Department of Pathology and Anatomical Sciences (MU)The Department of Pathology and Anatomical Sciences is part of the School of Medicine at the University of Missouri-Columbiahttps://hdl.handle.net/10355/9292024-03-28T08:01:28Z2024-03-28T08:01:28Z3D analysis of hip joint mobility and the evolution of locomotor abilities in miocene hominoidsHammond, Ashley S.https://hdl.handle.net/10355/446742022-09-28T16:53:49Z2013-01-01T00:00:00Z3D analysis of hip joint mobility and the evolution of locomotor abilities in miocene hominoids
Hammond, Ashley S.
The emergence of extant ape-like locomotor behaviors has become a defining issue in reconstructing ape evolution. Suspensory positional behaviors, such as antipronograde bridging, climbing, clambering and transfer, distinguish extant hominoids from Old World monkeys and most New World monkeys. It has been widely theorized that suspensory behaviors involve highly abducted hip joint postures, potentially permitting suspensory behaviors to be inferred from joint function rather than relying on isolated morphologies. This thesis tests whether adaptations for suspensory behaviors can be inferred in fossil nonhuman hominoids from the hip joint. The first study tests the association between suspensory behaviors and hip mobility in anesthetized living anthropoids (n=104). Suspensory taxa were found to have significantly higher passive ranges of abduction and external rotation compared to non-suspensory taxa. The second study developed a digital modeling technique to estimate range of hip abduction and then tested the accuracy of the modeling approach against the live animal data. Hip joint abduction and the abducted knee position were reconstructed in a large sample of extant anthropoids (n=252) and then quantitatively compared these simulations to the in vivo data for passive range of abduction. Suspensory taxa were significantly larger in both simulated abduction (degrees) and abducted knee position (mm), although there was overlap between locomotor groups. The results provided a hypothetical framework for how to interpret abduction modeled in fossil taxa. The final study modeled hip abduction in early Miocene hominoid Proconsul nyanzae, late Miocene crown hominoid Rudapithecus hungaricus, and several largebodied Plio-Pleistocene fossil cercopithecoids (Paracolobus mutiwa, Paracolobus chemeroni, Theropithecus oswaldi) using the validated modeling approach from the second study. Abduction simulations in Proconsul nyanzae and fossil cercopithecoids yielded abduction consistent with a non-suspensory locomotor reconstruct
2013-01-01T00:00:00ZAberrant DNA methylationof RUN domain containing 3B in lymphoid malignanciesBurmeister, Danehttps://hdl.handle.net/10355/439892022-09-28T16:54:41Z2013-01-01T00:00:00ZAberrant DNA methylationof RUN domain containing 3B in lymphoid malignancies
Burmeister, Dane
Heritable changes to DNA conformation can have significant impacts on gene expression without altering the DNA sequence. The RUN domain containing 3B gene (RUNDC3B) has been shown to be differentially expressed in cancer types such as, acute lymphoblastic leukemia. This differential expression has been linked to methylation of the gene. Combined bisulfite restriction analysis and methylation specific PCR were used to determine the methylation status of five regions spanning a CpG island (CGI) in the promoter region of RUNDC3B.This analysis was completed in cell lines from lymphoid malignancies, myeloid malignancies, various solid tumor cancers, and healthy lymphoid cell lines. To determine the effect of aberrant DNA methylation on RUNDC3B expression, real-time PCR was utilized. The lymphoid malignancies were found to have more prominent methylation and express RUNDC3B at lower levels than other malignant and healthy lymphoid cell lines. Sequence analysis of the CGI in the RUNDC3B promoter (RUNDC3B CGI) was performed to support the importance of this region as a regulatory element in several species. In this project we have extended our understanding of aberrant RUNDC3B CGI methylation to include cell lines representing 15 malignancies. Our data suggest that methylation located in the RUNDC3B CGI may serve as a biomarker for lymphoid malignancies. Additionally, the results provide the basis for continued analysis of the role of RUNDC3B repression in the pathogenesis of lymphoid malignancies.
July 2013.; A Thesis presented to the Faculty of the Graduate School at the University of Missouri--Columbia In Partial Fulfillment of the Requirements for the Degree Master of Science.; Thesis supervisor: Dr. Kristen H. Taylor.; Includes vita.
2013-01-01T00:00:00ZAdministration of apocynin in drinking water ameliorates transient cerebral ischemia-induced brain damage and behavioral deficits in miceLehmidi, Tareq Mohamed Elhadihttps://hdl.handle.net/10355/154052022-09-28T16:54:36Z2012-01-01T00:00:00ZAdministration of apocynin in drinking water ameliorates transient cerebral ischemia-induced brain damage and behavioral deficits in mice
Lehmidi, Tareq Mohamed Elhadi
[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Acute ischemic stroke is the third leading cause of death in developed countries and the most frequent cause of permanent disability in adults worldwide. Despite advances in the understanding of the pathophysiology of cerebral ischemia, therapeutic options remain limited. Inflammation following ischemic stroke is known to contribute to neurological injury. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) is well known as a major source for superoxide radical generation in leukocytes. Superoxide radicals play a significant role in brain ischemia-reperfusion (I/R) injury. Recently, several forms of this oxidase have been found in a variety of non-immune cells including neurons and glial cells. Apocynin is a NOX inhibitor that has been studied as a potential treatment in experimental stroke. The anti-inflammatory activity of apocynin has been demonstrated in a variety of cells and animal models of inflammation. Apocynin after metabolic conversion, inhibits the assembly of NADPH oxidase that is responsible for reactive oxygen species (ROS) production. In our study, apocynin was used to test whether suppression of ROS by the NADPH oxidase inhibitor can protect against ischemia-induced ROS generation. Focal cerebral ischemia was induced in mice (C57BL/6J male mice) that used a dietary preventative protocol in which apocynin was added into the drinking water so that animals received 50mg/kg dose each day for 5 days before surgery (Intraluminal filament MCAO). Mice used were subjected to 90-120 minutes of focal ischemia induced by MCAO followed by 24 hrs reperfusion. Drinking apocynin group prior to ischemia significantly attenuated infarct volume and improved functional outcome. The neuroprotective effects of apocynin against ROS production during early phase I/R and subsequent I/R-induced neuronal damage provide strong evidence that inhibition of NADPH oxidase could be a promising therapeutic mechanism to protect against stroke damage in the brain.
Title from PDF of title page (University of Missouri--Columbia, viewed on September 19, 2012).; The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.; Thesis advisor: Dr. Zezong Gu; Includes bibliographical references.; M.S. University of Missouri-Columbia 2012.; "May 2012"
2012-01-01T00:00:00ZAdrenalKrause, William J., II, 1942-https://hdl.handle.net/10355/10672018-10-22T23:30:18Z2009-01-01T00:00:00ZAdrenal
Krause, William J., II, 1942-
Histology blog entry for January 31, 2009 about the adrenal glands.
2009-01-01T00:00:00Z