Cílem této diplomové práce bylo nastudovat problematiku klasifikačních systémů v nemocnicích, které sledují především hospodářské požadavky hospitalizace. Následně bylo navrženo a naprogramováno webové rozhraní v prostředí Caché Server Pages (CSP), které poskytuje přístup k databázi CLINICOM. Pomocí webového rozhraní, je možno provádět klasifikaci pacientů do tříd MDC (Major Diagnostic Category), archivaci dat, výpočet DRG a další vybrané úkony. Webovou aplikaci by mohli využívat technicko-hospodářští pracovníci nemocnic a klinik jako jednoduchou pomůcku při své práci, respektive jako učební pomůcka biomedicínských oborů pří výuce zdravotnických informačních a klasifikačních systémů.

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Diplomová práce hodnotí historický proces implementace klasifikačního systému DRG v České republice a srovnává jej s vývojem analogických systémů v ostatních zemích světa. Na podkladě platné metodiky IR DRG užívané v ČR v roce 2006 analyzuje hospitalizační část lékařské péče poskytované ve Fakultní nemocnici v Motole. Zkoumá rozdíly v nákladovosti při srovnání rozdílných pacientských skupin (děti – dospělí, operovaní – léčení konzervativně) a ukazuje výhody užití DRG systému pro hodnocení kvality péče a nákladů z pohledu managementu nemocnice. V závěrečné části jsou popsány perspektivy využití klasifikačního systému DRG v prostředí českého zdravotního trhu.

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Reimbursement Decree and DRG mechanism and their influence on acute in-patient care Abstract The thesis focuses on Czech reimbursement mechanisms and their influence on volume of healthcare provided. The main Czech reimbursement legal documents are presented and formalized and their influence on volume of provided care tested. The thesis also offers a discussion of possible ineffectiveness which may be caused by the reimbursement decree for 2012. Keywords: healthcare, DRG, reimbursement mechanism

Ca2+-mediated regulation of gene expression plays an important role in neuronal plasticity. NFAT (Nuclear Factor of Activated T-cells) is a Ca2+/calcineurin (CaN)-dependent transcription factor that has been implicated in a number of neuronal functions including axon outgrowth, presynaptic remodeling and neural survival. NFAT is activated by Ca2+/CaN-dependent dephosphorylation, whereas re-phosphorylation by glycogen synthase kinase-3β (GSK3β) and several other protein kinases deactivates NFAT and triggers its export from the nucleus. In addition to electrically-mediated Ca2+ signals, neurotrophins can potently regulate NFAT function in neurons as well. However the mechanisms of NFAT activation by electrical activity and neurotrophins are not completely understood. In aim 1, I found that electrical stimulation produced a mitochondrial Ca2+ cycling-mediated prolonged [Ca2+]i elevation (plateau), which profoundly affected NFAT activity. The elimination of the [Ca2+]i plateau by blocking mitochondrial Ca2+ uptake or release strongly reduced nuclear import of NFAT. Furthermore, preventing Ca2+ mobilization from mitochondria diminished NFAT-mediated transcription. In aim 2, I found that NGF, a family of neurotrophins, potentiated NFAT-dependent transcription triggered by electrical activity through the TrkA-PI3K-Akt-GSK3β pathway and this effect was mediated primarily by NFATc3. Monitoring NFATc3 movement in DRG neurons in real time showed that NGF slowed the rate of NFATc3 nuclear export, which was mimicked by inhibiting GSK3β, whereas blockade of PI3K prevented this effect. Taken together, I proposed that mitochondrial Ca2+ cycling functions as a novel regulatory mechanism for NFAT activation and NFATc3 serves as an integrator of electrical activity and neurotrophin signaling in the regulation of gene expression in DRG neurons.

Financing healthcare is a problem not only in Germany but in many countries of Europe. Increasing total expenditure of health care resulted from many reasons, such as the aging population and the associated declining number of young people who contribute to the system. Another problem of financing health care, are ever increasing prices of medical devices, drugs, materials and energy. Since the beginning of the health system, Germany has been trying to stabilize the system through many reforms. The largest part of the revenues of the health system consists of contributions from members of statutory social insurance. Yet in Germany, financial participation in patients was implemented almost from the beginning of the health care system. Private costs are the second largest holder of health costs. Over the last 20 years, Germany has been among the countries that have a relatively balanced budget for financing health care. Among the most advanced countries in the world, which is seen in total expenditure of health care, had these expenses in recent years at around 11 percent of GDP.

Plasticity in dorsal root ganglion (DRG) neurons that promotes pain requires activity-dependent mRNA translation. Protein synthesis inhibitors block the ability of many pain-promoting molecules to enhance excitability in DRG neurons and attenuate behavioral signs of pain plasticity. In line with this, we have recently shown that phosphorylation of the 5' cap-binding protein, eIF4E, plays a pivotal role in plasticity of DRG nociceptors in models of hyperalgesic priming. However, mRNA targets of eIF4E phosphorylation have not been elucidated in the DRG. Brain-derived neurotrophic factor (BDNF) signaling from nociceptors in the DRG to spinal dorsal horn neurons is an important mediator of hyperalgesic priming. Regulatory mechanisms that promote pain plasticity via controlling BDNF expression that is involved in promoting pain plasticity have not been identified. We show that phosphorylation of eIF4E is paramount for Bdnf mRNA translation in the DRG. Bdnf mRNA translation is reduced in mice lacking eIF4E phosphorylation (eIF4E(S209A)) and pro-nociceptive factors fail to increase BDNF protein levels in the DRGs of these mice despite robust upregulation of Bdnf-201 mRNA levels. Importantly, bypassing the DRG by giving intrathecal injection of BDNF in eIF4E(S209A) mice creates a strong hyperalgesic priming response that is normally absent or reduced in these mice. We conclude that eIF4E phosphorylation-mediated translational control of BDNF expression is a key mechanism for nociceptor plasticity leading to hyperalgesic priming.

The thesis charts the rate of perioperative complications after removal of the uterus from non-malignant causes in two different medical facilities and compares them with the indicators in the DRG classification system to determine whether this is suitable for tool for the quality assesment of health care in health facilities.

Le système nerveux sensoriel somatique détecte et transmet les informations sensorielles périphériques par les neurones sensoriels dont le corps cellulaire est englobé dans les ganglions de la racine dorsale et les ganglions trijumeaux. Bien que cette hétérogénéité fonctionnelle a été mise en évidence, les mécanismes moléculaires qui la caractérisent sont moins connus. Dans l’optique de contribuer à la caractérisation moléculaire de la population neuronale du DRG, nous avons identifié un nouveau gène, stac2. Nous avons pu montrer que stac2 spécifie une sous population neuronale distincte dans le DRG. L’invalidation génétique de stac2 chez la souris n’a révélé aucun effet sur la survie ni sur la maturation neuronale. L’analyse comportementale des souris dépourvues de stac2 a montré un rôle important de stac2 dans la perception et la discrimination des températures fraîches ainsi que dans la sensibilisation périphérique au froid nocif. / The somatic sensory nervous system detects and transmits sensory information from peripheral by sensory neurons that have their cell body encompassed in the dorsal root and trigeminal ganglia. Although this functional heterogeneity has been demonstrated, the molecular mechanisms characterizing it are less known. In order to contribute to the molecular characterization of the neuronal population of DRG, we have identified a new gene, stac2. We have shown that stac2 specifies a distinct neuronal subpopulation in the DRG. The genetic invalidation of stac2 in mice showed no effect of stac2 on neuronal survival and maturation. The behavioral analysis of mice lacking stac2 showed an important role of this gene in the perception and discrimination of cold temperatures and in the peripheral sensitization to noxious cold.