Leadership Advancement: A Phenomenological Study of Non-Faculty Black Male Leadership in Higher Education

This transcendental phenomenological study examined the lived experiences of non-faculty Black male administrators and leadership advancement at predominantly White institutions (PWI) in Virginia. A transcendental phenomenological approach was used to address the central research question of what the leadership advancement experiences of non-faculty Black male administrators at predominately White institutions in Virginia. Critical race theory as it relates to education was used as the theoretical framework to guide the study. Purposeful and snowball sampling was used to select non-faculty Black male administrators from predominantly White institutions (PWI). Data collected through questionnaires, interviews, and focus groups revealed five major themes: cultural taxation, intersectionality, and understanding of Black culture, self-preservation, and cronyism. The data was analyzed using established phenomenological investigation methods of bracketing, horizontalization, clustering into themes, textural descriptions, and textural-structural synthesis (Moustakas, 1994). The study found that Black non-faculty male administrators at PWI leadership advancement was impacted by perceptions associated with gender and race, the history of education in the southern United States, inequity within systems created by White majority, and the lack of mentorship available. These factors create a disparity in leadership advancement for Blacks in higher education compared to their White counterparts

The Black Tradition of Excellence And the Challenge of the Eighties

Charter Day Convocation Speech by Lerone Bennett Jr

Inside the seed of school accountability: an African-centered analysis

I use Marimba Ani’s Asili concept as defined in Yurugu to examine the school accountability model. By school accountability model, I mean the school model that consists of privately managed “public schools” regulated by state testing programs. I argue that school accountability is essentially oppressive and its success depends on the falsification of African and African American history. Ani explains that Asili is a Kiswalhili term meaning “beginning,” “origin,” “source,” “nature (in the sense of the ‘nature’ of a person or thing),” “essence,” or “fundamental principle.” Furthermore, Ani writes that seed is an “ubiquitous African analogical symbol in African philosophical and cosmological explanations” and that a culture’s asili reveals its nature during times of ambivalence and conflict. I focus on Louisiana’s 1954 school laws and resolutions passed in reaction to the U.S. Supreme Court’s 1954 Brown decision and the White Citizen’s council’s 1950s Social Studies reform movement. I demonstrate that this is the time when we witness the major elements of the present accountability model suddenly unfold. For instance, Louisiana’s state testing program (for students and teachers), standardized social studies curriculum guides and tests, charter schools, and vouchers can all be traced to the resolutions passed during the weeks following the Brown decision. I examine the thoughts and activities of those who engineered the school accountability seed and thereby reveal its power seeking essence. Too, I trace the seed’s unfolding into a plant and its development to the present time, and I demonstrate its instinctual hostility toward African schools, African educators, African students, and liberating African thought. To the best of my knowledge this is the first major study that examines school accountability from an Afrocentric perspective

I Have A Dream

Martin Luther King Jr.’s iconic “I Have a Dream” speech has been the subject of much conversation and debate for 50 years. King’s dream was that of one person; however, he opened the door for everyone to have a dream. In the spirit of Martin Luther King Jr., our scholars were encouraged to write about their dreams and hopes for a better world. They were told to consider a social, community, or environmental issue they want to improve. Students were challenged to describe what they were thinking about doing and how their idea might make the world a better place.https://digitalcommons.njit.edu/stemshowcase/1013/thumbnail.jp

Current Genetic Epidemiology of β-Thalassemias and Structural Hemoglobin Variants in the Lazio Region (Central Italy) Following Recent Migration Movements

The aim of this study was to describe the changing pattern of mutational spectrum of β-thalassemia (β-thal) in the Lazio region (Central Italy), as consequence of recent demographic variations. From 1994 until present, 256 immigrant subjects with hemoglobin disorders (including 191 heterozygotes and 65 homozygotes or compound heterozygotes) coming from 44 different foreign countries, have been molecularly characterized. 14 β-globin gene mutations were identified and their frequencies reflect different ethnic origins: 8 of these mutations account for 76.97% of all molecular defects, while 6 of them are much rare, representing less than 2% of the total. These data differ, both in type and percentage, from the mutational spectrum detected in the native population in 1995. Since a few defects are prevalent in each country, a proper strategy for the identification of mutations in immigrant individuals relies on the prior knowledge of their frequency in native ethnic group

Multiple endocrine neoplasias type 2B and RET proto-oncogene

Multiple Endocrine Neoplasia type 2B (MEN 2B) is an autosomal dominant complex oncologic neurocristopathy including medullary thyroid carcinoma, pheochromocytoma, gastrointestinal disorders, marphanoid face, and mucosal multiple ganglioneuromas. Medullary thyroid carcinoma is the major cause of mortality in MEN 2B syndrome, and it often appears during the first years of life. RET proto-oncogene germline activating mutations are causative for MEN 2B. The 95% of MEN 2B patients are associated with a point mutation in exon 16 (M918/T). A second point mutation at codon 883 has been found in 2%-3% of MEN 2B cases. RET proto-oncogene is also involved in different neoplastic and not neoplastic neurocristopathies. Other RET mutations cause MEN 2A syndrome, familial medullary thyroid carcinoma, or Hirschsprung's disease. RET gene expression is also involved in Neuroblastoma. The main diagnosis standards are the acetylcholinesterase study of rectal mucosa and the molecular analysis of RET. In our protocol the rectal biopsy is, therefore, the first approach. RET mutation detection offers the possibility to diagnose MEN 2B predisposition at a pre-clinical stage in familial cases, and to perform an early total prophylactic thyroidectomy. The surgical treatment of MEN 2B is total thyroidectomy with cervical limphadenectomy of the central compartment of the neck. When possible, this intervention should be performed with prophylactic aim before 1 year of age in patients with molecular genetic diagnosis. Recent advances into the mechanisms of RET proto-oncogene signaling and pathways of RET signal transduction in the development of MEN 2 and MTC will allow new treatment possibilities

Microarray based analysis of an inherited terminal 3p26.3 deletion, containing only the CHL1 gene, from a normal father to his two affected children

<p>Abstract</p> <p>Background</p> <p>terminal deletions of the distal portion of the short arm of chromosome 3 cause a rare contiguous gene disorder characterized by growth retardation, developmental delay, mental retardation, dysmorphisms, microcephaly and ptosis. The phenotype of individuals with deletions varies from normal to severe. It was suggested that a 1,5 Mb minimal terminal deletion including the two genes <it>CRBN </it>and <it>CNTN4 </it>is sufficient to cause the syndrome.</p> <p>In addition the <it>CHL1 </it>gene, mapping at 3p26.3 distally to <it>CRBN </it>and <it>CNTN4</it>, was proposed as candidate gene for a non specific mental retardation because of its high level of expression in the brain.</p> <p>Methods and Results</p> <p>we describe two affected siblings in which array-CGH analysis disclosed an identical discontinuous terminal 3p26.3 deletion spanning less than 1 Mb. The deletion was transmitted from their normal father and included only the <it>CHL1 </it>gene. The two brothers present microcephaly, light mental retardation, learning and language difficulties but not the typical phenotype manifestations described in 3p- syndrome.</p> <p>Conclusion</p> <p>a terminal 3p26.3 deletion including only the <it>CHL1 </it>gene is a very rare finding previously reported only in one family. The phenotype of the affected individuals in the two families is very similar and the deletion has been inherited from an apparently normal parent. As already described for others recurrent syndromes with variable phenotype, these findings are challenging in genetic counselling because of an evident variable penetrance.</p

Genotype-phenotype correlation of 2q37 deletions including NPPC gene associated with skeletal malformations

Coordinated bone growth is controlled by numerous mechanisms which are only partially understood because of the involvement of many hormones and local regulators. The C-type Natriuretic Peptide (CNP), encoded by NPPC gene located on chromosome 2q37.1, is a molecule that regulates endochondral ossification of the cartilaginous growth plate and influences longitudinal bone growth. Two independent studies have described three patients with a Marfan-like phenotype presenting a de novo balanced translocation involving the same chromosomal region 2q37.1 and overexpression of NPPC. We report on two partially overlapping interstitial 2q37 deletions identified by array CGH. The two patients showed opposite phenotypes characterized by short stature and skeletal overgrowth, respectively. The patient with short stature presented a 2q37 deletion causing the loss of one copy of the NPPC gene and the truncation of the DIS3L2 gene with normal CNP plasma concentration. The deletion identified in the patient with a Marfan-like phenotype interrupted the DIS3L2 gene without involving the NPPC gene. In addition, a strongly elevated CNP plasma concentration was found in this patient. A possible role of NPPC as causative of the two opposite phenotypes is discussed in this study