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SOUSA, Auridéia Possidônio de. Síntese, caracterização e estudo de reatividade dos complexos cis-[Ru(bpy)2(4-bzpy)NO](PF6)3 e cis-[Ru(bpy)2(4-bzpy)CO](PF6)2 (onde bpy = 2,2’-bipiridina e 4-bzpy = 4-benzoilpiridina). 2015. 95 f. Dissertação (Mestrado em Química)-Universidade Federal do Ceará, Fortaleza, 2015. / Submitted by Celia Sena (celiasena@dqoi.ufc.br) on 2017-09-12T19:06:04Z No. of bitstreams: 1 2015_dis_apsousa.pdf: 2998037 bytes, checksum: fc4da604595d8a3a9ea76815a364ee13 (MD5) / Approved for entry into archive by Jairo Viana (jairo@ufc.br) on 2017-10-17T15:44:16Z (GMT) No. of bitstreams: 1 2015_dis_apsousa.pdf: 2998037 bytes, checksum: fc4da604595d8a3a9ea76815a364ee13 (MD5) / Made available in DSpace on 2017-10-17T15:44:16Z (GMT). No. of bitstreams: 1 2015_dis_apsousa.pdf: 2998037 bytes, checksum: fc4da604595d8a3a9ea76815a364ee13 (MD5) Previous issue date: 2015 / For a long time NO (nitric oxide) was known only as a toxic gas that in large concentrations caused damage to health. However, in the 1980s, studies have shown their participation in various physiological processes, including its activity as a mediation of the central nervous system, smooth muscle relaxation, participation in the ability of the immune system to destroy tumor cells and intracellular parasites, platelet adhesion and aggregation. Apparently, NO is not alone in many of these biological processes. Recently CO (carbon monoxide) is emerging as an important signaling molecule in these processes. Despite the beneficial effects, it is important to warn the danger of direct treatment with NO or CO gas, since it is difficult to determine the extent to which these gases are therapeutic, without causing toxic effects. This fact led recently the study of some metal complexes capable of releasing NO or CO in a controlled manner. This work was carried out the synthesis, characterization and evaluation of compounds of type cis-[Ru(bpy)2(4-bzpy)NO](PF6)3 and cis-[Ru(bpy)2(4-bzpy)CO](PF6)2 (where bpy = 2,2’-Bipyridina and 4-bzpy = 4-Benzoylpyridina). The characterization of the compounds was performed using electrochemical techniques (cyclic voltammetry), spectroscopic (vibrational spectroscopy in the IR region and electron spectroscopy), H and C nuclear magnetic resonance, X-ray diffraction monocrystals. The nitrosyl complex underwent reactivity testing as the release of NO0, showing good results as the electrochemical reduction, photochemical and biological front of a reducer. Once characterized, the carbonyl compound reactivity was also subjected to tests where the CO release was assessed by testing with myoglobin, using for this the spectrophotometric method. / Durante muito tempo o NO (óxido nítrico) foi conhecido apenas como um gás tóxico que em grandes concentrações causava danos à saúde. Entretanto, na década de 1980, estudos demonstraram sua participação em diversos processos fisiológicos, incluindo sua atividade como mediação do sistema nervoso central, relaxação da musculatura lisa, participação na capacidade do sistema imunológico de destruir células tumorais e parasitas intracelulares, adesão e agregação plaquetária. Ao que tudo indica, o NO não está sozinho nesses processos biológicos. Recentemente o CO (monóxido de carbono) vem surgindo como uma importante molécula sinalizadora em vários destes processos. Apesar dos efeitos benéficos, é importante alertar para o perigo do tratamento direto com NO ou CO gasosos, uma vez que é difícil determinar até que ponto estes gases são terapêuticos, sem provocar efeitos tóxicos. Esse fato estimulou, recentemente, o estudo de alguns complexos metálicos capazes de liberar NO ou CO de forma controlada. Assim, neste trabalho realizou-se a síntese, caracterização e avaliação de compostos do tipo cis-[Ru(bpy)2(4-bzpy)NO](PF6)3 e cis-[Ru(bpy)2(4-bzpy)CO](PF6)2 (onde bpy = 2,2’-Bipiridina e 4-bzpy = 4-Benzoilpiridina). A caracterização dos compostos foi realizada utilizando-se técnicas eletroquímicas (voltametria cíclica), espectroscópicas (espectroscopia vibracional na região do IV e espectroscopia eletrônica), ressonância magnética nuclear de 1H e 13C e difração de raios-X de monocristais. O nitrosilo complexo foi submetido a testes de reatividade quanto a liberação de NO0, apresentando bons resultados quanto a redução eletroquímica, fotoquímica e frente ao redutor biológico cisteína. Após caracterizado, o complexo carbonílico também foi submetido à testes de reatividade onde a liberação de CO foi avaliada através de ensaios com mioglobina, utilizando-se para isso o método espectrofotométrico.

CoordenaÃÃo de AperfeiÃoamento de NÃvel Superior / Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico / Estudos recentes, realizados no LFE da UFC, mostraram que o extrato aquoso da planta Alpinia zerumbet (Pers.) Burtt. et Smith (EaAz), conhecida popularmente como colÃnia, causa atividade vasodilatadora na aorta torÃcica isolada de rato. Objetivando encontrar o principio ativo desta planta, o EaAz foi fracionado com diferentes solventes e a atividade vasodilatadora das fraÃÃes foi avaliada em anÃis da aorta torÃcica isolada de rato. AlÃm disso, o mecanismo de aÃÃo da fraÃÃo acetato de etila obtida a partir do EaAz foi caracterizado. Ratos machos Wistar (250 a 300 g), oriundos do biotÃrio da UFC, foram sacrificados por deslocamento cervical e a aorta torÃcica removida e dissecada. Montaram-se os anÃis da aorta (4 a 5 mm) em cÃmeras orgÃnicas, contendo soluÃÃo de Krebs, aeradas com carbogÃnio e mantidas a 37ÂC, para a medida de variaÃÃes na tensÃo isomÃtrica. A integridade do endotÃlio foi avaliada utilizando-se a acetilcolina (ACh; 10-5 M) e, posteriormente, o EaAz e as fraÃÃes obtidas do EaAz, hexÃnica (FHxAz), acetato de etila (FAmAz), diclorometano (FDmAz) (0,15; 0,5; 1,5; 5; 15 e 50 g/mL) foram testados em preparaÃÃes contraÃdas com fenilefrina (Phe; 10-8 â 3x10-8 M). A fraÃÃo FAmAz, ACh e nitroprussiato de sÃdio foram testados em preparaÃÃes desprovidas de endotÃlio e tratadas com L-NAME (100 M), caribdotoxina (CTX; 100nM) mais apamina (100 nM), ODQ (30 M), catalase (500 U/mL), superÃxido dismutase (SOD; 500 U/mL) e PEG-catalase (500 U/mL). O EaAz e as fraÃÃes FHxAz e FAmAz foram capazes de relaxar, significativamente, a aorta torÃcica isolada de rato, apresentando os respectivos EC50 19,73, 11,15 e 9,08 (n = 5, 5 e 7, respectivamente, para cada grupo). Contudo, a fraÃÃo FDmAz nÃo apresentou atividade vasodilatadora. Depois, caracterizou-se a resposta vasodilatadora da fraÃÃo FamAz, resposta essa que foi abolida em preparaÃÃes desprovidas de endotÃlio e tratadas com L-NAME (n = 5), ODQ (n = 6) e PEG-Catalase (n = 2). Contudo, o efeito vasodilatador da fraÃÃo FAmAz permaneceu inalterado apÃs tratamento com CTX mais apamina, catalase e SOD na aorta torÃcica de rato (n = 5, 6 e 6, respectivamente, para cada grupo). Segundo nossos resultados, as fraÃÃes FAmAz e FHxAz apresentaram uma maior potÃncia na sua atividade vasodilatadora comparada ao EaAz. Este dado sugere que estas fraÃÃes, possivelmente, contÃm os princÃpios ativos responsÃveis pela atividade vasodilatadora do EaAZ. AlÃm disso, concluiu-se que a atividade vasodilatadora produzida pela FAmAz na aorta torÃcica de rato à dependente do endotÃlio e via NO-GMPc, talvez contando com a participaÃÃo das espÃcies reativas do oxigÃnio ao nÃvel intracelular / Recent studies conducted at the LFE showed that the aqueous extract from Alpinia zerumbet (Pers.) Burtt. et Smith (EaAz), popularly known as ColÃnia, causes vasodilation on isolated rat aortic rings. In order to find the active compound, the EaAz was diluted with different solvents and the vasodilator effect from the different fractions was analyzed on isolated rings of rat aorta. Additionally, the mechanism of action of the ethyl acetate fraction obtained from EaAz was characterized. Male rats Wistar (250 to 300g), provided by the vivarium of UFC, were terminated by cervical dislocation and the thoracic aorta was removed and dissected. The aortic rings (4 to 5 mm) were placed in chambers, which contained Krebs solution and carbogen and were kept at 37o C, in order to measure isometric tension variation. The endothelium integrity was assessed with acetylcholine (ACh; 10-5 M). Afterwards, the EaAz and the other fractions obtained from EaAz, hexane (FHxAz), ethyl acetate (FAmAz), dichloromethane (FDmAz) (0,15; 0,5; 1,5; 5; 15 and 50 g/mL) were tested in preparations that contained phenylephrine (Phe; 10-8 â 3x10-8 M). The FAmAz fraction, ACh and sodium nitroprussiate (SNP; 10-8 M) were tested in preparations without endothelium and treated with L-NAME (100 M), charybdotoxin (CTX; 100nM) plus apamine (100 nM), ODQ (30 M), catalase (500 U/mL), superoxide dismutase (SOD; 500 U/mL) and PEG-catalase (500 U/mL). The EaAz and the FHxAz and FAmAz fractions were able to relax significantly the isolated rat aortic rings, and EC50 was respectively 19,73, 11,15 and 9,08 (n = 5, 5 and 7, respectively, for each group). However, the FDmAz fraction did not present vasodilator activity. The vasodilatory effect of the FAmAz fraction was characterized. The vasodilator activity of the FAmAz fraction was impaired in preparation without endothelium and previously treated with L-NAME (n = 5), ODQ (n = 6) and PEG-Catalase (n = 2). However, the vasodilator activity of the FAmAz fraction remained unchanged after treatment with CTX plus apamin, catalase and SOD on the isolated rat aortic rings (n = 5, 6 and 6, respectively, for each group). The FAmAz and FHxAz fractions presented higher potency in their activity when compared to EaAz. This phenomenon suggests that these fractions possibly contain the active compound responsible for the EaAZ vasodilator effect. In addition, it was concluded that the vasodilator effect caused by the FAmAz fraction on the isolated rat aortic ring is endothelium-dependent and via NO-cGMP. We also believe that the intracellular reactive oxygen species play an important role on the vasodilator mechanism

Endothelium-derived vasodilators, i.e., nitric oxide (NO), prostacyclin (PGI2) and prostaglandin E2 (PGE2), play important roles in maintaining cardiovascular homeostasis. C-reactive protein (CRP), a biomarker of inflammation and cardiovascular disease, has been shown to inhibit NO-mediated vasodilation. The goal of this study was to determine whether CRP also affects endothelial arachidonic acid (AA)-prostanoid pathways for vasomotor regulation. Porcine coronary arterioles were isolated and pressurized for vasomotor study, as well as for molecular and biochemical analysis. AA elicited endothelium-dependent vasodilation and PGI2 release. PGI2 synthase (PGI2-S) inhibitor trans-2-phenyl cyclopropylamine blocked vasodilation to AA but not to serotonin (endothelium-dependent NO-mediated vasodilator). Intraluminal administration of a pathophysiological level of CRP (7 μg/mL, 60 min) attenuated vasodilations to serotonin and AA but not to nitroprusside, exogenous PGI2, or hydrogen peroxide (endothelium-dependent PGE2 activator). CRP also reduced basal NO production, caused tyrosine nitration of endothelial PGI2-S, and inhibited AA-stimulated PGI2 release from arterioles. Peroxynitrite scavenger urate failed to restore serotonin dilation, but preserved AA-stimulated PGI2 release/dilation and prevented PGI2-S nitration. NO synthase inhibitor L-NAME and superoxide scavenger TEMPOL also protected AA-induced vasodilation. Collectively, our results suggest that CRP stimulates superoxide production and the subsequent formation of peroxynitrite from basal released NO compromises PGI2 synthesis, and thus endothelium-dependent PGI2-mediated dilation, by inhibiting PGI2-S activity through tyrosine nitration. By impairing PGI2-S function, and thus PGI2 release, CRP could promote endothelial dysfunction and participate in the development of coronary artery disease.

Diss. (sammanfattning) Uppsala : Univ., 2002. / Härtill 5 uppsatser.

Doctor of Philosophy / Department of Anatomy and Physiology / Timothy I. Musch / Nitric oxide (NO) is synthesized via distinct NO synthase (NOS) enzymes and constitutes an essential cardiovascular signaling molecule. Whereas important vasomotor contributions of endothelial NOS (eNOS) have been well-described, the specific vasomotor contributions of nNOS-derived NO in healthy subjects during exercise are unknown. The purpose of this dissertation is to test the global hypothesis that nNOS-derived NO is a critical regulator of exercising skeletal muscle vascular control. Specifically, we utilized the selective nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) to investigate the effects of nNOS-derived NO on skeletal muscle vascular function within established rodent models of exercise performance. The first investigation (Chapter 2) identifies that nNOS inhibition with SMTC increases mean arterial pressure (MAP) and reduces rat hindlimb skeletal muscle blood flow at rest whereas there are no effects during low-speed (20 m/min) treadmill running. In Chapter 3 it is reported that nNOS inhibition with SMTC reduces blood flow during high-speed treadmill running (>50 m/min) with the greatest relative effects found in highly glycolytic fast-twitch muscles and muscle parts. Chapter 4 demonstrates that nNOS-derived NO modulates contracting skeletal muscle blood flow (increases), O2 consumption (VO2, increases), and force production (decreases) in the rat spinotrapezius muscle and thus impacts the microvascular O2 delivery-VO2 ratio (which sets the microvascular partial pressure of O2, PO2mv, and represents the pressure head that drives capillary-myocyte O2 diffusion). In Chapter 5 we report that systemic administration of the selective nNOS inhibitor SMTC does not impact lumbar sympathetic nerve discharge. This reveals that the SMTC-induced peripheral vascular effects described herein reflect peripheral nNOS-derived NO signaling as opposed to centrally-derived regulation. In conclusion, nNOS-derived NO exerts exercise-intensity and muscle fiber-type selective peripheral vascular effects during whole-body locomotor exercise. In addition, nNOS-derived NO modulates skeletal muscle contractile and metabolic function and, therefore, impacts the skeletal muscle PO2mv. These data identify novel integrated roles for nNOS-derived NO within healthy skeletal muscle and have important implications for populations associated with reduced NO bioavailability and/or impaired nNOS structure and/or function specifically (e.g., muscular dystrophy, chronic heart failure, advanced age, etc.).

Luk Wing Sze, Phoebe. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 173-190). / Abstracts in English and Chinese. / Abstract --- p.I / Acknowledgement --- p.XII / Publications Based on the Work in this Thesis --- p.XIII / Abbreviations --- p.IX / Table of Contents --- p.X / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1. --- Arthritis and Inflammation --- p.1 / Chapter 1.1.1. --- Tissue Reaction in Inflammation --- p.2 / Chapter 1.1.1.1. --- Mechanism of Vasodilatation --- p.2 / Chapter 1.1.1.2. --- Plasma Extravasation --- p.5 / Chapter 1.2. --- Neurogenic Inflammation --- p.8 / Chapter 1.2.1. --- Axon Reflex and Local Efferent Action of Primary Afferents --- p.9 / Chapter 1.2.2. --- Mediators of Neurogenic Inflammation --- p.10 / Chapter 1.2.3. --- Microvascular Effect of Substance P --- p.11 / Chapter 1.2.4. --- Microvascular Effect of Calcitonin Gene-Related Peptide --- p.13 / Chapter 1.3. --- Neurogenic Inflammation in the Joint --- p.16 / Chapter 1.3.1. --- Neuropeptides in Arthritic Knee --- p.16 / Chapter 1.3.2. --- Effects of Neuropeptides on Normal Knee --- p.16 / Chapter 1.3.3. --- Effects of Neuropeptides on Inflamed Knee --- p.17 / Chapter 1.3.4. --- Activation of Efferent Function of the Nerves --- p.19 / Chapter 1.4. --- Vanilloid Receptor --- p.20 / Chapter 1.4.1. --- The Use of Capsaicin as an Experimental Tool --- p.20 / Chapter 1.4.2. --- Identification of Vanilloid Receptor --- p.21 / Chapter 1.4.3. --- Molecular Biology of Vanilloid Receptor --- p.22 / Chapter 1.4.4. --- Electrophysiolgocial Properties of Vanilloid Receptors --- p.23 / Chapter 1.5. --- Activation of Vanilloid Receptors - A Detector of Physical Stimuli --- p.23 / Chapter 1.5.1. --- Exogenous Activators of Vanilloid Receptors --- p.25 / Chapter 1.5.2. --- Endogenous Activators of Vanilloid Receptors --- p.26 / Chapter 1.5.2.1. --- Anandamide as an Endovanilloid --- p.26 / Chapter 1.5.2.2. --- Other Possible Endovanilloid --- p.28 / Chapter 1.5.3. --- Biological Effects of Capsaicin --- p.29 / Chapter 1.5.3.1. --- Efferent Function: Neuropeptide Release --- p.29 / Chapter 1.5.3.2. --- Desensitization --- p.30 / Chapter 1.5.3.3. --- Neurotoxicity --- p.32 / Chapter 1.5.4. --- Biological Effects of Anandamide --- p.33 / Chapter 1.5.4.1. --- Vascular Effect of Anandamide --- p.33 / Chapter 1.5.4.2. --- Interaction of the Vanilloid and Cannabinoid System --- p.38 / Chapter 1.6. --- Aim of Study --- p.39 / Chapter Chapter 2 --- Methods --- p.40 / Chapter 2.1. --- Materials --- p.40 / Chapter 2.2. --- Protocols --- p.42 / Chapter 2.2.1. --- General Procedures --- p.42 / Chapter 2.2.2. --- Preparatory Procedure --- p.43 / Chapter 2.3. --- Measurement of Knee Joint Blood Flow --- p.46 / Chapter 2.3.1. --- Animal Preparation for Measuring Knee Joint Blood Flow --- p.48 / Chapter 2.3.2. --- Specific Procedures --- p.49 / Chapter 2.3.3. --- Image Analysis --- p.51 / Chapter 2.3.4. --- Data Analysis --- p.52 / Chapter 2.4. --- Quantification of Plasma Protein Extravasation --- p.52 / Chapter 2.4.1. --- Experimental Procedure --- p.53 / Chapter 2.4.2. --- Measurement of Evans Blue Content --- p.53 / Chapter 2.4.3. --- Measurement of Knee Joint Size --- p.54 / Chapter 2.5. --- Effect of Capsaicin on Acute Joint Inflammation --- p.54 / Chapter Chapter 3 --- Results --- p.55 / Chapter 3.1. --- Vanilloids on Knee Joint Blood Flow --- p.55 / Chapter 3.1.1. --- Capsaicin --- p.55 / Chapter 3.1.1.1. --- Cumulative Dosing of Capsaicin --- p.55 / Chapter 3.1.1.2. --- Time Course of Capsaicin-induced Vasodilatation --- p.55 / Chapter 3.1.1.3. --- VR1 Antagonists on Capsaicin-induced Vasodilatation --- p.57 / Chapter 3.1.1.4. --- NK1 Antagonists on Capsaicin-induced Vasodilatation --- p.58 / Chapter 3.1.1.5. --- CGRP Antagonist on Capsaicin-induced Vasodilatation --- p.60 / Chapter 3.1.1.6. --- Denervation on Capsaicin-induced Vasodilatation --- p.61 / Chapter 3.1.2. --- Anandamide --- p.62 / Chapter 3.1.2.1. --- Dose Responses of Anandamide --- p.62 / Chapter 3.1.2.2. --- Time Course of Anandamide-induced Vasodilatation --- p.63 / Chapter 3.1.2.3. --- VR1 Antagonist on Anandamide-induced Vasodilatation --- p.64 / Chapter 3.1.2.4. --- NK1 Receptor Antagonists on Anandamide-induced Vasodilatation --- p.65 / Chapter 3.1.2.5. --- CGRP Receptor Antagonist on Anandamide-induced Vasodilatation --- p.67 / Chapter 3.1.2.6. --- CB1 Receptor Antagonist on Anandamide-induced Vasodilatation --- p.67 / Chapter 3.1.2.7. --- CB2 Receptor Antagonist on Anandamide-induced Vasodilatation --- p.68 / Chapter 3.1.2.8. --- Anandamide Transporter Inhibitor on Anandamide-induced Vasodilatation --- p.69 / Chapter 3.1.2.9. --- Effects of Denervation on Anandamide-induced Vasodilatation --- p.70 / Chapter 3.2. --- Vanilloids on Plasma Extravasation --- p.71 / Chapter 3.2.1. --- Saline injection on Plasma Extravasation --- p.71 / Chapter 3.2.2. --- Capsaicin on Plasma Extravasation --- p.72 / Chapter 3.2.3. --- Capsaicin on Knee Joint Sizes --- p.73 / Chapter 3.2.4. --- Anandamide on Plasma Extravasation --- p.73 / Chapter 3.2.5. --- Anandamide on Knee Joint Size --- p.73 / Chapter 3.3. --- Effects of Vanilloid Agonists on Carrageenan-induced Acute Inflammation --- p.74 / Chapter 3.3.1. --- Capsaicin on Carrageenan-induced Plasma Extravasation --- p.74 / Chapter 3.3.2. --- Capsaicin on Carrageenan-induced Joint Swelling --- p.77 / Chapter 3.3.3. --- Anandamide on Carrageenan-induced Plasma Extravasation --- p.79 / Chapter 3.3.4. --- Anandamide on Carrageenan-induced Joint Swelling --- p.80 / Chapter Chapter 4 --- Discussion --- p.150 / Chapter 4.1. --- Capsaicin-induced Long Lasting Vasodilatation --- p.151 / Chapter 4.2. --- Capsaicin-induced Vasodilatation 一 a VR1 Mediated Effect? --- p.153 / Chapter 4.3. --- Substance P and CGRP in Capsaicin-induced Vasodilatation --- p.155 / Chapter 4.4. --- Anandamide-induced Vasodilatation --- p.157 / Chapter 4.5. --- VR1 in AEA-induced Vasodilatation --- p.159 / Chapter 4.6. --- Neuropeptides in AEA-induced Vasodilatation --- p.160 / Chapter 4.7. --- Cannabinoid Receptors in AEA-induced Vasodilatation --- p.161 / Chapter 4.8. --- Role of Anandamide Transporter in AEA-induced Vasodilatation --- p.163 / Chapter 4.9. --- A Neural Mechanism for Capsaicin- and AEA-induced Vasodilatation? --- p.164 / Chapter 4.10. --- Effects of Capsaicin and AEA on Plasma Extravasation --- p.167 / Chapter 4.11. --- Capsaicin and Anandamide in Acute Inflammation --- p.169 / Chapter 4.12. --- Conclusion --- p.170 / References --- p.173

The research to date, of transcutaneous electric nerve stimulation on cutaneous blood flow, is equivocal. The purpose of this report is to review the TENS body of knowledge, in particular synthesizing the literature on acupuncture stimulation of cutaneous blood flow with the two fold goal of creating a protocol to increase skin blood flow through the exogenous application of electrical stimulation, as well as creating an engaging engineering challenge for high school anatomy and physiology students. The hypothesis developed was TENS stimulation with electrode placement on specific acupuncture points would influence cutaneous blood flow as measured using laser Doppler flowmetry. The findings of this project did not support the hypothesis of TENS or Interferential electrical stimulation, in combination with acupuncture points or not, influencing skin blood flow. Perhaps this is due to the physiological differences between glabrous and non-glabrous skin and the different electrical resistances of each dermal layer, nerve stimulation, age and gender of subject or some combination thereof. These equivocal findings may also be the result of inconsistencies in testing protocols, such as subject preconditioning or not, subject’s position during administration of stimulation, electrode size and placement to name a few. Ultimately, this report provides a summary of the research to date, as well as outlining how this research could be adapted to supply engaging bio engineering challenges in the classroom including challenges to develop a model for delivering current to muscle; develop a model for skin blood flow management to name a few. / text

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.

Diss. (sammanfattning) Linköping : Linköpings universitet, 2007. / Härtill 5 uppsatser.