by Tai Fai Fok. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (p. 211-215). / Microfiche. Ann Arbor, Mich. UMI, 1998. 3 microfiches ; 11 x 15 cm.

Yip, Ka Yan. / "August 2011." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 87-113). / Abstracts in English and Chinese. / Acknowledgement --- p.III / Abstract --- p.V / 論文摘要 --- p.VI / Table of Contents --- p.VII / List of Figures --- p.IX / List of Abbreviations --- p.XI / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Hepatocellular carcinoma --- p.1 / Chapter 1.1.1 --- Overview --- p.1 / Chapter 1.1.2 --- Risk factors --- p.3 / Chapter 1.1.3 --- Treatment ofHCC --- p.12 / Chapter 1.2 --- Berberine - a compound derived from Traditional Chinese Medicine --- p.15 / Chapter 1.2.1 --- Traditional Chinese Medicine --- p.15 / Chapter 1.2.2 --- Berberine --- p.16 / Chapter 1.3 --- Cell cycle --- p.18 / Chapter 1.3.1 --- An Overview of cell cycle --- p.18 / Chapter 1.3.2 --- Cell cycle and carcinogenesis --- p.18 / Chapter 1.4 --- Molecular mechanism of apoptosis --- p.20 / Chapter 1.4.1 --- Overview of apoptosis --- p.20 / Chapter 1.4.2 --- Caspases cascade --- p.22 / Chapter 1.4.3 --- Bcl-2 family --- p.24 / Chapter 1.5 --- Apoptosis as a target of cancer therapy --- p.26 / Chapter 1.6 --- Aims of study --- p.27 / Chapter Chapter 2 --- Materials and Methods --- p.28 / Chapter 2.1 --- Cell culture and treatment --- p.28 / Chapter 2.1.1 --- Cell lines --- p.28 / Chapter 2.1.2 --- Berberine --- p.29 / Chapter 2.1.3 --- Chemicals and reagents --- p.29 / Chapter 2.1.4 --- Preparation of solutions --- p.29 / Chapter 2.1.5 --- Procedures --- p.31 / Chapter 2.2 --- Apoptosis detection by FITC Annexin V and PI co-staining --- p.33 / Chapter 2.2.1 --- Chemicals and reagents --- p.33 / Chapter 2.2.2 --- Procedures --- p.33 / Chapter 2.3 --- Gene expression in Berberine-induced apoptotic cells --- p.35 / Chapter 2.3.1 --- Chemicals and Reagents --- p.35 / Chapter 2.3.2 --- Procedures --- p.35 / Chapter 2.4 --- Protein expression in Berberine-induced apoptotic cells --- p.38 / Chapter 2.4.1 --- Chemicals and Reagents --- p.38 / Chapter 2.4.2 --- Preparation of solution --- p.39 / Chapter 2.4.3 --- Procedures --- p.41 / Chapter 2.5 --- Caspase cascade studies in berberine-induced apoptosis --- p.43 / Chapter 2.5.1 --- Chemicals and reagents --- p.43 / Chapter 2.5.2 --- Procedures --- p.43 / Chapter 2.6 --- Cell cycle study in berberine-induced apoptotic cells --- p.44 / Chapter 2.6.1 --- Chemicals and Reagents --- p.44 / Chapter 2.6.2 --- Preparation of solutions --- p.44 / Chapter 2.6.3 --- Procedures --- p.44 / Chapter Chapter 3 --- Results --- p.46 / Chapter 3.1 --- Berberine induces apoptosis in hepatocellular cells --- p.46 / Chapter 3.2 --- Gene expression in Berberine-induced apoptotic cells --- p.53 / Chapter 3.3 --- Caspase cascade studies in berberine-induced apoptosis --- p.58 / Chapter 3.4 --- Protein expression in Berberine-induced apoptotic cells --- p.62 / Chapter 3.5 --- Berberine caused G1 cell cycle arrest in HCC cell lines --- p.65 / Chapter Chapter 4 --- Discussion --- p.76 / References --- p.87

Neuroblastoma is one of the most common solid tumors in patients below the age of 15. In this PhD project, the possible anti-tumor effects of the soy isoflavones on neuroblastoma cells have been investigated. A number of aspects of neuroblastoma cancer cell biology, including cell proliferation, cell cycle regulation, cell differentiation and apoptosis, intracellular signaling mechanisms, tumor invasiveness and metastatic properties, have been examined. Furthermore, novel antitumor properties of the soy isoflavones on neuroblastoma have also been quested for, hoping that through this PhD project, a better understanding of the potential anti-tumor effects of soy isoflavones on neuroblastoma cells can be obtained. In Chapter Three, we have demonstrated that the major soy isoflavones daidzein and genistein exerted potent anti-proliferative effect on murine neuroblastoma Neuro-2a (BU-1) cells. These two compounds were shown to modulate cell cycle distribution in BU-1 cells in different ways, possible through their differential effects on the expression of cell cycle regulatory proteins such as cyclins and cyclin-dependent kinase inhibitors. The anti-tumor effect of daidzein was found to be fairly specific to tumor cells, as daidzein only exhibited little, if any, direct cytotoxicity to normal murine cells such as bone marrow cells, macrophages, and thymocytes. Furthermore, the anti-proliferative effect of daidzein was unlikely to be attributed to its direct cytotoxicity to the BU-1 cells, but might be coupled with its ability to trigger the apoptosis and differentiation in the neuroblastoma cells. Our results show that daidzein could induce DNA fragmentation, ultrastructural changes, and the enrichment of cytoplasmic mono- and oligo-nucleosomes in the treated-BU-1 cells. Moreover, daidzein was shown to induce neuronal differentiation in the BU-1 cells, as indicated by morphological changes, and increased expression of the neuronal differentiation marker microtubule-associated protein-2, and acetylcholine esterase activity. In addition, we have also demonstrated that the signals of daidzein might be mediated by the estrogen receptor and nuclear factor-kappa B pathways. In Chapter Four, daidzein was shown to exert a differential an proliferative effect on three human neuroblastoma cell lines, including SK-N-DZ and SH-SY5Y. The most sensitive cell line, LA-N-1, was chosen for further mechanistic studies. It was found that daidzein-induced growth-inhibitory effect was coupled with the induction of neurite outgrowth and altered mRNA expression of the N-myc-related transcription factors. Moreover, daidzein was observed to modulate the invasiveness and metastatic properties of LA-N-1 cells, as indicated by the reduction of colony-forming ability, cell migratory ability, in vivo tumorigenicity, tumor vascularity, and angiogenic factors expression. Our results clearly suggest that the major soy isoflavone daidzein can exert its pleiotropic anti-tumor effects on both marine and human neuroblastoma cells. In Chapter Five, we isolated two stable actively proliferating subclones from the human neuroblastoma SH-SY5Y cells. We compared the sensitivities of the parental SH-SY5Y cells and the active subclones to the growth inhibition exerted by a number of conventional cancer chemotherapeutic agents and the soy isoflavone derivatives. We found that the major soy isoflavones daidzein and genistein were rather selective to the active subclones and this phenomenon was not observed with other chemotherapeutic agents. The anti-tumor action mechanisms of genistein on the most active subclone, designated as SH-SY5Y cl.6 cells, were examined in detail. It was found that genistein could induce apoptosis in SH-SY5Y cl.6 cells, as indicated by the induction of ultrastructural changes, phosphatidylserine externalization, and cytoplasmic enrichment of mono- and oligo-nucleosomes. The genistein-induced apoptosis in SH-SY5Y cl.6 cells was found to be both mitochondria and caspases-dependent, as mitochondrial membrane depolarization, cytosolic release of apoptotic mitochondrial factors and activation of caspase-3 were observed. To sum up, our results show that the major soy isoflavones, particularly daidzein and genistein, exhibit pleiotropic anti-tumor effects on both murine and human neuroblastoma cells, and they are also selective to the actively proliferating human neuroblastoma cells. (Abstract shortened by UMI.) / Lo, Fai-Hang. / "September 2007." / Adviser: Leung Kwok-Nam. / Source: Dissertation Abstracts International, Volume: 69-02, Section: B, page: 0949. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (p. 255-287). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract in English and Chinese. / School code: 1307.

by Winnie Yeo. / Thesis (M.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 213-256). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

by Joseph Jao Yiu Sung. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (p. 201-220). / 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.

by Au Sze Ki. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves xii-xix). / Acknowledgement --- p.i / Table of Content --- p.ii / List of Abbreviation --- p.vi / Abstract --- p.viii / Chapter Chapter One : --- Introduction / Chapter 1.1. --- Osteosarcoma --- p.1 / Chapter 1.1.1. --- Definition --- p.1 / Chapter 1.1.2 --- "Incidence, geographic patterns of distribution and epidemiological consideration" --- p.1 / Chapter 1.1.3 --- "Age, sex and sites" --- p.3 / Chapter 1.1.4 --- Type and grade --- p.5 / Chapter 1.1.4.1. --- Grade --- p.5 / Chapter 1.1.4.2. --- Site --- p.5 / Chapter 1.1.4.3. --- Metastasis --- p.5 / Chapter 1.1.5 --- Histological features --- p.9 / Chapter 1.1.6 --- Clinical features --- p.9 / Chapter 1.1.7 --- Radiological features --- p.11 / Chapter 1.1.8. --- Molecuar genetics --- p.13 / Chapter 1.1.9 --- Treatment --- p.13 / Chapter 1.2 --- Biochemical Markers of Osteosarcoma --- p.14 / Chapter 1.2.1 --- Tumor marker --- p.14 / Chapter 1.2.2 --- Biochemical markers of bone turnover --- p.15 / Chapter 1.2.3 --- Change of biochemical marker in osteosarcoma --- p.17 / Chapter 1.3 --- Alkaline Phosphatase (ALP) --- p.17 / Chapter 1.3.1 --- ALPs Family --- p.20 / Chapter 1.3.2 --- Membrane binding --- p.22 / Chapter 1.3.3 --- Biochemical function and physiological role of ALP --- p.24 / Chapter 1.4 --- Normal values of serum ALP --- p.28 / Chapter 1.5 --- Clinical applications of ALP --- p.28 / Chapter 1.6 --- "Separation, identification and quantification of ALP isozymes" --- p.31 / Chapter 1.6.1 --- Themostability --- p.31 / Chapter 1.6.2 --- Inhibition studies --- p.31 / Chapter 1.6.3 --- Electrophoresis --- p.33 / Chapter 1.6.4 --- Isoelectric focusing --- p.34 / Chapter 1.6.5 --- Affinity precipitation --- p.34 / Chapter 1.6.6 --- Immunological studies --- p.35 / Chapter 1.7 --- Plasma BALP level as biochemical marker of osteosarcoma --- p.35 / Chapter 1.8 --- ALP in malignancies --- p.37 / Aim of study --- p.x / Chapter Chapter Two : --- Methods and Materials / Chapter 2.1 --- Plasma BALP measurement as a biochemical markerin osteosarcoma --- p.40 / Chapter 2.1.1 --- Patient groups --- p.40 / Chapter a) --- Normal subjects --- p.40 / Chapter b) --- Osteosarcoma patients --- p.40 / Chapter 2.1.2 --- Collection and preparation of patient bloods samples of patients --- p.40 / Chapter 2.1.3 --- Plasma total ALP measurement --- p.41 / Chapter a) --- Reagent --- p.41 / Chapter b) --- Procedure --- p.43 / Chapter 2.1.4 --- Plasma BALP measurements --- p.43 / Chapter a) --- Wheat germ lectin precipitation of BALP --- p.44 / Chapter i) --- Reagent / Chapter ii) --- Procedure / Chapter b) --- ABBOTT methods for plasma BALP activity measurement --- p.45 / Chapter c) --- COBAS MIRA methods for BALP measurement --- p.45 / Chapter d) --- ALKPHASE-B method of BALP measurement --- p.46 / Chapter 2.1.5 --- Inter-conversion of plasma BALP activity measurement in different methods --- p.47 / Chapter 2.1.6 --- Statistical analysis --- p.48 / Chapter 2.2 --- Alkaline phosphatase isozymes expression in human osteosarcoma --- p.48 / Chapter 2.2.1 --- In Vitro cultures of human SaOS-2 and U-2 OS osteosarcoma cell line --- p.48 / Chapter a) --- Reagent --- p.49 / Chapter b) --- Procedure --- p.50 / Chapter i) --- Storage of U-2 OS and SaOS-2 / Chapter ii) --- Subculture of confluent monolayer / Chapter 2.2.2 --- Protein assay --- p.51 / Chapter a) --- Standard Assay --- p.51 / Chapter i) --- Reagent / Chapter ii) --- Procedure / Chapter b) --- Mircoassay --- p.51 / Chapter i) --- Reagent / Chapter ii) --- Procedure / Chapter 2.2.3 --- Extraction of ALP from the cultured osteosarcoma cells --- p.52 / Chapter a) --- Reagent --- p.52 / Chapter b) --- Procedure --- p.52 / Chapter 2.2.4 --- "ALP extraction from human liver, placenta and osteosarcoma tissue" --- p.53 / Chapter a) --- Reagent --- p.53 / Chapter b) --- Procedure --- p.54 / Chapter 2.2.5 --- Isoelectric focusing of ALP --- p.55 / Chapter a) --- Preparation of the agarose IEF gel --- p.55 / Chapter b) --- Samples preparation --- p.56 / Chapter c) --- Isoelectric focusing --- p.57 / Chapter d) --- Protein detection --- p.59 / Chapter i) --- Reagent / Chapter ii) --- Procedure / Chapter e) --- Visualization of ALP isozyme --- p.60 / Chapter 2.2.6 --- Biochemical differentiation of ALP expressed in human osteosarcoma --- p.61 / Chapter a) --- Thermodenaturation of ALP --- p.61 / Chapter b) --- Ammino acid inhibition of ALP --- p.61 / Chapter 2.2.7 --- Immunohistostaining of placental ALP in human Osteosarcoma --- p.62 / Chapter a) --- Reagent --- p.62 / Chapter b) --- Preparation of human osteosarcoma cell line --- p.63 / Chapter c) --- Preparation of human osteosarcoma tissue --- p.63 / Chapter d) --- Immunohistostaining --- p.64 / Chapter Chapter Three : --- Results / Chapter 3.1 --- General information of the patients --- p.65 / Chapter 3.1.1 --- Age and sex distribution --- p.65 / Chapter 3.1.2 --- Sites --- p.65 / Chapter 3.1.3 --- Treatment and survival rate --- p.66 / Chapter 3.2 --- Clinical significance of plasma bone-specific alkaline phosphatase (BALP) activity measurementin osteosarcoma patients --- p.71 / Chapter 3.2.1 --- Plasma BALP activity measurement --- p.71 / Chapter 3.2.2 --- Normal reference of plasma BALP determination --- p.72 / Chapter 3.2.3 --- Diagnostic value of plasma BALP measurement in osteosarcoma --- p.75 / Chapter a) --- Plasma BALP level at admission --- p.75 / Chapter b) --- Plasma Total ALP level at admission --- p.78 / Chapter 3.2.4 --- Prognosis value of plasma BALP measurement in osteosarcoma Patients --- p.78 / Chapter a) --- Correlation of plasma BALP-Adm with the local relapse of the disease --- p.78 / Chapter b) --- Correlation of plasma BALP-Adm with survival rate of the patients --- p.90 / Chapter i) --- One year survival Rate / Chapter ii) --- two-year survival Rate / Chapter iii) --- Three-year survival rate / Chapter c) --- Correlation of the plasma BALP-Adm with the tumor volume --- p.90 / Chapter 3.2.5 --- Using plasma BALP measurement for monitoring of the disease --- p.91 / Chapter a) --- Effectiveness of pre-operative chemotherapy --- p.91 / Chapter b) --- Change of plasma BALP level during the treatment --- p.92 / Chapter i) --- Monitoring of pre-operative chemotherapy / Chapter ii) --- Detection of local recurrence and secondary metastasis / Chapter 3.3 --- Alkaline phosphatase isozyme expressionin osteosarcoma --- p.103 / Chapter 3.3.1 --- Isoelectric point (pI) gradient in isoelectric focusing (IEF)gel --- p.10? / Chapter 3.3.2 --- ALP isozyme standard --- p.103 / Chapter 3.3.3 --- Ectopic expression of ALP in human osteosarcoma cell line: U-2 OS and SaOS-2 --- p.104 / Chapter a) --- Isoelectric focusing separation --- p.104 / Chapter b) --- Biochemical differentiation of ALP extracts --- p.110 / Chapter 3.3.4 --- Alkaline phosphatase expression in osteosarcoma patient plasma sample --- p.110 / Chapter 3.3.5 --- Alkaline phosphatase isozyme expression in human osteosarcoma biopsy tissue --- p.111 / Chapter 3.3.6 --- Ectopic expression of placental ALP in human osteosarcoma by immunohistochemistry --- p.111 / Chapter a) --- Ectopic expression of placental ALP in human osteosarcoma cell line U-2 OS --- p.111 / Chapter b) --- Ectopic expression of placental ALP in human osteosarcoma tissue sections --- p.112 / Chapter Chapter Four : --- Discussion --- p.128 / Chapter Chapter Five : --- Conclusion --- p.142 / Bibliography --- p.xii / Appendix --- p.xx

Chan Ching-Man Loren. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 126-144). / Abstracts in English and Chinese. / Acknowledgement --- p.ii / Abstract --- p.iii / Table of Content --- p.vii / List of Figure --- p.ix / List of Abbreviations --- p.xii / Chapter Chapter One --- General Introduction / Chapter 1.1 --- Doxorubicin --- p.1 / Chapter 1.2 --- Antioxidants --- p.11 / Chapter 1.3 --- Flavonoids --- p.17 / Chapter 1.4 --- Protection against doxorubicin-induced cardiotoxicity by antioxidant --- p.25 / Chapter 1.5 --- Aim of research --- p.25 / Chapter Chapter Two --- Study of Cardioprotection Effect of Flavonoids Against Doxorubicin-induced Toxicity in Sprague-Dawley Rats / Chapter 2.1 --- Introduction --- p.27 / Chapter 2.2 --- Materials and Methods --- p.29 / Chapter 2.3 --- Results --- p.37 / Chapter 2.4 --- Discussion --- p.51 / Chapter ChapterThree --- Study of Effect of Flavonoids in Chemotherapy of Doxorubicinin Tumor-bearing Mice / Chapter 3.1 --- Introduction --- p.54 / Chapter 3.2 --- Materials and Methods --- p.56 / Chapter 3.3 --- Results --- p.63 / Chapter 3.4 --- Discussion --- p.80 / Chapter ChapterFour --- Study of the Effect of Flavonoids on Doxorubicin-induced Cytotoxicity on Human Tumor Cell Line and Doxorubicin-resistant Human Tumor Cell Line / Chapter 4.1 --- Introduction --- p.83 / Chapter 4.2 --- Materials and Methods --- p.86 / Chapter 4.3 --- Results --- p.94 / Chapter 4.4 --- Discussion --- p.120 / Chapter Chapter five --- Conclusion --- p.122 / References --- p.126

People with diabetes mellitus are more likely to die from cardiovascular causes than those without diabetes, and modifiable risk factors, such as hyperglycaemia, dyslipidaemia and hypertension can be targeted in intervention programs to decrease this risk. In addition to tertiary care for patients with diabetes, there is a need for simple programs to be implemented in the community that allow the benefits of improved metabolic and blood pressure control to be realised more widely. Pharmaceutical care comprises the detection, prevention and solution of drug-related problems in a quantifiable form, so that outcomes of care can be easily reviewed and monitored. Previous studies of pharmaceutical care programs in patients with diabetes do not provide conclusive evidence of the benefit of pharmaceutical care. The aim of this research was to evaluate the impact of the provision of pharmaceutical care to patients with diabetes mellitus in an Australian context. In order to develop a pharmaceutical care program, the characteristics of an Australian cohort of patients with diabetes were reviewed. The Fremantle Diabetes Study (FDS), was a community-based prospective observational study of diabetes care, control and complications in a postcode-defined region of 120 097 people surrounding the port city of Fremantle in Western Australia. It was intended that the FDS annual reviews would provide important local information in order to design and implement a prospective pharmaceutical care program. A pilot pharmaceutical care program was subsequently developed for use in a diabetes outpatient clinic. This program was then modified for use in a community-based sample of type 2 diabetes mellitus patients, drawn from the FDS cohort. / Demographic parameters, including ethnicity and treatment details, were reviewed at study entry for the full FDS cohort and then over time for a subset of patients that returned for four subsequent annual assessments. Insulin use was more common in patients of Southern European origin compared with the Anglo-Celt group irrespective of the level of glycaemia, at baseline. This difference persisted during subsequent follow-up but was not associated with improved glycaemic control. These findings demonstrated that there are important ethnic differences in the management of patients with type 2 diabetes mellitus. The pilot pharmaceutical care program was carried out in high-risk diabetes mellitus patients attending a hospital outpatient clinic. The patients had poor glycaemic control, dyslipidaemia, hypertension and/or were on three or more prescription medications. In the pharmaceutical care arm, a clinical pharmacist reviewed and monitored all aspects of the patients' drug therapy in collaboration with other health care professionals at six weekly intervals for six months. The control patients received usual outpatient care. Seventy-three patients were recruited into the study, of whom 48 (66%) were randomised to receive pharmaceutical care. One in six patients was taking complementary medicines. The pharmaceutical care program provided patients with important medication information that resulted in changes to drug therapy. However, the six-month program did not lead to an improvement in glycaemic control. The next phase of the study adapted the pilot hospital-based pharmaceutical care program to a community-based setting. / Two hundred and two type 2 diabetes mellitus FDS patients were recruited, of whom 101 (50%) were randomised to the pharmaceutical care program, and all were followed for 12-months. There were significant reductions in risk factors associated with coronary heart disease in the case but not the control group over time, specifically glycaemic control, lipid levels, and blood pressure. Glycosylated haemoglobin fell from 7.5% to 7.0% (P<0.0001), total cholesterol fell from 5 mmol/L to 4.6 mmol/L (P<0.0001), systolic blood pressure fell from 158 mmHg to 143 mmHg (P<0.0001) and diastolic blood pressure fell from 77mmHg to 71mmHg (P<0.0001). Multiple linear regression analysis confirmed that pharmaceutical care program involvement was an independent predictor of benefit after adjustment for key variables. The 10-year coronary heart disease risk for patients without a previous coronary event was reduced by 4.6% over the 12-month study period in the pharmaceutical care group (P<0.0001), while there was no change in the controls (P=0.23). This phase of the study showed that medium-term individualised pharmaceutical care reduced vascular risk factors in a community-based cohort of patients with diabetes and that provision of a multifactorial intervention can improve health outcomes in type 2 diabetes mellitus. As part of the pharmaceutical care program, a high level of complementary medicine use was found. As a result, a study of complementary medicine use was undertaken in 351 patients from the FDS. A convenience sample of FDS patients was interviewed regarding their use of complementary medicines. A literature search was conducted to assess the potential impact of these medicines on diabetes, concomitant medications or diabetes-related co-morbidities. / Eighty-three of 351 (23.6%) patients with diabetes had consumed at least one complementary medicine in the previous year and 42% (77/183) of the products potentially necessitated additional patient monitoring or could be considered potentially inappropriate for a diabetic patient. The data indicated the need for patient disclosure of complementary medicine use and adequate monitoring for complementary medicine-related adverse events, as part of the pharmaceutical care process. The pharmaceutical care model was established to provide a framework by which drug use could be improved to enhance patients' clinical and health-related quality of life outcomes. For the present study, a straightforward pharmaceutical care program was adapted from a hospital setting to a community setting, where the principal requirement was a clinical pharmacist who had completed a self-directed diabetes-training program. In this context, clinically relevant parameters improved over the course of the study period. Pharmaceutical care programs such as this can begin the process of translating the findings of large and expensive clinical trials into standard clinical practice.

No description available.

Hypertoni är en folksjukdom och en riskfaktor för hjärt-kärlsjukdom. Effektiva behandlingsmetoder finns men brist på följsamhet till behandlingsregimer vid hypertoni är ett stort problem, som utgör en risk för patienters hälsa. Bättre kunskap om vad som kan påverka patienternas följsamhet till hypertonibehandling är därmed av stor betydelse för sjuksköterskans hälsofrämjande arbete. Syftet med studien var att undersöka faktorer som påverkar patienters följsamhet till behandling vid hypertoni. Studien genomfördes som en litteraturstudie. Data bestod av 16 vetenskapliga artiklar som valdes ut, granskades och analyserades för att finna påverkande faktorer. De faktorer som framkom delades in i fem kategorier. Dessa var inställning till hypertoni och behandling, upplevelser av biverkningar, hälso- och sjukvårdens påverkan, omgivningens påverkan samt personliga faktorer. Misstro till diagnosen, behandling och hälso- och sjukvården samt rädsla för biverkningar utgjorde faktorer av vikt för följsamheten. Familjens engagemang var av betydelse för att hålla fast vid ordinationer och rekommendationer. En annan faktor av vikt var att patienter glömde ta sina läkemedel. Resurser i hälso- och sjukvården bör läggas på att utarbeta strategier för att effektivt kunna arbeta med hälsofrämjande arbete samt att optimera patientens delaktighet i beslut gällande den egna vården, detta för att öka följsamhet till behandling vid hypertoni. / Hypertension is a widespread disease and a risk factor for cardiovascular disease. Effective treatments are available but lack of compliance to treatment regimens in hypertension is considered a major problem that presents a risk to patient health. Better knowledge of what affect patients´ compliance to hypertension treatment is therefore of great importance to the nurse´s health promotion. The purpose of this study was to investigate factors that influence patients´ compliance to the treatment of hypertension. The study was conducted as a literature study. Data consisted of 16 scientific articles that were selected, reviewed and analyzed to find the influencing factors. The factors that emerged were divided into five categories. These were attitudes to hypertension and treatment, experiences of side effects, health care impact, impact of the surroundings and personal factors. Distrust of the diagnosis, treatment, health care and fear of side effects were factors of importance to compliance. The family´s involvement was important to adhere to prescriptions and recommendations. Another factor of importance was that the patients forgot to take their medicines. Resources in health care should be given to developing strategies to effectively work with health care promotion and to optimize the patient´s participation in decisions regarding their own care, this in order to increase compliance to hypertension treatment.