EMT

environment like a ship, instead of second in a dynamic and critical environment for the system as a hospital. Through the analysis of case happened, tabletop simulation, and the opinion of expert as doctors, firefighters, and rescue workers, we evaluate the hazard and we analyze the effect on the system, and how to interface The risk assessment is development the impact on systems, and how to interface with the national health system and its weakness. Analyzing the current system of response to events, there are analysis of the critical points. Moreover, It’s evaluate the current state of the art and the actors involved, their training and skill. Through the analysis of the critical points are identified solutions to optimize and improve the system. Keywords: Micro-organism; Bacterium; Virus; Drug; Outbreak; Epidemy; Biological evet; Biohazard; Bioweapon; Bioterrorism; HAZMAT; Risk; Hospital, Ship; Vessel; Port; First responder; University; Course; Emergency Medical Service; EMS; Firefighter;

Emergency management of biohazard events, outbreack on ship and hospital. Available from: https://www.researchgate.net/publication/317329024_Emergency_management_of_biohazard_events_outbreack_on_ship_and_hospital [accessed Jun 3, 2017].

Background: Reduced levels of magnesium can cause several diseases and increase cancer risk. Motivated by magnesium chloride’s (MgCl2) non-toxicity, physiological importance, and beneficial clinical applications, we studied its action mechanism and possible mechanical, molecular, and physiological effects in prostate cancer with different metastatic potentials.

Methods: We examined the effects of MgCl2, after 24 and 48 hours, on apoptosis, cell migration, expression of epithelial mesenchymal transition (EMT) markers, and V-H+-ATPase,
myosin II (NMII) and the transcription factor NF Kappa B (NFkB) expressions.

Results: MgCl2 induces apoptosis, and significantly decreases migration speed in cancer cells with different metastatic potentials. MgCl2 reduces the expression of V-H+-ATPase and myosin II that facilitates invasion and metastasis, suppresses the expression of vimentin and increases expression of E-cadherin, suggesting a role of MgCl2 in reversing the EMT. MgCl2 also significantly increases the chromatin condensation and decreases NFkB expression.

Conclusions: These results suggest a promising preventive and therapeutic role of MgCl2 for prostate cancer. Further studies should explore extending MgCl2 therapy to in vivo studies and other cancer types.

Keywords: Magnesium chloride, prostate cancer, migration speed, V-H+-ATPase, and EMT.

Uterine carcinosarcomas (UCS) are rare (3-4%) but highly aggressive, accounting for a disproportionately high (16.4%) mortality among uterine malignancies. Transforming growth factor beta (TGFβ) is a multifunctional cytokine that regulates important cellular processes including epithelial-mesenchymal transition (EMT). Existence of biphasic elements and a report demonstrating amplification of TGFβ at 19q13.1 prompted us to investigate the role of TGFβ signaling in UCS.Here we demonstrated the components of TGFβ pathway are expressed and functional in UCS. TGFβ-I induced significant Smad2/3 phosphorylation, migration and EMT responses in UCS cell lines which could be attenuated by the TGFβ receptor I (TGFβR-I) or TGFβ receptor I/II (TGFβR-I/II) inhibitor developed by Eli Lilly and company. Importantly, TGFβ-I induced proliferation was c-Myc dependent, likely through activation of cell cycle. c-Myc was induced by nuclear translocation of nuclear factor of activated T cells (NFAT-1) in ...

DOI: 10.13140/RG.2.2.14632.47360
Es de importancia destacar que la EMT es una estimulación de flujo eléctrico, no es una estimulación magnética, los pulsos magnéticos son portadores del flujo eléctrico modulado de modo no invasivo, generado por los inductores o bobinas sobre la superficie cortical.
En esta breve exposición se examinará el proceso experimental, parámetros, consecuencias y refutaciones.
Es común la difusión errónea sobre la EMT, en la que se suele resaltar erróneamente que el procedimiento es de estimulación magnética, ello es una referencia equívoca que podría ocasionar posibles riesgos a los sujetos expuestos a ello.

The Epithelial to Mesenchymal Transition (EMT) regulates cell plasticity during embryonic development and in disease. It is dynamically orchestrated by transcription factors (EMT-TFs), including Snail, Zeb, Twist and Prrx, all activated by TGF-β among other signals. Here we find that Snail1 and Prrx1, which respectively associate with gain or loss of stem-like properties and with bad or good prognosis in cancer patients, are expressed in complementary patterns during vertebrate development and in cancer. We show that this complementarity is established through a feedback loop in which Snail1 directly represses Prrx1, and Prrx1, through direct activation of the miR-15 family, attenuates the expression of Snail1. We also describe how this gene regulatory network can establish a hierarchical temporal expression of Snail1 and Prrx1 during EMT and validate its existence in vitro and in vivo, providing a mechanism to switch and select different EMT programs with important implications in development and disease.

Atypical protein kinase Cs (aPKC) are involved in cell cycle progression, tumorigenesis, cell survival and migration in many cancers. We believe that aPKCs play an important role in cell motility of melanoma by regulating cell signaling pathways and inducing epithelial to mesenchymal transition (EMT). We have investigated the effects of two novel aPKC inhibitors; 2-acetyl-1,3-cyclopentanedione (ACPD) and 3,4-diaminonaphthalene-2,7-disulfonic acid (DNDA) on cell proliferation, apoptosis, migration and invasion of two malignant melanoma cell lines compared to normal melanocytes. Molecular docking data suggested that both inhibitors specifically bind to protein kinase C-zeta (PKC-ζ) and PKC-iota (PKC-ι) and kinase activity assays were carried out to confirm these observations. Both inhibitors decreased the levels of total and phosphorylated PKC-ζ and PKC-ι. Increased levels of E-cadherin, RhoA, PTEN and decreased levels of phosphorylated vimentin, total vimentin, CD44, β-catenin and phosphorylated AKT in inhibitor treated cells. This suggests that inhibition of both PKC-ζ and PKC-ι using ACPD and DNDA downregulates EMT and induces apoptosis in melanoma cells. We also carried out PKC-ι and PKC-ζ directed siRNA treatments to prove the above observations. Immunoprecipitation data suggested an association between PKC-ι and vimentin and PKC-ι siRNA treatments confirmed that PKC-ι activates vimentin by phosphorylation. These results further suggested that PKC-ι is involved in signaling pathways which upregulate EMT and which can be effectively suppressed using ACPD and DNDA. Our results summarize that melanoma cells proliferate via aPKC/AKT/NF-κB mediated pathway while inducing the EMT via PKC-ι/Par6/RhoA pathway. Overall, results show that aPKCs are essential for melanoma progression and metastasis, suggesting that ACPD and DNDA can be effectively used as potential therapeutic drugs for melanoma by inhibiting aPKCs.

Cancer cell migration and invasion involves actin cytoskeleton reorganization, which is regulated by the WASP (Wiskott Aldrich Syndrome Protein) family of proteins such as WASP, N-WASP (Neural-WASP) and WASP interacting protein (WIP). In this study, we found that the expression of WIP was significantly upregulated in metastatic A5-RT3 cells compared to its parental non-tumorigenic HaCaT cells. Using A549 human lung adenocarcinoma cell line as the model system, we found that WIP regulates cell invasion , proliferation and anchorage-independent growth. Expression of WIP was enhanced during TGF-b1 induced epithelial-mesenchymal transition (EMT) and overexpression of WIP accelerated EMT while knocking down WIP attenuated EMT associated morphological changes. Knocking down WIP expression in A549 cells significantly reduced RhoA levels and WIP was found to interact with RhoA suggesting that WIP might be executing its function by regulating RhoA. Acquisition of invasive, proliferative properties and anoikis resistance is the central step in metastasis indicating a novel function of WIP in cancer progression.

The epithelial-mesenchymal transition (EMT) is a fundamental biological process that is involved in normal embryogenesis, would healing, and tissue repair, as well as numerous pathologies, including organ fibrosis, malignant transformation, and cancer progression. Both transcriptional and post-transcriptional regulatory mechanisms contribute to a complex and tightly controlled regulatory network during the EMT process, and a growing body of evidence now demonstrates that microRNAs (miRNAs) are crucial regulators of this network. miRNAs are a class of small non-coding RNAs that regulate gene expression through translational repression or mRNA degradation. A set of miRNAs have been discovered that have the potential to target multiple components of the signaling pathways and downstream effectors of the EMT. Our understanding of the roles that miRNAs play during the EMT process suggests that these miRNAs may eventually serve as novel biomarkers and therapeutic targets for various EMT-based pathological conditions. This review summarizes the current knowledge concerning how miRNAs mechanistically regulate the EMT and discusses the specific roles that miRNAs play in three EMT subtypes. We hope that a more comprehensive understanding of the functions of miRNAs in the EMT process will lead to the rapid development of novel diagnostic techniques and molecular-based strategies for controlling EMT.

Gradients of transmembrane potential coordinate cell-fate decisions and patterning during embryogenesis and wound-healing. Bioelectrical signaling may also be more important for adult pathologies than currently recognized. In this issue of Science Signaling, Lobikin et al. describe a role for bioelectric signals during the development of Xenopus leavis embryos to instruct an organism-level response reminiscent of neoplastic progression in melanoma.

Epithelial-mesenchymal transition (EMT) and dysregulated microRNAs (miRNAs) have important roles in driving chemoresistance. We previously reported that iASPP is a key EMT inducer and could increase cisplatin resistance in cervical cancer (CC) cells. Herein, we investigate the downstream mechanisms through which iASPP contributes to EMT and cisplatin resistance in CC. By using a lentiviral system, we investigated the effects of iASPP knockdown on CC cell growth and chemosensitivity of CC cells to cisplatin in vivo. We examined if miR-20a, which was up-regulated following iASPP overexpression, would influence metastatic phenotypes and cisplatin resistance in CC cells, and explored the possible molecular mechanisms involved. Knockdown of iASPP suppressed CC cell proliferation and sensitized CC cells to cisplatin in vivo. iASPP promotes miR-20a expression in a p53-dependent manner. Upregulation of miR-20a induced EMT and the recovery of CC cell invasion and cisplatin chemoresistance th...

This past month I told you about a partner I had. We couldn't seem to get out of each other's way. That wasn't his fault; we just didn't blend naturally. But what was indeed his fault were the g-forces he subjected me to on the way to the hospital on every run he drove. He accelerated too quickly, braked too hard, cornered too fast, and he never checked to see whether I was sitting or standing, starting an IV or reaching for equipment. As if his driving wasn't bad enough, the real roller coaster ride began when he would reach for his cell phone, or text or check messages. And I'm positive he has no idea he was doing anything wrong. Once upon a time, I worked for an EMS service in the northeast sector of this great country. One day while I was driving the ambulance to a call, my partner said, " I should install a string and pulley system in the cab to drop a grey wig on your head when you drive, grandma. " Well, I'm sorry to say I let him get to me. So I drove to the next call the way I used to drive my cab in New York City circa 1975. I'm not sure if I actually got it up on two wheels around one corner, but it was close. Of course when we got to the call it was a " no patient, " but it was the only time I received a

Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellula...

The Epithelial to Mesenchymal Transition (EMT) regulates cell plasticity during embryonic development and in disease. It is dynamically orchestrated by transcription factors (EMT-TFs), including Snail, Zeb, Twist and Prrx, all activated by TGF-β among other signals. Here we find that Snail1 and Prrx1, which respectively associate with gain or loss of stem-like properties and with bad or good prognosis in cancer patients, are expressed in complementary patterns during vertebrate development and in cancer. We show that this complementarity is established through a feedback loop in which Snail1 directly represses Prrx1, and Prrx1, through direct activation of the miR-15 family, attenuates the expression of Snail1. We also describe how this gene regulatory network can establish a hierarchical temporal expression of Snail1 and Prrx1 during EMT and validate its existence in vitro and in vivo, providing a mechanism to switch and select different EMT programs with important implications in ...

CDC42 interacting protein 4 (CIP4) is a CDC42 effector that coordinates membrane deformation and actin polymerization. The correlation of CIP4 overexpression with metastatic capacity has been characterized in several types of cancer. However, little information exists on how CIP4 function is regulated. CIP4 interacts with A-kinase (PKA) anchoring protein 350 (AKAP350) and CIP4 is also a PKA substrate. Here, we identified CIP4 T225 as the major CIP4 PKA phosphorylation site. In vitro and in vivo experiments using hepatocellular carcinoma (HCC) and breast cancer cells showed that expression of a CIP4(T225E) phosphomimetic mutant increased cancer cell metastatic capacity and that, conversely, expression of a CIP4(T225A) non-phosphorylatable mutant reduced invasive properties. PKA inhibition decreased to CIP4(T225A) cell-levels control but not CIP4(T225E) cell migratory and invasive efficiency. Concomitantly, our studies indicate that CIP4 T225 phosphorylation promotes the formation of functional invadopodia and enhances CIP4 localization at these structures. Our findings further provide mechanistic data indicating that CIP4 T225 phosphorylation facilitates CIP4 interaction with CDC42. Altogether this study identifies a signaling pathway that involves CIP4 phosphorylation by PKA during the acquisition of a metastatic phenotype in cancer cells.