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Thesis advisor: Paul Gray / "Compassion-focused therapy" (CFT) aims to increase the self-compassion of participants while reducing self-stigma. Although CFT is theorized to be effective for alcohol dependents, who suffer from high levels of self-criticism and self-hate, few clinical studies examine which factors facilitate the development of self-compassion and subsequently reduce harmful drinking. This qualitative study therefore values the subjective perspectives of female alcohol dependents as they participate in CFT in Northern Ireland. In doing so, it explores how self-compassion may be increased through modifications in self-labeling and self-concept. It is proposed that the development of a compassionate mindset, along with spirituality and mindfulness, grant alcohol dependents cautious optimism for the future. / Thesis (BA) — Boston College, 2015. / Submitted to: Boston College. College of Arts and Sciences. / Discipline: Departmental Honors. / Discipline: Sociology.

by Hon-chiu Leung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Bibliography: leaves 122-126. / Abstract --- p.i / Acknowledgement --- p.iv / Dedication --- p.v / Table of Contents --- p.vi / Introduction --- p.1 / Literature Review --- p.4 / Chapter 1) --- Ethanol production in bacteria / Chapter 1.1) --- Zymomonas mobilis --- p.4 / Chapter 1.2) --- Clostridium species --- p.7 / Chapter 1.3) --- "Enterobacter, Klebsiella, Serritia and Erwinia sp" --- p.9 / Chapter 1.4) --- Escherichia coli and Salmonella typhimurium --- p.10 / Chapter 2) --- Pyruvate decarboxylase of Z. mobilis / Chapter 2.1) --- Enzyme properties --- p.13 / Chapter 2.2) --- Cloning and expression of pdc gene --- p.15 / Chapter 3) --- Alcohol dehydrogenase (adh) gene / Chapter 3.1) --- "Cloning, chararterization and expression of adh genes" --- p.17 / Chapter 4) --- Gene transfer systems in Vibrio species --- p.21 / Chapter 5) --- Rationale and objectives of this study --- p.22 / Chapter Part I) --- Ethanol Production in terrestrial enteric bacteria / Chapter A) --- Introduction --- p.24 / Chapter B) --- Materials and Methods / Chapter 1) --- Bacterial strains and plasmids --- p.25 / Chapter 2) --- Media --- p.26 / Chapter 3) --- Solutions --- p.27 / Chapter 4) --- Isolation of plasmids / Chapter 4.1) --- Small Scale Isolation of plasmids --- p.30 / Chapter 4.2) --- Large Scale Isolation of plasmids --- p.32 / Chapter 5) --- Construction of a broad-host-range plasmid harbouring Zymomonas mobilis genes --- p.35 / Chapter 6) --- Transformation --- p.35 / Chapter 7) --- High Performance Liquid Chromatography of Organic Acids --- p.36 / Chapter 8) --- Maintenace of plasmids harbouring the genes of Zymomonas mobilis genes --- p.38 / Chapter 9) --- Ethanol tolerance of S. typhimurium strains --- p.38 / Chapter C) --- Results / Chapter 1) --- Construction of Salmonella typhimurium strains harbouring Z. mobilis genes --- p.39 / Chapter 2) --- Fermentative end products in culture medium --- p.48 / Chapter 3) --- Growth of hosts and transformants --- p.61 / Chapter 4) --- Ethanol tolerance of S. typhimurium strains --- p.65 / Chapter 5) --- Maintenance of plasmids --- p.67 / Chapter 6) --- Construction of broad-host-range plasmid harbouring Z. mobilis genes --- p.69 / Chapter D) --- Discussions / Chapter 1) --- Comparison of ethanol production in Escherichia coli and Salmonella typhimurium --- p.72 / Chapter 2) --- Ethanol tolerance of S. typhimurium strains --- p.74 / Chapter 3) --- Maintenance of plasmids --- p.76 / Chapter 4) --- Construction of broad-host-range plasmids harbouring Z. mobilis genes --- p.78 / Chapter Part II) --- Ethanol Production in marine enteric bacteria / Chapter A) --- Introduction --- p.79 / Chapter B) --- Materials and Methods / Chapter 1) --- Bacterial strains and plasmids --- p.80 / Chapter 2) --- Media --- p.80 / Chapter 3) --- Solutions --- p.80 / Chapter 4) --- Routine Identification Processes --- p.81 / Chapter 5) --- Systematic studies by Arbitrarily- Primed Polymerase Chain Reaction --- p.86 / Chapter 6) --- Optimal growth conditions --- p.88 / Chapter 7) --- Isolation of broad-host-range plasmid pIOl ( 64kb) --- p.89 / Chapter 8) --- Transformation of Vibrio sp. strain 60 --- p.90 / Chapter 9) --- Production of ethanol using different carbon sources in fermentation --- p.91 / Chapter C) --- Results / Chapter 1) --- Identification of Vibrio sp. strain 60 --- p.92 / Chapter 2) --- Optimal growth conditions --- p.101 / Chapter 3) --- Isolation of high molecular weight plasmid --- p.105 / Chapter 4) --- Ethanol production from different carbon sources --- p.107 / Chapter 5) --- Ethanol tolerance of Vibrio sp. strain 60 --- p.109 / Chapter 6) --- Salt tolerance of Vibrio sp. strain 60 --- p.111 / Chapter 7) --- Transformation of Vibrio sp. strain 60 --- p.113 / Chapter D) --- Discussions / Chapter 1) --- Strain identification by arbitrarily-primed PCR --- p.116 / Chapter 2) --- Isolation of high molecular weight plasmid --- p.118 / Chapter 3) --- Ethanol production of Vibrio sp. strain60 --- p.120 / References --- p.122

by Yu-Wai Ho. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1989. / Bibliography: leaves 122-129.

BACKGROUND: In the US 47.2% of adults have periodontitis. Alcohol affects the host response, impairs immune function, has toxic effects on the liver and affects with protein metabolism, and therefore may increase the risk of periodontitis. Alcohol may also interfere with homocysteine (Hcy) metabolism and result in hyperhomocysteinemia (HHcy), a risk factor for inflammatory diseases such as cardiovascular disease and possibly periodontal disease. Understanding the exact relationship between alcohol consumption, HHcy and periodontitis is incomplete. OBJECTIVES: To add to our understanding of the alcohol-periodontitis, periodontitis-Hcy and alcohol-Hcy associations longitudinally by addressing methodological issues that confound past research. Methods: The study used existing data from 562 male participants in the VA Dental Longitudinal Study (DLS) who answered food frequency questionnaires (FFQ), underwent periodontal examinations and had plasma . Hcy measurements (N=469). Periodontitis was defined using the CDC case definition (Eke et al., 2009) and categorized into none/mild/moderate or severe disease. HHcy was defined as Hcy ≥10.2 umol/L based on Spence et al., 2001. Alcohol intake was categorized as none, ≤ 1 drink/day, >1 but <2 drinks/day, or ≥ 2 drinks/day. RESULTS: In longitudinal analyses, the risk of developing severe periodontitis among alcohol consumers was 10-17% higher over a period of 19-years compared to non-drinkers after controlling for age, smoking, diabetes, education, and number of teeth present. These estimates were higher still among men with lower than average vitamin B6 or B12 intakes. However, these results were not statistically significant The analyses suggested that men with mild, moderate or severe periodontitis had greater hazards of developing HHcy compared to disease-free participants after adjusting for covariates, but these results were not statistically significant. Consuming more than 2 drinks of alcohol per day significantly increased the risk of developing HHcy by 76% (p= 0.037). SUMMARY: Our findings suggest that alcohol consumption may increase the hazards of developing severe periodontal disease especially if vitamin B complex intakes are low. These results also suggest that periodontal disease and alcohol consumption each increases the hazards of hyperhomocysteinemia. We believe this is the first prospective cohort study to examine associations among periodontitis, homocysteine and alcohol consumption.

Alcohol is the most widely used psychoactive drug on earth and continues to be responsible for a substantial burden of death and disability. Mitigating these harms is an important focus of any healthful society. Population-level alcohol policy strategies may be employed to decrease these harms and improve population health. To assist towards these goals, this dissertation has two research objectives relating to the estimation and mitigation of alcohol harms: (1) to complete a series of studies regarding the Alcohol Total Consumption Model (TCM) and (2) to specify and test a novel alcohol health harms estimator and alcohol policy scenario modeler, the International Model of Alcohol Harms and Policies (InterMAHP). The TCM is an important theory in alcohol studies and connects alcohol policies, per capita alcohol consumption and alcohol-attributable (AA) harms in a unified social theory. In brief, policies are expected to reflect on population-level consumption, which in turn is the most important predictor of alcohol harms. The TCM theorizes that change should flow directionally through the model – a policy expected to decrease consumption would be predicted to decrease alcohol harms. This theory has been critical towards informing alcohol control policies in the past five decades. In this dissertation, a series of studies were conducted to test the assumptions of the TCM, to test their continued viability. Study A is a comprehensive systematic review and series of meta-analyses that established the link between alcohol policies influencing day/hours of sale and outlet density and per capita consumption. Study B is a primary research study that examined the direct effect of a changed alcohol policy on alcohol-related ED visits, in the context of Saskatchewan. Studies C and D establish the link between alcohol consumption and AA mortality and morbidity through mathematical specification of InterMAHP. Next, the model was applied to the exemplar of AA mortality in Canada in 2016. Last, Study E extended InterMAHP functionalities to include modeling changes in AA harms expected from potential or realized per capita consumption changes resulting from policy change. An application was provided in the context of Québec. The results of this dissertation research provide some support, in a modern context, to the relationships defined in the TCM. The findings suggest that the TCM continues to be a largely appropriate conceptual model in consideration of alcohol policy-making. InterMAHP provides global alcohol researchers with a novel model towards estimating the health harms of alcohol. / Graduate / 2020-04-09

La producción de alcohol se encuentra relacionada directamente con la producción de Biocombustibles, debido al desplazamiento de importantes volúmenes de alcohol para su conversión en etanol o alcohol anhídrido; usado como complemento o sustituto de la gasolina. Esta situación ha generado que la caña de azúcar, principal materia prima para la elaboración de alcohol se convierta en un “bien escaso” y sea necesario buscar otras potenciales fuentes para su producción. En el Perú, existe también el potencial para producir el mencionado producto, usando los tubérculos como base, especialmente la papa; a través de la conversión de almidones en azúcares y su posterior fermentación y destilación en alcohol etílico. La presente investigación tiene por finalidad demostrar la viabilidad de la instalación de una planta de producción de alcohol de papa en la provincia de Chota, departamento de Cajamarca, con la intención de atender al mercado interno, con un producto de alta calidad, orientado al uso industrial, farmacéutico y cosmético. La metodología desarrollada comprende la determinación de viabilidad de Mercado, Organizacional, Técnico Operativa, Económica financiera y ambiental. Finalmente se concluye que es viable la instalación de una planta de producción de alcohol en la provincia de Chota. / Tesis

Magíster en Bioquímica, área de especialización en Bioquímica Toxicológica y Diagnóstico Molecular / Memoria para optar al Título de Bioquímico / Recientemente, se demostró que la metabolización de etanol a acetaldehído es indispensable para que su consumo sea reforzante; sin embargo, no se conoce el mecanismo cerebral por el cual se produce este efecto. Se ha postulado que el salsolinol, un producto racémico de la condensación no enzimática de acetaldehído con dopamina, es responsable del efecto reforzante del etanol. La concentración cerebral de salsolinol aumenta luego del consumo de etanol y el salsolinol es una molécula reforzante más potente que el acetaldehído y el etanol, probablemente activando al receptor μ de opioides. Sin embargo, el salsolinol de Sigma-Aldrich, caracterizado como reforzante en los estudios en la literatura, está compuesto por 4 isómeros: R- y S-salsolinol, y R- y S-isosalsolinol (este último es un producto secundario de la condensación no enzimática de acetaldehído y dopamina). Queda por esclarecer: cuál o cuáles de estas moléculas son reforzantes y si estas moléculas alcanzan su concentración reforzante cuando se consume etanol. Además, se ha reportado la existencia de una enzima R-salsolinol sintasa cuyos sustratos son dopamina y acetaldehído. Si la formación de R-salsolinol es responsable del efecto reforzante del etanol, esta enzima podría ser necesaria para que el etanol sea reforzante; sin embargo, no se ha publicado su secuencia aminoacídica. A partir de estos antecedentes se postula que un producto de la condensación de dopamina y acetaldehído es responsable del efecto reforzante del etanol, y este producto alcanza su concentración reforzante a través de su síntesis enzimática (por una R-salsolinol sintasa) o su síntesis no enzimática. Así, el primer objetivo de esta tesis fue detectar, caracterizar y purificar una enzima cerebral con actividad R-salsolinol sintasa en rata, que tenga como sustratos dopamina y acetaldehído. Se abordó la búsqueda de actividad R-salsolinol sintasa en las siguientes preparaciones de cerebro de ratas: homogeneizado completo, sobrenadante citosólico y proteínas purificadas en una resina modificada con dopamina. Se incubaron estas preparaciones con los sustratos dopamina y acetaldehído más cofactores que podrían ser requeridos por esta enzima. No se encontró actividad salsolinol sintasa en muestra alguna. Además, la revisión crítica de los artículos que reportan la presencia de la enzima como de peso molecular bajo 2 kDa y actividad de menor magnitud que la síntesis no enzimática, tornó su búsqueda infundada. Por lo tanto, se descartó esta línea de investigación. La búsqueda de una síntesis enzimática mostró que la velocidad de síntesis no enzimática de salsolinol podría ser suficiente para formar la cantidad reforzante de salsolinol. Luego de esta nueva evidencia, se siguió el objetivo alternativo en esta tesis: determinar cuál es el isómero de salsolinol reforzante, y si su concentración activa en el cerebro es alcanzable a partir de dopamina y acetaldehído. Primeramente, se determinó si las velocidades de síntesis no enzimática de los regioisómeros de salsolinol, salsolinol e isosalsolinol, son suficientemente rápidas para generar sus concentraciones reforzantes. Se midió la formación de salsolinol e isosalsolinol mediante cromatografía líquida de alta eficacia. Se calculó que la concentración reforzante de salsolinol, y no la de isosalsolinol, se alcanza en el cerebro partir de la concentración de acetaldehído reforzante; a través del uso de un modelo de estado estacionario que determina la concentración de salsolinol que se alcanza cuando sus velocidades de síntesis y de degradación se igualan. Debido a que las preparaciones de salsolinol (Sigma-Aldrich) usadas en estudios previos para determinar su efecto reforzante estaban contaminadas con isosalsolinol, era importante confirmar si el salsolinol sin isosalsolinol mantiene su efecto reforzante. Existe evidencia de que al menos un isómero de salsolinol activa al receptor μ de opioides y que, posiblemente, este sea el mecanismo que ejerce su efecto reforzante. Por esto, se realizó un estudio de acoplamiento molecular in silico de los 4 isómeros de salsolinol en el receptor μ de opioides (recientemente cristalizado) que pudiera identificar a cada isómero como activo o inactivo, antes de estudiarlos in vivo. Se observó que todos los isómeros de salsolinol calzan correctamente en el bolsillo de morfina del receptor μ de opioides. Esto no esclarece si cada isómero es agonista (o antagonista) del receptor. Para determinar in vivo si el salsolinol sin isosalsolinol es reforzante, se realizaron dos ensayos: (i) se estudió si, presionando una palanca, ratas se autoadministran intracerebralmente salsolinol; y (ii) se estudió si el salsolinol infundido intracerebralmente provoca una preferencia de lugar condicionada por esta infusión de salsolinol en ratas. La autoadministración intracerebral de salsolinol resultó negativa, posiblemente por la dificultad de la metodología. En el ensayo de preferencia de lugar, las ratas mostraron una tendencia a preferir el lado en el cuál se infundió salsolinol racémico, sin isosalsolinol, y no cuando se infundió la mezcla de ambos regioisómeros. Los resultados en este trabajo (i) indican que el salsolinol racémico no necesita de isosalsolinol para ser reforzante, sugieren que (ii) el isosalsolinol disminuye la capacidad reforzante del salsolinol, y que (iii) el salsolinol racémico alcanza su concentración reforzante no enzimáticamente y podría ser responsable del efecto reforzante del etanol. / Recently, it was shown that the metabolism of ethanol to acetaldehyde is essential for its consumption to be reinforcing; however the cerebral mechanism by which this effect occurs is not known. It has been postulated that salsolinol, a racemic non-enzymatic condensation product of acetaldehyde with dopamine, is responsible for the reinforcing effect of ethanol. The concentration of salsolinol in the brain increases after consumption of ethanol and salsolinol is a more powerfully reinforcing molecule than acetaldehyde and ethanol, possibly activating the μ-opioid receptor. However, the Sigma-Aldrich salsolinol that has been characterized in the literature studies comprises 4 isomers: R- and S-salsolinol, and R- and S-isosalsolinol (the latter is a secondary non-enzymatic condensation product of acetaldehyde and dopamine). Which of these molecules is reinforcing and if this molecule reaches its reinforcing concentration in the brain when ethanol is consumed remains to be elucidated. Furthermore, the existence of an enzyme R-salsolinol synthase whose substrates are acetaldehyde and dopamine has been reported. If the R-salsolinol formation is responsible for the reinforcing effect of ethanol, this enzyme may be necessary for ethanol to be reinforcing; however, its amino acid sequence has not been reported. From this background it is postulated that a condensation product of acetaldehyde and dopamine is responsible for the reinforcing effect of ethanol, and this product reaches its reinforcing concentration through either an enzymatic synthesis (by an R-salsolinol synthase) or a non-enzymatic synthesis. Thus, the first objective of this thesis was to detect, characterize and purify a brain enzyme with R-salsolinol synthase activity in rat, having dopamine and acetaldehyde as its substrates. The search for R-salsolinol synthase activity was addressed by using the following rat brain preparations: whole brain homogenates, cytosolic supernatant and proteins purified in a resin modified with dopamine. These preparations were incubated with the substrates dopamine and acetaldehyde, and cofactors that may be required by this enzyme. No salsolinol synthase activity was found in any sample. In addition, a critical review of articles reporting the presence of the enzyme with a molecular weight lower than 2 kDa and an activity of lesser magnitude than the non-enzymatic rate of synthesis, turned his search unfounded. Therefore, this line of research was discarded. The search for an enzymatic synthesis revealed that the rate of non-enzymatic synthesis of salsolinol may be sufficient for the formation of the reinforcing amount of salsolinol. After this new evidence, we followed the alternative objective in this thesis: to determine which salsolinol isomer is reinforcing and whether its active concentration in the brain can be reached from dopamine and acetaldehyde. Firstly, we investigated whether non-enzymatic synthesis rates of salsolinol and isosalsolinol were fast enough to generate its reinforcing concentrations. The formation of salsolinol and isosalsolinol was measured by high performance liquid chromatography. It was calculated that the reinforcing concentration of salsolinol, and not of isosalsolinol, can be reached in the brain if synthesized from the reinforcing concentrations of acetaldehyde; by means of a steady state model which determines the concentration of salsolinol achieved when its rate of synthesis and degradation are equal. Given that the salsolinol (Sigma-Aldrich) preparations used to determine its reinforcing effect in previous studies were contaminated with isosalsolinol, it was important to confirm that salsolinol without isosalsolinol retains its reinforcing effect. There is evidence that at least one salsolinol isomer activates the μ-opioid receptor and that, possibly, this is the mechanism that exerts its reinforcing effect. Therefore, we performed molecular docking studies of the 4 salsolinol isomers to the μ-opioid receptor (recently crystallized) aimed at identifying each isomer as active or inactive, before studying these in vivo. It was observed that all salsolinol isomers properly fit in the morphine pocket of the μ-opioid receptor. This result does not clarify if an isomer is an agonist (or antagonist) for this receptor. Subsequently, to determine in vivo if salsolinol without isosalsolinol is reinforcing, two assays were performed: (i) we studied if rats self-administered salsolinol directly in the brain by pressing a lever, and (ii) we examined whether salsolinol infused in the brain is capable of inducing a conditioned place preference in rats. The intracraneal salsolinol self-administration was negative, possibly because of the difficulty of the methodology. In the place preference test, rats showed a tendency to prefer the side on which racemic salsolinol without isosalsolinol was infused, and not when a mixture of both regioisomers was infused. The results in this study (i) indicate that racemic salsolinol does not need isosalsolinol to be reinforcing, suggest that (ii) the isosalsolinol decreases the salsolinol reinforcing capability, and (iii) racemic salsolinol reaches its reinforcing concentration non-enzymatically and could be responsible for the reinforcing effect of ethanol. / Fondecyt

No description available.

The term `quality' is regularly used by those who produce, promote and consume wine. However, the nature and features of wine quality are rarely explained. This study was designed to explore what drinkers consider to be the nature of wine quality and what they believe its features to be. Focus groups and individual and small group interviews were used to explore the conceptualisation and dimensions of wine quality, how that quality is assessed, and what its relevance may be. There were 105 informants, sourced from three states across Australia primarily by utilising friends and acquaintances of the researcher. Informants included consumers with a wide background of consumption practices and involvement levels, and also producers and those involved generally in the marketing, selling and promotion of wine. The study viewed wine as an aesthetic or quasi-aesthetic object and therefore also investigated drinkers' more general perceptions of the links between wine and other aesthetic products, placing the understanding of quality within that context.