Pain control in orthodontics using a micropulse vibration device: A randomized clinical trial

Objective:To investigate the relationship between a micropulse vibration device and pain perception during orthodontic treatment.Materials and Methods:This study was a parallel group, randomized clinical trial. A total of 58 patients meeting eligibility criteria were assigned using block allocation to one of two groups: an experimental group using the vibration device or a control group (n  =  29 for each group). Patients used the device for 20 minutes daily. Patients rated pain intensity on a visual analog scale at appropriate intervals during the weeks after the separator or archwire appointment. Data were analyzed using repeated measures analysis of variance at α  =  .05.Results:During the 4-month test period, significant differences between the micropulse vibration device group and the control group for overall pain (P  =  .002) and biting pain (P  =  .003) were identified. The authors observed that perceived pain was highest at the beginning of the month, following archwire adjustment.Conclusion:The micropulse vibration device significantly lowered the pain scores for overall pain and biting pain during the 4-month study period.     

Eicosanoids and control of mesangial cell contraction

Contraction of glomerular mesangial cells is stimulated in vitro by the vasoconstrictor metabolite of arachidonic acid, thromboxane A2. To establish the role of mesangial prostaglandin (PG) synthesis in the modulation of contractile responses, we studied the effects of the stable thromboxane A2/endoperoxide analogue U-46619 on cultured rat mesangial cells preincubated with 1) four structurally unrelated, nonsteroidal anti-inflammatory drugs, indomethacin, acetylsalicylic acid, meclofenamate, and piroxicam, to inhibit the synthesis of PGE2, the major mesangial metabolite of arachidonic acid; 2) exogenous PGE2 and the stable analogue of PGI2, iloprost; and 3) indomethacin in the presence of exogenous PGE2. Computer-assisted image analysis microscopy demonstrated enhancement of spontaneous and agonist-induced contraction by nonsteroidal anti-inflammatory drugs in individual cells grown on a glass substrate, from 37.2 +/- 7.3% to a maximum of 75.5 +/- 6.4% of the cells with piroxicam, at 1 microM U-46619. PGE2 and iloprost dose-dependently inhibited U-46619-induced contraction, to 5.0 +/- 2.8% and 12.5 +/- 4.7% of the cells, respectively, at 1 microM U-46619. PGE2 also completely reversed the effects of indomethacin. Both PGE2 and iloprost dose-dependently stimulated intracellular cyclic AMP (cAMP) accumulation during 3-minute incubations, an effect that was blocked by the inhibitor of adenylate cyclase, 2',5'-dideoxyadenosine. The latter reversed the inhibitory action of PGE2, enhancing spontaneous and agonist-induced contractility, thus indicating a modulatory role of cAMP. We conclude that endogenous arachidonate metabolism regulates mesangial cell contraction through elevation of intracellular cAMP.     

Therapeutic efficacy of granulocyte-macrophage colony-stimulating factor in patients with idiopathic acquired alveolar proteinosis

Alveolar proteinosis (AP) is characterized by excessive surfactant accumulation, and most cases are of unknown etiology. Standard therapy for AP is whole-lung lavage, which may not correct the underlying defect. Because the hematopoietic cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) is required for normal surfactant homeostasis, we evaluated the therapeutic activity of GM-CSF in patients with idiopathic AP. Fourteen patients received 5 microg/kg/d GM-CSF for 6 to 12 wk with serial monitoring of the alveolar-arterial oxygen gradient ([A-a]DO2), diffusing capacity of carbon monoxide, computed tomographic scans, and exercise testing. Patients not responding to 5 microg/kg/d GM-CSF underwent stepwise dose escalation, and responding patients were retreated at disease recurrence. Stored pretreatment sera were assayed for GM-CSF-neutralizing autoantibodies. According to prospective criteria, five of 14 patients responded to 5 microg/kg/d GM- CSF, and one of four patients responded after dose escalation (20 microg/kg/d). The overall response rate was 43% (mean improvement in [A-a]DO2 = 23.2 mm Hg). Responses lasted a median of 39 wk, and were reproducible with retreatment. GM-CSF was well-tolerated, with no late toxicity seen. The only treatment-related factor predictive of response was GM-CSF-induced eosinophilia (p = 0.01). Each of 12 patients tested had GM-CSF-neutralizing autoantibodies present in pretreatment serum. We conclude that GM- CSF has therapeutic activity in idiopathic AP, providing a potential alternative to whole-lung lavage.     

Electrocardiographic prediction of coronary artery patency after thrombolytic treatment in acute myocardial infarction: use of the ST segment as a non-invasive marker

The predictive value of the measurement of changes in ST segment elevation was assessed as a non-invasive marker of coronary artery reperfusion after thrombolytic treatment. Forty five patients with acute myocardial infarction (23 anterior, 22 inferior) of less than six hours' duration were given thrombolytic treatment by either the intravenous (n = 28) or the intracoronary route (n = 17). A proportional value for the shift in ST segment, termed the fractional change, was calculated both from 12 lead electrocardiograms and from the Holter tape for each patient. Coronary artery patency in an initial group of 22 patients (training group) was associated with a fractional change value of greater than or equal to 0.5 (100% specific, 88% sensitive by Holter analysis; 100% specific, 94% sensitive by 12 lead electrocardiogram). This rule performed well when it was applied to a test group of 17 patients (100% specific, 93% sensitive by Holter analysis; and 67% specific, 93% sensitive by 12 lead electrocardiogram). Linear discriminant analysis was then used to determine which features gave the best separation of those in whom there was reperfusion and those in whom there was not. This gave 100% specificity and 100% sensitivity when applied to the training group for either the 12 lead electrocardiogram or Holter monitoring. When it was applied to the test group, the sensitivity was maintained at 100%, but the specificity dropped to 33% irrespective of whether the basis of the test was Holter monitoring or the 12 lead electrocardiogram. These results suggest that a fractional change of >/= 0.5 calculated from a single lead showing myocardial injury is a useful non-invasive marker of reperfusion. The technique can be applied to either 12 lead electrocardiograms or Holter monitoring. The use of a more complex classification increased the sensitivity of the test at the expense of its specificity.     

Diurnal variation of blood pressure in elderly patients with essential hypertension

Twenty-one elderly patients with essential hypertension, all over 65 years of age, were subjected to automated noninvasive 24-hour blood pressure measurement. Readings were obtained every 7.5 minutes throughout the day. The data were analyzed with respect to: correlation between office and ambulatory pressure measurements; possible differences in the circadian blood pressure pattern; and the existence of hypertensive or atherosclerotic cardiovascular complications. In all patients, the office systolic pressures were significantly higher than the ambulatory daytime pressures; diastolic pressures were similar. At night, two patterns of blood pressure emerged. In one there was a further fall in both systolic and diastolic pressures to normotensive levels, whereas the other pattern revealed no change in diastolic pressure, although systolic pressure increased significantly to similar levels as measured in the office. The prevalence of hypertensive or atherosclerotic cardiovascular complications in the patients with the first pattern was significantly less than in the group of patients with the second pattern (chi square, P less than 0.025). The data reported herein indicate that ambulatory blood pressure monitoring may help in the overall clinical evaluation of elderly patients with hypertension.     

Effect of recombinant human interleukin-6 (rhIL-6) and rhIL-3 on hematopoietic regeneration as demonstrated in a nonhuman primate chemotherapy model

Using a recently developed hepsulfam-induced pancytopenia model in rhesus macaques, we have studied the effects of recombinant human interleukin-6 (rhIL-6) and rhIL-3 on marrow regeneration. Control animals were given hepsulfam (1.5 g/m2 by a single 30-minute intravenous [i.v.] injection, n = 4), while study animals received hepsulfam followed by rhIL-6, rhIL-3, or a combination of rhIL-6 and rhIL-3 (n = 3 per study group). Each cytokine was administered by once- daily subcutaneous (SC) injection (15 micrograms/kg/d) for 3 weeks beginning the day after chemotherapy (days 2 through 22). Mean platelet counts in control animals were < 100,000/microL on days 15 through 24, with 50% of the counts < 50,000/microL and two of four animals requiring platelet transfusion. In the rhIL-6- and rhIL-6/rhIL-3- treated groups, the nadir mean platelet counts were 164,000 +/- 58,700/microL and 162,300 +/- 23,800/microL, respectively, and occurred on day 15. Platelet counts in the rhIL-3-treated group were similar to those in controls. Mean absolute neutrophil counts (ANCs) < 1,000/microL occurred on days 10 through 29 in control animals, days 8 through 15 in rhIL-6-treated animals, and days 6 through 8 and 13 in rhIL-6/rhIL-3-treated animals. The frequency of ANCs < 500/microL was significantly less in the rhIL-6- and rhIL-6/rhIL-3-treated groups versus control groups (2.7 +/- 0.6 and 2.0 +/- 1.0 vs 7.0 +/- 1.4 occurrences, respectively; P < .05). rhIL-3-treated animals had ANCs similar to those in controls; one animal died with septicemia on day 21. Monkeys receiving rhIL-6 were significantly more anemic during the cytokine administration period; however, the anemia resolved by day 24. Coadministration of rhIL-3 and rhIL-6 partially corrected the anemia. The data indicate that rhIL-6 prevents significant thrombocytopenia and shortens the neutropenic period in this chemotherapy model.