published_or_final_version / Community Medicine / Master / Master of Public Health

Biotène® products have been developed with the intention of preventing tooth decay, plaque accumulation and oral infections in individuals with xerostomia (dry mouth). Not much is known about the effect of Biotène® chewing gums. Biotène® chewing gum contains host proteins. Due to these contents the manufacturer claims that Biotène® chewing gum is an “enzyme gum” that “boosts and strengthens the mouths natural defences”. The aim of this study was to investigate the effect of Biotène® chewing gum on saliva flow rates, saliva buffering capacity, plaque index, as well as salivary Streptococcus mutans and Lactobacilli counts, in healthy subjects with hyposalivation. One hundred and nine subjects with an age range of 18 to 23 years were screened for hyposalivation. Hyposalivation is a reduced salivary flow rate in a subject based on examination of the subject. Thirteen healthy subjects, who initially presented with hyposalivation, were included in the study. A baseline laboratory analysis of saliva was performed. Saliva was collected at rest and with masticatory stimulation, and measured. Resting saliva is saliva produced without any stimulation and can be obtained by allowing the subject to passively drool into a sputum jar. Stimulated saliva is produced as a result of stimulation of the salivary glands and may be obtained by allowing subject to chew inert rubber tubing while expectorating into a sputum jar. Buffering capacity was performed on both the saliva samples. Plaque index and DMFT was measured. Bacterial counts such as S. mutans and Lactobacilli counts were performed on the stimulated saliva. Subjects were given rubber tubing, xylitol chewing gum or Biotène® chewing gum to use for 2 weeks. A rubber tubing phase was introduced into the study to eliminate the effect of masticatory stimulation, which any chewing gum can provide. A xylitol-containing chewing gum (xylitol) phase was also introduced into the study in order to eliminate the effect of xylitol, as Biotène® chewing gum contains xylitol. A second laboratory analysis of saliva was performed. After a two weeks wash out period the second test product was given and the same procedure was repeated with the third product. The results showed that two weeks use of Biotène® chewing gum had no significant effect on the resting and stimulated saliva flows. It did not increase the buffering capacity of either the resting or stimulated saliva samples. Although it did not reduce the plaque index and S. mutans counts, it significantly reduced the Lactobacilli counts. Xylitol chewing gum, which was used as a control to eliminate the xylitol effect from the Biotène® chewing gum, significantly increased the stimulated saliva, reduced the plaque index and the salivary Lactobacilli count. Biotène® chewing gum which contains host proteins has no beneficial effects regarding saliva flow rate or against dental plaque and therefore against dental caries.

published_or_final_version / Nursing Studies / Master / Master of Nursing

published_or_final_version / Community Medicine / Master / Master of Public Health

Hypertensive left ventricular hypertrophy (LVH) increases the risk for the development of heart failure with systolic chamber dysfunction. However, the exact mechanisms and hence best therapeutic approach to prevent this transition process is uncertain. One potential mechanism is through excessive β-adrenergic receptor (-AR) activation, but the risks of β-AR blocker therapy may outweigh the benefits. Since activation of -AR augments function of the renin-angiotensin-aldosterone system, I therefore explored whether mineralocorticoid receptor (MR) blockade prevents the transition from hypertensive LVH to systolic chamber decompensation produced by excessive β-AR activation, and the mechanisms thereof. The role of hypertensive LVH as a predisposing factor to systolic chamber decompensation post-myocardial infarction (MI) is controversial. In the present thesis I therefore also evaluated this question. The effect of spironolactone (SPIRO, 80 mg.kg-1.day-1), an MR blocker, on LV chamber remodelling and function was evaluated in spontaneously hypertensive rats (SHR) in whom decompensation was induced by administering a low dose of the -AR agonist, isoproterenol (ISO) for 4.5 months. ISO administration resulted in an increased urinary aldosterone excretion and LV cavity dimensions, a right shift in LV diastolic pressure-volume relations, and a decreased LV relative wall thickness without further enhancing an increased myocardial norepinephrine (NE) release in SHR. ISO reduced LV systolic chamber function (decreased LV endocardial fractional shortening and the slope of the LV systolic pressure- volume relationship) without modifying intrinsic myocardial systolic function (as assessed from LV midwall fractional shortening and the slope of systolic stress-strain relationship). SPIRO abolished ISO-induced chamber dilatation, wall thinning and systolic dysfunction, but failed to modify blood pressure, volume preloads, intrinsic myocardial systolic function, or myocardial NE release. These results suggest that MR activation, through load-independent effects, may be critical in mediating the transition from compensated hypertensive LVH to dilatation and LV systolic chamber dysfunction. In SHR, ISO increased myocardial matrix metalloproteinase (MMP)-2 activity (zymography) after only 4-5 days of administration, a change that was associated with MMP-2, but not TIMP expression. The increased MMP-2 activity persisted until 4.5 months of the study and these changes were prevented by SPIRO. At 4.5 months, ISO resulted in increased non-cross-linked, but not cross-linked myocardial collagen concentrations in SHR, an effect that was abolished by SPIRO. Although at 4.5 months ISO administration was not associated with an increased cardiomyocyte apoptosis (TUNEL), an early (4-5 days) ISO-induced apoptotic effect was noted, which was prevented by SPIRO. Neither ISO nor SPIRO influenced cardiomyocyte length (image analysis and flow cytometry) in SHR. Thus MR blockade may prevent the adverse effects of β-AR activation in hypertensive LVH through alterations in the cardiac interstitium and cardiomyocyte apoptosis. Six-to-seven months after ligation of the left anterior descending coronary artery, LV myocardial systolic function as assessed from % shortening of the non-infarcted lateral wall segmental length determined over a range of filling pressures (ultrasonic transducers placed in the lateral wall in anaesthetized, open-chest, ventilated rats) and % thickening of the posterior wall (echocardiography) was reduced in infarcted SHR (SHR-MI) (p<0.05), but not in normotensive Wistar Kyoto (WKY-MI) animals as compared to corresponding controls (SHR-Sham, WKY-Sham). This change in regional myocardial function in SHR-MI, but not in WKY- MI, occurred despite a similar degree of LV dilatation in SHR-MI and WKY-MI rats and a lack of difference in LV relative wall thinning, LV wall stress, apoptosis (TUNEL) or necrosis (pathological score) between SHR-MI and WKY-MI rats. Although the change in regional myocardial function in the SHR-MI group was not associated with a greater reduction in resting global LV chamber systolic function (endocardial fractional shortening-FSend and end-systolic elastance [LV Ees] determined in the absence of an adrenergic stimulus), in the presence of an ISO challenge a reduction in LV Ees in SHR-MI compared to WKY-MI and SHR and WKY-Sham rats was noted (p<0.04). These data suggest that with chronic MI, the hypertensive heart is susceptible to development of viable tissue myocardial dysfunction, a change which cannot be attributed to excessive chamber dilatation, apoptosis or necrosis, but which in-turn, contributes toward a reduced cardiac adrenergic-inotropic reserve. The present thesis therefore suggests that MR blockade may prevent the transition from hypertensive LVH to systolic chamber decompensation, and that pre-existing hypertensive LVH increases the susceptibility to a depressed LV regional myocardial systolic function in the non-infarcted LV myocardium subsequent to MI, an effect that translates into a reduced inotropic reserve.

Includes bibliographical references (21 leaves). Previous studies have found that green tea and its antitoxidant constituents, the catechins, are hypocholesterolaemic in both epidemiological and animal intervetion studies. The main objectives of the present study were to investigate the mechanism by which green tea and its most abundant catechin constituent epigallocatechin gallate increase the low-density lipoprotein (LDL) receptor of HepG2 cells. In addition, it was hoped to determine if a crude catechin extract from green tea could lower plasma cholesterol levels in the hypercholesterolaemic rabbit and ascertain if this effect was due to an increase in the LDL receptor. The study provides evidence that green tea and its catechins exhibit hypocholesterolaemic properties and may therefore provide protection against heart disease.

Includes bibliographical references (21 leaves). / 1 v. (various pagings) : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Previous studies have found that green tea and its antitoxidant constituents, the catechins, are hypocholesterolaemic in both epidemiological and animal intervetion studies. The main objectives of the present study were to investigate the mechanism by which green tea and its most abundant catechin constituent epigallocatechin gallate increase the low-density lipoprotein (LDL) receptor of HepG2 cells. In addition, it was hoped to determine if a crude catechin extract from green tea could lower plasma cholesterol levels in the hypercholesterolaemic rabbit and ascertain if this effect was due to an increase in the LDL receptor. The study provides evidence that green tea and its catechins exhibit hypocholesterolaemic properties and may therefore provide protection against heart disease. / Thesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 2000

Graduation date: 1994

published_or_final_version / Nursing Studies / Master / Master of Nursing

Background: Research studies in recent years suggested possible role of dark chocolate in preventing cardiovascular diseases due to its high flavonal and procyanidins contents. Whether there is clear clinical benefit and the mechanisms mediating such benefits is controversial. Objective: This systematic review aims to comprehensively examine the current clinical evidence regarding effectiveness and the possible mechanisms of chocolate in reducing the risk and / or surrogate markers of cardiovascular diseases. Methods: Comprehensive electronic literature search was performed using Ovid, Medline and Cochrane database. Only English language literatures published during year 1950 - 2010 were reviewed. All intervention studies and observational studies of adult human subjects taking white or dark chocolate in relation to outcomes of cardiovascular risk were included. All review articles and meta-analysis were also included. Clinical diagnosis of cardiovascular disease and surrogate markers including blood pressure, vascular endothelial function as measured by flowed mediated vasodilation, and blood biomarkers such as lipid profile were studied as outcome variables. Results: The review outlines recent observational and interventional studies and meta-analysis to give an overview of the topic. For observational studies, a cohort studies and two case control studies were found. The observational studies showed that dark chocolate consumption was inversely associated with blood pressure, cardiovascular mortality and C-reactive protein. All interventional studies searched showed that dark chocolate increased FMD and improved platelet function. However, the effects of cocoa on intermediate outcomes such as blood pressure, antioxidant capacity and inflammatory marker changes were inconsistent among interventional studies. Three interventional studies indicated that there was a dose-dependent improvement in immediate outcome variables after 1 month or even 2 hours acute consumption of dark chocolate with procyanidins or cocoa drink with flavonol. However, publication bias and potential conflict of interests may be a potentially important factor in interpreting study results in the current literature. Conclusions: There are some clinical and scientific evidences that consumption of dark chocolate produces positive cardiovascular benefits. A small amount of dark chocolate may be good for the heart. However, gaps in our knowledge such as a lack of long-term RCT in clinical outcomes must be filled in before recommending habitual dark chocolate consumption for reduction of cardiovascular risk. / published_or_final_version / Community Medicine / Master / Master of Public Health