Neurocognitive functioning predicts frailty index in HIV.

Objective: To evaluate the association between a frailty index (i.e., scale of accumulated deficits) and neurocognitive functioning among persons living with HIV/AIDS (PLWHA).

Coagulation imbalance and neurocognitive functioning in older HIV-positive adults on suppressive antiretroviral therapy.

Objectives: The aim of this study was to compare plasma biomarkers of coagulation between HIV-infected individuals and HIV-uninfected controls and to assess the impact of disturbances in coagulation on neurocognitive functioning in HIV.

Design: A cross-sectional study of 66 antiretroviral therapy treated, virally suppressed, HIV-infected and 34 HIV-uninfected older (≥50 years of age) adults.

Methods: Participants completed standardized neurobehavioral and neuromedical assessments.

Dysregulated miRNA biogenesis downstream of cellular stress and ALS-causing mutations: a new mechanism for ALS.

Interest in RNA dysfunction in amyotrophic lateral sclerosis (ALS) recently aroused upon discovering causative mutations in RNA-binding protein genes. Here, we show that extensive down-regulation of miRNA levels is a common molecular denominator for multiple forms of human ALS. We further demonstrate that pathogenic ALS-causing mutations are sufficient to inhibit miRNA biogenesis at the Dicing step.

Albumin induces excitatory synaptogenesis through astrocytic TGF-β/ALK5 signaling in a model of acquired epilepsy following blood-brain barrier dysfunction.

Post-injury epilepsy (PIE) is a common complication following brain insults, including ischemic, and traumatic brain injuries. At present, there are no means to identify the patients at risk to develop PIE or to prevent its development. Seizures can occur months or years after the insult, do not respond to anti-seizure medications in over third of the patients, and are often associated with significant neuropsychiatric morbidities.

Exposure to vehicle emissions results in altered blood brain barrier permeability and expression of matrix metalloproteinases and tight junction proteins in mice.

Background: Traffic-generated air pollution-exposure is associated with adverse effects in the central nervous system (CNS) in both human exposures and animal models, including neuroinflammation and neurodegeneration. While alterations in the blood brain barrier (BBB) have been implicated as a potential mechanism of air pollution-induced CNS pathologies, pathways involved have not been elucidated.

Objectives: To determine whether inhalation exposure to mixed vehicle exhaust (MVE) mediates alterations in BBB permeability, activation of matrix metalloproteinases (MMP) -2 and -9, and altered tight junction (TJ) protein expression.

Oppenheim's myatonia congenita.

In 1900 the famous German neurologist Hermann Oppenheim published a two-page article on "Myatonia congenita" which led to a long-lasting and confusing discussion in neurology and neuropediatrics, and which was extensively quoted throughout the 20th century. As this article is only available in German, an English translation is presented here. Further publications of Oppenheim on the same subject are mentioned and some comments are made on the impact of his seminal article.

Injuries due to letter bombs.

In Austria in late 1993 ten letter bombs were sent to outstanding persons who have been engaged in the care of foreigners. Four of these bombs detonated, when they were opened by the addressee. The remaining six bombs were discovered in time and could be deactivated by specialists.

Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor gamma and the retinoid X receptor.

Induction of terminal differentiation represents a promising therapeutic approach to certain human malignancies. The peroxisome proliferator-activated receptor gamma (PPAR gamma) and the retinoid X receptor alpha (RXR alpha) form a heterodimeric complex that functions as a central regulator of adipocyte differentiation. Natural and synthetic ligands for both receptors have been identified.

c-fos is not essential for v-abl-induced lymphomagenesis.

Recent studies have suggested that cellular transformation by abl oncoproteins may be mediated by the ras signaling pathway. One of the main nuclear targets of this signal transduction cascade is the Fos and Jun family of transcription factors. To test the relevance of the c-fos proto-oncogene for v-abl-induced cancer development, we inoculated c-fos-deficient mice with the Abelson murine leukemia virus.

c-fos is required for malignant progression of skin tumors.

The proto-oncogene c-fos is a major nuclear target for signal transduction pathways involved in the regulation of cell growth, differentiation, and transformation. Using the multistep skin carcinogenesis model, we have directly tested the ability of c-fos-deficient mice to develop cancer. Upon treatment with a tumor promoter, c-fos knockout mice carrying a v-H-ras transgene were able to develop benign tumors with similar kinetics and relative incidence as wild-type animals.