• Temporal and spatial angiogenesis-associated gene expression in rat ischemic skin flaps

      Johnson, Thomas; Medical College of Georgia (Augusta University, 2008-04)
      Background: Emerging therapies designed to improve ischemic soft tissue flap survival include the use of angiogenic factors. However, endogenous expression patterns for these factors have not been characterized. The purpose of this study was to identify variations in gene expression patterns for angiogenesis-associated genes in ischemic rat skin flaps with respect to post operative time and distance from flap base. Methods: Caudally based dorsal random pattern skin flaps measuring 3x10 cm were created on fifteen male Sprague-Dawley rats. The rats were sacrificed at one, three, or seven days post surgery. Following euthanasia, flaps were harvested and sectioned into four 3x2.5 cm zones, with zone I located furthest from the flap base. Total RNA was isolated from each zone, amplified, labeled with biotin, and hybridized with oligoDNA microarrays containing probes for 113 angiogenesis-associated genes. Microarrays were imaged using chemiluminescence, and signal intensities were analyzed using web based software. In a previously published report, flap survival was assessed using orthogonal polarization spectral imaging, and the areas of the flap characterized by blood flow versus stasis ( absent capillary blood flow) were identified. Results: Orthogonal polarization spectral imaging results showed the transition of tissue from stasis to necrosis over time. The area of necrosis increased from day one to day seven as necrotic tissue replaced viable tissue in the stasis zone. Rat angiogenesis microarray analysis revealed significant modulation in the expression of multiple genes (p<0.05) in the areas of the skin flap characterized by advancing necrosis and stasis. A burst of gene modulation occurred from day one to day three in the most distal portion of the flap, and a similar burst occurred in the area characterized by stasis from day three to day seven. Six patterns of gene expression were defined. Patterns of angiogenesisassociated gene expression were different in the areas of blood flow compared to the areas of necrosis and stl!5is. Modulation of various gene functional groups also varied temporally and spatially. Conclusions: This study represents the first attempt to characterize endogenous spatial and temporal angiogenesis-associated gene expression patterns in ischemic skin flaps. The molecular analysis performed in this study correlates with the hemodynamic profile previously published. The gene expression patterns observed in this study may represent responses to hypoxia and necrosis as these processes proceeded proximally from the distal flap margin. In the future, molecular analysis of ischemic tissue may allow clinicians to distinguish hopeless tissue from a flap that may be rescued via pharmacological or surgical intervention. Additionally, molecular analysis in treated and untreated tissue may offer insight into the mechanisms by which pharmacological agents enhance flap survival.
    • Teratogenic activity of trypan blue in rats

      Ferris, Virginia W.; Department of Anatomy (1962-06)
    • Terminal competencies of the baccalaureate nursing graduate

      Eberhart, Aeris Dee; School of Nursing (1974-05)
    • The E2F1 corepressor BIN1 is a novel tumor suppressor RB1-binding cofactor for cell-cycle arrest and genomic instability

      Folk, Watson; Biomedical Sciences (Augusta University, 2020-04)
      The bridging integrator 1 protein (BIN1) exhibits tumor suppressor activities through multiple mechanisms, including by acting as a corepressor of the adenovirus E2-promoter binding cellular factor 1 (E2F1) transcription factor and sensitizing cells to genotoxic stress. By inhibiting E2F1-dependent cell-cycle progression, BIN1 displays an overlapping function with the well-known E2F1 corepressor retinoblastoma protein 1 (RB1). However, whether RB1 and BIN1 collaborate to inhibit E2F1 activity and whether E2F1 is involved in BIN1-dependent sensitization to DNA-damaging agents remain unresolved. Here, I report that BIN1 physically interacts with RB1 to cooperatively repress E2F1-mediated transactivation and that BIN1 interferes with the early stages of DNA damage responses in a manner dependent on BIN1/E2F1 interaction. BIN1 efficiently bound hypophosphorylated RB1, particularly when BIN1 contained exon 10. This was functionally meaningful because BIN1 inhibited serum-induced RB1 phosphorylation by blocking the physical binding of cyclin D1 to RB1 and stabilized hypophosphorylated RB1 on an E2F-sensitive gene promoter. BIN1 and RB1 cooperatively suppressed the transcription of a number of E2F1-sensitive genes, including ATM Ser/Thr kinase (ATM) and BRCA1, and reduced cellular DNA-end joining. Because BIN1 inhibits cellular poly(ADP-ribosyl)ation, simultaneous activation of RB1 and BIN1 induced ‘synthetic lethality’ in multiple cancer cell lines regardless of ‘BRCAness’. Furthermore, even in the absence of DNA damage, depletion of BIN1 enhanced E2F1-dependent ATM autophosphorylation, formation of the MRE11A/RAD50/NBS1 DNA-repair–promoting complex, and phosphorylation of histone H2AX (forming γH2AX, a biomarker of double-stranded DNA breaks). Similar to BIN1 reduction, RB1 deficit increased cancer-cell resistance to cisplatin. Our study reveals that by physically binding to RB1, BIN1 acts as a novel RB1 cofactor and stabilizes RB1 on an E2F-sensitive promoter. Additionally, we unveil that one of the likely mechanisms by which the tumor suppressors BIN1 and RB1 induce growth arrest is attributable to facilitating accumulation of genomic instability via inhibition of E2F1-dependent DNA-repair–promoting activities.
    • The Influence of Instructional Rounds on Teacher Metacognition in a Middle School Context: A Mixed Methods Study

      Hamilton, William B; Department of Advanced Studies and Innovation (Augusta University, 2020-05)
      This study investigated, quantified, and observed metacognitive transformation in middle school ELA and math teachers through the implementation of instructional rounds as a change agent in comparison to the traditional, one-stop workshop format of professional development. A mixed method design was utilized that addressed two research questions: How is teacher metacognition impacted through professional development, and what is the difference in teacher metacognition scores after receiving traditional professional development versus instructional rounds? The results of the study suggested that teacher metacognition is positively impacted by instructional rounds and there were positive attitudes towards instructional rounds as an alternative to traditional professional development. Additionally, the qualitative data indicated that instructional rounds did have a positive impact on instructional practices and supported a progressive maturation of teacher metacognition that could be ultimately transferred to the learner. First, the results elucidated that normal teaching practice is inherently metacognitive and embodies the metacognitive knowledge tenets: person, task, and strategy. Next, teacher collaboration supports the perpetuation of a metacognitive experience, which innately lends itself to reflection. Thirdly, teacher reflection fosters metacognitive goals, thereby resulting in regulation of actions or strategies. Finally, teacher action derived from goal setting is, by definition, metacognitive action. In summary, instructional rounds appeared to be an effective form of professional development that increased and matured teacher metacognition. Keywords: Instructional rounds, metacognition, professional development, teaching practice
    • The Influence of Instructional Rounds on Teacher Metacognition in a Middle School Context: A Mixed Methods Study

      Scoggins, Katherine; Department of Advanced Studies and Innovation (Augusta University, 2020-05)
      This study investigated, quantified, and observed metacognitive transformation in middle school ELA and math teachers through the implementation of instructional rounds as a change agent in comparison to the traditional, one-stop workshop format of professional development. A mixed method design was utilized that addressed two research questions: How is teacher metacognition impacted through professional development, and what is the difference in teacher metacognition scores after receiving traditional professional development versus instructional rounds? The results of the study suggested that teacher metacognition is positively impacted by instructional rounds and there were positive attitudes towards instructional rounds as an alternative to traditional professional development. Additionally, the qualitative data indicated that instructional rounds did have a positive impact on instructional practices and supported a progressive maturation of teacher metacognition that could be ultimately transferred to the learner. First, the results elucidated that normal teaching practice is inherently metacognitive and embodies the metacognitive knowledge tenets: person, task, and strategy. Next, teacher collaboration supports the perpetuation of a metacognitive experience, which innately lends itself to reflection. Thirdly, teacher reflection fosters metacognitive goals, thereby resulting in regulation of actions or strategies. Finally, teacher action derived from goal setting is, by definition, metacognitive action. In summary, instructional rounds appeared to be an effective form of professional development that increased and matured teacher metacognition.
    • The Influence of Instructional Rounds on Teacher Metacognition in a Middle School Context: A Mixed Methods Study

      Townsend, Holly; Department of Advanced Studies and Innovation (Augusta University, 2020-05)
      This study investigated, quantified, and observed metacognitive transformation in middle school ELA and math teachers through the implementation of instructional rounds as a change agent in comparison to the traditional, one-stop workshop format of professional development. A mixed method design was utilized that addressed two research questions: How is teacher metacognition impacted through professional development, and what is the difference in teacher metacognition scores after receiving traditional professional development versus instructional rounds? The results of the study suggested that teacher metacognition is positively impacted by instructional rounds and there were positive attitudes towards instructional rounds as an alternative to traditional professional development. Additionally, the qualitative data indicated that instructional rounds did have a positive impact on instructional practices and supported a progressive maturation of teacher metacognition that could be ultimately transferred to the learner. First, the results elucidated that normal teaching practice is inherently metacognitive and embodies the metacognitive knowledge tenets: person, task, and strategy. Next, teacher collaboration supports the perpetuation of a metacognitive experience, which innately lends itself to reflection. Thirdly, teacher reflection fosters metacognitive goals, thereby resulting in regulation of actions or strategies. Finally, teacher action derived from goal setting is, by definition, metacognitive action. In summary, instructional rounds appeared to be an effective form of professional development that increased and matured teacher metacognition.
    • THE ROLE OF GPR109A IN REGULATION OF RETINAL ANGIOGENESIS AND BLOOD-RETINAL BARRIER AS A POTENTIAL THERAPEUTIC TARGET IN DIABETIC RETINOPATHY

      Abdelrahman, Ammar; Department of Biochemistry and Molecular Biology (Augusta University, 2020-12)
      Currently, treatments of diabetic retinopathy (DR) have limited therapeutic benefits and limited accessibility to the growing diabetic population at risk because of the high expenses and complicated procedures. Inflammation, endothelial dysfunction, and microvascular damage are common features of diabetic complications including DR. GPR109A is the metabolite sensing receptor of beta-hydroxybutyrate (BHB) the principal ketone body in humans. Our previous studies have shown the role of GPR109A expression in promoting anti-inflammatory response in retinal pigmented epithelial (RPE) cells and the relevance of the receptor in DR. Expression of the GPR109A in microvascular endothelial cells (ECs) has been reported recently. However, the relevance of GPR109A expression and activation to retinal EC functions are yet to be studied. Our goal in this study was to identify the role of GPR109A expression and activation in barrier and angiogenic functions of retinal ECs in context of diabetic retinopathy. We used electrical cell impedance sensing (ECIS) technology to evaluate barrier functions in primary human retinal endothelial cells (HRECs) which constitute the inner BRB. Knocking down GPR109A in HRECs with siRNA decreased the transendothelial electrical resistance (TEER) compared to scrambled siRNA. Treating HRECs with BHB increased their TEER and counteracted VEGF-induced barrier disruption through activation of GPR109A and increasing zonula occludens-1 (ZO-1) expression. Treatment of STZ-diabetic mice with exogenous BHB for one month protected against the pathologic albumin leakage induced by diabetes and improved the visual acuity of this animal model of diabetes. Using the mouse model of oxygen induced retinopathy (OIR), we showed that Gpr109a-/- mice had slower vascular recovery from pathologic angiogenesis compared to age matched wild type mice. Moreover, physiologic revascularization of vaso-oblitrated retinas was impaired by loss of GPR109a and associated with dysregulated inflammatory and angiogenic signaling. Collectively, these data point to a role for GPR109A in the regulation of barrier and angiogenic mechanisms in retinal ECs and, promote the receptor as a potential druggable target for impacting these mechanisms in microvascular retinal diseases such as DR.
    • THE ROLE OF KYNURENINE, A TRYPTOPHAN METABOLITE THAT INCREASES WITH AGE, IN MUSCLE ATROPHY AND LIPID PEROXIDATION)

      Kaiser, Helen E.; Department of Cellular Biology and Anatomy (Augusta University, 2020-05)
      Loss of mobility and independence are risk factors for falls and mortality, and drastically reduce the quality of life among older adults. The cellular and molecular mechanisms underlying loss of muscle mass and strength with age (sarcopenia) are not well-understood; however, heterochronic parabiosis experiments show that circulating factors are likely to play a role. Kynurenine (KYN) is a circulating tryptophan metabolite that is known to increase with age and is implicated in several age-related pathologies. Here I tested the hypothesis that KYN contributes directly to muscle loss with aging. Results indicate that that KYN treatment of mouse and human myoblasts increased levels of reactive oxygen species (ROS) two-fold, and significantly increased lipid peroxidation enzymes. Small-molecule inhibition of the Aryl hydrocarbon receptor (Ahr), an endogenous KYN receptor, in vitro did not prevent KYN-induced increases in ROS, and homozygous Ahr knockout in vivo did not protect mice from KYN-induced stress, suggesting that KYN can directly increase ROS independent of Ahr activation. In vivo, wild-type mice treated with KYN had reduced skeletal muscle strength, size, and increased oxidative stress and lipid peroxidation. Old wild-type mice treated with 1MT, a small molecule that suppresses KYN production by IDO1, showed an increase in muscle fiber size, peak muscle strength, and oxidative stress. Protein analysis identified mitochondrial lipid peroxidation as a downstream mechanism that is increased upon KYN treatment. Lipid peroxidation enzymes increased with KYN have been shown to produce H2O2 outside of the electron transport chain. Our data suggest that IDO inhibition may represent a novel therapeutic approach for the attenuation of sarcopenia and possibly other age-associated conditions associated with KYN accumulation such as bone loss and neurodegeneration.
    • THE ROLE OF NEDDYLATION IN EARLY CARDIAC DEVELOPMENT

      Littlejohn, Rodney; Department of Cellular Biology and Anatomy (Augusta University, 2020-07)
      Background. Early cardiac development is a tightly regulated process, involving spatiotemporal coordination of multiple signaling pathways and heterogenous cell populations, both generated de novo and externally sourced. While the roles of transcription, environmental, and epigenetic factors have all been studied extensively in the context of heart development, the roles of post-translational protein modification in regulating this process remain to be elucidated. NEDD8 (neural precursor cell expressed developmentally downregulated 8) is a novel ubiquitin-like protein modifier. Conjugation of NEDD8 to protein targets, a process termed neddylation, has been shown to regulate cell proliferation, cell signaling, and protein homeostasis, and play important roles in multiple physiological and pathological events. We have previously shown that neddylation is developmentally downregulated in the developing heart and is essential for mid-to-late gestational ventricular chamber maturation. However, whether and how neddylation regulates early cardiogenic events remains unknown. Methods and results. Mice with constitutive, cardiac progenitor cell-specific, cardiomyocyte- and vascular smooth muscle cell-specific deletion of NAE1, a regulatory subunit of the NEDD8-specific E1 activating enzyme, were created. Constitutive deletion of NAE1 led to early embryonic lethality before E9.5. Nkx2.5Cre-mediated deletion of NAE1 decreased neddylated proteins in the heart, disrupted normal cardiogenesis and resulted in embryonic lethality by embryonic day (E) 12.5 due to heart failure. Similarly, SM22αCre-driven deletion of NAE1 also caused cardiac failure and embryonic lethality by E13.5. The striking cardiac phenotypes were associated with myocardial hypoplasia, ventricular hypo-trabeculation, and pronounced endocardial and/or epicardial defects in both models. Unbiased transcriptomic analysis revealed dysregulated expression of genes associated with cardiomyocyte differentiation, proliferation, and maturation in NAE1-deficient hearts. Indeed, inhibition of neddylation disturbed cardiomyocyte proliferation, and myofibril assembly in vitro and in vivo. Moreover, defects in cardiomyocyte differentiation and maturation were linked to downregulation of Nkx2.5 and Mef2c, two key transcription factors regulating early cardiogenesis. Conclusion. Collectively, our findings demonstrate that neddylation in cardiac progenitor cells and cardiomyocytes is essential in the regulation of cardiogenesis in transgenic mouse models. Our results uncover a previously unknown role of post-translational modification in the regulation of cardiac development via potential roles in mediating cardiomyocyte proliferation, differentiation, and maturation.
    • The therapeutic alliance, awareness, and medication compliance in the treatment of schizophrenia

      Chadwick, Nanenia Brannen; School of Graduate Studies (2001-04)
      Schizophrenia is one of the most debilitating and costly of the major illnesses in the UJ?ited States. Individuals diagnosed with schizophrenia are at-risk for impaired awareness, poor therapeutic alliance, and, failure to comply with medication regimens. Although awareness has been related to medication compliance, and the therapeutic alliance has been suggested as an explanation of medication compliance when individuals are not aware of their illness· symptoms, treatment response or social consequences of · their mental illness, findings of previous studies have been unclear concerning the influence of the therapeutic alliance on the relation between awareness and medication compliance. This cross-sectional correlational study was designed to test a hypothesized model in which the therapeutic alliance inflμences the relation between awareness and medication compliance in the treatment of a sample of individuals diagnosed with schizophrenia. The.settings for the study were two day treatment programs. Adults diagnosed with o!le of the types of schizophrenia and their primary therapists were invited to participate. Seventy-six patients and 12 primary therapists were offered the opportunity to participate, with 70 patients and 10 therapists who completed the·study. It was hypothesized that the therapeutic alliance would influence the relation . between awareness and medication compliance. Data were analyzed using hierarchical multiple regression anaiyses. The hypothesis was partially supported. The therapeutic alliance and awareness had significant main effects on medication compliance, but their interaction was not significant. In this sample, both the therapeutic alliance and awareness hc;!d additive effects on medication compliance, but their interaction did not significantly add to the prediction of medication compliance. The study suggests that primary therapists should spend time on both developing the therapeutic alliance and on improving patients' awareness of illness symptoms, treatment response, and social consequences of their mental illness in order to have the greatest effect on medication compliance for individuals diagnosed with schizophrenia.
    • Therapeutic induction of fetal hemoglobin in sickle cell disease: development of a novel prodrug AN-233

      Oseghale, Aluya; Biomedical Sciences (Augusta University, 2019-05)
      The reactivation of fetal hemoglobin (HbF) in sickle cell disease (SCD) ameliorates the clinical severity of the illness and improves patient's survival. Pharmacological induction of HbF has been a major strategy for SCD treatment and several research studies have focused on a wide variety of agents for their potential to induce HbF. However, hydroxyurea (HU) remains the only Food and Drug Administration (FDA)-approved drug proven to elevate HbF in about 50% of adults with SCD. Efficacy of HU has been very limited due to many side effects including bone marrow suppression, susceptibility to infections and long-term infertility. Our group reported potent HbF induction by sodium butyrate in erythroid cells through p38 MAPK activation. Nevertheless, oral administration of a butyrate (BA) derivative to SCD patients was ineffective due to rapid metabolic inactivation by the liver. Therefore, the need for better therapies exists. This project investigated a novel prodrug conjugate of BA and δ-aminolevulinate (ALA) denoted as AN-233. As an ester, AN-233 [1-(butyryloxy) ethyl-5-amino-4-oxopentanoate] undergoes cellular hydrolysis in an esterase dependent manner to yield two active drugs BA and ALA. In prior studies, oral administration of AN-233 to mice increased total hemoglobin but the effect on HbF was unknown. We proposed the hypothesis; that AN-233 upregulates γ-globin gene expression and elevates HbF synthesis via transcriptional and post-transcriptional mechanisms. We investigated AN-233 using in-vitro, in-vivo and ex-vivo model systems including K562 cell lines, sickle progenitors and β-YAC mice. Treatment of K562 cells showed AN-233 significantly increased mRNA levels. Flow cytometry analyses show the prodrug significantly increased HbF protein expression and Western blotting of whole cell lysates confirmed increased synthesis of HbF. Treatment of CD34+ stem cell-derived primary erythroid cells increased early stage (basophilic) erythroblasts by 2.4fold and decreased late stage (orthochromatophilic) erythroblasts by 2.5 fold. In sickle progenitors, AN-233 again elevated F-cell% by 1.5fold and HbF protein by over 2.6fold. Mechanistic studies in K562 cells show AN-233 significantly elevated heme biosynthesis, decreased phosphorylation of HRI and eIF2α thereby promoting the protein synthesis of globin chains. Additionally, AN-233 enhanced histone acetylation at the γ-globin promoter and LCR DNase hypersensitive site 2 (LCR HS2). Treatment of sickle progenitors with AN-233 decreased %sickled cells by up to 50%. The transcription factor BACH1 was reduced while NRF2 was increased in AN-233 treated K562 cells. In vivo, AN-233 increased F-cell% and F-cell MFI of treated β-YAC mice within 4-weeks. Our data support AN-233 as a potent HbF inducer in erythroid progenitors and in mice. The prodrug represents a drug candidate, which can be developed for the treatment of SCD patients.
    • Therapeutic Targeting of P2X7 After Traumatic Brain Injury

      Kimbler, Donald E.; Department of Neurosurgery (2012-02)
      Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP) and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches to alleviate increased ICP remain controversial and medical therapies are lacking due in part, to the absence of viable drug targets. In the present study, genetic inhibition (P2X7-/- mice) of the purinergic P2X7 receptor attenuated the expression of the pro-inflammatory cytokine, interleukin-iP (IL-ip) and reduced cerebral edema following controlled cortical impact, as compared to wild-type mice. Similarly, the clinically useful P2X7 inhibitor, brilliant blue G (BBG), inhibited the expression of IL-ip, limited edemic development and prevented the development of post-traumatic depression and anxiety. The beneficial effects of BBG were observed following either prophylactic administration via the drinking water for one week prior to injury or via an intravenous bolus administration up to four hours after TBI, suggesting a clinically-implementable therapeutic window. Notably, P2X7 localized within astrocytic end feet and administration of BBG decreased the expression of glial fibrillary acidic protein (GFAP), a reactive astrocyte marker, and reduced the expression of aquaporin-4 (AQP4), an astrocytic water channel that promotes cellular edema. Together, these data implicate P2X7 as a novel therapeutic target to prevent secondary neurological injury after TBI, a finding that warrants further investigation.
    • Therapeutic Targeting of P2X7 after Traumatic Brain Injury

      Kimbler Jr, Donald E; Department of Neuroscience and Regenerative Medicine (Georgia Health Sciences University, 2012-02)
      Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP) and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches to alleviate increased ICP remain controversial and medical therapies are lacking due in part, to the absence of viable drug targets. In the present study, genetic inhibition (P2X7-/- mice) of the purinergic P2x7 receptor attenuated the expression of the pro-inflammatory cytokine, interleukin-I~ (IL-1~) and reduced cerebral edema following controlled cortical impact, as compared to wild-type mice. Similarly, the clinically useful P2X7 inhibitor, brilliant blue G (BBG), inhibited the expression of IL-1~, limited edemic development and prevented the development of post-traumatic depression and anxiety. The beneficial effects of BBG were observed following either prophylactic administration via the drinking water for one week prior to injury or via an intravenous bolus administration up to four hours after TBI, suggesting a clinically-implementable therapeutic window. Notably, P2X7 localized within astrocytic end feet and administration of BBG decreased the expression of glial fibrillary acidic protein (GFAP), a reactive astrocyte marker, and reduced the expression of aquaporin-4 (AQP4), an astrocytic water channel that promotes cellular edema. Together, these data implicate P2X7 as a novel therapeutic target to prevent secondary neurological injury after TBI, a finding that warrants further investigation.
    • This retrospective study attempted to identity differences between student groups occurring before and after the restructuring of the Army occupational therapy assistant (OTA) program. Records of 168 students were reviewed (104 records of students in the pre-restructuring group, 64 in the post-restructuring group). Several areas were examined: (a) demographic data, (b) course attrition rates, (c) performance on level II fieldwork, and (d) national certification exam pass rates. Analyses of demographic data revealed that students in the post-restructuring group were significantly older (p<.OOl) and of higher rank (p<.001) than students in the pre-restructuring group. Analysis using a chi-square test revealed a significant decrease in the attrition rate (p<.001) after the restructuring. At-test revealed that students in the post-restructuring group performed significantly better on their level II fieldwork (p=.030). National certification exam pass rates for the groups could not be determined due to the confidential nature in which scores are reported

      Harrison-Weaver, Sandra; Medical College of Georgia (Augusta University, 1997-03)
      This retrospective study attempted to identity differences between student groups occurring before and after the restructuring of the Army occupational therapy assistant (OTA) program. Records of 168 students were reviewed (104 records of students in the pre-restructuring group, 64 in the post-restructuring group). Several areas were examined: (a) demographic data, (b) course attrition rates, (c) performance on level II fieldwork, and (d) national certification exam pass rates. Analyses of demographic data revealed that students in the post-restructuring group were significantly older (p<.OOl) and of higher rank (p<.001) than students in the pre-restructuring group. Analysis using a chi-square test revealed a significant decrease in the attrition rate (p<.001) after the restructuring. At-test revealed that students in the post-restructuring group performed significantly better on their level II fieldwork (p=.030). National certification exam pass rates for the groups could not be determined due to the confidential nature in which scores are reported
    • Tissue culture study of clinical specimens from an outbreak of rubella-like illness

      Reddick, Rhoda Anne; Department of Cell and Molecular Biology (1968-06)
    • Tissue culture study of clinical specimens from an outbreak of rubella-like illness

      Reddick, Rhoda Anne; Department of Cell and Molecular Biology (1965-06)
    • Tissue metabolism of thyroid hormones in hypothyroid and growth hormone treated hypothyroid mothers, their fetuses and their progenies

      Berdecia-Rodriguez, Joseph; Department of Physiology and Endocrinology (1990-05)
      Studies of Man et al. have shown that the children of hypothyroxinemic women have an .increased rate of mental and .motor retardation. A rat model which presents the ~etabolic and motor defects of these children developed by Hendrich et al. was used for these studies. The metabolism of T4 was studied i~ the progenies of Tx-only and GH-treated Tx dams utilizing a radioimmunoassay for T4 detection and equations based on those of Inglebleek .~d Malvaux. In the above mentioned study, the hypothyroid dams showed an impaired reproductive performance that included lower body weight gain, smaller liter size and greater mortality for their pups. Furthermore, maternal hypothyroidism had a detrimental effect on their offsprings body and tissue weights. The parameters of metabolism for T4 showed that the offsprings of hypothyroid mothers have a clear derangement in the utilization of this hormone at the ages studied (i.e., 5, 30, 60 days of age). The next step in our investigation wa~ to measure the iodothyronine concentrations intracellularly to determine how these J molecules were utilized. We developed a new technique for the extraction of iodothyronines based on HPLC fluorescence. The extracted iodothyronines were derivatized with dansyl chloride and then rap in our chromatographic system. The iodothyronine concentrations ·in the tissues {i.e., brain and liver) and plasma for the progenies of hypothyroid mothers at all ages {i.e,. 22 day, 10, 30, 60 day-olds} were consistently abnormal confirming what we saw with the metabolic studies of T4 done initially. The hypothyroid mothers had iodothyronine concentrations consistently abnormal in all tissues studies. The progenies of hypothyroid mothers appear to suffer an insult that causes a severe impairment in the metabolism of T4. This insult not only affects the metabolism of T4 but also affects the concentrations' of other iodothyronines in liver, brain and plasma