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ethylene oxide/hypoxia

Odkaz sa uloží do schránky
ČlánkyKlinické štúdiePatenty
6 výsledky
A novel triblock copolymer of epsilon-caprolactone (CL) and ethylene oxide (E), CL6E90CL6, intended for use in implantable drug-delivery systems, has been subjected to gamma irradiation, in the solid state and in aqueous solution, under different controlled environmental conditions, to assess its
Hypoxia can induce chemoresistance, which is a significant clinical obstacle in cancer therapy. Here, we assessed development of hypoxia-induced chemoresistance (HICR) against free versus polymeric cisplatin micelles in a triple negative breast cancer cell line, MDA-MB-231. We then explored two

Clinical significance of blood-device interaction in hemodialysis. A review.

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The syndrome of dialysis-associated leukopenia and complement activation by cellulosic membranes, including the so-called "first use syndrome", is reviewed and the pathophysiology of these phenomena is discussed. Subsequently the clinical side effects of hemodialysis, including dialysis-associated

[Interaction between blood and dialysis membrane].

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During contact between blood and dialysis membrane after the first 20-30 minutes of haemodialysis there occur the complement activation, ++intra-dialysis thrombocytopenia and leucopenia, especially neutropenia following their degranulation, which results in liberation of a number of proteases and

Adverse effects of dialyzers manifesting during the dialysis session.

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The intradialytic symptoms that can be linked to components of the extracorporeal circuit of greatest clinical importance are the Type A (anaphylactoid) reactions. Most of these are IgE-mediated reactions due to ethylene oxide and are preventable by adequate degassing of the dialyzer by the

Mitochondrial mechanisms of neuronal rescue by F-68, a hydrophilic Pluronic block co-polymer, following acute substrate deprivation.

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Global brain ischemia can lead to widespread neuronal death and poor neurologic outcomes in patients. Despite detailed understanding of the cellular and molecular mechanisms mediating neuronal death following focal and global brain hypoxia-ischemia, treatments to reduce ischemia-induced brain injury
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