The role of plasma gelsolin in cardiopulmonary bypass induced acute lung injury in infants and young children: a pilot study

Abstract Background Recent studies have analysed birth-related clavicular fractures to propose time frames for healing that could be applied to dating of all fractures in cases of suspected child abuse. Objective To assess differences in healing rates between femoral fractures and birth-related clavicular fractures in infants and young children. Materials and methods A retrospective 5-year pilot study of femoral fractures in children younger than 3 years of age was performed. Anonymised radiographs were independently scored by two radiologists for stages of fracture healing. In cases of reader disagreement, radiographs were independently scored by a third radiologist. Results In total, 74 radiographs (30 children) met the inclusion criteria. Fracture healing evolved over time with subperiosteal new bone formation (SPNBF) appearing first, followed by callus then remodelling. A power calculation for a single proportion, with a level of confidence of 95% and a margin of error of 5%, showed that in a definitive study, 359 radiographs would be required. Conclusion Although the overall pattern of healing is similar, in this small pilot study, the earliest times for SPNBF and callus formation in femoral fractures appeared to lag behind healing of birth-related clavicular fractures. Remodelling appeared earlier than remodelling of clavicular fractures. A power calculation has determined numbers of femoral radiographs (359) required for a definitive study.

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Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung injury via NF-κB signaling in bone marrow-derived macrophages

Bioscience Reports ◽

10.1042/bsr20181888 ◽

2019 ◽

Vol 39 (6) ◽

Cited By ~ 2

Author(s):

Tao Qiu ◽

Jiangqiao Zhou ◽

Tianyu Wang ◽

Zhongbao Chen ◽

Xiaoxiong Ma ◽

...

Keyword(s):

Bone Marrow ◽

Acute Lung Injury ◽

Lung Injury ◽

Stromal Cells ◽

Marrow Cell ◽

Marrow Transplant ◽

Cell Source ◽

Transplant Model ◽

Acute Inflammatory Disease

AbstractAcute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.

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Current and potential role of grain legumes on protein and micronutrient adequacy of the diet of rural Ghanaian infants and young children: using linear programming

Nutrition Journal ◽

10.1186/s12937-019-0435-5 ◽

2019 ◽

Vol 18 (1) ◽

Cited By ~ 7

Author(s):

Ilse de Jager ◽

Karin J. Borgonjen-van den Berg ◽

Ken E. Giller ◽

Inge D. Brouwer

Keyword(s):

Linear Programming ◽

Young Children ◽

Potential Role ◽

Grain Legumes ◽

Infants And Young Children

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H2O2 inhibits alveolar epithelial wound repair in vitro by induction of apoptosis

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00177.2003 ◽

2004 ◽

Vol 287 (2) ◽

pp. L448-L453 ◽

Cited By ~ 55

Author(s):

Thomas Geiser ◽

Masanobu Ishigaki ◽

Coretta van Leer ◽

Michael A. Matthay ◽

V. Courtney Broaddus

Keyword(s):

Acute Lung Injury ◽

Epithelial Cells ◽

Lung Injury ◽

Cell Viability ◽

Wound Repair ◽

Wound Edge ◽

Alveolar Epithelial ◽

Induction Of Apoptosis

Reactive oxygen species (ROS) are released into the alveolar space and contribute to alveolar epithelial damage in patients with acute lung injury. However, the role of ROS in alveolar repair is not known. We studied the effect of ROS in our in vitro wound healing model using either human A549 alveolar epithelial cells or primary distal lung epithelial cells. We found that H2O2 inhibited alveolar epithelial repair in a concentration-dependent manner. At similar concentrations, H2O2 also induced apoptosis, an effect seen particularly at the edge of the wound, leading us to hypothesize that apoptosis contributes to H2O2-induced inhibition of wound repair. To learn the role of apoptosis, we blocked caspases with the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp (zVAD). In the presence of H2O2, zVAD inhibited apoptosis, particularly at the wound edge and, most importantly, maintained alveolar epithelial wound repair. In H2O2-exposed cells, zVAD also maintained cell viability as judged by improved cell spreading and/or migration at the wound edge and by a more normal mitochondrial potential difference compared with cells not treated with zVAD. In conclusion, H2O2 inhibits alveolar epithelial wound repair in large part by induction of apoptosis. Inhibition of apoptosis can maintain wound repair and cell viability in the face of ROS. Inhibiting apoptosis may be a promising new approach to improve repair of the alveolar epithelium in patients with acute lung injury.

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