Functional cooperation of of IL-1β and RGS4 in the brachial plexus avulsion mediated brain reorganization

<p>Abstract</p> <p>Backgrounds</p> <p>There is considerable evidence that central nervous system is continuously modulated by activity, behavior and skill acquisition. This study is to examine the reorganization in cortical and subcortical regions in response to brachial plexus avulsion.</p> <p>Methods</p> <p>Adult C57BL/6 mice were divided into four groups: control, 1, 3 and 6 month of brachial plexus avulsion. IL-1β, IL-6 and RGS4 expression in cortex, brainstem and spinal cord were detected by BiostarM-140 s microarray and real-time PCR. RGS4 subcellular distribution and modulation were further analyzed by primary neuron culture and Western Blot.</p> <p>Results</p> <p>After 1, 3 and 6 months of brachial plexus avulsion, 49 (0 up, 49 down), 29 (17 up, 12 down), 13 (9 up, 4 down) genes in cerebral cortex, 40 (8 up, 32 down), 11 (7 up, 4 down), 137 (63 up, 74 down) in brainstem, 27 (14 up, 13 down), 33 (18 up, 15 down), 60 (29 up, 31 down) in spinal cord were identified. Among the regulated gene, IL-1β and IL-6 were sustainable enhanced in brain stem, while PKACβ and RGS4 were up-regulated throughout cerebral cortex, brainstem and spinal cord in 3 and 6 month of nerve injury. Intriguingly, subcellular distribution of RGS4 in above three regions was dependent on the functional correlation of PKA and IL-1β.</p> <p>Conclusion</p> <p>Data herein indicated that brachial plexus avulsion could efficiently initiate and perpetuate the brain reorganization. Network involved IL-1β and RGS4 signaling might implicate in the re-establish and strengthening of the local circuits at the cortical and subcortical levels.</p

Roles of microRNA on cancer cell metabolism

Advanced studies of microRNAs (miRNAs) have revealed their manifold biological functions, including control of cell proliferation, cell cycle and cell death. However, it seems that their roles as key regulators of metabolism have drawn more and more attention in the recent years. Cancer cells display increased metabolic autonomy in comparison to non-transformed cells, taking up nutrients and metabolizing them in pathways that support growth and proliferation. MiRNAs regulate cell metabolic processes through complicated mechanisms, including directly targeting key enzymes or transporters of metabolic processes and regulating transcription factors, oncogenes / tumor suppressors as well as multiple oncogenic signaling pathways. MiRNAs like miR-375, miR-143, miR-14 and miR-29b participate in controlling cancer cell metabolism by regulating the expression of genes whose protein products either directly regulate metabolic machinery or indirectly modulate the expression of metabolic enzymes, serving as master regulators, which will hopefully lead to a new therapeutic strategy for malignant cancer. This review focuses on miRNA regulations of cancer cell metabolism,including glucose uptake, glycolysis, tricarboxylic acid cycle and insulin production, lipid metabolism and amino acid biogenesis, as well as several oncogenic signaling pathways. Furthermore, the challenges of miRNA-based strategies for cancer diagnosis, prognosis and therapeutics have been discussed

The Relations between Chinese and English in the Era of Globalization

The authors study the ways to replenish the vocabulary of the modern Chinese language due to the penetration of English-American borrowings, adaptation/non-adaptation of the latter to the hieroglyphic environment, correlation of functional features of the English vocabulary and the intensity of replenishment of the vocabular

AGR3 Regulates Airway Epithelial Junctions in Patients with Frequent Exacerbations of COPD

Background: The mechanisms underlying differences in the susceptibility to chronic obstructive pulmonary disease (COPD) exacerbations between patients are not well understood. Recent studies have shown that the patients with frequent COPD exacerbations is related to specific protein expression in lung tissue. Anterior gradient 3 (AGR3) is expressed in airway epithelial cells in the lung and proteomic analysis revealed that its expression is decreased in patients with frequent COPD exacerbations. Moreover, the loss of epithelial integrity might facilitate trans-epithelial permeability of pathogens in such patients. This study was performed to determine that AGR3 protein play a role in COPD frequency exacerbators.Methods: Human lung tissues were collected from current-smoking patients (Control; n = 15) as well as patients with infrequent COPD exacerbations (IFCOPD; n = 18) and frequent COPD exacerbations (FCOPD; n = 8). While AGR3 protein expression was measured by immunohistochemistry and western blotting, AGR mRNA expression was determined by real time quantitative polymerase chain reaction (RT-qPCR). Furthermore, adherent junctions (AJs) and tight junctions (TJs) protein expression in human lung tissues were measured by immunohistochemistry. The effects of cigarette smoke extract (CSE) on AJ and TJ protein and mRNA expression in BEAS-2B cells were assessed by western blotting and RT-qPCR. In addition, the effect of AGR3 overexpression and knockdown on AJ and TJ protein expression was determined.Results: AGR3 was mainly expressed in the airway epithelium and AGR3-positive products were localized in the cytoplasm. Western blotting and RT-qPCR results showed that AGR3 protein (p = 0.009) and mRNA (p = 0.04) expression in the FCOPD group was significantly lower than that in the IFCOPD group. Moreover, E-cadherin, occludin, and zonula occludens-1 (ZO-1) expression was lower in the FCOPD group than in the IFCOPD group. The protein and mRNA expression of E-cadherin, occludin, and ZO-1 was decreased within 24 h post-CSE exposure. AGR3 overexpression rescued CSE-induced downregulation of E-cadherin, occludin, and ZO-1.Conclusion: Difference in AGR3 expression in the lung tissue might be correlated with increased susceptibility to COPD exacerbation. AGR3 can prevent CSE-induced downregulation of E-cadherin, occludin, and ZO-1 in airway epithelial cells. Loss of AGR3 might promote viral and bacterial infection and induce immune inflammation to increase COPD exacerbation

Deterministic generation of polarization-entangled photon pairs in a cavity-QED system

We propose a cavity-QED scheme that can deterministically generate Einstein-Podosky-Rosen polarization-entangled photon pairs. A four-level tripod atom successively couples to two high-Q optical cavities possessing polarization degeneracy, assisted by a classical $\pi$-polarized pump field. The stimulated Raman adiabatic passage process in the atom-cavity system is used to produce the polarization-entangled photon pairs. The proposal is particularly robust against atomic spontaneous decay, which should have potential applications in quantum information processing.Comment: 15 pages, 4figure