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In a world in which state-of-the-art technologies become obsolete in a matter of months and the most efficient systems may be easily used by competitors, there is just one area where a company can hope to establish and maintain a competitive edge: it is its people, who are the bearers of the intellectual capital. As a matter of fact the degree of any sector s competitive edge hangs on managements ability to manage company's intellectual capital, which in practice translates into an ability to manage people who are equipped with knowledge. The paper aims to show that management of knowledge will in the future play a crucial role in corporate activities, as it already does today, since knowledge is fast becoming a key resource in any company. The application of the latest methods, techniques and instruments to manage knowledge in a 21 century organization allows it to adapt to the fast changing environment and gain a competitive advantage. However, IT systems are merely a tool supporting knowledge. The key to efficiently and successfully managing knowledge lies not so much in corporate restructuring as in reprogramming the basic mental processes in executives and workers alike, which boils down to no less than a turnabout on corporate organizational structure.
EN
Tuberous sclerosis complex (TSC) is characterized by cortical developmental malformations that are associated with epilepsy and appearance of benign brain tumors – subependymal giant cell astrocytomas (SEGAs) which are composed of distinct cell types, including giant cells and dysplastic neurons. TSC results from mutations in TSC1 and TSC2, which lead to the mTOR pathway activation, and p70S6 kinase and ribosomal S6 protein phosphorylation. ERK pathway is also aberrantly activated in SEGAs. Clinical trials with the mTOR inhibitor – rapamycin have demonstrated reduction in size of SEGAs, but the molecular mechanisms are unknown. In the present study, we evaluated the effects of rapamycin and the ERK pathway inhibitor – UO126 on cell size, proliferation and viability of cell cultures derived from SEGA. Rapamycin or UO126 alone did not affect viability and proliferation of SEGA cells. However, treatment with both drugs reduced proliferation of SEGA cells. Staining of F-actin revealed decrease of cell size in SEGA cultures exposed to rapamycin alone or in combination with UO126, but treatment with UO126 alone did not infl uence cell size nor morphology. Our studies demonstrate that simultaneous inhibition of both mTOR and ERK signaling pathways reduces proliferation of SEGA cells. Moreover, inhibition of mTOR signaling with rapamycin diminishes a volume of giant SEGA cells. It implicates that inhibitors of mTOR and ERK pathways should be considered for clinical trials of SEGAs.
EN
BACKGROUND AND AIMS: Hypothesis that multiple sclerosis (MS) may be caused by chronic cerebrospinal venous insufficiency (CCVI) has gained public interest from both patients and physicians. However, there’s still lack of evidence for it. We have investigated presence of neuronal demyelination and degeneration, similar to these found in MS, in rat model of CCVI created by occlusion of jugular veins (JVs). METHODS: Twenty-five young female Wistar C rats were used. Complete ligation of both JVs (BO group), left JV (UO), or partial ligation (stenosis resulting in ~70% reduction of blood flow) of both JVs were performed. Blood flow in JVs was measured with Laser Doppler Flow Assessment. Neurological assessment using Neurologic Deficit Scale (NDS), 5-point EAE staging protocol, and gait analysis with CatWalk was performed. After 12 weeks, MRI for detecting demyelinating plaques as well as signs of bloodbrain barrier (BBB) disruption was performed. Histologic analysis of brain specimens was focused on markers of inflammation and demyelination. RESULTS: No neurologic deficits were found in all experimental animals. Both NDS, EAE and gait analysis did not differ from normal. MRI T2- and T1- weighted imaging as well as FLAIR sequence did not reveal any abnormalities in the brains of experimental rats. Histological analysis did not show any signs of inflammation or demyelination. CONCLUSIONS: Twelve-week CCVI in rats, both complete and partial, did not induce any changes resembling pathologies observed in MS. Therefore, linking CCVI with origin of MS remains controversial.
EN
Introduction: Neurological disorders are the most common cause of serious disability and have a major impact on financial healthrelated burden to society. Most of them are definitely associated with cell death: sudden or chronic. Conventional treatment methods yield disappointing results. Thus the discoveries in stem cell biology have fueled the interest in cell-based therapeutical approach. Based on experimental data cord blood has been proposed as a novel, autologous cell source for pediatric population. Non-invasive monitoring of cell fate following transplantation has been recently recommended as a basis for rational stem cell therapy. Subject: One year old child experienced devastating, cardiac arrest-induced cerebral ischemia. Despite a broad rehabilitation program diagnose of vegetative state has been established three months later. After next three months of continued rehabilitation no noticeable improvement has also been found and the child has been included into study. The protocol has been approved by the ethical commission of The Children’s Memorial Health Institute in Warsaw, Poland. Then the child’s own cord blood cells have been neurally-converted over 10 days in culture within GMP facility. Prior to transplantation cells were labeled with iron oxide (SPIO) for MR imaging. For scaling sensitivity of MR signal different concentrations of SPIO-labeled cells were scanned in the phantom. Then patient received monthly 3 subsequent cell infusions (1.2 x 107 cells each) to lateral ventricles. The follow up continued up to 6 months and included both clinical assessment and MR examinations. Results: High efficiency of neural cell conversion and SPIO labeling as well as no cytotoxicity were observed. The employed method of cell transplantation was found to be efficient to deliver cells to CNS as confirmed by MR imaging. Gradual decrease of SPIO signal intensity was observed over the period of follow up. No adverse events or abnormal reaction to cell implantation was detected. The follow up revealed mild functional improvement - decreased nystagmus, spasticity and the number of epileptic seizures. Moreover, the features of the child contact with parents has appeared, thus vegetative state can not be diagnosed any more. Conclusions: This report indicates that transplantation of autologous, neurally-committed cord blood-derived cells to the ventricular system of child is safe, feasible and able to result with mild functional improvement. Additionally cell-related MRI signal can be monitored for more than 4 months in transplanted brain hemisphere. Supported by MSHE grants no 0141/B/P01/2008/35 and 0142/B/ P01/2008/35.
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