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Biomedical subjects

S P Jones

Publications and source records attributed to S P Jones.

At least 19 recordsLinked to original sources
PubMed2003

A clinical investigation of force delivery systems for orthodontic space closure.

OBJECTIVE: To investigate the force retention, and rates of space closure achieved by elastomeric chain and nickel titanium coil springs. DESIGN: Randomized clinical trial. SETTING: Eastman Dental Hospital, London and Queen Mary's University Hospital, Roehampton, 1998-2000. SUBJECTS, MATERIALS AND METHODS: Twenty-two orthodontic patients, wearing the pre-adjusted edgewise appliance undergoing space closure in opposing quadrants, using sliding mechanics on 0.019 x 0.025-inch posted stainless steel archwires. Medium-spaced elastomeric chain [Durachain, OrthoCare (UK) Ltd., Bradford, UK] and 9-mm nickel titanium coil springs [OrthoCare (UK) Ltd.] were placed in opposing quadrants for 15 patients. Elastomeric chain only was used in a further seven patients. The initial forces on placement and residual forces at the subsequent visit were measured with a dial push-pull gauge [Orthocare (UK) Ltd]. Study models of eight patients were taken before and after space closure, from which measurements were made to establish mean space closure. MAIN OUTCOME MEASURES: The forces were measured in grammes and space closure in millimetres. RESULTS: Fifty-nine per cent (31/53) of the elastomeric sample maintained at least 50 per cent of the initial force over a time period of 1-15 weeks. No sample lost all its force, and the mean loss was 47 per cent (range: 0-76 per cent). Nickel titanium coil springs lost force rapidly over 6 weeks, following that force levels plateaued. Forty-six per cent (12/26) maintained at least 50 per cent of their initial force over a time period of 1-22 weeks, and mean force loss was 48 per cent (range: 12-68 per cent). The rate of mean weekly space closure for elastomeric chain was 0.21 mm and for nickel titanium coil springs 0.26 mm. There was no relationship between the initial force applied and rate of space closure. None of the sample failed during the study period giving a 100 per cent response rate. CONCLUSIONS: In clinical use, the force retention of elastomeric chain was better than previously concluded. High initial forces resulted in high force decay. Nickel titanium coil springs and elastomeric chain closed spaces at a similar rate.

Adolescent↗
PubMed2002

The effects of reconditioning on the slot dimensions and static frictional resistance of stainless steel brackets.

This study investigated the effects of reconditioning on the slot dimensions and the static frictional resistance of stainless steel brackets at 0, 5, and 10 degrees bracket/archwire angulation. A sample of 45 used, commercially reconditioned 0.018 x 0.030 inch stainless steel standard edgewise brackets was compared with a matched sample of 45 new brackets. The slot dimensions of 15 new and 15 reconditioned brackets were examined using a photomicroscope. With new brackets both the occluso-gingival slot width (mean = 0.0197 inch) and slot depth (mean = 0.0304 inch) exceeded the manufacturer's nominal dimensions of 0.018 x 0.030 inch. The reconditioning process resulted in a further increase in slot width (mean = 0.0205 inch), which was statistically significant (P = 0.028), and a reduction in slot depth (mean = 0.0291 inch), which was highly statistically significant (P = 0.002). This may be attributable to preferential metal removal by the electro-polishing phase of the reconditioning process. Friction testing of 30 new and 30 reconditioned brackets demonstrated that both showed an increase in binding effects as the bracket/archwire angulation was increased from 0 to 5-10 degrees. However, the changes in slot dimensions secondary to reconditioning did not result in a statistically significant difference in mean static frictional resistance when the two bracket types were compared. Although the brackets were altered physically by the reconditioning process, their performance during simulated sliding mechanics was not adversely affected. This implies that reconditioning may not result in clinically significant effects.

Dental Polishing↗
PubMed2001

Short-term exercise training improves body composition and hyperlipidaemia in HIV-positive individuals with lipodystrophy.

Exercise/physical activity is increasingly being advocated as a positive addition to the treatment regimen of HIV-positive individuals. We investigated the effects of 10 weeks' aerobic and resistance training on individuals with HIV-related lipodystrophy. These individuals demonstrated an improvement in exercise tolerance, body composition and blood lipid profiles. Potentially, such changes may contribute to an amelioration of some of the adverse metabolic effects associated with highly active antiretroviral therapy.

Adult↗
PubMed2001

Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function.

Up-regulation of proapoptotic genes has been reported in heart failure and myocardial infarction. To determine whether caspase genes can affect cardiac function, a transgenic mouse was generated. Cardiac tissue-specific overexpression of the proapoptotic gene Caspase3 was induced by using the rat promoter of alpha-myosin heavy chain, a model that may represent a unique tool for investigating new molecules and antiapoptotic therapeutic strategies. Cardiac-specific Caspase3 expression induced transient depression of cardiac function and abnormal nuclear and myofibrillar ultrastructural damage. When subjected to myocardial ischemia-reperfusion injury, Caspase3 transgenic mice showed increased infarct size and a pronounced susceptibility to die. In this report, we document an unexpected property of the proapoptotic gene caspase3 on cardiac contractility. Despite inducing ultrastructural damage, Caspase3 does not trigger a full apoptotic response in the cardiomyocyte. We also implicate Caspase3 in determining myocardial infarct size after ischemia-reperfusion injury, because its cardiomyocyte-specific overexpression increases infarct size.

Animals↗
PubMed2001

Simvastatin exerts both anti-inflammatory and cardioprotective effects in apolipoprotein E-deficient mice.

BACKGROUND: Simvastatin attenuates ischemia and reperfusion in normocholesterolemic animals by stabilizing endothelial nitric oxide synthase activity and inhibiting neutrophil-mediated injury. Because endothelial dysfunction is a detrimental effect of hypercholesterolemia, we examined whether short-term treatment with simvastatin could inhibit leukocyte-endothelium interaction and attenuate myocardial ischemia-reperfusion injury in apoE-deficient (apoE(-/-)) mice fed a high-cholesterol diet. METHODS AND RESULTS: We studied leukocyte-endothelium interactions in apoE(-/-) mice fed a normal or a high-cholesterol diet after short-term (ie, 18 hours) simvastatin treatment. We also studied simvastatin treatment in myocardial ischemia-reperfusion injury by subjecting apoE(-/-) mice to 30 minutes of ischemia and 24 hours of reperfusion. ApoE(-/-) mice fed a high-cholesterol diet exhibited higher blood cholesterol levels, which were not affected by short-term simvastatin treatment. However, the increased leukocyte rolling and adherence that occurred in cholesterol-fed apoE(-/-) mice (P<0.001 versus control diet) were significantly attenuated by simvastatin treatment (P<0.01 versus vehicle). Cholesterol-fed apoE(-/-) mice subjected to myocardial ischemia-reperfusion also experienced increased myocardial necrosis (P<0.01 versus control diet), which was significantly attenuated by simvastatin (P<0.01 versus vehicle). Simvastatin therapy also significantly increased vascular nitric oxide production in apoE(-/-) mice. CONCLUSIONS: Simvastatin attenuates leukocyte-endothelial cell interactions and ameliorates ischemic injury in hypercholesterolemic mice independently of lipid-lowering actions.

Animals↗
PubMed2001

Cardioprotective actions of acute HMG-CoA reductase inhibition in the setting of myocardial infarction.

A known risk factor for the development of coronary artery disease and subsequent myocardial infarction is hypercholesterolaemia. The widespread nature of this phenomenon in the western world has led to the development of agents which reduce serum cholesterol levels. One such class of agents, HMG-CoA reductase inhibitors (statins) are very effective in cholesterol reduction. Recently, clinical and experimental evidence has amassed suggesting that patients taking statins receive cardiovascular benefits that occur independent of cholesterol reduction. Experimental data suggest that statins may increase levels of nitric oxide (NO) in vivo. This review will address the 'cholesterol-independent' vasculoprotective and cardioprotective effects of statins in animal models. Upon completion, the reader will be familiar with the proposed cholesterol-independent pathways of statins and understand that the cholesterol-independent benefits may arise from enhanced production of NO.

Animals↗
PubMed2001

Root resorption in retained deciduous canine and molar teeth without permanent successors in patients with severe hypodontia.

AIMS: The ability to predict the morbidity of retained deciduous teeth with no permanent successors, a characteristic of hypodontia, would be of considerable value in treatment planning, but is hampered by lack of data. METHODS: This problem was studied using 356 orthopantomogram radiographs (OPGs) from the records of 249 patients who had attended a specialist hypodontia clinic, and had retained deciduous teeth with no permanent successors. Due to their clinical importance, canine and molar teeth were chosen for examination. Resorption was assessed subjectively by three experienced clinicians. RESULTS: Un-weighted Kappa values for reproducibility were > 0.8, and for interobserver error 0.60-0.83. Gender related differences were minimal. Regardless of gender or radiographic age, the lower canines appear to show the least amount of resorption and the upper first molars the most. The upper and lower second molars have particularly unpredictable life spans. Whilst the lower first molars have a predictable life span that is poor, the life span for the upper first molars is slightly worse. CONCLUSIONS: Lower canines have a predictable life span that appears to be good, as do upper canines, but of lesser duration than lower canines. Molars have poorer and less predictable life spans.

Adolescent↗
PubMed2001

An ex vivo investigation into the fluoride release and absorption profiles of three orthodontic adhesives.

Prevention of peri-bracket decalcification is essentially mediated by effective oral hygiene, which is patient dependent. The potential to compensate for poor oral hygiene may be through the release of free fluoride ions from direct bonding agents. It is well established that glass ionomer cements (GICs) release free fluoride ions which may be replenished by exposure to fluoride containing solutions. The aim of this ex vivo study was to compare the fluoride release and absorption profiles of a recently developed low fusion, monophase GIC, Limerick glass, with two materials in common clinical use, namely, Fuji-Ortho L.C. and Concise. Ten test specimens of each material were fabricated and stored in deionized water at 37 degrees C. The concentration of fluoride release was measured daily for the first 7 days after immersion and then weekly for 5 weeks. On day 42 the test specimens were recharged in 2 per cent sodium fluoride solution and fluoride release was measured initially after 24 hours and then every 48 hours. The recharge regimen was repeated for 3 weeks. Both Limerick glass and Fuji-Ortho L.C. demonstrated the characteristic fluoride release pattern of GIC with a rapid elution of fluoride after the first 24 hours followed by a more gradual release profile over the following 2 weeks. Fuji-Ortho L.C. released the greatest quantity of fluoride but the release profile of Limerick glass was more sustained. Concise released negligible amounts of fluoride. Limerick glass and Fuji-Ortho L.C. showed an increase (P < 0.01) in fluoride release following exposure to 2 per cent sodium fluoride that decreased both with time and subsequent exposures to fluoride supplement.

Absorption↗
PubMed2001

Acute exposure to a high cholesterol diet attenuates myocardial ischemia-reperfusion injury in cholesteryl ester transfer protein mice.

BACKGROUND: Previous experiments have demonstrated that acute exposure to a high-cholesterol diet (HCD) increases the severity of myocardial infarction in animals. Recent results suggest that the process is modulated by multiple genes and their interactions with circulating cholesterol. DESIGN: In the present study cholesteryl-ester-transfer-protein (CETP) transgenic mice were generated and fed a normal rodent-chow diet, HCD for 1 week, or a HCD for 6 weeks in order to define the role of CETP in myocardial infarction after acute exposure to a HCD. METHODS: Cholesterol levels in mice of all groups were measured. Separate groups of mice were exposed to 30 min of in-vivo occlusion of coronary artery and 2 h of reperfusion. We assessed the sizes of the ischemic zone and infarct using Evans blue and 2,3,5-triphenyltetrazolium chloride. RESULTS: The extent of infarction (percentage infarct/area at risk) was significantly less (P < 0.05) after 1 week of a HCD (18.7 +/- 7.0%) than those for the normal diet group (51.4 +/- 5.5%) and the group fed a HCD for 6 weeks (44.4 +/- 5.2%). Additionally, there was significantly less infiltration of neutrophils into the ischemic-reperfused mouse hearts for mice fed a HCD for 1 week. Levels of reduced and oxidized glutathione in the hearts of CETP mice were measured for separate groups of animals. The reduced:oxidized-glutathione ratio was significantly (P < 0.01) lower for mice fed a HCD for 1 week (1.5 +/- 0.1) than it was for mice fed a normal diet (3.6 +/- 0.3) and a HCD for 6 weeks (3.3 +/- 0.2). CONCLUSIONS: These data suggest that activity of CETP in hypercholesterolemic mice has an acute effect on size of infarct after 1 week of a HCD. This suggests that CETP induces tolerance of ischemia in the mice fed a HCD via mild oxidative stress.

Animals↗
PubMed2001

CD8(+)-T-cell depletion ameliorates circulatory shock in Plasmodium berghei-infected mice.

The Plasmodium berghei-infected mouse model is a well-recognized model for human cerebral malaria. Mice infected with P. berghei exhibit (i) metabolic acidosis (pH < 7.3) associated with elevated plasma lactate concentrations, (ii) significant (P < 0.05) vascular leakage in their lungs, hearts, kidneys, and brains, (ii) significantly (P < 0.05) higher cell and serum glutamate concentrations, and (iv) significantly (P < 0.05) lower mean arterial blood pressures. Because these complications are similar to those of septic shock, the simplest interpretation of these findings is that the mice develop shock brought on by the P. berghei infection. To determine whether the immune system and specifically CD8(+) T cells mediate the key features of shock during P. berghei malaria, we depleted CD8(+) T cells by monoclonal antibody (mAb) treatment and assessed the complications of malarial shock. P. berghei-infected mice depleted of CD8(+) T cells by mAb treatment had significantly reduced vascular leakage in their hearts, brains, lungs, and kidneys compared with infected controls treated with rat immunoglobulin G. CD8-depleted mice were significantly (P < 0.05) protected from lactic acidosis, glutamate buildup, and diminished HCO(3)(-) levels. Although the blood pressure decreased in anti-CD8 mAb-treated mice infected with P. berghei, the cardiac output, as assessed by echocardiography, was similar to that of uninfected control mice. Collectively, our results indicate that (i) pathogenesis similar to septic shock occurs during experimental P. berghei malaria, (ii) respiratory distress with lactic acidosis occurs during P. berghei malaria, and (iii) most components of circulatory shock are ameliorated by depletion of CD8(+) T cells.

Acidosis, Lactic↗
PubMed2001

Cardioprotective actions of endogenous IL-10 are independent of iNOS.

Myocardial ischemia-reperfusion (I/R) is a well-known stimulus for acute inflammatory responses that promote cell death and impair pump function. Interleukin-10 (IL-10) is an endogenous, potent anti-inflammatory cytokine. Recently, it has been proposed that IL-10 inhibits inducible nitric oxide synthase (iNOS) activity after myocardial I/R and consequently exerts cardioprotective effects. However, whether this actually occurs remains unclear. To test this hypothesis, we utilized iNOS-deficient (-/-), IL-10 -/-, and IL-10/iNOS -/- mice to examine the potential mechanism of IL-10-mediated cardioprotection after myocardial I/R. Wild-type, iNOS -/-, IL-10 -/-, and IL-10/iNOS -/- mice were subjected to in vivo myocardial ischemia (30 min) and reperfusion (24 h). Deficiency of iNOS alone did not significantly alter the extent of myocardial necrosis compared with wild-type mice. We found that deficiency of IL-10 resulted in a significantly (P < 0.05) larger infarct size than that in wild-type hearts. Interestingly, deficiency of both IL-10 and iNOS yielded significantly (P < 0.01) larger myocardial infarct sizes compared with wild-type animals. Histological examination of myocardial tissue samples revealed augmented neutrophil infiltration into the I/R myocardium of IL-10 -/- and IL-10/iNOS -/- mice compared with hearts of wild-type mice. These results demonstrate that 1) deficiency of endogenous IL-10 exacerbates myocardial injury after I/R; 2) the cardioprotective effects of IL-10 are not dependent on the presence or absence of iNOS; and 3) deficiency of IL-10 enhances the infiltration of neutrophils into the myocardium after I/R.

Animals↗
PubMed2001

Pretreatment with simvastatin attenuates myocardial dysfunction after ischemia and chronic reperfusion.

We have previously demonstrated that simvastatin attenuates myocardial cell necrosis after acute myocardial ischemia and reperfusion via induction of endothelial cell NO synthase. However, it remains unknown whether the cardioprotective effects of statins can persist after extended periods of reperfusion. Furthermore, it is unknown whether simvastatin therapy can attenuate postischemic cardiac dysfunction. Pretreatment with simvastatin attenuated myocardial injury after 30 minutes of myocardial ischemia and 24 hours of reperfusion. However, the protective effects are not recognized unless simvastatin is given at least 3 hours before myocardial ischemia. Subsequently, we pretreated mice with vehicle or simvastatin and subjected the mice to 30 minutes of myocardial ischemia and 6 months of reperfusion. Myocardial infarct size (percentage of left ventricle) was significantly reduced by 51% in the simvastatin-treated group compared with the vehicle-treated group. Left ventricular diastolic and systolic dilatation was significantly (P<0.05) reduced in simvastatin-treated mice compared with vehicle-treated mice. Additionally, the decrement in fractional shortening after 6 months of reperfusion was minimized in simvastatin-treated mice (P=NS versus baseline) compared with vehicle-treated mice (P<0.05 versus baseline). Left ventricular end-diastolic pressure was significantly (P<0.01) elevated in vehicle-treated mice (21+/-4 mm Hg) but not simvastatin-treated mice (5+/-2 mm Hg) compared with baseline values. These data demonstrate that simvastatin treatment before myocardial ischemia attenuates infarct size and preserves myocardial function after chronic reperfusion in mice.

Animals↗
PubMed2000

The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice.

Members of the mitogen-activated protein kinase (MAPK) cascade such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 are implicated as important regulators of cardiomyocyte hypertrophic growth in culture. However, the role that individual MAPK pathways play in vivo has not been extensively evaluated. Here we generated nine transgenic mouse lines with cardiac-restricted expression of an activated MEK1 cDNA in the heart. MEK1 transgenic mice demonstrated concentric hypertrophy without signs of cardiomyopathy or lethality up to 12 months of age. MEK1 transgenic mice showed a dramatic increase in cardiac function, as measured by echocardiography and isolated working heart preparation, without signs of decompensation over time. MEK1 transgenic mice and MEK1 adenovirus-infected neonatal cardiomyocytes each demonstrated ERK1/2, but not p38 or JNK, activation. MEK1 transgenic mice and MEK1 adenovirus-infected cultured cardiomyocytes were also partially resistant to apoptotic stimuli. The results of the present study indicate that the MEK1-ERK1/2 signaling pathway stimulates a physiologic hypertrophy response associated with augmented cardiac function and partial resistance to apoptotsis.

Actinin↗
PubMed2000

Myocardial ischemia/reperfusion injury in NADPH oxidase-deficient mice.

Previous studies have suggested that oxygen-derived free radicals are involved in the pathophysiology of myocardial ischemia/reperfusion (MI/R) injury. Specifically, neutrophils have been shown to mediate postischemic ventricular arrhythmias and myocardial necrosis. We hypothesized that MI/R injury would be reduced in the absence (-/-) of NADPH oxidase. Heterozygous control mice (n=23) and NADPH oxidase(-/-) mice (n=24) were subjected to 30 minutes of coronary artery occlusion and 24 hours of reperfusion. Myocardial area at risk per left ventricle was similar in heterozygous control hearts (55+/-3%) and NADPH oxidase(-/-) hearts (61+/-4%). Contrary to our hypothesis, the size of infarct area at risk was similar in the heterozygous control mice (42+/-4%) and NADPH oxidase(-/-) mice (34+/-5%) (P=not significant). In addition, echocardiographic examination of both groups revealed that left ventricle fractional shortening was similar in NADPH oxidase(-/-) mice (n=8; 27+/-2.5%) and heterozygous control mice (n=10; 23.3+/-3. 3%) after MI/R. Superoxide production, as detected by cytochrome c reduction, was significantly impaired (P<0.01) in NADPH oxidase(-/-) mice (n=6) compared with heterozygous mice (n=7) (0.04+/-0.03 versus 2.2+/-0.08 nmol O(2).min(-1).10(6) cells(-1)). Intravital microscopy of the inflamed mesenteric microcirculation demonstrated that leukocyte rolling and adhesion were unaffected by the absence of NADPH oxidase. Oyster glycogen-stimulated neutrophil transmigration into the peritoneum was also similar in both the heterozygous control mice and NADPH oxidase(-/-) mice (P:=not significant). These findings suggest that NADPH oxidase does not contribute to the development of myocardial injury and dysfunction after MI/R.

Animals↗
PubMed2000

Myocardial reperfusion injury in neuronal nitric oxide synthase deficient mice.

BACKGROUND: A substantial amount of data suggesting that endothelial cell nitric oxide synthase (eNOS) plays a cardioprotective role in animal models of ischemia-reperfusion injury has amassed. We have previously demonstrated that eNOS-deficient (-/-) mice exhibit significantly larger myocardial infarcts than do wild-type mice. Few investigations have examined the neuronal form of nitric oxide synthase in the heart. The two constitutive isoforms have been demonstrated to play differing roles in studies of cerebral ischemia-reperfusion. OBJECTIVE: To characterize the role of neuronal nitric oxide synthase (nNOS) in myocardial ischemia-reperfusion injury. METHODS: Wild-type and nNOS -/- mice were subjected to 20 min of coronary artery occlusion and 120 min of reflow. RESULTS: We found no significant difference between the two groups in terms of infarct size. Microscopic cross-sections from both groups were examined for infiltration of polymorphonuclear leukocyte. Hearts of nNOS -/- mice exhibited significantly (P < 0.05) more polymorphonuclear leukocytes than did hearts of wild-type mice. CONCLUSION: Despite the fact that eNOS plays a cardioprotective role in the ischemic-reperfused myocardium, we observed no change in size of myocardial infarcts when nNOS was genetically disrupted.

Animals↗