Introdução: A lesão axonal traumática (LAT) ou lesão axonal difusa (LAD) esta presente em grande parte dos traumatismos crânio-encefálicos (TCE), sendo importante causa de mortalidade e morbidade das suas vítimas. A LAT dispara uma sequência de mudanças neurodegenerativas encefálicas que são, paradoxalmente, acompanhadas por recuperação cognitiva. Objetivo: Avaliar quantitativamente a LAT, através da razão de transferência de magnetização (RTM) e de medidas volumétricas para caracterizar a evolução temporoespacial das mudanças macroscópicas e microscópicas e investigar possível correlação entre elas, auxiliando no entendimento da sua fisiopatologia. Este estudo ainda investigou correlação entre atrofia e dano axonal/mielínico e a evolução funcional. Métodos: Imagens 3D-T1, 3DGE (PRESTO) e de transferência de magnetização (ITM) foram obtidas de 26 pacientes vítimas de TCE moderado e grave e de 26 controles, de idade e sexo semelhantes. Os pacientes foram submetidos a RM com 2 (fase aguda tardia/subaguda), 6 (crônica precoce) e 12 (crônica tardia) meses do TCE. A RM foi realizada nos controles em apenas uma única ocasião. Através de métodos automatizados, calculou-se o volume da substancia cinzenta (SC), da substancia branca (SB) e do encéfalo total (ET), ajustando-os pelo volume intracraniano. A partir de histogramas da RTM obtidos das mesmas regiões, calculou-se a média e os percentis 25, 50 e 75% da RTM. As imagens PRESTO foram usadas na exclusão dos focos hemorrágicos da análise da RTM, nos pacientes. A evolução funcional foi medida pela escala prognostica de Glasgow (EPG), realizada um ano após o TCE. Resultados: A RTM media e o volume foram significativamente diferentes nos pacientes e nos controles. Os pacientes apresentaram RTM media maior (p < 0,05) e volume menor na SC e ET, desde o primeiro exame (fase aguda tardia/subaguda precoce). Na SB, valores menores tanto da RTM media (p=0,02) quanto do volume (p=0,009) foram observados nos pacientes apenas no terceiro exame (fase crônica tardia). Redução progressiva da RTM media dos pacientes foi observada em todos os compartimentos, estimada em 1,14% na SC, 1,38% na SB e 1,40% no ET durante todo o estudo. Houve também redução volumétrica gradual da SB e do ET, com taxa de atrofia total de 3,20% e 1,50%, respectivamente. Não houve relação entre redução da RTM media e atrofia. Nenhum dos parâmetros mostrou valor prognostico nas fases subaguda ou crônica precoce. Conclusões: A LAT resulta numa rarefação axonal/mielínica e redução volumétrica progressiva do tecido encefálico, que se perpetua por até um ano do trauma. As mudanças são mais expressivas e prolongada na SB. A redução do volume e da RTM media se mostraram independentes na LAT. Isso sugere que os dois parâmetros reflitam aspectos complementares da fisiopatologia da LAT, em níveis micro e macroestrutural / Introduction: Traumatic axonal injury (TAI) or diffuse axonal injury (DAI) is a frequent component of traumatic brain injury (TBI) and a major cause of mortality and morbidity in this population. It triggers a sequence of degenerative changes in the brain, that are paradoxically accompanied by cognitive recovery. Purposes: The present study used magnetization transfer ratio (MTR) and volumetric data to appreciate the spatiotemporal evolution of macroscopic and microscopic changes and investigate possible correlation between them, enhancing the knowledge about its pathophysiology. It also investigated correlation between atrophy and axonal/myelin damage and functional outcome. Methods: Volumetric T1-weighted, 3DGE (PRESTO) and magnetization transfer images (MTI) were obtained from 26 patients who experienced moderate to severe TBI and 26 age- and sex-matched controls. Patients were scanned at 2 (late acute/subacute stage), 6 (early chronic) and 12 months (late chronic) postinjury and controls, only once. Whole brain (WB), gray matter (GM) and white matter (WM) volumes were measured using automated technique and adjusted for intracranial volume. Histogram analysis was performed in the same regions, with calculation of the mean MTR and its 25, 50 and 75% percentiles. The PRESTO images were used to exclude the small lesions from the MTR analysis in the patients. Functional outcome was assessed 12 months after injury using the Glasgow Outcome Scale (GOS). Results: Mean MTR and volume were significantly different between patients and controls. Patients presented higher mean MTR values (p < 0,05) and smaller volume (p < 0,05) in the GM and WB, as of the first exam (late acute/subacute stage). In the WM, reduction of both, the mean MTR (p=.02) and volume (p=.009), was observed only in their third exam (late chronic stage). Progressive decrease of patients\' mean MTR was observed in all compartments, with rates of 1.14% for the GM, 1.38% for the WM and 1.40% for the WB across the study. Continuing reduction of the WM and WB volume was also observed, with total atrophy rate of 3.20% and 1.50%, respectively. No correlation between mean MT and the volumetric changes was found. None of the parameters showed prognostic value during the subacute and early chronic stages. Conclusions: TAI results in a progressive axonal/myelinic rarefaction and volumetric brain reduction that continues until a year postinjury. The changes are greater and lasts longer in the WM. The reduction in the volume and mean MTR were independent between them in TAI. This suggests that the two parameters reflect complementary aspects of the TAI pathologic lesion at macro and microstructural levels

Trauma de crânio leve (TCE leve) é definido como um déficit neurológico transitório que ocorre após um trauma incluindo história de náuseas, vômitos, cefaléia ou tontura acompanhada de alteração ou perda da consciência com duração inferior a 15 minutos, amnésia pós traumática e Escala de Coma de Glasgow entre 13 e 15. Apesar da alta taxa de sobrevida, pode cursar com alguma morbidade, principalmente nos três primeiros meses posteriores ao trauma e cerca de 18 % dos pacientes desenvolvem pelo menos uma síndrome psiquiátrica no primeiro ano após o acidente. O diagnóstico ainda é um desafio no sentido de minimizar-se gastos desnecessários com exames subsidiários entretanto, intervenções precoces podem evitar seqüelas. Nosso objetivo foi verificar o impacto do TCE leve na qualidade de vida de suas vítimas e diagnosticar as várias alterações neuropsicológicas que podem advir deste trauma. Esses alterações podem ser verificadas através de instrumentos de pesquisa. Inicialmente, foram avaliadas cinqüenta vítimas com TCE leve, atendidas no Hospital João XXIII, em Belo Horizonte - MG, as quais foram submetidas a dosagem de proteína S100B e tomografia de crânio (TCC) na admissão. Nessa fase, verificou-se que a proteína S100B tem valor preditivo negativo de 100%. Dezoito meses após o trauma, esses pacientes foram procurados em suas residências, quando foi lhes solicitado para que respondessem a quatro instrumentos de pesquisa [dois para diagnóstico de qualidade de vida (World Health Organization WHOQOL-100), e o Short Form-36 (SF-36), um para análise da presença de ansiedade e depressão (Escala Hospitalar de Ansiedade e Depressão (EHAD) e o Questionário de Sinais e Sintomas (QSS), baseado no Post Concussion Questionnaire] com o objetivo de pesquisar a presença de sinais e sintomas da síndrome pós-concussão. Também foram pesquisados aspectos sociodemográficos, como idade, escolaridade, estado civil, renda pessoal e origem desta renda. Os mesmos questionários foram preenchidos por um grupo de controle composto, necessariamente, por coabitantes dos pacientes, sem história de trauma craniano de qualquer gravidade e com idade a mais próxima possível da do paciente. Na avaliação pelo WHOQOL-100, pacientes apresentaram qualidade de vida inferior nos domínios nível de independência, ambiente e no total de domínios (p< 0,05). Na avaliação do SF-36, pacientes revelaram qualidade de vida inferior nos domínios capacidade funcional, vitalidade, saúde mental (p<0,001), dor, estado geral de saúde e aspectos mentais (p<0,05). Pacientes apresentaram mais ansiedade e estavam uma classe acima de seus controles pela EHAD. Pacientes referem ainda número maior de sinais e sintomas da síndrome pós-concussão do que seus respectivos controles. Não verificamos correlação entre a qualidade de vida, classificação na EHAD ou número de sinais e sintomas da SPC com as dosagens de proteína S100B ou com a presença de lesão na TCC realizadas na admissão / Mild head trauma (MHT) is defined as a transitory neurological deficit that happens after the trauma and includes a history of nausea, vomiting, headache or dizziness and loss or alteration of consciousness (less than 15 minutes), post-trauma amnesia, and Glasgow Coma Scale (GCS) at admission between 13 and 15. Despite the high survival rates, some morbidity has been observed in the three month period after this trauma. Approximately 18% of head trauma patients develop at least one psychiatric syndrome in the first year after the accident. The diagnostics difficulty and the risks of complications after the MHT continue to be a relevant problem at the emergency departments around the world. Limitations of active participation in daily life are alterations that influence life quality. Several of these alterations may be diagnosed through Interview Instruments. Our study was divided in two phases. In the first phase, 50 MHT patients admitted at Hospital João XXIII, Belo Horizonte-MG, Brazil, had protein S100B dosing and head CT taken at admission. Concentration values of S100B lower than 0.01 g/l were considered negative once this was the lowest value found in patients who did not show brain injuty signs in the CT scan. In that study it was found that protein S100B has 100% negative predictive value. In this second phase of the study, 18 months after the trauma, these patients were contacted at their homes and asked to answer four self- assessment questionnaires: two for quality of life diagnostic - World Health Organizations WHOQOL-100 and the Short Form-36 (SF36); one for the analysis of anxiety and depression - Hospital anxiety and depression scale-HADS; and one instrument developed by the author based on the Rivermead Post Concussion Questionnaire to evaluate the presence of post-concussion syndrome signs and symptoms. Several socio-demographic aspects were also analyzed, including income, source of income, means of transportation used, etc. The same questionnaires were filled by a control group formed necessarily by patients co-inhabitants, with no history of head trauma of any severity, and with closest age as possible to the patients. In the WHOQOL assessment patients showed a lower quality of life in the independence, environment, as well as in the total domains (p< 0,05). In the SF 36 assessment patients showed a lower quality of life in the functional capacity, vitality, and mental health domains (p<0,001); and also in pain, general health situation, and mental aspects (p<0,05). Patients showed more anxiety and, in the HADS Scale, showed at least a level higher, on average, than their controls. Patients also showed a higher number of post-concussion signs and symptoms than their respective controls. We did not find correlation between the later quality of life and protein S100B dosing at admission. We were not able to find correlation between the protein concentrations with the presence of brain lesions in the CCT scans taken at patients admission in the emergency department

Introdução: A cirurgia cardíaca resulta em taxa considerável de complicações neurológicas, incluindo delirium, disfunção cognitiva e acidente vascular cerebral isquêmico. Supõe que a fisiopatologia envolva embolia, aterotrombose, hipofluxo, redução do débito cardíaco e alterações da autorregulação cerebral. O balão de contrapulsação intra-aórtico (BIA) é um dispositivo de assistência circulatória comumente utilizado no perioperatório de pacientes de alto risco com o objetivo de otimização do débito cardíaco e da perfusão coronária. Apesar do benefício hemodinâmico do BIA, não é conhecido seu efeito na hemodinâmica encefálica. Objetivo: Avaliar os efeitos do BIA na hemodinâmica encefálica em pacientes de alto risco submetido a cirurgia cardíaca com circulação extracorpórea (CEC). Métodos: Trata-se de um subestudo do estudo clínico prospectivo e randomizado \"Balão de contra-pulsação intra-aórtico eletivo em pacientes de alto risco submetidos a cirurgia cardíaca\", realizado no Instituto do coração do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo entre 2014 e 2016. Dos 181 pacientes incluídos no estudo randomizado, 67 pacientes foram incluídos no subestudo. Os pacientes eram adultos, submetidos a cirurgia cardíaca de revascularização miocárdica (RM) com fração de ejeção menor ou igual a 40% e/ou EuroScore maior ou igual a 6. Os mesmos foram randomizados para uso do BIA logo após a indução anestésica ou para grupo controle. A velocidade de fluxo sanguíneo cerebral (VFSC) pelo ultrassom Doppler transcraniano e a pressão arterial (PA) pelo Finometer foram continuamente gravados por 5 minutos antes da cirurgia (T1), 24h após (T2) e 7 dias após (T3). O índice de autorregulação (ARI) foi estimado através da resposta ao degrau da VFSC a mudanças na PA, derivados da análise da função de transferência. As seguintes complicações clínicas neurológicas foram avaliadas: delirium, disfunção cognitiva e acidente vascular cerebral isquêmico. Resultados: Dos pacientes incluídos no estudo, 34 foram alocados para a estratégia de uso profilático do balão intra-aórtico e 33 para a estratégia controle. Não houve diferenças significativas entre os grupos BIA e controle respectivamente, nos três tempos de avaliação, em relação ao ARI (T1 - 5,5 ± 1,9 vs 5,7 ± 1,7; T2 - 4,0 ± 1,9 vs 4,1 ± 1,6; T3 - 5,7 ± 2,0 vs 5,7 ± 1,6, P= 0,978) e em relação à VFSC (T1 - 57,3 ± 19,4 vs 59,3 ± 11,8; T2 - 74,0 ± 21,6 vs 74,7 ± 17,5; T3 - 71,1 ± 21,3 vs 68,1 ± 15,1; P=0,952). O grupo BIA e o grupo controle apresentaram incidência semelhante de complicações neurológicas (delirium na unidade de terapia intensiva - 26,5% vs 24,2%, P=0,834, acidente vascular cerebral isquêmico - 3,0% vs 2,9%, P=1,00, e declínio cognitivo pós-operatório através das escalas Mini Mental State Examination MMSE - 16,7% vs 40,7%; P= 0,073 e Avaliação Cognitiva Montreal MoCA - 79,16% vs 81,5%; P= 1,000). Conclusões: O uso profilático do BIA em pacientes de alto risco submetidos à cirurgia de revascularização do miocárdio não altera a hemodinâmica encefálica e não está associado ao aumento de complicações neurológicas como delirium, declínio cognitivo e acidente vascular cerebral isquêmico / Introduction: Cardiac surgery is associated with a high incidence of neurologic complications, such as delirium, cognitive decline and stroke. The pathophysiology probably involves embolism, thrombosis, decreased cardiac output and abnormalities in cerebral autoregulation. The intraaortic balloon pump (IABP) is an assist device commonly in high-risk patients undergoing cardiac surgery aiming to increase the cardiac output and to improve the coronary perfusion. However, the effect of the IABP on the cerebral hemodynamic is unknown. Objectives: To assess the effect of IABP on cerebral hemodynamics in high-risk patients undergoing cardiac surgery with cardio-pulmonary bypass (CPB). Methods: This is a substudy of the randomized controlled trial \"Intraaortic Balloon Counterpulsation in Patients Undergoing Cardiac Surgery (IABCS trial)\", performed at the Heart Institute/University of Sao Paulo, from 2014 to 2016. Of the 181 patients included in the IABCS, 67 were included if they were submitted to cardiac surgery and if they had one of these two criteria: left ventricular ejection fraction equal or lower than 40% and/or EuroSCORE equal or higher than 6. Patients were allocated to the strategy of prohylatic IABP after anesthesia induction or to control. Cerebral blood flow velocity (CBFV) through transcranial Doppler and blood pressure (BP) through Finometer or intra-arterial line were continuously recorded over 5 minutes preoperatively (T1), after 24h (T2) and 7 days after surgery (T3). Autoregulation index (ARI) was estimated from the CBFV response to a step change in BP derived by transfer function analysis. The following complications neurologic were evaluated: delirium, cognitive decline and stroke. Results: Of the included patients, 34 were allocated to the IABP group and 33 to control group. There were no significant differences between the IABP and the control respectively in the following parameters: ARI (T1 - 5.5 ± 1.9 vs 5.7 ± 1.7; T2 - 4.0 ± 1.9 vs 4.1 ± 1.6; T3 - 5.7 ± 2.0 vs 5.7 ± 1.6, P= 0.978), CBFV (T1 - 57.3 ± 19.4 vs 59.3 ± 11.8; T2 - 74.0 ± 21.6 vs 74.7 ± 17.5; T3 - 71.1 ± 21.3 vs 68.1 ± 15.1; P=0.952). Both groups (IABP and control) had similar incidence of neurological complications (delirium - 26.5% vs 24.2%, P=0.834, stroke - 3.0% vs 2.9%, P=1.00, and cognitive decline through the scales Mini Mental State Examination MMSE - 16,7% vs 40,7%; P= 0.073 and Montreal Cognitive Assessment MoCA - 79.16% vs 81.5%; P= 1.000). Conclusions: The prophylactic use of IABP in high-risk patients undergoing cardiac surgery does not change the cerebral hemodynamic and is not associated with higher incidence of neurologic complications such as delirium, cognitive decline and stroke

Introdução: O traumatismo cranioencefálico (TCE) é o maior problema de saúde pública nos países ocidentais. A lesão axonial difusa (LAD) é uma das mais importantes causas de sequelas neurológicas e resultam do comprometimento da substância branca causada por forças rotacionais e/ou aceleração/ desaceleração no parênquima encefálico que tensiona e lesa os axônios. Apesar dos doentes com TCE apresentarem déficits neurológicos transitórios, as mudanças cognitivas podem ser persistentes, especialmente em lesões moderadas e severas. Até o momento poucos estudos analisaram aspectos neuropsicológicos de doentes com LAD. Método: Estudo unicêntrico, prospectivo, exploratório, com braço único e três níveis de medidas repetidas. Quarenta doentes com LAD de ambos os sexos, com idade entre 18 e 55 anos foram avaliados na fase 1 (até 3 meses após o trauma), fase 2 (6 meses) e fase 3 (12 meses). Na fase 1 avaliou-se os sintomas depressivos (BDI), ansiosos (IDATE), qualidade de vida (QV SF-36) e sobrecarga do cuidador (Zarit Burden Interview). Na fase foram avaliadas as mesmas variáveis, acrescida da avaliação cognitiva (QI, memória episódica verbal e visuoespacial, processos atencionais, funções executivas, coordenação motora). Na fase 3 repetimos o procedimento da fase 2. Resultados: Não houve diferença significativa dos sintomas depressivos, de ansiedade, sobrecarga do cuidador nas fases 1, 2 e 3. Constatamos melhora significativa na memória episódica verbal e visuoespacial (p < 0,05), dos processos atencionais (p < 0,05). O QI e a idade do doente foram preditores para desempenho dos doentes em diversos testes, o mesmo não foi observado em relação a gravidade do trauma. Conclusão: O estudo mostrou melhora espontânea da memória episódica e dos processos atencionais em doentes com LAD no primeiro ano após o trauma. Esses resultados foram independentes da gravidade do trauma e dos sintomas depressivos, ansiosos e da QV dos doentes. Esses achados podem estar associados à neuroplasticidade, evidenciando-se janela terapêutica importante no primeiro ano após o trama / Introduction: Traumatic brain injury (TBI) is a major public health problem in Western countries. Diffuse axonal injury (DAI) is one of the most important causes of neurological damage and result of white matter impairment caused by rotational forces and / or acceleration / deceleration in the brain parenchyma tenses and damages the axons. Although patients with TBI present transient neurological deficits, cognitive changes may be persistent, especially in moderate and severe injuries. To date few studies have examined neuropsychological aspects of patients with DAI. Method: single-center study, prospective, exploratory, with one arm design and three levels of repeated measures. Forty patients with LAD, both sexes, aged 18 to 55 were evaluated in phase 1 (up to 3 months after the trauma), phase 2 (6 months) and phase 3 (12 months). In phase 1 we evaluated depressive symptoms (BDI), anxiety (STAI), quality of life (QoL SF-36) and caregiver burden (Zarit Burden Interview). In phase 2 were evaluated the same variables, plus the cognitive assessment (IQ, verbal and visuospatial episodic memory, attentional processes, executive functions, motor coordination). In phase 3 we repeat the procedure from step 2. Results: No significant differences in depressive symptoms, anxiety, and caregiver burden in phases 1, 2 and 3. We found significant improvement in verbal and visuospatial episodic memory (p < 0.05), of the attentional processes (p < 0.05). The IQ and patient age were predictors for performance of patients in several tests, the same was not observed for the severity of the trauma. Conclusion: The study showed spontaneous improvement of episodic memory and attentional processes in patients with LAD in the first year after the trauma. These results were independent of the severity of the trauma and depressive symptoms, anxiety and QoL of the patients. These findings may be associated with neuroplasticity, demonstrating important therapeutic window in the first year after the trauma

Kar Wing To. / Thesis submitted in: December 1999. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 200-223). / Abstracts in English and Chinese. / Acknowledgements --- p.i / List of Abbreviations --- p.ii / Abstract --- p.v / 撮要 --- p.viii / List of Tables --- p.x / List of Figures --- p.xi / Contents --- p.xv / Chapter CHAPTER 1 --- INTRODUCTION / Chapter 1.1 --- The General Characteristics of Glial Cells --- p.1 / Chapter 1.1.1 --- Astrocytes --- p.1 / Chapter 1.1.2 --- Oligodendrocytes --- p.5 / Chapter 1.1.3 --- Microglial --- p.6 / Chapter 1.2 --- Brain Injury and Astrocyte Proliferation --- p.6 / Chapter 1.3 --- Reactive Astrogliosis and Glial Scar Formation --- p.9 / Chapter 1.4 --- Astrocytes and Immune Response --- p.10 / Chapter 1.5 --- Cytokines --- p.10 / Chapter 1.5.1 --- Cytokines and the Central Nervous System (CNS) --- p.12 / Chapter 1.5.2 --- Cytokines and brain injury --- p.13 / Chapter 1.5.3 --- Cytokines-activated astrocytes in brain injury --- p.13 / Chapter 1.5.4 --- Tumour Necrosis Factor-a --- p.14 / Chapter 1.5.4.1 --- Types of TNF-α receptor and their sturctures --- p.16 / Chapter 1.5.4.2 --- Binding to TNF-α --- p.17 / Chapter 1.5.4.3 --- Different Roles of the TNF-a Receptor Subtypes --- p.17 / Chapter 1.5.4.4 --- Role of TNF-α and Brain Injury --- p.19 / Chapter 1.5.4.5 --- TNF-α Stimulates Proliferation of Astrocytes and C6 Glioma Cells --- p.23 / Chapter 1.5.5 --- Interleukin-1 (IL-1) --- p.26 / Chapter 1.5.5.1 --- Interleukin-1 and Brain Injury --- p.27 / Chapter 1.5.6 --- Interleukin-6 (IL-6) --- p.28 / Chapter 1.5.6.1 --- Interleukin-6 and brain injury --- p.29 / Chapter 1.5.7 --- γ-Interferon (γ-IFN) --- p.30 / Chapter 1.5.7.1 --- γ-Interferon and Brain Injury --- p.30 / Chapter 1.6 --- Ion Channels and Astrocytes --- p.31 / Chapter 1.6.1 --- Roles of Sodium Channels in Astrocytes --- p.33 / Chapter 1.6.2 --- Role of Potassium Channels in Astrocytes --- p.33 / Chapter 1.6.3 --- Importance of Calcium Ion Channels in Astrocytes --- p.34 / Chapter 1.6.3.1 --- Function of Cellular and Nuclear Calcium --- p.34 / Chapter 1.6.3.2 --- Nuclear Calcium in Cell Proliferation --- p.36 / Chapter 1.6.3.3 --- Nuclear Calcium in Gene Transcription --- p.36 / Chapter 1.6.3.4 --- Nuclear Calcium in Apoptosis --- p.38 / Chapter 1.6.3.5 --- Spatial and Temporal Changes of Calcium-Calcium Oscillation --- p.39 / Chapter 1.6.3.6 --- Calcium Signalling in Glial Cells --- p.39 / Chapter 1.6.3.7 --- Calcium Channels in Astrocytes --- p.41 / Chapter 1.6.3.8 --- Relationship Between [Ca2+]i and Brain Injury --- p.43 / Chapter 1.6.3.9 --- TNF-α and Astrocyte [Ca2+]i --- p.45 / Chapter 1.6.3.10 --- Calcium-Sensing Receptor (CaSR) --- p.46 / Chapter 1.7 --- Protein Kinase C (PKC) Pathways --- p.49 / Chapter 1.7.1 --- PKC and Brain Injury --- p.50 / Chapter 1.7.2 --- Role of Protein Kinase C Activity in TNF-α Gene Expression in Astrocytes --- p.51 / Chapter 1.7.3 --- PKC and Calcium in Astrocytes --- p.52 / Chapter 1.8 --- Intermediate Early Gene (IEGs) --- p.54 / Chapter 1.8.1 --- IEGs Expression and Brain Injury --- p.54 / Chapter 1.8.2 --- IEGs Expression and Calcium --- p.55 / Chapter 1.9 --- The Rat C6 Clioma Cells --- p.56 / Chapter 1.10 --- The Aim of This Project --- p.58 / Chapter CHAPTER 2 --- MATERIALS AND METHODS / Chapter 2.1 --- Materials --- p.61 / Chapter 2.1.1 --- Sources of the Chemicals --- p.61 / Chapter 2.1.2 --- Materials Preparation --- p.65 / Chapter 2.1.2.1 --- Rat C6 Glioma Cell Line --- p.65 / Chapter 2.1.2.2 --- C6 Glioma Cell Culture --- p.65 / Chapter 2.1.2.2.1 --- Complete Dulbecco's Modified Eagle Medium (CDMEM) --- p.65 / Chapter 2.1.2.2.2 --- Serum-free Dulbecco's Modified Eagle Medium --- p.66 / Chapter 2.1.2.3 --- Phosphate Buffered Saline (PBS) --- p.66 / Chapter 2.1.2.4 --- Recombinant Cytokines --- p.67 / Chapter 2.1.2.5 --- Antibodies --- p.67 / Chapter 2.1.2.5.1 --- Anti-TNF-Receptor 1 (TNF-R1) Antibody --- p.67 / Chapter 2.1.2.5.2 --- Anti-TNF-Receptor 2 (TNF-R2) Antibody --- p.67 / Chapter 2.1.2.6 --- Chemicals for Signal Transduction Study --- p.68 / Chapter 2.1.2.6.1 --- Calcium Ionophore and Calcium Channel Blocker --- p.68 / Chapter 2.1.2.6.2 --- Calcium-Inducing Agents --- p.68 / Chapter 2.1.2.6.3 --- Modulators of Protein Kinase C (PKC) --- p.69 / Chapter 2.1.2.7 --- Reagents for Cell Proliferation --- p.69 / Chapter 2.1.2.8 --- Reagents for Calcium Level Measurement --- p.70 / Chapter 2.1.2.9 --- Reagents for RNA Extraction and Reverse Transcription-Polymerase Chain Reaction (RT-PCR) --- p.71 / Chapter 2.1.2.10 --- Sense and Antisense Used --- p.72 / Chapter 2.1.2.11 --- Reagents for Electrophoresis --- p.74 / Chapter 2.2 --- Methods --- p.74 / Chapter 2.2.1 --- Maintenance of the C6 Cell Line --- p.74 / Chapter 2.2.2 --- Cell Preparation for Assays --- p.75 / Chapter 2.2.3 --- Determination of Cell Proliferation --- p.76 / Chapter 2.2.3.1 --- Determination of Cell Proliferation by [3H]- Thymidine Incorporation --- p.76 / Chapter 2.2.3.2 --- Measurement of Cell Viability Using Neutral Red Assay --- p.77 / Chapter 2.2.3.3 --- Measurement of Cell Proliferation by MTT Assay --- p.77 / Chapter 2.2.3.4 --- Protein Assay --- p.78 / Chapter 2.2.3.5 --- Data Analysis --- p.79 / Chapter 2.2.3.5.1 --- The Measurement of Cell Proliferation by [3H]- Thymidine Incorporation --- p.79 / Chapter 2.2.3.5.2 --- The Measurement of Cell growth in Neutral Red and MTT Assays --- p.79 / Chapter 2.2.3.5.3 --- The Measurement of Cell Proliferationin Protein Assay --- p.79 / Chapter 2.2.4 --- Determination of Intracellular Calcium Changes --- p.80 / Chapter 2.2.4.1 --- Confocal Microscopy --- p.80 / Chapter 2.2.4.1.1 --- Procedures for Detecting Cell Activity by CLSM --- p.81 / Chapter 2.2.4.1.2 --- Precautions of CLSM --- p.82 / Chapter 2.2.5 --- Determination of Gene Expression by Reverse- Transcription Polymerase Chain Reaction (RT-PCR) --- p.83 / Chapter 2.2.5.1 --- RNA Preparation --- p.83 / Chapter 2.2.5.1.1 --- RNA Extraction --- p.83 / Chapter 2.2.5.1.2 --- Measurement of RNA Yield --- p.84 / Chapter 2.2.5.2 --- Reverse Transcription (RT) --- p.84 / Chapter 2.2.5.3 --- Polymerase Chain Reaction (PCR) --- p.85 / Chapter 2.2.5.4 --- Separation of PCR Products by Agarose Gel Electrophoresis --- p.85 / Chapter 2.2.5.5 --- Quantification of Band Density --- p.86 / Chapter CHAPTER 3 --- RESULTS / Chapter 3.1 --- Effects of Different Drugs on C6 Cell Proliferation --- p.87 / Chapter 3.1.1 --- Effects of Cytokines on C6 Cell Proliferation --- p.87 / Chapter 3.1.1.1 --- Effect of TNF-α on C6 Proliferation --- p.88 / Chapter 3.1.1.2 --- Effects of Other Cytokines on C6 Cell Proliferation --- p.92 / Chapter 3.1.2 --- The Signalling Pathway of TNF-α induced C6 Cell Proliferation --- p.92 / Chapter 3.1.2.1 --- The Involvement of Calcium Ions in TNF-α-induced C6Cell Proliferation --- p.95 / Chapter 3.1.2.2 --- The Involvement of Protein Kinase C in TNF-α- induced C6 Cell Proliferation --- p.96 / Chapter 3.1.3 --- Effects of Anti-TNF Receptor Subtype Antibodies on C6 Cell Proliferation --- p.102 / Chapter 3.2 --- The Effect of in Tumour Necrosis Factor-α on Changesin Intracellular Calcium Concentration --- p.102 / Chapter 3.2.1 --- Release of Intracellular Calcium in TNF-α-Treated C6 Cells --- p.104 / Chapter 3.2.2 --- Effects of Calcium Ionophore and Calcium Channel Blocker on TNF-α-induced [Ca2+]i Release --- p.107 / Chapter 3.2.3 --- Effects of Other Cytokines on the Change in [Ca2+]i --- p.109 / Chapter 3.2.4 --- The Role of PKC in [Ca2+]i release in C6 Glioma Cells --- p.109 / Chapter 3.2.4.1 --- Effects of PKC Activators and Inhibitors on the Changes in [Ca2+]i --- p.114 / Chapter 3.3 --- Determination of Gene Expression by RT-PCR --- p.114 / Chapter 3.3.1 --- Studies on TNF Receptors Gene Expression --- p.117 / Chapter 3.3.1.1 --- Effect of TNF-α on TNF Receptors Expression --- p.117 / Chapter 3.3.1.2 --- Effects of Other Cytokines on the TNF Receptors Expression --- p.119 / Chapter 3.3.1.3 --- Effects of Anti-TNF Receptor Subtype Antibodies on the TNF-a-induced Receptors Expression --- p.121 / Chapter 3.3.1.4 --- Effect of Calcium Ions on TNF Receptors Expression --- p.121 / Chapter 3.3.1.4.1 --- Effect of Calcium Ionophore on TNF Receptors Expression --- p.126 / Chapter 3.3.1.4.2 --- Effect of TNF-α Combination with A23187 on the Expression of TNF Receptors --- p.128 / Chapter 3.3.1.4.3 --- Effects of Calcium Ionophore and Channel Blocker on TNF Receptors Expression --- p.130 / Chapter 3.3.1.4.4 --- Effects of Calcium-Inducing Agents on TNF Receptors Gene Expressions --- p.130 / Chapter 3.3.1.5 --- Effects of PKC Activator and Inhibitor on TNF-α- induced TNF Receptors Expressions --- p.135 / Chapter 3.3.1.6 --- Effect of PKC and Ro31-8220 on IL-l-induced TNF Receptors Expressions --- p.138 / Chapter 3.3.2 --- Expression of Calcium-sensing Receptor upon Different Drug Treatments --- p.138 / Chapter 3.3.2.1 --- Effect of TNF-α on the Calcium-sensing Receptor Expression --- p.141 / Chapter 3.3.2.2 --- Effects of Other Cytokines on CaSR Expression --- p.143 / Chapter 3.3.2.3 --- Effect of A23187 on CaSR Expression --- p.143 / Chapter 3.3.2.4 --- Effect of TNF-α and A23187 Combined Treatment on CaSR Expression --- p.146 / Chapter 3.3.2.5 --- Effects of Calcium-inducing Agents on CaSR Expression --- p.149 / Chapter 3.3.2.6 --- Effects of PKC Activator and PKC Inhibitor on CaSR Expression --- p.149 / Chapter 3.3.3 --- Expression of PKC Isoforms upon Treatment with Different Drugs --- p.153 / Chapter 3.3.3.1 --- Effect of TNF-α on the PKC Isoforms Expression --- p.155 / Chapter 3.3.3.2 --- Effect of A23187 on the PKC Isoforms Expression --- p.155 / Chapter 3.3.3.3 --- Effect of TNF-α and Calcium Ionophore Combined Treatment on PKC Isoforms Expression --- p.157 / Chapter 3.3.3.4 --- Effects of Calcium-inducing Agents on PKC Isoforms Expression --- p.159 / Chapter 3.3.4 --- Expression of the Transcription Factors c-fos and c-junin Drug Treatments --- p.161 / Chapter 3.3.4.1 --- Effect of TNF-a on c-fos and c-jun Expression --- p.163 / Chapter 3.3.4.2 --- Effect of A23187 on c-fos and c-jun Expression --- p.163 / Chapter 3.3.4.3 --- Effect of TNF-a in Combination with A23187 on c- fos and c-jun Expression --- p.165 / Chapter 3.3.4.4 --- Effects of Calcium-inducing Agents on c-fos and c- jun Expression --- p.167 / Chapter 3.3.5 --- Effects of Different Drugs on Endogenous TNF-α Expression --- p.167 / Chapter 3.3.5.1 --- Effect of TNF-α on Endogenous TNF-α Expression --- p.169 / Chapter 3.3.5.2 --- Effect of A23187 on Endogenous TNF-α Expression --- p.169 / Chapter 3.3.5.3 --- Effect of TNF-α in Combination with A23187 on the Expression of Endogenous TNF-α --- p.172 / Chapter 3.3.5.4 --- Effects of Calcium-inducing Agents on Endogenous TNF-α Expression --- p.172 / Chapter 3.3.6 --- Effect of Different Drugs on LL-1 Expression --- p.175 / Chapter 3.3.6.1 --- Effect of TNF-a on IL-lα Expression --- p.177 / Chapter 3.3.6.2 --- Effect of A23187 on the IL-lα Expression --- p.177 / Chapter 3.3.6.3 --- Effect of Calcium Ionophore and TNF-α Combined Treatment on IL-1α Expression --- p.179 / Chapter 3.3.6.4 --- Effects of Calcium-inducing Agents on IL-lα Expression --- p.179 / Chapter 3.3.6.5 --- Effect of PKC Activator on the IL-1α Expression --- p.181 / Chapter CHAPTER 4 --- DISCUSSIONS AND CONCLUSIONS / Chapter 4.1 --- "Effects of Cytokines, Ca2+ and PKC and Anti-TNF-α Antibodies on C6 Glioma Cells Proliferation" --- p.184 / Chapter 4.2 --- The Role of Calcium in TNF-α-induced Signal Transduction Pathways --- p.186 / Chapter 4.3 --- Gene Expressions in C6 Cells after TNF-a Stimulation --- p.187 / Chapter 4.3.1 --- "Expression of TNF-α, TNF-Receptors and IL-1" --- p.187 / Chapter 4.3.2 --- CaSR Expression --- p.190 / Chapter 4.3.3 --- PKC Isoforms Expressions --- p.192 / Chapter 4.3.4 --- Expression of c-fos and c-jun --- p.193 / Chapter 4.4 --- Conclusion --- p.194 / REFERENCES --- p.200

Made available in DSpace on 2016-04-29T13:31:52Z (GMT). No. of bitstreams: 1 Sandra Regina Schewinsky.pdf: 10477872 bytes, checksum: f45db26602df9ae0747a68ec5641c178 (MD5) Previous issue date: 2008-05-05 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / The objective of this study is to the verify the following hypoteses: a) creative imagination stimulation reduces the memory déficits in persons who have suffered a Traumatic Brain Injury (TBI), b) the stimulation creative imagination and the memory déficits reduction are associated with the conscience level increase these persons. Many persons with TBI, mainly young people, have neuropsychological outcomes like by the memory and conscience. This ressearch is subsidized by basic concepts of social psychology presented in the work of Lev Semenovich Vygotsky, Alexander Romanovich Luria, Alexei Leontiev and from the reflections of George Mead, since these authors have analyzed the development of human psychological function though the perspective of society and culture. From this theoretical referential, the following aspects and analytical categories are detached, in agreement with the objectives of this study; the individual social genesis, human communication, creative imagination, memory, conscience, concepts formation and proximal development zone. It follows the nearly experimental orientation characterized by the case study, two young people attended in rehabilitation process, including a psychological treatment at the Department of Psychology, Division of Rehabilitation Medicine, Hospital das Clínicas, School of Medicine, University of São Paulo. The research consists in a psychological evaluation, in continuation the attendance whose objective is to stimulate the creative imagination of the person, with single activities and two persons participation, reinforcing the advantage of the work with Vygotsky s concept of proximal development zone, ending with the post-treatment psychological evaluation. The results suggest that the treatment for stimulation the imagination between the variables is inverse the increase in one of them reduces the other one, and the conscience has a synthesizings function for all the others, will be increased in this association. The research strengthens also the theoretical concepts of the mentioned authors above that mental functions act in interrelation and not isolately. The present study can collaborate with the psychological therapeutics which includes the neuropsychological rehabilitation / Esta pesquisa tem o objetivo de verificar as seguintes hipóteses: a) a estimulação da imaginação criativa diminui os déficits de memória em pessoas que sofreram Traumatismo Crânio Encefálico (TCE), b) a estimulação da imaginação criativa e a diminuição dos déficits de memória estão associadas à elevação do nível de consciência dos sujeitos vítimas de TCE. Um elevado número de pessoas, principalmente jovens, acometidas por esse traumatismo sofre de alterações neuropsicológicas, aquelas que afetam a memória e a consciência entre outras. Subsidiam esta investigação conceitos básicos da psicologia social extraídos da obra de Lev Semenovich Vygotsky, Alexander Romanovich Luria, Alexei Leontiev e das reflexões de George Mead, visto que esses autores analisaram o desenvolvimento das funções psicológicas humanas da perspectiva da sociedade e da cultura. Desse referencial teórico são destacados os seguintes aspectos e categorias analíticas, em consonância com os objetivos da pesquisa: gênese social do indivíduo, comunicação humana, imaginação criativa, memória, consciência, formação de conceitos e zona de desenvolvimento proximal. Esta pesquisa segue o delineamento quase-experimental caracterizado pelo estudo de caso, tendo dois jovens como sujeitos que realizaram processo de reabilitação incluindo o tratamento psicológico na Divisão de Medicina de Reabilitação do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo. A pesquisa consiste em avaliação psicológica, seguindo-se, então, o tratamento propriamente dito com objetivo de estimular a imaginação criativa dos sujeitos, incluindo atividades individuais e em dupla, reforçando a vantagem de se trabalhar com o conceito de zona de desenvolvimento proximal de Vygotsky, finalizando-se com a avaliação psicológica pós-tratamento. Os resultados sugerem que o tratamento de estimular a imaginação criativa trouxe benefícios aos sujeitos da pesquisa, confirmando as hipóteses de que a estimulação da imaginação está associada à redução dos déficits de memória, ou seja, a associação entre as variáveis é inversa, o aumento de uma diminui a outra, e que a consciência como função sintetizadora de todas as outras será aumentada nessa associação. O trabalho fortalece ainda os pressupostos dos autores citados de que as funções mentais atuam interrelacionadas, antes do que isoladamente. Pretende-se que a pesquisa presente possa colaborar com a terapêutica psicológica que engloba a reabilitação neuropsicológica

Made available in DSpace on 2016-01-26T12:51:49Z (GMT). No. of bitstreams: 1 sergioramin_tese.pdf: 5594028 bytes, checksum: 78bfa3ad01874a071e27eb7637a874df (MD5) Previous issue date: 2003-11-21 / Proton magnetic resonance spectroscopy is an noninvasive method that allows the detection of metabolic and biochemical detection of areas of the brain. This investigation focused on the clinical applications of proton MR spectroscopy in patients with focal brain lesions, considering the possibility of differentiate the normal brain tissue of pathological, neoplasic of non-neoplasic disorders, brain neoplasms to each other and similar lesions identified by the magnetic resonance imaging. A total of 308 proton magnetic resonance spectroscopies in 287 patients with focal brain lesions, 147 (51.2%) males and 140 (48.8%) females, was divided into three groups: Group I - 169 exams of patients with brain neoplasic; Group II - 58 exams of patients with non-neoplasic focal brain lesions, and Group III - 32 exams of individuals without lesions. Single voxel proton MR spectroscopy with echo time 136 ms was the method used. The qualitative analysis of the peaks of metabolites N-acetyl aspartate (Naa - 2,0 ppm), creatine (Cr - 3,0 ppm) and choline (Cho - 3,2ppm), expressed in graph, and quantitative by means of the calculation of the ratios Naa/Cr, Co/Cr and Co/Naa through height measurement of the peaks in the graph. The statistical analysis included Kruskal-Wallis test and principal component analysis. In most of spectroscopies performed in patients of Group I, there was an accentuated increase of Cho peak and reduction of Naa; in Group II slight increase of Cho and decrease of Naa was observed, while in the individuals of Group III Naa was the larger peak, corresponding to the double of the height of the Cho and Cr peaks. Lipids (0.9 and 1.3 ppm), that generally indicate necrosis, was detected more usually in malignant neoplasms (multiforme glioblastoma and metastases) and inflammatory process by toxoplasmosis. Aminoacids (0.9 ppm inverted) were detected only in pyogenic abscesses. Median values of Naa/Cr, Co/Cr and Cho/Naa ratios in Group I were 0.75, 3.00, and 4.00; 1.13, 1.20, and 0.92 in Group II; and 2.00, 0.76, and 0.40 in group III, respectively. With the ratios studied, it was possible differentiate significantly the three groups (p<0.001). The clinical application of the proton MR spectroscopy is useful to the elucidation of the etiological diagnosis of focal brain lesions. Metabolic pattern obtained by proton spectroscopy is distinct between normal brain tissue and pathological, occurring significant difference between neoplasic of non-neoplasic disorders. Proton magnetic resonance spectroscopy contribute to differentiate focal brain lesions similar to the magnetic resonance imaging exam. / A espectroscopia de prótons por ressonância magnética é um método não invasivo que possibilita a detecção de alterações metabólicas e bioquímicas de áreas do encéfalo. Este estudo teve como objetivo avaliar a aplicação clínica da espectroscopia de prótons por ressonância magnética em pacientes com lesões encefálicas focais, considerando-se a possibilidade de diferenciar tecido encefálico normal do patológico, lesões neoplásicas de não neoplásicas, neoplasias encefálicas entre si e lesões similares identificadas pela imagem por ressonância magnética. Foram estudados prospectivamente 308 exames de espectroscopia de prótons por ressonância magnética em 287 pacientes com lesões encefálicas focais, sendo 147 do sexo masculino (51,2%) e 140 do feminino (48,8%). Os exames foram divididos em três grupos: Grupo I - 169 exames de pacientes com neoplasias encefálicas; Grupo II - 58 exames de pacientes com lesões encefálicas focais não neoplásicas e Grupo III - 32 exames como grupo controle. Para realização da espectroscopia de prótons por RM foi utilizado o método single voxel com tempo de eco de 136 ms. Foram feitas análises qualitativa do comportamento dos picos dos metabólitos N-acetilaspartato (Naa - 2,0 ppm), creatina (Cr - 3,0ppm) e colina (Co - 3,2 ppm), expressos em gráfico, e quantitativa por meio do cálculo das razões Naa/Cr Co/Cr e Co/Naa, efetuado com base na amplitude do pico. A análise estatística incluiu teste de Kruskal-Wallis e análise de componentes principais. Na maioria das espectroscopias feitas em pacientes do Grupo I, houve aumento acentuado do pico de Co e redução do pico de Naa, nos exames do grupo II, leve aumento Co e redução de Naa, enquanto nos indivíduos do Grupo III nos exames o pico de Naa sempre foi o maior, correspondendo ao dobro da altura dos picos de Co e Cr. O metabólito lipídios (0,9 e 1,3 ppm), que geralmente indica necrose, foi detectado mais comumente em neoplasias malignas (glioblastoma multiforme e metástases) e processo inflamatório por toxoplasmose. Os aminoácidos (0,9 ppm invertido) foram detectados exclusivamente em abscessos piogênicos. Os valores das medianas das razões Naa/Cr, Co/Cr e Co/Naa nos exames dos pacientes do grupo I foram 0,75, 3,00 e 4,00; no grupo II 1,13, 1,20 e 0,92 e no grupo III 2,00, 0,76 e 0,40, respectivamente. Com as razões estudadas, foi possível diferenciar significantemente os três grupos (p<0,001). A aplicação clínica da espectroscopia de prótons por ressonância magnética é útil para a elucidação do diagnóstico etiológico de lesões encefálicas focais. O padrão metabólico obtido pela espectroscopia de prótons é distinto entre tecido encefálico normal e patológico, havendo também diferença significante entre lesões neoplásicas e não neoplásicas. A espectroscopia de prótons por ressonância magnética contribui para diferenciar lesões encefálicas focais similares ao exame de imagem por ressonância magnética

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Normal";mso-tstyle-rowband-size:0;mso-tstyle-colband-size:0;mso-style-noshow:yes;mso-style-priority:99;mso-style-qformat:yes;mso-style-parent:"";mso-padding-alt:0in 5.4pt 0in 5.4pt;mso-para-margin-top:0in;mso-para-margin-right:0in;mso-para-margin-bottom:10.0pt;mso-para-margin-left:0in;line-height:115%;mso-pagination:widow-orphan;font-size:11.0pt;font-family:"Calibri","sans-serif";mso-ascii-font-family:Calibri;mso-ascii-theme-font:minor-latin;mso-hansi-font-family:Calibri;mso-hansi-theme-font:minor-latin;mso-bidi-font-family:"Times New Roman";mso-bidi-theme-font:minor-bidi;}</style><![endif]-->Uvod: Traumatsko moždano o&scaron;tećenje (TMO) predstavlja globalni zdravstveni problem koji pogađa oko 10 miliona ljudi godi&scaron;nje &scaron;irom sveta. Te&scaron;ka traumatska moždana o&scaron;tećenja (TTMO) čine 10% svih TMO i imaju visoku stopu mortaliteta i neizvestan oporavak. Ranije prepoznavanje sistemskih faktora koji utiču na ishod lečenja može da ima značajan uticaj na pravovremeno započinjanje terapijskih mera i smanjivanje morbiditeta i mortaliteta. Cilj istraživanja: Identifikovati sistemske faktore koji imaju značajan uticaj na ishod lečenja povređenih sa TTMO u Jedinici intenzivnog lečenja (JIL) tokom prvog dana hospitalizacije. Metodologija: Ispitivanje je sprovedeno kao retrospektivno-prospektivna studija koja je obuhvatila 115 povređenih ispitanika sa TTMO koji su hospitalizovani u JIL Urgentnog centra Kliničkog centra Vojvodine (UC KCV) u periodu od 1.01.2014.-1.10.2017. Iz medicinske dokumentacije, za svakog ispitanika uključenog u istraživanje su uzeti u razmatranje i analizu sledeći parametri u toku prvih 24 časa od momenta prijema u JIL: demografske i op&scaron;te karakteristike ispitanika od značaja za istraživanje i sistemski prediktivni faktori (sistolni i srednji arterijski pritisak- SAP/MAP, glikemija-&Scaron;UK, telesna temperatura-TT, pH, parcijalni pritisak kiseonika-PaO2 i parcijalni pritisak ugljem dioksida- PaCO2) registrovani u pet vremenskih tačaka (0h, 6h, 12h,18h, 24h). Svi gore navedeni podaci su posmatrani i analizirani kao prediktorski faktori tj. nezavisne varijable u odnosu na zavisnu varijablu &bdquo;ishod lečenja&ldquo; definisanu kao Glazgovska skala ishoda (Glasgow outcome scale-GOS) nakon otpusta povređenih iz JIL na Kliniku za neurohirurgiju KCV i GOS nakon otpusta iz Klinike za neurohirurgiju KCV i &bdquo;tok lečenja&ldquo; definisan kroz dužinu boravka povređenih u JIL UC KCV, dužinu boravka na Klinici za neurohirurgiju KCV, odnosno ukupno trajanje hospitalizacije u KCV, kao i otpust kući ili u odgovarajući rehabilitacioni centar. Statistička analiza je izvr&scaron;ena pomoću statističkog paketa IBM SPSS 23. Podaci su predstavljeni tabelarno i grafički, a statistička značajnost određivana je na nivou p &lt; 0,05. Prikupljeni podaci su obrađeni adekvatnim statističkim metodima. Rezultati: Sistemski faktori koji su se izdvojili kao prediktori smrtnog ishoda (GOS 1) kod povređenih sa TTMO tokom prvog dana boravka u JIL su upotreba vazoaktivne potpore i glikemija. Upotreba vazoaktivne potpore povećava verovatnoću za smrtni ishod 4,7 puta (OR=0,214; 95%CI: 0,096-0,479; p&lt;0,05). i vrednosti glikemije &gt; 10 mmol/l povećavaju verovatnoću za smrtni ishod u nultom satu (OR= 0,240, 95%CI: 0,087-0,662; p=0,05) i u 24 satu (OR=0,206, 95%CI: 0,037 &ndash; 0,929; p=0,05). Sa svakim porastom telesne temperature za jednu jedinicu u posmatranom intervalu raste verovatnoća za pozitivan ishod (OR =2,118 , 95%CI: 1,097 &ndash; 4,091; p&lt;0,05) i vrednosti glikemije u intervalu od 4-8 mmol/l povećavaju verovatnoću za pozitivan ishod 2,5 puta. Sistemski faktori koji su se izdvojili u smislu predikcije ishoda lečenja ispitanika nakon otpusta iz JIL su vrednosti glikemije i telesna temperatura. Vrednost glikemije na prijemu u intervalu od 6,9 do 7,4 mmol/l povećavaju verovatnoću boljeg oporavka (GOS 4-5 vs. GOS 2-3). Niže vrednosti glikemiije u narednim vremenskim tačkama (6h, 12h, 18h) takođe povećavaju verovatnoću za bolji oporavak. Ukoliko je telesna temperatura u 6-om i 12-om satu, vi&scaron;a od 36,5 &deg;C veća je verovatnoća za bolji neurolo&scaron;ki oporavak, prilikom otpusta iz JIL, odnosno Klinike za neurohirurgiju KCV. Ispitanici koji su imali vi&scaron;e vrednosti telesne temperature su imali duže trajanje hospitalizacije (OR=4,096; 95%CI; 0,709-7,483;p&lt;0,05). Na dužinu boravka u JIL, kao i na otpust kući ili odgovarajući rehabilitacioni centar nije imao uticaj nijedan posmatrani sistemski faktor. Zaključak: Sistemski prediktivni faktori toka i ishoda lečenja povređenih sa TTMO su upotreba vazoaktivne potpore, glikemija i telesna temperatura.</p> / <p>Introduction: Traumatic brain injury (TBI) is a global health problem that affects about 10 million people worldwide annually. Severe traumatic brain injury (STBI) account for 10% of all TBI and has high morbidity and unreliable recovery. Early recognition of systemic factors that affect the treatment outcome can have a significant impact on the timely initiation of therapeutic measures and the reduction of morbidity and mortality. The objective of the research: to identify systemic factors that have a significant impact on the treatment outcome of the STBI patients in the Intensive Care Unit (ICU) during the first day of hospitalization. Methodology: The study was conducted as a retrospective-prospective study that included 115 injured patients with STBI who were hospitalized in the ICU, Emergency Center (EC) of the Clinical Center of Vojvodina (CCV) in the period from 01.01.2014 to 1.10.2017. From the medical documentation, for each participant involved in the research, the following parameters within the first 24 hours after the admission were considered and analyzed: demographic and general characteristics of the participants of importance for research and systemic predictive factors (systolic and mean arterial pressure-SAP / MAP, glycemia, body temperature -TT, pH, partial pressure of oxygen-PaO2 and partial pressure of carbon dioxide-PaCO2) registered at five time points (0h, 6h, 12h,18h, 24h). All of the above data were observed and analyzed as predictors, ie, independent variables in relation to the dependent variable &quot;treatment outcome&quot; defined as the Glasgow Outcome Scale (GOS) after the transfer from the ICU to the Clinic of neurosurgery of the CCV and GOS after discharge from a Clinic of neurosurgery and &quot;treatment course&quot; defined by length of stay in ICU, or the total duration of hospitalization in CCV, as well as the release to the home or the appropriate rehabilitation center. Statistical analysis was performed using the IBM SPSS 23 statistical package. The data are presented in tables and graphs, and the statistical significance was determined at p &lt;0.05. The collected data were processed with adequate statistical methods. Results: Systemic factors that had predictive value for the lethal outcome (GOS 1) in STBI during the first day of ICU stay were the use of vasopressors and glycemia. The use of vasopressors increases the likelihood of fatal outcome 4.7 times (OR= 0,214; 95%CI: 0,096-0,479; p&lt;0,05) and glycemic values &gt; 10 mmol/l increase the likelihood of fatal outcome on admission (OR=0,240, 95%CI: 0,087-0,662; p=0,05) and after 24 hours (OR=0,206, 95%CI: 0,037 &ndash; 0,929; p=0,05). With each increase in body temperature for one unit in the observed interval, the probability of a positive outcome increases (OR=2,118, 95%CI: 1,097 &ndash; 4,091;p&lt;0,05) and glycemic values in the range 4-8 mmol/l increase the probability of a positive outcome 2.5 times. Systemic factors that predict the treatment outcome of the patients after their discharge from ICU are glycemia and body temperature. The blood sugar on admission in the ICU in the range from 6.9 to 7.4 mmol/l increases the opportunity of a better recovery (GOS 4-5 vs. GOS 2-3). Lower glycemic values at the next time points (6h, 12h, 18h) also increase the opportunity of a better recovery. If the body temperature in the 6th and 12th-hour postadmission is higher than 36.5&deg; C, the greater opportunity for better neurological improvement when the patient is discharged from ICU, or from the Clinic of neurosurgery. Participants who had higher values of body temperature had a longer duration of hospitalization (OR 4.096; 95% CI; 0.709-7.483;p&lt;0,05). The length of the stay in ICU, as well as the release to the home or the appropriate rehabilitation center, was not affected by any observed systemic factor. Conclusion: Systemic predictive flow factors and outcome of treatment factors with STBI use of vasopressors, glycemia and body temperature.</p>

Thesis (doctoral)--University of Limburg, Maastricht, 1992. / Summary in Dutch. Includes bibliographical references (p. 109-119)

Diss. (sammanfattning) Umeå : Umeå universitet, 2010.