O uso de equipamentos e materiais na assistência à saúde contribui para a segurança do paciente e para o bom desempenho dos profissionais, porém não se pode desconsiderar o potencial de riscos trazido pela utilização destes e a possibilidade de ocorrências de eventos adversos (EA). O objetivo geral dessa investigação foi analisar o uso de equipamentos e materiais na assistência de enfermagem e sua relação com a ocorrência de EA. Trata-se de um estudo quantitativo, descritivo, com delineamento de pesquisa não-experimental, dividido em três etapas: 1ª) Revisão integrativa da literatura com busca nas bases de dados PubMed, CINAHL e LILACS; 2ª) Consulta às fichas informatizadas de notificação de EA de um hospital privado acreditado, registradas no período de 01/01/2011 a 30/06/2015, com vistas à seleção e análise dos eventos ocasionados pelo uso de equipamentos e materiais; 3ª) Elaboração, validação e aplicação de um instrumento de coleta para investigar os EA relacionados aos equipamentos e materiais e as estratégias utilizadas para propiciar o uso seguro desses dispositivos. Os principais resultados encontrados foram: 1ª) Seleção e análise de sete artigos, agrupados nas categorias: \"Métodos de registro, taxas de ocorrência e tipos de EA\" e \"EA ocorridos no transporte de pacientes críticos\" (ambos relacionados a equipamentos e materiais); 2ª) Constatado a notificação de 1.065 EA, sendo 180 (16,9% do total) relacionados ao uso de equipamentos e materiais na assistência de enfermagem: perda de sonda de alimentação (SNE, SNG, SOG e gastrostomia) (45,0%), perda de cateter venoso central (15,5%), lesão de pele (10,5%), extubação acidental (10,0%), perda de sonda vesical de demora (4,4%), erros de administração de medicamentos (bomba de infusão) (3,9%), perda de dreno (2,8%), tecnovigilância (2,8%), obstrução de cânula de traqueostomia (1,7%), perda de cateter de pressão arterial invasiva (1,7%), quedas (1,1%) e perda de cateter de analgesia (0,5%); 3ª) O instrumento foi elaborado, validado por cinco juízes e aplicado a 22 enfermeiros, apresentando as seguintes respostas: a) sobre o funcionamento inadequado ou o não funcionamento dos equipamentos, os mais citados foram bomba de infusão, cama elétrica, esfigmomanômetro, monitor multiparamêtrico, oxímetro de pulso e ventilador pulmonar mecânico; b) os EA provocados pela utilização inadequada ou incorreta de materiais foram lesão de pele, perda de sonda de alimentação, perda de cateter venoso central, perda de drenos, extubação acidental, perda de cateter de pressão arterial invasiva e perda de cateter de pressão intra-craniana; c) os EA ocorreram durante mudança de decúbito, administração de medicamentos, higiene corporal, transporte intra-hospitalar, atendimento de Urgências/Emergências e troca da fixação de cateteres e sondas; d) as estratégias preventivas prioritárias foram capacitação dos profissionais de enfermagem (na admissão e na aquisição de um novo equipamento ou material), utilização de protocolos assistenciais de enfermagem e manutenção preventiva / teste de qualidade prévio dos dispositivos. A aquisição de aparatos tecnológicos modernos se torna nula se não for acompanhada do investimento em capacitação dos profissionais de enfermagem das instituições de saúde e da preocupação em prevenir e minimizar a ocorrência de EA relacionados ao uso de equipamentos e materiais na assistência ao paciente / The use of equipment and materials in health care contributes to patient safety and to the good performance of professionals, but the potential for risks brought by the use of them and the possibility of adverse event (AE) occurrences cannot be ignored. This study aimed to analyze the use of equipment and materials in nursing care and its relationship to the AE occurrence. This is a quantitative, descriptive, non-experimental research design study, divided into three stages: 1) Integrative review with search in the databases PubMed, CINAHL and LILACS; 2) Consultation in computerized records of AE notification in an accredited private hospital, which were registered from January 1, 2011 to June 30, 2015, in order to select and to analyze events caused by the use of equipment and materials; 3) Development, validation and application of a data collection tool to investigate the AE related to equipment and materials and the strategies used to promote the safe use of these devices. The main results were: 1) Selection and analysis of seven articles, grouped into the following categories: \"Registration methods, occurrence rates and types of AE\" and \"AE occurred in the transport of critically ill patients\" (both related to equipment and materials); 2) After verifying the notification of 1,065 AE, and 180 (16.9% of the total) related to the use of equipment and materials in nursing care: feeding tube loss (SNE, SNG, SOG and gastrostomy) (45,0%), central venous catheter loss (15.5%), skin lesions (10.5%), accidental extubation (10.0%), bladder catheter loss (4.4%), medication administration errors (infusion pump) (3.9%), surgical drain loss (2.8%), technical surveillance (2.8%), tracheostomy tube obstruction (1.7%), invasive arterial pressure catheter loss (1,7%), falls (1.1%) and analgesia catheter loss (0.5%); 3) The instrument was developed, validated by five judges and applied to 22 nurses, with the following answers: a) about the improper functioning or non-functioning of equipment, the most common were infusion pump, electric bed, sphygmomanometer, multiparameter monitor , pulse oximeter and mechanical pulmonary ventilator; b) the AE caused by improper or incorrect use of materials were skin lesions, feeding tube loss, central venous catheters loss, surgical drain loss, accidental extubation, invasive arterial pressure catheter loss and intracranial pressure catheter loss; c) the EA occurred during change of decubitus, medication administration, personal hygiene, intra-hospital transport, Urgency/Emergency care and exchange of fixation of catheters and probes; d) priority preventive strategies were training of nursing professionals (on admission and in the purchase of new equipment or materials), use of nursing care protocols and preventive maintenance/quality prior testing of the devices. The acquisition of modern technological devices becomes invalid if it is not accompanied by investment in training of nursing professionals in health institutions and concerned to prevent and minimize the occurrence of adverse events related to the use of equipment and materials in patient care

O objetivo desta pesquisa foi identificar os efeitos adversos relatados por cirurgiões-dentistas (CD) e correlacioná-los com o uso de equipamentos motores. Trata-se de um estudo seccional, não experimental com análise quantitativa dos dados. O estudo foi realizado com 247 CD de Ribeirão Preto-SP. Na coleta dos dados, foi utilizado um questionário auto-aplicável composto por questões agrupadas em: questões sócio-demográficas, relativas a efeitos adversos (musculoesqueléticos, nervosos e vasculares), prática profissional e questões sobre o uso de equipamentos motores. Os dados foram analisados por meio de medidas de distribuição (freqüência), análise bivariada (Teste qui-quadrado e Exato de Fisher) e análise multivariável (Regressão logística). Os efeitos indesejáveis relatados pelos sujeitos e considerados mais intoleráveis foram: dor (67,65%), limitação de amplitude de movimento (7,84%) e parestesia / formigamento (6,86%). As regiões do corpo mais acometidas foram: pescoço, ombros e membros superiores direitos, perfazendo 76,8% das queixas. Os preditores estatisticamente significativos para os efeitos indesejáveis relatados em mãos foram sexo (RC = 0,513, p = 0,056) e pausa entre os atendimentos (RC = 0,514, p = 0,022). O equipamento mais utilizado foi o motor de alta rotação (94,7%), seguido pelos de baixa rotação com contra-ângulo (82,2%) e baixa rotação com peça reta (62,8%). Concluiu-se que embora os CD apresentassem sintomatologia característica de exposição a equipamentos motores que emitem vibração, estes sintomas não são suficientes para confirmar que os equipamentos motores são prejudiciais a sua saúde e que são fatores de risco para a ocorrência de LER/DORT. Os resultados deste estudo oferecem subsídios importantes para a conscientização do cirurgião-dentista sobre sua prática de trabalho e a necessidade de cuidar de sua saúde e levanta questionamentos que possibilitarão a realização de futuras investigações pela equipe multidisciplinar de Saúde do Trabalhador. / This study aimed to identify adverse effects reported by dental surgeons (DS) and correlate them to the use of motor equipment. We carried out a non experimental cross-sectional research with quantitative data analysis. The study involved 247 DS who work in Ribeirão Preto, Brazil. A self-applied questionnaire was used to assess the professionals. This instrument consisted of four parts, asking sociodemographic questions, questions about reported (muscle-skeletal, nervous and vascular) adverse effects, professional practice and questions related to motor equipment use. Data were analyzed through distribution (frequency) measures, bivariate analysis (chi-square and Fisher?s exact test) and multivariate analysis (logistic regression). Within the described undesirable effects, the ones these professionals considered most intolerable are pain (67.65%), movement range limitation (7.84%) and paresthesia/tingling (6.86%). The most affected body regions were neck, shoulders and right superior limbs, corresponding to 76.8% of complaints. The reported predictors statically significant for the undesirable effects on hands were gender (RC = 0,513, p = 0,056) and pause between appointments (RC = 0,514, p = 0,022). These professionals most frequently used high-speed rotating equipment (94.7%), followed low-speed rotation equipment with contra-angle (82.2%) and low-speed rotation equipment with a straight piece (62.8%). Although the symptoms these professionals present are characteristic of exposure to vibrating motor equipment, these symptoms are not sufficient to confirm that motor equipments cause damage to health and are factors of risk to the occurrence of RSI and WMSD. The results of this study offer important support to the consciousness of the Dental Surgeon about his(er) practice and the need to care of his(er) health and raises questions that can give rise to further research by the multidisciplinary team on the worker?s health.

Sun Qiang. / "December 1999." / Thesis (Ph.D.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (p. 119-139). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

吸煙是引起骨質疏鬆症的因素之一。臨床研究清楚表明吸煙者的骨密度降低，但其他干擾因素可能掩蓋了吸煙對骨頭的不良效果。使用動物模型用以研究吸煙和骨質疏鬆症之間是否有直接的因果關係與它潛在的機制是有必要的。為此，我們使用年輕和雌激素耗盡的小鼠作被動吸煙模型以及小鼠成骨細胞和破骨細胞株來作研究。 / 年輕的Balb/c小鼠暴露於2%或4% (v/v)的香煙煙霧中，代表中度和重度吸煙的人。骨代謝生物標誌物明顯增加，4%吸煙組在14週後股骨的微觀結構4%顯著下降，這相等於人類吸煙12年。此外，雌性Balb/c小鼠進行4%吸煙和/或卵巢切除術(OVX)。吸煙+OVX組增加血清中骨轉換指標水平。4%吸煙組的股骨生長板較薄。μ-CT數據進一步表明，相對骨體積(BV / TV)和結構模型指數(SMI)在吸煙組有顯著影響，而且在吸煙+ OVX組上有更大程度的影響。 / 在細胞研究中使用氯仿(CSE)和乙醇的香煙提取物(ESE)。CSE抑制小鼠細胞株RAW 264.7形成破骨細胞，並刺激小鼠成骨細胞株的分化和功能。這個與體內研究矛盾的結果暗示直接從煙霧中提取的化學成分並不是引起骨質疏鬆的元兇。影響骨代謝的很可能是其他從煙霧中生成的活性代謝物和一些吸煙引起的內源性激素物質。在吸煙引起的骨質流失中，這些代謝物或內源性物質可能是非常重要的。 / 有見及此，4%吸煙小鼠的血清用以研究其對成骨細胞和破骨細胞活動的影響。吸煙小鼠血清顯著降低在成骨細胞中鹼性磷酸酶(ALP)活性和鈣沉積，一些成骨細胞標記基因和蛋白表達均下降，而且 Wnt/β-catenin信號通路下調。此外，吸煙小鼠血清顯著增加形成破骨細胞的數量，組織蛋白酶K的基因和蛋白表達增加，在NF-κB和p-38 MAPK信號傳導途徑的信號分子表達增加。 / 總而言之，大量吸煙可能影響年輕小鼠和雌激素耗竭小鼠的骨代謝和微結構，通過類似的行動機制，人類也可能有同樣的骨疾病風險。這項研究揭示了吸煙導致的骨質疏鬆症在青少年和絶經後婦女的發病機制。這也給我們線索如何預防和治療與吸煙有關的骨骼疾病。這項研究還傳達了一個明確的信息：在年輕時應開始應控制吸煙。 / Cigarette smoking is one of the risk factors for osteoporosis. Clinical studies clearly showed that smokers have lower bone mineral density, but other confounding factors could mask the adverse actions of smoking on bones. Animal models are warranted to study the direct causal relationship between cigarette smoking and osteoporosis, and also the underlying mechanisms. In this regard, we used a mouse passive smoking model in both young and estrogen depleted mice, and the mouse osteoblast and osteoclast cell lines. / Young Balb/c mice were exposed to 2 or 4% (v/v) of cigarette smoke, similar to moderate or heavy smoking respectively in humans. Biomarkers for bone turnover were increased and bone microstructure of femur was significantly deteriorated after 4% smoking for 14 weeks which is similar to cigarette smoking for 12 years in humans. Furthermore, the effects of heavy smoking on ovariectomized mice were also investigated. Female Balb/c mice were subjected to 4% cigarette smoking and/or ovariectomy (OVX). Cigarette smoking together with OVX further increased the levels of bone turnover markers in serum. Femur growth plate was thinner in the 4% smoking group when compared to those in the SHAM- and OVX-operated groups. Micro-CT data further indicated that the relative bone volume (BV/TV) and structural model index (SMI) were significantly affected in the smoking groups, and to a greater extent in the 4% smoking + OVX group. / Chloroform (CSE) and ethanol smoke extracts (ESE) were used in cell studies. CSE suppressed the formation of osteoclasts, and stimulated the differentiation and function of mouse osteoblasts. These findings are contradictory to those found in in vivo study implying that chemical components directly extracted from cigarette smoke are not the culprits in causing bone disorder in animals. It is likely that other active metabolites from cigarette smoke and some endogenous hormonal substances released by cigarette smoking could affect bone metabolism. These active metabolites together with the endogenous bone hormones are perhaps crucial in smoking-induced bone loss in the body. / In view of this hypothesis, sera from 4% smoking mice were used to investigate their effects on osteoblast and osteoclast activities. It was found that the alkaline phosphatase (ALP) activity and calcium deposition in osteoblast were reduced significantly by the sera from smoking mice. Gene and protein expressions of some osteoblast markers were also decreased. The downregulation of Wnt/β-catenin signaling pathway was observed after the treatment with the serum obtained from the 4% smoking group. Moreover, the number of osteoclasts being formed was increased significantly by the smoking mouse serum. Cathepsin K gene and protein expressions were also induced. The increased expressions of the signaling molecules including NF-κB and p-38 MAPK were also observed. / In conclusion, heavy cigarette smoking could deteriorate bone metabolism and microstructures in young female and also estrogen depleted mice. The same kind of risk in bone disease may also apply to humans through similar mechanisms of action. This study sheds light in understanding the pathogenesis of smoking-induced bone disorders in teenagers and also postmenopausal women. It also gives us clues how to prevent and treat smoking related bone diseases. This study also conveys a clear message that cigarette smoking control should be started in young ages. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Chan, Lok Yi Ruby. / Thesis (Ph.D.) Chinese University of Hong Kong, 2014. / Includes bibliographical references (leaves 182-207). / Abstracts also in Chinese. / Chan, Lok Yi Ruby.

Wen Er Ya Jane. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 130-134). / Table of contents --- p.ii / List of tables --- p.iv / List of figures --- p.vi / Abstract --- p.vii / Glossary of abbreviations --- p.ix / Acknowledgments --- p.x / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- DEFINITIONS AND CLASSIFICATIONS...............................Error! Bookmark not defined / Chapter 1.1.1 --- Classification of drug-related problems --- p.2 / Chapter 1.1.2 --- Adverse drug reactions (ADRs) --- p.2 / Chapter 1.1.3 --- Drug interactions (DI) --- p.7 / Chapter 1.1.4 --- Therapeutic failures (TF) --- p.8 / Chapter 1.1.5 --- Non-compliance --- p.10 / Chapter 1.1.6 --- Drug overdoses (DO) or drug poisonings --- p.11 / Chapter 1.1.7 --- Drug-related hospitalizations (DRH) --- p.12 / Chapter 1.1.8 --- Other relevant definitions --- p.13 / Chapter 1.2 --- LITERATURE REVIEW --- p.16 / Chapter 1.2.1 --- Adverse drug reactions --- p.16 / Chapter 1.2.2 --- Hospital admission due to ADRs --- p.18 / Chapter 1.2.3 --- Drug-related hospitalizations (DRH) --- p.22 / Chapter 1.2.4 --- Discussion --- p.24 / Chapter 1.3 --- PURPOSE OF THIS STUDY --- p.27 / Chapter CHAPTER 2 --- METHODS --- p.30 / Chapter 2.1 --- BACKGROUND --- p.30 / Chapter 2.2 --- DATA COLLECTION --- p.31 / Chapter 2.2.1 --- The patients --- p.31 / Chapter 2.2.2 --- The drug history --- p.31 / Chapter 2.2.3 --- Patients knowledge of drugs they were taking --- p.33 / Chapter 2.2.4 --- Compliance --- p.33 / Chapter 2.2.5 --- Previous episodes of adverse drug reactions --- p.34 / Chapter 2.2.6 --- Diagnosis and outcome --- p.34 / Chapter 2.2.7 --- Laboratory Results --- p.34 / Chapter 2.2.8 --- Demographic characteristics of the patients --- p.35 / Chapter 2.2.9 --- The data sheet --- p.36 / Chapter 2.3. --- CASE REVIEW (REASSESSMENT) --- p.41 / Chapter 2.4 --- CODING OF DATA --- p.41 / Chapter 2.4.1 --- Coding of general data except diagnoses and drugs --- p.41 / Chapter 2.4.2 --- Coding of diagnoses --- p.42 / Chapter 2.4.3 --- Coding of drugs --- p.42 / Chapter 2.5 --- STATISTICAL ANALYSIS --- p.42 / Chapter CHAPTER 3 --- RESULTS --- p.43 / Chapter 3.1 --- THE PATIENTS --- p.43 / Chapter 3.1.1 --- Age and sex distributions --- p.43 / Chapter 3.1.2 --- Patients' ADL and living environments --- p.47 / Chapter 3.1.3 --- Baseline liver and renal function tests --- p.50 / Chapter 3.1.4 --- Diagnoses --- p.52 / Chapter 3.2 --- DRUG USE PRIOR TO ADMISSION --- p.54 / Chapter 3.2.1 --- Overview --- p.54 / Chapter 3.2.2 --- Consumption patterns for the prescribed drugs --- p.61 / Chapter 3.2.3 --- Sources and durations for the prescribed drugs --- p.69 / Chapter 3.2.4 --- Consumption patterns for self-medications --- p.71 / Chapter 3.2.5 --- Source and duration of the self-medications --- p.73 / Chapter 3.2.6 --- Drug overdose patterns --- p.75 / Chapter 3.3 --- PATIENTS' KNOWLEDGE OF THE EFFECTS AND SIDE-EFFECTS OF DRUGS --- p.74 / Chapter 3.3.1 --- Overview --- p.74 / Chapter 3.3.2 --- Patients' knowledge of the effects of their prescribed drugs --- p.74 / Chapter 3.3.3 --- Patients' knowledge of the side-effects of their prescribed drugs --- p.77 / Chapter 3.4 --- COMPLIANCE --- p.79 / Chapter 3.5 --- DRUG-RELATED HOSPITALIZATIONS (DRH) --- p.82 / Chapter 3.5.1 --- Overview --- p.82 / Chapter 3.5.2 --- Adverse drug reactions (ADRs) --- p.84 / Chapter 3.5.3 --- Outcome of ADRs --- p.98 / Chapter 3.5.4 --- "Therapeutic failures (Non-compliance, Inappropriate dose reduction)" --- p.100 / Chapter 3.5.5 --- Drug overdoses --- p.104 / Chapter CHAPTER 4 --- DISCUSSION --- p.106 / Chapter 4.1 --- ABOUT THE PATIENTS --- p.106 / Chapter 4.2 --- DISEASE PATTERNS AND DRUG CONSUMPTION PATTERNS --- p.107 / Chapter 4.2.1 --- Diagnoses on admission --- p.107 / Chapter 4.2.2 --- Drug consumption patterns --- p.109 / Chapter 4.2.3 --- About the sources and durations of the prescribed drugs --- p.112 / Chapter 4.2.4 --- About the self-medications --- p.113 / Chapter 4.3 --- ABOUT PATIENTS' KNOWLEDGE OF THE DRUGS --- p.114 / Chapter 4.4 --- ABOUT COMPLIANCE --- p.116 / Chapter 4.5 --- ABOUT ADRS AND DRUGS INTERACTIONS --- p.118 / Chapter 4.5.1 --- The incidence of ADRs --- p.118 / Chapter 4.5.2 --- The patterns of ADRs --- p.119 / Chapter 4.5.3 --- The drugs and ADRs --- p.119 / Chapter 4.5.4 --- Self-medications and ADRs --- p.121 / Chapter 4.5.5 --- The risk factors for ADRs --- p.122 / Chapter 4.5.6 --- Drug interactions --- p.125 / Chapter 4.6 --- ABOUT THERAPEUTIC FAILURES --- p.126 / Chapter 4.7 --- ABOUT DRUG OVERDOSES --- p.127 / Chapter 4.8 --- CONCLUSIONS --- p.128 / BIBLIOGRAPHY --- p.130

Segurança do paciente implica em reduzir riscos de dano desnecessário ao mínimo aceitável, causado pela assistência/cuidado e não pela doença, com utilização de boas práticas assistenciais, baseada em evidências científicas. As notificações de incidentes/eventos adversos configuram-se indicadores da qualidade dos serviços de saúde e sua ocorrência produz resultados indesejáveis que afetam a segurança do paciente. As notificações voluntárias de incidentes são instrumentos nos quais profissionais, instituições e indivíduos podem relatar problemas relacionados a segurança do paciente, e por meio da investigação e análise dos incidentes gerar informações uteis para melhoria dos processos assistenciais. Objetivo. Analisar as notificações de incidentes relacionados à segurança do paciente em um hospital público do interior do estado de São Paulo, de agosto de 2015 a julho de 2016. Método. Trata-se de um estudo descritivo, retrospectivo de análise documental, com abordagem quantitativa, com base nos dados do Serviço de Gerenciamento de Risco. Resultados. Foram analisadas 4.691 notificações. O enfermeiro foi a categoria profissional que mais notificou (n=3312; 71%), seguido do médico (n=373; 8%). O período mais frequente em que ocorreram as notificações foi o diurno. Houve diferença significativa da proporção de notificações entre os dias da semana. As notificações foram classificadas por motivo e os de maior prevalência neste estudo foram os relacionadas a medicamentos 807 (17%), seguido de lesões de pele 695 (15%), flebite 650 (14%) incidentes, artigos médico-hospitalar 630 (13%) e 299 (6%) quedas. A maior frequência de notificações ocorreu nas Unidades de Internação. Quanto a gravidade 344 eventos ocasionaram dano ao paciente, sendo a maioria de intensidade leve (n=224, 65%). Nos incidentes relacionados a medicamentos, contatou-se que os erros de medicamentos ocorreram com mais frequência (51%), seguido dos desvios de qualidade (27%). As ocorrências de flebite foram classificadas em grau, sendo o grau II o mais prevalente (47%), seguido do grau I (30%), o sexo masculino foi predominante, e o tempo de permanência do cateter prevalente foi menor que 72 horas, juntamente com dispositivos flexíveis de calibre 22 e curativo estéril com visualização. As quedas foram em sua maioria sem danos, mais frequentes no sexo masculino (59%), na enfermaria/quarto (61%) e no banheiro (20%). Quanto ao tipo de queda predominaram as da própria altura (44%), seguida do leito (20%). Nas lesões de pele predominou as lesões por pressão (94%), de estágio 2 (63%). Conclusão. As notificações espontâneas são uma importante fonte de informações, alerta para promoção da segurança no ambiente hospitalar e evidencia a magnitude do problema relacionado aos incidentes em saúde. A notificações estão muito centradas na figura do enfermeiro e todos os profissionais, principalmente os da linha de frente, devem compreender a importância das notificações para a assistência segura ao paciente. Há necessidade de fortalecer a cultura da segurança do paciente e os profissionais devem estar seguros que a notificação das falhas não implica em ações disciplinares. Falhas acontecem e é possível aprender a partir dos erros, a fim de evitá-los e promover ações que garantam uma prática mais segura / Patient safety implies in reducing risk of unnecessary damage to the minimum acceptable, caused by assistance/care and not by illness, using best practices, scientific evidence-based assistance. Notifications of incident/adverse events constitute indicators of quality of health services and their occurrence produce undesirable results that affect patient safety. Voluntary notifications of incidents are instruments in which professionals, institutions and individuals can report problems related to patient safety, and through research and analysis of incidents to generate useful information for improving assistance processes. Objective. Analyze incident notifications related to the patient\'s safety in a public hospital within the state of São Paulo, from August 2015 to July 2016. Method. It is a descriptive, retrospective study of documentary analysis, with quantitative approach, based on data from the risk Management service. Results. 4.691 notifications were analyzed. The nurse was the Professional category that most notified (n=3.312; 71%), followed by the Doctor (n=373; 8%). The most frequent period in which the notifications occurred was the daytime. There was significant difference in the proportion of notifications between the days of the week. The notifications were classified by reason and the most prevalence in this study were those related to medications 807 (17%), followed by skin lesions 695 (15%), Phlebitis 650 (14%) incidents, hospital medical articles 630 (13%) and 299 (6%) Falls. The highest frequency of notifications occurred in the internment units. In relation to severity, 344 events caused damage to the patient, being the most of light intensity (n=224; 65%). In drug related incidents, it was contacted that drug errors occurred more frequently (51%), followed by quality deviations (27%). The occurrences of phlebitis were classified in degree, the grade II being the most prevalent (47%), followed by grade I (30%), the male was prevalent, and the time remained of the prevalent catheter was less than 72 hours, along with devices Flexible 22 caliber and sterile dressing with visualization. The falls were mostly with no damage, more frequent in males (59%), in the infirmary/room (61%) and in the bathroom (20%). The type of fall predominated were those of the height (44%), followed by the bed (20%). In skin lesions, pressure lesions predominated (94%), stage 2 (63%). Conclusion. Spontaneous notifications are an important source of information, alert to promote safety in the hospital environment and evidence the magnitude of the problem related to health incidents. The notifications are very focused on the figure of the nurse and all professionals, especially the front line, must understand the importance of notifications for safe patient care. There is a need to strengthen the patient safety culture and practitioners should be assured that failure reporting does not entail disciplinary action. Failures happen and it is possible to learn from mistakes in order to avoid them and promote actions that ensure a safer practice

Wong Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves [110]-126). / Abstracts in English and Chinese. / ABSTRACT --- p.VI / ACKNOWLEDGEMENTS --- p.X / GLOSSARY --- p.XI / Chapter CHAPTER 1 --- INTRODUCTION AND LITERATURE REVIEW --- p.1 / Chapter 1.1 --- Sudden infant death syndrome --- p.1 / Chapter 1.1.1 --- Definition --- p.1 / Chapter 1.1.2 --- Epidemiology of sudden infant death syndrome --- p.1 / Chapter 1.1.3 --- Pathologic findings --- p.5 / Chapter 1.1.4 --- Theories of causation --- p.6 / Chapter 1.1.5 --- Associations of SIDS with temperature and hyperthermia --- p.8 / Chapter 1.1.6 --- Associations of sudden infant death syndrome with infection --- p.11 / Chapter 1.1.7 --- Association of sudden infant death syndrome with sleep state --- p.13 / Chapter 1.2 --- Overview of cytokines --- p.15 / Chapter 1.2.1 --- Definition --- p.15 / Chapter 1.2.2 --- Classification of cytokines --- p.15 / Chapter 1.2.3 --- Biological activities --- p.16 / Chapter 1.2.4 --- Cytokines and temperature --- p.20 / Chapter 1.2.5 --- Cytokines and infection --- p.22 / Chapter 1.2.6 --- Cytokines and smoking --- p.23 / Chapter 1.2.7 --- Cytokines and sleep/arousal --- p.23 / Chapter 1.3 --- Hypothesis and aims of the study --- p.27 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.28 / Chapter 2.1 --- Overview of methods in piglet experiments --- p.28 / Chapter 2.2 --- Pilot study design --- p.30 / Chapter 2.2.1 --- Study Groups --- p.30 / Chapter 2.2.2 --- Temperature controller --- p.33 / Chapter 2.2.3 --- PowerLab system --- p.34 / Chapter 2.2.4 --- Experimental set up --- p.36 / Chapter 2.2.5 --- Provisional ethical approval --- p.36 / Chapter 2.3 --- Problems and results of pilot experiments --- p.37 / Chapter 2.3.1 --- What is baseline body temperature of neonatal rat? --- p.38 / Chapter 2.3.2 --- What type of anaesthesic agent to use? --- p.39 / Chapter 2.3.3 --- What dose of ketamine to use? --- p.40 / Chapter 2.3.4 --- Dilution of ketamine --- p.41 / Chapter 2.3.5 --- Temperature calibration --- p.41 / Chapter 2.3.6 --- What is optimal neonatal rat age to use? --- p.44 / Chapter 2.3.7 --- Which method of blood collection to use? --- p.45 / Chapter 2.3.8 --- What method to raise body temperature? --- p.47 / Chapter 2.3.9 --- Summary results --- p.48 / Chapter 2.4 --- Final study design --- p.49 / Chapter 2.4.1 --- Study animal --- p.49 / Chapter 2.4.2 --- Final Study Groups --- p.50 / Chapter 2.4.3 --- Final ethical approval --- p.56 / Chapter 2.4.4 --- Muramyl dipeptide --- p.56 / Chapter 2.4.5 --- Recalibration of Temperature Controller --- p.57 / Chapter 2.4.6 --- Data collection --- p.58 / Chapter 2.4.7 --- Blood collection and Storage --- p.58 / Chapter 2.4.8 --- Study timetable --- p.59 / Chapter 2.5 --- Cytokines analysis --- p.59 / Chapter 2.5.1. --- Methods of Quantitative Enzyme Immunoassay --- p.59 / Chapter 2.5.2 --- Base theories of Enzyme-linked immunosorbent assay (ELISA) --- p.60 / Chapter 2.5.3 --- Procedure for cytokines assay --- p.61 / Chapter 2.6 --- Histology --- p.65 / Chapter 2.6.1. --- Macroscopic --- p.65 / Chapter 2.6.2. --- Microscopic --- p.65 / Chapter 2.7 --- Data handling and statistical analysis --- p.66 / Chapter CHAPTER 3 --- RESULTS --- p.67 / Chapter 3.1 --- Group (body weight) characteristics --- p.67 / Chapter 3.2 --- Serum concentration of IL- 6，IL-1 β --- p.69 / Chapter 3.3 --- Temperature --- p.78 / Chapter 3.4 --- Mortality rate --- p.80 / Chapter 3.5 --- Cardio-respiratory parameters --- p.85 / Chapter 3.6 --- Macroscopic findings at postmortem --- p.87 / Chapter 3.7 --- Histology --- p.91 / Chapter CHAPTER 4 --- DISCUSSION --- p.96 / Chapter 4.1 --- Study Model --- p.96 / Chapter 4.11 --- Core temperature of newborn rat --- p.95 / Chapter 4.12 --- Temperature calibration --- p.97 / Chapter 4.13 --- Respiratory and pulse rate measurements --- p.93 / Chapter 4.14 --- Measurement of sleep state --- p.99 / Chapter 4.2 --- Animal age and weight --- p.99 / Chapter 4.3 --- Cytokines response to heating --- p.101 / Chapter 4.4 --- Cytokine response to MDP --- p.104 / Chapter 4.5 --- "Hyperthermia, MDP and mortality" --- p.106 / Chapter 4.6 --- Further study --- p.107 / Chapter CHAPTER 5 --- CONCLUSION --- p.109 / Chapter 5.1 --- Small animal model of hyperthermia --- p.109 / Chapter 5.2 --- Hyperthermia and MDP elicit cytokine response --- p.109 / Chapter 5.3 --- Hyperthermia and MDP increase mortality rate --- p.109 / REFERENCES --- p.110 / APPENDICES --- p.A / Appendix 1: Experimental record --- p.A / Appendix 2 : Planned Study Timetable --- p.C / Appendix 3: PowerLab System --- p.E

Sam Sze Wing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 156-184). / Abstracts in English and Chinese. / Publications based on work in this thesis --- p.ii / Abstract --- p.iii / Acknowledgements --- p.vii / Chapter 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Corticosteroids --- p.2 / Chapter 1.1.1 --- Chemical Structure of Steroids --- p.3 / Chapter 1.1.2 --- Biosynthesis of Endogenous Corticosteroids --- p.3 / Chapter 1.1.2.1 --- Regulation of Cortisol synthesis and negative feedback system --- p.4 / Chapter 1.1.3 --- Biological Significance of Corticosteroids --- p.5 / Chapter 1.1.3.1 --- Involvement of corticosteroids as anti-inflammatory drugs --- p.6 / Chapter 1.1.3.2 --- Eicosanoid biosynthesis --- p.7 / Chapter 1.1.3.3 --- Lipoxygenase pathway --- p.9 / Chapter 1.1.3.4 --- Side-effects of prolonged use of corticosteroids --- p.9 / Chapter 1.2 --- Organisation of the Emetic Reflex --- p.11 / Chapter 1.2.1 --- Motor Pathway of Emetic Reflex --- p.12 / Chapter 1.2.1.1 --- Retching and vomiting --- p.12 / Chapter 1.2.1.2 --- Nausea --- p.13 / Chapter 1.2.2 --- Components of the Emetic Reflex --- p.14 / Chapter 1.2.2.1 --- The vomiting centre (VC) --- p.15 / Chapter 1.2.2.2 --- Area postrema (AP) / Chemoreceptor trigger zone (CTZ) --- p.15 / Chapter 1.2.2.3 --- The nucleus tractus solitarius (NTS) --- p.17 / Chapter 1.2.2.4 --- Gastrointestinal tract and vagus nerves --- p.17 / Chapter 1.2.2.5 --- Neurotransmitter receptors --- p.18 / Chapter 1.3 --- Chemotherapy-Induced Emesis --- p.19 / Chapter 1.3.1 --- Cancer as a cause of mortality in Man --- p.20 / Chapter 1.3.2 --- Chemotherapeutic Agents --- p.20 / Chapter 1.3.2.1 --- Different classes --- p.20 / Chapter 1.3.2.2 --- Emetogenic potential --- p.21 / Chapter 1.3.3 --- Cisplatin-Induced Emesis --- p.23 / Chapter 1.3.3.1 --- Unfavourable effects associated with chemotherapy-induced nausea and emesis --- p.24 / Chapter 1.3.3.2 --- Anticipatory nausea and vomiting --- p.24 / Chapter 1.3.3.3 --- Profile of cisplatin-induced emesis --- p.25 / Chapter 1.3.4 --- Animal Models of Cisplatin-Induced Acute and Delayed Emesis --- p.26 / Chapter 1.3.5 --- Mechanisms and Pathways Involves in Chemotherapy-Induced Emesis --- p.28 / Chapter 1.3.6 --- Anti-Emetic Drugs for the Treatment of Chemotherapy-Induced Emesis --- p.31 / Chapter 1.3.6.1 --- 5-HT3 receptor antagonists --- p.31 / Chapter 1.3.6.2 --- Dopamine receptor antagonists --- p.33 / Chapter 1.3.6.3 --- Benzodiazepines --- p.35 / Chapter 1.3.6.4 --- Cannabinoids --- p.35 / Chapter 1.3.6.5 --- Antihistamines and anticholinergics --- p.35 / Chapter 1.3.6.6 --- NK1 receptor antagonists --- p.37 / Chapter 1.3.6.7 --- Corticosteroids --- p.38 / Chapter 1.3.6.8 --- Multi-agent anti-emetic regimens --- p.39 / Chapter 1.4 --- Motion-Induced Emesis --- p.41 / Chapter 1.4.1 --- Incidence --- p.42 / Chapter 1.4.2 --- Mechanisms and Pathways Involved in Motion Sickness --- p.43 / Chapter 1.4.2.1 --- Importance of the vestibular apparatus --- p.44 / Chapter 1.4.2.2 --- Importance of the area postrema --- p.45 / Chapter 1.4.2.3 --- The nucleus tractus solitarius --- p.46 / Chapter 1.4.2.4 --- Hormone and neurotransmitters --- p.46 / Chapter 1.4.3 --- Animal models in Motion-Induced Emesis --- p.47 / Chapter 1.4.4 --- Anti-Emetic Drugs for the Treatment of Motion Sickness --- p.48 / Chapter 1.4.4.1 --- Anticholinergics --- p.49 / Chapter 1.4.4.2 --- Antihistamines --- p.49 / Chapter 1.4.4.3 --- Non-selective muscarinic and histamine receptor antagonists --- p.51 / Chapter 1.4.4.4 --- Sympathomimetics --- p.51 / Chapter 1.4.4.5 --- NK1i receptor antagonists --- p.51 / Chapter 1.4.4.6 --- 5-HT1A agonists --- p.52 / Chapter 1.4.4.7 --- 5-HT2 receptor agonist --- p.52 / Chapter 1.4.4.8 --- Arginine vasopressin (AVP) antagonists --- p.53 / Chapter 1.4.4.9 --- Opioid receptor agonists --- p.53 / Chapter 1.4.4.10 --- Dexamethasone and hormone levels --- p.54 / Chapter 1.4.4.11 --- Other anti-emetic drugs --- p.55 / Chapter 1.5 --- Aims of the Studies --- p.56 / Chapter 2 --- Methods --- p.59 / Chapter 2.1 --- Cisplatin-Induced Emesis Studies --- p.60 / Chapter 2.1.1 --- Animals --- p.60 / Chapter 2.1.2 --- Induction and Measurement of Emesis --- p.60 / Chapter 2.1.3 --- The Effects of Corticosteroids on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.63 / Chapter 2.1.4 --- "The Effects of Dexamethasone (1 mg/kg, i.p.) Administered as an Intervention Treatment on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.63 / Chapter 2.1.5 --- The Effects of Cortrosyn Depot (Tetracosactrin) on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.63 / Chapter 2.1.6 --- The Effects of Metyrapone on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.64 / Chapter 2.1.7 --- The Effects of Indomethacin on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.64 / Chapter 2.1.8 --- "The Effects of DFU and L-745,337 Administered as an Intervention Treatments on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.64 / Chapter 2.1.9 --- "The Effects of MK-886 (L-663,536) on Cisplatin-Induced Acute and Delayed Retching and Vomiting" --- p.65 / Chapter 2.1.10 --- The Effects of a Combination of Indomethacin and MK-886 on Cisplatin- Induced Acute and Delayed Retching and Vomiting --- p.65 / Chapter 2.1.11 --- Statistical Analysis --- p.66 / Chapter 2.2 --- Motion-Induced Emesis Studies --- p.67 / Chapter 2.2.1 --- Animals --- p.67 / Chapter 2.2.2 --- Measurement of Emesis --- p.67 / Chapter 2.2.3 --- Induction of Emesis in Motion-Naive Suncus murinus: Effects of Glucocorticoids --- p.68 / Chapter 2.2.4 --- Induction of Emesis in Motion-Sensitive Suncus murinus: Effects of Dexamethasone --- p.70 / Chapter 2.2.5 --- Preparation of Serum --- p.72 / Chapter 2.2.6 --- Measurement of Serum Cortisol by Enzyme-Linked Immunoassay (ELISA) --- p.72 / Chapter 2.2.6.1 --- Immunoassay kit --- p.72 / Chapter 2.2.6.2 --- Assay procedures --- p.73 / Chapter 2.2.7 --- Measurement of Serum Adrenocorticotrophin (ACTH) by Radioimmunoassay (RIA) --- p.75 / Chapter 2.2.7.1 --- Immunoassay kit --- p.75 / Chapter 2.2.7.2 --- Assay procedures --- p.76 / Chapter 2.2.8 --- Statistical Analysis --- p.79 / Chapter 3 --- Results --- p.81 / Chapter 3.1 --- Cisplatin-Induced Emesis --- p.82 / Chapter 3.1.1 --- General Profile of Emesis Induced by Cisplatin --- p.82 / Chapter 3.1.2 --- Antagonism of Cisplatin-Induced Emesis by Corticosteroids --- p.82 / Chapter 3.1.3 --- "The Effect of Dexamethasone (1 mg/kg, i.p.) Administered as an Intervention Treatment on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.84 / Chapter 3.1.4 --- The Effect of Cortrosyn Depot (Tetracosactrin) on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.85 / Chapter 3.1.5 --- The Effect of Metyrapone on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.85 / Chapter 3.1.6 --- "The Effect of Indomethacin, DFU and L-745,337 on Cisplatin-Induced Acute and Delayed Retching and Vomiting" --- p.86 / Chapter 3.1.7 --- The Effect of MK-886 on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.88 / Chapter 3.1.8 --- The Effect of Combination of Indomethacin and MK-886 on Cisplatin- Induced Acute and Delayed Retching and Vomiting --- p.89 / Chapter 3.2 --- Motion-Induced Emesis --- p.91 / Chapter 3.2.1 --- General Effect of Motion on Serum Cortisol and ACTH Levelsin Motion Naive Suncus murinus --- p.91 / Chapter 3.2.2 --- The Effect of Glucocorticoids on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion-Naive Male Suncus murinus --- p.92 / Chapter 3.2.2.1 --- Effect of dexamethasone --- p.92 / Chapter 3.2.2.2 --- Effect of betamethasone --- p.93 / Chapter 3.2.2.3 --- Effect of methylprednisolone --- p.93 / Chapter 3.2.3 --- The Effect of Glucocorticoids on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion Naive Female Suncus murinus --- p.94 / Chapter 3.2.3.1 --- Effect of dexamethasone --- p.94 / Chapter 3.2.3.2 --- Effect of betamethasone --- p.95 / Chapter 3.2.3.3 --- Effect of methylprednisolone --- p.95 / Chapter 3.2.4 --- The Effect of Dexamethasone on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion-Sensitive Suncus murinus --- p.96 / Chapter 3.2.4.1 --- Effect of dexamethasone on male motion-sensitive animals --- p.97 / Chapter 3.2.4.2 --- Effect of dexamethasone on female motion-sensitive animals --- p.97 / Chapter 4 --- Discussion --- p.131 / Chapter 4.1 --- "Cisplatin (5 mg/kg, i.p.)-Induced Emesis in Control Animals" --- p.132 / Chapter 4.2 --- Anti-Emetic Action of Corticosteroids in the Ferret --- p.133 / Chapter 4.3 --- Metyrapone Study --- p.138 / Chapter 4.4 --- Cortrosyn Depot Study --- p.139 / Chapter 4.5 --- Role of Cycloxygenase --- p.141 / Chapter 4.6 --- Role of 5-Lipoxygenase --- p.143 / Chapter 4.7 --- Duel Inhibition of Cycloxygenase and 5-Lipoxygenase --- p.144 / Chapter 4.8 --- Anti-Emetic Potential of Glucocorticoids in Suncus murinus --- p.145 / Chapter 4.9 --- General Summary --- p.149 / Appendix I --- p.152 / Appendix II --- p.154 / References --- p.156

by Wan Yu Kwan. / Thesis submitted in: December 1999. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 112-125). / Abstracts in English and Chinese. / Acknowledgement --- p.2 / Abstract --- p.3 / Table of Contents --- p.5 / Chapter Chapter 1 - --- Introduction --- p.7 / Chapter 1.1 --- Contribution of lifting techniques on risk assessment and training on manual materials handling --- p.7 / Chapter 1.2 --- Objectives --- p.12 / Chapter 1.3 --- Hypotheses --- p.12 / Chapter 1.4 --- Significance of Study --- p.13 / Chapter Chapter 2 - --- Literature Review --- p.14 / Chapter 2.1 --- Societal concerns on employee compensation --- p.14 / Chapter 2.2 --- Etiology of low back injury --- p.15 / Chapter 2.2.1 --- Compression forces on vertebral joints --- p.16 / Chapter 2.2.2 --- Shear forces on vertebral joints --- p.17 / Chapter 2.3 --- Lifting techniques --- p.18 / Chapter 2.3.1 --- Effect of lifting techniques on curvature of the spine --- p.22 / Chapter 2.3.2 --- Importance of leg muscles in manual lifting --- p.22 / Chapter 2.4 --- Prediction of low back injury in manual lifting --- p.24 / Chapter 2.4.1 --- Compression forces and moments --- p.26 / Chapter 2.4.2 --- Balance control --- p.29 / Chapter 2.4.3 --- Application of Surface electromyography in ergonomics --- p.31 / Chapter Chapter 3 - --- Method --- p.34 / Chapter 3.1 --- Subject recruitment --- p.34 / Chapter 3.2 --- Equipment --- p.35 / Chapter 3.2.1 --- Force platform --- p.35 / Chapter 3.2.2 --- Motion analysis system --- p.37 / Chapter 3.2.3 --- Surface electromyography --- p.38 / Chapter 3.3 --- Maximum voluntary contraction test --- p.40 / Chapter 3.3.1 --- MVC of vastus medialis --- p.41 / Chapter 3.3.2 --- MVC of medial gastrocnemius --- p.42 / Chapter 3.3.3 --- MVC of erector spinae --- p.43 / Chapter 3.4 --- Lifting techniques --- p.44 / Chapter 3.5 --- Experimental procedures --- p.48 / Chapter 3.6 --- Statistical analysis --- p.53 / Chapter Chapter 4 - --- Results and Dicussion --- p.54 / Chapter 4.1 --- No. of cases in the study --- p.54 / Chapter 4.2 --- Phases of lifting --- p.55 / Chapter 4.3 --- Process time --- p.56 / Chapter 4.4 --- Trunk inclination angles --- p.62 / Chapter 4.5 --- Hip joint angles --- p.67 / Chapter 4.6 --- Knee joint angles --- p.73 / Chapter 4.7 --- Center of mass of box --- p.79 / Chapter 4.8 --- Muscle activities --- p.84 / Chapter Chapter 5 - --- Conclusion --- p.109 / Chapter Chapter 6 - --- References --- p.112

by Yu Chung Wah. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 85-102). / Abstract also in Chinese. / Chapter Section 1 --- Literature review / Chapter 1.1 --- Physiology of anemia in the prematurity --- p.1 / Chapter 1.11 --- Erythropoiesis and Erythropoietin --- p.2 / Chapter 1.12 --- Postnatal changes in oxygen transport and delivery --- p.3-6 / Chapter 1.2 --- The concept of oxygen supply and demand --- p.6-7 / Chapter 1.3 --- Compensatory response and adverse effects of anemia --- p.8 -9 / Chapter 1.4 --- Treatments of anemia --- p.9 / Chapter 1.41 --- Red blood cell transfusion --- p.9-13 / Chapter 1.42 --- Recombinant human erythropoietin (rHuEpo) --- p.13 -14 / Chapter 1.5 --- Methods of cardiac output measurements --- p.15 / Chapter 1.51 --- Determination of cardiac output by invasive method --- p.15 -19 / Chapter 1.52 --- Determination of cardiac output by non-invasive methods --- p.20 -30 / Chapter 1.6 --- Methods of oxygen consumption measurements --- p.31 -37 / Chapter 1.7 --- Haemodynamic effects of red blood cell transfusion in preterm infants . --- p.38 -39 / Chapter Section 2 --- Introduction --- p.40 -42 / Chapter Section 3 --- Methodology --- p.43-47 / Chapter Section 4 --- Results --- p.48-51 / Chapter Section 5 --- Discussion --- p.52 -56 / Chapter Section 6 --- Conclusion --- p.57 / Chapter Section 7 --- Future Direction --- p.58 / Chapter Section 7 --- Tables and Figures --- p.59-84 / Chapter Section 8 --- References --- p.85 -102