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DE-627 |
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20250207182126.0 |
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231223s2006 xx ||||| 00| ||chi c |
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|a pubmed25n0555.xml
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|a (DE-627)NLM166388327
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|a (NLM)17083791
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a chi
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| 100 |
1 |
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|a Liu, Cui-qing
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Expression of nuclear factor-kappaB and its inhibitor in alveolar macrophages of patients with neonatal hyaline membrane disease
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| 264 |
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|c 2006
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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| 338 |
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|a Band
|b nc
|2 rdacarrier
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| 500 |
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|a Date Completed 03.08.2010
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|a Date Revised 24.11.2016
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|a published: Print
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|a Citation Status MEDLINE
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| 520 |
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|a OBJECTIVE: Inflammatory reaction and injury in immature lungs are associated with activation of nuclear factor-kappa B (NF-kappaB) to trigger proinflammatory cytokine release, but the mechanism thereof is not fully understood. The present study was conducted to understand possible relationship between expression of NF-kappaB and its inhibitor and severity and outcome of neonates with hyaline membrane disease (HMD)
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| 520 |
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|a METHODS: Serial samples of bronchoalveolar lavage fluid (BALF) were obtained during mechanical ventilation from 31 preterm infants with HMD. These infants were divided into two groups: survivors group [n = 22, birth weight (1500 +/- 320) g and gestational age (31.2 +/- 1.8) weeks] and nonsurvivors group [birth weight (1340 +/- 280) g, gestational age (30.8 +/- 2.1) weeks]. Nineteen preterm infants [birth weight (1470 +/- 280) g, gestational age (30.6 +/- 1.9) weeks] without respiratory disorders were enrolled as control subjects. Alveolar macrophages (AM) were isolated by differential adherence. AM was cultured and treated with lipopolysaccharide (LPS) for 1 hr. Then, nuclear extracts of AM were analyzed by electrophoretic mobility shift assay (EMSA) for NF-kappaB expression. NF-kappaB inhibitor (IkappaB-alpha protein) in cytoplasmic extracts was detected by using Western blotting and IL-1beta and IL-8 in BALF by enzyme-linked immunosorbent assay (ELISA)
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|a RESULTS: NF-kappaB complexes were observed by EMSA, they were characterized by competition with cold oligonucleotide and p65-specific antibodies. The addition of an excess of cold oligonucleotide, corresponding to the NF-kappaB binding site, turned off the signal of the band, showing that the band was specific. An excess of an irrelevant oligonucleotide (corresponding to the SP-1) did not show any effect. The addition of an anti-p65 antibody caused the supershift of the two upper bands. After EMSA, the NF-kappaB complexes were quantified by using a ImageQuant software. NF-kappaB expression in AM at 24 hrs was higher in all the patients with HMD as compared with control subjects (survives/control, 34.1 vs 11.4 RDU, P < 0.01; nonsurvivors/control, 55.2 vs 11.4 RDU, P < 0.01). The NF-kappaB expression in AM at 72 hrs was higher than that in control subjects but not for nonsurvivors (survivors/control, 47.8 vs 25.6 RDU, P < 0.01; nonsurvivors/control, 21.8 vs 25.6, P > 0.05). The NF-kappaB expression in AM from nonsurvivors was depressed at 72 hrs as compared to 24 hrs (21.8 vs 55.2, P < 0.01), whereas the NF-kappaB expression in AM from survivors was still higher at 72 hrs than that at 24 hrs (47.8 vs 34.1, t = 4.43, P < 0.01)
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|a CONCLUSION: Altered NF-kappaB activation in AM of BALF of neonates with HMD was observed, and it may be mediated by decreased IkappaB synthesis, increased IkappaB degradation, or both. In HMD nonsurvivors NF-kappaB translocation was hampered upon LPS activation
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| 650 |
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|a Comparative Study
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4 |
|a Journal Article
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| 650 |
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7 |
|a I-kappa B Proteins
|2 NLM
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| 650 |
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7 |
|a Interleukin-1beta
|2 NLM
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| 650 |
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7 |
|a Interleukin-8
|2 NLM
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| 650 |
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7 |
|a Lipopolysaccharides
|2 NLM
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| 650 |
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7 |
|a NF-kappa B
|2 NLM
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| 650 |
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|a NFKBIA protein, human
|2 NLM
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| 650 |
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|a NF-KappaB Inhibitor alpha
|2 NLM
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| 650 |
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7 |
|a 139874-52-5
|2 NLM
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| 700 |
1 |
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|a Cao, Lei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zheng, Hua-cheng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Jia, Xi-qun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Kang, Li-min
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Lan-feng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liu, Su-zhe
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Zhonghua er ke za zhi = Chinese journal of pediatrics
|d 1960
|g 44(2006), 8 vom: 06. Aug., Seite 602-6
|w (DE-627)NLM136249191
|x 0578-1310
|7 nnns
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| 773 |
1 |
8 |
|g volume:44
|g year:2006
|g number:8
|g day:06
|g month:08
|g pages:602-6
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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|a GBV_ILN_20
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|a GBV_ILN_22
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|a GBV_ILN_24
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|a GBV_ILN_31
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|a GBV_ILN_39
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|a GBV_ILN_40
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|a GBV_ILN_50
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|a GBV_ILN_61
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|a GBV_ILN_65
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|a GBV_ILN_69
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|a GBV_ILN_70
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|a GBV_ILN_72
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|a GBV_ILN_120
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|a GBV_ILN_130
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|a GBV_ILN_227
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|a GBV_ILN_244
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|a GBV_ILN_285
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|a GBV_ILN_294
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|a GBV_ILN_350
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|a GBV_ILN_665
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|a GBV_ILN_813
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|a AR
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|d 44
|j 2006
|e 8
|b 06
|c 08
|h 602-6
|