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Artykuły w czasopismach na temat "S555n"
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Drake, Joshua, Anna Nichenko, Orion Wiloughby, Matt Brisendine, Garrett Hays, Grace DiGirolamo, Zach Weingrad i Ryan McMillan. "PHOSPHORYLATION OF ULK1 AT S555 IS REQUIRED FOR METABOLIC ADAPTATIONS TO CALORIC RESTRICTION". Innovation in Aging 6, Supplement_1 (1.11.2022): 424–25. http://dx.doi.org/10.1093/geroni/igac059.1668.
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Abstract Unc-51 Like Autophagy Activating Kinase 1 (Ulk1) is responsible for initiating selective degradation of damaged/dysfunctional mitochondria (mitophagy) once phosphorylated at S555 in response to energetic stress. Mitophagy is integral for mitochondrial health and Ulk1 has been implicated to be important for metabolic adaptation to exercise. Caloric restriction (CR), which extends lifespan and healthspan, has profound metabolic benefits, including improved mitochondrial health. However, the contribution of Ulk1 in adaptation to CR is unknown. To decipher a functional role of Ulk1(S555) in adaptations to CR we used CRISPR-Cas9 generated, loss-of-function Ulk1(S555A) mice, in which Ulk1 cannot be phosphorylated at S555. 6-month-old, male and female homozygous Ulk1(S555A) mice and C57BL6/J (wild type, WT) mice were placed on a 40% CR diet for 8 weeks. Body mass in both male and female Ulk1(S555A) and WT mice was reduced with CR (p < 0.001), however female Ulk1(S555A) were heavier than their WT counterparts (p=0.02). Via nuclear magnetic resonance (NMR), male and female Ulk1(S555A) mice did not lose fat mass during CR. In addition, periovarian (female) and epididymal (male) fat mass was greater in Ulk1(S555A) compared to WT mice post-CR (p < 0.001). Furthermore, fasting blood glucose increased in male and female Ulk1(S555A) post-CR (p < 0.0001), suggesting altered substrate metabolism. In support of this notion, glucose oxidation in both quadriceps muscle and liver of male mice increased in WT following CR but not in Ulk1(S555A) mice (interaction effect p< 0.002). In sum, these data suggest that phosphorylation of Ulk1 at S555 is required for metabolic adaptations to CR.
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Guan, Yuntian, Mei Zhang, Christie Lacy, Soham Shah, Frederick H. Epstein i Zhen Yan. "Endurance Exercise Training Mitigates Diastolic Dysfunction in Diabetic Mice Independent of Phosphorylation of Ulk1 at S555". International Journal of Molecular Sciences 25, nr 1 (3.01.2024): 633. http://dx.doi.org/10.3390/ijms25010633.
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Millions of diabetic patients suffer from cardiovascular complications. One of the earliest signs of diabetic complications in the heart is diastolic dysfunction. Regular exercise is a highly effective preventive/therapeutic intervention against diastolic dysfunction in diabetes, but the underlying mechanism(s) remain poorly understood. Studies have shown that the accumulation of damaged or dysfunctional mitochondria in the myocardium is at the center of this pathology. Here, we employed a mouse model of diabetes to test the hypothesis that endurance exercise training mitigates diastolic dysfunction by promoting cardiac mitophagy (the clearance of mitochondria via autophagy) via S555 phosphorylation of Ulk1. High-fat diet (HFD) feeding and streptozotocin (STZ) injection in mice led to reduced endurance capacity, impaired diastolic function, increased myocardial oxidative stress, and compromised mitochondrial structure and function, which were all ameliorated by 6 weeks of voluntary wheel running. Using CRISPR/Cas9-mediated gene editing, we generated non-phosphorylatable Ulk1 (S555A) mutant mice and showed the requirement of p-Ulk1at S555 for exercise-induced mitophagy in the myocardium. However, diabetic Ulk1 (S555A) mice retained the benefits of exercise intervention. We conclude that endurance exercise training mitigates diabetes-induced diastolic dysfunction independent of Ulk1 phosphorylation at S555.
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Stockklausner, Clemens, Christin Maria Duffert, Nicole Dickemann, Anne Christine Klotter, Isabelle Nadine Kuhlee, Carolin Kerber i Andreas E. Kulozik. "The Predominant Activation of Alternative Signaling Pathways Explains the Differential Propensity of Different c-Mpl Gain-of-Function Mutations to Promote Myeloproliferative Malignancies". Blood 124, nr 21 (6.12.2014): 1578. http://dx.doi.org/10.1182/blood.v124.21.1578.1578.
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Abstract Thrombopoiesis is tightly regulated by the binding of thrombopoietin (THPO) to its receptor c-Mpl that leads to the clearance of THPO from the plasma thus establishing a negative feedback loop. Several mutations in the c-Mpl receptor gene have been linked to a gain-of-function resulting in thrombocytosis. We focused on a comparison of gain-of-function mutation in the extracellular part of the c-Mpl receptor, where ligand binding and receptor dimerization occur, with the S505N, W515K and W515L mutations in the transmembrane and juxtamembrane region, respectively. Interestingly, the latter mutations are known to also promote myeloproliferative malignancies and AML, whereas the P106L mutation causes hereditary thrombocytosis without a known predisposition to hematologic malignancies. We have now performed functional analyses of these gain-of-function mutations to address the question of how the different propensity to induce malignancy can be explained. We first analyzed the post-translational processing of the normal and the P106L mutated receptor in comparison to the receptors carrying the S505N, W515K and W515L mutations in transfected HeLa and BA/F3 cells. The normal and the S505N, W515K and W515L mutated c-Mpl receptors were properly glycosylated during their transport through the Golgi apparatus, whereas the P106L mutated receptor did not enter the Golgi and was not fully glycosylated. The plasma membrane expression, assayed by confocal microscopy and FACS, of the S515N, W515K and W515L mutated receptors was comparable to the normal receptor, whereas the P106L mutated receptor was not detectable on the cell surface. Functional analyses of the THPO/c-Mpl signaling pathways in THPO stimulated c-Mpl transfected BA/F3 cells showed activation of the ERK1/2 pathway in all mutants but only weaker activation of the PI3K/m-TOR and Stat3/5 signaling pathways for the P106L mutant. By contrast, cells transfected with the normal receptor gene and the S505N, W515K and W515L c-Mpl mutants showed predominant up-regulation of the PI3K/m-TOR and Stat3/5 pathways. These results show that (1) the activation of c-Mpl by THPO does not absolutely require surface expression of the receptor (2) different c-Mpl gain-of-function mutations activate separable downstream pathways and (3) the predominant activation of the PI3K/m-TOR and Stat3/5 pathways correlates with the propensity to induce hematopoietic malignancy. Further, it is interesting to note that the c-Mpl P106L gain-of-function mutant is known to cause 10 to 20-fold elevated thrombopoietin (THPO) plasma levels in patients and is shown here not to be properly glycosylated and transported to the cell surface. By contrast, patients with the other gain-of-function mutations analyzed here show normal or even reduced THPO plasma concentrations and normal post-translational processing and cell surface expression. In conclusion, we propose that c-Mpl gain-of-function mutations exert their effect by predominantly activating either the PI3K/m-TOR and Stat3/5 or the ERK signaling pathways and that the predominant activation of PI3K/m-TOR and Stat3/5 correlates with the propensity to induce malignancy. Furthermore, THPO clearance and maintenance of the negative feedback loop regulating THPO plasma levels, but not signaling activity of the c-Mpl receptor necessarily require proper glycosylation, intracellular trafficking and cell surface expression. Disclosures No relevant conflicts of interest to declare.
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Levy, Gabriel, Serge Carillo, Benjamin Papoular, Bruno Cassinat, Jean-Marc Zini, Emilie Leroy, Leila N. Varghese i in. "MPL mutations in essential thrombocythemia uncover a common path of activation with eltrombopag dependent on W491". Blood 135, nr 12 (19.03.2020): 948–53. http://dx.doi.org/10.1182/blood.2019003240.
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Abstract Mutations in the MPL gene encoding the human thrombopoietin receptor (TpoR) drive sporadic and familial essential thrombocythemias (ETs). We identified 2 ET patients harboring double mutations in cis in MPL, namely, L498W-H499C and H499Y-S505N. Using biochemical and signaling assays along with partial saturation mutagenesis, we showed that L498W is an activating mutation potentiated by H499C and that H499C and H499Y enhance the activity of the canonical S505N mutation. L498W and H499C can activate a truncated TpoR mutant, which lacks the extracellular domain, indicating these mutations act on the transmembrane (TM) cytosolic domain. Using a protein complementation assay, we showed that L498W and H499C strongly drive dimerization of TpoR. Activation by tryptophan substitution is exquisitely specific for position 498. Using structure-guided mutagenesis, we identified upstream amino acid W491 as a key residue required for activation by L498W or canonical activating mutations such as S505N and W515K, as well as by eltrombopag. Structural data point to a common dimerization and activation path for TpoR via its TM domain that is shared between the small-molecule agonist eltrombopag and canonical and novel activating TpoR mutations that all depend on W491, a potentially accessible extracellular residue that could become a target for therapeutic intervention.
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Porret, Naomi A., Elisabeth Oppliger Leibundgut, Serge Carillo, Bruno Cassinat, Francois Girodon, Éric Lippert, Valérie Ugo i in. "Interlaboratory Quality Control Round of MPL Mutation Detection in Fourteen European Laboratories: A MPN&MPNr-EuroNet Study",. Blood 118, nr 21 (18.11.2011): 3859. http://dx.doi.org/10.1182/blood.v118.21.3859.3859.
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Abstract Abstract 3859 The MPL gene is located on chromosome 1p34 and encodes the thrombopoietin receptor. It includes 12 exons and is a key factor for growth and survival of megacaryocytes. Acquired mutations in this gene activate the thrombopoietin receptor constitutively. MPL515 somatic mutations are stem cell-derived events that involve both myeloid and lymphoid progenitors. Two distinct exon 10 mutations are found in 15% of JAK2-V617F negative myeloproliferative neoplasms (MPN),), i.e. 3% of essential thrombocythemia (ET) and 10% of primary myelofibrosis (PMF).: W515L, W515K and the rare W515A variant. A hereditary mutation, S505N, is associated with familial thrombocytosis. MPL mutation detection is a helpful new tool to detect clonality in JAK2 V617F negative MPN and to establish the diagnosis of MPN. As many laboratories use very different methods and interpretations, standardization is highly warranted. Particularly the methodology is diverse and the results need to be comparable, requiring comprehensive testing. This quality control project was established within workgroup 2 of the MPN&MPNr-EuroNet network, (www.mpneuronet.eu, supported by the European program COST (CoOperation in Science and Technology)). The lab from the ‘Hopital H. Mondor AP-HP Paris' provided 29 samples containing randomized concentrations (between 100% and 1%) of the four mutations MPL W515L, W515K, W515A and S505N. The plasmids used for this quality control experiment spanned exons 9, intron 9 and exon10 of the MPL with S505N, W515L, W515K and W515A mutants diluted first with wild-type plasmid gene and then diluted in human genomic DNA. Thirteen European laboratories tested these 29 samples, each using their own chosen methods (14 altogether). The following methods were used: Mutascreen W515L/K Kit (Ipsogen, France):(n=4), allelic discrimination real-time PCR (n=2), high resolution melting (HRM) (n=7) and sequencing (n=2, 1 Sanger, 1 pyrosequencing)). There were no false positive results in any of the labs. All labs using the Mutascreen W515L/K Kit detected all W515L and W515K mutations, from 100% mutated down to 1% mutated plasmids. The allelic discrimination assays which were also designed for W515L and W515K only, detected the mutations down to 2%. The HRM methods were all designed differently. All except one (which did not recognize S505N) detected all 4 mutations with a sensitivity, down to 5% mutated plasmids, with few exceptions detecting either lower or higher amounts. The Sanger sequencing and pyrosequencing assays had a detection limit of 5–10%, with the pyrosequencing assay not being designed for the S505N mutation. All participating labs detected the most frequent MPL mutations in MPN W515L and W515K, with many designs not including W515A and S505N. Achieved sensitivities differed between methods with cutoffs of 1% to 10% (1.5% for the Ipsogen kit). Most laboratories reported the results as either positive or negative. However, the percentages of mutated alleles reported by a few labs differed greatly from each other and from the original dilutions (range 2–50 times) In conclusion, these results show that the diverse methods for MPL mutation detection used by different European labs yielded comparable specificity with varying sensitivity. Smaller clones might be missed by the less sensitive methods, and quantification of mutated alleles should be interpreted very carefully until standardised reference material for MPL mutation testing will be available. More extensive interlaboratory testing including patient samples is needed to identify the most robust assays suitable for diagnostic mutation detection and particularly for quantification of mutated alleles. Disclosures: No relevant conflicts of interest to declare.
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Stockklausner, Clemens, Christin Maria Duffert, Ziwei Zhou, Anne Christine Klotter, Isabelle Nadine Kuhlee i Andreas E. Kulozik. "Mpl Gain-of-Function Mutations Can be Classified By Differential Subcellular Processing, Molecular Mechanisms, Mode of Inheritance and Clinical Impact". Blood 126, nr 23 (3.12.2015): 1634. http://dx.doi.org/10.1182/blood.v126.23.1634.1634.
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Abstract The interaction between the c-Mpl receptor and its ligand thrombopoietin (TPO) on the cell surface is crucial for the regulation of thrombopoiesis. Several mutations in the c-Mpl receptor gene have been linked to a gain-of-function resulting in thrombocytosis. We have analyzed the known gain-of-function mutations in the extracellular part of the Mpl receptor, K39N and P106L, as well as the S505N, W515K and W515L mutations in the transmembrane and juxtamembrane region, respectively. Interestingly, the latter mutations can occur as autosomal dominant and/or as somatic mutations and are known to be associated with myeloproliferative malignancies and AML, whereas the abundant K39N and the P106L mutations are the cause of autosomal recessive hereditary thrombocytosis without a known predisposition to hematologic malignancies. To date, these differences in clinical impact and mode of inheritance are poorly understood. Starting from these clinical observations, we have performed functional analyses of the described gain-of-function mutations to address the key functional properties that might explain the observed clinical differences. Three crucial stages of the c-Mpl receptor life cycle were addressed: (1) post-translational processing of the immature receptor protein and its subcellular distribution, (2) membranous expression of the mature receptor and (3) receptor internalization upon stimulation with its ligand TPO. We first analyzed the post-translational processing of the normal, the K39N and the P106L mutated receptor in comparison with receptors carrying the S505N, the W515K and W515L mutations in a HeLa cell culture model. The normal, the K39N, S505N, W515K and W515L mutated c-Mpl receptors were properly glycosylated during their transport through the Golgi apparatus, whereas the P106L mutated receptor did not enter the Golgi and was not fully glycosylated. The K39N mutant was fully glycosylated but did show different running behavior on the SDS Gel, most likely caused by post-translational modifications different from glycosylation. The S505N, the W515K and the W515L mutated receptors displayed stable surface expression in confocal microscopy and FACS analysis, whereas the P106L mutated receptor was not detectable on the cell surface. After stimulation with TPO, a decrease in mean receptor surface protein could be observed for the wild type and all mutants that were expressed on the surface, namely S505N, W515K and W515L, however not significant (p>0.05). Interestingly, our functional analyses of the TPO/c-Mpl signaling pathways in TPO stimulated c-Mpl transfected BA/F3 cells showed activation of the ERK1/2 pathway in all mutants but only weaker activation of the PI3K/m-TOR and Stat3/5 signaling pathways for the P106L mutant. By contrast, cells transfected with the wild type, the S505N, W515K and W515L c-Mpl mutants showed predominant up-regulation of the PI3K/m-TOR and Stat3/5 pathways. These results show that first, both impaired and regular receptor glycosylation and correlating subcellular distribution may occur in c-Mpl gain-of function mutants. Second, the c-Mpl gain-of-function mutants differ substantially in surface expression levels. Third, our results suggest differences in the maintenance of the TPO negative feedback loop across c-Mpl gain-of-function mutants. Indeed, in contrast to P106L, it seems likely that the TPO negative feedback-loop is preserved in the S505N, the W515K and the W515L mutants. In line with this, highly elevated TPO serum levels have only been described for P106L, but not for the other gain-of-function mutations. We hypothesize that maintenance of the TPO negative feedback-loop is sufficient to prevent dysregulation of TPO levels but not transmission of a harmful c-Mpl gain-of-function effect. Instead, the predominant activation of the PI3K/m-TOR and Stat3/5 pathways might explain the different propensity to induce hematopoietic malignancy. In summary, our findings suggest the existence of different disease causing molecular mechanisms behind the mutations' respective clinical correlates and provide the basis for an important extension to the current classification of c-Mpl mutations that is primordially based on clinical observations. Disclosures No relevant conflicts of interest to declare.
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Ardicli, Sena, Hale Samli, Deniz Dincel, Bahadir Soyudal i Faruk Balci. "Individual and combined effects of <i>CAPN1</i>, <i>CAST</i>, <i>LEP</i> and <i>GHR</i> gene polymorphisms on carcass characteristics and meat quality in Holstein bulls". Archives Animal Breeding 60, nr 3 (8.09.2017): 303–13. http://dx.doi.org/10.5194/aab-60-303-2017.
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Abstract. The objective of this study was to determine the association of single nucleotide polymorphisms (SNPs) with carcass characteristics and meat quality traits in selected candidate genes in Holstein bulls. Five SNPs in four genes, i.e. calpain 1 (CAPN1), calpastatin (CAST), leptin (LEP) and growth hormone receptor (GHR), were genotyped in 400 purebred bulls using PCR-RFLP. Statistically significant associations were as follows: CAPN1 G316A with live weight, carcass weight, back fat thickness, m. longissimus thoracis et lumborum area and carcass measurements; CAPN1 V530I with pH and L∗; CAST S20T with live weight, inner chest depth and b∗ value; and GHR with ph, a∗ and h∗. In addition, significant genotypic interactions were observed for dressing percentage (LEP A80V × CAST S20T), pH (CAPN1 V530I × GHR S555G and LEP A80V × GHR S555G) and rump width (CAPN1 V530I × CAST S20T). There was no association between the LEP A80V marker and any of the traits evaluated, nor was there any association of the tested SNPs with chest width, C∗ and marbling score. The present results could therefore be indicative for future studies on meat yield and quality.
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Bridgford, Jessica L., Su Min Lee, Christine M. M. Lee, Paola Guglielmelli, Elisa Rumi, Daniela Pietra, Stephen Wilcox i in. "Novel drivers and modifiers of MPL-dependent oncogenic transformation identified by deep mutational scanning". Blood 135, nr 4 (23.01.2020): 287–92. http://dx.doi.org/10.1182/blood.2019002561.
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Abstract The single transmembrane domain (TMD) of the human thrombopoietin receptor (TpoR/myeloproliferative leukemia [MPL] protein), encoded by exon 10 of the MPL gene, is a hotspot for somatic mutations associated with myeloproliferative neoplasms (MPNs). Approximately 6% and 14% of JAK2 V617F− essential thrombocythemia and primary myelofibrosis patients, respectively, have “canonical” MPL exon 10 driver mutations W515L/K/R/A or S505N, which generate constitutively active receptors and consequent loss of Tpo dependence. Other “noncanonical” MPL exon 10 mutations have also been identified in patients, both alone and in combination with canonical mutations, but, in almost all cases, their functional consequences and relevance to disease are unknown. Here, we used a deep mutational scanning approach to evaluate all possible single amino acid substitutions in the human TpoR TMD for their ability to confer cytokine-independent growth in Ba/F3 cells. We identified all currently recognized driver mutations and 7 novel mutations that cause constitutive TpoR activation, and a much larger number of second-site mutations that enhance S505N-driven activation. We found examples of both of these categories in published and previously unpublished MPL exon 10 sequencing data from MPN patients, demonstrating that some, if not all, of the new mutations reported here represent likely drivers or modifiers of myeloproliferative disease.
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Kim, Ung-Jun, Ho-Jong Lee, In-Sun Choi, Seong-Ho Kang, Sook-Jin Jang, Dae-Soo Moon i Geon Park. "Primary Myelofibrosis with MPL S505N Mutation: The First Case Reported in Korea". Laboratory Medicine Online 8, nr 4 (2018): 167. http://dx.doi.org/10.3343/lmo.2018.8.4.167.
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Aung, Lynn, Tommy Petros, Jessica Geiger i Sara Graham. "Agree to Disagree? Equianalgesic Consensus Amongst Hospice and Palliative Providers (S555)". Journal of Pain and Symptom Management 63, nr 5 (maj 2022): 936–37. http://dx.doi.org/10.1016/j.jpainsymman.2022.02.178.
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Shoaf, M. Todd. "Urban in the sky : a vertical transition /". Thesis, This resource online, 1994. http://scholar.lib.vt.edu/theses/available/etd-12052009-020340/.
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Skinner, Daniel B. "Microwave heating of a coating on a temperature-sensitive substrate". Thesis, This resource online, 1995. http://scholar.lib.vt.edu/theses/available/etd-03142009-040544/.
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Simonson, Timothy D. "Distribution, ecology, and reproductive biology of the orangefin madtom (Noturus gilberti)". Thesis, Virginia Polytechnic Institute and State University, 1987. http://hdl.handle.net/10919/80168.
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Distribution of the orangefin madtom (Noturus gilberti) was determined from 347 sites sampled in Virginia and North Carolina. This species inhabited 264 stream kilometers, over twice the reported range, in the following systems: Craig Creek, Roanoke River, Dan River, Big Chestnut Creek, South Mayo River, Pigg River, and Smith River. The orangefin madtom was somewhat common; 33% (Dan River) to 70% (Craig Creek) of the sites sampled were occupied.
Negative interspecific associates of orangefin madtoms included chubs, mountain redbelly dace, rosyside dace, crescent shiners, and crayfish; only Roanoke darters were considered positive associates. Sand and silt levels were significantly lower at sites with N. gilberti, while percentage of small cobble, local gradient, and depth were significantly higher. Discriminant function analysis identified large gravel, local gradient, silt, and occurrence of rosyside dace and crayfish, as significant predictors of the occurrence of the orangefin madtom.
Seasonal samples from Craig Creek consisted of three age groups. The smallest individual captured was 33 mm total length (TL) and the largest was 111 mm TL. Mortality appeared moderate from age I until summer of the third year, when most individuals apparently died shortly after spawning. Spawning habitat of orangefin madtoms in Craig Creek appeared to be fast-water riffles dominated by small cobble substrate.
Attempts to induce N. gilberti spawning in the laboratory were unsuccessful due to high mortality of captive fish. Field-collected margined madtom egg masses, however, were successfully hatched, and subsequent survival was significantly greater for fry fed ground trout chow versus live brine shrimp nauplii.Master of Science
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Simmons, Sarah. "The development of schooling in Floyd County, Virginia 1831-1900". Diss., Virginia Polytechnic Institute and State University, 1987. http://hdl.handle.net/10919/53659.
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This dissertation addresses the cultural, economic, and geographic factors that politically affected the development of schooling in Floyd County, located in southwest Virginia, from its formation in 1831 to the beginning of the twentieth century. Floyd County was formed in 1831 during Virginia's quasi-system of education. This quasi-system was created due to the "peopling" of early Virginia. Colonial Virginia provided educational opportunities for the rich and poor. The General Assembly, which was dominated by the planter-aristocrats, opposed state education. These aristocrats saw no reason to tax themselves for educational opportunities they would not patronize. As settlers of Swiss, German, and Scotch-Irish descent migrated into the backcountry of Virginia, they brought with them a desire for universal education. The conflicts between the eastern and western portion of the state resulted in the Literary Fund Act of 1818 which provided funds to educate Virginia's poor. The wealthy continued to educate their own with the middle class left to their own devices. This quasi-system of education lasted until the Civil War. At the end of the war, conservatives, still in control of the General Assembly, were forced to accept state supported education due to the Underwood Constitutional mandate. Separate schools for blacks and whites were begun under the state plan in 1870. By July 1876, Floyd County had 52 schools in operation; but this expansion faced ruin when the General Assembly used funds to pay off the state's debt. The debt issue split Virginians into two political camps, Funders and Readjusters. It was not until the Readjuster victory in the early 1880's that Virginia's state system began to stabilize.
Political decisions continued to affect education in the late nineteenth century. District boards hired teachers and located schools for political and social reasons which were often tied to community loyalties. Superintendents licensed and examined teachers based on their own standards. The General Assembly denied teachers the right to meet during school terms. No public money could be used to finance their meetings. What education teachers did receive was financed by local efforts and Peabody funds. By the 1890's, over 4000 teachers in Virginia had not attended State Summer Normals. Floyd County had a higher percentage of teachers attending Normals due to its third superintendent bringing a Normal to Jacksonville in 1889.
By 1900, schooling in Floyd County had survived its first 30 years, but with only partial success. Political entanglements, dating back over two centuries, had affected public education at the state and local level with the results that by the beginning of the twentieth century, half of the school age population in Virginia had never attended school.Ed. D.
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Simmons, James H. "A life-cycle analysis of the advanced program management system (APMS) prototype". Master's thesis, This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-12232009-020133/.
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Sikkema, Kathleen J. "Skills training with heterosexual females for the prevention of HIV infection, other sexually transmitted diseases, and sexual assault". Diss., Virginia Tech, 1991. http://hdl.handle.net/10919/38871.
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Slack, Rebecca A. "Open space preservation in rural residential development". Thesis, This resource online, 1996. http://scholar.lib.vt.edu/theses/available/etd-12172008-063233/.
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Shields, Jean-Philippe. "Élaboration du modèle conceptuel flexible et extensible d'une architecture logicielle orientée-objet permettant la parallélisation et la distribution d'une architecture de simulation séquentielle". Thesis, Université Laval, 2007. http://www.theses.ulaval.ca/2007/24474/24474.pdf.
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