Energy Spectra of Anti-nucleons in Finite Nuclei

The quantum vacuum in a many-body system of finite nuclei has been investigated within the relativistic Hartree approach which describes the bound states of nucleons and anti-nucleons consistently. The contributions of the Dirac sea to the source terms of the meson-field equations are taken into account up to the one-nucleon loop and one-meson loop. The tensor couplings for the $\omega$- and $\rho$-meson are included in the model. The overall nucleon spectra of shell-model states are in agreement with the data. The calculated anti-nucleon spectra in the vacuum differ about 20 -- 30 MeV with and without the tensor-coupling effects.Comment: 4 pages, to appear in the Proceedings of MENU 2004 (Beijing, Aug. 29 -- Sept. 4, 2004

Tick-borne encephalitis virus induces chemokine RANTES expression via activation of IRF-3 pathway.

BACKGROUND: Tick-borne encephalitis virus (TBEV) is one of the most important flaviviruses that targets the central nervous system (CNS) and causes encephalitides in humans. Although neuroinflammatory mechanisms may contribute to brain tissue destruction, the induction pathways and potential roles of specific chemokines in TBEV-mediated neurological disease are poorly understood. METHODS: BALB/c mice were intracerebrally injected with TBEV, followed by evaluation of chemokine and cytokine profiles using protein array analysis. The virus-infected mice were treated with the CC chemokine antagonist Met-RANTES or anti-RANTES mAb to determine the role of RANTES in affecting TBEV-induced neurological disease. The underlying signaling mechanisms were delineated using RANTES promoter luciferase reporter assay, siRNA-mediated knockdown, and pharmacological inhibitors in human brain-derived cell culture models. RESULTS: In a mouse model, pathological features including marked inflammatory cell infiltrates were observed in brain sections, which correlated with a robust up-regulation of RANTES within the brain but not in peripheral tissues and sera. Antagonizing RANTES within CNS extended the survival of mice and reduced accumulation of infiltrating cells in the brain after TBEV infection. Through in vitro studies, we show that virus infection up-regulated RANTES production at both mRNA and protein levels in human brain-derived cell lines and primary progenitor-derived astrocytes. Furthermore, IRF-3 pathway appeared to be essential for TBEV-induced RANTES production. Site mutation of an IRF-3-binding motif abrogated the RANTES promoter activity in virus-infected brain cells. Moreover, IRF-3 was activated upon TBEV infection as evidenced by phosphorylation of TBK1 and IRF-3, while blockade of IRF-3 activation drastically reduced virus-induced RANTES expression. CONCLUSIONS: Our findings together provide insights into the molecular mechanism underlying RANTES production induced by TBEV, highlighting its potential importance in the process of neuroinflammatory responses to TBEV infection

Prognostic Importance of Circulating Tumor Cells in Nonsmall Cell Lung Cancer: A Prospective Study

Purpose: To investigate the prognostic value of circulating tumor cells (CTCs) and to predict the treatment response in a non-small cell lung cancer (NSCLC).Methodology: A single-center prospective study involving 93 patients with NSCLC was conducted. Blood samples were analyzed for CTC count before and after chemotherapy. Clinical relevance of CTCs with patient`s characteristics and treatment response were determined.Results: Higher levels of CTCs were associated with severe stage of NSCLC (p = 0.003), tumor histology (p = 0.014) and metastases (p = 0.013). Significant difference in CTC count was observed in favorable (CTCs < 5) and unfavorable (CTCs ≥ 5) groups. Progression-free survival (PFS) was 5.8 months (range: 5.32 to 6.43) and 2.2 months (range: 1.85 to 3.01) in the favorable and unfavorable groups, respectively (HR: 3.88, 95% CI, p < 0.001). Similarly, overall survival (OS) was 7.3 months (95% CI, 6.51 to 7.92) and 3.9 months (95% CI, 1.99 to 5.13), respectively (HR: 4.8, 95% CI, p < 0.001). Multivariate  regression analysis revealed CTCs as strong predictors of OS and PFS. Significant reduction (p < 0.001) in CTC count was also observed after one cycle of chemotherapy.Conclusion: Patients with low CTC count live longer and remain progression-free for a longer period of time than those with high CTC count. High CTCs can be detected in severe forms of lung cancer and can be used as a valid prognostic marker. However, this assertion requires validation in larger prospective clinical cohorts.Keywords: Circulating tumor cells, Non-small cell lung cancer, Circulating tumor cell, Prognosi

Zika virus promotes CCN1 expression via the CaMKIIα-CREB pathway in astrocytes.

Zika virus (ZIKV) infection in the human central nervous system (CNS) causes Guillain-Barre syndrome, cerebellum deformity, and other diseases. Astrocytes are immune response cells in the CNS and an important component of the blood-brain barrier. Consequently, any damage to astrocytes facilitates the spread of ZIKV in the CNS. Connective tissue growth factor/Nephroblastoma overexpressed gene family 1 (CCN1), an important inflammatory factor secreted by astrocytes, is reported to regulate innate immunity and viral infection. However, the mechanism by which astrocyte viral infection affects CCN1 expression remains undefined. In this study, we demonstrate that ZIKV infection up-regulates CCN1 expression in astrocytes, thus promoting intracellular viral replication. Other studies revealed that the cAMP response element (CRE) in the CCN1 promoter is activated by the ZIKV NS3 protein. The cAMP-responsive element-binding protein (CREB), a transacting factor of the CRE, is also activated by NS3 or ZIKV. Furthermore,a specific inhibitor of CREB, i.e. SGC-CBP30, reduced ZIKV-induced CCN1 up-regulation and ZIKV replication. Moreover, co-immunoprecipitation, overexpression, and knockdown studies confirmed that the interaction between NS3 and the regulatory domain of CaMKIIα could activate the CREB pathway, thus resulting in the up-regulation of CCN1 expression and enhancement of virus replication. In conclusion, the findings of our investigations on the NS3-CaMKIIα-CREB-CCN1 pathway provide a foundation for understanding the infection mechanism of ZIKV in the CNS

Global synchronization for delayed complex networks with randomly occurring nonlinearities and multiple stochastic disturbances

This is the post print version of the article. The official published version can be obained from the link - Copyright 2009 IOP Publishing LtdThis paper is concerned with the synchronization problem for a new class of continuous time delayed complex networks with stochastic nonlinearities (randomly occurring nonlinearities), interval time-varying delays, unbounded distributed delays as well as multiple stochastic disturbances. The stochastic nonlinearities and multiple stochastic disturbances are investigated here in order to reflect more realistic dynamical behaviors of the complex networks that are affected by the noisy environment. By utilizing a new matrix functional with the idea of partitioning the lower bound h1 of the time-varying delay, we employ the stochastic analysis techniques and the properties of the Kronecker product to establish delay-dependent synchronization criteria that ensure the globally asymptotically mean-square synchronization of the addressed stochastic delayed complex networks. The sufficient conditions obtained are in the form of linear matrix inequalities (LMIs) whose solutions can be readily solved by using the standard numerical software. A numerical example is exploited to show the applicability of the proposed results.This work was supported in part by the Engineering and Physical Sciences Research Council (EPSRC) of the UK under Grant GR/S27658/01, an International Joint Project sponsored by the Royal Society of the UK, the National 973 Program of China under Grant 2009CB320600, the National Natural Science Foundation of China under Grant 60804028, the Specialized Research Fund for the Doctoral Program of Higher Education for New Teachers under Grant 200802861044, the Teaching and Research Fund for Excellent Young Teachers at Southeast University of China, and the Alexander von Humboldt Foundation of Germany