No description available.

No description available.

No description available.

No description available.

The measurement of vital signs is a risk-free, inexpensive, and reproducible clinical practice that enables identification of physiological deterioration of patients before an adverse event occurs. However, studies show that manual clinical measurements of respiratory rate are intermittent, biased, and inaccurate. Therefore, a contactless planar capacitive sensor was developed and evaluated against a clinical reference method. Results show that the sensor is accurate (i.e. strong agreement with an average ICC value of 0.99 and an average BSI coefficient of 2.76 < 4 breaths/min clinical threshold) and unbiased (i.e. average mean difference of -0.02 breaths/min). The sensor has promise for respiratory rate monitoring of bedridden patients even during shallow breathing. Future work includes addressing technology limitations, conducting a clinical pilot with a diverse patient population, and exploring potential in sleep quality assessment.

The measurement of vital signs is a risk-free, inexpensive, and reproducible clinical practice that enables identification of physiological deterioration of patients before an adverse event occurs. However, studies show that manual clinical measurements of respiratory rate are intermittent, biased, and inaccurate. Therefore, a contactless planar capacitive sensor was developed and evaluated against a clinical reference method. Results show that the sensor is accurate (i.e. strong agreement with an average ICC value of 0.99 and an average BSI coefficient of 2.76 < 4 breaths/min clinical threshold) and unbiased (i.e. average mean difference of -0.02 breaths/min). The sensor has promise for respiratory rate monitoring of bedridden patients even during shallow breathing. Future work includes addressing technology limitations, conducting a clinical pilot with a diverse patient population, and exploring potential in sleep quality assessment.

This study addressed the location of the breathing movement and its relationship to stress levels. Sixty-three Ball State students voluntarily participated by completing the A-State and A-Trait forms of the State-Trait Anxiety Inventory (STAI). Under the pretense that they would be questioned about music later, each participant also listened to preselected music for about 4 minutes in both seated and reclining positions. The participants were unaware that their breathing was being observed. During the listening portion of the study from behind a one-way mirror, 3 trained observers rated each breath as either thoracic or non-thoracic. The percentage of total breaths that were thoracic was calculated for each subject in both positions. Interrater reliability was determined inadequate for data of participants in the reclining position. The scores on the STAI and the percentage of thoracic breaths were the variables analyzed. A Pearson R correlation was then used to test the hypotheses. Null hypothesis 1, that there is no relationship between percentage of total breaths that are thoracic in a seated position and scores for AState, was upheld. Also, no relationship was found between percentage of total breaths that are thoracic in a seated position and scores for A-Trait, therefore, null hypothesis 2 was also upheld. This study also found that 71% of the participants breathing style is primarily thoracic. These findings and procedural effects on the outcome as well as implications for further research were discussed. / Fisher Institute for Wellness

Neuroepithelial cells (NECs) of the zebrafish gill filament have been previously identified as bimodal O2 and CO2/H+ sensors that depolarize in response to chemostimuli via inhibition of background K+ channels. To further elucidate the signaling pathway underlying CO2/H+ chemoreception in the NECs we employed microspectrofluorometric techniques to examine the effects of hypercapnia on [Ca2+]i and pHi. NECs increased their [Ca2+]i in response to acidic hypercapnia (5% CO2, pH 6.6) and isocapnic acidosis (normocapnia, pH 6.6), but not to isohydric hypercapnia (5% CO2, pH 7.8). The acid- induced increase in [Ca2+]i persisted in the absence of extracellular Ca2+, and Ca2+ channel blockers (Cd2+, Ni2+ and nifedipine). NECs exhibited a rapid and reversible drop in pHi in response to acidic hypercapnia and isohydric hypercapnia. Isocapnic acidosis also induced intracellular acidification within NECs, but it was less severe than the drop in pHi elicited by acidic hypercapnia and isohydric hypercapnia. The rate and magnitude of intracellular acidification was reduced by the CA-inhibitor, acetazolamide, without effect on the acid-induced increase in [Ca2+]i. Acetate was used to investigate the relationship between pHi and [Ca2+]i. Acetate induced intracellular acidification without augmentation of [Ca2+]i. The results of this thesis demonstrate that (1) extracellular acidification, but not CO2, is critical to the hypercapnia-induced increase in [Ca2+]i (2) the increase in [Ca2+]i is independent of the drop in pHi (3) the increase in [Ca2+]i is not mediated by the influx of Ca2+ across the plasma membrane.

No description available.

The LD(_50) of 10-day-old blowflies differed significantly in two different stocks, and were found to be 38.12 ± 0.07ºC for the Durham stock and 40.8 ± 0.18ºC for the Cambridge stock. A transitory increase in heat resistance occurred following the exposure of adult blowflies to a sublethal heat shock. This thermotolerance was apparent 1h after the application of heat shock, was maximal 2-3 h later and had disappeared after 6 h. Oxidative phosphorylation by flight muscle mitochondria from non-thermotolerant control flies was impaired by an LD(_50) dose in vivo. Respiration using glycerol-3- phosphate was more heat sensitive than that with pyruvate plus proline. State III respiration was markedly inhibited, acceptor control (RCI) was lost with (G 3P) as substrate and so ADP:0 ratios were not measurable; whereas with pyruvate + proline as substrates, although State III respiration was inhibited by 50% and acceptor control was significantly reduced, ADP:0 remained measurable. Uncoupling of oxidative phosphorylation was obvious only with pyruvate + proline where State IV was significantiy increased. The development of thermotolerance protected oxidative phosphorylation against heat damage. With G-3-P respiration State III was largely restored and acceptor control was not significantly different from controls, but ADP:0 remained lower. With pyruvate + proline as substrates State III respiration was inhibited, but State IV was also lower without evidence of uncoupling of oxidative phosphorylation. Acceptor control was restored to control levels but ADP:0 values were lower. The lower ADP:0 ratios indicate some impairment of mitochondrial function occurred. The effect of experimental temperature in vitro on respiratory performance of mitochondria from non-pretreated control and thermotolerant LD(_50) flies was also determined between 19 and 39ºC. State III respiration was markedly temperature- dependent in mitochondria from non-pretreated control flies with both substrates; it was maximal at 24-29ºC and fell progressively at higher measuring temperatures. In mitochondria from thermotolerant flies, State III respiration was less temperature dependent with both substrates, but this effect was more marked for G-3-P. The effect of experimental temperature on State IV respiration was similar in mitochondria from non- pretreated control and thermotolerant LD(_50) flies with the same substrate, but differed between the two substrates. With G 3P as substrate, respiration rate rose with temperature with a Q(_10) of approximately 1.5; however, with pyruvate + proline as substrate, the trend was for respiration rate to fall as experimental temperature rose. Differences in the temperature sensitivities of mitochondria from control and thermotolerant flies, in terms of acceptor control, were found. Using G-3-P, acceptor control was lost in mitochondria from control flies above 29ºC, but was still measurable at 34ºC in mitochondria from thermotolerant flies. With pyruvate + proline as substrate acceptor control was demonstrable in mitochondria from both non-pre-treated control and thermotolerant flies at all experimental temperatures. The thermal sensitivities of the respiratory complexes were studied using the inhibitors rotenone and antimycin A. In mitochondria from LD(_50) treated control flies respiration uncoupled with FCCP was not restored to State II levels. However, in LD(_50) treated mitochondria from thermotolerant flies respiration uncoupled with FCCP was not different from State III respiration. These data suggest that the reduction in State III respiration after heating is owing to an inhibition of oxidation rather than phosphorylation. Complex I, NADH coenzyme Q reductase, was shown to be the most temperature sensitive of the respiratory complexes.