Unilateral double facial artery: an anatomic variant and clinical implications.

Background: This paper reports a rare anatomical variant of the facial artery (FA) - namely, a double FA pattern - which has significant implications in a wide range of surgical and aesthetic medicine disciplines.

Case: The study involves a case report and literature review of the FA and its variants. The case is that of a 61-year-old female cadaver with a unilateral FA variant branching pattern discovered during a cadaveric dissection for an anatomy course.

Hilar Abnormality in the Left Lung: Left Pulmonary Artery Posterior to the Left Mainstem Bronchus.

The thoracic cavity contains vital cardiovascular and pulmonary structures. Few congenital anatomical variations in the bronchial tree and pulmonary vasculature have been reported. Understanding such variants is crucial during surgical procedures that involve the thorax.

Anomalous Extensor Indicis Proprius Muscle Extending Beyond the Extensor Retinaculum: A Case Report.

Case: During dissection of the upper limb of a cadaver in preparation for a first-year anatomy course, an extensor indicis proprius (EIP) variant was discovered with its muscle belly extending distal to the extensor retinaculum and beyond what has been previously described in the literature.

Conclusion: EIP is commonly used as a tendon transfer for extensor pollicis longus rupture. Few anatomic variants of EIP have been reported in the literature, but such variants should be considered because of their consequences to the success of tendon transfer and potential implications for diagnosis of an otherwise unexplained mass of the wrist.

Reversal of prenatal heroin-induced alterations in hippocampal gene expression via transplantation of mesenchymal stem cells during adulthood.

Neurobehavioral teratology is the study of typically subtle neurobehavioral birth defects. Our previously described mouse model demonstrated septohippocampal cholinergic innervation-related molecular and behavioral deficits after prenatal exposure to heroin. Since the alterations are below malformation level, they are likely to represent consequences of regulatory processes, feasibly gene expression.

Metal-induced neurotoxicity in a RAGE-expressing C. elegans model.

Environmental and occupational metal exposure poses serious global concerns. Metal exposure have severally been associated with neurotoxicity and brain damage. Furthermore, receptor for advanced glycation end products (RAGE) is also implicated in neurological disorders, particularly those with altered glucose metabolism.

System-specific neurodegeneration following glucotoxicity in the C. elegans model.

Hyperglycemia-related neuropathy leads to the onset and exacerbation of several pathologies. The C. elegans model has been used to study this phenomenon and its underlying mechanisms using a broad evaluation for neurodegeneration.

-An Emerging Model to Study Metal-Induced RAGE-Related Pathologies.

The receptor for advanced glycation end products (RAGE), a multi-ligand receptor, is mostly associated with promoting inflammation and oxidative stress. In addition to advanced glycation end products (AGEs), its ligands include High mobility group box 1 protein (HMGB-1), S-100 proteins and beta-sheet fibrils. The effects of several metals and metalloids on RAGE expression and activation have been recently studied: in vivo and in vitro exposure to methylmercury, selenium, zinc, manganese, and arsenic was associated with a variety of RAGE-related alterations and behavioral impairments, which are mostly dependent upon the administration procedure (local vs.

A C. elegans Model for the Study of RAGE-Related Neurodegeneration.

The receptor for advanced glycation products (RAGE) is a cell surface, multi-ligand receptor belonging to the immunoglobulin superfamily; this receptor is implicated in a variety of maladies, via inflammatory pathways and induction of oxidative stress. Currently, RAGE is being studied using a limited number of mammalian in vivo, and some complementary in vitro, models. Here, we present a Caenorhabditis elegans model for the study of RAGE-related pathology: a transgenic strain, expressing RAGE in all neurons, was generated and subsequently tested behaviorally, developmentally, and morphologically.

C. elegans as a model in developmental neurotoxicology.

Due to many advantages Caenorhabditis elegans (C. elegans) has become a preferred model of choice in many fields, including neurodevelopmental toxicity studies. This review discusses the benefits of using C.

Neurotoxic effect of active ingredients in sunscreen products, a contemporary review.

Sunscreen application is the main strategy used to prevent the maladies inflicted by ultraviolet (UV) radiation. Despite the continuously increasing frequency of sunscreen use worldwide, the prevalence of certain sun exposure-related pathologies, mainly malignant melanoma, is also on the rise. In the past century, a variety of protective agents against UV exposure have been developed.

Neurotoxicity of fragrance compounds: A review.

Fragrance compounds are chemicals belonging to one of several families, which are used frequently and globally in cosmetics, household products, foods and beverages. A complete list of such compounds is rarely found on the ingredients-list of such products, as "fragrance mixtures" are defined as "trade secrets" and thus protected by law. While some information regarding the general toxicity of some of these compounds is available, their neurotoxicity is known to a lesser extent.

AGEs/RAGE-Related Neurodegeneration: daf-16 as a Mediator, Insulin as an Ameliorant, and C. elegans as an Expedient Research Model.

Advanced glycation end-products (AGEs) are nonenzymatically glycated proteins, lipids, and nucleic acids. These compounds both originate exogenously and are formed endogenously, and they are associated, along with one of their receptors (RAGE), with a variety of pathologies and neurodegeneration. Some of their deleterious effects include affecting insulin signaling and FOXO-related pathways in both receptor-dependent and -independent manners.

Advanced Glycation End-Products and Their Receptors: Related Pathologies, Recent Therapeutic Strategies, and a Potential Model for Future Neurodegeneration Studies.

Advanced glycation end products (AGEs) are the result of a nonenzymatic reaction between sugars and proteins, lipids, or nucleic acids. AGEs are both consumed and endogenously formed; their accumulation is accelerated under hyperglycemic and oxidative stress conditions, and they are associated with the onset and complication of many diseases, such as cardiovascular diseases, diabetes, and Alzheimer's disease. AGEs exert their deleterious effects by either accumulating in the circulation and tissues or by receptor-mediated signal transduction.

An avian model for ascertaining the mechanisms of organophosphate neuroteratogenicity and its therapy with mesenchymal stem cell transplantation.

Introduction: A fast and simple model which uses animals lower on the evolutionary scale is beneficial for progress in neuroteratological research. Here, we established this novel model and applied it in the study of the detrimental effects of pre-hatch exposure to chlorpyrifos on neurogenesis and several neurotransmitter systems in the chick and their reversal, using mesenchymal stem cell (MSC) transplantation.

Methods: Chicken eggs were injected with the organophosphate chlorpyrifos, 10mg/kg eggs - a dose below the threshold for dysmorphology - on incubation days (ID) 0 and 5 and subsequently the embryos were subjected to intravenous transplantation of MSC on ID 13.

The teratogenicity and behavioral teratogenicity of di(2-ethylhexyl) phthalate (DEHP) and di-butyl phthalate (DBP) in a chick model.

Phthalates are industrial chemicals widely used in consumer products, plastics and children toys, and the risk of exposure to phthalates, especially prenatal exposure, is a growing concern justifying the development of an animal model to better understand their effect. The present study was designed to evaluate the suitability of a chick model for phthalate DEHP teratogenicity and neurobehavioral teratogenicity, a model which is simple and devoid of potential confounding factors such as maternal toxicity, maternal-fetal unit and maternal-neonatal interactions; major findings were confirmed in the DBP study. Prehatch exposure to DEHP in doses ranging from 20 to 100 mg/kg, reduced the percent hatching from 80% in control eggs to 65%, and increased late hatchings from 12.

Reversal of chlorpyrifos neurobehavioral teratogenicity in mice by allographic transplantation of adult subventricular zone-derived neural stem cells.

Neurobehavioral teratogenicity can be reversed with transplantation of neural stem cells. However, the usefulness of this therapy would be greatly enhanced by employing adult stem cells. In pursuit of this this goal, we developed a model that uses subventricular zone (SVZ) cells.

An avian model for the reversal of neurobehavioral teratogenicity with neural stem cells.

A fast and simple model which uses lower animals on the evolutionary scale is beneficial for developing procedures for the reversal of neurobehavioral teratogenicity with neural stem cells. Here, we established a procedure for the derivation of chick neural stem cells, establishing embryonic day (E) 10 as optimal for progression to neuronal phenotypes. Cells were obtained from the embryonic cerebral hemispheres and incubated for 5-7 days in enriched medium containing epidermal growth factor (EGF) and basic fibroblast growth factor (FGF2) according to a procedure originally developed for mice.

Neurobehavioral teratogenicity of perfluorinated alkyls in an avian model.

Perfluorinated alkyls are widely-used agents that accumulate in ecosystems and organisms because of their slow rate of degradation. There is increasing concern that these agents may be developmental neurotoxicants and the present study was designed to develop an avian model for the neurobehavioral teratogenicity of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS). Fertilized chicken eggs were injected with 5 or 10mg/kg of either compound on incubation day 0.

Reversal of chlorpyrifos neurobehavioral teratogenicity in mice by nicotine administration and neural stem cell transplantation.

Identifying the mechanisms underlying the adverse effects of developmental neurotoxicants enables the design of therapies that can potentially reverse neurobehavioral deficits in adulthood. We administered chlorpyrifos (CPF), a model organophosphate pesticide to pregnant mice and identified visuospatial deficits in adult offspring using performance in the Morris maze. We then evaluated two strategies to reverse the effects, nicotine administration and transplantation of neural stem cells.

Neurobehavioral teratogenicity of sarin in an avian model.

Nerve gas organophosphates like sarin are likely to be used in urban terrorism, leading to widespread exposures of pregnant women and young children. Here, we established a model for sarin neurobehavioral teratogenicity in the developing chick so as to explore the consequences of apparently subtoxic sarin exposure and the mechanisms underlying synaptic and behavioral deficits. Chicken eggs were injected with sarin (2, 6 and 12 microg/kg) on incubation days 2 and 6, treatments that did not decrease hatching and did not evoke dysmorphology.

A mechanism-based complementary screening approach for the amelioration and reversal of neurobehavioral teratogenicity.

The identification of mechanisms and outcomes for neurobehavioral teratogenesis is critical to our ability to develop therapies to ameliorate or reverse the deleterious effects of exposure to developmental neurotoxicants. We established mechanistically-based complementary models for the study of cholinergic systems in the mouse and the chick, using both environmental neurotoxicants (chlorpyrifos, perfluoroalkyls) and drugs of abuse (heroin, nicotine, PCP). Behavioral evaluations were made using the Morris maze in the mouse, evaluating visuospatial memory related to hippocampal cholinergic systems, and imprinting in the chick, examining behavior dependent on cholinergic innervation of the IMHV.

Exposure of developing chicks to perfluorooctanoic acid induces defects in prehatch and early posthatch development.

There is increasing concern over the widespread use of perfluorinated chemicals, which accumulate in various tissues and penetrate the mammalian fetus. A chick model was established for the rapid evaluation of teratogenicity of these chemicals, an important issue because developmental defects often occur at lower exposures than those required for adult systemic toxicity. Chicken eggs were injected with varying doses of perfluorooctanoic acid prior to incubation.