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1 ion manifested later than cardiovascular and respiratory dysfunction.
2 n be fatal, including premature death due to respiratory dysfunction.
3 s and showed a higher level of mitochondrial respiratory dysfunction.
4 targets of alcohol-induced toxicity causing respiratory dysfunction.
5 oteomic changes that accompany mitochondrial respiratory dysfunction.
6 g injury (ALI) results in severe, persistent respiratory dysfunction.
7 resents a reliable tool for the diagnosis of respiratory dysfunction.
8 f activating 5-HT1A receptors on post-C5 SCI respiratory dysfunction.
9 nd young children with NMD may contribute to respiratory dysfunction.
10 ld asthmatic children and adults with severe respiratory dysfunctions (7, 5, and 3 mug.h(-1), respect
12 al injury and the magnitude of mitochondrial respiratory dysfunction after lipopolysaccharide treatme
14 ore sensitive to MPTP-mediated mitochondrial respiratory dysfunction and complex I inhibition than ce
15 tation would alter hemorrhagic shock-induced respiratory dysfunction and correlate with nuclear facto
16 n of mild hypothermia attenuates cardiac and respiratory dysfunction and counteracts sympathetic acti
17 in Clara cells of SP-B -/- mice resulted in respiratory dysfunction and invariable neonatal death, r
18 g mutations have a higher incidence of awake respiratory dysfunction and lower levels of cerebrospina
19 eased production of reactive oxygen species, respiratory dysfunction, and loss of cytochrome c oxidas
20 agmentation, cardiomyocyte and mitochondrial respiratory dysfunction, and rapidly progressive and let
21 mitochondria showed increasing irreversible respiratory dysfunction as well as diminished calcium bu
23 educed fetal growth, cardiovascular disease, respiratory dysfunction, asthma, sensitization to common
25 postnatal mortality, infertility and strong respiratory dysfunction caused by defective mucociliary
27 mplications of pain, nausea and vomiting and respiratory dysfunction, differences between anaesthetic
28 mild hypothermia impacts on circulatory and respiratory dysfunction during experimental endotoxemia.
30 l material in stimulating IgE production and respiratory dysfunction in a C57BL/6 murine model of AHR
32 d functionally abnormal mitochondria induced respiratory dysfunction in Mfn2-deficient mouse embryoni
33 tory muscle weakness is the primary cause of respiratory dysfunction in neuromuscular disease (NMD),
34 ible for a distinct program of mitochondrial respiratory dysfunction, in addition to the activation o
37 nd, consequently, suggest that mitochondrial respiratory dysfunction is not essential for HD pathogen
39 opioid receptors as a possible source of the respiratory dysfunction manifested in panic attacks occu
42 ubiquitination and death, forelimb motor and respiratory dysfunction, reactive astrocytosis, and redu
44 SCI for preventing PhMN loss and consequent respiratory dysfunction that occurs during secondary deg
45 on Assessment Method for ICU), for renal and respiratory dysfunction (using the ordinal renal and res
47 certain clinical features, like dysphonia or respiratory dysfunction, were exclusively detected in th
48 ld result in survival of infants with severe respiratory dysfunction who would otherwise have died.
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