FREQUENCY OF TRAUMAS IN LIBURNIAN POPULATION

<p><b>Copyright information:</b></p><p>Taken from "The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment"</p><p>http://www.biomedcentral.com/1471-2210/7/16</p><p>BMC Pharmacology 2007;7():16-16.</p><p>Published online 20 Dec 2007</p><p>PMCID:PMC2234403.</p><p></p>o αand α) and αC4 (corresponding to α) gene products (Table 3). The reactions amplified fragments of the expected size from each set of primers. αC10/C4 primers amplified 233 bp products from SH-SY5Y mRNA that were sensitive to digestion by II (specific for the αproduct). Restriction digestion with XI of the 630 bp product of α 2C4 primer amplification gave three fragments of 271, 225 and 78 bp. All reactions were performed in the presence (+) or absence (-) of reverse transcriptase (RT) to rule out the possibility of DNA contamination. Lane M designates the 100 bp ladder; the 500 bp fragment is indicated by an arrow in each panel

The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment-0

<p><b>Copyright information:</b></p><p>Taken from "The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment"</p><p>http://www.biomedcentral.com/1471-2210/7/16</p><p>BMC Pharmacology 2007;7():16-16.</p><p>Published online 20 Dec 2007</p><p>PMCID:PMC2234403.</p><p></p>tudent's -test (GraphPad Prism, San Diego, CA), while the α-selective antagonist, ARC-239, had no effect. The results represent the mean ± S.E. of 2–9 experiments, performed in duplicate

The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment-5

<p><b>Copyright information:</b></p><p>Taken from "The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment"</p><p>http://www.biomedcentral.com/1471-2210/7/16</p><p>BMC Pharmacology 2007;7():16-16.</p><p>Published online 20 Dec 2007</p><p>PMCID:PMC2234403.</p><p></p>0 nM propranolol. Isolation of the membrane fraction and immunoblotting for GRK2 and GRK3 was conducted as described in . EPI exposure significantly increased the level of GRK3 and GRK2 expressed in the membrane fractions from SHβAR4 cells compared to vehicle-treated controls (*< 0.05; n = 3). Inclusion of propranolol (P) with EPI treatment prevented the increased translocation of both GRK isoforms (< 0.01 as compared to EPI treatment), while propranolol treatment alone was without effect. In contrast, EPI failed to increase mobilization of GRK to the plasma membrane of wt SH cells (n = 4–7). Data represent mean ± S.E.; comparisons were made by ANOVA with Tukey's post-hoc test

The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment-7

<p><b>Copyright information:</b></p><p>Taken from "The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment"</p><p>http://www.biomedcentral.com/1471-2210/7/16</p><p>BMC Pharmacology 2007;7():16-16.</p><p>Published online 20 Dec 2007</p><p>PMCID:PMC2234403.</p><p></p>o αand α) and αC4 (corresponding to α) gene products (Table 3). The reactions amplified fragments of the expected size from each set of primers. αC10/C4 primers amplified 233 bp products from SH-SY5Y mRNA that were sensitive to digestion by II (specific for the αproduct). Restriction digestion with XI of the 630 bp product of α 2C4 primer amplification gave three fragments of 271, 225 and 78 bp. All reactions were performed in the presence (+) or absence (-) of reverse transcriptase (RT) to rule out the possibility of DNA contamination. Lane M designates the 100 bp ladder; the 500 bp fragment is indicated by an arrow in each panel

The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment-1

<p><b>Copyright information:</b></p><p>Taken from "The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment"</p><p>http://www.biomedcentral.com/1471-2210/7/16</p><p>BMC Pharmacology 2007;7():16-16.</p><p>Published online 20 Dec 2007</p><p>PMCID:PMC2234403.</p><p></p>o αand α) and αC4 (corresponding to α) gene products (Table 3). The reactions amplified fragments of the expected size from each set of primers. αC10/C4 primers amplified 233 bp products from SH-SY5Y mRNA that were sensitive to digestion by II (specific for the αproduct). Restriction digestion with XI of the 630 bp product of α 2C4 primer amplification gave three fragments of 271, 225 and 78 bp. All reactions were performed in the presence (+) or absence (-) of reverse transcriptase (RT) to rule out the possibility of DNA contamination. Lane M designates the 100 bp ladder; the 500 bp fragment is indicated by an arrow in each panel