (7.0%) versus 10 (3.3%), adjusted odds ratio (aOR) 2.37, 95% CI 1.08–5.21]. The prevalence of HPV16 was higher in cases than controls [20 (6.7%) versus 8 (2.7%), aOR 2.84, 95% CI 1.21–6.68]. The risk of LSCC associated with HPV16 DNA positivity was even higher in patients aged 55 years or younger (aOR 3.52, 95% CI 1.07–11.54), males (aOR 4.74, 95% CI 1.33–16.90), never-smokers (aOR 5.57, 95% CI 1.41–22.10), and never-drinkers (aOR 3.72, 95% CI 1.09–12.72). HPV DNA was partly or fully integrated in all 20 HPV16-positive cases but was episomal in all 8 HPV16-positive controls; however, the HPV16-positive cases and controls had similar viral loads (P = 0.28). P16 immunostaining was positive in 31 of the 300 cases (10.3%) and negative in all 300 controls.
Conclusion
These results suggest that prior infection with HPV16 may play a role in the etiology of some LSCC. This larger case–control study will offer for the first time the possibility to address in depth the understanding of a tissue-specific role of HPV in laryngeal carcinogenesis. Further studies with larger samples are needed to confirm these findings.
doi:10.1093/annonc/mdx027
PMCID: PMC5406756  PMID: 28327951
human papillomavirus; head and neck cancer; laryngeal cancer; risk; viral load; physical status
5.  Adiposity and blood pressure among 55 000 relatively lean rural adults in southwest of China 
Chen, X | Du, H | Zhang, J | Chen, X | Luo, G | Que, X | Zhang, N | Bian, Z | Guo, Y | Li, L | Chen, Z | Wu, X
Journal of Human Hypertension  2015;29(9):522-529.
Obesity is a strong determinant of blood pressure. Uncertainty remains, however, about which indices of adiposity most strongly predict blood pressure, particularly among those who were relatively lean, such as those from rural China. We analyzed cross-sectional data on 55 687 (38.3% men) participants aged 30–79 years who were enrolled into the China Kadoorie Biobank from a rural county in southwest of China during 2004–2008. Measured body mass index (BMI) and waist circumference (WC) were related to blood pressure in multivariable linear regression analyses. The overall mean values of BMI, WC, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were 23.3 kg m−2, 78.0 cm, 129.2 mm Hg and 77.2 mm Hg, respectively. There was a strongly positive, and apparently linear, relationship of BMI and WC with blood pressure, with 1 s.d. higher BMI associated with 4.3/2.3 mm Hg higher SBP/DBP and 1 s.d. WC associated with 3.8/2.1 mm Hg (P<0.0001). Additional adjustment for WC only slightly attenuated the association of BMI with blood pressure, whereas additional adjustment for BMI almost completely eliminated the association of WC with blood pressure. Our findings suggest that in relatively lean Chinese adults, general adiposity is more strongly assciated with blood pressure than central adiposity.
doi:10.1038/jhh.2014.129
PMCID: PMC4537884  PMID: 25652532
6.  Humoural immune response and pathological analysis in patients with false immune diagnosis of cystic echinococcosis 
Parasite Immunology  2014;36(4):170-176.
The patients with false immune diagnosis of hydatid disease were investigated for the humoural immune response to analyse the possible reasons and mechanism leading to false immune diagnosis. Two hundred and thirty-nine patients with nature-unknown cysts and 30 healthy controls were detected by immunological assays (four hydatid antigen-based immunogold filtration assay and enzyme-linked immune absorbent assay) and ultrasound. Sensitivity of and specificity of immunological assay and ultrasound were calculated, respectively. The serological diagnosis was compared with surgical pathology to screen the patients with false immune diagnosis for the immunoglobulin measurement and pathological analysis. The history and cyst characteristics were also reviewed. The results indicate the immunoglobulin has little influence on false immunodiagnosis. The false-negative immunodiagnosis was caused by the cysts' inactive status while the false positive caused by previous rupture, antigen cross-reaction. The clinical diagnosis of cystic echinococcosis requires a combination of immunodiagnosis and ultrasonography, which is the necessary complementary confirmation.
doi:10.1111/pim.12096
PMCID: PMC4312899  PMID: 24372157
false negative; false positive; humoural immune response; hydatid disease; immunological assay
7.  A novel nickel complex works as a proteasomal deubiquitinase inhibitor for cancer therapy 
Zhao, C | Chen, X | Zang, D | Lan, X | Liao, S | Yang, C | Zhang, P | Wu, J | Li, X | Liu, N | Liao, Y | Huang, H | Shi, X | Jiang, L | Liu, X | He, Z | Dou, QP | Wang, X | Liu, J
Oncogene  2016;35(45):5916-5927.
Based on the central role of the ubiquitin–proteasome system (UPS) in the degradation of cellular proteins, proteasome inhibition has been considered an attractive approach for anticancer therapy. Deubiquitinases (DUBs) remove ubiquitin conjugates from diverse substrates; therefore, they are essential regulators of the UPS. DUB inhibitors, especially the inhibitors of proteasomal DUBs are becoming a research hotspot in targeted cancer therapy. Previous studies have shown that metal complexes, such as copper and zinc complexes, can induce cancer cell apoptosis through inhibiting UPS function. Moreover, we have found that copper pyrithione inhibits both 19S proteasome-associated DUBs and 20S proteasome activity with a mechanism distinct from that of the classical 20S proteasome inhibitor bortezomib. In the present study, we reveal that (i) nickel pyrithione complex (NiPT) potently inhibits the UPS via targeting the 19S proteasome-associated DUBs (UCHL5 and USP14), without effecting on the 20S proteasome; (ii) NiPT selectively induces proteasome inhibition and apoptosis in cultured tumor cells and cancer cells from acute myeloid leukemia human patients; and (iii) NiPT inhibits proteasome function and tumor growth in nude mice. This study, for the first time, uncovers a nickel complex as an effective inhibitor of the 19S proteasomal DUBs and suggests a potentially new strategy for cancer treatment.
doi:10.1038/onc.2016.114
PMCID: PMC5497060  PMID: 27086925
8.  Cooperative polariton dynamics in feedback-coupled cavities 
Nature Communications  2017;8:1437.
The emerging field of cavity spintronics utilizes the cavity magnon polariton (CMP) induced by magnon Rabi oscillations. In contrast to a single-spin quantum system, such a cooperative spin dynamics in the linear regime is governed by the classical physics of harmonic oscillators. It makes the magnon Rabi frequency independent of the photon Fock state occupation, and thereby restricts the quantum application of CMP. Here we show that a feedback cavity architecture breaks the harmonic-oscillator restriction. By increasing the feedback photon number, we observe an increase in the Rabi frequency, accompanied with the evolution of CMP to a cavity magnon triplet and a cavity magnon quintuplet. We present a theory that explains these features. Our results reveal the physics of cooperative polariton dynamics in feedback-coupled cavities, and open up new avenues for exploiting the light–matter interactions.
Rabi oscillations of magnons typically do not have few photon control of single spin quantum systems. Here, the authors use a feedback cavity architecture to increase magnon-photon cooperativity, enabling increased control of light-matter interactions in magnonic systems via cooperative polariton dynamics.
doi:10.1038/s41467-017-01796-7
PMCID: PMC5681655  PMID: 29127391
9.  Childhood internalizing behaviour: analysis and implications 
The concept of ‘internalizing behaviour’ reflects a child’s emotional or psychological state and typically includes depressive disorders, anxiety disorders, somatic complaints and teenage suicide. Genetic and environmental causes have been largely implicated, although research continues to explore social etiological factors. Some research suggests females may be especially vulnerable to internalizing disorders, while data across ethnicities are somewhat variable. Regarding treatment, cognitive-behavioural therapies and use of pharmacological approaches (i.e. selective serotonin reuptake inhibitors) have both shown great promise in reducing symptoms of internalizing disorders. However, given the role of the social environment, prevention programmes aimed at reducing exposure to drugs, violence/abuse and environmental toxins are highly important. Internalizing disorders are associated with a host of deleterious outcomes (e.g. school drop-out, substance use and potentially suicide) as well as psychopathological outcomes (e.g. co-morbid anxiety or depression, externalizing disorders – including suicide). Children with mental health problems suffer educationally and are more likely to become entangled in the justice and welfare systems. Clearly, early treatment and prevention programmes for internalizing disorders need to be a priority from a public health perspective as well as from a family and community perspective.
doi:10.1111/j.1365-2850.2011.01743.x
PMCID: PMC5675073  PMID: 22070805
behaviour problems; children; internalizing behaviour
10.  The miR-181d-regulated metalloproteinase Adamts1 enzymatically impairs adipogenesis via ECM remodeling 
Cell Death and Differentiation  2016;23(11):1778-1791.
The extracellular matrix (ECM) maintenance is crucial to the structural integrity of adipocytes and whole adipose tissue formation. However, the potential impact of the ECM on adipocyte lineage commitment is unclear. Herein, we demonstrate that forced expression of matrix-associated metalloproteinase Adamts1 (a disintegrin and metalloproteinase with thrombospondin motifs 1), which we show is targeted by microRNA-181d (miR-181d) during BMP4-induced adipocytic lineage commitment, markedly impairs adipocyte commitment. Conversely, siRNA-induced inhibition of Adamts1 promotes adipocyte commitment. Adamst1 metalloprotease activity is required for this inhibition and is determined to function via remodeling ECM components followed by activating FAK–ERK signaling pathway during the commitment process. Furthermore, ablation of Adamts1 in adipose tissue increases adipose tissue mass, reduces insulin sensitivity, and disrupts lipid homeostasis. This finding is consistent with Adamts1 decreased expression in the adipose tissue of obese mice and an inverse correlation of Adamts1 expression with body mass index in humans. Collectively, our results indicate that Adamts1 acts as an ECM ‘modifier', with miR-181d-induced downregulation, that regulates adipocyte lineage commitment and obesity.
doi:10.1038/cdd.2016.66
PMCID: PMC5071569  PMID: 27447109
11.  Performance of the ATLAS track reconstruction algorithms in dense environments in LHC Run 2 
Aaboud, M. | Aad, G. | Abbott, B. | Abdallah, J. | Abdinov, O. | Abeloos, B. | Abidi, S. H. | AbouZeid, O. S. | Abraham, N. L. | Abramowicz, H. | Abreu, H. | Abreu, R. | Abulaiti, Y. | Acharya, B. S. | Adachi, S. | Adamczyk, L. | Adelman, J. | Adersberger, M. | Adye, T. | Affolder, A. A. | Agatonovic-Jovin, T. | Agheorghiesei, C. | Aguilar-Saavedra, J. A. | Ahlen, S. P. | Ahmadov, F. | Aielli, G. | Akatsuka, S. | Akerstedt, H. | Åkesson, T. P. A. | Akimov, A. V. | Alberghi, G. L. | Albert, J. | Albicocco, P. | Alconada Verzini, M. J. | Aleksa, M. | Aleksandrov, I. N. | Alexa, C. | Alexander, G. | Alexopoulos, T. | Alhroob, M. | Ali, B. | Aliev, M. | Alimonti, G. | Alison, J. | Alkire, S. P. | Allbrooke, B. M. M. | Allen, B. W. | Allport, P. P. | Aloisio, A. | Alonso, A. | Alonso, F. | Alpigiani, C. | Alshehri, A. A. | Alstaty, M. | Alvarez Gonzalez, B. | Álvarez Piqueras, D. | Alviggi, M. G. | Amadio, B. T. | Amaral Coutinho, Y. | Amelung, C. | Amidei, D. | Santos, S. P. Amor Dos | Amorim, A. | Amoroso, S. | Amundsen, G. | Anastopoulos, C. | Ancu, L. S. | Andari, N. | Andeen, T. | Anders, C. F. | Anders, J. K. | Anderson, K. J. | Andreazza, A. | Andrei, V. | Angelidakis, S. | Angelozzi, I. | Angerami, A. | Anisenkov, A. V. | Anjos, N. | Annovi, A. | Antel, C. | Antonelli, M. | Antonov, A. | Antrim, D. J. | Anulli, F. | Aoki, M. | Aperio Bella, L. | Arabidze, G. | Arai, Y. | Araque, J. P. | Araujo Ferraz, V. | Arce, A. T. H. | Ardell, R. E. | Arduh, F. A. | Arguin, J.-F. | Argyropoulos, S. | Arik, M. | Armbruster, A. J. | Armitage, L. J. | Arnaez, O. | Arnold, H. | Arratia, M. | Arslan, O. | Artamonov, A. | Artoni, G. | Artz, S. | Asai, S. | Asbah, N. | Ashkenazi, A. | Asquith, L. | Assamagan, K. | Astalos, R. | Atkinson, M. | Atlay, N. B. | Augsten, K. | Avolio, G. | Axen, B. | Ayoub, M. K. | Azuelos, G. | Baas, A. E. | Baca, M. J. | Bachacou, H. | Bachas, K. | Backes, M. | Backhaus, M. | Bagnaia, P. | Bahrasemani, H. | Baines, J. T. | Bajic, M. | Baker, O. K. | Baldin, E. M. | Balek, P. | Balli, F. | Balunas, W. K. | Banas, E. | Banerjee, Sw. | Bannoura, A. A. E. | Barak, L. | Barberio, E. L. | Barberis, D. | Barbero, M. | Barillari, T. | Barisits, M.-S. | Barklow, T. | Barlow, N. | Barnes, S. L. | Barnett, B. M. | Barnett, R. M. | Barnovska-Blenessy, Z. | Baroncelli, A. | Barone, G. | Barr, A. J. | Barranco Navarro, L. | Barreiro, F. | Barreiro Guimarães da Costa, J. | Bartoldus, R. | Barton, A. E. | Bartos, P. | Basalaev, A. | Bassalat, A. | Bates, R. L. | Batista, S. J. | Batley, J. R. | Battaglia, M. | Bauce, M. | Bauer, F. | Bawa, H. S. | Beacham, J. B. | Beattie, M. D. | Beau, T. | Beauchemin, P. H. | Bechtle, P. | Beck, H. P. | Becker, K. | Becker, M. | Beckingham, M. | Becot, C. | Beddall, A. J. | Beddall, A. | Bednyakov, V. A. | Bedognetti, M. | Bee, C. P. | Beermann, T. A. | Begalli, M. | Begel, M. | Behr, J. K. | Bell, A. S. | Bella, G. | Bellagamba, L. | Bellerive, A. | Bellomo, M. | Belotskiy, K. | Beltramello, O. | Belyaev, N. L. | Benary, O. | Benchekroun, D. | Bender, M. | Bendtz, K. | Benekos, N. | Benhammou, Y. | Benhar Noccioli, E. | Benitez, J. | Benjamin, D. P. | Benoit, M. | Bensinger, J. R. | Bentvelsen, S. | Beresford, L. | Beretta, M. | Berge, D. | Bergeaas Kuutmann, E. | Berger, N. | Beringer, J. | Berlendis, S. | Bernard, N. R. | Bernardi, G. | Bernius, C. | Bernlochner, F. U. | Berry, T. | Berta, P. | Bertella, C. | Bertoli, G. | Bertolucci, F. | Bertram, I. A. | Bertsche, C. | Bertsche, D. | Besjes, G. J. | Bessidskaia Bylund, O. | Bessner, M. | Besson, N. | Betancourt, C. | Bethani, A. | Bethke, S. | Bevan, A. J. | Beyer, J. | Bianchi, R. M. | Biebel, O. | Biedermann, D. | Bielski, R. | Biesuz, N. V. | Biglietti, M. | Billoud, T. R. V. | Bilokon, H. | Bindi, M. | Bingul, A. | Bini, C. | Biondi, S. | Bisanz, T. | Bittrich, C. | Bjergaard, D. M. | Black, C. W. | Black, J. E. | Black, K. M. | Blair, R. E. | Blazek, T. | Bloch, I. | Blocker, C. | Blue, A. | Blum, W. | Blumenschein, U. | Blunier, S. | Bobbink, G. J. | Bobrovnikov, V. S. | Bocchetta, S. S. | Bocci, A. | Bock, C. | Boehler, M. | Boerner, D. | Bogavac, D. | Bogdanchikov, A. G. | Bohm, C. | Boisvert, V. | Bokan, P. | Bold, T. | Boldyrev, A. S. | Bolz, A. E. | Bomben, M. | Bona, M. | Boonekamp, M. | Borisov, A. | Borissov, G. | Bortfeldt, J. | Bortoletto, D. | Bortolotto, V. | Boscherini, D. | Bosman, M. | Bossio Sola, J. D. | Boudreau, J. | Bouffard, J. | Bouhova-Thacker, E. V. | Boumediene, D. | Bourdarios, C. | Boutle, S. K. | Boveia, A. | Boyd, J. | Boyko, I. R. | Bracinik, J. | Brandt, A. | Brandt, G. | Brandt, O. | Bratzler, U. | Brau, B. | Brau, J. E. | Breaden Madden, W. D. | Brendlinger, K. | Brennan, A. J. | Brenner, L. | Brenner, R. | Bressler, S. | Briglin, D. L. | Bristow, T. M. | Britton, D. | Britzger, D. | Brochu, F. 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With the increase in energy of the Large Hadron Collider to a centre-of-mass energy of 13 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\text {TeV}$$\end{document}TeV for Run 2, events with dense environments, such as in the cores of high-energy jets, became a focus for new physics searches as well as measurements of the Standard Model. These environments are characterized by charged-particle separations of the order of the tracking detectors sensor granularity. Basic track quantities are compared between 3.2 fb\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$^{-1}$$\end{document}-1 of data collected by the ATLAS experiment and simulation of proton–proton collisions producing high-transverse-momentum jets at a centre-of-mass energy of 13 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\text {TeV}$$\end{document}TeV. The impact of charged-particle separations and multiplicities on the track reconstruction performance is discussed. The track reconstruction efficiency in the cores of jets with transverse momenta between 200 and 1600 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\text {GeV}$$\end{document}GeV is quantified using a novel, data-driven, method. The method uses the energy loss, \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text { d}}{} \textit{E}/d\textit{x}$$\end{document}dE/dx, to identify pixel clusters originating from two charged particles. Of the charged particles creating these clusters, the measured fraction that fail to be reconstructed is \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$0.061 \pm 0.006\ {\text {(stat.)}} \pm 0.014\ {\text {(syst.)}}$$\end{document}0.061±0.006(stat.)±0.014(syst.) and \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$0.093 \pm 0.017\ {\text {(stat.)}}\pm 0.021\ {\text {(syst.)}}$$\end{document}0.093±0.017(stat.)±0.021(syst.) for jet transverse momenta of 200–400 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\text {GeV}$$\end{document}GeV and 1400–1600 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\text {GeV}$$\end{document}GeV, respectively.
doi:10.1140/epjc/s10052-017-5225-7
PMCID: PMC5638380
12.  Effects of vacuum sealing drainage on the treatment of cranial bone-exposed wounds in rabbits 
This study was designed to assess the efficacy of vacuum sealing drainage (VSD) on skull exposure wounds in rabbits and to investigate the underlying mechanism of the process. Full-thickness excisional circular wounds 2×2 cm with or without periosteum involvement were created in 88 New Zealand white rabbits (mean body weight: 3.0±0.65 kg). Animals were randomly divided into 4 groups: periosteum-intact wounds treated with traditional dressing (p+control), periosteum-intact wounds treated with VSD (p+VSD), periosteum-lacking wounds treated with traditional dressing (p–control) and periosteum-lacking wounds treated with VSD (p–VSD). The wounds treated with traditional dressing were covered with Vaseline gauze, while VSD treatment was accompanied with continuous –120 mmHg pressure. Finally, wound tissues were harvested for analysis of hydroxyproline content and histologic detection. VSD hastened the wound healing process significantly (P<0.05) compared to the corresponding control groups. VSD alleviated the inflammation reaction, accelerated re-epithelialization and facilitated the organization of collagen fibers into neat rows. During the wound healing process, the hydroxyproline content increased overtime [i.e., postoperative days (POD) 7, POD 10 and POD 15] in all four groups, and it peaked in the p+VSD group. VSD also promoted angiogenesis via increasing number and quality of collagen. We concluded that VSD can promote healing in bone-exposed wounds via increasing hydroxyproline content and vessel density, reducing inflammatory responses and generating ordered collagen arrangement.
doi:10.1590/1414-431X20175837
PMCID: PMC5625544
Cranial bone-exposed wound; Vacuum sealing drainage; Periosteum; Wound healing; Efficacy
13.  Mesenchymal stromal cell injection promotes vocal fold scar repair without long-term engraftment 
Cytotherapy  2016;18(10):1284-1296.
Background
Regenerative medicine holds promise for restoring voice in patients with vocal fold scarring. As experimental treatments approach clinical translation, several considerations remain. Our objective was to evaluate efficacy and biocompatibility of four bone marrow mesenchymal stromal cell (BM-MSC) and tunable hyaluronic acid based hydrogel (HyStem-VF) treatments for vocal fold scar using clinically acceptable materials, a preclinical sample size and a dosing comparison.
Methods
Vocal folds of 84 rabbits were injured and injected with four treatment variations (BM-MSC, HyStem-VF, and BM-MSC in HyStem-VF at two concentrations) 6 weeks later. Efficacy was assessed with rheometry, real-time polymerase chain reaction (PCR) and histology at 2, 4 and 10 weeks following treatment. Lung, liver, kidney, spleen and vocal folds were screened for biocompatibility by a pathologist.
Results and discussion
Persistent inflammation was identified in all hydrogel-injected groups. The BM-MSC alone treatment appeared to be the most efficacious and safe, providing an early resolution of viscoelasticity, gene expression consistent with desirable extracellular matrix remodeling (less fibronectin, collagen 1α2, collagen 3, procollagen, transforming growth factor [TGF]β1, alpha smooth muscle actin, interleukin-1β, interleukin-17β and tumor necrosis factor [TNF] than injured controls) and minimal inflammation. Human beta actin expression in BM-MSC–treated vocal folds was minimal after 2 weeks, suggesting that paracrine signaling from the BM-MSCs may have facilitated tissue repair.
doi:10.1016/j.jcyt.2016.07.005
PMCID: PMC5031418  PMID: 27637759
elasticity; fibrosis; hyaluronic acid; hydrogel; mesenchymal stromal cells; rheology; viscosity; vocal cord
14.  Combination curcumin and (−)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway 
Jin, G | Yang, Y | Liu, K | Zhao, J | Chen, X | Liu, H | Bai, R | Li, X | Jiang, Y | Zhang, X | Lu, J | Dong, Z
Oncogenesis  2017;6(10):e384-.
Tumor microenvironment has a crucial role in cancer development and progression, whereas the mechanism of how it regulates angiogenesis is unclear. In this study, we simulated the colorectal carcinoma microenvironment by conditioned medium (CM) of colorectal carcinoma cell lines (SW620, HT-29, HCT116) supernatant or colorectal carcinoma tissue homogenate supernatant to induce normal endothelial cells (NECs). We found that colorectal carcinoma CM promoted tumor angiogenesis by coercing NECs toward tumor endothelial cells (TECs) with the activation of the JAK/STAT3 signaling pathway. Antibody array analysis showed HT-29 supernatant contained numerous angiogenesis-related proteins, especially IL-8. Interestingly, the production of IL-8 in NECs induced by HT-29 CM was also increased. We also verified the crucial role of IL-8 in promoting the CM-induced angiogenesis, as IL-8 repression by neutralizing antibody abolished the transition of NECs toward TECs. Curcumin and (−)-epigallocatechin-3-gallate (EGCG) are broadly investigated in cancer chemoprevention. However, poor bioavailability hurdles their application alone, and the mechanism of their anti-angiogenesis still need to be illuminated. Here, we found that curcumin combination with EGCG attenuated the tumor CM-induced transition of NECs toward TECs by inhibiting JAK/STAT3 signaling pathway. Furthermore, the combination of curcumin and EGCG markedly reduced tumor growth and angiogenesis in the colorectal carcinoma PDX mouse model, and the combined anti-angiogenic effect was better than that of curcumin or EGCG alone. Taken together, our findings provide a new mechanism of tumor angiogenesis, and the combination of curcumin and EGCG represents a potential anti-angiogenic therapeutic method for colorectal carcinoma.
doi:10.1038/oncsis.2017.84
PMCID: PMC5668882  PMID: 28967875
15.  Hypoxia stimulates neural stem cell proliferation by increasing HIF-1α expression and activating Wnt/β-catenin signaling 
Evidence indicates that after brain injury, neurogenesis is enhanced in regions such as hippocampus, striatum, and cortex. To study the role of hypoxia-inducible factor-1 (HIF−1α) and Wnt signaling in cerebral ischemia/hypoxia-induced proliferation of neural stem cells (NSCs), we investigated the proliferation of NSCs, expression of HIF−1α, and activation of Wnt signaling under conditions of pathologic hypoxia in vitro. NSCs were isolated from 30-day-old Sprague–Dawley rats and subjected to 0.3% oxygen in a microaerophilic incubation system. Cell proliferation was evaluated by measuring the diameter of neurospheres and by bromodeoxyuridine incorporation assays. Real-time quantitative PCR and Western blotting were used to detect mRNA and protein levels of HIF-1α, β-catenin, and cyclin D1 in the NSCs. The results showed that hypoxia increased NSC proliferation and the levels of HIF-1α, β−catenin, and cyclin D1 (p < 0.05). Blockade of the Wnt signaling pathway decreased hypoxia-induced NSC proliferation, whereas activation of this pathway increased hypoxia-induced NSC proliferation (p < 0.05). Knockdown of HIF-1α with HIF-1α siRNA decreased β−catenin nuclear translocation and cyclin D1 expression, and inhibited proliferation of NSCs (p < 0.05). These findings indicate that pathologic hypoxia stimulates NSC proliferation by increasing expression of HIF-1α and activating the Wnt/β-catenin signaling pathway. The data suggest that Wnt/β-catenin signaling may play a key role in NSC proliferation under conditions of pathologic hypoxia.
PMCID: PMC5614483  PMID: 28838333
Wnt; Hypoxia inducible factor-1 alpha; Neurogenesis; Neural stem cells
16.  Critical role of Myc activation in mouse hepatocarcinogenesis induced by the activation of AKT and RAS pathways 
Oncogene  2017;36(36):5087-5097.
MYC activation at modest levels has been frequently found in hepatocellular carcinoma. However, its significance in hepatocarcinogenesis has remained obscure. Here we examined the role of Myc activation in mouse liver tumours induced by hepatocytic expression of myristoylated AKT (AKT) and/or mutant HRASV12 (HRAS) via transposon-mediated gene integration. AKT or HRAS alone required 5 months to induce liver tumours, whereas their combination generated hepatocellular carcinoma within 8 weeks. Co-introduction of AKT and HRAS induced lipid-laden preneoplastic cells that grew into nodules composed of tumour cells with or without intracytoplasmic lipid, with the latter being more proliferative and associated with spontaneous Myc expression. AKT/HRAS-induced tumorigenesis was almost completely abolished when MadMyc, a competitive Myc inhibitor, was expressed simultaneously. The Tet-On induction of MadMyc in preneoplastic cells significantly inhibited the progression of AKT/HRAS-induced tumours; its induction in transformed cells suppressed their proliferative activity with alterations in lipid metabolism and protein translation. Transposon-mediated Myc overexpression facilitated tumorigenesis by AKT or HRAS, and when it was co-introduced with AKT and HRAS, diffusely infiltrating tumours without lipid accumulation developed as early as 2 weeks. Examination of the dose-responses of Myc in the enhancement of AKT/HRAS-induced tumorigenesis revealed that a reduction to one-third retained enhancing effect but three-times greater introduction damped the process with increased apoptosis. Myc overexpression suppressed the mRNA expression of proteins involved in the synthesis of fatty acids, and when combined with HRAS introduction, it also suppressed the mRNA expression of proteins involved in their degradation. Finally, the MYC-positive human hepatocellular carcinoma was characterized by the cytoplasm devoid of lipid accumulation, prominent nucleoli and a higher proliferative activity. Our results demonstrate that in hepatocarcinogenesis induced by both activated AKT and HRAS, activation of endogenous Myc is an enhancing factor and adequate levels of Myc deregulation further facilitate the process with alterations in cellular metabolism.
doi:10.1038/onc.2017.114
PMCID: PMC5596209  PMID: 28481866
17.  Tunneling anisotropic magnetoresistance driven by magnetic phase transition 
Nature Communications  2017;8:449.
The independent control of two magnetic electrodes and spin-coherent transport in magnetic tunnel junctions are strictly required for tunneling magnetoresistance, while junctions with only one ferromagnetic electrode exhibit tunneling anisotropic magnetoresistance dependent on the anisotropic density of states with no room temperature performance so far. Here, we report an alternative approach to obtaining tunneling anisotropic magnetoresistance in α′-FeRh-based junctions driven by the magnetic phase transition of α′-FeRh and resultantly large variation of the density of states in the vicinity of MgO tunneling barrier, referred to as phase transition tunneling anisotropic magnetoresistance. The junctions with only one α′-FeRh magnetic electrode show a magnetoresistance ratio up to 20% at room temperature. Both the polarity and magnitude of the phase transition tunneling anisotropic magnetoresistance can be modulated by interfacial engineering at the α′-FeRh/MgO interface. Besides the fundamental significance, our finding might add a different dimension to magnetic random access memory and antiferromagnet spintronics.
Tunneling anisotropic magnetoresistance is promising for next generation memory devices but limited by the low efficiency and functioning temperature. Here the authors achieved 20% tunneling anisotropic magnetoresistance at room temperature in magnetic tunnel junctions with one α′-FeRh magnetic electrode.
doi:10.1038/s41467-017-00290-4
PMCID: PMC5587625  PMID: 28878205
18.  Infrared probe of pseudogap in electron-doped Sr2IrO4 
Scientific Reports  2017;7:10494.
We report on infrared spectroscopy experiments on the electronic response in (Sr1−xLax)2IrO4 (x = 0, 0.021, and 0.067). Our data show that electron doping induced by La substitution leads to an insulator-to-metal transition. The evolution of the electronic structure across the transition reveals the robustness of the strong electronic correlations against the electron doping. The conductivity data of the metallic compound show the signature of the pseudogap that bears close similarity to the analogous studies of the pseudogap in the underdoped cuprates. While the low energy conductivity of the metallic compound is barely frequency dependent, the formation of the pseudogap is revealed by the gradual suppression of the featureless conductivity below a threshold frequency of about 17 meV. The threshold structure develops below about 100 K which is in the vicinity of the onset of the short-range antiferromagnetic order. Our results demonstrate that the electronic correlations play a crucial role in the anomalous charge dynamics in the (Sr1−xLax)2IrO4 system.
doi:10.1038/s41598-017-10725-z
PMCID: PMC5585243
19.  CYP4A in tumor-associated macrophages promotes pre-metastatic niche formation and metastasis 
Oncogene  2017;36(35):5045-5057.
Tumor-associated macrophages (TAMs) play an essential role in metastasis. However, what enables TAMs to have a superior capacity to establish pre-metastatic microenvironment in distant organs is unclear. Here we have begun to uncover the effects of cytochrome P450 (CYP) 4A in TAMs on lung pre-metastatic niche formation and metastasis. CYP4A+ TAM infiltration was positively associated with metastasis, pre-metastatic niche formation and poor prognosis in breast cancer patients. The pharmacological inhibition of CYP4A reduced lung pre-metastatic niche formation (evidenced by a decrease in vascular endothelial growth factor receptor 1 positive (VEGFR1+) myeloid cell recruitment and pro-metastatic protein expression) and metastatic burden, accompanied with TAM polarization away from the M2 phenotype in spontaneous metastasis models of 4T1 breast cancer and B16F10 melanoma. Co-implantation of 4T1 cells with CYP4A10high macrophages promoted lung pre-metastatic niche formation and metastasis. Depletion of TAMs disrupted lung pre-metastatic niches and thereby prevented metastasis. Treatment with the CM from CYP4A10high M2 macrophages (M2) increased pre-metastatic niche formation and metastatic burden in the lungs, whereas CYP4A inhibition attenuated these effects. In vitro TAM polarization away from the M2 phenotype induced by CYP4A inhibition decreased VEGFR1+ myeloid cell migration and fibronectin expression, accompanied with downregulation of STAT3 signaling. Conversely, overexpression of CYP4A or exogenous addition of 20-hydroxyeicosatetraenoic acid promoted M2 polarization and cytokine production of macrophages and thereby enhanced migration of VEGFR1+ myeloid cells, which were reversed by siRNA or pharmacological inhibition of STAT3. Importantly, a combined blocking M2 macrophage-derived factors TGF-β, VEGF and SDF-1 abolished VEGFR1+ myeloid cell migration and fibroblast activation induced by CYP4A. In summary, CYP4A in TAMs is crucial for lung pre-metastatic niche formation and metastasis, and may serve as a potential therapeutic target in human cancer.
doi:10.1038/onc.2017.118
PMCID: PMC5582214  PMID: 28481877
20.  Risperidone-induced topological alterations of anatomical brain network in first-episode drug-naive schizophrenia patients: a longitudinal diffusion tensor imaging study 
Psychological medicine  2016;46(12):2549-2560.
Background
It remains unclear whether the topological deficits of the white matter network documented in cross-sectional studies of chronic schizophrenia patients are due to chronic illness or to other factors such as antipsychotic treatment effects. To answer this question, we evaluated the white matter network in medication-naive first-episode schizophrenia patients (FESP) before and after a course of treatment.
Method
We performed a longitudinal diffusion tensor imaging study in 42 drug-naive FESP at baseline and then after 8 weeks of risperidone monotherapy, and compared them with 38 healthy volunteers. Graph theory was utilized to calculate the topological characteristics of brain anatomical network. Patients’ clinical state was evaluated using the Positive and Negative Syndrome Scale (PANSS) before and after treatment.
Results
Pretreatment, patients had relatively intact overall topological organizations, and deficient nodal topological properties primarily in prefrontal gyrus and limbic system components such as the bilateral anterior and posterior cingulate. Treatment with risperidone normalized topological parameters in the limbic system, and the enhancement positively correlated with the reduction in PANSS-positive symptoms. Prefrontal topological impairments persisted following treatment and negative symptoms did not improve.
Conclusions
During the early phase of antipsychotic medication treatment there are region-specific alterations in white matter topological measures. Limbic white matter topological dysfunction improves with positive symptom reduction. Prefrontal deficits and negative symptoms are unresponsive to medication intervention, and prefrontal deficits are potential trait biomarkers and targets for negative symptom treatment development.
doi:10.1017/S0033291716001380
PMCID: PMC5242555  PMID: 27338296
First-episode schizophrenia; longitudinal studies; networks; schizophrenia; topology; white matter
21.  Fiducial, total and differential cross-section measurements of t-channel single top-quark production in pp collisions at 8 TeV using data collected by the ATLAS detector 
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T. | Bajic, M. | Baker, O. K. | Baldin, E. M. | Balek, P. | Balestri, T. | Balli, F. | Balunas, W. K. | Banas, E. | Banerjee, Sw. | Bannoura, A. A. E. | Barak, L. | Barberio, E. L. | Barberis, D. | Barbero, M. | Barillari, T. | Barisits, M-S. | Barklow, T. | Barlow, N. | Barnes, S. L. | Barnett, B. M. | Barnett, R. M. | Barnovska-Blenessy, Z. | Baroncelli, A. | Barone, G. | Barr, A. J. | Navarro, L. Barranco | Barreiro, F. | da Costa, J. Barreiro Guimarães | Bartoldus, R. | Barton, A. E. | Bartos, P. | Basalaev, A. | Bassalat, A. | Bates, R. L. | Batista, S. J. | Batley, J. R. | Battaglia, M. | Bauce, M. | Bauer, F. | Bawa, H. S. | Beacham, J. B. | Beattie, M. D. | Beau, T. | Beauchemin, P. H. | Bechtle, P. | Beck, H. P. | Becker, K. | Becker, M. | Beckingham, M. | Becot, C. | Beddall, A. J. | Beddall, A. | Bednyakov, V. A. | Bedognetti, M. | Bee, C. P. | Beemster, L. J. | Beermann, T. A. | Begel, M. | Behr, J. K. | Bell, A. S. | Bella, G. | Bellagamba, L. | Bellerive, A. | Bellomo, M. | Belotskiy, K. | Beltramello, O. | Belyaev, N. L. | Benary, O. | Benchekroun, D. | Bender, M. | Bendtz, K. | Benekos, N. | Benhammou, Y. | Noccioli, E. Benhar | Benitez, J. | Benjamin, D. P. | Bensinger, J. R. | Bentvelsen, S. | Beresford, L. | Beretta, M. | Berge, D. | Kuutmann, E. Bergeaas | Berger, N. | Beringer, J. | Berlendis, S. | Bernard, N. R. | Bernius, C. | Bernlochner, F. U. | Berry, T. | Berta, P. | Bertella, C. | Bertoli, G. | Bertolucci, F. | Bertram, I. A. | Bertsche, C. | Bertsche, D. | Besjes, G. J. | Bylund, O. Bessidskaia | Bessner, M. | Besson, N. | Betancourt, C. | Bethani, A. | Bethke, S. | Bevan, A. J. | Bianchi, R. M. | Bianco, M. | Biebel, O. | Biedermann, D. | Bielski, R. | Biesuz, N. V. | Biglietti, M. | De Mendizabal, J. Bilbao | Billoud, T. R. V. | Bilokon, H. | Bindi, M. | Bingul, A. | Bini, C. | Biondi, S. | Bisanz, T. | Bjergaard, D. M. | Black, C. W. | Black, J. E. | Black, K. M. | Blackburn, D. | Blair, R. E. | Blazek, T. | Bloch, I. | Blocker, C. | Blue, A. | Blum, W. | Blumenschein, U. | Blunier, S. | Bobbink, G. J. | Bobrovnikov, V. S. | Bocchetta, S. S. | Bocci, A. | Bock, C. | Boehler, M. | Boerner, D. | Bogaerts, J. A. | Bogavac, D. | Bogdanchikov, A. G. | Bohm, C. | Boisvert, V. | Bokan, P. | Bold, T. | Boldyrev, A. S. | Bomben, M. | Bona, M. | Boonekamp, M. | Borisov, A. | Borissov, G. | Bortfeldt, J. | Bortoletto, D. | Bortolotto, V. | Bos, K. | Boscherini, D. | Bosman, M. | Sola, J. D. Bossio | Boudreau, J. | Bouffard, J. | Bouhova-Thacker, E. V. | Boumediene, D. | Bourdarios, C. | Boutle, S. K. | Boveia, A. | Boyd, J. | Boyko, I. R. | Bracinik, J. | Brandt, A. | Brandt, G. | Brandt, O. | Bratzler, U. | Brau, B. | Brau, J. E. | Madden, W. D. Breaden | Brendlinger, K. | Brennan, A. J. | Brenner, L. | Brenner, R. | Bressler, S. | Bristow, T. M. | Britton, D. | Britzger, D. | Brochu, F. 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Detailed measurements of t-channel single top-quark production are presented. They use 20.2 fb\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$^{-1}$$\end{document}-1 of data collected by the ATLAS experiment in proton–proton collisions at a centre-of-mass energy of 8 TeV at the LHC. Total, fiducial and differential cross-sections are measured for both top-quark and top-antiquark production. The fiducial cross-section is measured with a precision of 5.8% (top quark) and 7.8% (top antiquark), respectively. The total cross-sections are measured to be \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sigma _{\text {tot}} (tq) = 56.7^{+4.3}_{-3.8}\;\mathrm{pb}$$\end{document}σtot(tq)=56.7-3.8+4.3pb for top-quark production and \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sigma _{\text {tot}} (\bar{t} q) = 32.9^{+3.0}_{-2.7}\;\mathrm{pb}$$\end{document}σtot(t¯q)=32.9-2.7+3.0pb for top-antiquark production, in agreement with the Standard Model prediction. In addition, the ratio of top-quark to top-antiquark production cross-sections is determined to be \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$R_t=1.72 \pm 0.09$$\end{document}Rt=1.72±0.09. The differential cross-sections as a function of the transverse momentum and rapidity of both the top quark and the top antiquark are measured at both the parton and particle levels. The transverse momentum and rapidity differential cross-sections of the accompanying jet from the t-channel scattering are measured at particle level. All measurements are compared to various Monte Carlo predictions as well as to fixed-order QCD calculations where available.
doi:10.1140/epjc/s10052-017-5061-9
PMCID: PMC5589447
22.  Low dose arsenite confers resistance to UV induced apoptosis via p53-MDM2 pathway in ketatinocytes 
Zhou, Y | Zeng, W | Qi, M | Duan, Y | Su, J | Zhao, S | Zhong, W | Gao, M | Li, F | He, Y | Hu, X | Xu, X | Chen, X | Peng, C | Zhang, J
Oncogenesis  2017;6(8):e370-.
Chronic arsenite and ultraviolet (UV) exposure are associated with skin tumor. To investigate the details by low concentrations of arsenite and UV induced carcinogenesis in skin, hTERT-immortalized human keratinocytes were used as a cellular model with exposure to low concentrations of sodium arsenite and UV. The effect of NaAsO2 on UV treatment-induced apoptosis was measured by flow cytometry and Hoechst staining. We found that the cell apoptosis induced by UV exposure was significantly attenuated after exposure to low-dose arsenite, and knockdown of p53 could block UV-induced apoptosis indicating that this phenomenon depended on p53. Interestingly, the expression of murine double minute 2 (MDM2), including its protein and transcriptional levels, was remarkably high after exposure to low-dose arsenite. Moreover, low-dose arsenite treatment dramatically decreased the MDM2 gene promoter activity, suggesting that this effect has been mediated through transcription. In addition, treatment of PD98059 reversed low-dose arsenite-induced MDM2 expression, and the inhibition of ERK2 expression could significantly block MDM2 expression as a consequence, and p53 expression automatically was increased. To validate the role of p53 in exposure to low-dose arsenite, the expression of p53 was examined by immunohistochemistry in the skin of Sprague−Dawley rats model by chronic arsenite exposure for 6 months and in patients with arsenic keratosis, and the results showed that the expression of p53 was decreased in those samples. Taken together, our results demonstrated that low-dose arsenite-induced resistance to apoptosis through p53 mediated by MDM2 in keratinocytes.
doi:10.1038/oncsis.2017.67
PMCID: PMC5608918  PMID: 28785074
23.  Topological cell clustering in the ATLAS calorimeters and its performance in LHC Run 1 
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The reconstruction of the signal from hadrons and jets emerging from the proton–proton collisions at the Large Hadron Collider (LHC) and entering the ATLAS calorimeters is based on a three-dimensional topological clustering of individual calorimeter cell signals. The cluster formation follows cell signal-significance patterns generated by electromagnetic and hadronic showers. In this, the clustering algorithm implicitly performs a topological noise suppression by removing cells with insignificant signals which are not in close proximity to cells with significant signals. The resulting topological cell clusters have shape and location information, which is exploited to apply a local energy calibration and corrections depending on the nature of the cluster. Topological cell clustering is established as a well-performing calorimeter signal definition for jet and missing transverse momentum reconstruction in ATLAS.
doi:10.1140/epjc/s10052-017-5004-5
PMCID: PMC5586976
24.  Measurements of electroweak \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Wjj $$\end{document}Wjj production and constraints on anomalous gauge couplings with the ATLAS detector 
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Measurements of the electroweak production of a W boson in association with two jets at high dijet invariant mass are performed using \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s} =$$\end{document}s= 7 and 8 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\text {TeV}$$\end{document}TeV proton–proton collision data produced by the Large Hadron Collider, corresponding respectively to 4.7 and 20.2 fb\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$^{-1}$$\end{document}-1 of integrated luminosity collected by the ATLAS detector. The measurements are sensitive to the production of a W boson via a triple-gauge-boson vertex and include both the fiducial and differential cross sections of the electroweak process.
doi:10.1140/epjc/s10052-017-5007-2
PMCID: PMC5586972