Thesis (Ph. D.)--Case Western Reserve University, 2006. / [School of Medicine] Department of Neurosciences. Includes bibliographical references. Available online via OhioLINK's ETD Center.

No description available.

Thesis (Ph. D.)--University of Virginia, 2001. / Spine title: Cell death in olfactory development. Includes bibliographical references (leaves 124-151). Also available online through Digital Dissertations.

Tsim Ting Yuk. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 119-135). / Abstracts in English and Chinese. / ABSTRACT --- p.i / 摘要 --- p.iii / 英漢譯名對照 --- p.v / ABBREVIATIONS --- p.vi / ACKNOWLEDGMENTS --- p.viii / Chapter 1. --- Introduction / Chapter 1.1. --- Olfactory system --- p.1 / Chapter 1.1.1. --- Olfactory bulb (OB) --- p.1 / Chapter 1.1.2. --- Accessory olfactory bulb (AOB) --- p.3 / Chapter 1.2. --- Stem cells --- p.5 / Chapter 1.3. --- Sexual differentiation --- p.8 / Chapter 1.3.1. --- Sexual dimorphic olfactory system --- p.8 / Chapter 1.3.2. --- Androgen receptor (AR) & estrogen receptor beta (ERβ) --- p.13 / Chapter 1.3.3. --- Aromatase --- p.15 / Chapter 1.3.4. --- Oligomycin sensitivity-conferringrotein (OSCP) --- p.18 / Chapter 1.4. --- rogrammed cell death (PCD) --- p.18 / Chapter 1.4.1. --- CD in the olfactory development --- p.18 / Chapter 1.4.2. --- Caspase 3 --- p.22 / Chapter 1.4.3. --- B cell leukemia/ Lymphoma 2 (Bcl-2) --- p.23 / Chapter 1.5. --- Axon guidance molecules --- p.25 / Chapter 1.5.1. --- Growth cone --- p.25 / Chapter 1.5.2. --- Mechanisms of growth cone advance --- p.26 / Chapter 1.5.3. --- Semaphorins --- p.28 / Chapter 1.5.4. --- Neuropilin --- p.31 / Chapter 1.5.5. --- lexin --- p.32 / Chapter 1.5.6. --- Collapsin response mediatorroteins (CRMPs) --- p.32 / Chapter 1.6. --- Olfactory markerroteins --- p.33 / Chapter 1.6.1. --- Markerroteins in ORNs --- p.33 / Chapter 1.6.2. --- Growth associatedrotein (GAP-43) --- p.34 / Chapter 1.6.3. --- Is the expression of GAP-43 in rat OB sexually dimorphic? --- p.36 / Chapter 1.6.4. --- Olfactory markerrotein (OMP) --- p.38 / Chapter 1.6.5. --- Golf --- p.39 / Chapter 1.7. --- Miscellaneous genes --- p.40 / Chapter 1.7.1. --- Substance (SP) --- p.40 / Chapter 1.7.2. --- Gonadotropin releasing hormone (GnRH) --- p.41 / Chapter 1.7.3. --- Metabotropic glutamate receptor 2 (mGluR2) --- p.42 / Chapter 1.7.4. --- Insulin-like growth factor binding protein-2 (IGFBP2) --- p.43 / Chapter 2. --- Materials and methods / Chapter 2.1. --- Animal study --- p.46 / Chapter 2.2. --- RNA extraction --- p.46 / Chapter 2.3. --- Quantitation of total RNA --- p.49 / Chapter 2.4. --- Reverse Transcription (RT) --- p.50 / Chapter 2.5. --- olymerase Chain Reaction (PCR) --- p.51 / Chapter 2.6. --- urification ofCRroducts --- p.55 / Chapter 2.7. --- Confirmation ofCRroducts --- p.56 / Chapter 2.8. --- Quantitation of cDNA --- p.57 / Chapter 2.9. --- Radioactive labeledCR --- p.58 / Chapter 2.10. --- Electrophoresis ofCRroducts --- p.59 / Chapter 2.11. --- Statistical analysis --- p.60 / Chapter 3. --- Results / Chapter 3.1. --- Standard curve construction --- p.61 / Chapter 3.2. --- β-actin --- p.62 / Chapter 3.3. --- Sexual differentiation related genes --- p.64 / Chapter 3.3.1. --- AR --- p.64 / Chapter 3.3.2. --- ERβ --- p.65 / Chapter 3.3.3. --- Aromatase --- p.65 / Chapter 3.3.4. --- OSCP --- p.66 / Chapter 3.4. --- CD related genes --- p.66 / Chapter 3.4.1. --- Bcl-2α --- p.66 / Chapter 3.4.2. --- Caspase 3 --- p.67 / Chapter 3.5. --- Axon guidance molecules and related genes --- p.67 / Chapter 3.5.1. --- SemaIII --- p.67 / Chapter 3.5.2. --- Neuropilin-1 --- p.68 / Chapter 3.5.3. --- lexin-1 --- p.68 / Chapter 3.5.4. --- CRMP-1 --- p.69 / Chapter 3.5.5. --- CRMP-2 --- p.70 / Chapter 3.5.6. --- CRMP-3 --- p.70 / Chapter 3.5.7. --- CRMP-4 --- p.71 / Chapter 3.6. --- Olfactory markerrotein genes --- p.71 / Chapter 3.6.1. --- GAP-43 --- p.71 / Chapter 3.6.2. --- OMP --- p.72 / Chapter 3.6.3. --- Golf --- p.72 / Chapter 3.7. --- Miscellaneous genes --- p.73 / Chapter 3.7.1. --- SubstanceP --- p.73 / Chapter 3.7.2. --- GnRH --- p.73 / Chapter 3.7.3. --- mGluR2 --- p.74 / Chapter 3.7.4. --- IGFBP-2 --- p.74 / Chapter 3.8. --- Graphs and tables --- p.75 / Chapter 4. --- Discussion / Chapter 4.1. --- Quantitation of cDNA and normalization of CR results --- p.97 / Chapter 4.2. --- Sexual differentiation related genes --- p.98 / Chapter 4.3. --- CD related genes --- p.100 / Chapter 4.4. --- Axon guidance molecule and related genes --- p.103 / Chapter 4.5. --- Olfactory markerrotein genes --- p.109 / Chapter 4.6. --- Miscellaneous genes --- p.112 / Chapter 5. --- References --- p.119

Thesis (Ph. D.)--University of Washington, 1997. / Vita. Includes bibliographical references (leaves [90]-110).

Developmental signaling pathways have many diverse roles throughout the life of an organism. The proper regulation of these pathways is essential for normal development, and misregulation can lead to diseases such as cancer. Heparan sulfate proteoglycans function to modulate growth factor signaling in many biological processes by acting as co-receptors, or by influencing ligand distribution. The heparan sulfate proteoglycan Trol, the Drosophila Perlecan homolog, is known to modulate signaling in a population of neuroblasts in the developing Drosophila central nervous system. My studies aim to determine the function Trol has in regulating signaling pathways during development. trol mutants are examined to determine how various mutant alleles impact signaling in several different developmental contexts. The role growth factor pathways play during induction of a Drosophila prostate cancer model is also examined. Gene expression profiles are determined for two types of prostate model overproliferation. Trol is shown to be able to differentially regulate multiple signaling pathways during several developmental processes. The Drosophila prostate cancer model is also shown to have many characteristics similar to those of human prostate cancer, and that signaling and proteoglycan expression are impacted by aberrant overgrowth in the model. My results indicate that Trol is able to specifically modulate different signaling pathways depending on the tissue and developmental context.

Revised; Originally Published: 2009 / 2 pp. / This publication discusses water in in dry bulb onion production in Arizona.

Thesis PlanB (M.S.)--University of Wisconsin--Stout, 2009. / Includes bibliographical references.

Light - body - space - Bulb Instalation includes sixty incandescent bulbs (25 W), which flashing in certain interval. Bulbs covered all floor and their intensity of light create and change space around. Spectator has an opportunity to enter to the quickly changing field of instalation, which can confused him.

Olfactory Granule cells (GCs) are a population of inhibitory interneurons responsible for maintaining normal olfactory bulb (OB) function and circuitry. Through dendrodendritic synapses with the OBs projection neurons, the GCs regulate information sent to the olfactory cortices. Throughout adulthood, GCs continue to integrate into the OB and contribute to olfactory circuitry. However, only ~50% will integrate and survive longterm. Factors aiding in the survival and morphological development of these neurons are still being explored. The neurotrophin brain-derived neurotrophic factor (BDNF) aids in the survival and dendritic spine maturation/maintenance in several populations of CNS neurons. Investigators show that increasing BDNF in the adult-rodent SVZ stimulates proliferation and increases numbers of new OB GCs. However, attempts to replicate these experiments failed to find that BDNF affects proliferation or survival of adult-born granule cells (abGCs). BDNFs regulation of dendritic spines in the CNS is well characterized. In the OB, absence of BDNF’s receptor on abGCs hinders normal spine development and demonstrates a role for BDNF /TrkB signaling in abGCs development. In this study, we use transgenic mice over-expressing endogenous BDNF in the OB (TgBDNF) to determine how sustained increased in BDNF affect the morphology of olfactory GCs and the survival and development of abGCs. Using protein assays, we discovered that TgBDNF mice have higher BDNF protein levels in their OB. We employed a Golgi-cox staining technique to show that increased BDNF expression leads to an increase in dendritic spines, mainly the mature, headed-type spine on OB GCs. With cell birth-dating using 5-bromo-2’- deoxyuridine (BrdU), immunofluorescent cell markers, TUNEL staining and confocal microscopy, we demonstrate that over-expression of BDNF in the OB does not increase survival of abGCs or reduce cell death in the GC population. Using virally labeled abGCs, we concluded that abGCs in TgBDNF mice had similar integration patterns compared to wild-type (WT) mice, but maintained increases in apical headed-type spine density from 12 to 60 days PI. The evidence combined demonstrates that although increased BDNF does not promote cell survival, BDNF modifies GC morphology and abGC development through its regulation of dendritic spine development, maturation and maintenance in vivo. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2018. / FAU Electronic Theses and Dissertations Collection