Telephone vs Face-to-Face Interviews for Quantitative Food Frequency Assessment

Objective To develop and test a quantitative food frequency method for administration by telephone.Design A comparison study of telephone and face-to-face interviews was conducted among a representative sample of the five major ethnic groups in Oahu, Hawaii. Two interviews were administered 4 to 6 months apart by trained interviewers using identical questionnaires and color photographs of food items showing three different portion sizes. The order of the interviewing methods was randomly assigned. The questionnaire included 115 food items selected to estimate 80% or more of usual dietary intakes. Frequencies and quantities of each item consumed during the past year were obtained.Subjects/setting Subjects were recruited from the Health Surveillance Program of the Hawaii State Department of Health and consisted of 167 men and 158 women, aged 45 to 74 years, who provided a telephone number. Eighty percent of the face-to-face interviews were conducted in the subjects’ homes and 20% were conducted at the workplace or the University of Hawaii Cancer Research Center, if requested.Statistical analyses The paired t test was used to compare the mean daily intakes obtained by the telephone and face-to-face methods. Agreement was measured by the intraclass correlation coefficient (ICC), Pearson correlation coefficient, and weighted κ statistic.Results The means of energy and each nutrient were slightly higher in the first interview than the second, regardless of the interviewing method. Because of close correspondence among all 3 statistical measures of agreement, only the ICCs are reported. The ICCs ranged from .61 for protein and vitamin A to .69 for dietary cholesterol among men, and from .61 for vitamin C to .74 for saturated fat among women. Agreement was not significantly affected by age, gender, ethnicity, order of interview, or educational level.Applications Telephone interviews to obtain quantitative food frequencies are cost-efficient methods for estimating usual dietary intakes among persons in widely scattered geographic areas. Photographs of the foods in 3 portion sizes mailed in advance help the respondents estimate amounts eaten. J Am Diet Assoc. 1998;98:44-48.     

The Effects of Perfluorodecanoic Acid on Hepatic Stearoyl-Coenzyme A 1 Desaturase and Mixed Function Oxidase Activities in Rats

The Effects of Perfluorodecanoic Acid on Hepatic Stearoyl-CoenzymeA Desaturase and Mixed Function Oxidase Activities in Rats.VANRAFELGHAM, M. J., AND ANDERSON, M. E. (1988). Fundam. Appl.Toxicol. 11, 503-510. Perfluorodecanoic acid (PFDA) causes adioxin-lilce toxic syndrome and alters the hepatic oleate/stearateratio in rats. The acute toxic effects of a single ip dose (50mg/kg) of PFDA on hepatic stearoyl-CoA desaturase and mixedfunction oxidases were studied in male Fischer-344 rats, 14days after dosing. PFDA causes a marked decrease in food intakein rats, resulting in severe body weight loss with delayed lethality(2-3 weeks after dosing). To distinguish the effects of hypophagiafrom those caused by PFDA, pair-fed control rats were used inaddition to ad libitum-fed controls. Stearoyl-CoA desaturaseactivity, responsible for the conversion of stearoyl-CoA tooleoyl-CoA, was absent in both PFDA dosed rats and their pair-fedcontrols at Day 14. Electron transfer through the desaturasesystem was significantly reduced in PFDA-treated rats only,and in these rats there was a significant reduction in microsomalcytochrome an important component of this electron transfersystem. Pentobarbital sleeping times were significantly prolongedin both the PFDA-dosed and pairfed rats, as compared with thead libitumfed controls. This effect was more pronounced in PFDA-dosedrats. Waking plasma pentobarbital concentration was similarin all treatment groups. Hepatic microsomal cytochrome PASOcontent was unaffected. Aminopyrine N-de-methylase activitywas greatly reduced in PFDA-dosed rats. Although pairfed controlsalso had reduced demethylase activity, it was not as pronouncedas in PFDA-dosed rats, and was probably due to the fasted conditionof these animals. Although the mechanism of action of PFDA isnot known, it is possible that PFDA affects microsomal enzymesby altering the structure and/or function of the membranes inwhich they are located, through effects on lipid metabolism.     

Feasibility assessment of shear wave elastography to lumbar back muscles

Low back pain is often associated with tensional changes in the paraspinal muscles detected by palpatory procedures. Shear wave elastography (SWE), recently introduced, allows the stiffness of muscles to be assessed noninvasively. The aim of this work was to study the feasibility of using SWE on the three main lumbar back muscles (multifidus, longissimus, and iliocostalis) in vivo after analyzing their muscular architecture ex vivo. We determined the orientation of fibers in the multifidus, longissimus, and iliocotalis muscles in seven fresh cadavers using gross anatomy and B‐Mode ultrasound imaging. We then quantified the stiffness of these three muscles at the L3 level ex vivo and in 16 healthy young adults. Little pennation was observed in the longissimus and iliocostalis, in which the direction of fibers was almost parallel to the line of spinous processes. The multifidus appeared as a multiceps and multipennate muscle. Given the random layering of millimetric fascicles, tendons, and fatty spaces, the multifidus had multiple fiber orientations. Muscular fascicles and fibers were oriented from 9° to 22° to the line of spinous processes. The shear moduli related to stiffness were 6.9 ± 2.7 kPa for the longissimus, 4.9 ± 1.4 kPa for the iliocostalis, and 5.4 ± 1.6 kPa for the multifidus. SWE is a feasible method for quantifying the stiffness of the lumbar back muscles. Clin. Anat. 30:774–780, 2017. © 2017Wiley Periodicals, Inc.     

Mechanism-Specific Antiarrhythmic Effects of the Potassium Channel Activator Levcromakalim Against Repolarization-Dependent Tachycardias

Mechanism-Specific Action of Levcromakalim. Introduction: The hypothesis that levcromakalim. a potassium channel (I_K-ATP.) activator with antihypertensive properties, has a mechanism-specific antiarrhythmic action against repolarization-dependent ventricular tachycardias (VTs) was tested in dogs. Methods and Results: A low dose of leveromakalim (0.01 mg/kg) was selected, which decreased blood pressure by 25% but had almost no electrophysiologic effect on AV nodal or ventricular conduction or effective refractory period. In dogs with chronic AV block, the antiarrhythmic action of this dose of levcromakalim was evaluated in three models of abnormal impulse formation: (I) dsotalol (2 mg/kg) induced torsades de pointes VT, initiated by early afterdepolarizations (EADs). (2) sustained ouabain-induced VTs, which are dependent on delayed after depolarizations (DADs), and (3) VT occurring 24 hours after left anterior descending coronary artery occlusion, which are likely based on abnormal automaticity. Levcromakalim abolished d-sotalol induced U waves, ventricular ectopic beats, and self-terminating bouts of torsades de pointes. Induction of torsades de pointes by pacing was also completely prevented. The cycle length of the idioventricular rhythm, which was lengthened after d-sotalol from 1490 ± 515 to 1700 ± 610 msec (P < 0.05), remained similar after levcromakalim (1655 ± 580 msec). The QT(U) duration, which was increased after d-sotalol from 410 ± 55 to 550 ± 40 msec (P < 0.05), normalized to 405 ± 70 msec (P < 0.05). Lcvcromakulim did not suppress but rather enhanced ouabain-induced VT by decreasing the cycle length slightly from 315 ± 35 to 290 ± 35 msec (P < 0.05). Pretreatment with a beta Mocker prevented this acceleration in rate. Finally, levcromakalim had no effect on VT 24 hours after infarction. Conclusion: A low dose of levcromakalim has specific antiarrhythmic properties against repolarization-dependent arrhythmias, but it does not affect VTs based on other mechanisms of abnormal impulse formation.     

The neural bases of prosody: Insights from lesion studies and neuroimaging

This paper reviews the major findings and hypotheses to emerge in the literature concerned with speech prosody. Both production and perception of prosody are considered. Evidence from studies of patients with lateralized left or right hemisphere damage are presented, as well as relevant data from anatomical and functional imaging studies.     

Systolic Arterial Pressure Recovery After Ventricular Fibrillation/Flutter in Humans

Although the elective induction of cardiac arrest for implantable defibrillator insertion under general anesthesia is widely used, the hemodynamics of recovery of arterial blood pressure after cardiac arrest is not well-defined. Accordingly, the time course of recovery of systolic arterial pressure was studied in seven patients during the repetitive induction of ventricular fibrillation (n = 6) or ventricular flutter (n = 1). The mean number of episodes of cardiac arrest was 7 ± 2, and the mean drop in systolic pressure was 84 ± 16mmHg. The mean recovery time for systolic pressure was 10 ± 6 seconds, the average systolic pressure recovery rate was 13 ± 14 mmHg/sec, and the mean percent systolic pressure recovery was 94%± 9%. A negative logarithmic relation was found to exist between the rate of systolic arterial pressure recovery and the duration of ventricular fibrillation or flutter with a correlation coefficient of 0.68 to 0.97 (P < 0.05) in five of the seven patients. A linear relation between the time for systolic pressure recovery and duration of asystole was also defined. These results are consistent with the view that prolongation of ventricular fibrillation or flutter increases the duration of arterial pressure recovery through a negative effect on left ventricular contractility. Increased understanding of these relations may lead to increased safety of implantable defibrillator insertion.