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1.  Interrogation of gossypol therapy in glioblastoma implementing cell line and patient-derived tumour models 
British Journal of Cancer  2014;111(12):2275-2286.
Background:
Glioblastoma (GBM), being a highly vascularised and locally invasive tumour, is an attractive target for anti-angiogenic and anti-invasive therapies. The GBM/endothelial cell response to gossypol/temozolomide (TMZ) treatment was investigated with a particular aim to assess treatment effects on cancer hallmarks.
Methods:
Cell viability, endothelial tube formation and GBM tumour cell invasion were variously assessed following combined treatment in vitro. The U87MG-luc2 subcutaneous xenograft model was used to investigate therapeutic response in vivo. Viable tumour response to treatment was interrogated using immunohistochemistry. Combined treatment protocols were also tested in primary GBM patient-derived cultures.
Results:
An endothelial/GBM cell viability inhibitory effect, as well as an anti-angiogenic and anti-invasive response, to combined treatment have been demonstrated in vitro. A significantly greater anti-proliferative (P=0.020, P=0.030), anti-angiogenic (P=0.040, P<0.0001) and pro-apoptotic (P=0.0083, P=0.0149) response was observed when combined treatment was compared with single gossypol/TMZ treatment response, respectively. GBM cell line and patient-specific response to gossypol/TMZ treatment was observed.
Conclusions:
Our results indicate that response to a combined gossypol/TMZ treatment is related to inhibition of tumour-associated angiogenesis, invasion and proliferation and warrants further investigation as a novel targeted GBM treatment strategy.
doi:10.1038/bjc.2014.529
PMCID: PMC4264441  PMID: 25375271
GBM; gossypol; TMZ; angiogenesis; apoptosis; invasion
2.  L-Stepholidine rescues memory deficit and synaptic plasticity in models of Alzheimer's disease via activating dopamine D1 receptor/PKA signaling pathway 
Hao, J-R | Sun, N | Lei, L | Li, X-Y | Yao, B | Sun, K | Hu, R | Zhang, X | Shi, X-D | Gao, C
Cell Death & Disease  2015;6(11):e1965-.
It is accepted that amyloid β-derived diffusible ligands (ADDLs) have a prominent role in triggering the early cognitive deficits that constitute Alzheimer's disease (AD). However, there is still no effective treatment for preventing or reversing the progression of the disease. Targeting α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor trafficking and its regulation is a new strategy for AD early treatment. Here we investigate the effect and mechanism of L-Stepholidine (L-SPD), which elicits dopamine D1-type receptor agonistic activity, while acting as D2-type receptor antagonist on cognition and synaptic plasticity in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic (APP/PS1) mice, and hippocampal cultures or slices treated with ADDLs. L-SPD could improve the hippocampus-dependent memory, surface expression of glutamate receptor A (GluA1)-containing AMPA receptors and spine density in hippocampus of APP/PS1 transgenic mice. L-SPD not only rescued decreased phosphorylation and surface expression of GluA1 in hippocampal cultures but also protected the long-term potentiation in hippocampal slices induced by ADDLs. Protein kinase A (PKA) agonist Sp-cAMPS or D1-type receptor agonist SKF81297 had similar effects, whereas PKA antagonist Rp-cAMPS or D1-type receptor antagonist SCH23390 abolished the effect of L-SPD on GluA1 trafficking. This was mediated mainly by PKA, which could phosphorylate serine residue at 845 of the GluA1. L-SPD may be explored as a potential therapeutic drug for AD through a mechanism that improves AMPA receptor trafficking and synaptic plasticity via activating D1/PKA signaling pathway.
doi:10.1038/cddis.2015.315
PMCID: PMC4670924  PMID: 26539912
3.  Subtypes of major depression: latent class analysis in depressed Han Chinese women 
Psychological medicine  2014;44(15):3275-3288.
Background
Despite substantial research, uncertainty remains about the clinical and etiological heterogeneity of major depression (MD). Can meaningful and valid subtypes be identified and would they be stable cross-culturally?
Method
Symptoms at their lifetime worst depressive episode were assessed at structured psychiatric interview in 6008 women of Han Chinese descent, age ≥30 years, with recurrent DSM-IV MD. Latent class analysis (LCA) was performed in Mplus.
Results
Using the nine DSM-IV MD symptomatic A criteria, the 14 disaggregated DSM-IV criteria and all independently assessed depressive symptoms (n=27), the best LCA model identified respectively three, four and six classes. A severe and non-suicidal class was seen in all solutions, as was a mild/moderate subtype. An atypical class emerged once bidirectional neurovegetative symptoms were included. The non-suicidal class demonstrated low levels of worthlessness/guilt and hopelessness. Patterns of co-morbidity, family history, personality, environmental precipitants, recurrence and body mass index (BMI) differed meaningfully across subtypes, with the atypical class standing out as particularly distinct.
Conclusions
MD is a clinically complex syndrome with several detectable subtypes with distinct clinical and demographic correlates. Three subtypes were most consistently identified in our analyses: severe, atypical and non-suicidal. Severe and atypical MD have been identified in multiple prior studies in samples of European ethnicity. Our non-suicidal subtype, with low levels of guilt and hopelessness, may represent a pathoplastic variant reflecting Chinese cultural influences.
doi:10.1017/S0033291714000749
PMCID: PMC4180813  PMID: 25065911
Atypical depression; China; depression; latent class analysis; melancholia; suicidal ideation
4.  Square Kilometre Array Telescope—Precision Reference Frequency Synchronisation via 1f-2f Dissemination 
Scientific Reports  2015;5:13851.
The Square Kilometre Array (SKA) project is an international effort to build the world’s largest radio telescope, with a one-square-kilometre collecting area. In addition to its ambitious scientific objectives, such as probing cosmic dawn and the cradle of life, the SKA demands several revolutionary technological breakthroughs, such as ultra-high precision synchronisation of the frequency references for thousands of antennas. In this report, with the purpose of application to the SKA, we demonstrate a frequency reference dissemination and synchronisation scheme in which the phase-noise compensation function is applied at the client site. Hence, one central hub can be linked to a large number of client sites, thus forming a star-shaped topology. As a performance test, a 100-MHz reference frequency signal from a hydrogen maser (H-maser) clock is disseminated and recovered at two remote sites. The phase-noise characteristics of the recovered reference frequency signal coincide with those of the H-maser source and satisfy the SKA requirements.
doi:10.1038/srep13851
PMCID: PMC4563364  PMID: 26349544
5.  The consensus sequence of FAMLF alternative splice variants is overexpressed in undifferentiated hematopoietic cells 
The familial acute myeloid leukemia related factor gene (FAMLF) was previously identified from a familial AML subtractive cDNA library and shown to undergo alternative splicing. This study used real-time quantitative PCR to investigate the expression of the FAMLF alternative-splicing transcript consensus sequence (FAMLF-CS) in peripheral blood mononuclear cells (PBMCs) from 119 patients with de novo acute leukemia (AL) and 104 healthy controls, as well as in CD34+cells from 12 AL patients and 10 healthy donors. A 429-bp fragment from a novel splicing variant of FAMLF was obtained, and a 363-bp consensus sequence was targeted to quantify total FAMLF expression. Kruskal-Wallis, Nemenyi, Spearman's correlation, and Mann-Whitney U-tests were used to analyze the data. FAMLF-CS expression in PBMCs from AL patients and CD34+ cells from AL patients and controls was significantly higher than in control PBMCs (P<0.0001). Moreover,FAMLF-CS expression in PBMCs from the AML group was positively correlated with red blood cell count (rs =0.317, P=0.006), hemoglobin levels (rs =0.210, P=0.049), and percentage of peripheral blood blasts (rs =0.256, P=0.027), but inversely correlated with hemoglobin levels in the control group (rs =–0.391, P<0.0001). AML patients with high CD34+ expression showed significantly higherFAMLF-CS expression than those with low CD34+ expression (P=0.041). Our results showed thatFAMLF is highly expressed in both normal and malignant immature hematopoietic cells, but that expression is lower in normal mature PBMCs.
doi:10.1590/1414-431X20154430
PMCID: PMC4512098  PMID: 26083996
FAMLF; Gene expression; Leukemia; Real-time polymerase chain reaction; Alternative splicing
6.  Measurement of pion, kaon and proton production in proton–proton collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s} = 7$$\end{document}s=7 TeV 
Adam, J. | Adamová, D. | Aggarwal, M. M. | Rinella, G. Aglieri | Agnello, M. | Agrawal, N. | Ahammed, Z. | Ahmed, I. | Ahn, S. U. | Aimo, I. | Aiola, S. | Ajaz, M. | Akindinov, A. | Alam, S. N. | Aleksandrov, D. | Alessandro, B. | Alexandre, D. | Molina, R. Alfaro | Alici, A. | Alkin, A. | Alme, J. | Alt, T. | Altinpinar, S. | Altsybeev, I. | Prado, C. Alves Garcia | Andrei, C. | Andronic, A. | Anguelov, V. | Anielski, J. | Antičić, T. | Antinori, F. | Antonioli, P. | Aphecetche, L. | Appelshäuser, H. | Arcelli, S. | Armesto, N. | Arnaldi, R. | Aronsson, T. | Arsene, I. C. | Arslandok, M. | Augustinus, A. | Averbeck, R. | Azmi, M. D. | Bach, M. | Badalà, A. | Baek, Y. W. | Bagnasco, S. | Bailhache, R. | Bala, R. | Baldisseri, A. | Ball, M. | Pedrosa, F. Baltasar Dos Santos | Baral, R. C. | Barbano, A. M. | Barbera, R. | Barile, F. | Barnaföldi, G. G. | Barnby, L. 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Cortés | Cortese, P. | Cosentino, M. R. | Costa, F. | Crochet, P. | Albino, R. Cruz | Cuautle, E. | Cunqueiro, L. | Dahms, T. | Dainese, A. | Danu, A. | Das, D. | Das, I. | Das, S. | Dash, A. | Dash, S. | De, S. | Caro, A. De | Cataldo, G. de | Cuveland, J. de | Falco, A. De | Gruttola, D. De | Marco, N. De | Pasquale, S. De | Deisting, A. | Deloff, A. | Dénes, E. | D’Erasmo, G. | Bari, D. Di | Mauro, A. Di | Nezza, P. Di | Corchero, M. A. Diaz | Dietel, T. | Dillenseger, P. | Divià, R. | Djuvsland, Ø. | Dobrin, A. | Dobrowolski, T. | Gimenez, D. Domenicis | Dönigus, B. | Dordic, O. | Dubey, A. K. | Dubla, A. | Ducroux, L. | Dupieux, P. | Ehlers, R. J. | Elia, D. | Engel, H. | Erazmus, B. | Erhardt, F. | Eschweiler, D. | Espagnon, B. | Estienne, M. | Esumi, S. | Eum, J. | Evans, D. | Evdokimov, S. | Eyyubova, G. | Fabbietti, L. | Fabris, D. | Faivre, J. | Fantoni, A. | Fasel, M. | Feldkamp, L. | Felea, D. | Feliciello, A. | Feofilov, G. | Ferencei, J. | Téllez, A. Fernández | Ferreiro, E. G. | Ferretti, A. | Festanti, A. | Figiel, J. | Figueredo, M. A. S. | Filchagin, S. | Finogeev, D. | Fionda, F. M. | Fiore, E. M. | Fleck, M. G. | Floris, M. | Foertsch, S. | Foka, P. | Fokin, S. | Fragiacomo, E. | Francescon, A. | Frankenfeld, U. | Fuchs, U. | Furget, C. | Furs, A. | Girard, M. Fusco | Gaardhøje, J. J. | Gagliardi, M. | Gago, A. M. | Gallio, M. | Gangadharan, D. R. | Ganoti, P. | Gao, C. | Garabatos, C. | Garcia-Solis, E. | Gargiulo, C. | Gasik, P. | Germain, M. | Gheata, A. | Gheata, M. | Ghosh, P. | Ghosh, S. K. | Gianotti, P. | Giubellino, P. | Giubilato, P. | Dziadus, E. Gladysz | Glässel, P. | Ramirez, A. Gomez | Zamora, P. González | Gorbunov, S. | Görlich, L. | Gotovac, S. | Grabski, V. | Graczykowski, L. K. | Grelli, A. | Grigoras, A. | Grigoras, C. | Grigoriev, V. | Grigoryan, A. | Grigoryan, S. | Grinyov, B. | Grion, N. | Grosse-Oetringhaus, J. F. | Grossiord, J.-Y. | Grosso, R. | Guber, F. | Guernane, R. | Guerzoni, B. | Gulbrandsen, K. | Gulkanyan, H. | Gunji, T. | Gupta, A. | Gupta, R. | Haake, R. | Haaland, Ø. | Hadjidakis, C. | Haiduc, M. | Hamagaki, H. | Hamar, G. | Hanratty, L. D. | Hansen, A. | Harris, J. W. | Hartmann, H. | Harton, A. | Hatzifotiadou, D. | Hayashi, S. | Heckel, S. T. | Heide, M. | Helstrup, H. | Herghelegiu, A. | Corral, G. Herrera | Hess, B. A. | Hetland, K. F. | Hilden, T. E. | Hillemanns, H. | Hippolyte, B. | Hristov, P. | Huang, M. | Humanic, T. J. | Hussain, N. | Hussain, T. | Hutter, D. | Hwang, D. S. | Ilkaev, R. | Ilkiv, I. | Inaba, M. | Ionita, C. | Ippolitov, M. | Irfan, M. | Ivanov, M. | Ivanov, V. | Izucheev, V. | Jacobs, P. M. | Jahnke, C. | Jang, H. J. | Janik, M. A. | Jayarathna, P. H. S. Y. | Jena, C. | Jena, S. | Bustamante, R. T. Jimenez | Jones, P. G. | Jung, H. | Jusko, A. | Kalinak, P. | Kalweit, A. | Kamin, J. | Kang, J. H. | Kaplin, V. | Kar, S. | Uysal, A. Karasu | Karavichev, O. | Karavicheva, T. | Karpechev, E. | Kebschull, U. | Keidel, R. | Keijdener, D. L. D. | Keil, M. | Khan, K. H. | Khan, M. M. | Khan, P. | Khan, S. A. | Khanzadeev, A. | Kharlov, Y. | Kileng, B. | Kim, B. | Kim, D. W. | Kim, D. J. | Kim, H. | Kim, J. S. | Kim, M. | Kim, M. | Kim, S. | Kim, T. | Kirsch, S. | Kisel, I. | Kiselev, S. | Kisiel, A. | Kiss, G. | Klay, J. L. | Klein, C. | Klein, J. | Klein-Bösing, C. | Kluge, A. | Knichel, M. L. | Knospe, A. G. | Kobayashi, T. | Kobdaj, C. | Kofarago, M. | Köhler, M. K. | Kollegger, T. | Kolojvari, A. | Kondratiev, V. | Kondratyeva, N. | Kondratyuk, E. | Konevskikh, A. | Kouzinopoulos, C. | Kovalenko, O. | Kovalenko, V. | Kowalski, M. | Kox, S. | Meethaleveedu, G. Koyithatta | Kral, J. | Králik, I. | Kravčáková, A. | Krelina, M. | Kretz, M. | Krivda, M. | Krizek, F. | Kryshen, E. | Krzewicki, M. | Kubera, A. M. | Kučera, V. | Kucheriaev, Y. | Kugathasan, T. | Kuhn, C. | Kuijer, P. 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The measurement of primary \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\pi ^{\pm }$$\end{document}π±, \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$K^{\pm }$$\end{document}K±, \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p$$\end{document}p and \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\overline{{p}}}$$\end{document}p¯ production at mid-rapidity (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$|y| <$$\end{document}|y|< 0.5) in proton–proton collisions at \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\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$=$$\end{document}= 7 TeV performed with a large ion collider experiment at the large hadron collider (LHC) is reported. Particle identification is performed using the specific ionisation energy-loss and time-of-flight information, the ring-imaging Cherenkov technique and the kink-topology identification of weak decays of charged kaons. Transverse momentum spectra are measured from 0.1 up to 3 GeV/\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$c$$\end{document}c for pions, from 0.2 up to 6 GeV/\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$c$$\end{document}c for kaons and from 0.3 up to 6 GeV/\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$c$$\end{document}c for protons. The measured spectra and particle ratios are compared with quantum chromodynamics-inspired models, tuned to reproduce also the earlier measurements performed at the LHC. Furthermore, the integrated particle yields and ratios as well as the average transverse momenta are compared with results at lower collision energies.
doi:10.1140/epjc/s10052-015-3422-9
PMCID: PMC4446008  PMID: 26041975
7.  Association between nutritional risk and routine clinical laboratory measurements and adverse outcomes: a prospective study in hospitalized patients of wuhan tongji hospital 
Background/Objectives:
Nutritional risk screening (NRS-2002) and routine clinical laboratory measurements (RCLMs) had been shown to have a predictive value in adverse outcomes in some studies, respectively. This study analyzed the association between NRS-2002 and RCLMs and estimated their prospective value in predicting adverse outcomes.
Subjects/Methods:
A total of 916 hospitalized patients were screened on admission with NRS-2002 and Subjective Global Assessment; RCLMs, which include blood test, kidney and liver function and electrolytes, were recorded. Diagnosis, nutritional support, surgery, radiotherapy, chemotherapy, complications, mortality and hospital stay during hospitalization were collected. The X2-test, odds ratios with 95% confidence intervals, kappa (k) statistic and regression analyses were conducted.
Results:
An overall 48.1% of the 916 patients were at nutritional risk on admission. Comparing ‘at risk' with ‘no risk', a significantly higher incidence of abnormality was found not only in nutritional markers but also in other parameters of RCLMs (OR ranged from 1.5 to 3.5). Regression analyses showed that ‘at risk' determined at admission was not a significant predictor of adverse outcomes after adjusting for other confounding factors, although it was a strong predictor in univariate analysis, whereas hypoalbuminemia, low total lymphocyte count, abnormality of hepatic and renal function were predictors after adjusting for confounders.
Conclusions:
The findings suggest that NRS-2002 might be a global index of ‘sickness' rather than be only a nutritional screening tool. It being rated once at admission is insufficient and should be repeated for using it as a predictor, whereas RCLMs routinely measured at admission may be able to be used to predict adverse outcomes.
doi:10.1038/ejcn.2014.239
PMCID: PMC4424800  PMID: 25369828
9.  Production of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mathbf {\Sigma (1385)^{\pm }}$$\end{document}Σ(1385)± and \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mathbf {\Xi (1530)^{0}}$$\end{document}Ξ(1530)0 in proton–proton collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mathbf {\sqrt{s}=}$$\end{document}s= 7 TeV 
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G. | Yamaguchi, Y. | Yang, H. | Yang, P. | Yang, S. | Yano, S. | Yasnopolskiy, S. | Yi, J. | Yin, Z. | Yoo, I.-K. | Yushmanov, I. | Zaccolo, V. | Zach, C. | Zaman, A. | Zampolli, C. | Zaporozhets, S. | Zarochentsev, A. | Závada, P. | Zaviyalov, N. | Zbroszczyk, H. | Zgura, I. S. | Zhalov, M. | Zhang, H. | Zhang, X. | Zhang, Y. | Zhao, C. | Zhigareva, N. | Zhou, D. | Zhou, F. | Zhou, Y. | Zhuo, Zhou | Zhu, H. | Zhu, J. | Zhu, X. | Zichichi, A. | Zimmermann, A. | Zimmermann, M. B. | Zinovjev, G. | Zoccarato, Y. | Zyzak, M.
The production of the strange and double-strange baryon resonances (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\Sigma (1385)^{\pm }$$\end{document}Σ(1385)±, \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\Xi (1530)^{0}$$\end{document}Ξ(1530)0) has been measured at mid-rapidity (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\left| y \right| $$\end{document}y\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$<0.5$$\end{document}<0.5) in proton–proton collisions at \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 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$=$$\end{document}= 7 TeV with the ALICE detector at the LHC. Transverse momentum spectra for inelastic collisions are compared to QCD-inspired models, which in general underpredict the data. A search for the \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\phi (1860)$$\end{document}ϕ(1860) pentaquark, decaying in the \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\Xi \pi $$\end{document}Ξπ channel, has been carried out but no evidence is seen.
doi:10.1140/epjc/s10052-014-3191-x
PMCID: PMC4424041  PMID: 25983644
10.  TLR4-mediated inflammation promotes foam cell formation of vascular smooth muscle cell by upregulating ACAT1 expression 
Cell Death & Disease  2014;5(12):e1574-.
Vascular smooth muscle cell (VSMC) foam cell formation is an important hallmark, especially in advanced atherosclerosis lesions. Acyl-coenzyme A:cholesterol acyltransferase 1 (ACAT1) promotes foam cell formation by promoting intracellular cholesteryl ester synthesis. The present study tests the hypothesis that oxidized low-density lipoprotein (oxLDL) increases the ACAT1 expression by activating the Toll-like receptor 4 (TLR4)-mediated inflammation, and ultimately promotes VSMC foam cell formation. Wild-type, ApoE−/−, TLR4−/− and ACAT1−/− mice on a C57BL/6J background were used. Increased TLR4, proinflammatory cytokines and ACAT1 were observed in high-fat (HF) diet-induced atherosclerotic plaque formation and in oxLDL-stimulated VSMCs. ACAT1 deficiency impeded the HF diet-induced atherosclerotic plaque formation and impaired the TLR4-manipulated VSMC foam cell formation in response to oxLDL. TLR4 deficiency inhibited the upregulation of myeloid-differentiating factor 88 (MyD88), nuclear factor-κB (NF-κB), proinflammatory cytokines and ACAT1, and eventually attenuated the HF diet-induced atherosclerotic plaque formation and suppressed the oxLDL-induced VSMC foam cell formation. Knockdown of MyD88 and NF-κB, respectively, impaired the TLR4-manipulated VSMC foam cell formation in response to oxLDL. Rosiglitazone (RSG) attenuated HF diet-induced atherosclerotic plaque formation in ApoE−/− mice, accompanied by reduced expression of TLR4, proinflammatory cytokines and ACAT1 accordingly. Activation of peroxisome proliferator-activated receptor γ (PPARγ) suppressed oxLDL-induced VSMC foam cell formation and inhibited the expression of TLR4, MyD88, NF-κB, proinflammatory cytokines and ACAT1, whereas inhibition of PPARγ exerted the opposite effect. TLR4−/− mice and VSMCs showed impaired atherosclerotic plaque formation and foam cell formation, and displayed no response to PPARγ manipulation. In conclusion, our data showed that oxLDL stimulation can activate the TLR4/MyD88/NF-κB inflammatory signaling pathway in VSMCs, which in turn upregulates the ACAT1 expression and finally promotes VSMC foam cell formation.
doi:10.1038/cddis.2014.535
PMCID: PMC4454165  PMID: 25522268
11.  Relevant mouse model for human monocytic leukemia through Cre/lox-controlled myeloid-specific deletion of PTEN 
Leukemia  2010;24(5):1077-1080.
doi:10.1038/leu.2010.34
PMCID: PMC4134872  PMID: 20220776
12.  Differential Expression of Vitamin E and Selenium-Responsive Genes by Disease Severity in Chronic Obstructive Pulmonary Disease 
COPD  2013;10(4):450-458.
Antioxidant nutritional status is hypothesized to influence chronic obstructive pulmonary disease (COPD) susceptibility and progression. Although past studies relate antioxidants to gene expression, there are no data in patients with COPD. This study investigated the hypothesis that antioxidant status is compromised in patients with COPD, and antioxidant-responsive genes differentially express in a similar pattern.
Lung tissue samples from patients with COPD were assayed for vitamin E and gene expression. Selenium and vitamin E were assayed in corresponding plasma samples. Discovery based genome-wide expression analysis compared moderate, severe, and very severe COPD (GOLD II-IV) patients to mild and at-risk/normal (GOLD 0-I). Hypotheses-driven analyses assessed differential gene expression by disease severity for vitamin E-responsive and selenium-responsive genes.
GOLD II-IV COPD patients had 30% lower lung tissue vitamin E levels compared to GOLD 0-I participants (p = 0.0082). No statistically significant genome-wide differences in expression by disease severity were identified. Hypothesis-driven analyses of 109 genes found 16 genes differentially expressed (padjusted<0.05) by disease severity including 6 selenium-responsive genes (range in fold-change -1.39 to 2.25), 6 vitamin E-responsive genes (fold-change -2.30 to 1.51), and 4 COPD-associated genes.
Lung tissue vitamin E in patients with COPD was associated with disease severity and vitamin E-responsive genes were differentially expressed by disease severity. While nutritional status is hypothesized to contribute to COPD risk, and is of therapeutic interest, evidence to date is mainly observational. The findings reported herein are novel, and support a role of vitamin E in COPD progression.
doi:10.3109/15412555.2012.761958
PMCID: PMC4060420  PMID: 23875740
Antioxidants; gene expression; tocopherol; selenium; COPD
13.  A step-by-step guide to the systematic review and meta-analysis of diagnostic and prognostic test accuracy evaluations 
Liu, Z | Yao, Z | Li, C | Liu, X | Chen, H | Gao, C
British Journal of Cancer  2013;108(11):2299-2303.
In evidence-based medicine (EBM), systematic reviews and meta-analyses have been widely applied in biological and medical research. Moreover, the most popular application of meta-analyses in this field may be to examine diagnostic (sensitivity and specificity) and prognostic (hazard ratio (HR) and its variance, standard error (SE) or confidence interval (CI)) test accuracy. However, conducting such analyses requires not only a great deal of time but also an advanced professional knowledge of mathematics, statistics and computer science. Regarding the practical application of meta-analyses for diagnostic and prognostic markers, the majority of users are clinicians and biologists, most of whom are not skilled at mathematics and computer science in particular. Hence, it is necessary for these users to have a simplified version of a protocol to help them to quickly conduct meta-analyses of the accuracy of diagnostic and prognostic tests. The aim of this paper is to enable individuals who have never performed a meta-analysis to do so from scratch. The paper does not attempt to serve as a comprehensive theoretical guide but instead describes one rigorous way of conducting a meta-analysis for diagnostic and prognostic markers. Investigators who follow the outlined methods should be able to understand the basic ideas behind the steps taken, the meaning of the meta-analysis results obtained for diagnostic and prognostic markers and the scope of questions that can be answered with Systematic Reviews and Meta-Analyses (SRMA). The presented protocols have been successfully tested by clinicians without meta-analysis experience.
doi:10.1038/bjc.2013.185
PMCID: PMC3681011  PMID: 23695015
systematic review; meta-analysis; prognostic marker; diagnostic marker; sensitivity and specificity; hazard ratio
14.  Lactobacillus reuteri-Specific Immunoregulatory Gene rsiR Modulates Histamine Production and Immunomodulation by Lactobacillus reuteri 
Journal of Bacteriology  2013;195(24):5567-5576.
Human microbiome-derived strains of Lactobacillus reuteri potently suppress proinflammatory cytokines like human tumor necrosis factor (TNF) by converting the amino acid l-histidine to the biogenic amine histamine. Histamine suppresses mitogen-activated protein (MAP) kinase activation and cytokine production by signaling via histamine receptor type 2 (H2) on myeloid cells. Investigations of the gene expression profiles of immunomodulatory L. reuteri ATCC PTA 6475 highlighted numerous genes that were highly expressed during the stationary phase of growth, when TNF suppression is most potent. One such gene was found to be a regulator of genes involved in histidine-histamine metabolism by this probiotic species. During the course of these studies, this gene was renamed the Lactobacillus reuteri-specific immunoregulatory (rsiR) gene. The rsiR gene is essential for human TNF suppression by L. reuteri and expression of the histidine decarboxylase (hdc) gene cluster on the L. reuteri chromosome. Inactivation of rsiR resulted in diminished TNF suppression in vitro and reduced anti-inflammatory effects in vivo in a trinitrobenzene sulfonic acid (TNBS)-induced mouse model of acute colitis. A L. reuteri strain lacking an intact rsiR gene was unable to suppress colitis and resulted in greater concentrations of serum amyloid A (SAA) in the bloodstream of affected animals. The PhdcAB promoter region targeted by rsiR was defined by reporter gene experiments. These studies support the presence of a regulatory gene, rsiR, which modulates the expression of a gene cluster known to mediate immunoregulation by probiotics at the transcriptional level. These findings may point the way toward new strategies for controlling gene expression in probiotics by dietary interventions or microbiome manipulation.
doi:10.1128/JB.00261-13
PMCID: PMC3889603  PMID: 24123819
15.  TRPV1 activation impedes foam cell formation by inducing autophagy in oxLDL-treated vascular smooth muscle cells 
Cell Death & Disease  2014;5(4):e1182-.
Vascular smooth muscle cells (VSMCs) are an important origin of foam cells besides macrophages. The mechanisms underlying VSMC foam cell formation are relatively little known. Activation of transient receptor potential vanilloid subfamily 1 (TRPV1) and autophagy have a potential role in regulating foam cell formation. Our study demonstrated that autophagy protected against foam cell formation in oxidized low-density lipoprotein (oxLDL)-treated VSMCs; activation of TRPV1 by capsaicin rescued the autophagy impaired by oxLDL and activated autophagy–lysosome pathway in VSMCs; activation of TRPV1 by capsaicin impeded foam cell formation of VSMCs through autophagy induction; activation of TRPV1 by capsaicin induced autophagy through AMP-activated protein kinase (AMPK) signaling pathway. This study provides evidence that autophagy plays an important role in VSMC foam cell formation and highlights TRPV1 as a promising therapeutic target in atherosclerosis.
doi:10.1038/cddis.2014.146
PMCID: PMC4001301  PMID: 24743737
AMP-activated protein kinase; autophagy; foam cell; transient receptor potential vanilloid subfamily 1; vascular smooth muscle cell
16.  GluR6-FasL-Trx2 mediates denitrosylation and activation of procaspase-3 in cerebral ischemia/reperfusion in rats 
Cell Death & Disease  2013;4(8):e771-.
Global cerebral ischemia/reperfusion (I/R) facilitates the activation of procaspase-3 and promotes apoptosis in hippocampus. But the mechanisms have remained uncharacterized. Protein S-nitrosylation and denitrosylation is an important reversible posttranslational modification, which is a common mechanism in signal transduction and affects numerous physiological and pathophysiological events. However, it is not known whether S-nitrosylation/denitrosylation modification of procaspase-3 serves as a component of apoptosis and cell death induced by cerebral I/R. Here we show that procaspase-3 is significantly denitrosylated and activated after I/R in rat hippocampus. NS102, a glutamate receptor 6 (GluR6) antagonist, can inhibit the denitrosylation of procaspase-3 and diminish the increased Fas ligand (FasL) and thioredoxin (Trx)-2 expression induced by cerebral I/R. Moreover, downregulation of FasL expression by antisense oligodeoxynucleotides inhibits the denitrosylation and activation of procaspase-3. Auranofin, a TrxR inhibitor or TrxR2 antisense oligodeoxynucleotide, has similar effects. In primary hippocampal cultures, Lentiviral-mediated knockdown of FasL and TrxR2 before the oxygen and glucose deprivation/reoxygenation further verifies that FasL and TrxR2 are involved in the denitrosylation of procaspase-3. In situ TUNEL staining and cresyl violet staining validate that inhibiting denitrosylation of procaspase-3 may exert neuroprotective effect on apoptosis and cell death induced by cerebral I/R in hippocampal CA1 pyramidal neurons. This is the first evidence that cerebral I/R mediates procaspase-3 denitrosylation and activation through GluR6-FasL-Trx2 pathway, which leads to neuronal apoptosis and cell death.
doi:10.1038/cddis.2013.299
PMCID: PMC3763460  PMID: 23949220
brain ischemic; FasL; Trx2; Procaspase-3; denitrosylation; neuroprotection.
17.  Cdk5 targets active Src for ubiquitin-dependent degradation by phosphorylating Src(S75) 
The non-receptor tyrosine kinase Src is a critical regulator of cytoskeletal contraction, cell adhesion, and migration. In normal cells, Src activity is stringently controlled by Csk-dependent phosphorylation of Src(Y530), and by Cullin-5-dependent ubiquitinylation, which affects active Src(pY419) exclusively, leading to its degradation by the proteosome. Previous work has shown that Src activity is also limited by Cdk5, a proline-directed kinase, which has been shown to phosphorylate Src(S75). Here we show that this phosphorylation promotes the ubiquitin-dependent degradation of Src, thus restricting the availability of active Src. We demonstrate that Src(S75) phosphorylation occurs in vivo in epithelial cells, and like ubiquitinylation, is associated only with active Src. Preventing Cdk5-dependent phosphorylation of Src(S75), by site-specific mutation of S75 or by Cdk5 inhibition or suppression, increases Src(Y419) phosphorylation and kinase activity, resulting in Src-dependent cytoskeletal changes. In transfected cells, ubiquitinylation of Src(S75A) is about 35% that of wild-type Src-V5, and its half-life is approximately 2.5-fold greater. Cdk5 suppression leads to a comparable decrease in the ubiquitinylation of endogenous Src and a similar increase in Src stability. Together, these findings demonstrate that Cdk5-dependent phosphorylation of Src(S75) is a physiologically significant mechanism of regulating intracellular Src activity.
doi:10.1007/s00018-011-0638-1
PMCID: PMC3167940  PMID: 21442427
Cdk5; Src; Signal transduction; Ubiquitination; Kinase activity
18.  Precise and Continuous Time and Frequency Synchronisation at the 5×10-19 Accuracy Level 
Scientific Reports  2012;2:556.
The synchronisation of time and frequency between remote locations is crucial for many important applications. Conventional time and frequency dissemination often makes use of satellite links. Recently, the communication fibre network has become an attractive option for long-distance time and frequency dissemination. Here, we demonstrate accurate frequency transfer and time synchronisation via an 80 km fibre link between Tsinghua University (THU) and the National Institute of Metrology of China (NIM). Using a 9.1 GHz microwave modulation and a timing signal carried by two continuous-wave lasers and transferred across the same 80 km urban fibre link, frequency transfer stability at the level of 5×10−19/day was achieved. Time synchronisation at the 50 ps precision level was also demonstrated. The system is reliable and has operated continuously for several months. We further discuss the feasibility of using such frequency and time transfer over 1000 km and its applications to long-baseline radio astronomy.
doi:10.1038/srep00556
PMCID: PMC3412274  PMID: 22870385
19.  PAP-LMPCR for improved, allele-specific footprinting and automated chromatin fine structure analysis 
Nucleic Acids Research  2008;36(3):e19.
The analysis of chromatin fine structure and transcription factor occupancy of differentially expressed genes by in vivo footprinting and ligation-mediated-PCR (LMPCR) is a powerful tool to understand the impact of chromatin on gene expression. However, as with all PCR-based techniques, the accuracy of the experiments has often been reduced by sequence similarities and the presence of GC-rich or repeat sequences, and some sequences are completely refractory to analysis. Here we describe a novel method, pyrophosphorolysis activated polymerization LMPCR or PAP-LMPCR, which is capable of generating accurate and reproducible footprints specific for individual alleles and can read through sequences previously not accessible for analysis. In addition, we have adapted this technique for automation, thus enabling the simultaneous and rapid analysis of chromatin structure at many different genes.
doi:10.1093/nar/gkm1159
PMCID: PMC2241904  PMID: 18208840
20.  Construction of bovine whole-genome radiation hybrid and linkage maps using high-throughput genotyping 
Animal Genetics  2007;38(2):120-125.
High-density whole-genome maps are essential for ordering genes or markers and aid in the assembly of genome sequence. To increase the density of markers on the bovine radiation hybrid map, and hence contribute to the assembly of the bovine genome sequence, an Illumina® BeadStation was used to simultaneously type large numbers of markers on the Roslin-Cambridge 3000 rad bovine–hamster whole-genome radiation hybrid panel (WGRH3000). In five multiplex reactions, 6738 sequence tagged site (STS) markers were successfully typed on the WGRH3000 panel DNA. These STSs harboured SNPs that were developed as a result of the bovine genome sequencing initiative. Typically, the most time consuming and expensive part of creating high-density radiation hybrid (RH) maps is genotyping the markers on the RH panel with conventional approaches. Using the method described in this article, we have developed a high-density whole-genome RH map with 4690 loci and a linkage map with 2701 loci, with direct comparison to the bovine whole-genome sequence assembly (Btau_2.0) in a fraction of the time it would have taken with conventional typing and genotyping methods.
doi:10.1111/j.1365-2052.2006.01564.x
PMCID: PMC2063635  PMID: 17302794
bovine; illumina; map; single nucleotide polymorphism
21.  Childhood sexual abuse and the risk for recurrent major depression in Chinese women 
Psychological Medicine  2011;42(2):409-417.
Background
Studies in Western countries have repeatedly shown that women with a history of childhood sexual abuse (CSA) are at increased risk for developing major depression (MD). Would this relationship be found in China?
Method
Three levels of CSA (non-genital, genital, and intercourse) were assessed by self-report in two groups of Han Chinese women: 1970 clinically ascertained with recurrent MD and 2597 matched controls. Diagnostic and other risk factor information was assessed at personal interview. Odds ratios (ORs) were calculated by logistic regression and regression coefficients by linear or Poisson regression.
Results
Any form of CSA was significantly associated with recurrent MD [OR 3.26, 95% confidence interval (CI) 1.95–5.45]. This association strengthened with increasing CSA severity: non-genital (OR 2.47, 95% CI 1.17–5.23), genital (OR 2.77, 95% CI 1.32–5.83) and intercourse (OR 13.35, 95% CI 1.83–97.42). The association between any form of CSA and MD remained significant after accounting for parental history of depression, childhood emotional neglect (CEN), childhood physical abuse (CPA) and parent–child relationship. Among the depressed women, those with CSA had an earlier age of onset, longer depressive episodes and an increased risk for generalized anxiety disorder (GAD; OR 1.92, 95% CI 1.39–2.66) and dysthymia (OR 2.16, 95% CI 1.52–3.09).
Conclusions
In Chinese women CSA is strongly associated with MD and this association increases with greater severity of CSA. Depressed women with CSA have an earlier age of onset, longer depressive episodes and increased co-morbidity with GAD and dysthymia. Although reporting biases cannot be ruled out, our results are consistent with the hypothesis that, as in Western countries, CSA substantially increases the risk for MD in China.
doi:10.1017/S0033291711001462
PMCID: PMC3250087  PMID: 21835095
Childhood sexual abuse; co-morbidity; major depression
22.  Patterns of co-morbidity with anxiety disorders in Chinese women with recurrent major depression 
Psychological Medicine  2011;42(6):1239-1248.
Background
Studies conducted in Europe and the USA have shown that co-morbidity between major depressive disorder (MDD) and anxiety disorders is associated with various MDD-related features, including clinical symptoms, degree of familial aggregation and socio-economic status. However, few studies have investigated whether these patterns of association vary across different co-morbid anxiety disorders. Here, using a large cohort of Chinese women with recurrent MDD, we examine the prevalence and associated clinical features of co-morbid anxiety disorders.
Method
A total of 1970 female Chinese MDD patients with or without seven co-morbid anxiety disorders [including generalized anxiety disorder (GAD), panic disorder, and five phobia subtypes] were ascertained in the CONVERGE study. Generalized linear models were used to model association between co-morbid anxiety disorders and various MDD features.
Results
The lifetime prevalence rate for any type of co-morbid anxiety disorder is 60.2%. Panic and social phobia significantly predict an increased family history of MDD. GAD and animal phobia predict an earlier onset of MDD and a higher number of MDD episodes, respectively. Panic and GAD predict a higher number of DSM-IV diagnostic criteria. GAD and blood-injury phobia are both significantly associated with suicidal attempt with opposite effects. All seven co-morbid anxiety disorders predict higher neuroticism.
Conclusions
Patterns of co-morbidity between MDD and anxiety are consistent with findings from the US and European studies; the seven co-morbid anxiety disorders are heterogeneous when tested for association with various MDD features.
doi:10.1017/S003329171100273X
PMCID: PMC3339636  PMID: 22126712
Co-morbid anxiety disorders; major depression
23.  Cognitive trio: relationship with major depression and clinical predictors in Han Chinese women 
Psychological Medicine  2013;43(11):2265-2275.
Background
Previous studies support Beck's cognitive model of vulnerability to depression. However, the relationship between his cognitive triad and other clinical features and risk factors among those with major depression (MD) has rarely been systematically studied.
Method
The three key cognitive symptoms of worthlessness, hopelessness and helplessness were assessed during their lifetime worst episode in 1970 Han Chinese women with recurrent MD. Diagnostic and other risk factor information was assessed at personal interview. Odds ratios (ORs) were calculated by logistic regression.
Results
Compared to patients who did not endorse the cognitive trio, those who did had a greater number of DSM-IV A criteria, more individual depressive symptoms, an earlier age at onset, a greater number of episodes, and were more likely to meet diagnostic criteria for melancholia, postnatal depression, dysthymia and anxiety disorders. Hopelessness was highly related to all the suicidal symptomatology, with ORs ranging from 5.92 to 6.51. Neuroticism, stressful life events (SLEs) and a protective parental rearing style were associated with these cognitive symptoms.
Conclusions
During the worst episode of MD in Han Chinese women, the endorsement of the cognitive trio was associated with a worse course of depression and an increased risk of suicide. Individuals with high levels of neuroticism, many SLEs and high parental protectiveness were at increased risk for these cognitive depressive symptoms. As in Western populations, symptoms of the cognitive trio appear to play a central role in the psychopathology of MD in Chinese women.
doi:10.1017/S0033291713000160
PMCID: PMC3807662  PMID: 23425530
Cognitive trio; Han Chinese women; major depression; suicide; symptoms
24.  The structure of the symptoms of major depression: exploratory and confirmatory factor analysis in depressed Han Chinese women 
Psychological Medicine  2013;44(7):1391-1401.
Background
The symptoms of major depression (MD) are clinically diverse. Do they form coherent factors that might clarify the underlying nature of this important psychiatric syndrome?
Method
Symptoms at lifetime worst depressive episode were assessed at structured psychiatric interview in 6008 women of Han Chinese descent, age ⩾30 years with recurrent DSM-IV MD. Exploratory factor analysis (EFA) and confirmatoryfactor analysis (CFA) were performed in Mplus in random split-half samples.
Results
The preliminary EFA results were consistently supported by the findings from CFA. Analyses of the nine DSM-IV MD symptomatic A criteria revealed two factors loading on: (i) general depressive symptoms; and (ii) guilt/suicidal ideation. Examining 14 disaggregated DSM-IV criteria revealed three factors reflecting: (i) weight/appetite disturbance; (ii) general depressive symptoms; and (iii) sleep disturbance. Using all symptoms (n = 27), we identified five factors that reflected: (i) weight/appetite symptoms; (ii) general retarded depressive symptoms; (iii) atypical vegetative symptoms; (iv) suicidality/hopelessness; and (v) symptoms of agitation and anxiety.
Conclusions
MD is a clinically complex syndrome with several underlying correlated symptom dimensions. In addition to a general depressive symptom factor, a complete picture must include factors reflecting typical/atypical vegetative symptoms, cognitive symptoms (hopelessness/suicidal ideation), and an agitated symptom factor characterized by anxiety, guilt, helplessness and irritability. Prior cross-cultural studies, factor analyses of MD in Western populations and empirical findings in this sample showing risk factor profiles similar to those seen in Western populations suggest that our results are likely to be broadly representative of the human depressive syndrome.
doi:10.1017/S003329171300192X
PMCID: PMC3967839  PMID: 23920138
Atypical symptoms; China; cognitive symptoms; depression; factor analysis
25.  Targeting autophagy overcomes Enzalutamide resistance in castration-resistant prostate cancer cells and improves therapeutic response in a xenograft model 
Oncogene  2014;33(36):4521-4530.
Macro-autophagy is associated with drug resistance in various cancers and can function as an adaptive response to maintain cell survival under metabolic stresses, including androgen deprivation. Androgen deprivation or treatment with androgen receptor (AR) signaling inhibitor (ARSI), Enzalutamide (MDV-3100, ENZA) or bicalutamide induced autophagy in androgen-dependent and in castration-resistant CaP (castration-resistant prostate cancer (CRPC)) cell lines. The autophagic cascade triggered by AR blockage, correlated with the increased light chain 3-II/I ratio and ATG-5 expression. Autophagy was observed in a subpopulation of C4-2B cells that developed insensitivity to ENZA after sustained exposure in culture. Using flow cytometry and clonogenic assays, we showed that inhibiting autophagy with clomipramine (CMI), chloroquine or metformin increased apoptosis and significantly impaired cell viability. This autophagic process was mediated by AMP-dependent protein kinase (AMPK) activation and the suppression of mammalian target of rapamycin (mTOR) through Raptor phosphorylation (Serine 792). Furthermore, small interfering RNA targeting AMPK significantly inhibited autophagy and promoted cell death in CaP cells acutely or chronically exposed to ENZA or androgen deprivation, suggesting that autophagy is an important survival mechanism in CRPC. Lastly, in vivo studies with mice orthotopically implanted with ENZA-resistant cells demonstrated that the combination of ENZA and autophagy modulators, CMI or metformin significantly reduced tumor growth when compared with control groups (P<0.005). In conclusion, autophagy is as an important mechanism of resistance to ARSI in CRPC. Antiandrogen-induced autophagy is mediated through the activation of AMPK pathway and the suppression of mTOR pathway. Blocking autophagy pharmacologically or genetically significantly impairs prostate cancer cell survival in vitro and in vivo, implying the therapeutics potential of autophagy inhibitors in the antiandrogen-resistance setting.
doi:10.1038/onc.2014.25
PMCID: PMC4155805  PMID: 24662833

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