Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “COLLAPSE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed2006

A new mechanism for gravitational-wave emission in core-collapse supernovae.

We present a new theory for the gravitational-wave signatures of core-collapse supernovae. Previous studies identified axisymmetric rotating core collapse, core bounce, postbounce convection, and anisotropic neutrino emission as the primary processes and phases for the radiation of gravitational waves. Our results, which are based on axisymmetric Newtonian supernova simulations, indicate that the dominant emission process of gravitational waves in core-collapse supernovae may be the oscillations of the protoneutron star core. The oscillations are predominantly of mode character, are excited hundreds of milliseconds after bounce, and typically last for several hundred milliseconds. Our results suggest that even nonrotating core-collapse supernovae should be visible to current LIGO-class detectors throughout the Galaxy, and depending on progenitor structure, possibly out to megaparsec distances.

Journal Article↗
PubMed2001

Solvent-induced collapse of alpha-synuclein and acid-denatured cytochrome c.

The effects of solution conditions on protein collapse were studied by measuring the hydrodynamic radii of two unfolded proteins, alpha-synuclein and acid-denatured ferricytochrome c, in dilute solution and in 1 M glucose. The radius of alpha-synuclein in dilute solution is less than that predicted for a highly denatured state, and adding 1 M glucose causes further collapse. Circular dichroic data show that alpha-synuclein lacks organized structure in both dilute solution and 1 M glucose. On the other hand, the radius of acid-denatured cytochrome c in dilute solution is consistent with that of a highly denatured state, and 1 M glucose induces collapse to the size and structure of native cytochrome c. Taken together, these data show that alpha-synuclein, a natively unfolded protein, is collapsed even in dilute solution, but lacks structure.

Circular Dichroism↗
PubMed1998

Podocytes undergo phenotypic changes and express macrophagic-associated markers in idiopathic collapsing glomerulopathy.

Collapsing glomerulopathy (CG), a severe form of focal segmental glomerulosclerosis (FSG), is characterized by tuft retraction and consolidation in numerous glomeruli and changes in podocyte morphology and topography. Other glomeruli are less affected. Collapsing glomerulopathy is also characterized by tubulointerstitial atrophy and fibrosis. The pathophysiology of the glomerular and tubulointerstitial lesions is poorly understood. We studied renal tissue of five Black and three White patients, all human immuno-deficiency virus (HIV) negative, with nephrotic syndrome, renal failure, and histological evidence of CG. Immunohistochemistry identified normal podocyte phenotypes by podocalyxin, vimentin and complement receptor 1 (CR1) labeling. Three monoclonal antibodies were used to further characterize podocyte epitopes: anti-CD68 clone KP1, anti-CD68 clone PG-M1 and anti-M130 clone M18 (Ber-MAC3). Light microscopy of collapsed glomeruli showed podocyte swelling, vacuolization, multinucleation, "cobblestone-like" alignment around the glomerular tuft, and pseudo-crescent formation in Bowman's space. In collapsed glomeruli, podocalyxin, vimentin and CR1 labeling tagged both normal and vacuolated podocytes still attached to the GBM, but labeling was not found in cobblestone-like podocytes or in podocytes detached from the GBM. Conversely, numerous podocytes undergoing detachment and shedding into Bowman's space expressed macrophagic-associated epitopes. Cells with macrophagic-associated epitopes clumped in cystically dilated tubules and were aligned in tubules of smaller caliber. Their appearance was that of viable cells. There was no morphologic indication that these cells expressing macrophage-associated antigens originated from outside the glomeruli or outside the tubules. We conclude that in CG podocytes detach from the GBM, lose their normal podocytic phenotype and acquire macrophage differentiation antigens. The presence of cells with such antigens in tubular lumens suggests that detached metaplastic podocytes progress along the tubule or, alternatively, that CG tubular cells also undergo metaplastic changes into macrophage-like cells.

Adult↗
PubMed1990

Collapse and rebound of a gas-filled spherical bubble immersed in a diagnostic ultrasonic field.

This work is concerned with the influence of the finite-amplitude distortion of a driving diagnostic ultrasonic field on the collapse and rebound of a gas-filled spherical microbubble, present in the exposed compressible liquid. Such an analysis is especially important since one of the mechanisms for cavitation damage comes from the very large gas pressures generated at bubble collapse and in the subsequent pressure wave formed by bubble rebound. Gilmore's model [F.R. Gilmore, "The growth or collapse of a spherical bubble in a viscous compressible liquid," Hydrodynamics Lab. Rep. No. 26-4, California Institute of Technology, Pasadena, CA (1952)] for bubble dynamics is used to obtain the motion of the bubble interface when subjected to a pulsed diagnostic ultrasonic field of large amplitude. Knowledge of the bubble motion allows one to derive the pressure distribution around the bubble. Numerical results over a range of initial bubble sizes, acoustic pressures, and frequencies relevant to medical use show that the strength of the pressure spikes radiated by the rebounding bubble depends upon (i) the acoustic frequency (f), (ii) the initial bubble size (R0), and (iii) the magnitude of the pressure amplitude of the fundamental (PF) in a Fourier series description of the distorted pulse. As the pressure spikes propagate outward from the bubble wall, their strength is attenuated as the reciprocal of the distance from the center of collapse.

Air Pressure↗
PubMed1997

Magnetic Collapse in Transition Metal Oxides at High Pressure: Implications for the Earth

Magnetic collapse in transition metal ions is predicted from first-principles computations at pressures reached in the Earth's lower mantle and core. Magnetic collapse would lead to marked changes in geophysically important properties, such as elasticity and conductivity, and also to different geochemical behavior, such as element partitioning, than estimated by extrapolating low-pressure data, and thus change the understanding of Earth's structure and evolution. Magnetic collapse results from band widening rather than from changes in crystal field splitting under pressure. Seismic anomalies in the outer core and the lowermost mantle may be due to magnetic collapse of ferrous iron, dissolved in iron liquid in the outer core, and in solution in magnesiowustite in the lowermost mantle.

Journal Article↗
PubMed1993

Role of intracellular calcium in NI-35-evoked collapse of neuronal growth cones.

A myelin-associated protein from the central nervous system, the neurite growth inhibitor NI-35, inhibits regeneration of lesioned neuronal fiber tracts in vivo and growth of neurites in vitro. Growth cones of cultured rat dorsal root ganglion neurons arrested their growth and collapsed when exposed to liposomes containing NI-35. Before morphological changes, the concentration of free intracellular calcium ([Ca2+]i) showed a rapid and large increase in growth cones exposed to liposomes containing NI-35. Neither an increase in [Ca2+]i nor collapse of growth cones was detected in the presence of antibodies to NI-35. Dantrolene, an inhibitor of calcium release from caffeine-sensitive intracellular calcium stores, protected growth cones from collapse evoked by NI-35. Depletion of these caffeine-sensitive intracellular calcium stores prevented the increase in [Ca2+]i evoked by NI-35. The NI-35-evoked cascade of intracellular messengers that mediates collapse of growth cones includes the crucial step of calcium release from intracellular stores.

Animals↗
PubMed2003

Central retinal artery and vein collapse pressure in eyes with chronic open angle glaucoma.

AIMS: To determine central retinal vessel collapse pressure in chronic open angle glaucoma. METHODS: For 19 eyes with chronic open angle glaucoma and 27 eyes of a control group, central retinal vessel collapse pressure was measured by a Goldmann contact lens fitted with a pressure sensor in its holding grip. RESULTS: Central retinal vein collapse pressure was significantly (p=0.001) higher in the glaucoma group than in the control group (26.1 (SD 26.4) relative units versus 6.1 (8.4) relative units). CONCLUSIONS: Measured by a new ophthalmodynamometer, central retinal vein collapse pressure measurements may be abnormally high in eyes with chronic open angle glaucoma.

Adult↗
PubMed2006

Collapse dynamics of smectic-A bubbles.

The collapse dynamics of smectic-A bubbles are analyzed experimentally and theoretically. Each bubble is expanded from a flat film stretched at the end of a hollow cylinder and deflated through a pressure release by means of a capillary tube. Its total collapse time can be varied between 0.1s and 20s by suitably choosing the length and the internal diameter of the capillary. This experiment allowed us to show that the collapse takes place in two steps: an initial one, which lasts a fraction of a second, where the meniscus destabilizes and fills up with focal conics, followed by a much longer period during which the bubble collapses and exchanges material with the meniscus. By measuring simultaneously the Laplace pressure and the internal pressure inside the bubble, we were able to fully characterize the shear-thinning behavior of the smectic phase within the meniscus. We emphasize that this method is generic and could be applied as well to other systems such as soap bubbles, on condition that inertial effects are negligible.

Algorithms↗
PubMed1977

Effect of lung collapse on compensatory lung growth.

The effect of unilateral lung collapse on compensatory lung growth was studied in 3-wk-old (young) and 10-wk-old (adult) male Long-Evans rats. Under light halothane anesthesia, left lung collapse was produced by injection of dental plastic through a thracheostomy cannula. The rats were killed either 5 days or 4 wk later. At 5 days postcollapse, the 3-wk-old rats had an increase in DNA over sham controls (21%) (P less than 0.05), with no significant change in the protein/DNA ratio. At 4 wk postcollapse, increases in DNA over shamoperated controls were observed in both the 3-wk-old (58%) and the 10-wk-old (28%) rats, whereas the protein/DNA ratio at both ages was significantly less than that of sham controls (P less than 0.05). Thus, unilateral lung collapse stimulates growth of the contralateral lung by cellular hyperplasia, not hypertrophy, both in the young and adult rat. The hyperplasia begins within 5 days after collapse and is greater by 4 wk. The extent of hyperplasia is greater in the young than in the adult rat.

Animals↗
PubMed1981

Human lung pressure-volume relationships: alveolar collapse and airway closure.

We investigated the effect of airway closure and alveolar collapse on the large-volume deflation and inflation transpulmonary pressure-volume (Ptp-V) curves of five postmortem excised human lungs. For stepwise static cycles, no inflection occurred on the deflation curve, while either one or two inflections occurred on the inflation curve. These relations were stimulated by a multicompartment model, which assumed a bimodal distribution of compartmental collapse-pressure differences. The simulations indicate that alveolar collapse can occur without causing an inflection on the deflation curve and that hysteresis in reopening of collapsed alveoli on inflation can account for a major portion of Ptp-V hysteresis. In contrast, for slow dynamic cycles, an inflection occurred on the experimental deflation Ptp-V curve, and when inflations were begun at sufficiently low volumes, volume did not change until a threshold pressure difference was reached about which PtP began to oscillate as lung volume increased. These differences in the stepwise static and dynamic Ptp-V curves can result from sustained airway closure on deflation and popping-opening on inflation.

Humans↗
PubMed1998

Dynamics of lung collapse and recruitment during prolonged breathing in porcine lung injury.

Oleic acid (OA) injection, lung lavage, and endotoxin infusion are three commonly used methods to induce experimental lung injury. The dynamics of lung collapse and recruitment in these models have not been studied, although knowledge of this is desirable to establish ventilatory techniques that keep the lungs open. We measured lung density by computed tomography during breath-holding procedures. Lung injury was induced with OA, lung lavage, or endotoxin in groups of six mechanically ventilated pigs. After a stabilization period, repetitive computed tomography scans of the same slice were obtained during prolonged expirations with and without positive end-expiratory pressure and during prolonged inspirations after 5 and 30 s of expiration. Lung collapse and recruitment occurred mainly within the first 4 s of breath-holding procedures in all three lung injury models, and some collapse and recruitment occurred even within 0.6 s. OA-injured lungs were significantly more unstable than lungs injured by bronchoalveolar lavage or endotoxin infusion. In this experimental setting, expiration times <0.6 s are required to avoid cyclic alveolar collapse during mechanical ventilation without extrinsic positive end-expiratory pressure.

Animals↗
PubMed1994

Effects of sleep deprivation and sleep fragmentation on upper airway collapsibility in normal subjects.

Sleep deprivation can induce or worsen nocturnal respiratory disturbances. In patients with sleep apnea hypopnea, sleep abnormalities consist of repetitive episodes of arousals and awakenings that lead to sleep fragmentation. Because the propensity for upper airway collapse is increased in these patients, we wondered if sleep fragmentation could increase upper airway collapsibility and contribute to the pathogenesis of this disease. In eight normal subjects, upper airway collapsibility was assessed during sleep by progressively decreasing the pressure in a nasal mask while recording airflow, mask, and esophageal pressures. The critical pressure was determined by the relationship between breath-by-breath values of maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding mask pressure. Critical pressure was measured twice in each subject: after one night of total sleep deprivation and after one night of sleep fragmentation using auditory stimuli. The two measures were done in random order 1 wk apart. A polysomnographic recording was obtained the night after each measurement of critical pressure. Sleep architecture was identical after sleep deprivation and fragmentation. Sleep-related breathing abnormalities were more frequent after sleep fragmentation than after sleep deprivation. Critical pressure was -17.1 +/- 6.8 cm H2O (mean +/- SEM) after sleep deprivation, and -12.3 +/- 6.3 cm H2O after sleep fragmentation (p < 0.05), corresponding to an earlier closing of the upper airway. We conclude that sleep fragmentation leads to a higher upper airway collapsibility than does sleep deprivation.

Adult↗
PubMed1991

Upper airway collapsibility in snorers and in patients with obstructive hypopnea and apnea.

During sleep, mild reduction in inspiratory airflow is associated with snoring, whereas obstructive hypopneas and apneas are associated with more marked reductions in airflow. We determined whether the degree of inspiratory airflow reduction was associated with differences in the collapsibility of the upper airway during sleep. Upper airway collapsibility was defined by the critical pressure (Pcrit) derived from the relationship between maximal inspiratory airflow and nasal pressure. In 10 asymptomatic snorers, six patients with obstructive hypopneas, and 10 patients with obstructive apneas, during nonrapid eye movement sleep, Pcrit ranged from -6.5 +/- 2.7 cm H2O to -1.6 +/- 1.4 and 2.5 +/- 1.5 cm H2O, respectively (mean +/- SD, p less than 0.001). Moreover, higher levels of Pcrit were associated with lower levels of maximal inspiratory airflow during tidal breathing during sleep (p less than 0.005). We conclude that differences in upper airway collapsibility distinguish among groups of normal subjects who snore and patients with periodic hypopneas and apneas. Moreover, the findings suggest that small differences in collapsibility (Pcrit) along a continuum are associated with reduced airflow and altered changes in pattern of breathing.

Airway Obstruction↗
PubMed2004

Quantitative assessment of tracheal collapsibility in infants with tracheomalacia.

Infantile tracheomalacia is a potentially life-threatening disease requiring prolonged artificial respiratory support. Diagnosis and management of this disease may be further improved by establishing a suitable objective and quantitative assessment protocol for tracheal collapsibility. It is our hypothesis that tracheal collapsibility can be represented by the relationship between intraluminal pressure and the cross-sectional area of the trachea. To test this hypothesis, static pressure/area relationships of the trachea were obtained from anesthetized and paralyzed infants, who were diagnosed as having tracheomalacia by endoscopic observation. These relationships were fitted on a linear regression model, followed by calculation of the estimated closing pressure. The tracheal closing pressure ranged from -8 to -27 cm H(2)O, suggesting easy collapsibility of the trachea during crying or coughing and noncollapsibility during the spontaneous respiratory cycle, which coincided with the infants' symptoms. It is our conclusion that tracheal collapsibility of infants with tracheomalacia can be quantitatively assessed by the static pressure/area relationship of the trachea obtained under general anesthesia and paralysis.

Airway Resistance↗
PubMed1973

Contributions of loss of lung recoil and of enhanced airways collapsibility to the airflow obstruction of chronic bronchitis and emphysema.

We investigated the contributions of intrinsic disease of the airways, loss of lung recoil and enhanced airway collapsibility to the airflow obstruction of 17 patients with chronic bronchitis and emphysema. Airways conductance at low flow (G(aw)), maximum expiratory flow (V(E, MAX)) and static lung recoil pressure [P(st) (l)] were measured at different lung volumes, and conductance-static recoil pressure and maximum flow-static recoil pressure curves constructed. Low values of DeltaG(aw)/DeltaP(st) (l) and DeltaV(E), max/DeltaP(st) (l) were attributed to intrinsic airways disease. Airway collapsibility was assessed by comparing G(aw) with upstream conductance on forced expiration and by the intercept of the maximum flow-static recoil curve on the static recoil pressure axis (P(tm)'). All patients had reduced G(aw) at all volumes but in seven DeltaG(aw)/DeltaP(st) (l) was normal. On forced expiration, maximum flow in all patients was reduced more than could be accounted for by loss of lung recoil. DeltaV(E, MAX)/DeltaP(st) (l) was reduced in the patients in whom DeltaG(aw)/P(st) (l) was low. In contrast DeltaV(E, MAX)/DeltaP(st) (l) was normal in three and only slightly reduced in another three of the seven patients with normal DeltaG(aw)/DeltaP(st) (l). In these patients G(aw) greatly exceeded upstream conductance and P(tm)' was increased.We conclude that loss of lung recoil could account for the reduction in resting airways dimensions in 7 of the 17 patients. Enhanced airway collapsibility commonly contributed to reduction in maximum flow. In three patients the airflow obstruction could be entirely accounted for by loss of lung recoil and enhanced airway collapsibility.

Adult↗
PubMed2000

Site of airway collapse in obstructive sleep apnea after uvulopalatopharyngoplasty.

The objective of this prospective study was to determine the site and pattern of upper airway collapse by a multiple-catheter technique in subjects demonstrated to have obstructive sleep apnea (OSA) after uvulopalatopharyngoplasty (UPPP). Standard diagnostic nocturnal polysomnography (PSG) was done on all subjects. The PSG recordings included electroencephalogram, electrooculogram, electrocardiogram, chin and leg electromyograms, nasal and oral airflow, and abdominal effort. Polysomnography with a multiport flexible airway Gaeltec catheter was performed in 22 subjects. The Gaeltec flexible airway catheter has 4 high-fidelity pressure sensors to aid in determining the primary site of airway collapse. The primary site of airway collapse was determined by differential pressure gradients between pressure ports and by visual inspection of the pressure tracings. Forty-two subjects with prior UPPP from a total of 60 (39 men and 3 women, ages 33 to 61) agreed to be to studied by the standard PSG technique. Thirty-five subjects complained of excessive daytime sleepiness. Ten had mild OSA, 10 had moderate OSA, 12 had severe OSA, and 10 were "normal." Of the 22 subjects who had airway catheter monitoring, 3 of the normals were reclassified as having upper airway resistance (mean peak negative esophageal pressure of -28 cm H2O); 2 patients demonstrated airway obstruction in the nasopharynx, 2 at the oropharynx, and 11 at the level of the hypopharynx. Postoperative nocturnal PSG data were compared to data gathered prior to UPPP. The mean respiratory disturbance index (RDI) for the catheter group was 54 events per hour prior to UPPP, and the mean RDI after surgery was 44. There was no correlation between the severity of OSA and the stage of sleep. We conclude that the majority of patients who complain of excessive daytime sleepiness following UPPP have OSA with the primary site of obstruction at the level of the hypopharynx. The severity of airway collapse is variable during each stage of sleep. Esophageal pressure monitoring during sleep should be considered when evaluating symptoms of persistent OSA in patients who have had UPPP.

Adult↗
PubMed2002

Surgery of the nasal columella in external valve collapse.

The authors describe and discuss their experience with the collapse of the external nasal valve, focusing on the role that surgery of the columella plays in solving this problem. Thirty-seven cases were treated. In all but I there had been a previous septorhinoplasty. Seven patients had concomitant internal valve collapse. A modified alarplasty associated with columelloplasty was adopted in the cases with severe collapse. When the reduction of the nostril opening was mild to moderate, the surgical strategy varied depending on the width of the columella base: alarplasty in cases with a narrow to normal columella, and columelloplasty in the presence of a wide columella base. The authors' philosophy tends to minimize intervention on the nasal valve areas. Their results demonstrate that when the collapse and its functional effect are not too severe, a good result can be achieved by working only on the columella, especially if its base is significantly wide.

Humans↗
PubMed1992

Pediatric tracheobronchomalacia and major airway collapse.

Based on histopathologic, endoscopic, and clinical findings of the flaccid airway, new descriptive terms--major airway collapse types 1 through 3--are proposed to better define tracheobronchomalacia. A typing and grading system is offered to objectively analyze and compare clinical cases. Endoscopic and anesthetic techniques are presented for use in children with respiratory distress suggestive of tracheobronchomalacia. Spontaneous ventilation with laryngoscopic insufflation of anesthetic gases and the use of small-diameter telescopes without bronchoscopes are key elements for the examination of the dynamic pediatric airway. Pitfalls of classic bronchoscopy techniques are described that can lead to a missed diagnosis. Between 1987 and 1990, over 200 telescopic bronchoscopies were performed at Wilford Hall US Air Force Medical Center on 129 children 3 years old and younger with respiratory distress. By means of the described techniques, 38 children (30%) with major airway collapse were identified. Major airway collapse was associated with a variety of endoscopic and cardiac abnormalities. With the emergence of sophisticated neonatal pediatric respiratory care, a growing number of premature infants with major airway collapse are surviving. Early, precise endoscopic diagnosis allows optimal management.

Abnormalities, Multiple↗