334 research outputs found
Functions and of personnel management and its realization in a company "Varner Baltija" LLC
No full textDarba tēma ir Personāla vadības funkcijas un to realizācija uzņēmumā SIA „Varner Baltija”.
Darba mērķis ir izpētīt, analizēt un novērtēt personāla vadīšanas būtību, funkcijas un to realizāciju SIA „Varner Baltija” „Dressmann” veikalu attīstībā un sniegt priekšlikumus personāla vadīšanas funkciju uzlabošanai un uzņēmuma attīstībai.
Darba mērķa sasniegšanai tika izvirzīti uzdevumi – izpētīt teorētiski personāla vadīšanas būtību, funkcijas un noskaidrot praktiski personāla vadīšanas efektivitāti uzņēmuma attīstībā, ar anketēšanas un intervēšanas palīdzību noskaidrot personāla un vadītāju viedokli.
Darba apjoms ir 53 lapaspuses, tajā ir 14 attēli, 3 tabulas un 4 pielikumi
Atslēgvārdi: personāla vadība, personālvadība, “Varner Baltija”.Bachelor thesis.
Functions and of personnel management and its realization in a company „Varner Baltija” LLC
The goal of this scientific work is to analyze and evaluate the essence, functions and its realization of personnel management in a company “Varner Baltija” LLC “Dressmann” shops’ development and to give proposals to improve functions of personnel management in this company.
To reach this goal, author has set following tasks – explore theoretical nature of personnel management, find out the effectiveness personnel management in company development, find out personnel’s and managers’ opinions using survey and interview
The thesis is written in Latvian language. This thesis consists of 53 pages, and it includes 14 pictures, 3 tables and 4 appendices.
Keywords: personnel management, human recourse management, “Varner Baltija”
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Do Tumor Cells or the Tumor Microenvironment Determine the Phenotype of Tumor-Associated Macrophages?
No full textTumor-associated macrophages (TAMs) create an immunosuppressive tumor microenvironment (TME) that will promote tumor progression. The goal of this project is to understand whether the pattern of TAMs in a tumor is determined by the tumor cells or by the host tissue environment. Knowing how the phenotype of TAMs is determined will help us better target TAMs to improve cancer patient’s outcome. Moreover, another goal of this project is to understand whether the TAMs that develop in a primary tumor have the same phenotype as those that develop in subsequent metastases. Comparing gene expression profiles between TAMs in different tissues can provide future directions to improve cancer therapies so that we can better target TAMs in order to effectively eradicate primary and metastatic tumors. Using flow cytometry to examine like tumors growing in different tissues, we found that subcutaneous, orthotopic, and intravenous LLC tumor models all have similar TAM profiles that are distinct from genetically engineered CC10Cre KrasG12D p53-/- spontaneous lung tumor models. In addition, using single-cell sequencing to investigate the PyMT primary mammary gland tumors and metastatic lung tumor the and CC10Cre KrasG12D p53-/- spontaneous lung tumors, we can conclude that the TAM profile of the primary tumor and subsequent metastasized tumor have similar TAM profiles. As a result, we can conclude that the TAM profile is dependent on the tumor cells themselves instead of the microenvironment
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An Analysis of Novel Macrophage Targeted Therapeutics That Impact Macropinocytosis and Mitochondrial Permeability
No full textMacrophages are innate immune cells that play key roles in infection, immunity and cancer. Understanding the mechanisms that control macrophage contributions to cancer can help to develop strategies to improve cancer therapy. Oncogenic mutations allow cancer cells to take up nutrients through a process called macropinocytosis or “cell-drinking”, which promotes cancer cell survival and proliferation. The role of macropinocytosis has been studied in various cancers but has been less well explored in macrophages. Macropinocytosis in macrophages may help these cells to survive in the harsh tumor microenvironment. Thus, one of the goals of this project is to investigate macrophage macropinocytosis by studying the uptake of Tetramethyl rhodamine (TMR-dextran) in macrophages. My hypothesis is that PI3Kgamma plays a role in promoting macropinocytosis in macrophages. Through macropinocytosis assays using TMR-dextran, we found that PI3Kgamma inhibition successfully suppressed macropinocytosis in iWT macrophages. To further study macrophages, we tested the effect of 3G8, a small molecular drug that inhibits FLT3, CKIT and CSF1R, on mitochondrial function. We had found that 3G8 can also stimulates release of mitochondrial ROS. My hypothesis is that 3G8 activates the mitochondrial permeability transition pore (thereby releasing ROS and impacting cell signaling). Through mitochondrial permeability transition pore activity (mPTP) assays, we observed that 3G8 induced opening of the mPTP in macrophages and tumor cells. Understanding the mechanisms by which these inhibitors function in macrophages could help with the development of anti-cancer therapeutics and thus reduce the effects of cancer
Abstract 3966: Targeting integrin αvβ3-expressing cancer stem cells to manipulate tumor-associated macrophages
No full textAbstract
Tumor associated macrophages are involved in regulation of cancer growth and aggressiveness. Whereas M1 macrophages trigger an inflammatory response and inhibit tumor growth, M2 macrophages secrete pro-tumor cytokines into the microenvironment to support tumor progression. A macrophage switch from M1 to M2 has been associated with lung cancer progression, and cancer stem cells have been implicated as a driver of this reprogramming.
We recently reported that integrin αvβ3 expression is induced on lung adenocarcinoma cells during drug resistance and is both necessary and sufficient to reprogram these tumors to a stem-like state. Given the role that cancer stem cells play in switching M1 to M2 macrophages, we asked whether αvβ3 expression on lung adenocarcinoma cells account for this macrophage conversion. The M1/M2 macrophage ratio in αvβ3-positive tumors was markedly decreased relative to tumors lacking αvβ3. We next treated mice bearing αvβ3-positive tumors with a monoclonal antibody (LM609) targeting this receptor to assess its ability to alter the macrophage phenotype within these tumors. LM609 was able to selectively eliminate the αvβ3-positive cancer stem cells via antibody-dependent cell-mediated cytotoxicity (ADCC), and this not only increased the M1 macrophage population, but also markedly enhanced the sensitivity of these tumors to the effects of therapy.
These findings reveal that αvβ3-expressing cancer stem cells favor the pro-tumor M2 macrophage phenotype. Eliminating αvβ3-positive cancer stem cells via ADCC serves to both increase pro-inflammatory macrophages within the tumor microenvironment and prolong tumor sensitivity to therapy.
Citation Format: Hiromi I. Wettersten, Toshiyuki Minami, Megan M. Kaneda, Laetitia Seguin, Judith A. Varner, Sara M. Weis, David A. Cheresh. Targeting integrin αvβ3-expressing cancer stem cells to manipulate tumor-associated macrophages [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3966. doi:10.1158/1538-7445.AM2017-3966</jats:p
Abstract B03: Integrin agonists reduce infiltration of tumor-associated macrophages to promote T-cell mediated anti-tumor immunity
No full textAbstract
Tumors associated macrophages (TAMs) mediate neovascularization and promote tumor growth. Integrin CD11b/CD18 is highly expressed on cells of myeloid and granulocytic lineage and mediates their adhesion, migration and tissue recruitment functions. CD11b+ TAMs are present at high numbers in several types of human cancers, including breast and non-small cell lung cancer, and are associated with reduced T-cell mediated anti-tumor immunity. This suggests that reducing infiltration of CD11b+ TAMs could have a therapeutic benefit. Recently, we have developed a novel small molecule CD11b agonist termed leukadherin-1 (LA1) that binds to and allosterically activates integrin CD11b on leukocytes. We also reported that CD11b activation is a more effective strategy for reducing CD11b+ cell tissue infiltration, as compared to integrin antagonists. LA1 binding transiently increases leukocyte adhesion to the vascular endothelium and reduces their transmigration in vivo. Here, we show that LA1 mediated CD11b activation reduced the number of CD11b+ TAMs in two different murine tumor models that was accompanied with diminished primary tumor growth. LA1 treated animals also had significantly reduced tumor angiogenesis and prolonged survival. These improved aspects were accompanied with reduction in vessel density as indicated by reduced intratumoral expression levels of CD31 and αSMA and increased numbers of CD8+ T cells indicating an anti-tumor immune profile response fostering tumor suppression. Our data provide a rationale for using allosteric CD11b agonists to target TAMs as a novel therapeutic approach for treating cancer.
Citation Format: Samia Q. Khan, Mohd. H. Faridi, Shehryar J. Khaliqdina, Antonio J. Barbosa, Judith A. Varner, Vineet Gupta. Integrin agonists reduce infiltration of tumor-associated macrophages to promote T-cell mediated anti-tumor immunity. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Immunology and Immunotherapy; 2016 Oct 20-23; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2017;5(3 Suppl):Abstract nr B03.</jats:p
Cell adhesion in sponges: Potentiation by a cell surface 68 kDa proteoglycan-binding protein
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