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Biomedical subjects

L Jerome

Publications and source records attributed to L Jerome.

At least 19 recordsLinked to original sources
PubMed2005

The effects of stereotype threat on cognitive function in ecstasy users.

Stereotype threat occurs when individuals, believed to be intellectually inferior, perform badly on cognitive tests they perceive to confirm stereotypes about them. Due to the wide media coverage of studies purporting to show cognitive deficits in ecstasy users it is possible that they experience stereotype threat. This study tested ecstasy and non-ecstasy using polysubstance misusers on a variety of cognitive tests after they had been exposed to stereotype threat. This priming consisted of exposing them to information about the long-term effects of ecstasy which either stated that ecstasy caused memory loss or that it did not. Ecstasy users that had been primed that ecstasy did not cause cognitive deficits performed better than the other three groups on the delayed portion of the prose recall task from the Rivermead Behavioural Memory Test battery. There were no other statistically significant differences between any of the groups on any of the other cognitive tests used. This suggests that stereotype threat exists in ecstasy users and may be influencing their performance in experiments designed to identify cognitive deficits. In order to prevent this occurring in future studies, experimenters must be careful how they conduct their experiments and discuss their results with the media.

Adolescent↗
PubMed2003

Deregulation of the IGF axis in cancer: epidemiological evidence and potential therapeutic interventions.

The IGF system performs a fundamental role in the regulation of cellular proliferation, differentiation and apoptosis. These diverse biological actions are mediated primarily by IGF association with the type I IGF receptor (IGF-IR), which is in turn regulated by a group of high-affinity IGF-binding proteins (IGFBP-1 to -6). All of the IGFBPs can have growth-inhibitory effects by competitively binding IGFs and preventing their association with the IGF-IR. IGFBP-3 is the most abundant binding protein in the circulation and controls the actions of the IGFs by regulating their distribution and bioavailability to target tissues. Disruptions in the balance of IGF system components leading to excessive proliferation and survival signals have been implicated in the development of different tumor types. Epidemiological evidence indicates that increased levels of IGF-I, reduced levels of IGFBP-3 or an increased ratio of IGF-I to IGFBP-3 in the circulation are associated with an increased risk for the development of several common cancers, including those of the breast, prostate, lung and colon. The results of preclinical studies indicate that a diversity of interventions which antagonize IGF-IR signaling or augment IGFBP-3 function inhibit tumor cell growth in models of human cancers. A more comprehensive understanding of the interplay between cellular targets of the IGF system and antineoplastic agents will facilitate the development of novel strategies for the prevention and treatment of cancer.

Antineoplastic Agents↗
PubMed2001

Defining roles for HOX and MEIS1 genes in induction of acute myeloid leukemia.

Complex genetic and biochemical interactions between HOX proteins and members of the TALE (i.e., PBX and MEIS) family have been identified in embryonic development, and some of these interactions also appear to be important for leukemic transformation. We have previously shown that HOXA9 collaborates with MEIS1 in the induction of acute myeloid leukemia (AML). In this report, we demonstrate that HOXB3, which is highly divergent from HOXA9, also genetically interacts with MEIS1, but not with PBX1, in generating AML. In addition, we show that the HOXA9 and HOXB3 genes play key roles in establishing all the main characteristics of the leukemias, while MEIS1 functions only to accelerate the onset of the leukemic transformation. Contrasting the reported functional similarities between PREP1 and MEIS1, such as PBX nuclear retention, we also show that PREP1 overexpression is incapable of accelerating the HOXA9-induced AML, suggesting that MEIS1 function in transformation must entail more than PBX nuclear localization. Collectively, these data demonstrate that MEIS1 is a common leukemic collaborator with two structurally and functionally divergent HOX genes and that, in this collaboration, the HOX gene defines the identity of the leukemia.

Acute Disease↗