Malignant Dysrhythmias - Brugada Type 1 Pattern Formation in the Presence of Fever.

Brugada is a malignant cardiac dysrhythmia characterized by ST elevations in precordial leads V1 to V3. It is an autosomal dominant disease, and patients are usually asymptomatic. Often the initial presenting symptom of this syndrome is syncope or sudden cardiac death (SCD). In patients with this syndrome, the only definitive treatment is the implantation of a cardioverter-defibrillator device (ICD). Previously it has been reported that Brugada type EKG patterns have been observed in patients who have used sodium channel blocking medications/drugs and in patients who are febrile. In this case, a 58 year-old male presented to our emergency department with a fever of five days duration and a non-productive cough. The patient was initially diagnosed with bilateral pneumonia, however during the initial workup his EKG demonstrated a Brugada type EKG pattern. The patient did not have any history of cardiac disease, nor was there any history of syncope or SCD in his family. The patient was eventually discharged from the hospital four days after his initial presentation and instructed to follow up with cardiology. Brugada type EKG patterns are known to occur in patients in febrile states and in those patients using certain types of medications. In those patients who present under the above mentioned conditions who are otherwise asymptomatic, the literature does not support the implantation of an ICD.

Selenite triggers rapid transcriptional activation of p53, and p53-mediated apoptosis in prostate cancer cells: Implication for the treatment of early-stage prostate cancer.

Supra-nutritional selenium supplementation has emerged as an attractive new approach to intervene in a range of human cancers, in particular prostate cancer. However, scanty information is currently available on molecular mechanisms underlying selenium's anticancer action. The tumor suppressor p53 plays an important role in preventing transformation by transcriptional regulation of a range of genes that are involved in vital cell functions such as DNA repair, cell cycle arrest, and induction of apoptosis. Here we report that incubation of LNCaP human prostate cancer cells (p53 +/+) with a natural form of selenium triggers rapid transcriptional activation of p53, and up-regulation of the expression of p53-target genes as well as induction of miR-34 class of microRNAs. Moreover, blocking p53 function by transfection of cells with a dominant-negative, mutated p53 gene, or by siRNA, significantly reduced selenium-induced expression of p53-target genes and induction of apoptosis. Since majority of the early-stage human prostate cancers bear functional p53 gene (p53+/+), our findings indicate that the anticancer action of selenium may involve transactivation of p53 as a potential mechanism, and suggest that selenite may be useful not only for prevention but also for treatment of human prostate cancer.