Influence of Fever and hospital-acquired infection on the incidence of delayed neurological deficit and poor outcome after aneurysmal subarachnoid hemorrhage.

Although fever and infection have been implicated in the causation of delayed neurological deficits (DND) and poor outcome after aneurysmal subarachnoid hemorrhage (SAH), the relationship between these two often related events has not been extensively studied. We reviewed these events through of our retrospective database of patients with SAH. Multivariate logistic regression was used to determine independent predictors of DND and poor outcome.

Metabolic disorders of the brain: part II.

Metabolic disorders of the brain are extensive and to encompass these disorders in two articles is impossible. The aim of this article to provide a brief overview of the non-organelle based metabolic disorders affecting the brain. Due to its complexity, classification of the metabolic disorders of brain is not easy.

Metabolic disorders of the brain: part I.

Due to nonspecific clinical presentation, diagnosis of metabolic disorders affecting the brain is very challenging for physicians. It is always the constellation of the clinical examination, biochemical assay and imaging that helps in reaching the diagnosis of metabolic disorders. Diagnosis of these disorders or even limiting the differential diagnosis on imaging may pose a formidable challenge to the radiologist.

The relative contribution of pro-apoptotic p53-target genes in the triggering of apoptosis following DNA damage in vitro and in vivo.

The p53 pathway displays a large degree of redundancy in the expression of a number of pro-apoptotic mechanisms following DNA damage that, among others, involves increased expression of several pro-apoptotic genes through transactivation. Spatial and temporal cellular contexts contribute to the complexity of the regulation of apoptosis, hence different genes may show a cell- and tissue-dependent specificity with regard to the regulation of cell death and act in concert or show redundancy with one and another. We used siRNA technology to assess the effect of multiple ablations of documented pro-apoptotic p53 target genes (PPG) in the colorectal cancer cell line HCT116 and generated mice deficient in both of the extrinsic and intrinsic PPGs genes Dr5 and Puma following treatment with chemotherapeutics and ionizing radiation.

Malformations of cortical development.

The advent of high resolution MRI techniques has revolutionized the imaging of cortical malformations. Today, specific gene defects have been identified to be responsible for several of the developmental cortical malformations. In this article we have discussed the developmental cortical malformations under stages of proliferation, migration and organization.

Malformations of dorsal induction.

Dorsal induction includes the formation and closure of neural tube, occurs during 3-5 weeks of gestation. Neurulation occurs in two phases, primary neurulation (formation of the neural plate and subsequently neural tube) and secondary neurulation (formation of distal cord and sacral and coccygeal segments). Failure of dorsal induction leads to anencephaly, exencephaly, cephaloceles, Chiari malformation and spinal dysraphism.

Tumor necrosis factor alpha induces p53 up-regulated modulator of apoptosis expression in colorectal cancer cell lines.

Purpose: Inflammatory bowel disease (IBD)-associated colorectal carcinogenesis involves dysregulation of multiple cellular pathways, including p53 signaling and cytokine action. The purpose of the current study was to evaluate the effects of tumor necrosis factor alpha (TNF-alpha) on p53 and p53 up-regulated modulator of apoptosis (PUMA), a downstream effector of p53 in the apoptotic pathway in colorectal cancer cells.

Methods: The cell lines HT29 (which express mutant p53) and HCT116 (which express wild-type p53) were treated with TNF-alpha (0, 50, 100, or 500 ng/mL) for 1, 12, 24, or 48 hours.