Identification of sensitivity genes involved in teratogen-induced neural tube defects

Due to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to [email protected], referencing the URI of the item.Includes bibliographical references.Neural tube defects (NTDs) are common human congenital anomalies affecting 1 per 1000 live-born infants in the United States. NTDs are medical conditions that result from improper formation of the brain and spinal cord. There is evidence to suggest that NTDs have a strong genetic component to their development. My project is designed to examine differential expression patterns of genes within the neural tube cells of inbred LM/Bc mouse fetuses following exposure to the known teratogenic agent, Valproic acid (VPA). In this project I am comparing gene expression patterns in both control and treated mice and attempting to identify those genes whose expression patterns have been significantly altered. My experimental methods include isolating total RNA from Lm/Bc mouse neural tissue, reverse transcribing the RNA into cDNA and PCR amplifying the cDNA using a radioactively end labeled primer in order to visualize the amplified fragment. The labeled cDNA fragment is then loaded onto a denaturing gel and separated by electrophoresis. The gel is then exposed to film and examined. Differentially expressed cDNAs are then isolated from the gel and sequenced. The results of this project show the identification of differentially expressed genes that may regulate the occurrence of NTDs

Identification of sensitivity genes involved in teratogen-induced neural tube defects

Due to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to [email protected], referencing the URI of the item.Includes bibliographical references.Neural tube defects (NTDs) are common human congenital anomalies affecting 1 per 1000 live-born infants in the United States. NTDs are medical conditions that result from improper formation of the brain and spinal cord. There is evidence to suggest that NTDs have a strong genetic component to their development. My project is designed to examine differential expression patterns of genes within the neural tube cells of inbred LM/Bc mouse fetuses following exposure to the known teratogenic agent, Valproic acid (VPA). In this project I am comparing gene expression patterns in both control and treated mice and attempting to identify those genes whose expression patterns have been significantly altered. My experimental methods include isolating total RNA from Lm/Bc mouse neural tissue, reverse transcribing the RNA into cDNA and PCR amplifying the cDNA using a radioactively end labeled primer in order to visualize the amplified fragment. The labeled cDNA fragment is then loaded onto a denaturing gel and separated by electrophoresis. The gel is then exposed to film and examined. Differentially expressed cDNAs are then isolated from the gel and sequenced. The results of this project show the identification of differentially expressed genes that may regulate the occurrence of NTDs

Perfectionism, self-stigma, and coping in students with dyslexia: The central role of perfectionistic self-presentation

Dyslexia is a prevalent condition, and a significant percentage of students in higher education are dyslexic. Despite this, few studies have investigated dyslexia in university students and what personality dispositions may predict how students feel about help-seeking for dyslexia and how they cope with dyslexia. Against this background, the present study investigated perfectionism, self-stigma, and coping in 115 university students with dyslexia examining the relationships of dispositional perfectionism (self-oriented and socially prescribed perfectionism) and perfectionistic self-presentation with self-stigma of seeking help and adaptive versus maladaptive coping with dyslexia. Results from regression and mediation analyses showed that perfectionistic self-presentation predicted higher levels of self-stigma and maladaptive coping, and lower levels of adaptive coping. Furthermore, both forms of dispositional perfectionism predicted higher levels of self-stigma and maladaptive coping, and lower levels of adaptive coping, via perfectionistic self-presentation (dispositional perfectionism => perfectionistic self-presentation => self-stigma and coping). The findings suggest that perfectionistic self-presentation plays a central role in the relationships of perfectionism, self-stigma, and coping in students with dyslexia, and that impression management aimed at presenting a perfect self-image (and hiding imperfections) represents a significant risk for students’ seeking help for and successful coping with dyslexia