Individual, seizure-related, and psychosocial predictors of depressive symptoms among people with epilepsy over six months.

Depression is the most frequently diagnosed psychiatric disorder among people with epilepsy. A variety of risk factors for depression among people with epilepsy have been identified; however, few studies have examined these risk factors over time. The primary purpose of this study was to explore the relationship between demographic characteristics, seizure-related factors, and psychosocial factors and depressive symptoms over 6 months.

WebEase: development of a Web-based epilepsy self-management intervention.

People with epilepsy must adopt many self-management behaviors, especially regarding medication adherence, stress management, and sleep quality. In response to the need for theory-based self-management programs that people with epilepsy can easily access, the WebEase Web site was created and tested for feasibility, acceptability, and usability. This article discusses the theoretical background and developmental phases of WebEase and lessons learned throughout the development process.

A telephone-based self-management program for people with epilepsy.

The study was conducted to test the feasibility of a telephone-based self-management program for adults with epilepsy. The program was based on social cognitive theory and principles of motivational interviewing (MI). Twenty-two adults with epilepsy were recruited from hospital-based epilepsy clinics.

Evaluation of WebEase: an epilepsy self-management Web site.

People with epilepsy have various education needs and must adopt many self-management behaviors in order to control their condition. This study evaluates WebEase, an Internet-based, theory-driven, self-management program for adults with epilepsy. Thirty-five participants took part in a 6-week pilot implementation of WebEase.

A descriptive analysis of seizure events among adults who participated in a computer-based assessment.

The purpose of this study was to document seizure events associated with the use of a computer-based assessment and to describe the contextual factors surrounding these seizure episodes. Study participants were adults with epilepsy who were enrolled at research sites in Atlanta and Boston. Subjects were asked to complete a computer-based assessment at 3 time points.

Use of computers and the Internet for health information by patients with epilepsy.

The purpose of this study was to describe computer and Internet use among an online group and a clinic-based group of people with epilepsy. Greater than 95% of the online group and 60% of the clinic group have access to computers and the Internet. More than 99% of the online group and 57% of the clinic group used the Internet to find health information.

Human immunodeficiency virus-encoded Tat activates glycogen synthase kinase-3beta to antagonize nuclear factor-kappaB survival pathway in neurons.

The pathogenesis of human immunodeficiency virus type 1 (HIV-1)-associated dementia is mediated by neuronal dysfunction and death, brought about by the action of soluble neurotoxic factors that are released by virally infected macrophages and microglia. Paradoxically, many candidate HIV-1 neurotoxins also possess the ability to activate nuclear factor-kappa B (NF-kappaB), which has a potent pro-survival effect in primary neurons. The present study explored this conundrum and investigated why NF-kappaB might fail to protect neurons that are exposed to candidate HIV-1 neurotoxins.

Inhibition of mixed lineage kinase 3 prevents HIV-1 Tat-mediated neurotoxicity and monocyte activation.

The HIV-1 gene products Tat and gp120 are toxic to neurons and can activate cells of myeloid origin, properties that are thought to contribute to the clinical manifestations of HIV-1-associated dementia (HAD). To investigate the intracellular signaling mechanisms involved in these events, the effect of Tat and gp120 on mixed lineage kinase (MLK) 3 activation was examined. Tat and gp120 were shown to induce autophosphorylation of MLK3 in primary rat neurons; this was abolished by the addition of an inhibitor of MLK3 (CEP1347).