The syndrome known as Gastric Dilation Air Sacculitis (GDAS) has recently been described by Lumsden et al. (2002) for Chinook salmon (Oncorhynchus tshawytscha, Walbaum), in seawater (SW) culture in New Zealand. The syndrome is characterised by distended abdomens, gastric dilation and air sacculitis, increased feed conversion ratios (FCR) and mortality. Consequently, financial returns on affected stocks are greatly reduced. A study into the epidemiology and physiology of the syndrome was initiated, working with the major aquaculture company, The New Zealand King Salmon Company (NZKS). The study revealed causative factors of GDAS. GDAS was experimentally induced only in saltwater by feeding a commercially manufactured low-cohesion pelleted diet. Control groups were fed a different diet with high physical cohesion. Low-cohesion pellets have previously been associated with a high incidence of GDAS in commercial sea cages. These data implicated osmoregulatory stress and physical properties of the feed in GDAS development. In addition, gastrointestinal (GI) physiology in GDAS -affected and -control fish was characterised. The process of GDAS development in O. tshawytscha is characterised by a loss of smooth muscle tone of the stomach as it distends. Laplace's law (P= 2T/r, where P is the distending pressure, T is the tension in the wall and r is the radius of the cylinder) predicts that unless muscle mass increases, the ability of the stomach wall to contract will be lost and consequently a loss of GI motor function will result. Therefore, GI circular smooth muscle integrity in terms of (1) stimulated and maximal contractility, (2) osmoregulatory ability of the intestine and the (3) control of the GI system was studied in pathologically affected (+ve) and unaffected (-ve) smolt. Affected fish showed changes in GI circular smooth muscle function and osmoregulatory dysfunction. Feeding different diets induced distinct gastric evacuation patterns. The intestinal brake hypothesis is presented and argued to be the probable mechanism for GDAS development. GDAS (+ve) serum showed the presence of factors capable of contracting gut smooth muscle. In addition, potential humoral mediators of the intestinal brake in fish were investigated.

INTRODUCTION : S'il est fortement pressenti que la viscerosensibilité chimique intestinale, c'est-à-dire la détection des macronutriments dans le contenu intestinal est un des paramètres clé de la régulation de la prise alimentaire pendant la digestion, nos connaissances sur ces phénomènes sont encore très fragmentaires. On ignore notamment les mécanismes précis responsables de la détection des nutriments dans l'intestin et les modalités de transmission (nerveuse ou humorale) des signaux ainsi générés vers les centres de régulation du comportement alimentaire. OBJECTIF : L'objet de ces travaux a été de préciser les mécanismes de la détection des nutriments dans l'intestin et de déterminer l'implication du nerf vague dans la transmission des informations de la viscerosensibilité chimique intestinale vers le système nerveux central. RESULTATS : Les résultats obtenus ici confirment le modèle selon lequel l'intestin peut être perçu comme un organe sensoriel capable, pendant la digestion, de détecter la présence de certains macronutriments. Le nerf vague participe activement à la transmission de l'information générée au niveau de l'intestin vers le système nerveux central. CONCLUSIONS : Le système viscérosensoriel chimique intestinal est une composante sensorielle à part entière qui exerce un puissant rôle dans le contrôle de la prise alimentaire. Les avancées dans la compréhension de ces mécanismes et de leur rôle dans l'homéostasie énergétique ouvriront sans nul doute de nouvelles voies dans le développement de thérapies contre l'obésité.

Women seem to be largely protected against certain ‘welfare disorders’ such as cardiovacular disease and osteoporosis, during their fertile years.The metabolic changes observed during women’s non-menstrual states, i.e. during pregnancy, after the menopause and during use of oral contraceptives, indicate the importance of sex steroids and an undisturbed biological rhythm. Treatment with monophasic, combined oral contraceptives constitutes a model for the non-cyclic state.Growth hormone (GH) is a pituitary hormone that has major metabolic effects. The pattern of GH exposure to the target organ is of vital importance for the effects and changes in rhythm could possibly induce metabolic changes.Growth hormome, cholecystokinin (CCK), osteocalcin and angiotensinogen were used as markers for metabolic effects and the concentrations in serum were recorded in women during non-menstrual states. The clinical material comprised a total of 60 women: 18 healthy non-pregnant, 25 pregnant, one lactating woman and 16 postmenopausal women. Using a portable pump and a non-thrombogenic venous catheter, blood samples could be collected at 30-min intervals during 24-h periods. Furthermore, the effects of estrogen and GH in the regulation of angiotensinogen were investigated in an experimental model in the rat.Oral contraceptives were found to alter the secretion of GH towards a pattern of lower and more frequent peaks, though the total amount secreted during 24 h was unchanged. Oral contraceptives seem to induce a suppression of the 24-h concentrations of CCK, which may be important with respect to weight gain in some women. Osteocalcin in serum display a significant circadian variation. This emphasizes the need for careful timing of single point measurements and the value of continuous blood sampling. Oral contraceptives may reduce osteocalcin serum concentrations. The long-term effects on bone are unknown. During late pregnancy osteocalcin levels are extremely low, which could indicate osteoblast inhibition and reduced bone turnover. The mode of GH administration is important for the plasma concentration of angiotensinogen in the non-pregnant rat. Estrogen effects on this protein may be mediated via a modification of GH secretion. Oral contraceptives not only increase angiotensinogen concentrations in serum but also markedly enhance their variability. Further studies are needed to elucidate the relation between the individual pattern of angiotensinogen and hypertension. / <p>S. 1-42: sammanfattning, s. 43-88: 6 uppsatser</p> / digitalisering@umu

The syndrome known as Gastric Dilation Air Sacculitis (GDAS) has recently been described by Lumsden et al. (2002) for Chinook salmon (Oncorhynchus tshawytscha, Walbaum), in seawater (SW) culture in New Zealand. The syndrome is characterised by distended abdomens, gastric dilation and air sacculitis, increased feed conversion ratios (FCR) and mortality. Consequently, financial returns on affected stocks are greatly reduced. A study into the epidemiology and physiology of the syndrome was initiated, working with the major aquaculture company, The New Zealand King Salmon Company (NZKS). The study revealed causative factors of GDAS. GDAS was experimentally induced only in saltwater by feeding a commercially manufactured low-cohesion pelleted diet. Control groups were fed a different diet with high physical cohesion. Low-cohesion pellets have previously been associated with a high incidence of GDAS in commercial sea cages. These data implicated osmoregulatory stress and physical properties of the feed in GDAS development. In addition, gastrointestinal (GI) physiology in GDAS -affected and -control fish was characterised. The process of GDAS development in O. tshawytscha is characterised by a loss of smooth muscle tone of the stomach as it distends. Laplace's law (P= 2T/r, where P is the distending pressure, T is the tension in the wall and r is the radius of the cylinder) predicts that unless muscle mass increases, the ability of the stomach wall to contract will be lost and consequently a loss of GI motor function will result. Therefore, GI circular smooth muscle integrity in terms of (1) stimulated and maximal contractility, (2) osmoregulatory ability of the intestine and the (3) control of the GI system was studied in pathologically affected (+ve) and unaffected (-ve) smolt. Affected fish showed changes in GI circular smooth muscle function and osmoregulatory dysfunction. Feeding different diets induced distinct gastric evacuation patterns. The intestinal brake hypothesis is presented and argued to be the probable mechanism for GDAS development. GDAS (+ve) serum showed the presence of factors capable of contracting gut smooth muscle. In addition, potential humoral mediators of the intestinal brake in fish were investigated.

Submitted by Automa??o e Estat?stica (sst@bczm.ufrn.br) on 2017-12-04T21:15:19Z No. of bitstreams: 1 AmandaFernandesDeMedeiros_DISSERT.pdf: 1948827 bytes, checksum: 087502936007b7e2996629625be441ef (MD5) / Approved for entry into archive by Arlan Eloi Leite Silva (eloihistoriador@yahoo.com.br) on 2017-12-08T21:43:18Z (GMT) No. of bitstreams: 1 AmandaFernandesDeMedeiros_DISSERT.pdf: 1948827 bytes, checksum: 087502936007b7e2996629625be441ef (MD5) / Made available in DSpace on 2017-12-08T21:43:18Z (GMT). No. of bitstreams: 1 AmandaFernandesDeMedeiros_DISSERT.pdf: 1948827 bytes, checksum: 087502936007b7e2996629625be441ef (MD5) Previous issue date: 2017-11-03 / Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico (CNPq) / A obesidade ? uma das Doen?as Cr?nicas N?o Transmiss?veis de maior impacto na sa?de p?blica. A semente de tamarindo (Tamarindus indica L.) vem sendo estudada por possuir inibidor de tripsina, e, entre os atributos relacionados a esse inibidor parcialmente purificado (ITT), tem-se a sua rela??o com a saciedade, por aumentar colecistocinina (CCK) plasm?tica em animais eutr?ficos e seu efeito na redu??o da concentra??o circulante de leptina em animais com obesidade, entretanto sem aumento plasm?tico de CCK. Neste estudo, o ITT foi purificado, caracterizado e avaliado quanto ?s suas propriedades frente aos horm?nios CCK e leptina em ratos Wistar com obesidade. Para purifica??o e caracteriza??o desse inibidor, foram realizados: fracionamento do extrato bruto proteico com sulfato de am?nio; cromatografia de afinidade Tripsina-Sepharose; Cromatografia L?quida de Alta Efici?ncia (HPLC); determina??o da massa molecular por MS-ESI; sequenciamento parcial por MALDI-TOF com ISD; ensaio de estabilidade de temperatura e pH; estimativa dos par?metros de especificidade; eletroforese bidimensional (2-DE) e dosagens de CCK e leptina plasm?tica, por ELISA, em ratos com obesidade, submetidos ? gavagem oral (730 ?g/kg) do inibidor de tripsina purificado (ITTp) comparando-os a ratos com obesidade sem tratamento. Desse modo, o ITT purificado por HPLC foi denominado ITTp. Com o refinamento do m?todo, obtiveram-se, com base no ITTp, dois picos proteicos, as fra??es: Fr 1 e Fr 2. As massas moleculares m?dias dessas fra??es proteicas foram de [M+H]+ = 19594,690 Da e de [M+H]+ = 19578,266 Da, respectivamente. Ap?s redu??o e alquila??o, estimou-se a presen?a de 4 ciste?nas para Fr 1 e Fr 2. As sequ?ncias parciais obtidas para Fr 1 e Fr 2 foram de 54 e 53 res?duos de amino?cidos identificados e exatamente com a mesma sequ?ncia para ambas, sugerindo-se tratar da mesma mol?cula. O ITTp se mostrou resistente ? varia??o de temperatura at? 80?C, reduzindo cerca de 30% de sua atividade antitr?ptica quando em 100 ?C, e resistente aos extremos de pH. Para o ITTp estimou-se a IC50 de 2,7 x 10-10 mol.L-1 e a Ki de 2,9 x 10-11 mol.L-1. Na eletroforese bidimensional com ITTp foram revelados pontos isoel?tricos entre pH 5 e 6, al?m de um spot pr?ximo ao pH 8. Dessa forma, foi constatado que se trata de um inibidor de tripsina da fam?lia Kunitz. No experimento in vivo foi confirmada a a??o de ITTp sobre a redu??o de leptina plasm?tica, mas sem efeito sobre CCK em animais com obesidade, como j? atestado em estudos pr?vios com o ITT. A caracteriza??o bioqu?mica desse inibidor e os seus efeitos sobre CCK e leptina, observados em experimentos in vivo, constituem relatos in?ditos e promissores para uma prov?vel aplica??o biotecnol?gica. / Obesity is one of the non-communicable chronic diseases with a great impact on public health. The tamarind (Tamarindus indica L.) seed has been studied for its trypsin inhibitor and one of the attributes of this partially purified inhibitor (TTI) is its relationship with satiety, increasing cholecystokinin (CCK) in eutrophic and reducing leptin in obese animals. In this study the ITT was purified, characterized and evaluated for its properties against CCK and leptin in obese Wistar rats. For the purification and characterization of this inhibitor, the crude protein extract was fractionated with ammonium sulfate followed by trypsin-Sepharose affinity chromatography, two-dimensional electrophoresis (2-DE) and High Efficiency Liquid Chromatography (HPLC). TTIp molecular mass was determined by MS-ESI. Partial sequencing of TTIp was established by MALDI-ISD. Inhibitory specificity, stability to temperature and pH was characterized for TTIp. Plasma CCK and leptin was evaluated in rats submitted to oral gavage with TTIp (730 ?g / kg) comparing them to untreated obese rats. TTI was purified by HPLC with a single protein peak (ITTp). After refinement of the methods, two protein fractions were observed: Fr 1 and Fr 2, with average mass of [M+H]+ = 19594.690 Da and [M+H]+ = 19578.266 Da, respectively. The presence of 4 cysteines was estimated after reduction and alkylation of Fr 1 e Fr 2. The protein fractions showed 54 and 53 amino acid residues with exactly the same sequence. TTIp presented resistance to temperature variations, reducing about 30% of its anti-tryptic activity at 100 ?C, and resistance to pH extremes. TTIp IC50 was 2.7 x 10-10 mol.L-1 and Ki was 2.9 x 10-11 mol.L-1. The 2-DE revealed spots with isoelectric points between pH 5 and 6, and a spot near pH 8. TTIp characteristics are compatible with trypsin inhibitors from the Kunitz family. In the in vivo experiment, ITTp action on leptin reduction was confirmed, but no effect on CCK was observed in animals with obesity, corroborating previous studies using unpurified TTI. Biochemical knowledge of this molecule and the in vivo experiments shown here are novel and provide essential information for a biomolecule of possible biotechnological application.

Os azo corantes atualmente são considerados um assunto preocupante no que se refere à saúde pública e ambiental, pois quando lançados nos efluentes industriais contaminam o meio ambiente. Infelizmente, o método convencional de tratamento de efluentes têxteis, bem como de águas brutas que os recebem não são capazes de remover de maneira eficaz os corantes bem como sua toxicidade. Dentro deste contexto, este trabalho teve como objetivo avaliar a eficiência do tratamento de amostras aquosas por fotoeletrocatálise em comparação com a cloração convencional como método alternativo de degradação de azo corantes, usando os corantes Disperse Orange 1, Disperse Red 1 e Disperse Red 13 como modelo. Adicionalmente, foi avaliada a citotoxicidade dos corantes originais em condrócitos bovinos e células HepG2 em cultura em monocamadas e 3D. Para tanto, soluções desses corantes originais, clorados e fotoeletrocatalisados foram avaliadas utilizando ensaios de genotoxicidade/mutagenicidade, citotoxicidade e ecotoxicidade. Todos os corantes originais e clorados foram genotóxicos para as células HepG2 no ensaio cometa. Para o ensaio com Salmonella, a cloração reduziu a mutagenicidade dos corantes para a linhagem YG1041 e aumentou o efeito para a linhagem TA98, exceto o Disperse Red 13 que teve a mutagenicidade reduzida para as duas linhagens após cloração. A fotoeletrocatálise removeu tanto a genotoxicidade quanto a mutagenicidade. Somente o Disperse Orange 1 induziu apoptose pelo ensaio com anexina V, mas essa citotoxicidade foi removida após os tratamentos. Os corantes Disperse Red 1 e Disperse Red 13 foram tóxicos para D. similis enquanto somente o Disperse Red 1 foi tóxico para V. fischeri, sendo que os tratamentos por cloração e fotoeletrocatálise diminuíram a toxicidade apresentada. Os corantes Disperse Orange 1 e Disperse Red 13 passaram a ser tóxicos para V. fischeri após cloração, sendo que a fotoeletrocatálise do Disperse Red 13 também gerou produtos tóxicos para esse organismo. Assim, embora seja um método de tratamento promissor, atenção deve ser dada na avaliação e aplicação da fotoeletrocatálise como um método alternativo à cloração. Os corantes originais Disperse Orange 1 e Disperse Red 13 diminuíram a atividade mitocondrial dos condrócitos, sendo que o Disperse Red 13 também diminuiu a produção de lactato. Todos os corantes reduziram a atividade mitocondrial das células HepG2 em monocamadas, ao passo que o Disperse Orange 1 deixou de exercer esse efeito no cultivo em 3D. Somente o Disperse Red 13 diminuiu a atividade de desidrogenases das células HepG2 e tal efeito foi observado tanto no cultivo em monocamadas quanto em 3D. / The azo dyes are currently considered as a concern regarding the environmental and public health, since when released in industrial effluents they pollute the environment. Unfortunately, the conventional method of treatment of textile effluents is not able to effectively remove both dyes and their toxicity. Within this context, this study aimed to evaluate the effectiveness of the treatment of aqueous samples by photoelectrocatalysis compared to conventional chlorination as an alternative method of degradation of azo dyes, using the dyes Disperse Orange 1, Disperse Red 1 and Disperse Red 13 as a model. Additionally, we evaluated the cytotoxicity of the original dyes using HepG2 cells and chondrocytes cultured in monolayer and in 3D. To this end, solutions of these original dyes, chlorinated and photoelectrocatalysed were evaluated using tests of genotoxicity / mutagenicity, cytotoxicity and ecotoxicity. All the dyes, original and chlorinated, were genotoxic to HepG2 cells in the comet assay. For the test with Salmonella, chlorination reduced the mutagenicity of the dyes for the YG1041 strain and increased the effect for the TA98 strain, except Disperse Red 13, which had the mutagenic effect reduced for both strains after chlorination. The photoelectrocatalysis removed both genotoxicity and mutagenicity. Only Disperse Orange 1 induced apoptosis by annexin V assay, but this cytotoxicity was removed after treatment. The dye Disperse Red 1 and Disperse Red 13 were toxic to D. similis while only the Disperse Red 1 was toxic to V. fischeri, and the treatment by chlorination and photoelectrocatalysis decreased the toxicity showed. The dyes Disperse Orange 1 and Disperse Red 13 began toxic to V. fischeri after chlorination, and the photoelectrocatalysis of the Disperse Red 13 generated toxic products for this organism. So, while it is a promising treatment method, attention should be given in the evaluation and application of photoelectrocatalysis as an alternative to chlorination. The dyes Disperse Orange 1 and Disperse Red 13 decreased the mitochondrial activity of chondrocytes, and the dye Disperse Red 13 also decreased the production of lactate. All the dyes reduced the mitochondrial activity of the HepG2 cells cultured in monolayer, while the Disperse Orange 1 did no show this effect in 3D. Only Disperse Red 13 decreased the activity of dehydrogenases of HepG2 cells and this effect was observed both in monolayer and in 3D.

Os azo corantes atualmente são considerados um assunto preocupante no que se refere à saúde pública e ambiental, pois quando lançados nos efluentes industriais contaminam o meio ambiente. Infelizmente, o método convencional de tratamento de efluentes têxteis, bem como de águas brutas que os recebem não são capazes de remover de maneira eficaz os corantes bem como sua toxicidade. Dentro deste contexto, este trabalho teve como objetivo avaliar a eficiência do tratamento de amostras aquosas por fotoeletrocatálise em comparação com a cloração convencional como método alternativo de degradação de azo corantes, usando os corantes Disperse Orange 1, Disperse Red 1 e Disperse Red 13 como modelo. Adicionalmente, foi avaliada a citotoxicidade dos corantes originais em condrócitos bovinos e células HepG2 em cultura em monocamadas e 3D. Para tanto, soluções desses corantes originais, clorados e fotoeletrocatalisados foram avaliadas utilizando ensaios de genotoxicidade/mutagenicidade, citotoxicidade e ecotoxicidade. Todos os corantes originais e clorados foram genotóxicos para as células HepG2 no ensaio cometa. Para o ensaio com Salmonella, a cloração reduziu a mutagenicidade dos corantes para a linhagem YG1041 e aumentou o efeito para a linhagem TA98, exceto o Disperse Red 13 que teve a mutagenicidade reduzida para as duas linhagens após cloração. A fotoeletrocatálise removeu tanto a genotoxicidade quanto a mutagenicidade. Somente o Disperse Orange 1 induziu apoptose pelo ensaio com anexina V, mas essa citotoxicidade foi removida após os tratamentos. Os corantes Disperse Red 1 e Disperse Red 13 foram tóxicos para D. similis enquanto somente o Disperse Red 1 foi tóxico para V. fischeri, sendo que os tratamentos por cloração e fotoeletrocatálise diminuíram a toxicidade apresentada. Os corantes Disperse Orange 1 e Disperse Red 13 passaram a ser tóxicos para V. fischeri após cloração, sendo que a fotoeletrocatálise do Disperse Red 13 também gerou produtos tóxicos para esse organismo. Assim, embora seja um método de tratamento promissor, atenção deve ser dada na avaliação e aplicação da fotoeletrocatálise como um método alternativo à cloração. Os corantes originais Disperse Orange 1 e Disperse Red 13 diminuíram a atividade mitocondrial dos condrócitos, sendo que o Disperse Red 13 também diminuiu a produção de lactato. Todos os corantes reduziram a atividade mitocondrial das células HepG2 em monocamadas, ao passo que o Disperse Orange 1 deixou de exercer esse efeito no cultivo em 3D. Somente o Disperse Red 13 diminuiu a atividade de desidrogenases das células HepG2 e tal efeito foi observado tanto no cultivo em monocamadas quanto em 3D. / The azo dyes are currently considered as a concern regarding the environmental and public health, since when released in industrial effluents they pollute the environment. Unfortunately, the conventional method of treatment of textile effluents is not able to effectively remove both dyes and their toxicity. Within this context, this study aimed to evaluate the effectiveness of the treatment of aqueous samples by photoelectrocatalysis compared to conventional chlorination as an alternative method of degradation of azo dyes, using the dyes Disperse Orange 1, Disperse Red 1 and Disperse Red 13 as a model. Additionally, we evaluated the cytotoxicity of the original dyes using HepG2 cells and chondrocytes cultured in monolayer and in 3D. To this end, solutions of these original dyes, chlorinated and photoelectrocatalysed were evaluated using tests of genotoxicity / mutagenicity, cytotoxicity and ecotoxicity. All the dyes, original and chlorinated, were genotoxic to HepG2 cells in the comet assay. For the test with Salmonella, chlorination reduced the mutagenicity of the dyes for the YG1041 strain and increased the effect for the TA98 strain, except Disperse Red 13, which had the mutagenic effect reduced for both strains after chlorination. The photoelectrocatalysis removed both genotoxicity and mutagenicity. Only Disperse Orange 1 induced apoptosis by annexin V assay, but this cytotoxicity was removed after treatment. The dye Disperse Red 1 and Disperse Red 13 were toxic to D. similis while only the Disperse Red 1 was toxic to V. fischeri, and the treatment by chlorination and photoelectrocatalysis decreased the toxicity showed. The dyes Disperse Orange 1 and Disperse Red 13 began toxic to V. fischeri after chlorination, and the photoelectrocatalysis of the Disperse Red 13 generated toxic products for this organism. So, while it is a promising treatment method, attention should be given in the evaluation and application of photoelectrocatalysis as an alternative to chlorination. The dyes Disperse Orange 1 and Disperse Red 13 decreased the mitochondrial activity of chondrocytes, and the dye Disperse Red 13 also decreased the production of lactate. All the dyes reduced the mitochondrial activity of the HepG2 cells cultured in monolayer, while the Disperse Orange 1 did no show this effect in 3D. Only Disperse Red 13 decreased the activity of dehydrogenases of HepG2 cells and this effect was observed both in monolayer and in 3D.

Smith-Magenis syndrome (SMS) is a complex disorder caused by haploinsufficiency of RAI1 and characterized by sleep disturbances, behavioral abnormalities, mental retardation, and obesity in teens and adults. Rai1+/- mice are obese after 20 weeks. Dup(17)(p11.2) syndrome is a complex disorder associated with overexpression of RAI1. A transgenic mouse model of dup(17)(p11.2) syndrome overexpresses Rai1 and results in a mouse that is growth delayed. In order to characterize the obese phenotypes of mouse models of SMS and the role of RAI1 in obesity, daily food intake and serum levels of insulin, glucose, PPY, and leptin were measured; adiposity was studied by characterizing fat deposition; and gene expression was studied in the hypothalamus. These studies show that Rai1+/- mice are hyperphagic, consume more during the inactive light phase, and have altered satiety genes in the hypothalamus. Adiposity studies have shown WT females have a higher body fat content and visceral fat proportion than males, but Rai1-Tg and Rai1+/- females have similar fat deposition patterns as WT males. Hypothalamic gene expression studies show that many genes and pathways are affected by Rai1 and Rai1 dosage, including many genes associated with obesity and satiety.

As one of the major building blocks in a wireless receiver, the Analog-to-Digital Interface (ADI) provides link and transition between the analog Radio Frequency (RF) frontend and the baseband Digital Signal Processing (DSP) module. The rapid development of the radio technologies raises new design challenges for the receiver ADI implementation. Requirements, such as power consumption optimization, multi-standard compatibility, fast settling capability and wide signal bandwidth capacity, are often encountered in a low voltage ADI design environment. Previous research offers ADI design schemes that emphasize individual merit. A systematic ADI design methodology is, however, not suffciently studied. In this work, the ADI design for two receiver systems are employed as research vehicles to provide solutions for different ADI design issues. A zero-crossing demodulator ADI is designed in the 0.35µm CMOS technology for the Bluetooth receiver to provide fast settling. Architectural level modi&#64257;cation improves the process variation and the Local Oscillation (LO) frequency offset immunity of the demodulator. A 16.2dB Signal-to-Noise Ratio (SNR) at 0.1% Bit Error Rate (BER) is achieved with less than 9mW power dissipation in the lab measurement. For ADI in the 802.11b/Bluetooth dual-mode receiver, a con&#64257;gurable time-interleaved pipeline Analog-to-Digital-Converter (ADC) structure is adopted to provide the required multi-standard compatibility. An online digital calibration scheme is also proposed to compensate process variation and mismatching. The prototype chip is fabricated in the 0.25µm BiCMOS technology. Experimentally, an SNR of 60dB and 64dB are obtained under the 802.11b and Bluetooth receiving modes, respectively. The power consumption of the ADI is 20.2mW under the 802.11b receiving mode and 14.8mW under the Bluetooth mode. In this dissertation, each step of the receiver ADI design procedure, from system level optimization to the transistor level implementation and lab measurement, is illustrated in detail. The observations are carefully studied to provide insight on receiver ADI design issues. The ADI design for the Ultra-Wide Band (UWB) receiver is also studied at system level. Potential ADI structure is proposed to satisfy the wide signal bandwidth and high speed requirement for future applications.

Obesity is pandemic. Pharmacological treatment development depends on modeling the regulation of feeding, particularly by free fatty acids (FFA). Most models have been employed in the rat in vivo, and show FFA-stimulated intestinal satiety signals are dependent on the fat’s acyl chain-length, involve cholecystokinin (CCK) secretion, and are mediated by vagal afferents. I hypothesized that an in vitro mouse model could be employed, with sensitivity to measure afferent responses to nutrient stimuli. Male C57BL/6N mice were killed, the intestine harvested en bloc, and a jejunal section dissected with neurovascular mesenteric arcade emanating centrally. The tissue was placed in a Krebs-superfused chamber, the lumen cannulated with the outlet open to drain, and Krebs or other mediators were continuously perfused intraluminally. The dissected afferent nerve was placed in a suction electrode for extracellular recording. Afferent responses to distension and the perfusion of mediators (e.g. CCK or FFA) were tested. Preparations from normal mice (no surgery), or from mice following chronic subdiaphragmatic vagotomy or sham operation, were used to assess vagal afferent contributions. Luminally-perfused CCK (100 nM) increased afferent firing. This response was abolished with the CCK-1 receptor antagonist lorglumide (10 µM). The short-chain fatty acid (SCFA) sodium butyrate (30 mM) potentiated firing. The long-chain fatty acid (LCFA) sodium oleate (1-300 mM) activated concentration-dependent firing (EC50=25.35 mM) that was significantly greater at 30 mM than that evoked by butyrate. Lorglumide (30 µM) abolished the oleate (30 mM) response. The L-type Ca2+ channel (LTCC) inhibitor nicardipine (3 µM), intraluminally, potentiated the oleate response, while bath application abolished it. Vagotomy attenuated the oleate response. Vagotomy abolished the intraluminal CCK (100 nM) response, and attenuated the response to bath-superfused CCK. These findings support FFA chain-length-dependent mesenteric afferent activation and CCK involvement in oleate-induced firing, and suggest LTCC mediation of excitatory and inhibitory oleate response transduction pathways. The murine oleate response was shown to be mostly vagally-mediated, with some spinal contribution, and both vagal and spinal contributions to CCK responses were suggested. These data provide a basis for further investigation in vitro of cellular and molecular mechanisms of afferent satiety signals, and ultimately of obesity pathogenesis. / Thesis (Master, Physiology) -- Queen's University, 2010-06-29 15:56:08.387