bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of clinical and ventilatory parameters on morphology of bronchopulmonary dysplasia
Authors: Gorenflo M. , Vogel M. , Herbst L. , Bassir C. , Kattner E. , Obladen M. 
Published: March 2007

AbstractOur aim was to assess multiple factors which contribute to bronchopulmonary dysplasia (BPD) in prematurely born neonates. Specific morphologic features might relate to cumulative oxygen dose Barotrauma, prematurity, infection, and persistent ductus arteriosus (PDA). Seventy‐two patients dying from BPD as defined by the histopathologic criteria of Stocker were analyzed retrospectively. Median (range) gestational age was 28 (25‐35) weeks, and median survival was 16 (5‐386) days. The infants were ventilated for 15 (5‐149) days with a mean inspired oxygen fraction (FiO2,) of 0.78. The cumulative oxygen dose and mean airway pressures were determined. The presence of neonatal infection, PDA, and interstitial lung emphysema (ILE) was assessed. Baseline lung disease was estimated as proposed by Palta. At autopsy, the degree of hyaline membranes, epithelial cell necrosis, emphysema, atelectasis, interstitial cell proliferation, and lung fibrosis was scored semiquantitatively (0 to 3+). The influence of neonatal infection, PDA, gestational age, survival, oxygen dose, or barotrauma on morphological findings was examined by multivariate analysis. We found “acute” BPD in 22, “reparative” in 34 and long‐standing‐healed in 16 cases. ILE within the first week was associated with interstitial cell proliferation and lung fibrosis in infants surviving more than 28 days. Initial barotrauma contributes to lung fibrosis in infants with BPD. © 1995 Wiley‐Liss, Inc.
Vitamin A status and airway infection in mechanically ventilated very‐low‐birth‐weight neonates
Authors: Shenai Jayant P. , Chytil Frank , Parker Robert A. , Stahlman Mildred T. 
Published: March 2007

AbstractVitamin A (retinol) plays an important role in immunity. Respiratory and enteral infections in children are associated with low serum vitamin A concentrations that improve during recovery. To test the hypothesis that airway infection in very‐low‐birth‐weight (VLBW) neonates likewise may be associated with a change in vitamin A status, we examined 20 VLBW neonates (selection criteria: birth weight 700–1300 g, gestational age 26–30 weeks, need for supplemental oxygen and mechanical ventilation for >72 hr after birth) who were enrolled in the control group of a randomized clinical trial of vitamin A supplementation reported earlier. We studied changes in weekly measurements of plasma concentrations of vitamin A and retinol‐binding protein (RBP) during 4 weeks following enrollment in the trial (postnatal day 4) and compared changes between periods with and without airway infections. Seventeen infants had 22 episodes of documented airway infection. Staphylococcus epidermidis was the predominant organism. Plasma vitamin A concentrations decreased during 19 out of 22. With airway infection (mean change: −4.1 to −18.6 μg/dL), while they increased during 37 out of 58 periods without airway infection (mean change: −0.2 to +5.8 μg/dl; P < 0.001). The mean (±SD) plasma vitamin A concentrations before, during, 1 week after, and 2 weeks after an episode of airway infection were 20.9 ± 8.3, 9.7 ± 4.1,12.8 ± 8.9, and 16.2 ± 7.2 μg/dL, respectively. The mean value during airway infection was significantly lower than those before and two weeks after airway infection (P < 0.05). All of the individual plasma vitamin A concentrations during airway infection were low (<20.0 μg/dL). Airway infection had no significant effect on plasma RBP concentrations. We conclude that airway infection in mechanically ventilated VLBW neonates is associated with low plasma vitamin A concentrations that improve during recovery. We speculate that the depletion of marginal liver stores of vitamin A from its increased tissue utilization during airway infection may account for this change in the vitamin A status. Further studies are needed to establish the cause and effect relationship between vitamin A deficiency and airway infection in these infants. © 1995 Wiley‐Liss, Inc.
The cost of childhood asthma to Australian families
Authors: Toelle Brett G. , Peat Jennifer K. , Mellis Craig M. , Woolcock Ann J. 
Published: March 2007

AbstractThere have been no estimates of the actual cost of asthma care to Australian families. Previous estimates have been of the total cost to the community and have relied upon data collected by government departments and agencies. It was the aim of this investigation to estimate the cost of childhood asthma from the parents perspective in Australian families. A total of 238 asthmatic children aged 8–12 years were identified through prevalence studies of asthma in Sydney and Belmont, N.S.W. Children were selected if they had wheezed in the previous 12 months, had used asthma medicines or had airway hyperresponsiveness when tested. The study sample had wide range of asthma severity. Data were collected retrospectively and prospectively. Parents completed questionnaire which asked about health insurance and special asthma equipment costs in the previous 12 months. Every 2 weeks for total of 3 months between February and June parents completed further questionnaires which assessed costs incurred because of their child's asthma, together with time spent obtaining treatment. Items included doctor consultations and tests, alternative practitioner consultations and tests, medications and alternative therapies purchased, hospital and ambulance use, and the cost of childcare as consequence of asthma. We collected two or more months of prospective data from total of 193 children. The mean annual cost of asthma to the family was A$212.48 per asthmatic child and 13.4 hr were spent obtaining treatment. For the group of children who had not visited doctor in the previous year, the mean annual cost was A$85.60 and 13.1 hr were spent obtaining treatment. For the group of children who had been admitted to hospital in the previous year, the mean annual cost was A$884.34 and 153.0 hr were spent obtaining treatment. We conclude that the cost of asthma and the time spent obtaining treatment increases with increasing severity of the illness. In cases in which the child's asthma is severe enough to require hospitalisation in the previous 12 months, the cost to the family may be considerable. © 1995 Wiley‐Liss, Inc.
Tryptase immunoreactive mast cell hyperplasia in bronchopulmonary dysplasia
Authors: Lyle Robert E. , Tryka A. Francine , Griffin W. Sue , Taylor Bonnie J. 
Published: March 2007

AbstractBronchopulmonary dysplasia (BPD), the most common cause of chronic lung disease in prematurely born infants, is histologically characterized by various degrees of airway and alveolar septal fibrosis. Tryptase, serine protease specific to mast cells, has been shown to have potent fibroblast mitogenic properties and in addition has been shown to be increased in adult fibrotic lung disorders. Based on this analogy, the distribution of pulmonary mast cells exhibiting tryptase immunoreactivity was investigated by immunoperoxidase staining in autopsy specimens of infants dying with BPD. Morphologically normal lung specimens from similarly aged infants dying of sudden infant death syndrome (SIDS) served as controls. Tryptase–positive mast cell counts were performed at 250× from at least 10 random fields in bronchial, peribronchiolar, and alveolar regions. Compared to controls, in lung sections exhibiting typical histologic features of long‐standing BPD, tryptase positive cells were significantly increased in bronchial (23.9 ± 3.6 vs 14.4 ± 2.3) and peribronchiolar (15.3 ± 3.2 vs 4.63 ± 0.6) regions compared to controls (P < 0.05, Student's t test). In particular, alveolar regions exhibiting moderate to severe degrees of septal fibrosis exhibited dramatic increase in the number of tryptase‐positive cells (9.83 ± 1.89 vs 0.34 ± 0.18, P = 0.003). These findings of tryptase‐positive mast cell hyperplasia in BPD suggest potential roles of mast cells as well as tryptase in the pathogenesis of this disease. © 1995 Wiley‐Liss, Inc.
Bronchial artery embolization in the management of hemoptysis in cystic fibrosis
Authors: Cipolli M. , Perini S. , Valletta E. A. , Mastella G. 
Published: March 2007

AbstractMassive hemoptysis and/or recurrent expectoration of measurable amounts of blood are common complications of chronic bronchopulmonary infections in cystic fibrosis (CF). When conservative treatment fails to control bleeding, surgery or bronchial artery embolization (BAE) is frequently considered. We present our experience and long‐term follow up of BAE in 14 CF patients (age range 15–39 years) with massive (6 subjects) and/or recurrent (8 subjects) hemoptysis not responsive to medical treatment. Seven had chronic hypercapnic respiratory failure. After angiographic evaluation, polyvinyl alcohol particles (halon) were injected to embolize obviously enlarged bronchial arteries. Seventeen procedures were performed in 14 patients and 36 bronchial arteries were embolized. All the patients stopped bleeding immediately upon BAE. Most of the patients had postembolization fever, dysphagia, and transient chest pain which were managed symptomatically. After median follow‐up period of 10.5 months (range 0.5–38 months), no recurrence of hemoptysis was observed in 8 patients who are still alive. In 3 patients hemoptysis recurred and they underwent reembolization after 3,22, and 25 months, respectively. Three subjects died of respiratory failure within 5 months from BAE. Presently, 50% of patients studied had a ≥ 1 year interval free of major hemoptysis after the first BAE. Our experience indicates that massive and/or recurrent hemoptysis in C:F patients can be safety and effectively managed by BAE if the procedure is performed by skilled practitioner. The procedure was well tolerated and resulted in prolonged and satisfactory bleeding control in most patients. © 1995 Wiley‐Liss, Inc.
Effects of streptozotocin‐induced diabetes on postpneumonectomy lung growth and connective tissue levels
Authors: Ofulue A. Felix , Thurlbeck William M. 
Published: March 2007

AbstractDiabetes is generally accompanied by abnormal levels of growth hormone and adrenal steroids, hormones known to modulate postpneumonectomy (post‐PNX) compensatory lung growth. Thus, we examined the possibility that diabetes may affect post‐PNX lung growth processes. Left PNX was performed in young diabetic rats (streptozotocin‐induced; 75 mg/kg body weight) (DM‐PNX) and in control rats (C‐PNX), for comparison with sham‐operated control rats (C‐SHAM). The rats were permitted free access to food and water. Examination at day 7 after surgery showed that right lung absolute dry weight and absolute DNA, collagen and elastin contents were increased in C‐PNX and DM‐PNX rats (but only C‐PNX values reached those of both lungs in C‐SHAM rats). Body weights (BW) of DM‐PNX rats were lower than those of C‐PNX and C‐SHAM rats. Lung DNNBW in C‐PNX and DM‐PNX rats were comparable, and matched values for both lungs in C‐SHAM rats. Lung dry weight/BW, collagen/BW, and elastin/BW in DM‐PNX rats exceeded values in C‐PNX rats and even more for values of both lungs in C‐SHAM rats. Data of another experiment, comparing DM‐PNX rats with body weight‐matched (by food limitation) PNX and control rats (WMC‐PNX and WMC‐SHAM rats, respectively) indicated comparable lung absolute DNA contents in DM‐PNX and WMC‐PNX rats (which matched values for both lungs in WMC‐SHAM rats), however, lung absolute collagen and elastic contents were greater in the DM‐PNX rats. These findings demonstrate that an underlying diabetic state per se does not prevent post‐PNX compensatory hyperplastic lung growth, but can result in increased connective tissue contents. © 1995 Wiley‐Liss, Inc.
Symptomatic increase in intracranial pressure following pancreatic enzyme replacement therapy for cystic fibrosis
Authors: Nasr Samya Z. , Schaffert Denise 
Published: March 2007

AbstractA newly diagnosed 5‐month‐old infant with cystic fibrosis (CF) developed signs and symptoms of increased intracranial pressure (ICP) within days of starting pancreatic enzyme replacement therapy. Symptoms promptly resolved on two occasions after stopping enzyme replacement. At 10 months of age, enzyme replacement was well tolerated. © 1995 Wiley‐Liss, Inc.
The effect of inhaled adrenaline on lung function of recurrently wheezy infants less than 18 months old
Authors: Henderson A. J. W. , Arnott J. , Young S. , Warshawski T. , Landau L. I. , Lesouëf P. N. 
Published: March 2007

AbstractInhaled bronchodilators have been shown not to improve lung function in infants with wheeze. This observation has led to the suggestion that airway wall edema may be more important than bronchoconstriction in infants with airway narrowing. Inhaled adrenaline is used to relieve upper airway edema in children with croup and has been demonstrated to improve clinical scores and lower pulmonary resistance in some infants with wheeze associated with bronchiolitis. The aim of the present study was to examine the effect of inhaled adrenaline on lung function in a group of infants with recurrent wheeze. Eleven infants aged 10 to 18 months with a history of recurrent wheeze were studied during an asymptomatic interval. Respiratory function was assessed (1) by measuring maximal expiratory flow at functional residual capacity (V̇maxFRC) during a forced partial expiratory maneuver and (2) by measuring conductance of the respiratory system Grs using a single expiratory occlusion technique. Following baseline measurements, the infants received 0.5 mg/kg adrenaline by nebulizer and serial lung function tests were repeated at 5 min intervals. Ten infants had abnormal baseline lung function (median V̇maxFRC 44.2% predicted; median Grs 34% predicted). Using a random effects model, V̇maxFRC and Grs declined significantly at 10 and 5 min after adrenaline, respectively. No significant improvements from baseline were observed in either measurement for up to 30 min following adrenaline delivery. It is concluded that inhaled adrenaline did not relieve airways obstruction in this group of asymptomatic infants with recurrent wheeze. Pediatr Pulmonol. 1995; 20:9–15. © 1995 Wiley‐Liss, Inc.
Effect of chestwall distortion on the measurement of pulmonary mechanics in preterm infants
Authors: Neto Galdino Silva , Gerhardt Tilo , Claure Nelson , Duara Shahnaz , Bancalari Eduardo 
Published: March 2007

AbstractThe purpose of this study was to determine the effect of chestwall distortion (CWD) on the measurement of pulmonary compliance (CL) and resistance (RL). Inductance plethysmography was used in 15 preterm infants to determine CWD as total compartmental displacement ratio (TCDR) and out of phase movement between ribcage and abdomen as phase shift (PS). Flow was measured by pneumotachography and esophageal pressure change (Pe) with a water‐filled catheter. CL and RL were calculated by linear regression analysis. Seven infants (mean ± SD: BW, 1,484 ± 186 g, GA 32.4 ± 2.2 weeks, age 8.7 ± 4.7 days) had a breathing pattern characterized by episodes with a high degree of CWD, followed by periods with minimal CWD (distortion group). In this group lung function measurements were analyzed separately during periods with and without CWD. The remaining 8 infants (BW, 1,244 ± 233 g, GA 30.4 ± 2.4 weeks, age 7.4 ± 3.1 days) always breathed with minimal CWD, and the measurements in this group (non‐distortion group) were used as a reference for the values obtained in the distortion group. Measurements of TCDR, PS, CL, RL, and tidal volume (VT) obtained in the absence of CWD were not significantly different between distortion and non‐distortion groups. The measurements obtained in the presence of CWD showed a significantly higher TCDR and PS, but CL and RL were not significantly different from the CL and RL measurements obtained in the distortion and non‐distortion groups in the absence of CWD. The only signficant effect of CWD was a reduction in VT. The results indicate that the moderate degree of CWD observed in the study population does not significantly contribute to the variability in CL and RL measurements in preterm infants. Pediatr Pulmonol. 1995; 20:34–39. © 1995 Wiley‐Liss, Inc.
High levels of complement‐activation capacity in sera from patients with cystic fibrosis correlate with high levels of IgG3 antibodies to Pseudomonas aeruginosa antigens and poor lung function
Authors: Pressler Tacjana , Jensen Elsebeth T. , Espersen Frank , Pedersen Svend S. , Høiby Niels 
Published: March 2007

AbstractHeat‐stable opsonins from sera of cystic fibrosis (CF) patients were investigated for their ability to activate complement. Complement activation by Pseudomonas aeruginosa after opsonization with patient serum was examined in a complement‐consumption assay. Absorption of patients' sera with formalin‐treated and boiled bacteria removed specific antibodies and the complement activation decreased. We found a positive correlation between serum complement‐activation ability and IgG3 antibody levels to lipopolysaccharide (LPS), alginate, and a crude mixture of P. aeruginosa antigens (sonicate) in a group of patients with high levels of anti‐Pseudomonas precipitins. In the same group of patients a significant negative correlation was found between complement activation and lung function. Eighteen patients have been followed longitudinally with serum samples covering the pre‐infection, the early, and the late stages of chronic infection. Patients with poor lung function showed significantly higher levels of complement‐activation capacity. We conclude that patients with high levels of specific IgG3 antibodies are able to induce a high level of complement activation and then develop more aggressive pulmonary tissue damage, probably secondary to local immune complex formation. Pediatr Pulmonol. 1995; 20:71–77. © 1995 Wiley‐Liss, Inc.
Congenital central hypoventilation syndrome: Cardiorespiratory responses to moderate exercise, simulating daily activity
Authors: Silvestri Jean M. , Weese‐Mayer Debra E. , Flanagan Erin A. 
Published: March 2007

AbstractChildren with congenital central hypoventilation syndrome (CCHS) lack normal awake ventilatory responses to hypoxia and hypercarbia, yet engage in daily activities typical of similarly aged children. Our patients with CCHS are assessed annually with a walking treadmill protocol to assess physiologic responses to different levels of simulated daily activity. We hypothesized that children with CCHS (compared with age‐ and sex‐matched healthy controls) would (1) exercise for shorter durations and reach lower peak speed and incline on the treadmill; (2) become more hypoxemic, more hypercarbic, and develop less tachycardia during activity; and (3) take longer to return to baseline oxygenation, ventilation, and heart rate than normal children. Seven children with CCHS [mean age, 6.9 ± 3.0 (SD) years] who required 24 h/day ventilatory support (diaphragm pacers while awake and mechanical ventilation asleep) and 7 controls performed a walking protocol on a treadmill with progressive increments in speed and incline. Hemoglobin saturations (SaO2), end‐tidal carbon dioxide concentrations (ETCO2), and heart rates (HR) were recorded at baseline conditions, during activity and during recovery. There were no significant differences between children with CCHS and controls in baseline values, duration of activity, peak speed, and incline achieved during walking and recovery time to baseline once the treadmill had stopped. However, children with CCHS became significantly more hypoxemic and hypercarbic during activity (P < 0.05), and they had a lower percent increase in HR during treadmill walking than controls (P < 0.05). These results offer the clinician an opportunity to adjust clinical management in children with CCHS by providing specific recommendations to parents about appropriate levels of activity for their children with CCHS. Although such was not the intent of the current research, this study will suggest further investigation into improved ventilatory support for these children during exercise. Pediatr Pulmonol. 1995; 20:89–93. © 1995 Wiley‐Liss, Inc.
Carotid bodies and ventilatory response to hypoxia in aminophylline‐treated piglets
Authors: Cattarossi Luigi , Haxhiu‐Poskurica Besa , Haxhiu Musa A. , Litmanovitz Ita , Martin Richard J. , Carlo Waldemar A. 
Published: March 2007

AbstractPeripheral chemoreceptors may be immature in neonatal animals, exhibiting maturational changes in the perinatal period. Even though methylxanthines are respiratory stimulants, many premature neonates do not respond to them. Thus, we hypothesized that carotid body activity is necessary for aminophylline to reverse hypoxia‐induced respiratory depression. We exposed 16 anesthetized newborn piglets (age 2‐7 days) to hypoxia (inhalation of 12% oxygen) for 5 min. Aminophylline (15 mg/kg iv) was administered either prior to (11 piglets) or following (5 piglets) carotid body denervation (CBD). Before CBD, hypoxia elicited transient initial increases in tidal volume (from 79 ± 4 to 99 ± 1% of maximum, mean ± SE), minute ventilation (from 64 ± 5 to 93 ± 4%), and peak phrenic electroneurogram (from 63 ± 8 to 91 ± 6%, all P < 0.05). This was followed by a decrease in tidal volume, minute ventilation and phrenic electroneurogram (all P < 0.05). Prior to CBD, aminophylline pretreatment prevented the decrease in all the measures of respiratory output during late hypoxia. After CBD, hypoxia induced an initial and sustained depression of ventilation (tidal volume from 100 to 33 ± 14%; frequency from 94 ± 4 to 42 ± 17%; minute ventilation from 100 to 32 ± 14%, all P < 0.05)and phrenic electroneurogram (peak phrenic from 100 to 47 ± 18%; minute phrenic from 85 ± 6 to 55 ± 21%, both P < 0.05). Administration of aminophylline after CBD did not prevent the profound respiratory depression elicited by hypoxia in the chemodenervated piglets. We conclude that aminophylline prevents respiratory depression during late hypoxia, however, in the absence of afferent input generated by the carotid bodies, aminophylline does not reverse respiratory depression induced by hypoxia in anesthetized newborn piglets. Pediatr Pulmonol. 1995; 20:94–100. © 1995 Wiley‐Liss, Inc.
Blunted peripheral chemoreceptor response to hyperoxia in a group of infants with bronchopulmonary dysplasia
Authors: Katz‐Salamon Miriam , Jonsson Baldvin , Lagercrantz Hugo 
Published: March 2007

AbstractInfants with BPD often suffer from chronic hypoxia and require supplemental oxygen (O2). This might affect the sensitivity of peripheral chemoreceptors. Therefore, we assessed peripheral chemoreceptor function in 25 infants with bronchopulmonary dysplasia (BPD) of varying severity, using the hyperoxic test. These infants were compared with 35 preterm infants who did not develop BPD. All infants were tested during the 40th week of postconceptional age and their mean postnatal age was 81.5 ± 16.3 days. Sixty percent (15/25) of the BPD infants lacked a hyperoxic response, while the proportion of nonresponders to O2, among the other groups was 20% (7/35). The intensity of this response was negatively correlated to time spent on a ventilator and positively to time without supplemental oxygen. The intensity of chemoreceptor function was closely related to the severity of BPD; none of the infants with the most severe form of BPD (grade 3) showed a ventilatory response to hyperoxia. Furthermore, infants with BPD needed significantly longer time to increase their saturation than did non‐BPD infants (4.7 and 9.3 sec, respectively). We conclude that many infants with BPD, particularly those with the most severe form of the disease, have abnormally functioning peripheral chemoreceptors. Pediatr Pulmonol. 1995; 20:101–106. © 1995 Wiley‐Liss, Inc.