Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 7 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 7 uppsatser.

Made available in DSpace on 2014-06-11T19:28:03Z (GMT). No. of bitstreams: 0 Previous issue date: 2002-02-25Bitstream added on 2014-06-13T18:32:31Z : No. of bitstreams: 1 sousa_cp_me_arafo.pdf: 282394 bytes, checksum: da271e59dd6d66efadb106512dc6504c (MD5) / O objetivo deste trabalho foi avaliar a prevalência e severidade do crescimento gengival em pacientes brasileiros sob terapia com nifedipina, por meio do uso do Novo Índice Clínico para Crescimento Gengival Induzido por Drogas(Índice DIGO). O estudo foi realizado em 35 pacientes sob terapia com nifedipina (grupo teste ) e em um grupo controle de 35 pacientes. Foram feitos os registros das variáveis demográficas (idade e sexo do paciente), farmacológicas (dose e tempo de uso da nifedipina) e das variáveis periodontais (índice de placa, índice gengival, profundidade de sondagem, nível de inserção clínico, sangramento à sondagem) e do crescimento gengival. O teste Z (nível de significância a 5% e p<0.05) e a correlação de Spearman foram usados para a comparação dos resultados entre os grupos teste e controle. Os resultados mostraram que o crescimento gengival foi observado em 68% dos pacientes e que não houve associação entre o crescimento gengival e as variáveis demográficas e as variáveis farmacológicas. No entanto, houve associação entre o crescimento gengival e as variáveis periodontais, exceto para o índice de placa. Podemos concluir que a inflamação gengival apresentou influência no crescimento gengival associado à nifedipina. / The aim of this study was to evaluate the occurrence of nifedipine induced GO in patients and the risk factors associated using a New Clinical Index for Drug Induced Gingival Overgrowth (DIGO) and the relation between The study was carried out with 35 patients under treatment with nifedipine (test group) and 35 patients without treatment (control group). There was assessed the characteristics of demographic (age, gender), pharmacological (dose, time of use), periodontal variables (plaque index, gingival index, probing depth, attachment level, bleeding on probing) and gingival overgrowth of the sample. The test Z (significance level at 5% - p< 0.05) and the Spearman correlation were used to compare data in test and control groups. Gingival overgrowth was noticed in 68% of patients. The statistical analyses showed no association between the gingival overgrowth and demographic and pharmacological variables, except for the plaque index. However, there was an association between the gingival overgrowth and periodontal variables. Further, it is possible to conclude that the presence of gingival inflammation was the main factor of risk to promote nifedipine-induced gingival overgrowth.

Abstract Radiotherapy is used in the treatment of breast cancer in order to reduce local recurrence rate. However, radiation is known to cause both acute and delayed side-effects on normal tissues. A common late complication of radiotherapy is fibrosis of skin and other organs. Fibrosis has been described as excessive accumulation of extracellular matrix components, especially collagens. Collagens are a group of extracellular matrix proteins that provide connective tissues with tensile strength. Type I and III collagens are the major structural proteins in skin. Alterations in collagen synthesis occur in various pathological conditions, during ageing and in association with diverse medical therapies. Collagens are degraded by matrix metalloproteinase enzymes (MMPs). The activity of MMPs is restrained by their specific tissue inhibitors (TIMPs). Elastic fibres constitute about 2–4% of skin dry weight. Despite their low quantity, elastic fibres are responsible for the resilient and elastic properties of skin. Dermal elastic fibres may be affected by intrinsic ageing, by extrinsic reasons such as photodamage and in several connective tissue diseases. The effect of radiotherapy on human skin type I and III collagen synthesis was investigated in a group of women who had been treated for breast cancer surgically and with radiotherapy. The levels of MMP-9, MMP-2/TIMP-2 complex, TIMP-1 and TIMP-2 in irradiated skin were also analysed. The effect of radiotherapy on elastic fibres was analysed using skin samples. The physio-mechanical properties of radiotherapy-treated skin were studied using ultrasound and elastometer devices, and compared with those of non-treated skin. In addition, skin samples were stained for haematoxylin-eosin, tenascin and mast cells. Factor VIII immunostaining was performed to visualize dermal blood vessels. Wound regeneration in irradiated skin was also studied using suction blister as a model. The synthesis of type I and III collagens was markedly increased as a result of radiotherapy. An increased amount of cross-linked type I collagen was detected in irradiated skin, and collagen turnover was also increased in irradiated skin. No difference in the amount or structure of the elastic fibres could be found between radiotherapy-treated and non-treated skin. A slight increase of skin thickness and stiffness was found in irradiated skin compared to non-treated skin. Increased tenascin expression was found in irradiated skin. The number of dermal blood vessels visualized by FVIII immunostaining was slightly higher in irradiated than in control skin. The amount of mast cells positive for tryptase, Kit receptor and chymase was increased in the upper dermis of irradiated skin. No difference in epidermal regeneration was found between irradiated and non-treated skin. The results of this study suggest that alteration of collagen metabolism contributes to dermal side effects of therapeutic irradiation.

The role of cholesterol-rich diet and of high protein supplement on the development of a glomerular lesion was studied in male guinea pigs. The possible pathogenesis of lipid-induced glomerulosclerosis was investigated. Four experiments were carried out. Four groups of guinea pigs were used in experiment I: CONT group was kept on normal guinea pig chow for 70 days; HC group was kept on 2% cholesterol diet for 70 days; HP group was kept on 50% casein diet for 70 days, and HCHP group received 2% cholesterol diet for 30 days and 2% cholesterol/50% casein diet for another 40 days. In experiment II two groups were used: CONT group and acetyl phenylhydrazine (APH)-treated group in which haemolytic anaemia was induced. In the third experiment the same dietary regimens as described in experiment I were used. In experiment IV three groups, namely CONT, HC, and HCHP, were employed. The animals in experiment IV were sacrificed after 5, 10, and 30 days. The first experiment explored the role of high cholesterol - and high cholesterol/high protein diet in the development of glomerulosclerosis. The other three experiments were designed to learn about the possible mechanism of lipid-induced glomerulosclerosis. Lipid analyses of plasma, erythrocytes and kidney tissue as well as complete blood count, erythrocyte osmotic fragility and blood cell morphology studies were performed. Kidney histology, histochemistry, immunohistochemistry, electron microscopy, morphometry, and renal and liver function tests were also carried out. De novo cholesterol synthesis was assessed by measuring HMG COA reductase activity and incorporation of tritiated water into cholesterol in the kidneys. Cholesterol-fed animals showed decreased weight gain, increased cholesterol concentration in plasma, erythrocytes, and kidney tissue. Haemolytic anaemia was documented after 70 days on this dietary regimen. Glomerular proliferation lesion was first noted at day 30 and progressed by day 70. Moderate proteinuria and haematuria were observed at day 70. Addition of protein to the high cholesterol diet led to a further decrease in weight gain. It also increased the mortality rate to 40% by day 70. The glomerular lesion, proteinuria and haematuria, and possibly haemolysis were more marked in the HCHP group. No causal relationship was found between liver function, immune complexes, haemolysis and glomerulosclerosis. Serum phosphate levels did not differ among the groups. The lipid found in the kidney of both HC and HCHP groups was mostly of plasma origin, since the kidney cholesterol de novo synthesis was suppressed in these two groups compared to the CONT group. There was a concommitant increase in the lipid content of kidney tissue and the mesangial expansion (MA/GTA) at day 30. No significant increase in the intraglomerular monocyte/macrophage was found at day 30 in the HCHP group compared to the HC group. However, a significant correlation (r=0.678, p 0.001) was found between the number of these cells and MA/GTA ratio among the four experimental groups at day 70. These data indicate that lipid deposits in kidney tissue may induce a glomerulosclerotic lesion in the absence of monocytes. However, these cells likely augment the proliferation of mesangial cells. We postulate that high protein diet could worsen the lipid-induced glomerular lesion by increasing delivery of abnormal lipoproteins to the kidney which could trigger mesangial cellular proliferation directly and indirectly by a macrophage-mediated process. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

Indiana University-Purdue University Indianapolis (IUPUI) / Introduction: Regenerative endodontic therapy in immature teeth with necrotic pulps triggers continued root development thereby improving the prognosis of these teeth. Several agents are under consideration for the disinfection and conditioning phases of this therapy. Triple antibiotic paste (TAP, i.e. equal parts of ciprofloxacin, metronidazole, minocycline) is used for canal disinfection and 17% EDTA solution is used for dentin conditioning. However, TAP and EDTA cause demineralization and their effect on surface loss and surface roughness of radicular dentin during regenerative procedures has not been quantified. Surface loss may be correlated with reduced tooth strength and surface roughness may be correlated with stem cell attachment. Objectives: The aim of this in vitro study was to quantitatively investigate the surface loss and surface roughness on human radicular dentin after treatment with two concentrations of TAP followed by EDTA. Materials and Methods: Human radicular dentin specimens were prepared from extracted human anterior teeth and randomized into six experimental groups. Group 1: saline control; Group 2: 17% EDTA; Group 3: TAP 1 mg/mL; Group 4: TAP 1 mg/mL and 17% EDTA; Group 5: TAP 1,000 mg/mL; Group 6: TAP 1,000 mg/mL and 17% EDTA for 5 minutes. After TAP is applied to Groups 3-6, all groups were incubated for 4 weeks. Then, groups 2, 4, and 6 were treated with EDTA for 5 minutes. Dentin surface loss (μm) and surface roughness (Ra, μm) were quantified after various treatments using non-contact and contact profilometry, respectively. Data were analyzed by one-way analysis of variance (α = 0.05) Hypothesis: It was hypothesized that there would be a significant difference in surface loss or surface roughness between at least two treatment groups. Results: All treatment groups showed significantly higher surface loss compared to untreated control. Dentin treated with 1g/mL TAP caused significant increase in surface loss and surface roughness compared to dentin treated with 1 mg/mL TAP. However, only 1g/mL TAP treated dentin showed significantly higher surface roughness compared to untreated control. The use of EDTA after both concentrations of TAP did not have significant additive effect on surface loss and surface roughness of dentin. Conclusion: The use of 1 mg/mL TAP can minimize surface loss and surface roughness of radicular dentin compared to higher concentrations. The use of EDTA after TAP may not cause additional surface loss and surface roughness of dentin.

Alcohol is a major public health problem globally. According to the World Health Organization (WHO) report, alcohol accounts for 2.5 million deaths (4% of total) and 69.4 million (4.5% of total) of Disability-Adjusted Life Years (DALYs), (WHO, 2002, 2011). In South Africa, alcohol was found to be the third highest contributor to death and disability (Parry, 2007/8). Among the many far-reaching consequences of alcohol use in South Africa, Fetal Alcohol Syndrome (FAS) in certain regions in the country, rates among the highest in the world (May et al., 2007). Despite higher comparative levels of FAS in rural areas, almost one third of the population in urban sites (Gauteng) demonstrates that FAS is not exclusively a problem of South African rural areas. This study hypothesized that higher knowledge levels about the effects of alcohol on pregnancy may deter use among women. Employing secondary data analysis from a 2006 cross-sectional household survey, this study explored the prevalence of alcohol use among urban women (18-44 years) in the Tshwane Municipality, in general and in pregnancy. It also examined the relationship between knowledge of alcohol effects on pregnancy and alcohol use. A significant association was found between employment status, pregnancy outcome and general alcohol use among women. An almost significant association was found between knowledge of alcohol effects on pregnancy and past month alcohol use, knowledge levels and alcohol use during pregnancy. Findings partially support the hypothesis. However, knowledge of alcohol effects on pregnancy alone cannot deter women from using alcohol. Multiple influencing factors should be considered in planning prevention programmes for urban women’s alcohol use. Further research with larger sample sizes of pregnant women is suggested to explore the associations conclusively.

by Chan Hung Chuen. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 143-151). / Abstract also in Chinese. / Acknowledgments --- p.i / Abstract --- p.ii / Abstract (Chinese version) --- p.v / Abbreviations --- p.viii / Content --- p.ix / Chapter CHAPTER ONE --- INTRODUCTION / Chapter 1. --- Free radical and free radical-mediated antitumor drugs --- p.1 / Chapter 2. --- Mitomycin C (MC) / Chapter 2.1 --- Drug actions of MC --- p.2 / Chapter 2.2 --- Adverse side effects of MC --- p.5 / Chapter 3. --- Doxorubicin (DOX) / Chapter 3.1 --- Drug actions of DOX --- p.7 / Chapter 3.2 --- Adverse side effects of DOX --- p.8 / Chapter 4. --- Antioxidants --- p.14 / Chapter 5. --- Effects of exogenous ATP on the antitumor activity of Doxorubicin and Mitomycin C / Chapter 5.1 --- Glutathione (GSH) and related enzymes --- p.17 / Chapter 5.2 --- Glutathione (GSH) and Anticancer Quinones --- p.19 / Chapter 5.3 --- Glutathione and the cardiac toxicity of the anticancer drugs --- p.20 / Chapter 5.4 --- Glutathione depletion in tumor cells by exogenous ATP --- p.21 / Chapter 6. --- Aim of research --- p.24 / Chapter CHAPTER TWO --- THE EFFECT OF ANTIOXIDANTS ON DOXORUBICIN- OR MITOMYCIN C-INDUCED CYTOTOXICITY ON HUMAN TUMOR AND NORMAL CELL LINES / Chapter 2.1 --- Introduction --- p.26 / Chapter 2.2 --- Materials and Methods --- p.28 / Chapter 2.3 --- Results --- p.36 / Chapter 2.4 --- Discussion --- p.60 / Chapter CHAPTER THREE --- STUDY OF CARDIOPROTECTIVE EFFECTS OF ANTIOXIDANTS AGAINST DOXORUBICIN- OR MITOMYCIN C-INDUCED TOXICITY BY LANGENDORFF PERFUEED ISOLATED RAT HEART MODEL / Chapter 3.1 --- Introduction --- p.64 / Chapter 3.2 --- Materials and Methods --- p.67 / Chapter 3.3 --- Results --- p.75 / Chapter 3.4 --- Discussion --- p.76 / Chapter CHAPTER FOUR --- THE EFFECT OF ANTIOXIDANTS DURING CHEMOTHERAPY OF DOXORUBICIN OR MITOMYCIN C IN TUMOR-BEARING MICE / Chapter 4.1 --- Introduction --- p.78 / Chapter 4.2 --- Materials and Methods --- p.80 / Chapter 4.3 --- Results --- p.83 / Chapter 4.4 --- Discussion --- p.93 / Chapter CHAPTER FIVE --- HISTOLOGICAL STUDY AND LIPID PEROXIDATION STUDY OF PROTECTIVE EFFECT OF ANTIOXIDANTS IN TUMOR-BEARING MICE TREATED WITH DOXORUBICIN OR MITOMYCIN C / Chapter 5.1 --- Introduction --- p.95 / Chapter 5.2 --- Materials and Methods --- p.98 / Chapter 5.3 --- Results --- p.103 / Chapter 5.4 --- Discussion --- p.117 / Chapter CHAPTER SIX --- EFFECT OF EXOGENOUS ATP ON THE ANTITUMOR ACTIVITY OF DOXORUBICIN AND MITOMYCIN C ON CULTURED HUMAN HEPATOMA CELLS / Chapter 6.1 --- Introduction --- p.122 / Chapter 6.2 --- Materials and Methods --- p.124 / Chapter 6.3 --- Results --- p.126 / Chapter 6.4 --- Discussion --- p.136 / Chapter CHAPTER SEVEN --- CONCLUSION / Chapter 7.1 --- Conclusion --- p.139 / Chapter 7.2 --- Future perspective --- p.141 / Bibliography --- p.142