The effect of amalgam bonding on the stiffness of teeth weakened by cavity preparation.

OBJECTIVE: The objective of this study is to evaluate the effect of amalgam bonding on the stiffness of teeth weakened by cavity preparation. METHODS: Strain gages were bonded to maxillary premolars. The rigidity was tested by applying a load to a sequence of sound, prepared and restored teeth as follows: sound tooth, MOD preparation, amalgam restoration, amalgam removed recovering the MOD preparation, bonded amalgam restoration, bonded amalgam removed recovering the MOD preparation, bonded composite restoration. The relative stiffness (RS) and relative deformation (RD) of each condition for each cusp to that of the sound tooth was determined. RESULTS: The premolar cusps were deformed 1.80, 2.14, and 2.32 times more than the cusps of the sound tooth for the three succeeding MOD preparations. For these three preparations, the stiffness of the premolar cusps was 0.58, 0.48, and 0.46 relative to a stiffness of 1.00 for the sound tooth. The deformation was 1.77, 1.27, and 1.16 for the non-bonded amalgam, the bonded amalgam, and the bonded composite, respectively, corresponding to a mean RS of 0.59, 0.80, and 0.88. The calculated mean stiffness parameter C (standard deviation) was 2.6% (6.9) for the amalgam restoration, 62.5% (12.8) for the bonded amalgam restoration, and 77.8% (15.8) for the bonded composite restoration. The stiffness parameter C measured the extent to which the procedure returned the stiffness of the restored tooth to the original stiffness of the intact tooth (100%). SIGNIFICANCE: Cavity preparation reduced the stiffness and weakened the tooth. Restoring the prepared tooth with unbonded amalgam did not restore the lost tooth stiffness. Restoring the prepared tooth with bonded amalgam or with bonded composite recovered a significant portion of the lost tooth stiffness. It was concluded that bonding amalgam to tooth structure could partly restore the strength and rigidity lost by the cavity preparation. This might lead to a reduction in cuspal flexure and the incidence of tooth fracture due to fatigue.     

Evaluation of the integrated 3-hour plasma cortisol concentration as a test for Cushing's syndrome

Twenty-four hour urinary free cortisol and mean and integrated 13h00-16h00 plasma cortisol levels were measured in 9 patients with proven Cushing's syndrome (5 with Cushing's disease, 2 with ectopic adrenocorticotrophic hormone production due to bronchial carcinoma and 2 with adrenal adenomas) and in 21 patients without Cushing's syndrome. The 24-hour urinary free cortisol levels and mean and integrated 13h00-16h00 plasma cortisol estimations clearly distinguished patients with Cushing's syndrome from those without. However, adequate suppression on dexamethasone suppression tests (false negatives) were obtained in 3 of the 9 patients with Cushing's syndrome. Since the integrated 13h00-16h00 plasma cortisol estimation is cheaper and simpler than the mean 13h00-16h00 plasma cortisol estimation, we recommend it as an adjunct in the diagnosis of Cushing's syndrome.     

Glatiramer acetate in the treatment of multiple sclerosis

Glatiramer acetate is an immunomodulating drug used in the treatment of multiple sclerosis. It consists of a copolymer of amino acid residues in the same stoichiometric proportions as in myelin basic protein. Its mechanism of action is not entirely known and is probably multifaceted, with deletion of some immune cell populations and stimulation of others in these patients. Some mechanisms involve neuroprotectant effects. There is ample evidence of its efficacy in relapsing-remitting disease, using both clinical and imaging measures of disease activity, and in this paper we review the clinical and basic studies of this drug. Finally we discuss how some of its neuroprotectant effects may be useful in neurodegeneration such as is seen in more advanced cases of multiple sclerosis and other diseases such as amyotrophic lateral sclerosis and Parkinson’s disease.     

Absence of relaxation to lactate in human placental vessels of pregnancies with severe preeclampsia

OBJECTIVE: Our objective was to determine whether the observed relaxation to lactate and other agents in placental vessels of normal pregnancies is altered in severe preeclampsia.STUDY DESIGN: Isolated placental arteries and veins from women with severe preeclampsia and uncomplicated term pregnancies were precontracted with prostaglandin F_2α under 5% oxygen and 5% carbon dioxide with the balance nitrogen (Po₂ 35 to 38 torr) and then exposed to lactate (1 to 10 mmol/L, pH 7.4, n = 8 to 15), arachidonic acid (0.01 to 10 μmol/L, n = 6 to 13), nitroglycerin (1 nmol to 1 μmol/L, n = 4 to 12), or forskolin (0.01 to 10 μmol/L, n = 6 to 9). The response to lactate was also examined in placental vessels from appropriate-for-gestational-age preterm deliveries (n = 8) for comparison with a similar group with severe preeclampsia (n = 8). The t test and analysis of variance statistics were used.RESULTS: Relaxation to lactate was markedly inhibited in both placental arteries and veins of women with severe preeclampsia compared with vessels from uncomplicated term or preterm pregnancies. Responses to the other relaxing agents were not altered in the severely preeclampsia vessels.CONCLUSIONS: In severe preeclampsia absence of lactate-induced dilatation of placental vessels may contribute to the fetal complications associated with impaired blood flow and vasospasm.     

The heat shock/oxidative stress connection

Involvement of free-radical oxidations in the aging process has been a topic of interest since Harman's original contribution. Because of the close association between aging and Alzheimer disease (AD) and the qualitative similarity in the neuropathology of both conditions, it has been proposed by many investigators that oxidative stress may be important in AD. If such modality of injury was indeed involved, one should expect to find markers of oxidation and heat shock (since free radicals are key mediators of heat-shock induction) in brains of patients with AD. In fact, several studies documented abnormal expression of antioxidant enzymes and heat-shock proteins (HSP) along with other markers of oxidation in AD brains. We showed that abnormally expressed antioxidant enzymes are topographically associated with senile plaques and neurofibrillary tangles, and that the activity of these enzymes is (contrary to what one would expect) markedly reduced. These findings have recently been confirmed by other investigators. Despite a large amount of evidence that suggests an association between oxidative stress and the pathogenesis of AD, it is not yet known whether oxidative stress is a cause or consequence of the disorder. Future research efforts regarding the oxidative stress hypothesis of AD should include attempts, at generating AD pathology by oxidative means in laboratory animals, determining the role and integrity of the heat-shock response in AD, as well as that of various antioxidant systems, growth factors, and hormones with antioxidant and neuroprotective properties.     

Chlorinated hydrocarbon levels in human serum: Effects of fasting and feeding

Twenty healthy adult humans had serum samples drawn on four occasions within a 24-hr period: after a 12 hr overnight fast, 4–5 hr after a high fat breakfast, at midafternoon, and the next morning after another 12 hr fast. Nonfasting samples had 22% to 29% higher mean concentrations (p < 0.05) than did fasting samples for polychlorinated biphenyls (PCBs, 4.81 vs 3.74 ng/g serum wt), hexachlorobenzene (HCB, 0.163 vs 0.134 ng/g serum wt), andp,p-dichlorodiphenyldichloroethylene (p,p-DDE, 6.74 vs 5.37 ng/g serum wt) measured by electron capture gas liquid chromatography. Total serum lipids were estimated from measurements of total cholesterol, free cholesterol, triglycerides, and phospholipids and were 20% higher in nonfasting samples than in fasting samples (7.05 g/L vs 5.86 g/L). When PCBs, HCB, andp,p-DDE concentrations were corrected by total serum lipids, results from fasting and nonfasting samples were not statistically different. Because of the differences in these chlorinated hydrocarbon concentrations observed with different sample collection regimens, meaningful comparison of analytical results requires standardizing collection procedures or correcting by total serum lipid levels.     

In vivo and in vitro analysis of chloroquine resistance in Plasmodium falciparum isolates from Senegal

To determine the predictive value of chloroquine (CQ) resistance markers in Senegal, Plasmodium falciparum DNA polymorphisms in pfmdr1and pfcrt were examined in relation to clinical outcome. Despite CQ treatment, 17% of patients had parasitemia after 28 days. Examination of molecular markers of CQ resistance revealed that 64% of all isolates had the T76 resistant allele at the pfcrt locus, while 30% carried the Y86 resistant allele at the pfmdr1 locus. The pfcrt T76 allele was present not only in all in vivo resistant isolates, 89% of in vitro resistant isolates, but also in 35% of in vitro sensitive isolates. The pfmdr1 N86Y polymorphism did not correlate with in vitro or in vivo CQ resistance. Our data suggest that the pfcrt T76 allele alone is required but not a sufficient predictor for in vivo CQ resistance.