Increased sensitization in urban vs. rural environment – Rural protection or an urban living effect?

In a population-based longitudinal cohort study, we tested the hypothesis that children growing up in a high-traffic polluted urban area (UA) in the Athens' basin have higher prevalence of allergies and sensitization when compared with those growing up in a Greek provincial rural area (RA). We recruited 478 and 342 children aged 8-10 living in the UA and the RA, respectively. Respiratory health was assessed by a parent-completed questionnaire in three phases: 1995-96 (phase 1), 1999-2000 (phase 2), 2003-04 (phase 3) and skin-prick testing to common indoor and outdoor aeroallergens was performed at phases 1 and 2. Reported asthma and eczema did not differ between the two areas, whereas reported hay fever was persistently more prevalent in the UA than in the RA (16.5%, 17.0%, 18.2% vs. 7.0%, 8.3%, 9.6%, respectively). Sensitization was more prevalent in the UA at both phases (19.0% vs. 12.1% in phase 1, 20.0% vs. 14.1% in phase 2). Residential area contributed independently to sensitization to >or=1 aeroallergens (OR: 0.29; 95% CI: 0.13-0.66; p = 0.003) and to polysensitization (OR: 0.28; 95% CI: 0.10-0.82; p = 0.020) in phase 1. These associations were independent of farming practices. No significant contributions were found in phase 2. Our results suggest that long-term exposure to urban environment is associated with a higher prevalence of hay fever but not of asthma or eczema. The negative association between rural living and the risk of atopy during childhood, which is independent of farming practices, implies that it is mainly driven by an urban living effect.     

Controlling for occasion-specific effects when assessing the test–retest reliability of self-report health questionnaires

OBJECTIVE: This study proposes a method for self-report health questionnaires to adjust test-retest reliability for changes during the test-retest interval based on an external measure, and to distinguish such changes from random response errors. METHODS: In our application, eighty participants completed the Symptoms of Illness Checklist (SIC) on two occasions, two weeks apart, immediately before interviews given on each occasion by one of two physicians in a crossover design. The physician interview scores served as external measures, and structural equation modeling was used to estimate the parameters of a model that corrected for the occasion-specific effect of participants' responses using information from the interviews. RESULTS: Correcting for changes in symptoms during the test-retest interval increased SIC test-retest reliability from .744 to .804 and significantly improved model fit (chi2(diff)(1) = 30.78, p < .001). CONCLUSIONS: The results suggest methods that can improve the evaluation of self-report health questionnaire test-retest reliability by identifying changes using an external measure, and distinguishing these from random response errors; these increased the estimated SIC test-retest reliability and indicated that the SIC was indeed able to measure changes over the studied time interval. This method can be applied across a broad range of questionnaires.     

Investigation of tinnitus induced by sound and its relationship to ongoing tinnitus

Tinnitus was temporarily induced by monaurally presented sound, and its level monitored using a dichotic loudness-matching task. The first experiment found no effect of varying the level, bandwidth, or center frequency of an inducing noise on the level or duration of the induced tinnitus; nor was there any difference when tones or different noises were used to induce tinnitus. The rated loudness of the tinnitus, however, increased with the level and decreased with the center frequency of the noise. The second experiment investigated tinnitus induced by a 1-kHz, 95-dB SPL tone in 53 subjects with thresholds in the normal range, but with varying degrees of ongoing tinnitus that ranged from no discernible sound sensation at all, through an apparently normal but usually inaudible noise or ringing, to constant or near-constant tinnitus. Individual differences in induced tinnitus were found that were related to differences in ongoing tinnitus; for example, the levels of induced and ongoing tinnitus were positively correlated. The results suggest that some kinds of ongoing tinnitus may arise from the auditory process responsible for induced tinnitus.     

Upper gastrointestinal tract dysfunction in bulimia

Bulimia nervosa is a health problem of increasing magnitude that is estimated to affect 2–5% of the American adolescent and young adult female population. Because of the magnitude of this clinical problem and because of the importance of the upper gastrointestinal tract in its expression, a intradepartmental program of health care for patients affected with the disease was initiated. Eleven consecutive symptomatic bulimic individuals have been evaluated jointly by the gastroenterology and the psychiatry departments of the University of Pittsburgh. Five of these 11 individuals were found to have clinically important upper gastrointestinal pathology including ulcerative esophagitis, erosive gastritis, duodenal ulcer, and delayed gastric emptying. These gastrointestinal conditions could have been either a result of or have contributed to the symptomatology of these five patients. These data suggest that bulimic subjects have clinically important gastroenterological disease processes that require specific diagnosis and treatment independent of the psychiatric treatment provided for the bulimic condition.This work was supported in part by grants from NIDDK AM 32556.     

Genetic Tools in the Study of Drug Self-administration

Recent studies have shown that large genetic differences exist in the extent to which orally delivered ethanol will come to serve as a positive reinforcer under operantly defined conditions. In addition, these studies suggest that a significant correlation exists between results from two-bottle choice studies of ethanol drinking and operant self-administration studies of ethanol functioning as a reinforcer. The present paper reports further genetic influences on ethanol self-administration which were found using Long Sleep and Short Sleep mice, bred selectively for high and low duration of loss of the righting reflex in responses to ethanol, respectively. It was possible to establish ethanol as a reinforcer in Long Sleep mice but not in Short Sleep mice. These results indicate that neurosensitivity to ethanol may determine the absolute amount of ethanol consumption but is not highly related to the ability of ethanol to serve as a positive reinforcer. In addition, this paper presents genetic correlations which indicate that (a) ethanol preference and self-administration are highly correlated across genotype; (b) sensitivity to ethanol and self-administration of this drug are not highly genetically correlated; (c) ethanol is not self-administered in operant studies solely for its caloric value; and (d) there exist important genetic determinants of drug reinforced behavior.     

Tetrahymena extract protects Paramecium from oxygen-free radicals

Cells of Paramecium tetraurelia will age and die, while cells of Tetrahymena thermophilia are immortal. Both are free-living, ciliated protozoa. Whole cells and homogenates of both Paramecium and Tetrahymena were treated with iron(+2) to induce peroxidation of membrane lipids and other cellular constituents. Paramecium is far more susceptible to such peroxidative damage than Tetrahymena. Indeed, addition of Tetrahymena extract protects Paramecium from peroxidative damage. Tetrahymena’s protective molecules block the initial attack of oxygen-free radicals on Paramecium constituents. A portion of the protective molecules are high molecular weight and temperature sensitive, but others are of small size. Some of the protective molecules are tightly bound to membranes or cytoskeletal elements pelleted from Tetrahymena sonicates.     

Response of lower esophageal contractility to changing concentrations of halothane or isoflurane: A multicenter study

A multiple-center study was performed to determine the relationship between lower esophageal contractility, clinical signs, and anesthetic concentration as expressed by minimum alveolar concentration (MAC). One hundred four American Society of Anesthesiologists Class I through III patients were exposed to isoflurane (with and without nitrous oxide) or halothane in concentrations of 0.5, 1.0, and 1.5 MAC. Heart rate and systolic blood pressure were continuously monitored. Both the amplitude and frequency of spontaneous and provoked lower esophageal contractions were measured in situ by using a 24-F probe equipped with provoking and measuring balloons. Combined results demonstrated statistically significant correlations (P<0.001) between lower esophageal contractility and MAC. Spontaneous lower esophageal contractions decreased from 1.10±0.12 (SEM) contractions per minute (0.5 MAC) to 0.42±0.05 (1 MAC) to 0.18±0.05 (1.5 MAC). Provoked lower esophageal contractility values decreased from 45±4 mm Hg (0.5 MAC) to 29±3 (1 MAC) to 19±2 (1.5 MAC). Heart rate changes did not correlate with MAC, and systolic blood pressure correlated in only one of three centers. Intracenter and intercenter analyses failed to demonstrate a significant relationship between lower esophageal contractility and heart rate or systolic blood pressure. No intracenter differences in either amplitude or frequency of lower esophageal contractions were observed, despite differences in volatile agents, induction techniques and agents, patient populations, and duration of anesthesia. Our studies indicate that lower esophageal contractility may be an indicator of anesthetic depth as reflected by MAC, but further studies are needed to quantify the effects of surgical stimulus, intravenous anesthetics, vasodilators, anticholinergics, calcium channel blockers, beta-adrenergic agonists, and the presence of a nasogastric tube.     

Increased incidence of gap junctional coupling between spinal motoneurones following transient blockade of NMDA receptors in neonatal rats

Neonatal rat motoneurones are electrically coupled via gap junctions and the incidence of this coupling declines during postnatal development. The mechanisms involved in this developmental regulation of gap junctional communication are largely unknown. Here we have studied the role of NMDA receptor-mediated glutamatergic synaptic activity in the regulation of motoneurone coupling. Gap junctional coupling was demonstrated by the presence of graded, short latency depolarising potentials following ventral root stimulation, and by the transfer of the low molecular weight tracer Neurobiotin to neighbouring motoneurones. Sites of close apposition between the somata and/or dendrites of the dye-coupled motoneurones were identified as potential sites of gap junctional coupling. Early postnatal blockade of the NMDA subtype of glutamate receptors using the non-competitive antagonist dizocilpine maleate (MK801) arrested the developmental decrease in electrotonic and dye coupling during the first postnatal week. These results suggest that the postnatal increase in glutamatergic synaptic activity associated with the onset of locomotion promote the loss of gap junctional connections between developing motoneurones.     

Erythromycin-Induced Immune Hemolytic Anemia

A 3-year-old female receiving Pediazole (erythromycin ethylsuccinate and sulfisoxazole) for tonsillitis and otitis media developed severe hemolytic anemia. No serum drug-dependent antibodies could be demonstrated with an in vitro 'immune-complex' method using Pediazole, pure erythromycin ethylsuccinate or pure sulfisoxazole. However, a method using red cells coated with erythromycin base showed in vitro lysis of the erythromycin-coated red cells. This is only the second case of immune hemolytic anemia associated with erythromycin and the first where in vitro drug-dependent hemolysis was demonstrable.     

In vivo vs in vitro anticariogenic behavior of glass-ionomer and resin composite restorative materials.

OBJECTIVE: To evaluate the in vivo vs the in vitro anticariogenic potential of glass-ionomer and resin composite restoratives, utilizing a standardized interfacial gap model. METHODS: (a) In vitro study. Box shaped cavities were prepared at the buccal surfaces of extracted premolars limited to enamel. The incisal cavity walls received no treatment and were covered with 40 microm-thick metal spacers. The cavities were restored with a glass-ionomer (Ketac-Fil, n=8) and a fluoride-free resin composite (Scotchbond MP Plus/Z100, n=8). After 4 weeks immersion in an acidic gel (pH 4), thin sections were produced and examined under polarized-light microscopy.(b) In vivo study. Four low caries activity volunteers, with first four premolars, each planned to be extracted for orthodontic reasons, participated in the study. Cavities were prepared as before and filled contralaterally per patient with glass-ionomer (n=8) and resin composite (n=8). After 6 months in vivo, the teeth were extracted, sectioned and investigated by polarized-light microscopy, Raman microspectroscopy and SEM-EDS X-ray microanalysis. Unpaired t-test (lesion dimensions) and one-way ANOVA and Newman-Keuls tests (Ca, P wt%, Ca/P ratios) were used to identify statistically significant differences in lesion analysis (alpha=0.05). RESULTS: (a) In vitro study. All restorations developed lesions at incisal and cervical margins. At gap-free regions glass-ionomers showed reduced lesion dimensions compared to those of composites (p<0.05). At regions with gaps, no significant differences were found in lesion depth between the restorative groups tested. Lesion length was increased in composite, and decreased in glass-ionomer, whereas lesion depth in both restorative groups was increased in comparison to gap-free regions (p<0.05).(b) In vivo study. No lesions were observed at gap-free regions. At gap regions, 75.5% of glass-ionomer and 62.5% of composite restorations developed lesions. The lesion dimensions were significantly greater in glass-ionomer (p<0.05). A reduction in PO4(3-), CO3(2-), Ca and P was found in lesions compared to intact tissues. No F was detected and no CaF2 lattice vibrations were found at the enamel margins facing the gap adjacent to glass-ionomers. SIGNIFICANCE: In the presence of a standardized interfacial gap, no preventive effect was exerted in vivo from the glass-ionomer to protect the adjacent enamel wall from secondary caries attack. The lack of any correlation between the in vivo and in vitro models tested implies that artificial caries experiments have a negligible clinical relevance in predicting the in vivo effect.