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Claudia Schumacher

Publications and source records attributed to Claudia Schumacher.

2 recordsLinked to original sources

The support of adenosine release from adenosine kinase deficient ES cells by silk substrates.

Adenosine kinase deficient (Adk-/-) embryonic stem cells (ESCs) encapsulated in synthetic polymers have previously been shown to provide therapeutic adenosine release and transient seizure suppression in epileptic rats. Here we explored the utility of biopolymer-substrates to promote long-term adenosine release from Adk-/- ESCs. Three different substrates were studied: (1) type I collagen (Col-1), (2) silk-fibroin (SF), and (3) poly(L-ornithine) (PO) coated tissue culture plastic. Adk-/- or wild type (wt) ESC-derived glial precursor cells were seeded on the substrates and cultured either in proliferation medium containing growth factors or in differentiation medium devoid of growth factors. In proliferation medium cell proliferation was higher and metabolic activity lower on Col-1 and PO substrates as compared to SF. Cells from both genotypes readily differentiated into astrocytes after growth factor removal on all substrates. Adk-/- cells cultured on biopolymers released significantly more adenosine than their wt counterparts at all developmental stages. Adenosine release was similar on SF and PO substrates and the amounts released from Adk-/- cells (>20 ng/ml) were considered to be of therapeutic relevance. Taken together, these results suggest that silk matrices are particularly suitable biomaterials for ESC encapsulation and for the design of adenosine releasing bioincubators for the treatment of epilepsy.

Adenosine↗

Small-dose nitric oxide improves oxygenation during one-lung ventilation: an experimental study.

UNLABELLED: Inhaled nitric oxide (NO) at 20 or 40 ppm does not improve arterial oxygenation during one-lung ventilation (OLV). The authors hypothesized that NO at smaller concentrations might improve oxygenation. Twelve piglets weighing 26 to 32 kg were studied. When PaO(2) had reached a plateau during OLV, NO at doses of 4, 8, 16, and 32 ppm were randomly administered for 30 min. Hemodynamic data were determined by invasive monitoring. Blood gas analysis and, in six animals, ventilation-perfusion analysis by the multiple inert gas elimination technique were used to characterize pulmonary gas exchange. NO at 4, 8, 16, and 32 ppm improved PaO(2) during OLV. NO at 4 ppm had a more intense effect on arterial oxygenation than doses of 8, 16, and 32 ppm (DeltaPaO(2), 42 +/- 35 mm Hg versus 22 +/- 20 mm Hg, 13 +/- 18 mm Hg, and 15 +/- 16 mm Hg; P < 0.05). NO at 4 ppm reduced intrapulmonary shunt flow, whereas a larger concentration exhibited no statistically significant effect. The authors conclude that NO improves arterial oxygenation more effectively at smaller doses than at larger doses. This dose-dependent effect remains to be confirmed in acute hypoxemia during OLV. IMPLICATIONS: Inhaled nitric oxide at 4 ppm improves arterial oxygenation during one-lung ventilation to a greater extent than larger doses, and this effect is caused by a reduction in intrapulmonary shunt.

Animals↗