Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P39060 (endostatin)
 2,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Preterm infants exposed to oxygen and mechanical ventilation are at risk for bronchopulmonary dysplasia (BPD), a multifactorial chronic lung disorder characterized by arrested alveolar development and nonsprouting, dysmorphic microvascular angiogenesis. The molecular regulation of this BPD-associated pathological angiogenesis remains incompletely understood. In this study, the authors used focused microarray technology to characterize the angiogenic gene expression profile in postmortem lung samples from short-term ventilated preterm infants (born at 24 to 27 weeks' gestation) and age-matched control infants. Microarray analysis identified differential expression of 13 of 112 angiogenesis-related genes. Genes significantly up-regulated in ventilated lungs included the antiangiogenic genes thrombospondin-1, collagen XVIII alpha-1, and tissue inhibitor of metalloproteinase-1 (TIMP1), as well as endoglin, transforming growth factor-alpha, and monocyte chemoattractant protein-1 (CCL2). Increased expression of thrombospondin-1 in ventilated lungs was verified by real-time polymerase chain reaction (PCR) and immunolocalized primarily to intravascular platelets and fibrin aggregates. Down-regulated genes included proangiogenic angiogenin and midkine, as well as vascular endothelial growth factor (VEGF)-B, VEGF receptor-2, and the angiopoietin receptor TEK/Tie-2. In conclusion, short-term ventilated lungs show a shift from traditional angiogenic growth factors to alternative, often antisprouting regulators. This angiogenic shift may be implicated in the regulation of dysmorphic angiogenesis and, consequently, deficient alveolarization characteristic of infants with BPD.
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PMID:Angiogenesis-related gene expression profiling in ventilated preterm human lungs. 2071 99

Pulmonary diffusing capacity for carbon monoxide (DLCO) has been an important pulmonary function test used since the 1950's. It measures the uptake of CO from the alveolar space into pulmonary capillary blood, following the same path as oxygen. It's used to evaluate/follow the progress of various lung diseases. In the eighties, a new test was developed similar to the DLCO test: pulmonary diffusing capacity for nitric oxide (DLNO). About 81-90% of the variance in DLNO is shared by DLCO in patients with cardiopulmonary disease and in healthy subjects. When DLNO is abnormally low, so is DLCO, and when DLNO is normal, so is DLCO (Kappa Statistic=0.69, n=251). The probability that DLNO and DLCO will be abnormally low when a cardiopulmonary disease is present (sensitivity) is 79% and 68%, respectively. The DLNO test avoids many technical issues associated with the measurement of DLCO: (1) DLNO is relatively unaffected by inspired oxygen concentration or ambient pressure, (2) DLNO is unaffected by carboxyhemoglobin, (3) DLNO is minimally affected by hemoglobin (Hb) concentration, thus correcting for Hb is not needed. (4) DLNO is more affected by lung volume compared to DLCO, thus DLNO divided by alveolar volume (KNO) is a better measure than KCO in those with restrictive lung disease, and (5) DLNO is a more stable measure over time compared to DLCO. Therefore, DLNO has several advantages over DLCO in the management of patients and could replace the DLCO test in most cases moving forward.
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PMID:Can the measurement of pulmonary diffusing capacity for nitric oxide replace the measurement of pulmonary diffusing capacity for carbon monoxide? 2788 96