The Mathematics Teaching Efficacy Belief Instrument (MTEBI) for preservice teachers resulted from the modification of the Science Teaching Efficacy Belief Instrument STEBI‐B. The MTEBI consists of 21 items, 13 items on the Personal Mathematics Teaching Efficacy (PMTE) subscale and eight items on the Mathematics Teaching Outcome Expectancy (MTOE) subscale. Possible scores on the PMTE scale range from 13 to 65; MTOE scores may range from 8 to 40. The first version of the MTEBI had 23 items like the STEBI‐B; however, subsequent analysis in this validation required two items be dropped. Reliability analysis produced an alpha coefficient of 0.88 for the PMTE scale and an alpha coefficient of 0. 75 for the MTOE scale (n = 324). Confirmatory factor analysis indicates that the two scales (PMTE and MTOE) are independent, adding to the construct validity of the MTEBI.
Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (CIH) and associated with dysregulation of lipid metabolisms and atherosclerosis. Causal relationships between OSA and metabolic abnormalities have not been established because of confounding effects of underlying obesity. The goal of the study was to determine if CIH causes lipid peroxidation and dyslipidemia in the absence of obesity and whether the degrees of dyslipidemia and lipid peroxidation depend on the severity of hypoxia. Lean C57BL/6J mice were exposed to CIH for 4 wk with a fractional inspired O2 (FI(O2)) nadir of either 10% (moderate CIH) or 5% (severe CIH). Mice exposed to severe CIH exhibited significant increases in fasting serum levels of total cholesterol (129 +/- 2.9 vs. 113 +/- 2.8 mg/dl in control mice, P < 0.05) and low-density lipoprotein cholesterol (85.7 +/- 8.9 vs. 56.4 +/- 9.7 mg/dl, P < 0.05) in conjunction with a 1.5- to 2-fold increase in lipoprotein secretion, and upregulation of hepatic stearoyl coenzyme A desaturase 1 (SCD-1). Severe CIH also markedly increased lipid peroxidation in the liver (malondialdehyde levels of 94.4 +/- 5.4 vs. 57.4 +/- 5.2 nmol/mg in control mice, P < 0.001). In contrast, moderate CIH did not induce hyperlipidemia or change in hepatic SCD-1 levels but did cause lipid peroxidation in the liver at a reduced level relative to severe CIH. In conclusion, CIH leads to hypercholesterolemia and lipid peroxidation in the absence of obesity, and the degree of metabolic dysregulation is dependent on the severity of the hypoxic stimulus.
Obstructive sleep apnea is the result of repeated episodes of upper airway obstruction during sleep. Recent evidence indicates that alterations in upper airway anatomy and disturbances in neuromuscular control both play a role in the pathogenesis of obstructive sleep apnea. We hypothesized that subjects without sleep apnea are more capable of mounting vigorous neuromuscular responses to upper airway obstruction than subjects with sleep apnea. To address this hypothesis we lowered nasal pressure to induce upper airway obstruction to the verge of periodic obstructive hypopneas (cycling threshold). Ten patients with obstructive sleep apnea and nine weight-, age-, and sex-matched controls were studied during sleep. Responses in genioglossal electromyography (EMG(GG)) activity (tonic, peak phasic, and phasic EMG(GG)), maximal inspiratory airflow (V(I)max), and pharyngeal transmural pressure (P(TM)) were assessed during similar degrees of sustained conditions of upper airway obstruction and compared with those obtained at a similar nasal pressure under transient conditions. Control compared with sleep apnea subjects demonstrated greater EMG(GG), V(I)max, and P(TM) responses at comparable levels of mechanical and ventilatory stimuli at the cycling threshold, during sustained compared with transient periods of upper airway obstruction. Furthermore, the increases in EMG(GG) activity in control compared with sleep apnea subjects were observed in the tonic but not the phasic component of the EMG response. We conclude that sustained periods of upper airway obstruction induce greater increases in tonic EMG(GG), V(I)max, and P(TM) in control subjects. Our findings suggest that neuromuscular responses protect individuals without sleep apnea from developing upper airway obstruction during sleep.
The etiology of excessive daytime sleepiness in patients with sleep-disordered breathing (SDB) is not well defined. In this study, we examined the relationships between several clinical and polysomnographic parameters and the degree of hypersomnolence in 741 patients with SDB (apnea-hypopnea index [AHI] >/= 10 events/h). The study sample was obese (body mass index [BMI]: 35.3 +/- 8.5 kg/m2) and had evidence of moderate SDB (AHI: 47.6 +/- 29.3 events/h). Hypersomnolence was quantified with the multiple sleep latency test (MSLT) and survival analysis was used to assess the risk factors for hypersomnolence. In a multivariate proportional hazards model, AHI and nocturnal hypoxemia were independent predictors of hypersomnolence (MSLT < 10 min). The adjusted relative risks (RR) of hypersomnolence were 1.00, 1.30, and 1.65 for patients with an AHI of 10 to 29.9, 30 to 59.9, and >/= 60 events/h, respectively. A positive association between hypersomnolence and oxyhemoglobin desaturation (DeltaSaO2) was observed with RR of 1.00, 1.18, 1.43, and 1.94 for a DeltaSaO2 of = 5%, 5.1 to 10%, 10.1 to 15%, and > 15%, respectively. Sleep fragmentation, as assessed by the distribution of sleep stages, was also an independent predictor of hypersomnolence. Using stage 1 sleep as a reference, an increase in stage 2 and slow wave sleep (SWS) were protective from hypersomnolence. For a 10% increase in stage 2 or SWS the adjusted RR for hypersomnolence were 0.93 and 0.79, respectively. REM sleep showed no significant association with the degree of hypersomnolence. These results suggest that AHI, nocturnal hypoxemia, and sleep fragmentation are independent determinants of hypersomnolence in SDB.
We used intracellular microelectrode techniques and equivalent electrical circuit analysis to examine the changes in individual membrane resistances and electromotive forces that accompany stimulation of C1 secretion across canine tracheal epithelium, Tissues were pretreated with indomethacin (10-6 M, mucosal solution) to reduce basal C1 secretion rate. Subsequent addition of epinephrine (10 -6 M, submucosal solution) increased the rate of electrogenic C1 secretion as indicated by an increase in the short-circuit current (Iso) and decrease in the transepithelial resistance (Rt). The reduction in Rt was due to decreases in both Ra and Rb (the resistances of the apical and basolateral cell membranes, respectively).At the apical membrane, a nearly 10-fold decrease in R, was accompanied by reversal of the electromotive force (E,) from + 11 +9 mV to -31_+3 mV. Variations in C1 secretion rate induced by indomethacin and epinephrine disclosed a direct relation between R~ and E,. In the presence of indomethacin R~ was high and E, was consistent with the chemical potential difference for Na across the apical membrane (ca, + 60 mV), reflecting the predominance of Na absorption across indomethacin-treated tissues. In the presence of epinephrine, R, was low and E, was consistent with the chemical potential difference for C1 across this barrier (-31 mV), reflecting the dominance of C1 secretion across epinephrine-treated tissues. These findings suggest that the conversion from absorption to secretion primarily involves a secretogogue-induced decrease in apical membrane resistance to C1.At the basolateral membrane, epinephrine decreased R b threefold without markedly altering the electromotive force across this barrier (Eb). To the extent that R b and E b represent the resistance and chemical potential difference for K diffusion across the basolateral membrane, the inverse relation between Rb and Isc suggests that stimulation is associated with increased basolateral membrane K permeability without marked changes in intracellular K activity.Key words tracheal epithelium 9 C1 secretion 9 electrophysiology 9 equivalent electrical circuit -epinephrine
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