Bad actor reporting has recently grown in popularity as an effective method for social media attacks and harassment, but many mitigation strategies have yet to be investigated. In this study, we created a simulated social media environment of 500,000 users, and let those users create and review a number of posts. We then created four different post-removal algorithms to analyze the simulation, each algorithm building on previous ones, and evaluated them based on their accuracy and effectiveness at removing malicious posts. This thesis work concludes that a trust-reward structure within user report systems is the most effective strategy for removing malicious content while minimizing the removal of genuine content. This thesis also discusses how the structure can be further enhanced to accommodate real-world data and provide a viable solution for reducing bad actor online activity as a whole.

Maternal consumption of alcohol (ethanol) during pregnancy can inhibit prenatal growth, resulting in fetuses that are small for gestational age. Those prenatal growth deficiencies can have lasting consequences for early childhood development and are often reflected by low weight and stature. Those alcohol-induced pre- and post-natal growth deficiencies ("failure to thrive") are among the abnormal developmental criteria used to identify Fetal Alcohol Syndrome (FAS). FAS is characterized by minor facial abnormalities and deficiencies of the central nervous system as well. A deficiency in prenatal growth is often referred to as an intrauterine growth restriction (IUGR), a general term that refers to stunted fetal growth that may be a result of genetic or environmental factors.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system. The pattern of facial defects that occur as a result of ethanol exposure during development primarily affects the midline of the face, altering morphology of the eyes, nose, and lips. Ethanol damage to cranial neural crest cells (CNCC) early in embryonic development is responsible for these minor midline abnormalities. Regulation of the gene sonic hedgehog (shh) during this period of development has been observed to rescue these ethanol-affected CNCC from fated cell death, an association that has not yet been examined as it applies to human cells.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system (CNS). The developing brain is particularly vulnerable to the toxicity of ethanol, given the broad time frame of susceptibility from neurulation, when the neural tube is formed, all the way through to birth. The cerebellum is an area of the brain particularly vulnerable to prenatal ethanol exposure. Mechanisms proposed for this drastic reduction in brain cells include apoptosis, oxidative stress, and damage to the radial glia stem cell progenitor pool. Physical dexterity, coordination, and visuospatial processing are all affected by these stressors, and eyeblink classical conditioning tests have proven that ethanol-induced damage goes beyond motor coordination by permanently impacting learning and memory.

Prenatal exposure to alcohol (ethanol) in human and animal models results in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The basal ganglia, one of the central nervous system components, are affected by exposure to ethanol during development. When exposed to alcohol in utero, the basal ganglia decrease in size resulting in poor motor coordination and defects in executive functioning.

Maternal consumption of alcohol (ethanol) can result in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The eye and ocular system development is particularly susceptible to the effects of prenatal alcohol exposure and can result in visual impairment or blindness.

The term Fetal Alcohol Syndrome (FAS) was first published in 1973 in an article published in the British medical journal The Lancet. In that article, a group of pediatricians and psychiatrists at the University of Washington Medical School helped to define the morphological defects and developmental delays that can affect children born to alcoholic mothers. Those observations include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing brain that can result in behavioral, learning, and cognitive abnormalities.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) is part of this group and was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities and defects of the central nervous system (CNS). The CNS is particularly vulnerable to the effects of ethanol during prenatal development. Severe exposure correlates with gross morphological abnormalities and an overall decrease in white matter. Mechanisms for how ethanol affects the development of the CNS are complicated, but damage to neural stem cell progenitor pools that give rise to neurons and glia is strongly suspected to be a major factor. Damage to this population of cells at any point during CNS development can result in abnormalities in the formation and maturation of these cells, from the initial differentiation through the maturation of neuronal networks. This damage can lead to a wide variety of cognitive deficiencies, functional impairments, and behavioral problems depending on the area of the brain impacted by prenatal ethanol exposure.

A variety of developmental defects occur as a result of prenatal exposure to alcohol (ethanol) in utero. In humans, those defects are collectively classified as Fetal Alcohol Spectrum Disorders, with Fetal Alcohol Syndrome (FAS) representing the more severe defects. FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). In addition to those defects, prenatal exposure to alcohol impacts cardiogenesis, the developmental stage of heart formation.

Prenatal exposure to alcohol (ethanol) can result in a continuum of developmental abnormalities that are highly variable depending on the severity, duration, frequency, and timing of exposure during gestation. Defects of the corpus callosum (CC) have proven to be a reliable indicator of prenatal alcohol exposure as it affects the brain. Structural abnormalities of the CC occur along a continuum, like most alcohol-induced anomalies, whereby more severe prenatal exposure results in a greater expression of the abnormal trait. A variety of cognitive deficiencies are associated with defects of the fetal CC, the morphology of which can vary greatly between individuals and can be observed through neuroimaging over a broad transect of life stages.