Metal-organic framework-based high-performance column chip for micro gas chromatography: hybrid function for simultaneous preconcentration and separation of volatile organic compounds.

Numerous attempts have been made to replace commercial bulky gas chromatography (GC) systems with compact GC systems for monitoring volatile organic compounds in indoor air. However, recently developed compact GC systems are still too bulky in terms of user convenience, portability, and on-site analysis. Hence, an advanced miniaturization of compact GC systems is needed. Importantly, the small and high-performance gas pretreatment chip devices should be developed for compact GC systems. This paper reports the development of a metal-organic framework (MOF)-coated hybrid micro gas chromatography column chip (hybrid GC chip) capable of preconcentration and separation on harmful volatile organic compounds at low-concentration in one single chip device. The hybrid GC chip, 2 cm × 2 cm in size, was fabricated using a microelectromechanical systems process. The synthesized MOF-5 particles were coated on the inner wall of the fabricated hybrid GC chip and acted as an adsorbent and a stationary phase. The developed hybrid GC chip afforded high preconcentration factors with 1033-1237 and high separation resolutions with 3.8-13.3. The developed column showed good performance as a gas preconcentrator and separation column, and is the first device to perform both roles in one single chip device.

S-endoglin expression is induced in hyperoxia and contributes to altered pulmonary angiogenesis in bronchopulmonary dysplasia development.

Altered pulmonary angiogenesis contributes to disrupted alveolarization, which is the main characteristic of bronchopulmonary dysplasia (BPD). Transforming growth factor ß (TGFß) plays an important role during lung vascular development, and recent studies have demonstrated that endoglin is engaged in the modulation of TGFß downstream signalling. Although there are two different isoforms of endoglin, L- and S-endoglin, little is known about the effect of S-endoglin in developing lungs. We analysed the expression of both L- and S-endoglin in the lung vasculature and its contribution to TGFß-activin-like kinase (ALK)-Smad signalling with respect to BPD development. Hyperoxia impaired pulmonary angiogenesis accompanied by alveolar simplification in neonatal mouse lungs. S-endoglin, phosphorylated Smad2/3 and connective tissue growth factor levels were significantly increased in hyperoxia-exposed mice, while L-endoglin, phosphor-Smad1/5 and platelet-endothelial cell adhesion molecule-1 levels were significantly decreased. Hyperoxia suppressed the tubular growth of human pulmonary microvascular endothelial cells (ECs), and the selective inhibition of ALK5 signalling restored tubular growth. These results indicate that hyperoxia alters the balance in two isoforms of endoglin towards increased S-endoglin and that S-endoglin attenuates TGFß-ALK1-Smad1/5 signalling but stimulates TGFß-ALK5-Smad2/3 signalling in pulmonary ECs, which may lead to impaired pulmonary angiogenesis in developing lungs.