Biomedical subjects
Publications and source records attributed to S C Smith.
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Reactive oxygen and nitrogen intermediates (ROI, RNI), such as superoxide anion, nitric oxide (NO) and peroxynitrite, are present in villous trophoblasts and mediate TNF-alpha-induced apoptosis in other cell types. We therefore proposed that ROI/RNI mediate cytokine-induced apoptosis of cultured villous cytotrophoblasts. Treatment of cultures of highly purified term cytotrophoblasts with TNF-alpha and IFN-gamma had no effect on NO synthase (NOS) protein expression measured by immunoblot analysis: iNOS was not expressed and eNOS expression was unaffected. NO production assessed by nitrite levels was below detection limits of the Griess reaction and the NOS inhibitors L-NAME and L-NMMA did not decrease cytokine-stimulated apoptosis. Trophoblasts produced ROI and expressed Cu/Zn superoxide dismutase (SOD) protein but neither was affected by cytokine treatment. ROI scavengers (exogenous SOD, ascorbic acid and butylated hydroxyanisole) also had no effect on cytokine-stimulated apoptosis. Nitrotyrosine immunoblot analysis indicated peroxynitrite production but again cytokines did not reproducibly alter expression patterns or band intensities. Exogenous peroxynitrite stimulated cytotrophoblast apoptosis but only at high levels (1000 microM). We conclude that, although present in cultured villous cytotrophoblasts, ROI/RNI are not induced by TNF-alpha and IFN-gamma and do not mediate cytokine-induced apoptosis.
OBJECTIVE: The purpose of this in vitro study was to evaluate the potential use of pulsed CO2 laser radiation to remove selectivity residues of orthodontic bonding resin that remain after debonding of fixed orthodontic appliances. SUMMARY BACKGROUND DATA: Current techniques used for removal of orthodontic bonding resin after removal of fixed appliances include rotary instruments, debonding pliers, and ultrasonic scalers. These techniques, however, are time-consuming and inefficient, and may damage tooth enamel. METHODS: A standardized cylinder of orthodontic bonding resin was bonded to the buccal surfaces of 100 extracted premolar teeth, which were then divided into 10 groups of 10 specimens each. In 9 groups, the resin was ablated using 1 of 9 different laser parameters, while in the remaining control group, the resin was removed with a slow speed tungsten carbide bur. Specimens were evaluated by light microscopy and scanning electron microscopy (SEM) to assess the amount of resin remaining and the extent of the damage to the underlying enamel. RESULTS: The 2 W/100 ms combination was optimal, with a high efficiency of resin removal and the least enamel damage. Higher laser powers increased the extent of enamel damage without enhancing resin removal. CONCLUSIONS: This laser technique appears promising, however, further studies of the extent of thermal changes at the level of the dental pulp are necessary to establish more fully the risk-benefit ratio.
Trophoblasts, the fetal cells that line the villous placenta and separate maternal blood from fetal tissue, express both Fas antigen and the tumor necrosis factor (TNF) receptor p55 (TNFRp55), two members of the TNF receptor family that contain a cytoplasmic "death domain" that mediates apoptotic signals. We show that Fas mRNA expressed by cultured villous cytotrophoblasts isolated from term placentas encodes transmembrane sequences and that the protein is full-length (approximately 45 kDa), suggesting that the product is an active plasma membrane-anchored receptor. Its location on the cell surface was confirmed by cellular ELISA analysis of live cells. Although cytotrophoblast apoptosis was induced by TNFalpha, and both anti-Fas antibody (CH11) and FasL-expressing T lymphocyte hybridoma (activated A1.1) cells induced HeLa cell apoptosis, neither CH11 antibody nor activated A1.1 cells stimulated apoptosis in term or first-trimester cytotrophoblasts or in term syncytiotrophoblasts. We conclude that Fas- but not TNFRp55-mediated apoptosis is blocked in primary villous trophoblasts. These data suggest that the Fas response is specifically inactivated by unknown mechanisms to avoid autocrine or paracrine killing by Fas ligand constitutively expressed on neighboring cyto- or syncytiotrophoblasts.
Compelling evidence from clinical trials confirms the benefits of secondary prevention for patients with known coronary disease. Preventive therapies initiated after myocardial infarction can extend overall survival, reduce subsequent myocardial infarction, decrease the need for revascularization, and improve quality of life. All patients with atherosclerotic cardiovascular disease should be considered for lipid lowering therapy, antiplatelet agents, beta-blockers, and control of hypertension. Long-term therapy with angiotensin-converting enzyme inhibitors should be continued in patients with systolic dysfunction. Hormone replacement therapy has not been shown to benefit postmenopausal women when initiated after myocardial infarction. Smoking cessation, weight control, exercise, and appropriate diet represent important behavioral modifications.
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We compared the quality of reference measurements for serum potassium in four reference laboratories from three different European countries, using a panel of 60 native patients' samples. The reference methods were based on either ion chromatography (one laboratory) or flame atomic emission spectrometry (three laboratories). Performance specifications for serum potassium measurements were defined as a maximum overall coefficient of variation (CV) of 1.5%, a maximum bias of 0.65% and a maximum total error of 3.0%. The overall imprecision for all laboratories was in the range of 0.7 to 1.3%, and was thus below the proposed specification of 1.5%. However, two laboratories reported 12 and 13 quadruplicates with CVs exceeding this limit. The mean bias (expressed as deviation from the overall mean of all laboratories) for all reference laboratories was < 0.65%. In the lower concentration range, however, one laboratory exceeded this limit. No laboratory measured samples with a total error above 3.0%. From these results, it can be concluded that the reference measurements, and, thus, also the reference methodologies, based on ion chromatography and flame atomic emission spectrometry were equivalent, and able to satisfy current analytical specifications for serum potassium measurements.
Cardiovascular disease remains the number one killer in the United States, despite advances made in diagnosis and therapy. A major shift to expand treatment beyond symptomatic obstructions and infarctions toward comprehensive therapies aimed at treatment of the underlying disease process could decrease the death rate and cost of cardiovascular disease enormously. In the past 5 years, major trials have clearly demonstrated that aggressive intervention with lipid-lowering therapy can dramatically alter the course of disease. Aspirin, smoking cessation, exercise, diet, and other medical and lifestyle interventions can also decrease risk. Successful therapies are not being implemented, however. Making prevention the primary approach to treatment will require increased resource allocation, use of health provider teams, integration of healthcare delivery systems, and expanded emphasis on educating patients about prevention.
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More than 13 million individuals have coronary artery disease (CAD), and in approximately 2 million patients with congestive heart failure, CAD is the underlying cause. The cost of treating cardiovascular disease has spiraled, yet only a small percentage of the total cost is spent on preventive medical therapies and lifestyle changes that can reduce the morbidity, mortality, and disability caused by heart disease. Recent trials of cholesterol-lowering therapies have clearly shown that this treatment approach, particularly the use of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, can significantly reduce mortality from cardiovascular events and the need for expensive hospitalization and revascularization procedures. The challenge for clinicians is to apply the important lessons learned from these clinical trials to patient care. Recent data indicate that less than half of patients with CAD receive cholesterol-lowering therapy, and few meet the low-density lipoprotein (LDL) cholesterol goal. Clinicians treating CAD need to emphasize primary and secondary prevention and recognize the key role of cholesterol-lowering therapy.
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Fourteen-day-old chickens were inoculated with selected Campylobacter coli and C. jejuni strains. C. jejuni strains were of two subgroups based on a polymorphism detected using a DNA probe and represented the profiles typical for the majority of strains of either chicken or human origin. All C. coli strains previously isolated from humans colonised chickens, whereas from 4/7 C. jejuni strains of human origin, failed to colonise. Of 12 Campylobacter strains of chicken origin, 10 established a persistent colonisation in the chickens, and 2 strains colonised poorly or not at all. Four strains that failed to colonise chickens were each inoculated into groups of five birds. Three strains again did not colonise any of the chickens and the fourth strain colonised four out of the five chickens, but was poorly excreted. When infected chickens were placed in the same enclosure to facilitate interchange of strains, C. jejuni strain 331 was found to be dominant and colonised all 12 chickens by 21 days, displacing all other strains. C. jejuni strain 331, was then inoculated into groups of five birds with previously established colonisation by C. jejuni and C. coli strains. Strain 331 was able to replace the C. jejuni strain in all five birds but established co-colonisation with C. coli strain. Naturally occurring co-colonisation by two C. jejuni strains was detected in one chicken out of 200 tested. There was no obvious correlation between the type of DNA polymorphism in strains of chicken origin and their ability to colonise chickens.
Recent decades have witnessed significant advances in the use of interventional procedures and medical therapies for relief of symptoms associated with obstructive coronary artery disease (CAD). At the same time, however, little progress has been made in understanding and implementing preventive therapy and risk reduction. Our traditional focus on treatment of severe coronary obstruction has addressed only part of the problem. We now need to adopt a more comprehensive approach aimed at the entire spectrum of atherosclerotic disease. Numerous clinical trials have demonstrated that risk-reduction strategies can produce marked decreases in the incidence of cardiovascular events as well as in total mortality. Despite this strong body of evidence, risk-reduction therapies continue to be underutilized. Comprehensive changes in healthcare delivery systems are needed to ensure that risk-reduction strategies become a routine part of care for patients with cardiovascular disease.
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Ventricular free-wall rupture is a well-known catastrophic complication of acute myocardial infarction. A significant number of patients present in a subacute fashion and can be successfully treated with surgery if diagnosed promptly. We present a case of subacute free-wall rupture that occurred after an undiagnosed myocardial infarction. The findings at pericardiocentesis were unusual in that the fluid was sanguinous but not frank hemopericardium. This patient represents the first known reported case to present without frank hemopericardium who survived and was successfully treated surgically. The absence of frank hemopericardium should not exclude the diagnosis of free-wall rupture.