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At least 937 records · Page 52Linked to original sources
PubMed2005

Factors affecting older african american women's decisions to join the PLCO Cancer Screening Trial.

PURPOSE: The purpose of this study is to describe the factors associated with the decisions of older African American women to join the PLCO (Prostate, Lung, Colorectal and Ovarian) Cancer Screening Trial when recruited. METHODS: African American women between ages 55 and 74 years who were never diagnosed with a PLCO cancer were eligible for our study. Two methods of recruitment were used. First, mailings were sent to a random sample of women describing the PLCO followed by a telephone call to determine interest in the PLCO. If women were not interested in PLCO but consented to participate in our study, they were interviewed immediately. Second, we followed up with African American women who responded to mass mailings sent out before the start of our study by the Pittsburgh PLCO office. Women completed an interview about their cancer and clinical trial knowledge, attitudes, beliefs, and behaviors. The responses of women who joined the PLCO Trial are contrasted with the responses of women who did not join. RESULTS: Numerous factors were associated with the decision of older African American women to join the PLCO, including perceptions of cancer prevention and detection, the experience of having a loved one with cancer, knowledge of and experience with clinical trials, and beliefs regarding the benefits and risks of clinical trial participation. CONCLUSION: Minority recruitment to cancer clinical trials could be increased by designing interventions focused on individual, organizational, and community needs.

Black or African American↗
PubMed2002

Effects of hypoxia on respiratory neural output and lower esophageal sphincter pressure in piglets.

We have previously documented anatomic and functional relationships between ventilatory and autonomic neural output. Therefore, we hypothesized in this study that hypoxia-induced changes in respiratory neural output are associated with changes in autonomic regulation of lower esophageal sphincter (LES) pressure. Respiratory neural output, heart rate, and LES pressure were measured before and during a 3-min exposure to 8% oxygen (balance nitrogen) in 12 3- to 7-d-old piglets. Respiratory neural output was determined from diaphragmatic electromyogram and LES pressure from an esophageal catheter. Studies were repeated after atropine administration in eight animals. Hypoxic exposure resulted in significant increases in diaphragmatic amplitude, respiratory rate, and minute diaphragmatic activity as well as heart rate. The biphasic response of diaphragm amplitude peaked at 1 min, whereas the responses of respiratory frequency and heart rate were sustained. Hypoxia caused a 50% increase in LES pressure (p < 0.05), which was eliminated by i.v. atropine administration. Development of apnea during subsequent hyperoxic exposure was always followed by a decline in LES pressure. Hypoxia-induced increase in respiratory neural output and accompanying increase in heart rate are associated with enhanced constrictive output to the LES. Blockade by atropine implicates a peripheral cholinergic mechanism for this LES response. We speculate that whereas hypoxia in the presence of enhanced respiratory neural output seems to be protective against reflux, decreased respiratory drive and accompanying apnea may be associated with a decline in LES tone and predispose to gastroesophageal reflux.

Animals↗
PubMed2002

Epilepsy and the ketogenic diet: assessment of ketosis in children using breath acetone.

High-fat ketogenic diets increase ketones (acetoacetate, beta-hydroxybutyrate, and acetone) and are used to treat refractory seizures. Although ketosis is an integral aspect of these therapeutic regimens, the direct importance of ketosis to seizure control needs further investigation. An examination of this relationship requires a reliable, minimally invasive measure of ketosis that can be performed frequently. In the present study, we examined the use of breath acetone as a measure of ketosis in children with refractory seizures on a classic ketogenic diet. Results were compared with breath acetone levels in epilepsy and healthy controls. Children on the ketogenic diet had significantly higher fasting breath acetone compared with epilepsy or healthy controls (2530 +/- 600 nmol/L versus 19 +/- 9 nmol/L and 21 +/- 4 nmol/L, respectively; p < 0.05). One hour after consumption of a ketogenic breakfast meal, breath acetone increased significantly in epilepsy and healthy controls (p < 0.05), but not in children on a ketogenic diet. Children who were on the ketogenic diet for longer periods of time had a significantly lower fasting breath acetone (R(2) = 0.55, p = 0.014). In one child on the ketogenic diet, breath acetone was determined hourly over a 9-h period, both by gas chromatography and by a prototype hand-held breath acetone analyzer. Preliminary results using this hand-held breath acetone analyzer are encouraging. Breath acetone may be a useful tool in examining the relationship between ketosis and seizure control and enhancing our understanding of the mechanism of the ketogenic diet.

Acetone↗
PubMed2002

Inhibition of Na(+)/H(+) exchanger type 3 reduces duration of apnea induced by laryngeal stimulation in piglets.

Reflexes from the larynx induce cessation of breathing in newborn animals. The magnitude of respiratory inhibition is inversely related to the level of central chemical input. Recent studies indicate that selective inhibition of Na(+)/H(+) exchanger type 3 (NHE3) activates CO(2)/H(+)-sensitive neurons, resembling the responses evoked by hypercapnic stimuli. Hence, the use of NHE3 inhibitors may reduce reflexly mediated respiratory depression and duration of apnea in the neonatal period. This possibility was examined in decerebrate, vagotomized, ventilated, and paralyzed piglets by testing the effects of i.v. administration of NHE3 blocker S8218 on the response of phrenic nerve amplitude, frequency, and duration of apnea induced by graded electrical stimulation of the superior laryngeal nerve. Superior laryngeal nerve stimulation caused a significant decrease in phrenic nerve amplitude, frequency, minute phrenic activity, and inspiratory time (all p < 0.01) that was proportional to the level of electrical stimulation. Increased levels of stimulation were more likely to induce apnea both during and after cessation of stimulation. NHE3 blocker S8218 reduced the superior laryngeal nerve stimulation-induced decrease in phrenic nerve amplitude, minute phrenic activity, and phrenic nerve frequency (all p < 0.05) and reduced superior laryngeal nerve stimulation-induced apnea and duration of poststimulation apnea (p < 0.05). In six other pigs the brain concentrations of S8218 were measured at different intervals after i.v. administration of the drug and were found to be higher in the brain tissue than plasma at all intervals. These findings suggest that the use of NHE3 blockers may decrease the duration of apnea and possibly reduce the pathophysiologic consequences of potentially life-threatening apnea in infants.

Animals↗
PubMed2003

The basomedial hypothalamus modulates the ventilatory response to hypoxia in neonatal rats.

We sought to examine the role of the basomedial hypothalamus in the regulation of breathing in neonatal rats. Small basomedial hypothalamic lesions were produced by a lesioning agent, goldthioglucose, in 5-d-old male rat pups, and 2 d later, baseline ventilation and the ventilatory responses to hypoxia and hypercapnia were examined. When compared with vehicle-injected controls, goldthioglucose-lesioned rat pups had a significantly slower respiratory rate and longer expiratory time at baseline. Lesioned rats displayed an impaired increase in breathing frequency in response to hypoxia, and augmented increases in tidal volume and respiratory drive (the ratio of tidal volume to inspiratory time) during hypoxia relative to controls. Hypercapnic responses were not affected. These data demonstrate that cells in a restricted area of the hypothalamus specifically influence the respiratory response to hypoxia.

Animals↗
PubMed2006

Short-term mechanical ventilation increases airway reactivity in rat pups.

We used a rat pup model to delineate whether mechanical ventilation of 95% O2). After each intervention, they were returned to their mothers. On d 10 of life, all animals were anesthetized, paralyzed, and ventilated to measure pulmonary function. Total lung resistance (RL) and dynamic lung compliance (Cdyn) were measured in response to increasing intravenous doses of methacholine (0.03-1 microg/g) by head-out body plethysmography. Injection of methacholine caused a dose-dependent increase in RL and decrease in Cdyn. The response of both RL and Cdyn to methacholine was significantly potentiated by prior exposure to mechanical ventilation when compared with unventilated normoxic controls. The addition of hyperoxia to mechanical ventilation did not further potentiate responses to methacholine. Mechanical ventilation did not alter lung myosin or the number of inflammatory cells in airways of room air ventilated versus unventilated control animals. We conclude that a brief period of mechanical ventilation in rat pups increases airway reactivity 48 h after such exposure in the presence as well as absence of hyperoxic exposure. This represents a potentially important model to investigate the mechanisms involved in airway hyperreactivity induced by neonatal lung injury.

Airway Resistance↗
PubMed1996

Phenolic and tyrosyl ring iodothyronine deiodination and thyroid hormone concentrations in the human central nervous system.

In the present study we investigated the biochemical properties of in vitro phenolic (5'D) and tyrosyl (5D) ring deiodination and the tissue concentrations of T4, T3, and rT3 in adult human central nervous system (CNS) tissue. All samples were obtained from nontumoral tissue at autopsy (n = 6) or neurosurgical operation (n = 5). Both phenolic and tyrosyl ring deiodinase activities were demonstrable in all samples obtained intraoperatively, whereas only tyrosyl ring deiodination was evident in the tissues obtained postmortem. The phenolic ring deiodination pathway corresponded to the type II 5'-deiodinase isoenzyme with regard to its high affinity for T4 and rT3 (Km = 2.2 and 2.4 nmol/L, respectively), its insensitivity to 6-propyl-n-2-thiouracil (PTU), and the sequential reaction mechanism. No PTU-sensitive 5'-deiodination of rT3 was demonstrable. Tyrosyl ring deiodination of both T4 and T3 showed typical type III 5D kinetics (Ka, 6.5 nmol/L for T4 and 3.4 nmol/L for T3) and was PTU insensitive. Nanomolar concentrations of tissue T4, T3, and rT3 were detected in samples obtained both intraoperatively and postmortem. They were very similar to the absolute values of the apparent Km for T4, T3, and rT3 in the phenolic and tyrosyl ring deiodination pathways. In conclusion, we have demonstrated the coexistence of both phenolic and tyrosyl ring deiodinase activities in the human CNS. Their kinetic characteristics, substrate specificity, and reaction mechanisms are very similar to the corresponding type II 5'- and type III 5-iodothyronine deiodinase activities in rat brain. In contrast to the findings in the rat CNS, no PTU-sensitive phenolic ring deiodinase (i.e. type I 5'D) activity was found in the human CNS. This may explain the relatively high tissue concentrations of rT3.

Adolescent↗
PubMed2003

Elevated polyunsaturated fatty acids in blood serum obtained from children on the ketogenic diet.

The authors analyzed blood metabolites in nine children with epilepsy prior to starting the ketogenic diet (KD) and 3 to 4 weeks after KD therapy. Elevated beta-hydroxybutyrate and cortisol levels were observed in all children on the KD. Free fatty acids increased 2.2-fold on the KD, with significant elevations in most polyunsaturated fatty acids (PUFA; arachidonate increased 1.6- to 2.9-fold and docosahexaenoate increased 1.5- to 4.0-fold). The rise in total serum arachidonate correlated with improved seizure control. Elevated PUFA may represent a key anticonvulsant mechanism of the KD.

3-Hydroxybutyric Acid↗