Preventive dental prosthesis for the patient with bulimia

Bulimia is a distinct diagnostic eating disorder with its most noted manifestation being the rapid ingestion of large quantities of food followed by its elimination through the mouth. Because of the dental implications of highly acidic stomach contents chronically being regurgitated, the dentist is in a unique position to help identify the patient with bulimia. Dental erosion is not only the most easily noted but also the most destructive of the many oral problems caused by bulimia. This report of case describes a preventive dental prosthesis that can be used by the patient with bulimia to protect those teeth that are most affected by dental erosion. The construction of the prosthesis is easily completed with materials in the dental office and provides a great service to the patient with bulimia.     

The Fagerström Test for Nicotine Dependence: a revision of the Fagerstrom Tolerance Questionnaire

We examine and refine the Fagerström Tolerance Questionnaire (FTQ; Fagerström, 1978). The relation between each FTQ item and biochemical measures of heaviness of smoking was examined in 254 smokers. We found that the nicotine rating item and the inhalation item were unrelated to any of our biochemical measures and these two items were primary contributors to psychometric deficiencies in the FTQ. We also found that a revised scoring of time to the first cigarette of the day (TTF) and number of cigarettes smoked per day (CPD) improved the scale. We present a revision of the FTQ: the Fagerström Test for Nicotine Dependence (FTND).     

Flecainide

Flecainide. Flecainide is a Class IC antiarrhythmic agent whose primary electrophysiologic effect is a slowing of conduction in a wide range of cardiac tissues. It is well absorbed and effective in suppressing isolated premature ventricular contractions (PVCs) or nonsustained ventricular arrhythmia but has only a modest efficacy when electrophysiologic testing is used as an endpoint. Us adverse effect on mortality in the CAST trial suggested a propensity to proarrhythmia-a phenomenon to which the Class IC agents appear particularly prone. Despite the applicability of the CAST study only to patients with a prior myocardial infarction, there has been a shift away from flecainide in ventricular arrhythmia, but the low noncardiac side effect profile of the agent allows for its continued use in a wide variety of supraventricular arrhythmias. ( J Cardiovasc Electrophysiol, Vol. 5, pp. 964–981. November 1994 )     

A Subset of Patients With Recurrent Spontaneous Abortion Is Deficient in Transforming Growth Factor β-2-Producing “Suppressor Cells” in Uterine Tissue Near the Placental Attachment Site

PROBLEM : To determine if patients with unexplained recurrent miscarriage have a deficiency of decidual immunosuppressor cells that produce transforming growth factor β type 2, as has been found in mice with abortion due to rejection and/or trophoblast failure. METHODS : Decidual biopsy specimens were taken as near to the placental attachment site as possible under ultrasound guidance from first trimester legal termination (control) patients with recurrent miscarriage and non-viable pregnancy, and from patients with sporadic missed abortion. The tissue was tested for TGFβ-2⁺ suppressor cells by in situ hybridization, immunohistochemistry, and analysis of supernatants. RESULTS : TGFβ-2-related suppressor molecules similar but not identical to those identified in pregnant mice were released by decidual lymphoid cells. Fifty percent of 14 recurrent miscarriage patients showed a lack of suppressor cells and 59% were subnormal in comparison to 20 controls and 5 sporadic miscarriage patients, where 80–85% of the patients had detectable suppressor cells. CONCLUSIONS : Suppressor cell deficiency is compatible with a role for rejection and/or trophoblast failure in some patients with recurrent miscarriage. Presence of suppressor cells in most patients with missed abortion (4/5) is compatible with an alternative cause of fetal death, similar to findings reported in genetic fetal death mice.