Fractal morphology, imaging and mass spectrometry of single aerosol particles in flight.

The morphology of micrometre-size particulate matter is of critical importance in fields ranging from toxicology to climate science, yet these properties are surprisingly difficult to measure in the particles' native environment. Electron microscopy requires collection of particles on a substrate; visible light scattering provides insufficient resolution; and X-ray synchrotron studies have been limited to ensembles of particles. Here we demonstrate an in situ method for imaging individual sub-micrometre particles to nanometre resolution in their native environment, using intense, coherent X-ray pulses from the Linac Coherent Light Source free-electron laser. We introduced individual aerosol particles into the pulsed X-ray beam, which is sufficiently intense that diffraction from individual particles can be measured for morphological analysis. At the same time, ion fragments ejected from the beam were analysed using mass spectrometry, to determine the composition of single aerosol particles. Our results show the extent of internal dilation symmetry of individual soot particles subject to non-equilibrium aggregation, and the surprisingly large variability in their fractal dimensions. More broadly, our methods can be extended to resolve both static and dynamic morphology of general ensembles of disordered particles. Such general morphology has implications in topics such as solvent accessibilities in proteins, vibrational energy transfer by the hydrodynamic interaction of amino acids, and large-scale production of nanoscale structures by flame synthesis.

Early nasojejunal tube feeding versus nil-by-mouth in acute pancreatitis: A randomized clinical trial.

BACKGROUND/OBJECTIVES: There is substantial evidence of superiority of enteral nutrition (EN) to parenteral nutrition in acute pancreatitis (AP) treatment, but few studies evaluated its effectiveness compared to no intervention. The objective of our trial was to compare the effects of EN to a nil-by-mouth (NBM) regimen in patients with AP. METHODS: Patients with AP were randomized to receive either EN via a nasojejunal tube initiated within 24 h of admission or no nutritional support. Systemic inflammatory response syndrome (SIRS) was assessed as the primary outcome. Secondary outcomes included mortality, organ failure, local complications, infected pancreatic necrosis, surgical interventions, length of hospital stay, adverse events and inflammatory response intensity. Outcomes were compared using Student's t-test and Mann-Whitney U test as appropriate. RESULTS: 214 patients were randomized in total, 107 to each group. SIRS occurrence was similar between groups, with 48 (45%) versus 51 (48%), respectively (RR 0.94; 95% CI 0.71-1.26). No significant reduction of persistent organ failure (RR 0.81; 95% CI 0.52-1.27) and mortality (RR 0.59; 95% CI 0.28-1.23) was present in the EN group. There were no significant differences in other outcomes between the groups. When analyzing the occurrence of SIRS and mortality in subgroup of patients with severe disease no significant differences were noted. CONCLUSION: Our results showed no significant reduction of persistent organ failure and mortality in patients with AP receiving early EN compared to patients treated with no nutritional support (NCT01965873).

Nanoscale spin reversal by non-local angular momentum transfer following ultrafast laser excitation in ferrimagnetic GdFeCo.

Ultrafast laser techniques have revealed extraordinary spin dynamics in magnetic materials that equilibrium descriptions of magnetism cannot explain. Particularly important for future applications is understanding non-equilibrium spin dynamics following laser excitation on the nanoscale, yet the limited spatial resolution of optical laser techniques has impeded such nanoscale studies. Here we present ultrafast diffraction experiments with an X-ray laser that probes the nanoscale spin dynamics following optical laser excitation in the ferrimagnetic alloy GdFeCo, which exhibits macroscopic all-optical switching. Our study reveals that GdFeCo displays nanoscale chemical and magnetic inhomogeneities that affect the spin dynamics. In particular, we observe Gd spin reversal in Gd-rich nanoregions within the first picosecond driven by the non-local transfer of angular momentum from larger adjacent Fe-rich nanoregions. These results suggest that a magnetic material's microstructure can be engineered to control transient laser-excited spins, potentially allowing faster (~ 1 ps) spin reversal than in present technologies.

Femtosecond dark-field imaging with an X-ray free electron laser.

The emergence of femtosecond diffractive imaging with X-ray lasers has enabled pioneering structural studies of isolated particles, such as viruses, at nanometer length scales. However, the issue of missing low frequency data significantly limits the potential of X-ray lasers to reveal sub-nanometer details of micrometer-sized samples. We have developed a new technique of dark-field coherent diffractive imaging to simultaneously overcome the missing data issue and enable us to harness the unique contrast mechanisms available in dark-field microscopy. Images of airborne particulate matter (soot) up to two microns in length were obtained using single-shot diffraction patterns obtained at the Linac Coherent Light Source, four times the size of objects previously imaged in similar experiments. This technique opens the door to femtosecond diffractive imaging of a wide range of micrometer-sized materials that exhibit irreproducible complexity down to the nanoscale, including airborne particulate matter, small cells, bacteria and gold-labeled biological samples.

Nanoplasma dynamics of single large xenon clusters irradiated with superintense x-ray pulses from the linac coherent light source free-electron laser.

The plasma dynamics of single mesoscopic Xe particles irradiated with intense femtosecond x-ray pulses exceeding 10(16) W/cm2 from the Linac Coherent Light Source free-electron laser are investigated. Simultaneous recording of diffraction patterns and ion spectra allows eliminating the influence of the laser focal volume intensity and particle size distribution. The data show that for clusters illuminated with intense x-ray pulses, highly charged ionization fragments in a narrow distribution are created and that the nanoplasma recombination is efficiently suppressed.

Elastographic parameters of liver steatosis and fibrosis predict independently the risk of incident chronic kidney disease and acute myocardial infarction in patients with type 2 diabetes mellitus.

AIMS: The aim of this prospective study was to examine the relationship between controlled attenuation parameter (CAP) and liver stiffness measurements (LSM) with the risk of developing a composite endpoint inclusive of incident acute myocardial infarction (AMI), cerebrovascular insult (CVI) or chronic kidney disease (CKD) in people with type 2 diabetes mellitus (T2DM). METHODS: This study included 238 T2DM outpatients without chronic liver diseases. RESULTS: The patient population was followed for a median period of 7.6 years. Kaplan-Meier survival analyses showed that there was a higher proportion of patients who developed the aforementioned composite outcome (P < 0.001 by the log-rank test), as well as CKD (P < 0.001) or AMI alone (P = 0.014) among those with elevated CAP values (≥238 dB/m) at baseline. Similarly, Kaplan-Meier survival analyses showed that there was a higher proportion of patients who developed the composite outcome (P < 0.001), as well as CKD (P < 0.001), or AMI alone (P < 0.001) among those with elevated LSM values (≥7.0/6.2 kPa). In multivariable regression analyses, the presence of elevated CAP (adjusted-hazard ratio 2.34, 95% CI 1.32-4.15) and elevated LSM (adjusted-hazard ratio 2.84, 95% CI 1.92-4.21), independently of each other, were associated with a higher risk of developing the composite outcome, as well as incident AMI or CKD alone after adjusting for traditional cardiovascular risk factors and diabetes-related variables. CONCLUSIONS: Our study shows that the elastographic parameters of liver steatosis and fibrosis independently predict the long-term risk of developing chronic vascular complications in T2DM patients.

Significant liver fibrosis, as assessed by fibroscan, is independently associated with chronic vascular complications of type 2 diabetes: A multicenter study.

AIMS: The aim of this study was to investigate whether controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), as assessed by vibration-controlled transient elastography (VCTE), are associated with chronic vascular complications of diabetes mellitus type 2 (T2DM). METHODS: We studied 442 outpatients with established T2DM, and who underwent VCTE and extensive assessment of chronic vascular complications of diabetes. RESULTS: A quarter of analyzed patients had a previous history of myocardial infarction and/or ischemic stroke, and about half of them had at least one microvascular complication (chronic kidney disease (CKD), retinopathy or polyneuropathy). The prevalence of liver steatosis (i.e., CAP ≥ 238 dB/m) and significant liver fibrosis (i.e., LSM ≥ 7.0/6.2 kPa) was 84.2% and 46.6%, respectively. Significant liver fibrosis was associated with an increased likelihood of having myocardial infarction (adjusted-odds ratio 6.61, 95%CI 1.66-37.4), peripheral polyneuropathy (adjusted-OR 4.55, 95%CI 1.25-16.6), CKD (adjusted-OR 4.54, 95%CI 1.24-16.6) or retinopathy (adjusted-OR 1.81, 95%CI 1.62-1.97), independently of cardiometabolic risk factors, diabetes-related variables, and other potential confounders. Liver steatosis was not independently associated with any macro-/microvascular diabetic complications. CONCLUSIONS: Significant liver fibrosis is strongly associated with the presence of macro-/microvascular complications in patients with T2DM. These results offer a new perspective on the follow-up of people with T2DM.

Toxic epidermal necrolysis associated with carvedilol treatment.

OBJECTIVE: To report a case of fatal toxic epidermal necrolysis associated with carvedilol treatment. CASE SUMMARY: Two days after the initiation of carvedilol treatment, a 70-year old woman presented with skin eruptions in the form of maculous rash with blisters that rapidly progressed to epidermal necrolysis. Although the suspected drug was withdrawn, the reaction was extremely rapid in its development with fatal outcome. DISCUSSION: Carvedilol is not a drug commonly associated with TEN. To our knowledge there are no cases of carvedilol related TEN reported in the literature. CONCLUSION: Because of the close temporal relationship between the initiation of carvedilol treatment and the appearance of skin eruptions, and because carvedilol was the only new medication the patient had taken, the etiology of TEN was most likely a reaction to this drug. Physicians should be aware of this extremely rare but serious ADR.

Systematic evaluation of FRAP experiments performed in a confocal laser scanning microscope--part II: Multiple diffusion processes.

A procedure for a systematic evaluation of fluorescence recovery after photo-bleaching (FRAP) data is presented that allows one to determine distributions of diffusion coefficients. The method provides a straightforward and calibration-free way to quantify multiple diffusion processes when FRAP is measured as a function of time and space by means of confocal laser scanning microscopy. It is verified utilizing FRAP experiments on mixtures of differently sized fluorescent micro-spheres as realizations of discrete D distributions.

Manipulation of oxygen radical-scavenging capacity in mice alters host sensitivity to tumor necrosis factor toxicity but does not interfere with its antitumor efficacy.

The role of oxygen free radicals in the toxicity and antitumor effect of tumor necrosis factor was investigated in vivo. Treatment of non-tumor-bearing mice and mice bearing methylcholanthrene-induced sarcomas with bovine CuZn superoxide dismutase or recombinant human CuZn superoxide dismutase afforded significant protection to these mice from a subsequent challenge with recombinant human tumor necrosis factor (rhTNF). Pretreatment with superoxide dismutase increased survival rates, at 48 h after rhTNF injection, in non-tumor-bearing mice from 22 to 65% and in tumor-bearing mice from 25 to 79%. Protection from rhTNF toxicity was not associated with any reduction in the therapeutic efficacy of rhTNF against methylcholanthrene-induced sarcomas in either s.c. or visceral sites (e.g., cure rates in mice bearing s.c. tumors which were treated with rhTNF without or with superoxide dismutase pretreatment were 18 and 39%, respectively). Furthermore, the administration of L-buthionine-S,R-sulfoximine, an inhibitor of glutathione synthesis, to mice bearing s.c. tumors resulted in increased rhTNF toxicity but no improvement in therapeutic efficacy. Tumor necrosis factor toxicity is mediated by the release of oxygen free radicals, probably from activated neutrophils, but its antitumor effect in methylcholanthrene-induced sarcomas is not dependent on their generation.

Mechanism of modification of rat brain lysophospholipase A activity by cationic amphiphilic drugs.

The three psychotropic cationic amphiphilic drugs, chlorpromazine, desmethylimipramine and propranolol were found to have biphasic effects on rat brain lysophospholipase A, stimulating the enzyme at low, and inhibiting it non-competitively at higher concentrations. Low concentrations (less than or equal to 50 microM) of the drugs prevented the formation of micelles of lysophosphatidylcholine, whereas high concentrations caused a phase transition of the substrate with formation of a highly ordered membranous lattice. A possible mechanism of stimulation and inhibition of the enzyme activity by cationic amphiphilic drugs is proposed. Stimulation is explained by a decrease in the concentration of substrate micelles, which are inhibitory for the activity, whereas inhibition may be caused by adsorption of the enzyme onto the membranous lattice formed by the substrate in the presence of high cationic amphiphilic drug concentrations.

The mechanism of modification by propranolol of the metabolism of phosphatidyl-CMP (CDP-diacylglycerol) and other lipids in the rat pineal gland.

The mechanism underlying the alteration of phospholipid metabolism in rat pineal gland in vitro produced by propranolol and tertiary amine local anesthetics was investigated. 0.1 mM propranolol did not affect either the levels or specific activity of [32P]ATP in glands. In the presence of the drug, the incorporation of cytidine, but not of inorganic phosphate, into phosphatidyl-CMP (CDP-diacylglycerol) was dependent on the cytidine concentration. The incorporation of glycerol into phosphatidyl-CMP, phosphatidylinositol and phosphatidylglycerol was enhanced by propranolol, whereas labeling of phosphatidylcholine was decreased. When both 1 mM propranolol and 1 mM inositol were present, labeling of phosphatidylinositol was further increased, stimulation of phosphatidyl-CMP and phosphatidylglycerol labeling was reduced and incorporation into phosphatidylcholine and triacylglycerol was depressed. The incorporation of [3H]inositol into pineal lipids was also enhanced by propranolol. 10 microM propranolol inhibited rat liver phosphatidic acid phosphohydrolase by 50%, while local anesthetics were less potent in the decreasing order: dibucaine greater than tetracaine greater than lidocaine greater than procaine. The propranolol-induced accumulation of phosphatidyl-CMP was prevented by supplying adequate freely diffusible inositol in the medium. The phosphatidyl-CMP which accumulated was not utilized for the enhanced formation of phosphatidylinositol brought about by norepinephrine. The results indicate that propranolol and local anesthetics redirect pineal phospholipid metabolism in part by inhibition of phosphatidic acid phosphohydrolase.

Alterations in the metabolism of choline-containing phospholipids by lithium and carbachol in SH-SY5Y neuroblastoma cells.

To investigate choline phospholipid metabolism in the human neuroblastoma cell line SH-SY5Y, cultures labeled with [14C-methyl]choline were incubated for up to 30 min in Krebs-Ringer-glucose-N-2-hydroxyethyl-piperazine-N1-2-ethane sulfonic acid (HEPES) buffer with or without 10 mmol/L LiCl. When desired, 1 mmol/L of the muscarinic agonist carbamoylcholine was present during the last minute of incubation. When cells were exposed for 10 min to lithium, radioactivity in phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin was 40%-140% higher than in controls incubated in buffer only. This contrasted with the results from carbamoylcholine-containing incubations, which gave radioactivities lower than or equal to controls. Carbamoylcholine added to the LiCl-containing incubations yielded results only minimally different from LiCl alone. Phosphorylcholine radioactivity was also elevated by about 50% after 10 min incubation with LiCl with or without added carbamoylcholine, but was not increased in incubations with the agonist by itself. Similar changes were observed for intracellular choline but after only 5 min. These data suggest that carbamoylcholine does not stimulate phosphatidylcholine degradation, whereas LiCl can significantly affect its metabolism and may affect signal transduction via second messengers in human neuroblastoma cells.

Ultrastructure of an identified molluscan neuron in organ culture and cell culture following axotomy.

We examined the ultrastructure of neuron 5 from the buccal ganglion of the mollusc Helisoma trivolvis after axotomy and organ culture, and after isolation of the same neuron in culture. Buccal ganglia containing axotomized neurons 5 were cultured either in host snails or in Leibovitz medium conditioned with ganglia. In addition, some neurons 5 were isolated from buccal ganglia by micro-dissection and plated into culture. Neuron 5 and its processes were identified in both whole mounts and plastic sections of buccal ganglia after intracellular injection with Lucifer Yellow or horseradish peroxidase. Five days after axotomy of neuron 5, thick sections of buccal ganglia stained with toluidine blue revealed that densely staining basophilic bodies (Nissl bodies) within the cytoplasm had dispersed, i.e., they had undergone chromatolysis. Coincident with chromatolysis was an overall increase in diffuse basophilic staining within the cytoplasm of neuron 5 when maintained in organ culture. The dispersion of Nissl bodies viewed by light microscopy correlated with a more freely arranged rough endoplasmic reticulum and associated polysomes within neuron 5 as seen by electron microscopy. Isolated neurons 5 did not possess densely staining Nissl bodies when examined after 2 days in vitro, thus indicating that chromatolysis occurred earlier in isolated neurons. Furthermore, no increase in diffuse cytoplasmic basophilia was observed within isolated neurons 5 cultured in vitro. However, isolated neurons 5 exhibited a marked increase in the number of lipid-like bodies (0.5-1.5 micron in diameter) that were particularly evident in scanning electron micrographs. Scanning and transmission electron micrographs revealed that the isolated neurons were free of associated glia, but non-neuronal cells (hemocytes) would attach themselves to the somata and neurites. Glia surrounding neuron 5 within buccal ganglia exhibited a marked hypertrophy following axotomy and organ culture. Hypertrophy of glia was absent, however, if ganglia were axotomized and left within the animal or axotomized ganglia were implanted into host animals and examined 5 days later by electron microscopy. These observations indicate that, following axotomy, a molluscan neuron may exhibit different morphological features depending on its microenvironment. In addition, the hypertrophy of glia surrounding neurons in Helisoma was not associated with axotomy per se, but with organ culture.

Routine chest radiographs in pediatric intensive care: a prospective study.

The clinical value of routine chest radiographs was prospectively evaluated in a pediatric intensive care unit. Physicians were asked to predict findings of clinical impact in 353 routine morning chest radiographs performed in 101 patients after examining the patients. In 81 instances (23%), the clinical impact of the chest radiographs was incorrectly predicted and significant alterations in management would have potentially been missed had the chest radiographs not been available. These 81 chest radiographs included 72 unpredicted radiographic changes of clinical significance, and nine chest radiographs in which a significant radiographic change was incorrectly predicted. Thirty five (43.2%) of these 81 chest radiographs had unpredicted pulmonary findings and 46 (56.8%) showed unpredicted appliance malpositions. Incorrect predictions were significantly associated with radiographs from patients who were younger, intubated, mechanically ventilated, and had indwelling central venous catheters. Level of training of the predicting physicians did not affect prediction accuracy. In analysis of 43 routine postintubation chest radiographs and 39 routine postcentral venous catheter placement chest radiographs, appliance malpositions were disclosed in 34.9% and 43.6%, respectively. Routine daily and post-appliance placement chest radiographs have significant clinical value in the pediatric intensive care unit.

Modifications of phospholipid metabolism induced by chlorpromazine, desmethylimipramine and propranolol in C6 glioma cells.

The effects of chlorpromazine (CPZ), desmethylimipramine (DMI) and propranolol (PRO) on phospholipid metabolism in C6 glioma cells were studied by following the incorporation of 32Pi, [U-14C]glycerol, [2-3H]glycerol and [1-14C]oleate into lipids. The drugs produced a dose-dependent increase in the incorporation of 32Pi and [U-14C]glycerol, but not of [1-14C] oleate, into total phospholipids, that reached a plateau at 200 microM CPZ and 500 microM DMI and PRO. The three drugs shifted the incorporation of precursors from neutral [phosphatidylcholine (PC) and phosphatidylethanolamine (PE)] to acidic phospholipids [phosphatidic acid (PA), phosphatidylinositol (PI), phosphatidylglycerol, phosphatidylinositol-4-phosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2)] in a dose-dependent, qualitatively similar manner. The incorporation of [2-3H]glycerol into diacylglycerol was also depressed markedly by CPZ. Addition of 1 mM 1,2-dioleoylglycerol, 1-oleoyl-2-acetylglycerol or oleate only partially reversed the decrease in PC labeling caused by CPZ. 12-O-Tetradecanoylphorbol-13-acetate counteracted this effect of CPZ completely but greatly increased PC labeling even in the absence of the drug. Polyphosphoinositides rapidly incorporated 32Pi at early times reaching a plateau in about 40 min. The labeling rate of PI was not parallel to that of PIP or PIP2 and continued to increase even after the polyphosphoinositides had reached a plateau. CPZ increased PI labeling much more than that of PIP and PIP2. These data suggest that cationic amphiphilic drugs may act by inhibiting CTP:phosphocholine cytidylyltransferase, thus decreasing incorporation of precursors into PC and PE; inhibiting PA phosphohydrolase with increased formation of phosphatidyl-CMP, the intermediate for the synthesis of acidic phospholipids; and stimulating the inositol exchange reaction, forming a pool of PI that is not available for PIP and PIP2 synthesis.

Stimulation of luteinizing hormone release by melittin and phospholipase A2 in rat pituitary cells.

Gonadotropin release in rat pituitary monolayer cultures was stimulated by phospholipase A2, as well as by its activator melittin. A dose-dependent stimulation of luteinizing hormone secretion by melittin was observed in a dose range of 10(-8) to 10(-4) M. A higher dose (1 mM) melittin had a sub-optimal effect. The stimulatory action of melittin was calcium-dependent and blocked by phospholipase A2 inhibitors, chloroquine and quinacrine. Similar to melittin, phospholipase A2 enhanced the effect of LH release in a dose range of 0.1-100 units/ml. The effect of this enzyme was also calcium-dependent with optimal calcium concentrations at 1.5 mM, as obtained also for melittin. In superfusion experiments, the stimulatory action of melittin and phospholipase A2 was reproducible in their effects on LH release in gonadotrophs. In addition, melittin (10(-7) M) stimulated LH and 3H-arachidonic acid efflux in superfused pituicytes following prelabelling with radiolabelled arachidonate. These data suggest that phospholipase A2, which releases arachidonic acid from phospholipids, may participate in controlling gonadotropin secretion in gonadotrophs, since arachidonic acid and its metabolites have previously been found to enhance gonadotropin release.

Effect of sodium arsenite on iNOS expression and vascular hyporeactivity associated with cecal ligation and puncture in the rat.

Induction of the heat shock response protects animals from either endotoxemia or peritonitis. In endotoxemia, heat shock protein (HSP) induction is associated with reversal of vascular hyporeactivity and inhibition of iNOS expression. Recent studies suggest differences in the inflammatory mechanisms during endotoxemia and peritonitis animal models and their response to therapeutic interventions. We therefore studied the effect of the HSP inducer sodium arsenite (SA) on vascular reactivity and iNOS expression in rats undergoing cecal ligation and puncture (CLP). CLP resulted in suppression of the pressor effect of norepinephrine (NE) in vivo (measured by changes in blood pressure in response to NE boluses) and ex vivo (changes in contraction force in isolated mesenteric arteries in response to NE concentrations), and in the expression of iNOS protein. Pretreatment of the rats with SA resulted in reversal of CLP-induced vascular hyporeactivity in vivo and ex vivo, and inhibition of iNOS expression after 22 h. SA pretreatment improved 7-day survival after CLP from 18.2% to 70% (P < 0.005). Glucocorticoid receptor inhibition did not affect the effect of HSP induction on iNOS expression. The similarity of the effect of HSP on vascular reactivity and iNOS expression in two distinct sepsis models suggests that this effect may be clinically important and that a causative relationship between HSP induction, iNOS inhibition, and reversal of vascular reactivity is likely.

Effect of tyrosine kinase inhibition on sepsis-induced vascular hyporesponsiveness, inos mrna expression and NF-kappaB nuclear translocation in rats.

The dependence of the critical steps in the sepsis cascade on the transcription factor NF-kappaB andation to nitric oxide (NO) production are controversial. Tyrosine kinase (TK) is involved in several of the steps, and TK inhibitors (TKI) inhibit lipopolysaccharide (LPS)-induced vascular hyporesponsiveness in septic animals. We studied the relationship of TK inhibition, hemodynamics, vascular contraction, iNOS mRNA expression and NF-kappaB translocation in anesthetized endotoxic rats. The TKI AG556 (2.5 mg/kg i.p.), given 1 h before i.v. endotoxin (LPS) resulted in attenuation of early (<60 min) and late (60-120 min) hypotension, improved contraction of mesenteric arteries to norepinephrine 4 h after LPS, and attenuated tissue iNOS mRNA expression. LPS-induced NF-kappaB translocation was unaffected. The observed dissociation between NF-kappaB translocation and the salutary effect of TKI in vivo and ex vivo and its effect on iNOS mRNA expression suggest that although NF-kappaB may be involved in the sepsis cascade, it may not be essential for some of the molecular and vascular consequences of septic shock.

Noninvasive positive-pressure ventilation facilitates tracheal extubation after laryngotracheal reconstruction in children.

Tracheal extubation after laryngotracheal reconstruction in children may be complicated by postoperative tracheal edema and pulmonary dysfunction. The replacement of a tracheal tube in this situation may exacerbate the existing injury to the tracheal mucosa, complicating subsequent attempts at tracheal extubation. We present two cases where noninvasive positive-pressure ventilation was employed to treat partial airway obstruction and respiratory failure in two children following laryngotracheal reconstruction. Noninvasive positive-pressure ventilation served as a bridge between mechanical ventilation via a tracheal tube and spontaneous breathing, providing airway stenting and ventilatory support while tracheal edema and pulmonary dysfunction were resolved. Under appropriate conditions, noninvasive positive-pressure ventilation may be useful in the management of these patients.