| 1. |
- Donaldsson, Snorri, et al.
(author)
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Comparison of Respiratory Support After Delivery in Infants Born Before 28 Weeks Gestational Age The CORSAD Randomized Clinical Trial
- 2021
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In: JAMA pediatrics. - : AMER MEDICAL ASSOC. - 2168-6203 .- 2168-6211. ; 175:9, s. 911-918
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Journal article (peer-reviewed)abstract
- IMPORTANCE Establishing stable breathing is a key event for preterm infants after birth. Delivery of pressure-stable continuous positive airway pressure and avoiding face mask use could be of importance in the delivery room. OBJECTIVE To determine whether using a new respiratory support system with low imposed work of breathing and short binasal prongs decreases delivery room intubations or death compared with a standard T-piece system with a face mask. DESIGN, SETTING, AND PARTICIPANTS In this unblinded randomized clinical trial, mothers threatening preterm delivery before week 28 of gestation were screened. A total of 365 mothers were enrolled, and 250 infants were randomized before birth and 246 liveborn infants were treated. The trial was conducted in 7 neonatal intensive care units in 5 European countries from March 2016 to May 2020. The follow-up period was 72 hours after intervention. INTERVENTIONS Infants were randomized to either the new respiratory support system with short binasal prongs (n = 124 infants) or the standard T-piece system with face mask (n = 122 infants). The intervention was providing continuous positive airway pressure for 10 to 30 minutes and positive pressure ventilation, if needed, with the randomized system. Main Outcomes and Measures The primary outcome was delivery room intubation or death within 30 minutes of birth. Secondary outcomes included respiratory and safety variables. RESULTS Of 246 liveborn infants treated, the mean (SD) gestational age was 25.9 (1.3) weeks, and 127 (51.6%) were female. A total of 41 infants (33.1%) receiving the new respiratory support system were intubated or died in the delivery room compared with 55 infants (45.1%) receiving standard care. The adjusted odds ratio was statistically significant after adjusting for stratification variables (adjusted odds ratio, 0.53; 95% CI, 0.30-0.94; P = .03). No significant differences were seen in secondary outcomes or safety variables. CONCLUSIONS AND RELEVANCE In this study, using the new respiratory support system reduced delivery room intubation in extremely preterm infants. Stabilizing preterm infants with a system that has low imposed work of breathing and binasal prongs as interface is safe and feasible.
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| 2. |
- Li, Yinghua
(author)
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Ureaplasma urealyticum induced pulmonary inflammation in the development of chronic lung disease of prematurity
- 2001
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Doctoral thesis (other academic/artistic)abstract
- Chronic lung disease (CLD) of prematurity is a prolonged respiratory failure in very-lowbirthweight neonates. This disorder is multifactorial and associated with an early increase in the numbers of neutrophils and alveolar macrophages, together with. morphological abnormalities in epithelial and endothelial cells. Infection and associated inflammatory responses in the lungs play important roles in the development of CLD. Ureaplasma urealyticum has been postulated to be of importance in this context, but this is still a matter for debate. Treatment of neonates with steroids provides some improvement. Proinflammatory cytokines have been implicated as being involved in the development of CLD. In the present study, production of TNF-alpha and IL-6 by both a human and a rat macrophage cell line was found to increase after stimulation with U. urealyticum antigen. This induction was down-regulated by dexamethasone, budesonide and recombinant IL-10 (rIL-10) in the human macrophage cell line. In tracheobronchial aspirate fluid (TAF) macrophages, U. urealyticum antigen enhanced the production, of TNF-alpha 14-84% and IL-6 46-268%. In the rat alveolar macrophage cell line, steroids inhibited the increases in IL-6 and TNF-alpha production caused by U. urealyticum antigen, whereas rat rIL- 10 was without effect. Nitric oxide (NO) has been suggested to be an important mediator of inflammation associated with pulmonary infections. We discovered that U. urealyticum antigen stimulates alveolar macrophages directly to increase their production of NO in a dose- and time-dependent manner. This effect was further enhanced by IFN-gamma, while being attenuated by budesonide and dexamethasone. The NO was regulated at transcriptional levels as measured by inducible NO synthase (iNOS). The NO formed in response to U. urealyticum caused a 6-fold reduction in the growth rate of this organism itself after 10 hours of infection. Vascular endothelial growth factor (VEGF) and intercellular adhesion molecule-1 (ICAM-1) may be involved in both early and later pathological changes in the lung during the development of CLD. We found that U. urealyticum antigen enhances expression of VEGF, cell surface and soluble ICAM-1 by human macrophages in a dose-dependent manner, an effect which is also inhibited by budesonide and dexamethasone. The extent of this up-regulation of ICAM-1 was reduced by 86% when TNF-alpha was prevented from exerting its action by an anti-TNF-alpha antibody. In addition, U. urealyticum antigen triggered activation of nuclear factor -kappaB (NF-kappaB). This observation suggests a possible mechanism for the increases in cytokine production, and expression of iNOS, growth factor and cellular adhesion molecule evoked by this antigen. In our clinical study, levels of TGF-beta I in TAF from infants who developed CLD were found to be significantly elevated during the first week of postnatal life and remain elevated at 2 weeks and even beyond 4 weeks of age. These levels of TGF-beta I were not significantly decreased by treatment with steroids in 6 infants with CLD. IL-10 was detected in 12/44 (27%) TAF samples from 24 infants who developed CLD, compared to 6/57 (11 %) TAF samples from 22 preterm infants who did not develop this disease. These findings indicate that infection by U. urealyticum may be an important causative factor in the development of CLD. NO is probably involved in host defenses against such infection. The down- regulatory effect by steroids might in part explain the beneficial results of treating neonates with CLD with these agents. TGF-beta1 might play an important role in the fibrotic response observed in the CLD lung.
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| 3. |
- Piao, Yinghua, et al.
(author)
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An extensive Raman spectroscopic investigation of ultrathin Co1-xNixSi2 films grown on Si(100)
- 2012
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In: Journal of Vacuum Science & Technology. A. Vacuum, Surfaces, and Films. - : American Vacuum Society. - 0734-2101 .- 1520-8559. ; 30:4, s. 041511-041518
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Journal article (peer-reviewed)abstract
- Ultrathin silicide films were formed by starting from 1-8 nm thick Co1-xNix (x = 0, 0.25, 0.5, 0.75, and 1) at 350 degrees C-900 degrees C. For each composition x, there exists a critical thickness above which the transition temperature from monosilicides CoSi and NiSi to a disilicide-like phase increases with increasing film thickness. Below this thickness, the disilicide phase seems to form without exhibiting the monosilicides within the detection resolution limits of transmission electron microscopy and Raman spectroscopy. Raman spectroscopic analysis seems to indicate that Ni could be dissolved in the CoSi lattice to a certain fraction despite the fact that CoSi and NiSi are distinct with different crystallographic structures. Moreover, the disorder-induced Raman scattering in NiSi2 is found to be enhanced by Co incorporation. The observed annealing behaviors are attributed to variations in free energy change for phase transition caused by differences in metal thickness.
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| 4. |
- Zhang, Jiayi, et al.
(author)
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Spectral and Energy Efficiency of Cell-Free Massive MIMO Systems with Hardware Impairments
- 2017
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In: 2017 9TH INTERNATIONAL CONFERENCE ON WIRELESS COMMUNICATIONS AND SIGNAL PROCESSING (WCSP). - : Institute of Electrical and Electronics Engineers (IEEE). - 9781538620625
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Conference paper (peer-reviewed)abstract
- Cell-free massive multiple-input multiple-output (MIMO), with a large number of distributed access points (APs) that jointly serve the user equipments (UEs), is a promising network architecture for future wireless communications. To reduce the cost and power consumption of such systems, it is important to utilize low-quality transceiver hardware at the APs. However, the impact of hardware impairments on cell-free massive MIMO has thus far not been studied. In this paper, we take a first look at this important topic by utilizing well-established models of hardware distortion and deriving new closed-form expressions for the spectral and energy efficiency. These expressions provide important insights into the practical impact of hardware impairments and also how to efficiently deploy cell-free systems. Furthermore, a novel hardware-quality scaling law is presented. It proves that the impact of hardware impairments at the APs vanish as the number of APs grows. Numerical results validate that cell-free massive MIMO systems are inherently resilient to hardware impairments.
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| 5. |
- Zhang, Jiao, et al.
(author)
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Wnt inhibitory factor-1 functions as a tumor suppressor through modulating Wnt/β-catenin signaling in neuroblastoma
- 2014
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In: Cancer Letters. - : Elsevier. - 0304-3835 .- 1872-7980. ; 348:1–2, s. 12-19
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Journal article (peer-reviewed)abstract
- Neuroblastoma is the most common extracranial solid tumor in childhood and is associated with serious morbidity and mortality. The effective treatment of neuroblastoma remains one of the major challenges in pediatric oncology. The Wnt signaling pathway has been shown to play a significant role in the pathogenesis of adult and pediatric tumors. WIF-1 has been identified as an important Wnt antagonist which inhibits Wnt/β-catenin signaling by directly binding to Wnt proteins. However, the expression and function of WIF-1 in neuroblastoma remains unknown. The present study showed that WIF-1 was downregulated with high level promoter methylation in neuroblastoma cells, and was significantly upregulated after exposure to demethylating agent. This finding suggests that downregulation of WIF-1 was associated with its promoter methylation in neuroblastoma. To further study the potential function of WIF-1 in neuroblastoma, we constructed a plasmid that over-expressed WIF-1 and transfected the plasmid into one neuroblastoma cell line SK-N-SH. We found that restoration of WIF-1 inhibited the growth and proliferation of neuroblastoma cells in vitro. Morever, Wnt/β-catenin signaling activity and target genes expression were reduced by WIF-1 restoration. These results provide support that WIF-1 is downregulated and functions as a tumor suppressor by antagonizing Wnt/β-catenin signaling in neuroblastoma, suggesting a potential role as a therapeutic target in neuroblastoma.
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