Organizational Possibilities of Shaping Top Management of Enterprise

The paper deals with problems of the organizational shaping of the management of an industrial enterprise with a functional or divisional structure, Preceeding from an assumption that effective development of an enterprise is a supreme goal the author considers various ways and model organizational solutions of managing an enterprise. His analys is is supported by examples of organizational structural solutions applied in several large West German enterprises. The analysis ends with evaluation of the presented alternatives regarding the organizational shaping of an enterprise management

State and Trends of Strategie Planning Development

The article presents the main problems concerning strategic planning as a procedure aiming at systematic shaping of the enterprise’s future. The author remarks that the enterprise while drafting its strategic plans faces also such problems as lowering of its growth rate, stagnation and shrinking. Numerous exogeneous factors cause increasingly bigger difficultiss in planning, but simultaneously the demand for it continues to grow. It encompasses four main complexes: (1) general planning of goals; (2) strategic planning; (3) operational planning; and (4) planning of financial effects. In the general planning of goals, the main role is played by the goal of preserving the enterprise's capital assets and promoting its effective development. The article points simultaneously at ever-growing difficulties in achieving growth of the enterprise. A significant role in the strategic planning is played by: "portfolio" concept, analysis of weak and strong sides of the enterprise, early warning systems, and scenario method. Application of the strategic planning is connected with the central organizational task, which is proper adjustment of the organizational structure of the requirements of strategies of enterprise growth, shrinkage, and restructuralization. The article tackles also some personnel problems, which must be solved in conditions of the strategic planning in the enterprise.Zadanie pt. „Digitalizacja i udostępnienie w Cyfrowym Repozytorium Uniwersytetu Łódzkiego kolekcji czasopism naukowych wydawanych przez Uniwersytet Łódzki” nr 885/P-DUN/2014 dofinansowane zostało ze środków MNiSW w ramach działalności upowszechniającej naukę

Aufbau und Funktionsweise von betrieblichen Fruehwarnsystemen in der Industrie: Arbeitsbericht, Inst. fuer Unternehmungsplanung, Justus-Liebig-Univ. Giessen

Available from Bibliothek des Instituts fuer Weltwirtschaft, ZBW, Duesternbrook Weg 120, D-24105 Kiel C 142434 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

Human Cytomegalovirus Infection Alters PC3 Prostate Carcinoma Cell Adhesion to Endothelial Cells and Extracellular Matrix

The genome and antigens of human cytomegalovirus (HCMV) are frequently found in prostatic carcinoma. However, whether this infection is causative or is an epiphenomenon is not clear. We therefore investigated the ability of HCMV to promote metastatic processes, defined by tumor cell adhesion to the endothelium and extracellular matrix proteins. Experiments were based on the human prostate tumor cell line PC3, either infected with the HCMV strain Hi (HCMV(Hi)) or transfected with cDNA encoding the HCMV-specific immediate early protein IEA1 (UL123) or IEA2 (UL122). HCMV(Hi) upregulated PC3 adhesion to the endothelium and to the extracellular matrix proteins collagen, laminin, and fibronectin. The process was accompanied by enhancement of β(1)-integrin surface expression, elevated levels of integrin-linked kinase, and phosphorylation of focal adhesion kinase. IEA1 or IEA2 did not modulate PC3 adhesion or β(1)-integrin expression. Based on this in vitro model, we postulate a direct association between HCMV infection and prostate tumor transmigration, which is not dependent on IEA proteins. Integrin overexpression, combined with the modulation of integrin-dependent signalling, seems to be, at least in part, responsible for a more invasive PC3(Hi) tumor cell phenotype. Elevated levels of c-myc found in IEA1-transfected or IEA2-transfected PC3 cell populations might promote further carcinogenic processes through accelerated cell proliferation

Human cytomegalovirus infection alters PC3 prostate carcinoma cell adhesion to endothelial cells, extracellular matrix

The genome, antigens of human cytomegalovirus (HCMV) are frequently found in prostatic carcinoma. However, whether this infection is causative or is an epiphenomenon is not clear. We therefore investigated the ability of HCMV to promote metastatic processes, defined by tumor cell adhesion to the endothelium, extracellular matrix proteins. Experiments were based on the human prostate tumor cell line PC3, either infected with the HCMV strain Hi (HCMVHi) or transfected with cDNA encoding the HCMV-specific immediate early protein IEA1 (UL123) or IEA2 (UL122). HCMVHi upregulated PC3 adhesion to the endothelium, to the extracellular matrix proteins collagen, laminin, fibronectin. The process was accompanied by enhancement of β1-integrin surface expression, elevated levels of integrin-linked kinase, phosphorylation of focal adhesion kinase. IEA1 or IEA2 did not modulate PC3 adhesion or β1-integrin expression. Based on this in vitro model, we postulate a direct association between HCMV infection, prostate tumor transmigration, which is not dependent on IEA proteins. Integrin overexpression, combined with the modulation of integrin-dependent signalling, seems to be, at least in part, responsible for a more invasive PC3Hi tumor cell phenotype. Elevated levels of c-myc found in IEA1-transfected or IEA2-transfected PC3 cell populations might promote further carcinogenic processes through accelerated cell proliferation

CXCR4 Chemokine Receptor Mediates Prostate Tumor Cell Adhesion through α(5) and β(3) Integrins

The mechanisms leading to prostate cancer metastasis are not understood completely. Although there is evidence that the CXC chemokine receptor (CXCR) 4 and its ligand CXCL12 may regulate tumor dissemination, their role in prostate cancer is controversial. We examined CXCR4 expression and functionality, and explored CXCL12-triggered adhesion of prostate tumor cells to human endothelium or to extracellular matrix proteins laminin, collagen, and fibronectin. Although little CXCR4 was expressed on LNCaP and DU-145 prostate tumor cells, CXCR4 was still active, enabling the cells to migrate toward a CXCL12 gradient. CXCL12 induced elevated adhesion to the endothelial cell monolayer and to immobilized fibronectin, laminin, and collagen. Anti-CXCR4 antibodies or CXCR4 knock out significantly impaired CXCL12-triggered tumor cell binding. The effects observed did not depend on CXCR4 surface expression level. Rather, CXCR4-mediated adhesion was established by α(5) and β(3) integrin subunits and took place in the presence of reduced p38 and p38 phosphorylation. These data show that chemoattractive mechanisms are involved in adhesion processes of prostate cancer cells, and that binding of CXCL12 to its receptor leads to enhanced expression of α(5) and β(3) integrins. The findings provide a link between chemokine receptor expression and integrin-triggered tumor dissemination

CXCR4 chemokine receptor mediates prostate tumor cell adhesion through alpha5 and beta3 integrins

The mechanisms leading to prostate cancer metastasis are not understood completely. Although there is evidence that the CXC chemokine receptor (CXCR) 4 and its ligand CXCL12 may regulate tumor dissemination, their role in prostate cancer is controversial. We examined CXCR4 expression and functionality, and explored CXCL12-triggered adhesion of prostate tumor cells to human endothelium or to extracellular matrix proteins laminin, collagen, and fibronectin. Although little CXCR4 was expressed on LNCaP and DU-145 prostate tumor cells, CXCR4 was still active, enabling the cells to migrate toward a CXCL12 gradient. CXCL12 induced elevated adhesion to the endothelial cell monolayer and to immobilized fibronectin, laminin, and collagen. Anti-CXCR4 antibodies or CXCR4 knock out significantly impaired CXCL12-triggered tumor cell binding. The effects observed did not depend on CXCR4 surface expression level. Rather, CXCR4-mediated adhesion was established by alpha5 and beta3 integrin subunits and took place in the presence of reduced p38 and p38 phosphorylation. These data show that chemoattractive mechanisms are involved in adhesion processes of prostate cancer cells, and that binding of CXCL12 to its receptor leads to enhanced expression of alpha5 and beta3 integrins. The findings provide a link between chemokine receptor expression and integrin-triggered tumor dissemination