Book Review

Review of the following: THOMAS SZASZ, OUR RIGHT TO DRUGS: THE CASE FOR A FREE MARKET. (Praeger 1992) [164 pp.] Notes, bibliography, name index, notes, preface, subject index. LC: 91-30378; ISBN: 0-275-94216-3. [Cloth $19.95. P.O. Box 5007, Westwood CT 06881-9990.

The Identification of Variables and Factors Related to Preservice Teacher Candidates’ Passing a State Teacher Certification Examination at an HBCU

This study sought to examine the outcome of teacher education candidates’ performance on a state content exam. Seventeen participants from the class of 2012 were identified for the study of which 12 participants fully participated in the study. This study utilized data collected from the participants through the Teacher Quality Enhancement Subcontract Grant Summer/Fall/Spring 2011-2012 Workshop Series held at the private HBCU. The research design used a QUAN- QUAL-QUAN to triangulate the data through three methods of data collection: GACE early childhood education (ECE) data, GACE ECE survey questionnaire and class of 2012 member interviews. The findings from the survey items related to program quality for the participants’ mean was 3.05 (n = 12) on a 1 to 5 Likert scale. The findings from the survey items related to motivation for the participants’ mean was 4.35 (n = 12) on a 1 to 5 Likert scale. A limitation was the total participants that were available for the case study of majors for the degree in the class of 2012 (n = 17). Recommendations for future studies include a concentrated study from public and private HBCUs and/or minority serving institutions with teacher preparation programs enrolling more than 30 candidates of color in their graduating classes

Avoiding the Dissertation Syndrome: Reflections from New Docs

Abstract From the reflective experiences shared by participants in focus groups at GERA and informal settings, the relevance the conceptual factors related to the completion of doctoral students seems to be a consistent matter. The Council of Graduate Schools (CGS) has posted research based and reflective information related to Graduate Schools attempts to address these pressing issues of doctoral degree completion (“Chapter 3: What University Administrators Can Do to Improve Completion Rates” Retrieved from www.gsnet.org). The voices of doctoral degree attendees and recent graduates should be centrifugal in the development of a symposium on the dissertation syndrome (2011). As a result the foci for this symposium will be to hear the voices of recent completers of a doctoral program and review results from a soon to be defended case study on faculty engagement and academic scholarship as factors in the relationship between doctoral candidates and faculty. Additionally, the attendees will be offered a survey based upon the theory of the dissertation syndrome

FASTER MT: Isolation of Pure Populations of a and α Ascospores from Saccharomyces cerevisiae

The budding yeast Saccharomyces cerevisiae has many traits that make it useful for studies of quantitative inheritance. Genome-wide association studies and bulk segregant analyses often serve as first steps toward the identification of quantitative trait loci. These approaches benefit from having large numbers of ascospores pooled by mating type without contamination by vegetative cells. To this end, we inserted a gene encoding red fluorescent protein into the MATa locus. Red fluorescent protein expression caused MATa and a/α diploid vegetative cells and MATa ascospores to fluoresce; MATα cells without the gene did not fluoresce. Heterozygous diploids segregated fluorescent and nonfluorescent ascospores 2:2 in tetrads and bulk populations. The two populations of spores were separable by fluorescence-activated cell sorting with little cross contamination or contamination with diploid vegetative cells. This approach, which we call Fluorescent Ascospore Technique for Efficient Recovery of Mating Type (FASTER MT), should be applicable to laboratory, industrial, and undomesticated, strains

The Risk of Exposure to Diagnostic Ultrasound in Postnatal Subjects

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135382/1/jum2008274565.pd

American Institute of Ultrasound in Medicine

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24836/1/0000262.pd

MutLα heterodimers modify the molecular phenotype of Friedreich ataxia

This article has been made available through the Brunel Open Access Publishing Fund.Background: Friedreich ataxia (FRDA), the most common autosomal recessive ataxia disorder, is caused by a dynamic GAA repeat expansion mutation within intron 1 of FXN gene, resulting in down-regulation of frataxin expression. Studies of cell and mouse models have revealed a role for the mismatch repair (MMR) MutS-heterodimer complexes and the PMS2 component of the MutLα complex in the dynamics of intergenerational and somatic GAA repeat expansions: MSH2, MSH3 and MSH6 promote GAA repeat expansions, while PMS2 inhibits GAA repeat expansions. Methodology/Principal Findings: To determine the potential role of the other component of the MutLα complex, MLH1, in GAA repeat instability in FRDA, we have analyzed intergenerational and somatic GAA repeat expansions from FXN transgenic mice that have been crossed with Mlh1 deficient mice. We find that loss of Mlh1 activity reduces both intergenerational and somatic GAA repeat expansions. However, we also find that loss of either Mlh1 or Pms2 reduces FXN transcription, suggesting different mechanisms of action for Mlh1 and Pms2 on GAA repeat expansion dynamics and regulation of FXN transcription. Conclusions/Significance: Both MutLα components, PMS2 and MLH1, have now been shown to modify the molecular phenotype of FRDA. We propose that upregulation of MLH1 or PMS2 could be potential FRDA therapeutic approaches to increase FXN transcription. © 2014 Ezzatizadeh et al.This article has been made available through the Brunel Open Access Publishing Fund

From CFTR biology toward combinatorial pharmacotherapy:expanded classification of cystic fibrosis mutations

More than 2000 mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) have been described that confer a range of molecular cell biological and functional phenotypes. Most of these mutations lead to compromised anion conductance at the apical plasma membrane of secretory epithelia and cause cystic fibrosis (CF) with variable disease severity. Based on the molecular phenotypic complexity of CFTR mutants and their susceptibility to pharmacotherapy, it has been recognized that mutations may impose combinatorial defects in CFTR channel biology. This notion led to the conclusion that the combination of pharmacotherapies addressing single defects (e.g., transcription, translation, folding, and/or gating) may show improved clinical benefit over available low-efficacy monotherapies. Indeed, recent phase 3 clinical trials combining ivacaftor (a gating potentiator) and lumacaftor (a folding corrector) have proven efficacious in CF patients harboring the most common mutation (deletion of residue F508, ΔF508, or Phe508del). This drug combination was recently approved by the U.S. Food and Drug Administration for patients homozygous for ΔF508. Emerging studies of the structural, cell biological, and functional defects caused by rare mutations provide a new framework that reveals a mixture of deficiencies in different CFTR alleles. Establishment of a set of combinatorial categories of the previously defined basic defects in CF alleles will aid the design of even more efficacious therapeutic interventions for CF patients