Thesis (M. Litt.)--Madras University. / In Tamil. Includes bibliographical references (p. [93]-95).

Thesis (Ph. D.)--University of Texas at Austin, 2002. / Vita. Includes bibliographical references. Available also from UMI Company.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1981. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 214-227).

Thesis (Ph. D.)--University of Hong Kong, 2004. / Also available in print.

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

The 4.6 Mb circular E. coli chromosome is compacted by segregation into 400-500 supercoiled domains, created by both active and passive mechanisms like transcription and DNA-binding proteins. We find that transposable prophage Mu, transcriptionally silent by definition, is organized into an independent domain as determined by the close proximity of Mu termini L and R separated by a 37 kb Mu genome. Cre-loxP recombination is used in this study in vivo and in vitro. Critical to formation/maintenance of the Mu 'domain' configuration are a strong gyrase site SGS at the center of Mu, the Mu L end, the MuB protein, and the E. coli nucleoid-associated proteins IHF, Fis and HU. The Mu domain was observed at two structurally different chromosomal locations, and was specific to the Mu prophage, i.e. was not observed for the [mathematical symbol] prophage. A model is proposed that by employing its cis-elements to create a domain barrier for segregation and compaction of its genome, the large selfish DNA element Mu profits from the transposition-ready arrangement of its ends, while simultaneously providing a fitness advantage to the host. / text

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Thesis (Ph. D.)--University of Texas at Austin, 2006. / Vita. Includes bibliographical references.

Memoria para optar al título de Químico Farmacéutico / El alcoholismo es un problema mundial de salud pública, por lo que es importante comprender sus bases neuro-farmacológicas para identificar nuevos blancos terapéuticos. Uno de los problemas del alcoholismo es la recaída, que corresponde a la pérdida de control sobre el consumo de alcohol cuando el paciente vuelve a beber después de un período de abstinencia. Estudios en modelos animales de alcoholismo han asociado un mayor valor placentero del alcohol al momento de la recaída. Este incremento del valor hedonístico del alcohol podría estar asociado a un mayor nivel del receptor (mu) μ-opioide (OPMR) en el circuito cerebral de recompensa. Para determinar el rol del OPMR en la recaída al consumo de alcohol, en este trabajo se presentan estudios destinados a evaluar la capacidad inhibitoria de distintas secuencias de RNAs de interferencia tipo horquilla (shRNAs) dirigidas a disminuir la expresión de OPMR in vitro, para ser utilizadas posteriormente en futuros estudios en modelos in vivo. Para ello se clonó el gen del receptor μ-opioide de rata (OPMRr) en el plásmido de expresión pHIV-GFP, generando pHIV-OPMRr-GFP. Se transfectaron células HEK-293T, que naturalmente no expresan OPMRr, con pHIV-OPMRr-GFP y se verificó la expresión de OPMRr mediante Western blot. Para lograr el silenciamiento de la expresión OPMRr se co-transfectó pHIV-OPMRr-GFP con cuatro secuencias distintas (A, B, C y D) de shRNAs dirigidos al RNA mensajero del OPMRr. Las secuencias A y D otorgaron el mayor grado de silenciamiento, inhibiendo en un 73% y 75% respectivamente la expresión de OPMRr. Se generaron lentivirus codificantes de los shRNAs más potentes en reducir su expresión para posteriores ensayos in vivo. En conclusión, mediante el uso de técnicas de biología molecular se clonó y expresó el gen del OPMRr en células en cultivo. Además, se identificaron 2 secuencias de shRNAs capaces de silenciar en más de un 70% la expresión del cDNA codificante para OPMRr y se generaron sus correspondientes lentivirus / Alcoholism is a worldwide public health problem. Therefore, it is important to understand its neuropharmacological bases to identify new therapeutic targets. One of the main problems of alcoholism is relapse, which is the loss of control over ethanol consumption when the patients start to drink again after a period of abstinence. Studies carried out on animal models of alcoholism have established an enhanced pleasurable value of ethanol consumption at the time of relapse. This alcohol enhanced hedonistic value could be associated to an increase in the μ-opioid receptor (OPMR) levels on the brain reward circuit. To determine the role of OPMR on ethanol consumption relapse, the ability of different short hairpin RNAs (shRNAs) to decrease OPMR expression in vitro was assessed. The best shRNAs are intended to be used in future in vivo studies. First, the rat μ-opioid receptor (OPMRr) gene was cloned into the expression plasmid pHIV-GFP, generating the pHIV-OPMRr-GFP plasmid. HEK-293T cells, which naturally do not express OPMRr, were transfected with pHIV-OPMRr-GFP and the OPMRr expression was determined by Western blot. To assess the silencing of the OPMRr in vitro, the pHIV-OPMRr-GFP plasmid was co-transfected with 4 shRNAs sequences (A, B, C y D) designed against the OPMRr messenger RNA. shRNAs A and D exhibit the highest silencing ability, inhibiting OPMRr expression by 73% and 75% respectively. For future in vivo assays, lentiviral vectors codifying for these shRNAs were generated. In conclusion, using molecular biology techniques it was possible to clone and express the gene of the OPMRr in HEK-293T cells. Two shRNAs sequences that inhibit the OPMRr cDNA expression over a 70% were identified and lentiviral vectors that codify for these shRNAs were generated / FONDECYT 11130241

Magnetoencephalography was used to investigate the effect of directed attention on changes in sensorimotor mu (8-12Hz) response (mu reactivity) to non-painful electrical stimulation of the median nerve in healthy adults. Results indicated attention-related sex differences in mu reactivity, with females showing i) prolonged mu suppression when attending to somatosensory stimuli indicating active processing of the sensory stimuli; ii) task-dependent attentional modulation of the mu response, which was absent in males, and iii) a trend for greater neuronal excitability of the primary somatosensory region suggesting greater physiological responsiveness to stimulation overall. Sex-related differences in attentional modulation of sensorimotor rhythms suggest that females and males use different top-down control strategies when processing somatosensory information. These sex differences in attention may underlie well-documented sex-related biases in pain processing wherein females typically report greater sensitivity to experimental and clinical pain.