By generating a docetaxel-cross-resistant PacR cancer cell line (PacR/DCT), we further clarified the role of FOXO3a in glycolysis-associated mediation of P-glycoprotein/ABCB1hyperactivity that induces docetaxel cross-resistance.
Subjects with either C/T or C/C (n = 16) genotypes showed a three-fold greater improvement than T/T MDR1C3435T genotype (n = 6) (mean decrease of 15.1 +/- 12.6, or 50.7% from baseline, versus 4.5 +/- 5.1, or 15.6% from baseline) in parent-rated ABC Hyperactivity scores over 8 weeks (p = 0.03).
These results suggest the systemic hyperactivity of P-gp in RE patients, including brain P-gp over-expression should be suspected when persistent subtherapeutic levels of AEDs in plasma are detected.
In the child study, the highest dose group showed benefit over placebo on the ABC-C<sub>FX</sub> Irritability subscale (<i>p</i> = 0.03) and Parenting Stress Index (PSI, <i>p</i> = 0.03) and trends toward benefit on the ABC-C<sub>FX</sub> Social Avoidance and Hyperactivity subscales (both <i>p</i> < 0.1) and CGI-I (<i>p</i> = 0.119).
These are the first reported results to show that berry extracts can inhibit MRP-1 function that causes apoptotic tumor cell death by accumulation of GSSG in the nucleus of EOMA cells where NADPH oxidase is hyperactive and causes pathological angiogenesis.
The aims of this study were to 1) investigate the expression and co-localisation of the K(ATP) channel subunits, Kir6.2 and SUR1, in human L- and K-cells and 2) investigate if a common hyperactive variant of the Kir6.2 subunit, Glu23Lys, exerts a functional impact on glucose-sensing tissues in vivo that may affect the overall glycaemic control in children with new-onset type 1 diabetes.
These substitutions, which could be grouped into three different "hot spots," were gain of function (GOF) mutations since they conferred hyperactivity to CgPdr1p revealed by constitutive high expression of ABC-transporter genes.
In aggregate, our data link the loss of Abi-1 function to hyperactive SFKs/STAT3/NF-κB signaling and suggest that this signaling axis may represent a regulatory module involved in the molecular pathophysiology of PMF.
The excessive proliferation of the myeloid marrow compartment in Philadelphia chromosome (Ph)-positive acute and chronic leukemias has been largely attributed to a hyperactive and autonomously acting hybrid tyrosine kinase BCR-ABL, a product of the fusion between the second exon of the c-ABL proto-oncogene and 5' portions of the BCR gene on chromosome 22.
Consistent with the observation of age-related hyperactivity of CA3, learning failed to increase DGC-SLIN connectivity in 17-month-old mice, whereas downregulation of ABLIM3 expression was sufficient to restore DGC-SLIN connectivity, increase PV+ SLIN activation and improve the precision of remote memories.
Compared with the <i>in situ</i>-osmolarity culture, hyper-osmolarity culture significantly decreased cell proliferation and telomerase activity, increased SA-β-Gal activity and cell fraction in the G<sub>0</sub>/G<sub>1</sub> phase, up-regulated expression of senescence markers (p16 and p53) and down-regulated expression of matrix molecules (aggrecan and collagen II), and increased intracellular ROS accumulation.
Angiotensin-converting enzyme (ACE) is assumed to influence the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis, which shows hyperactivity in depressed patients.
Angiotensin-converting enzyme (ACE) is thought to influence the activity of the hypothalamic-pituitary-adrenocortical system, which shows hyperactivity in the majority of patients with major depressive disorder (MDD).
The HPA axis stimulating properties of higher ACE and consecutively higher AT-II and/or lower substance P concentrations may be crucial factors for the HPA system hyperactivity during major depressive episodes.
Sympathetic hyperactivity and poor sleep quality are reported in myocardial infarction (MI) patients and angiotensin-converting enzyme inhibitors (ACEI) can improve long-term survival in these patients.