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PubMed2004

Proteinuria in rats induced by serum from patients with collapsing glomerulopathy.

BACKGROUND: Primary collapsing glomerulopathy recurs postransplant, raising the possibility of circulating factors implicated in the pathogenesis of the disease. METHODS: To determine the presence of circulating factors in collapsing glomerulopathy patients, we tested serum from those patients in an in vivo assay. Eleven groups of rats received serum from collapsing glomerulopathy patients, idiopathic focal segmental glomerulosclerosis (FSGS) or healthy subjects in its native form, isolated IgG, or serum without IgG. The presence of proteinuria and creatinine clearance were determined. Histopathologic analysis included light, immunofluorescence, and electron microscopy. RESULTS: Collapsing glomerulopathy rats developed proteinuria while rats injected with serum from FSGS and healthy subjects did not. Rats injected with serum of collapsing glomerulopathy in its native form developed marked proteinuria (99.2 +/- 42 mg/24 hours at day 5, P= 0.0001, compared to the baseline), and decreased in creatinine clearance. Rats receiving isolated IgG or serum without IgG from collapsing glomerulopathy developed mild proteinuria (46.5 +/- 8.4 mg/24 hours and 30.9 +/- 11 mg/24 hours, respectively, at day 5 (P= 0.0001). Glomerular tuft retraction and podocyte damage were seen only in collapsing glomerulapthy rats. No abnormalities were found in rats injected with serum from FSGS or healthy subjects. CONCLUSION: Circulating factors in the serum of collapsing glomerulopathy patients produce podocyte damage, whereas such factors are not present in noncollapsing FSGS. IgG eluates from collapsing glomerulopathy produce proteinuria when injected into the rat. Such factors remain in the circulation when serum of patients is adsorbed into protein A, raising the possibility that there are more than one circulating factor present in patients with collapsing glomerulopathy.

Adolescent↗
PubMedDate not supplied

Upper airway dysfunction associated with collapse of the apex of the corniculate process of the left arytenoid cartilage during exercise in 15 horses.

OBJECTIVE: To report dynamic collapse of the apex of the left corniculate process under the right corniculate process into the airway at the dorsal apposition of the paired arytenoid cartilages during exercise as a cause of upper airway dysfunction in horses. DESIGN: Retrospective study. ANIMALS: Fifteen horses with a history of poor performance and/or upper respiratory tract noise during exercise. METHODS: Video recordings of all horses referred for upper airway evaluation using high-speed treadmill videoendoscopy (HSTV) between January 1998 and December 2003 were reviewed. Records of horses that developed dynamic collapse of the apex of the left corniculate process into the airway were included. Clinical history, age, gender, breed, and use of the horse were retrieved. RESULTS: Of 309 horses referred for examination for poor performance and/or upper respiratory tract noise during exercise, 15 (4.9%) had collapse of the apex of the left corniculate process under the right and into the airway at the dorsal apposition between the paired arytenoid cartilages during HSTV. There were 3 females and 13 males, aged from 2 to 5 years. Five horses had previous surgery for left recurrent laryngeal neuropathy (RLN): 2 had nerve muscle pedicle graft and 3 had laryngeal prosthesis. During HSTV, all 15 horses had progressive collapse of the apex of the left corniculate process under the right at the dorsal apposition of the 2 arytenoid cartilages, and into the dorsal aspect of the rima glottidis. Review of video recordings revealed that collapse of the apex of the corniculate process was followed by progressive collapse of the left aryepiglottic fold and left vocal fold. The ventral aspect of the left corniculate cartilage maintained abduction in all horses. Two horses also had progressive collapse of the right vocal fold, 1 had rostral displacement of the palatopharyngeal arch, and another had dorsal displacement of the soft palate. CONCLUSIONS: Dynamic collapse of the apex of the left corniculate process of the arytenoid cartilage under the right is an uncommon cause of upper airway dysfunction in horses and the pathogenesis is unclear. We speculate that the left arytenoideus transversus muscle is unable to support the dorsal apposition between the arytenoid cartilages. This loss of support allows the elastic cartilage of the left corniculate process to collapse under the right and into the airway, as inspiratory pressure increases during exercise. This condition may be associated with an unusually advanced neuropathy of the adductor components of the left recurrent laryngeal nerve and may be an unusual manifestation of RLN; however, this is speculative and further investigation is required to determine its cause. CLINICAL RELEVANCE: Dynamic collapse of the apex of the left corniculate process and into the airway at the dorsal apposition between the paired arytenoid cartilages can only be diagnosed during HSTV. It is an uncommon cause of upper airway dysfunction but may affect the athletic potential of racing Thoroughbreds and Standardbreds.

Animals↗
PubMed2000

The Rayleigh-like collapse of a conical bubble

Key to the dynamics of the type of bubble collapse which is associated with such phenomena as sonoluminescence and the emission of strong rebound pressures into the liquid is the role of the liquid inertia. Following the initial formulation of the collapse of an empty spherical cavity, such collapses have been termed "Rayleigh-like." Today this type of cavitation is termed "inertial," reflecting the dominant role of the liquid inertia in the early stages of the collapse. While the inertia in models of spherical bubble collapses depends primarily on the liquid, experimental control of the liquid inertia has not readily been achievable without changing the liquid density and, consequently, changing other liquid properties. In this paper, novel experimental apparatus is described whereby the inertia at the early stages of the collapse of a conical bubble can easily be controlled. The collapse is capable of producing luminescence. The similarity between the collapses of spherical and conical bubbles is investigated analytically, and compared with experimental measurements of the gas pressures generated by the collapse, the bubble wall speeds, and the collapse times.

Journal Article↗
PubMed1999

Role of cdk5 and tau phosphorylation in heterotrimeric G protein-mediated retinal growth cone collapse.

During axonal growth, repulsive guidance cues cause growth cone collapse and retraction. In the chick embryo, membranes from the posterior part of the optic tectum containing ephrins are original collapsing factors for axons growing from the temporal retina. We investigated signal transduction pathways in retinal axons underlying this membrane-evoked collapse. Perturbation experiments using pertussis toxin (PTX) showed that membrane-induced collapse is mediated via G(o/i) proteins, as is the case for semaphorin/collapsin-1-induced collapse. Studies with Indo-1 revealed that growth cone collapse by direct activation of G(o/i) proteins with mastoparan did not cause elevation of the intracellular Ca(2+) level, and thus this signal transduction pathway is Ca(2+) independent. Application of the protein phosphatase inhibitor okadaic acid alone induced growth cone collapse in retinal culture, suggesting signals involving protein dephosphorylation. In addition, pretreatment of retinal axons with olomoucine, a specific inhibitor of cdk5 (tau kinase II), prevented mastoparan-evoked collapse. Olomoucine also blocks caudal tectal membrane-mediated collapse. These results suggest that rearrangement of the cytoskeleton is mediated by tau phosphorylation. Immunostaining visualized complementary distributions of tau phospho- and dephosphoisoforms within the growth cone, which also supports the involvement of tau. Taking these findings together, we conclude that cdk5 and tau phosphorylation probably lie downstream of growth cone collapse signaling mediated by PTX-sensitive G proteins.

Animals↗
PubMed1993

Left ventricular diastolic collapse in regional left heart cardiac tamponade. An experimental echocardiographic and hemodynamic study.

OBJECTIVES: This study was designed to describe the hemodynamic abnormalities associated with the appearance of left ventricular diastolic collapse in the setting of regional left heart cardiac tamponade. BACKGROUND: Cardiac tamponade after heart surgery is frequently associated with localized pericardial effusion. Although right ventricular diastolic collapse and right atrial collapse are reliable echocardiographic findings in patients with circumferential pericardial effusion and tamponade, they are often not present in postoperative patients with localized pericardial effusion and regional left heart tamponade. Left ventricular diastolic collapse has been described in such patients, but the degree of hemodynamic alteration that exists with this finding is not known. METHODS: Acute regional left heart tamponade was produced 14 times in seven spontaneously breathing anesthetized dogs by infusing fluid into an isolated compartment created in the pericardial space adjacent to the left ventricular free wall. Continuous echocardiographic imaging and hemodynamic monitoring of left ventricular, systemic arterial, right atrial, pulmonary capillary wedge and pericardial pressures were performed. Measurements at baseline were compared with those made at the onset of left ventricular diastolic collapse and at decompensated tamponade. RESULTS: Left ventricular diastolic collapse was noted in all 14 episodes of regional tamponade. It occurred when pressure in the left pericardial compartment exceeded left ventricular diastolic pressure by 3.0 +/- 1.9 mm Hg. At the onset of left ventricular diastolic collapse, cardiac output and mean arterial pressure were significantly reduced from the control value (p < 0.05). Systolic hypotension was noted only twice at this stage, respiratory variation in systolic pressure > 10 mm Hg only once. The appearance of this sign was also associated with elevated left heart filling pressures. CONCLUSIONS: Left ventricular diastolic collapse is a reliable sign of regional left ventricular tamponade and is associated with a reduction in cardiac output. This echocardiographic finding usually occurs before the development of arterial hypotension and pulsus paradoxus. Thus, left ventricular diastolic collapse is potentially more reliable than hypotension or pulsus paradoxus in the diagnosis of regional left ventricular tamponade.

Acute Disease↗
PubMed2006

Specificity of the initial collapse in the folding of the cold shock protein.

The two-state folding reaction of the cold shock protein from Bacillus caldolyticus (Bc-Csp) is preceded by a rapid chain collapse. A fast shortening of intra-protein distances was revealed by Förster resonance energy transfer (FRET) measurements with protein variants that carried individual pairs of donor and acceptor chromophores at various positions along the polypeptide chain. Here we investigated the specificity of this rapid compaction. Energy transfer experiments that probed the stretching of strand beta2 and the close approach between the strands beta1 and beta2 revealed that the beta1-beta2 hairpin is barely formed in the collapsed form, although it is native-like in the folding transition state of Bc-Csp. The time course of the collapse could not be resolved by pressure or temperature jump experiments, indicating that the collapsed and extended forms are not separated by an energy barrier. The co-solute (NH4)2SO4 stabilizes both native Bc-Csp and the collapsed form, which suggests that the large hydrated SO4(2-) ions are excluded from the surface of the collapsed form in a similar fashion as they are excluded from folded Bc-Csp. Ethylene glycol increases the stability of proteins because it is excluded preferentially from the backbone, which is accessible in the unfolded state. The collapsed form of Bc-Csp resembles the unfolded form in its interaction with ethylene glycol, suggesting that in the collapsed form the backbone is still accessible to water and small molecules. Our results thus rule out that the collapsed form is a folding intermediate with native-like chain topology. It is better described as a mixture of compact conformations that belong to the unfolded state ensemble. However, some of its structural elements are reminiscent of the native protein.

Ammonium Sulfate↗
PubMed1999

Collapsing glomerulopathy: clinical characteristics and follow-up.

In 1986, Weiss et al reported a group of patients with nephrotic syndrome, progressive chronic renal failure, and the histopathologic features of glomerular capillary collapse. Similar lesions are often described in human immunodeficiency virus (HIV) nephropathy. We evaluated 893 consecutive nontransplant renal biopsies performed in our department and the follow-up of the patients at our outpatient service. Sixteen specimens were identified with the pathological features of collapsing glomerulopathy (focal segmental or global glomerular capillary collapse and visceral epithelial cell hyperplasia), with no evidence of HIV infection and/or intravenous drug abuse. Their clinical characteristics were analyzed and compared with a group of 29 patients with noncollapsing focal segmental glomerulosclerosis (FSGS). The follow-up period of both patient groups was 5 +/- 1.46 years. The Kaplan-Meier life table method was used to present survival of the patients. The age of both groups was similar, 34 +/- 4 years (mean +/- standard error of the mean) for patients with collapsing glomerulopathy and 35 +/- 3 years for those with FSGS. The serum creatinine level was greater in patients with collapsing glomerulopathy (183 +/- 31 micromol/L) compared with those with FSGS (115 +/- 18 micromol/L), but the difference was not significant (P = 0.0504). The difference in proteinuria was not significant (P = 0.7668); it was 5.83 +/- 0.74 g/d in patients with collapsing glomerulopathy and 5.42 +/- 0.84 g/d in those with focal sclerosing glomerulonephritis. The difference in systolic (P = 0.4) and diastolic blood pressure (P = 0.556) was also not significant. Survival of the patients with collapsing glomerulopathy was worse than that of patients with FSGS (P = 0.025). Renal function survived 5 years in 40% of the patients with FSGS, but patients with collapsing glomerulopathy had no renal function survival. Our data suggest that idiopathic collapsing glomerulopathy is a distinct clinicopathologic entity with similar clinical features to focal sclerosing glomerulonephritis, but a worse prognosis and a rapidly progressive course toward end-stage renal disease.

Adolescent↗
PubMedDate not supplied

Pathogenesis and diagnosis of delayed vertebral collapse resulting from osteoporotic spinal fracture.

BACKGROUND CONTEXT: In recent years there have been an increasing number of reports on surgical cases involving delayed neurological deficits caused by vertebral collapse after osteoporotic vertebral fracture. PURPOSE: We do not yet know which patients are most susceptible to delayed vertebral collapse and subsequent neurological deficits, or whether this pathological condition can be prevented or predicted. In this study, we investigated the mechanism of progression and radiographic features characteristic of this disease, and we report here the predictive or risk factors for delayed osteoporotic vertebral collapse. STUDY DESIGN: Retrospectively, we investigated the pathogenesis and diagnosis of delayed vertebral collapse with neurological deficit resulting from osteoporosis. PATIENT SAMPLE: A total of 28 patients (7 men and 21 women) with neurological deficits resulting from vertebral collapse caused by osteoporotic vertebral fractures were the subjects for this study. OUTCOME MEASURES: Comparisons and investigations about clinical features and radiographic findings between the patient group of delayed vertebral collapse with neurological deficits and the group of osteoporotic spinal fracture with no neurological deficits. METHODS: The following factors were examined: the cause of injury; the length of time from injury, or the onset of pain, to the onset of neurological symptoms; radiographic findings obtained during the above period; the clinical course of vertebral fracture on plain X-ray films; time of appearance of the intravertebral cleft, and its localization and changes. RESULTS: Six patients were hospitalized and prescribed a period of 2 weeks of bed rest followed by the fitting of a corset; seven outpatients were corseted but not prescribed bed rest; 15 patients were given medication only at an outpatient clinic. At radiography, intravertebral clefts were detected in 22 patients (79%) during the period from the appearance of pain to the onset of neurological deficit. In 14 patients (50%) who were radiographed every 1 to 2 weeks from the injury to the onset of neurological symptoms, the course of progression to collapse of the vertebral body could be observed. CONCLUSION: Initial correct diagnosis and immobilization are important in preventing the delayed collapse with neurological deficit. The presence of an intravertebral cleft and instability of the affected vertebra represent risk factors for vertebral collapse with neurological deficit, requiring careful observation.

Aged↗
PubMed2005

Effect of metal ions on monolayer collapses.

A Langmuir monolayer of stearic acid on pure water and in the presence of certain divalent metal ions such as Cd and Pb at pH approximately 6.5 of the subphase water collapses at constant area, while for other divalent ions such as Mg, Co, Zn, and Mn at the same subphase pH the monolayer collapses nearly at constant pressure. Films of stearic acid with Cd, Pb, Mn, and Co in the subphase (at pH approximately 6.5) have been transferred onto hydrophilic Si(001) using a horizontal deposition technique, just after and long after collapse. Electron density profiles obtained from X-ray reflectivity analysis show that a three-molecular-layer structure starts to form just after constant area collapse, where in the lowest molecular layer, in contact with the substrate, molecules are in asymmetric configuration, i.e., both hydrocarbon tails are on the same side of the metal-bearing headgroup that touches the substrate, while the molecules above the first layer are in symmetric conformation of the tails with respect to the headgroups. Further along collapse, when the surface pressure starts to rise again with a decrease in area, more layers with molecules in the symmetric configuration are added, but the coverage is poor. On the other hand, only bimolecular layers form after constant pressure collapse, with the lower and upper layers having molecules in asymmetric and symmetric configurations, respectively, and the upper molecular layer density increases with compression of the monolayer after collapse. A "Ries mechanism" for constant area collapse and a "folding and sliding mechanism" for constant pressure collapse have been proposed.

Journal Article↗
PubMed1994

Collapsing glomerulopathy: a clinically and pathologically distinct variant of focal segmental glomerulosclerosis.

Sixteen patients with renal biopsy findings of extensive focal glomerular capillary collapse, visceral epithelial cell hypertrophy and hyperplasia, and variable degrees of tubulointerstitial injury in the absence of evidence for human immunodeficiency virus (HIV) infection or intravenous drug abuse were prospectively identified by renal biopsy. The pathologic process was designated collapsing glomerulopathy to distinguish it from other patterns of focal glomerular sclerosis. The clinical and pathologic characteristics of these 16 patients were analyzed and compared to a group of 25 patients with noncollapsing focal segmental glomerulosclerosis (FSGS). Thirteen of 16 patients with collapsing glomerulopathy were black as compared with 11 of 25 with FSGS (P = 0.018). The most common findings at presentation were hypertension and manifestations of the nephrotic syndrome. Although the duration of symptoms prior to presentation was no longer in the collapsing glomerulopathy group, the presenting mean serum creatinine was higher in patients with collapsing glomerulopathy than in those with noncollapsing FSGS (3.5 +/- 3.4 mg/dl vs. 1.3 0.6 mg/dl, P = 0.001). Twenty-four-hour urine protein excretion was also higher in the collapsing glomerulopathy group (13.2 +/- 7.7 g/day vs. 4.6 +/- 4.5 g/day FSGS, P = 0.005). The collapsing glomerulopathy patients had a mean age of 41.4 +/- 19.1 (range 19 to 81), a male-to-female ratio of 11:5 and a black-to-white ratio of 13:3. Renal survival, evaluated by life-table analysis, was markedly worse in collapsing glomerulopathy patients than in FSGS patients (P = 0.0004). It is proposed that collapsing glomerulopathy is a distinct entity characterized by black racial predominance, massive proteinuria, relatively rapidly progressive renal insufficiency, and distinctive pathologic findings.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Collapsing glomerulopathy.

Collapsing glomerulopathy is a morphologic variant of focal segmental glomerulosclerosis (FSGS) characterized by segmental and global collapse of the glomerular capillaries, marked hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial disease. The cause of this disorder is unknown, but nearly identical pathologic findings are present in idiopathic collapsing glomerulopathy and human immunodeficiency virus (HIV)-associated nephropathy, and collapsing glomerulopathy has been associated with parvovirus B19 infection and treatment with pamidronate. The pathogenesis of collapsing glomerulopathy involves visceral epithelial cell injury leading to cell cycle dysregulation and a proliferative phenotype. Clinically, collapsing glomerulopathy is characterized by black racial predominance, a high incidence of nephrotic syndrome, and rapidly progressive renal failure. Collapsing glomerulopathy also may recur after renal transplantation or present de novo, often leading to loss of the allograft. The optimal treatment for collapsing glomerulopathy is unknown. Treatments may include steroids or cyclosporine in addition to aggressive blood pressure control, angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, and lipid lowering agents. The role of other immunosuppressive agents such as mycophenolate mofetil in the treatment of collapsing FSGS remains to be defined. Prospective clinical trials are needed to define optimal therapy of this aggressive form of FSGS.

Capillaries↗
PubMed2001

Growth cone collapse through coincident loss of actin bundles and leading edge actin without actin depolymerization.

Repulsive guidance cues can either collapse the whole growth cone to arrest neurite outgrowth or cause asymmetric collapse leading to growth cone turning. How signals from repulsive cues are translated by growth cones into this morphological change through rearranging the cytoskeleton is unclear. We examined three factors that are able to induce the collapse of extending Helisoma growth cones in conditioned medium, including serotonin, myosin light chain kinase inhibitor, and phorbol ester. To study the cytoskeletal events contributing to collapse, we cultured Helisoma growth cones on polylysine in which lamellipodial collapse was prevented by substrate adhesion. We found that all three factors that induced collapse of extending growth cones also caused actin bundle loss in polylysine-attached growth cones without loss of actin meshwork. In addition, actin bundle loss correlated with specific filamentous actin redistribution away from the leading edge that is characteristic of repulsive factors. Finally, we provide direct evidence using time-lapse studies of extending growth cones that actin bundle loss paralleled collapse. Taken together, these results suggest that actin bundles could be a common cytoskeletal target of various collapsing factors, which may use different signaling pathways that converge to induce growth cone collapse.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Venous collapse and the respiratory variability in systemic venous return.

OBJECTIVE: Venous collapse limits systemic venous return, but its effects on beat to beat respiratory venous return variations are less well known. The aim of this study was to investigate the effects of venous collapse on respiratory variations in venous return. METHODS: A model of venous collapse which included both an increase in haemodynamic resistance to flow and an increase in vessel compliance was incorporated in a previously described cardiovascular model. Respiration was simulated by 5 mm Hg swings of intrathoracic pressure (PTH) at different mean pressures such that the abdominal vena cava and jugular vein were either fully collapsed (mean PTH -11 mm Hg), in the transition zone between collapse and distension (mean PTH -6 mm Hg), or fully distended (mean PTH 9 mm Hg). The mean and standard deviations over each respiratory cycle of the venous return volume (flow integral over heart cycle) and the abdominal vena caval volume were recorded. RESULTS: Different venous return volume variabilities in the three operating zones of the vena cava were identified: (1) reduced variability in the collapsed zone associated with the increased haemodynamic resistance [venous return 93(SD 6) ml, abdominal vena caval volume 30(3) ml. absolute right atrial pressure -6.3(1.1) mm Hg]; (2) increased variability in the transition zone [venous return 86(24) ml, abdominal vena caval volume 81(15) ml, right atrial pressure -2.2(0.8) mm Hg]; (3) low variability in the distended zone [venous return 42(11) ml, abdominal vena caval volume 120(2) ml, right atrial pressure 10.1(1.1) mm Hg]. The greater the change in compliance with collapse the greater the increase in flow variability in the transition zone; with no change in compliance there was no increased flow variability in the transition zone. CONCLUSIONS: The results suggest that venous collapse increases the respiratory variations in venous return in the transition zone. As venous return variations contribute to arterial pressure variations, the collapsible nature of the great veins may influence respiratory variations in systemic arterial pressure.

Blood Circulation↗
PubMedDate not supplied

Induction of ventricular collapse by an axial flow blood pump.

An important consideration for clinical application of rotary blood pump based ventricular assist is the avoidance of ventricular collapse due to excessive operating speed. Because healthy animals do not typically demonstrate this phenomenon, it is difficult to evaluate control algorithms for avoiding suction in vivo. An acute hemodynamic study was thus conducted to determine the conditions under which suction could be induced. A 70 kg calf was implanted with an axial flow assist device (Nimbus/UoP IVAS; Nimbus Inc., Rancho Cordova, CA) cannulated from the left ventricular apex to ascending aorta. On initiation of pump operation, several vasoactive interventions were performed to alter preload, afterload, and contractility of the left ventricle. Initially, dobutamine increased contractility and heart rate ([HR] = 139; baseline = 70), but ventricular collapse was not achievable, even at the maximal pump speed of 15,000 rpm. Norepinephrine decreased HR (HR = 60), increased contractility, and increased systemic vascular resistance ([SVR] = 24; baseline = 15), resulting in ventricular collapse at a pump speed of 14,000 rpm. Isoproterenol (beta agonist) increased HR (HR = 103) and decreased SVR (SVR = 12), but ventricular collapse was not achieved. Inferior vena cava occlusion reduced preload, and ventricular collapse was achieved at speeds as low as 11,000 rpm. Esmolol (beta1 antagonist) decreased HR (HR = 55) and contractility, and ventricular collapse was achieved at 11,500 rpm. Episodes of ventricular collapse were characterized initially by the pump output exceeding the venous return and the aortic valve remaining closed throughout the cardiac cycle. If continued, the mitral valve would remain open throughout the cardiac cycle. Using these unique states of the mitral and aortic valves, the onset of ventricular collapse could reliably be identified. It is hoped that the ability to detect the onset of ventricular collapse, rather than the event itself, will assist in the development and the evaluation of control algorithms for rotary ventricular assist devices.

Adrenergic alpha-Agonists↗
PubMed2005

Investigations for the diagnostic recording of nasal wing collapse.

BACKGROUND: The inspiratory medial movement of the nasal wing at high flow velocities is a protective physiologic mechanism. If this collapse of the nasal wing occurs at lower flow velocities, it may result in nasal obstruction. "Nasal wing collapse" is generally a clinical diagnosis. However, in the pressure-flow relationship of rhinomanometry, the medial movement of the nasal wing can be documented in the inspiratory arm of the graph. The diagnostic impact of this hysteresis was investigated. METHODS: The pressure-flow curves of three box models and three nasal models with a moveable valve (analogous to the nasal wing) in the entrance area as well as three volunteers with unstable nasal wings were investigated. We recorded synchronously the pressure-flow relationship and by endoscopy the movement of the valve in the box models and the nasal wing in the volunteers on video. For evaluation, we used the frame by frame analysis of the tape. RESULTS AND CONCLUSIONS: The medial movement of the nasal wing causes a hysteresis in the inspiratory arm of the pressure-flow curve. At this point, the graph runs on or between two border curves, termed the "no collapse curve" (for the maximally opened valve or a stable nasal wing) and the "collapse curve" (for the subtotally closed valve or a collapsed nasal wing), respectively. Analogous to the nasal wing motion, the descending course of hysteresis runs in two phases, and the ascending course runs in three phases. The medial movement of the nasal wing is expressed by a deviation of the graph from the "no collapse curve." The flow, at which the graph leaves this curve, depends on the elasticity module of the nasal wing. The extent of nasal wing collapse is reflected by the approximation of the pressure-flow curve to the "collapse curve" of the graph. The hysteresis appears because of a late opening of the collapsed nasal wing.

Adult↗
PubMed2006

Comparison of conventional and collapsed region operation of capacitive micromachined ultrasonic transducers.

We report experimental results from a comparative study on collapsed region and conventional region operation of capacitive micromachined ultrasonic transducers (CMUTs) fabricated with a wafer bonding technique. Using ultrasonic pulse-echo and pitch-catch measurements, we characterized single elements of 1-D CMUT arrays operating in oil. The experimental results from this study agreed with the simulation results: a CMUT operating in the collapsed region produced a higher maximum output pressure than a CMUT operated in the conventional region at 90% of its collapse voltage (3 kPa/V vs. 16.1 kPa/V at 2.3 MHz). While the pulse-echo fractional bandwidth (126%) was higher in the collapsed region operation than in the conventional operation (117%), the pulse-echo amplitude in collapsed region operation was 11 dB higher than in conventional region operation. Furthermore, within the range of tested bias voltages, the output pressure monotonously increased with increased bias during collapsed region operation. It was also found that in the conventional mode, short AC pulses (larger than the collapse voltage) could be applied without collapsing the membranes. Finally, while no significant difference was observed in reflectivity of the CMUT face between the two regions of operation, hysteretic behavior of the devices was identified in the collapsed region operation.

Journal Article↗
PubMed1984

Right ventricular and right atrial collapse in patients with cardiac tamponade--a combined echocardiographic and hemodynamic study.

To determine the hemodynamic derangement associated with right ventricular diastolic collapse and to assess the value of right ventricular and right atrial collapse in identifying cardiac tamponade, two-dimensional echocardiograms were recorded simultaneously with measurement of right atrial, pulmonary capillary wedge, intrapericardial, and systemic arterial pressures and cardiac output in 16 patients as they underwent pericardiocentesis. Twelve patients (group I) had evidence of right ventricular or right atrial collapse or both on their echocardiograms and hemodynamic evidence of cardiac tamponade before pericardiocentesis. All hemodynamic parameters improved after pericardiocentesis (p less than or equal to .05). Continuous monitoring during pericardiocentesis in three of these patients showed significant improvement in all parameters except heart rate (p less than or equal to .02) at the point of disappearance of right ventricular diastolic collapse, with further improvement in cardiac output as pericardiocentesis continued (p less than .01). Right atrial collapse persisted after right ventricular collapse disappeared but was no longer present when pericardiocentesis was completed. Three patients (group II) had no right ventricular or right atrial collapse, no hemodynamic evidence of cardiac tamponade, and no improvement in hemodynamic parameters after pericardiocentesis. A single patient (group III) was found to have elevated right heart pressures and right ventricular hypertrophy before pericardiocentesis. Although there was hemodynamic evidence of cardiac tamponade in this patient, there was no evidence of right ventricular or right atrial collapse. In this study, the sensitivity of right ventricular collapse as a marker for cardiac tamponade was 92%, its specificity 100%, its accuracy 94%, and its predictive value 100%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Conditions before collapse of the contralateral hip in osteonecrosis of the femoral head.

BACKGROUND: Osteonecrosis of the femoral head is a disease which may cause rapid femoral head collapse in relatively young patients. Clinical results of prosthesis replacement in osteonecrosis patients are generally poorer than in age-matched patients with other diagnoses. The ultimate goal in treating these patients is therefore to preserve not replace the involved femoral head. The purposes of this study were to analyze outcomes by examining osteonecrotic hips before collapse and to justify the role of early surgical intervention for osteonecrosis of the femoral head. METHODS: Between 1993 and 1997, there were 275 consecutive patients with osteonecrosis of the femoral head who received joint replacement on 1 side. Among these patients, 100 contralateral hips with evidence of osteonecrosis in the stage before collapse were included in this study. Demographic information, laboratory data, and radiographs were reviewed and compared between patients whose collapse time was less than 1 year, between 1 and 2 years, and more than 2 years, and those who had no collapse at the latest follow-up. RESULTS: At the final follow-up, the overall collapse rate was 78%, and the collapse time was generally within 2 years. Patients with younger age (less than 50 years old), higher activity levels, and higher serum triglyceride levels were at higher risk of rapid collapse. CONCLUSION: In conclusion, we found that the disease progression rate is high in patients who have bilateral femoral head involvement. Early surgical intervention to preserve the femoral head should be adopted to prevent early femoral head collapse in these patients. In addition, risk factors such as high activity levels and abnormal lipid metabolism should also possibly be addressed in the therapeutic modality.

Adult↗