Risk Management of a Business Entity

Tato diplomová práce se zabývá řízením rizik společnosti Motortec s.r.o, podnikající v oblasti prodeje a servisu osobních a užitkových vozidel. Práce je rozdělena na část teoretickou, ve které jsou uvedeny všechny důležité pojmy, vztahující se k práci a část analytickou, ve které je aplikován proces řízení rizik. Proces obsahuje identifikaci, analýzu a následné ošetření zjištěných rizik. Identifikace rizik proběhla pomocí Porterovy analýzy pěti konkurenčních sil, SLEPT analýzy a 7S analýzy. Dále byla zpracována SWOT analýza. Definovaná rizika byla ohodnocena skórovací metodou a rozčleněna podle jejich závažnosti. V poslední části jsou navrhnuta opatření ke snížení hlavních rizik, ohrožujících sledovanou společnost.The thesis deals with the risk management in Motortec s.r.o., a company that operates in the field of sales and maintenance service of passenger and commercial vehicles. The thesis is divided into the theoretical part, in which all the essential terms are defined that relate to the thesis itself, and an analytical part that employs the process of risk management. The process includes identification, analysis and subsequent remedies to risks identified. The identification of risks has been carried out using Porter's five forces analysis, SLEPT analysis and McKinsey 7S Framework. SWOT analysis has been carried out subsequently. The risks defined have been assessed using a scoring method and grouped into categories based on their severity. The last part includes measures to reduce the major risks that threaten the examined company.

The metastasis promoting protein S100A4 is increased in idiopathic inflammatory myopathies

Objectives. The S100A4 protein is known as a metastasis promoting factor; however, its involvement in non-malignant diseases such as RA and psoriasis has been recently described. The aim of this study was to investigate the expression and possible role of S100A4 in idiopathic inflammatory myopathies. Methods. S100A4 protein expression was detected by immunohistochemistry in muscle tissue from control individuals (n = 11) and patients with PM and DM (n = 8/6). IF staining was used to co-localize S100A4 with selected cells. Cytokine expression and protein synthesis in S100A4-treated cells were analysed by RT-PCR and ELISA. Results. S100A4 protein was significantly up-regulated in muscle tissue of patients with inflammatory myopathies compared with control individuals and was associated particularly with the presence of mononuclear infiltrates. Only few regenerating muscle fibres in PM/DM expressed S100A4. Then we analysed the effect of S100A4 on human myocytes and peripheral blood mononuclear cells (PBMCs). Although S100A4 did not affect myocytes, stimulation of PBMCs with S100A4 significantly induced the expression and synthesis of TNF-α, IL-1β and IL-6, but not of IFN-α. We showed that S100A4 is not directly involved in perforin/granzyme B-induced apoptosis and that it does not modulate the expression of Bax and Bcl2 mRNA in myocytes and PBMCs. Conclusion. Increased expression of S100A4 in inflamed muscle tissue highlights its potential role in the pathogenesis of inflammatory myopathies. S100A4 may act as a cytokine-like factor indirectly promoting muscle fibre damage by stimulating mononuclear cells to increase the synthesis of pro-inflammatory cytokine

Hemodynamics in Ruptured Intracranial Aneurysms

Incidental detection of unruptured intracranial aneurysms (UIA) has increased in the recent years. There is a need in the clinical community to identify those that are prone to rupture and would require preventive treatment. Hemodynamics in cerebral blood vessels plays a key role in the lifetime cycle of intracranial aneurysms (IA). Understanding their initiation, growth, and rupture or stabilization may identify those hemodynamic features that lead to aneurysm instability and rupture. Modeling hemodynamics using computational fluid dynamics (CFD) could aid in understanding the processes in the development of IA. The neurosurgical approach during operation of IA allows direct visualization of the aneurysm sac and its sampling in many cases. Detailed analysis of the quality of the aneurysm wall under the microscope, together with histological assessment of the aneurysm wall and CFD modeling, can help in building complex knowledge on the relationship between the biology of the wall and hemodynamics. Detailed CFD analysis of the rupture point can further strengthen the association between hemodynamics and rupture. In this chapter we summarize current knowledge on CFD and intracranial aneurysms

Posouzení finanční situace podniku

Abstract Zámečník, J. Evaluation of the financial situation in a business company. Bachelor thesis. Brno, 2014. Aim of this bachelor thesis is to evaluate the financial situation and management of the company called AMB Finance s.r.o between the years 2008-2012. Methods of financial analysis were used to meet the objective. The input data are the financial statements balance sheets and the profit and loss statement. The thesis is divided into two parts. The literature retrieval and practical part. In the literature retrieval section the calculation methods used, substance and the application of the financial analysis are described. In the practical part theoretical knowledge is applied on the chosen company and its financial situation is evaluated using horizontal, vertical analysis, differential analysis, ratio indicators analysis and bankruptcy prediction models. The paper concludes with the overall evaluation of the financial situation of the company and proposed recommendations that would lead to the improvement in the financial situation of the company

Activism and the perception of the lives of LGBT individuals in the Czech Republic in the perspective of two generations of LGBT men

Katedra sociologieDepartment of SociologyFaculty of Social SciencesFakulta sociálních vě

Toxic myopathies

Poškození kosterního svalu toxickou látkou je podkladem rozvoje toxické myopatie. Ve velké většině se jedná o toxické působení léků, méně již návykových látek, biologických či chemických toxinů. Toxická látka může poškodit kontraktilní elementy (aktin, myosin) či jiné bílkoviny svau, jednotlivé organely (např. mikrotubuly), poškodí metabolizmus svalové buňky (např. mitochondrie), membránu svalu s iontovými kanály. Jednotlivé patofyziologické mechanizmy vedou k různým patologickým i klinickým obrazům toxické myopatie. Stále přibývá léků s myotoxickým působením a rovněž přibývají nemocní s různě výraznou myopatií lékově podmíněnou. Nejčastější poškození svalu léky je při použií statinů. K nebolestivé myopatii vede léčba chlorochinem. Terapie zidovudinem (léčba HIV) může vés k proximální svalové slabosti s bolestmi a poruchou mitochondrií. Dlouhodobá léčba kortikosteroidy je příčinou nebolestivého oslabení proximálních svalů s výraznou atrofií vláken typu II. Myopatie kriticky nemocných je charakterizována svalovou slabostí, rozvojem atrofií, charakteristickým EMG nálezem. Ve svalové biopsii je nápadné chybění silných vláken (myozinu). Včasné rozpoznání myopatie a identifikace toxického léku je základem léčby i prevence toxických myopatií.Damage of skeletal muscle by a toxic substance can lead to toxic myopathy. In most cases there is a toxic effect of medicaments, in a lesse extent effects of abuse substances, biological or chemical toxins. A toxic substance can damage contractile elements (actin, myosin) or some other muscle proteins, individual organells (e.g. microtubulls), can disturb muscle cell metabolism (e.g. mitochondrias), muscle membrane with ionic channels. Individual patophysiological mechanisms lead to various pathological or clinical pictures of toxic myopathies. There is an increasing number of medicaments with myotoxic effects and there are more patients with variably marked myopathy with pharmacological cause. The most common pharmacologically induced toxic myopathy is attributed by statins. The painless myopathy is associated with therapeutic use of chlorochin. Therapy with zidovudine (used in HIV therapy) may be associated with proximal muscle weakness, with muscle pain and mitochondrial damage. Long-lasting steroid therapy may cause painless weakness of proximal muscles with prominent typ II fibre atrophy. Critically ill myopathy is characterized by muscle weakness, development of muscle atrophy, characteristic EMG findings. In muscle biopsy is a prominent loss of thick fibers (myosine). Early disclosure of myopathy and identification of the toxic medicament is a basis of therapy and prevention of toxic myopathies