Toxicity of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) on oligodendrocytes during embryonic zebrafish development.

Polybrominated diphenyl ethers (PBDEs) are flame retardants heavily utilized across plastic, textile and electronic industries. Although these PBDEs are effective in protecting property and human life from fire, their high production volumes have led PBDEs to become pervasive environmental contaminants and pose an ecological and health risk as high levels have been noted in environmental media including water and sediment, wildlife and human tissue. Here we investigate the developmental neurotoxicity of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), one of the more dominant PBDE congeners found in human tissue, on oligodendrocytes in the hindbrain and spinal cord.

Butyl Benzyl Phthalate (BBP) disrupts neuromast development in embryonic zebrafish.

Butyl benzyl phthalate (BBP) is found in common household and industrial products world-wide. Phthalates are not covalently bound to plastics and continuously leach into the soil, sediment and aquatic environments. The lateral line system of fish is a mechanosensory system composed of neuromasts essential for survival behaviors including rheotaxis, schooling and predator avoidance.

Di-butyl phthalate disrupts muscle, motor and sensory neuron development in embryonic zebrafish.

Phthalates are added to plastics to enhance its flexibility, durability and transparency. Phthalates are not covalently bound to plastics and leach into the environment. Phthalates are now pervasive and ubiquitously present in the atmosphere, soil and sediment, surface and wastewater.

Hindbrain defects induced by Di-butyl phthalate (DBP) in developing zebrafish embryos.

Di-butyl phthalate (DBP) is a globally used plasticizer found in alarmingly high concentrations in soil and water ecosystems. As phthalates are non-covalently bound to plastic polymers, phthalates easily leach into the aquatic environment. The effects of DBP on aquatic organisms is concerning, most notably, studies have focused on the endocrine-disrupting effects.

Di-butyl phthalate (DBP) induces defects during embryonic eye development in zebrafish.

Di-butyl phthalate (DBP) is a phthalate ester (PAEs) added during the manufacturing of plastics to make them stronger, yet more pliable. DBP is noncovalently bound to plastics resulting in leaching into the environment. Concerning concentrations of DBP have been noted in surface and groundwater, aquatic ecosystems, soil and atmospheric environments globally.

Di-butyl phthalate (DBP) induces craniofacial defects during embryonic development in zebrafish.

Di-butyl phthalate (DBP) is commonly added to make plastics softer and more pliable and is found in a variety of consumer and industrial products. Alarmingly high levels of DBP have been detected in water and sediment as DBP leaches from products. These levels are concerning and have led the Environmental Protection Agency to label DBP as a priority environmental pollutant and the European Commission to label DBP as a priority substance.

Butyl benzyl phthalate (BBP) induces caudal defects during embryonic development.

Butyl benzyl phthalate (BBP) is commonly added during the manufacturing of plastics to increase flexibility and elasticity. However, BBP leaches off of plastic and environment presence has been detected in soil, groundwater and sediment potentially effecting organisms in the environment. Given the widespread uses of BBP in household, consumer goods and the presence of BBP in the environment, studies on developmental toxicity are needed.

Glyphosate induces cardiovascular toxicity in Danio rerio.

Glyphosate is a broad spectrum herbicide used aggressively in agricultural practices as well as home garden care. Although labeled "safe" by the chemical industry, doses tested by industry do not mimic chronic exposures to sublethal doses that organisms in the environment are exposed to over long periods of time. Given the widespread uses of and exposure to glyphosate, studies on developmental toxicity are needed.

Using Photovoice and Asset Mapping to Inform a Community-Based Diabetes Intervention, Boston, Massachusetts, 2015.

Introduction: Diabetes self-management takes place within a complex social and environmental context.  This study's objective was to examine the perceived and actual presence of community assets that may aid in diabetes control.

Methods: We conducted one 6-hour photovoice session with 11 adults with poorly controlled diabetes in Boston, Massachusetts.

Glyphosate induces neurotoxicity in zebrafish.

Glyphosate based herbicides (GBH) like Roundup(®) are used extensively in agriculture as well as in urban and rural settings as a broad spectrum herbicide. Its mechanism of action was thought to be specific only to plants and thus considered safe and non-toxic. However, mounting evidence suggests that GBHs may not be as safe as once thought as initial studies in frogs suggest that GBHs may be teratogenic.

Evaluation of the developmental toxicity of lead in the Danio rerio body.

Lead has been utilized throughout history and is widely distributed and mobilized globally. Although lead in the environment has been somewhat mitigated, the nature of lead and its extensive uses in the past prohibit it from being completely absent from our environment and exposure to lead is still a public health concern. Most studies regarding lead toxicity have focused on the brain.

Neural alterations from lead exposure in zebrafish.

Lead was used extensively as a gas additive and pesticide, in paints, batteries, lead shot, pipes, canning and toy manufacturing. Although uses of lead have been restricted, lead persists in our environment especially in older homes, and generally in soil and water. Although extensive studies have determined that fetal and childhood exposures to lead have been associated with childhood and adolescent memory impairments and learning disabilities, there are limited studies investigating early neural and morphological effects that may lead to these behavioral and learning abnormalities.

Brief embryonic strychnine exposure in zebrafish causes long-term adult behavioral impairment with indications of embryonic synaptic changes.

Zebrafish provide a powerful model of the impacts of embryonic toxicant exposure on neural development that may result in long-term behavioral dysfunction. In this study, zebrafish embryos were treated with 1.5mM strychnine for short embryonic time windows to induce transient changes in inhibitory neural signaling, and were subsequently raised in untreated water until adulthood.

A zebrafish assay for identifying neuroprotectants in vivo.

In this study, we developed an in vivo method to determine drug effects on oxidation-induced apoptosis in the zebrafish brain caused by treatment with L-hydroxyglutaric acid (LGA). We confirmed that LGA-induced apoptosis was caused by oxidation by examining the presence of an oxidative product, nitrotyrosine. Next, we examined the effects of 14 characterized neuroprotectants on LGA-treated zebrafish, including: D-methionine (D-Met), Indole-3-carbinol, deferoxamine (DFO), dihydroxybenzoate (DHB), deprenyl, L-NAME (N(G)-nitro-L-arginine methyl ester), n-acetyl L-cysteine (L-NAC), 2-oxothiazolidine-4-carboxylate (OTC), lipoic acid, minocycline, isatin, cortisone, ascorbic acid and alpha-tocopherol.

Neurotoxicity assessment using zebrafish.

Introduction: Transparency is a unique attribute of zebrafish that permits direct assessment of drug effects on the nervous system using whole mount antibody immunostaining and histochemistry.

Methods: To assess pharmacological effects of drugs on the optic nerves, motor neurons, and dopaminergic neurons, we performed whole mount immunostaining and visualized different neuronal cell types in vivo. In addition, we assessed neuronal apoptosis, proliferation, oxidation and the integrity of the myelin sheath using TUNEL staining, immunostaining and in situ hybridization.

An early Fgf signal required for gene expression in the zebrafish hindbrain primordium.

We have explored the role of fibroblast growth factor (Fgf) signaling in regulating gene expression in the early zebrafish hindbrain primordium. We demonstrate that a dominant negative Fgf receptor (FgfR) construct disrupts gene expression along the entire rostrocaudal axis of the hindbrain primordium and, using an FgfR antagonist, we find that this Fgf signal is required at early gastrula stages. This effect cannot be mimicked by morpholino antisense oligos to Fgf3, Fgf8 or Fgf24--three Fgf family members known to be secreted from signaling centers at the midbrain-hindbrain boundary (MHB), in rhombomere 4 and in caudal mesoderm at gastrula stages.

Dynamic expression and regulation by Fgf8 and Pou2 of the zebrafish LIM-only gene, lmo4.

We report the expression of zebrafish lmo4 during the first 48 h of development. Like its murine ortholog, lmo4 is expressed in somitic mesoderm, branchial arches, otic vesicles, and limb (pectoral fin) buds. In addition, however, we report zebrafish lmo4 expression in the developing eye, cardiovascular tissue, and the neural plate and telencephalon.

Dynamic expression and regulation by Fgf8 and Pou2 of the zebrafish LIM-only gene, lmo4.

We report the expression of zebrafish lmo4 during the first 48 h of development. Like its murine ortholog, lmo4 is expressed in somitic mesoderm, branchial arches, otic vesicles, and limb (pectoral fin) buds. In addition, however, we report zebrafish lmo4 expression in the developing eye, cardiovascular tissue, and the neural plate and telencephalon.