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Full-Text Articles in Medicine and Health Sciences
Simulated Diabetic Ketoacidosis Therapy In Vitro Elicits Brain Cell Swelling Via Sodium-Hydrogen Exchange And Anion Transport., Keeley L Rose, Andrew J Watson, Thomas A Drysdale, Gediminas Cepinskas, Melissa Chan, C Anthony Rupar, Douglas D Fraser
Simulated Diabetic Ketoacidosis Therapy In Vitro Elicits Brain Cell Swelling Via Sodium-Hydrogen Exchange And Anion Transport., Keeley L Rose, Andrew J Watson, Thomas A Drysdale, Gediminas Cepinskas, Melissa Chan, C Anthony Rupar, Douglas D Fraser
Obstetrics & Gynaecology Publications
A common complication of type 1 diabetes mellitus is diabetic ketoacidosis (DKA), a state of severe insulin deficiency. A potentially harmful consequence of DKA therapy in children is cerebral edema (DKA-CE); however, the mechanisms of therapy-induced DKA-CE are unknown. Our aims were to identify the DKA treatment factors and membrane mechanisms that might contribute specifically to brain cell swelling. To this end, DKA was induced in juvenile mice with the administration of the pancreatic toxins streptozocin and alloxan. Brain slices were prepared and exposed to DKA-like conditions in vitro. Cell volume changes were imaged in response to simulated DKA therapy. …
Long Non-Coding Rna Malat1 Regulates Hyperglycaemia Induced Inflammatory Process In The Endothelial Cells., Prasanth Puthanveetil, Shali Chen, Biao Feng, Anirudh Gautam, Subrata Chakrabarti
Long Non-Coding Rna Malat1 Regulates Hyperglycaemia Induced Inflammatory Process In The Endothelial Cells., Prasanth Puthanveetil, Shali Chen, Biao Feng, Anirudh Gautam, Subrata Chakrabarti
Pathology Publications
To examine whether the long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is altered in the endothelial cells in response to glucose and the significance of such alteration. We incubated human umbilical vein endothelial cells with media containing various glucose levels. We found an increase in MALAT1 expression peaking after 12 hrs of incubation in high glucose. This increase was associated with parallel increase in serum amyloid antigen 3 (SAA3), an inflammatory ligand and target of MALAT1 and was further accompanied by increase in mRNAs and proteins of inflammatory mediators, tumour necrosis factor alpha (TNF-α) and interleukin …