VLCFA triggers an oxidative stress characterized by an overproduc

VLCFA triggers an oxidative stress characterized by an overproduction of ROS and RNS associated

with lipid peroxidation, protein carbonylation, increased superoxide dismutase (SOD) activity, decreased catalase activity and glutathione level. SiRNA knockdown of Abcd1 or Acox1 increased ROS and RNS production even in the absence of VLCFA, and especially potentialized VLCFA-induced ROS overproduction. Moreover, mainly in cells with reduced Acox1 level, the levels of VLCFA and neutral lipids were strongly enhanced both in untreated and VLCFA – treated cells. Our data obtained on 158N murine oligodendrocytes selleck chemicals llc highlight that VLCFA induce an oxidative stress, and demonstrate that Abcd1 or Acox1 knockdown contributes to disrupt RedOx equilibrium supporting a link between oxidative stress and the deficiency of Abcd1 or Acox1 peroxisomal proteins. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Acute promyelocytic leukemia (APL) is a hematological malignancy driven by the PML/RARA oncogene. The prognosis for patients with APL was revolutionized by two treatments:

retinoic acid (RA) and As2O3 (arsenic trioxide). These were both shown a posteriori to target PML/RARA, explaining click here their exquisite specificity for APL. Arsenic, as a single agent, cures up to 70% of patients, whereas APL patients treated with the combination of RA and As2O3 reach a stunning 90% cure rate. Recent physiopathological models highlight the key role of RA- and As2O3-triggered PML/RARA degradation, and the molecular mechanisms underlying As2O3-induced PML/RARA degradation have been recently clarified. As discussed below, arsenic binding, oxidation, sumoylation on PML nuclear bodies, and RNF4-mediated ubiquitination all contribute to the As2O3-triggered ALOX15 catabolism of PML/RARA.”
“Purpose: We examined the association between urological cancer mortality rates and the presence of physicians. We hypothesized that cancer mortality rates increase with a low physician population density since this would decrease the detection of

cancers at an early stage.

Materials and Methods: Mortality rates for prostate cancer, bladder cancer, kidney and renal pelvis cancer, and cancer at all sites for white patients in United States counties from 2003 to 2007 were obtained from the National Vital Statistics System. High and low rate groups of counties were reviewed for each type of cancer. The high rate groups consisted of 15 or 25 counties with the highest cancer mortality rates. The low rate groups consisted of counties, selected from the same states as high rate groups, with the lowest mortality rates. Levels of physicians per 10,000 general population, income, poverty and no health insurance were compared between the high and low cancer rate groups.

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