Neurotoxicity of diesel exhaust extracts in zebrafish and its implications for neurodegenerative disease.

Long-term air pollution (AP) exposure, including diesel exhaust exposure, is increasingly being recognized as a major contributor to the development of neurodegenerative diseases such as Parkinson's and Alzheimer's disease. How AP increases the risk of neurodegeneration is not well understood but might include direct neurotoxicity and CNS inflammation. We investigated the impact of diesel exhaust particulate extract (DEPe) exposure on the brain and the mechanisms by which microglia and astroglia might mediate neuronal changes.

Air Pollution and the Risk of Parkinson's Disease: A Review.

Parkinson's disease, as well as other neurodegenerative disorders, are primarily characterized by pathological accumulation of proteins, inflammation, and neuron loss. Although there are some known genetic risk factors, most cases cannot be explained by genetics alone. Therefore, it is important to determine the environmental factors that confer risk and the mechanisms by which they act.

Straight from the horse's mouth: Increasing self-report in mental health assessment in individuals with intellectual disability.

Background: Mental health conditions are common among individuals with intellectual disability. Under recognition of mental health disorders leading to unmet treatment needs is common in this population. This article addresses one major contributing factor, the lack of cognitively accessible self-report measures for individuals with intellectual disability.

Diesel exhaust exposure alters the expression of networks implicated in neurodegeneration in zebrafish brains.

Neurodegenerative diseases are a major cause of disability in the world, but their etiologies largely remain elusive. Genetic factors can only account for a minority of risk for most of these disorders, suggesting environmental factors play a significant role in the development of these diseases. Prolonged exposure to air pollution has recently been identified to increase the risk of Alzheimer's and Parkinson's diseases, but the molecular mechanisms by which it acts are not well understood.

Studying the Pathophysiology of Parkinson's Disease Using Zebrafish.

Parkinson's disease is a common neurodegenerative disorder leading to severe disability. The clinical features reflect progressive neuronal loss, especially involving the dopaminergic system. The causes of Parkinson's disease are slowly being uncovered and include both genetic and environmental insults.

Diesel Exhaust Extract Exposure Induces Neuronal Toxicity by Disrupting Autophagy.

The vast majority of neurodegenerative disease cannot be attributed to genetic causes alone and as a result, there is significant interest in identifying environmental modifiers of disease risk. Epidemiological studies have supported an association between long-term exposure to air pollutants and disease risk. Here, we investigate the mechanisms by which diesel exhaust, a major component of air pollution, induces neurotoxicity.

A novel transgenic zebrafish line allows for in vivo quantification of autophagic activity in neurons.

The pathophysiology of most neurodegenerative diseases includes aberrant accumulation of protein aggregates. Recent evidence highlights the role of protein degradation pathways in neurodegeneration. Concurrently, genetic tools have been generated to enable zebrafish, Danio rerio, to be used as an animal model to study neurodegenerative processes.

Neurotoxicity of the Parkinson Disease-Associated Pesticide Ziram Is Synuclein-Dependent in Zebrafish Embryos.

Background: Exposure to the commonly used dithiocarbamate (DTC) pesticides is associated with an increased risk of developing Parkinson disease (PD), although the mechanisms by which they exert their toxicity are not completely understood.

Objective: We studied the mechanisms of ziram's (a DTC fungicide) neurotoxicity in vivo.

Methods: Zebrafish (ZF) embryos were utilized to determine ziram's effects on behavior, neuronal toxicity, and the role of synuclein in its toxicity.

Strategic Grassland Bird Conservation throughout the Annual Cycle: Linking Policy Alternatives, Landowner Decisions, and Biological Population Outcomes.

Grassland bird habitat has declined substantially in the United States. Remaining grasslands are increasingly fragmented, mostly privately owned, and vary greatly in terms of habitat quality and protection status. A coordinated strategic response for grassland bird conservation is difficult, largely due to the scope and complexity of the problem, further compounded by biological, sociological, and economic uncertainties.

High expression of CAI2, a 9p21-embedded long noncoding RNA, contributes to advanced-stage neuroblastoma.

Neuroblastoma is a pediatric cancer with significant genomic and biologic heterogeneity. p16 and ARF, two important tumor-suppressor genes on chromosome 9p21, are inactivated commonly in most cancers, but paradoxically overexpressed in neuroblastoma. Here, we report that exon γ in p16 is also part of an undescribed long noncoding RNA (lncRNA) that we have termed CAI2 (CDKN2A/ARF Intron 2 lncRNA).

Chimeras of p14ARF and p16: functional hybrids with the ability to arrest growth.

The INK4A locus codes for two independent tumor suppressors, p14ARF and p16/CDKN2A, and is frequently mutated in many cancers. Here we report a novel deletion/substitution from CC to T in the shared exon 2 of p14ARF/p16 in a melanoma cell line. This mutation aligns the reading frames of p14ARF and p16 mid-transcript, producing one protein which is half p14ARF and half p16, chimera ARF (chARF), and another which is half p16 and half non-p14ARF/non-p16 amino acids, p16-Alternate Carboxyl Terminal (p16-ACT).

A+KIDS, a web-based antipsychotic registry for North Carolina youths: an alternative to prior authorization.

Objective: The rise in use of antipsychotics among U.S. children is well documented.

Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease.

Parkinson disease (PD) is a neurodegenerative disorder particularly characterized by the loss of dopaminergic neurons in the substantia nigra. Pesticide exposure has been associated with PD occurrence, and we previously reported that the fungicide benomyl interferes with several cellular processes potentially relevant to PD pathogenesis. Here we propose that benomyl, via its bioactivated thiocarbamate sulfoxide metabolite, inhibits aldehyde dehydrogenase (ALDH), leading to accumulation of the reactive dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL), preferential degeneration of dopaminergic neurons, and development of PD.

Clinical usefulness of the diagnostic manual-intellectual disability for mental disorders in persons with intellectual disability: results from a brief field survey.

Objective: The National Association for the Dually Diagnosed, in collaboration with the American Psychiatric Association, adapted the DSM-IV-TR for use with individuals with intellectual disability. This article presents the findings of a study to examine the utility of the Diagnostic Manual-Intellectual Disability (DM-ID) in clinical practice.

Method: In a survey conducted during the summer of 2006, clinicians reported on the extent to which the DM-ID was user friendly, whether it allowed the clinician to arrive at an appropriate diagnosis of the patient, if the clinician was able to arrive at a more specific diagnosis than with the DSM-IV-TR, and if it helped avoid the use of "not otherwise specified" (NOS) diagnostic categories.

Inactivation of SHIP1 in T-cell acute lymphoblastic leukemia due to mutation and extensive alternative splicing.

To understand the mechanism behind aberrant Akt activation in T-ALL, PIK3CA, PTEN and SHIP1 expression and genotype were assessed. No cell lines or primary ALLs harbored PIK3CA mutations. PTEN was expressed in just one-third of the cell lines, but in two-thirds of the primary ALLs, though in the inactivated (phosphorylated) form.

The diagnosis and treatment of individuals with mental illness and developmental disabilities: an overview.

Background: The assessment and treatment psychiatric disorders among individuals with developmental disorders is in a state of flux. Clinicians working in this field confront two heterogeneous conditions based on separate but overlapping biopsychosocial bodies of scientific and clinical experiences.

Methods: The paper is a review of the relevant literature and an effort to synthesize sokme of the major problem areas in differential diagnosis and treatment planning.

Treatment models for treating patients with combined mental illness and developmental disability.

The presence of co-occurring psychiatric disorders among individuals with developmental disability (DD) requires clinicians to adjust and modify standard mental health assessment and treatment planning. In particular, assessment includes input from a multi-disciplinary team and as a result, diagnosis is frequently a synthesis of data from many different points of view. Treatment planning and implementation commonly include a collection of highly specialized, individualized programs that focus on the long term management of both disorders.

Antipsychotic withdrawal-induced relapse predicts future relapses in institutionalized adults with severe intellectual disability.

Severe intellectual and developmental disabilities are frequently associated with aggression toward self and others, destruction of property, and disruption. Antipsychotic medications are a mainstay of treatment of such behaviors. National and state guidelines suggest stopping these medications or decreasing their dosages when possible if patients have maintained stability.

The genome of epsilon15, a serotype-converting, Group E1 Salmonella enterica-specific bacteriophage.

The genome sequence of the Salmonella enterica serovar Anatum-specific, serotype-converting bacteriophage epsilon15 has been completed. The nonredundant genome contains 39,671 bp and 51 putative genes. It most closely resembles the genome of phiV10, an Escherichia coli O157:H7-specific temperate phage, with which it shares 36 related genes.

Relapse of aggressive and disruptive behavior in mentally retarded adults following antipsychotic drug withdrawal predicts psychotropic drug use a decade later.

Background: Mental retardation is frequently associated with aggression toward self and others. Antipsychotic medications are frequently used as a major treatment of such aggression. However, national and state policies and guidelines are weighted toward stopping or decreasing the doses of these medications whenever possible, although exceptions are permitted.

Minimally effective doses of conventional antipsychotic medications used to treat aggression, self-injurious and destructive behaviors in mentally retarded adults.

Retrospective review of records from 1990 to 1997 revealed unsuccessful attempts to withdraw antipsychotic medications from a total of 34 intellectually disabled individuals. The lowest dose of antipsychotic medication necessary to maintain symptom suppression and the dose at which relapse occurred were noted. Target behaviors observed indicating relapse included increased self-injurious behavior, aggression, and destructive/disruptive behaviors.

Olanzapine for self-injurious, aggressive, and disruptive behaviors in intellectually disabled adults: a retrospective, open-label, naturalistic trial.

Background: The effectiveness of olanzapine in treating challenging behaviors in the intellectually disabled and its ability to substitute for conventional antipsychotic drugs were evaluated.

Method: A total of 20 institutionalized adults with a mean age of 42.7 years (range, 18-55 years) with intellectual disability and aggression, self-injurious behavior, destructive/disruptive behavior, or combinations of these behaviors were studied.