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“Hyperthermia is a common complication during anesthesia of bears, and it can be life threatening. The objective of this study was to evaluate the effectiveness of active cooling on core body temperature for treatment of hyperthermia in anesthetized brown bears (Ursus arctos). In addition, body temperature after reversal with atipamezole was also evaluated. Twenty-five adult and subadult brown bears were captured with a combination of zolazepam-tiletamine and xylazine or medetomidine. A core temperature capsule was inserted into the bears’ stomach or 15 cm into their rectum or a combination of both.
In six bears with gastric temperatures bigger than = 40.0 degrees C, an active cooling protocol was performed, and the temperature change over 30 min was BYL719 nmr analyzed. The cooling protocol consisted CBL0137 price of
enemas with 2 L of water at approximately 5 degrees C/100 kg of body weight every 10 min, 1 L of intravenous fluids at ambient temperature, water or snow on the paws or the inguinal area, intranasal oxygen supplementation, and removing the bear from direct sunlight or providing shade. Nine bears with body temperature bigger than 39.0 degrees C that were not cooled served as control for the treated animals. Their body temperatures were recorded for 30 min, prior to administration of reversal. At the end of the anesthetic procedure, all bears received an intramuscular dose of atipamezole. In 10 bears, deep rectal temperature change over 30 min
after administration of atipamezole was evaluated. The active cooling protocol used in hyperthermic bears significantly decreased their body temperatures within 10 min, and it produced a significantly greater decrease in their temperature than that recorded in the control group.”
“Elevated expression and activity of the epidermal growth factor receptor (EGFR) is associated Buparlisib supplier with development and progression of head and neck cancer (HNC) and a poor prognosis. Clinical trials with EGFR tyrosine kinase inhibitors (e.g., erlotinib) have been disappointing in HNC. To investigate the mechanisms mediating resistance to these agents, we developed an HNC cell line (HN5-ER) with acquired erlotinib resistance. In contrast to parental HN5 HNC cells, HN5-ER cells exhibited an epithelial-mesenchymal (EMT) phenotype with increased migratory potential, reduced E-cadherin and epithelial-associated microRNAs (miRNA), and elevated vimentin expression. Phosphorylated receptor tyrosine kinase profiling identified Axl activation in HN5-ER cells. Growth and migration of HN5-ER cells were blocked with a specific Axl inhibitor, R428, and R428 resensitized HN5-ER cells to erlotinib. Microarray analysis of HN5-ER cells confirmed the EMT phenotype associated with acquired erlotinib resistance, and identified activation of gene expression associated with cell migration and inflammation pathways.