Call number: LD2668 .T4 1957 R43 / Master of Science

Student Number : 9201775F - MSc dissertation - School of Chemistry - Faculty of Science / The base/light-induced cyclisation (condensation) reaction between alkyl and carbonyl substituents on biaryl compounds discovered in the University of the Witwatersrand laboratories was used to synthesise benzo[c]carbazoles. Specifically, 5,7-dimethyl-7H-benzo[c]carbazole was synthesised from 2-methyl-1H-indole in 79 % yield over four steps. The reaction sequence involved bromination of 2-methyl-1H-indole at C-3 to give 3-bromo-2-methyl-1H-indole. The subsequent methylation of the amino group to give 3-bromo-1,2-dimethyl-1H-indole was followed by Suzuki coupling with acetophenone-2-boronic acid under non-aqueous reaction conditions to give 1-[2-(1,2-dimethyl-1H-indol-3-yl)phenyl]. Lastly, tBuOK/hν–induced cyclisation of the product yielded the desired benzo[c]carbazole. 10-Methoxy-5,7-dimethyl-7H-benzo[c]carbazole was synthesized analogously in 75% yield from 5-methoxy-2-methyl-1H-indole.

A antecipação de potássio (K) do milho segunda safra na cultura da soja é um sistema de adubação que pode apresentar aproveitamento do K-fertilizante pela sucessão soja - milho similar ao parcelamento de potássio para cada cultura, sem alterar o desempenho da sucessão soja - milho em região de Cerrado. A viabilidade da antecipação do K de base e cobertura do milho na cultura da soja se dá pela aplicação a lanço, que reduz o tempo de reabastecimento da semeadora durante o plantio. Isto permite rápida semeadura do milho para garantir seu desenvolvimento em época de precipitação pluviométrica adequada. O objetivo desta tese foi avaliar o desempenho da sucessão soja - milho, assim como o aproveitamento de K-fertilizante (acúmulo e recuperação), em razão da aplicação de doses de potássio feitas a lanço em dois sistemas de adubação (antecipação e parcelamento). Os estudos de campo foram feitos nas safras 2014/15 e 2015/16 no estado do Tocantins. Os tratamentos foram as doses 0, 60, 120 e 180 kg ha-1 de K2O com aplicação parcelada (40% - soja e 60% - milho) e antecipada, uma única vez na soja. As avaliações foram acúmulo de biomassa, potássio e magnésio (Mg) na parte aérea das plantas, a concentração K e Mg na folha diagnóstica, e a produtividade de soja e milho. Foram quantificados também, o acúmulo e a recuperação de potássio proveniente do fertilizante por meio de rubídio como traçador de potássio. Os resultados mostraram que antecipação de potássio não alterou a produtividade de grãos das culturas de soja e milho. No entanto, as doses de potássio mostraram efeito positivo na nutrição de K e negativo na de Mg, independente do sistema de adubação. O aproveitamento de K-fertilizante pela sucessão soja-milho foi similiar e até superior (22%) para a antecipação de potássio. Portanto, justifica-se ao produtor fazer a aplicação de potássio uma única vez, por ganhar agilidade durante a semeadura do milho. / Early application is a practice that brings potassium (K) fertilizer from corn to soybean in the soybean - corn succession. Recovery of K-fertilizer by these crops might be similar between early (to soybean) and split (soybean and corn) application, without change crops performance at Cerrado\'s region. Broadcast application allow these practices because planter stops is reduced: avoiding recharges of fertilizer during corn sowing and ensure a good plant development until the end of rainy season. So, the aim of this dissertation was assess crop`s performance, and uptake and recovery of K from fertilizer in the soybean - corn affected by potassim application at two practices (split application and early). Field study was conducted in the rainy season 2014/15 and 2015/16 at Tocantins State, Brazil. Treatments are rates 0, 60, 120 e 180 kg ha-1of K2O with two practices: spplit application (40% - soja e 60% - milho) and early application (once in soybean). Evaluations were aboveground biomass, potassium and magnesium (Mg) accumulation, and leaf K and Mg content, and yield of soybean and corn. Potassium uptake and recovery from fertilizer was meseuared by rubidium as a tracr of potassium. Results showed that early application did not change grain yield for soybean and corn. However, regardless practice, the rate of potassium showed positive effect on K plant nutrition, whilst negative effect was observed on Mg. Overall, K recovery from fertilizer by soybean - corn succession was similar and higher (22%) for early application. Therefore, farmers can do early application for improve corn sowing.

by Paul Li Wai Ching. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1990. / Includes bibliographical references. / Acknowledgements --- p.i / Summary --- p.ii / Index to Figures --- p.V / Index to Tables --- p.vii / Abbreviations --- p.viii / CONTENTS / Chapter Chapter 1 --- INTRODUCTION --- p.1 / Chapter Chapter 2 --- LITERATURE REVIEW : SALT AND HYPERTENSION / Chapter 2.1. --- Summary of evidence linking salt and hypertension --- p.4 / Chapter 2.1.1. --- Epidemiological studies --- p.4 / Chapter 2.1.2. --- Dietary intervention studies --- p.7 / Chapter 2.1.3. --- Experimental studies --- p.9 / Chapter 2.2. --- Cellular sodium transport --- p.10 / Chapter 2.2.1. --- The Sodium Pump --- p.10 / Chapter 2.2.2. --- Defects in sodium transport in hypertension --- p.14 / Chapter 2.3. --- Hypothesis linking salt to the pathogenesis of hypertension --- p.15 / Chapter 2.4. --- Evidence for the presence of natriuretic Hormone --- p.18 / Chapter 2.4.1. --- Indirect evidence --- p.18 / Chapter 2.4.2. --- Direct evidence --- p.18 / Chapter 2.4.3. --- The source and properties of natriuretic hormone --- p.20 / Chapter 2.4.4. --- Other natriuretic factors --- p.21 / Chapter Chapter 3 --- REGULATION OF THE SODIUM PUMP / Chapter 3.1. --- General introduction --- p.24 / Chapter 3.2. --- Regulation of the sodium pump by intracellular sodium --- p.24 / Chapter 3.3. --- "Effects of ethanol on Na+,K+-ATPase activity" --- p.26 / Chapter 3.4. --- "Effects of potassium depletion on Na+,K+-ATPase activity" --- p.27 / Chapter 3.4.1. --- In vivo studies of sodium pump regulation by potassium --- p.27 / Chapter 3.4.2. --- In vitro studies of sodium pump regulation by potassium --- p.29 / Chapter 3.5. --- Effects of cardiac glycosides on the sodium pump --- p.30 / Chapter 3.5.1. --- In vivo studies of sodium pump regulation by cardiac glycosides --- p.31 / Chapter 3.5.2. --- In vitro studies of sodium pump regulation by cardiac glycosides --- p.33 / Chapter 3.6. --- Effects of dietary salt on the sodium pump --- p.35 / Chapter 3.6.1. --- Acute effects of salt-loading --- p.35 / Chapter 3.6.2. --- Chronic effects of salt-loading --- p.36 / Chapter Chapter 4 --- AIMS OF THE STUDY --- p.39 / Chapter Chapter 5 --- MEASUREMENT OF THE SODIUM PUMP ACTIVITY / Chapter 5.1. --- General introduction --- p.41 / Chapter 5.2. --- The measurement of sodium pump activity --- p.42 / Chapter 5.2.1. --- The sodium pump transport activity --- p.42 / Chapter 5.2.2. --- Quantitation of the number of sodium pump sites --- p.45 / Chapter 5.2.3. --- The measurement of enzyme activity --- p.47 / Chapter (a) --- Introduction --- p.47 / Chapter (b) --- Preparation of tissues and detergent treatment --- p.48 / Chapter (c) --- Measurement of ATPase activity by measuring the rate of release of inorganic phosphate --- p.49 / Chapter (d) --- The coupled-enzyme assay --- p.53 / Chapter (e) --- The K+-stimulated 3-0-MFPase assay --- p.54 / Chapter Chapter 6 --- METHODS - ESTABLISHMENT AND EVALUATION / Chapter 6.1. --- Chemicals --- p.57 / Chapter 6.2. --- "Measurement of Na+,K+-ATPase activity by the rate of release of inorganic phosphate" --- p.58 / Chapter 6.3. --- "Automated coupled-enzyme assay of Na+,K+-ATPase activity" --- p.62 / Chapter 6.4. --- "The measurement of Na+,K+-ATPase activity by the potassium-stimulated 3-0-MFPase assay" --- p.67 / Chapter 6.5. --- Determination of protein concentration --- p.70 / Chapter 6.6. --- Statistical analysis --- p.73 / Chapter 6.7. --- Results --- p.73 / Chapter 6.7.1. --- Evaluation of the inorganic phosphate release method --- p.73 / Chapter 6.7.2. --- Evaluation of the coupled-enzyme method --- p.78 / Chapter 6.7.3. --- Evaluation of the K+-stimulated 3-0-MFPase method --- p.89 / Chapter 6.7.4. --- Evaluation of the protein determination method --- p.94 / Chapter 6.8. --- Discussion --- p.96 / Chapter Chapter 7 --- "THE EFFECTS OF DIGOXIN TREATMENT ON Na+,K+-ATPase ACTIVITY OF DIFFERENT TISSUES" / Chapter 7.1. --- Introduction --- p.101 / Chapter 7.2. --- Materials and Methods --- p.103 / Chapter 7.2.1. --- Animals and diets --- p.103 / Chapter 7.2.2. --- Drugs --- p.103 / Chapter 7.2.3. --- Pharmacokinetics of digoxin --- p.103 / Chapter 7.2.4. --- The digoxin regimes --- p.104 / Chapter 7.2.5. --- Preparation and deoxycholate treatment of tissue homogenates --- p.105 / Chapter 7.2.6. --- "Measurement of Na+,K+-ATPase activity" --- p.107 / Chapter 7.2.7. --- Digoxin radioimmunoassay --- p.107 / Chapter 7.2.8. --- Measurement of plasma electrolytes --- p.109 / Chapter 7.3. --- Results --- p.110 / Chapter 7.3.1. --- The pharmacokinetics of digoxin in the rat --- p.110 / Chapter 7.3.2. --- Plasma digoxin levels --- p.110 / Chapter 7.3.3. --- Effects of digoxin treatment on body weight --- p.113 / Chapter 7.3.4. --- Effects of digoxin treatment on plasma electrolytes --- p.117 / Chapter 7.3.5. --- "Effects of digoxin treatment on tissue Na+,K+-ATPase activity" --- p.119 / Chapter 7.4. --- Discussion --- p.129 / Chapter Chapter 8 --- THE SALT-LOADING EXPERIMENT / Chapter 8.1. --- Introduction --- p.140 / Chapter 8.2. --- Materials and Methods --- p.142 / Chapter 8.2.1. --- Animals --- p.142 / Chapter 8.2.2. --- The salt-loading protocol --- p.142 / Chapter 8.2.3. --- Preparation of crude tissue homogenates --- p.143 / Chapter 8.2.4. --- "Measurement of Na+,K+-ATPase activity" --- p.144 / Chapter 8.2.5. --- Analysis of urinary electrolytes --- p.144 / Chapter 8.2.6. --- Measurements of body weight and wet weight of kidney --- p.145 / Chapter 8.3. --- Results --- p.145 / Chapter 8.3.1. --- Effects of salt loading on the body weight --- p.145 / Chapter 8.3.2. --- Effects of salt loading on 24-hour urinary sodium excretion --- p.148 / Chapter 8.3.3. --- Effects of salt loading on the wet weight of kidney --- p.152 / Chapter 8.3.4. --- "Effects of salt loading on tissue Na+,K+-ATPase activity" --- p.152 / Chapter 8.4. --- Discussion --- p.163 / Chapter Chapter 9 --- CONCLUSIONS AND FUTURE WORK --- p.175 / REFERENCES --- p.183

by So Siu Cheung, Eddie. / "September 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

In this thesis, I focus on studies of the mechanism of inactivation in KcsA. Allosteric coupling between the pH gate and the selectivity filter in the protein is hypothesized to be the cause of inactivation. Allosteric coupling refers to changes at one site of a protein due to perturbations at a remote site. In chapter 3, I measured the potassium affinities at the selectivity filter at neutral and low pH, which corresponds to the closed and open conformation at the pH gate. The results show a three order of magnitude shift in the potassium affinity. This is direct evidence that the pH gate and the selectivity filter are coupled, in support of the activation-coupled inactivation hypothesis. The allosteric coupling factor, defined as the ratio of the affinities, can be used as a benchmark to study other factors in the allosteric process, such as the membrane and specific residues. Because of the potential deleterious effect of the acidic pH on the protein and membrane, we studied a mutant E118A&H25R, in which the pH gate is mutated to be open. Thus we were able to measure the K+ affinity change in the open and closed conformation at the pH gate at neutral pH. The results confirmed that the opening of the pH gate results in an energetic stabilization of the collapsed (K+-unbound) state, and shifts the K+ affinity towards looser binding. In chapter 4, I tested the important role of residue F103 in mediating allosteric coupling, as suggested by electrophysiology and crystallography studies. I mutated this residue and measured the allosteric coupling factor on the mutant. The affinity at low pH is much tighter than wild-type and the coupling factor is significantly reduced. From the spectra, I observe local structural changes on I100 and T74 as a result of F103A mutation, implying the interaction among F103, I100 and T74 to mediate the allosteric coupling. F103 is distant from the pH gate and the selectivity filter; its effect on the coupling and inactivation behaviors confirms that inactivation involves coupling between the pH gate and the selectivity filter. In chapter 5, I developed a method to probe those allosteric participants, such as F103 in KcsA by NMR measurements. I tested this method on KcsA, dissecting KcsA into various functional compartments. Various allosteric participants T75Cg T74Cg I100 were identified. The importance of residue T74 for the coupling was confirmed by electrophysiology and NMR thermodynamics characterization. In chapter 6, we applied SSNMR to probe the structural and magnetic properties of superatom clusters.

No description available.

Banca: José Roberto de Oliveira e Silva / Banca:Wilma Pereira Bastos Ramos / Banca: Gerhard Malnic / Banca: Sonia Malheiros Lopes Sanioto / Banca: Frida Zaladek Gil / Resumo: Estudamos o efeito da Angiotensina II sobre a secreção de potásssio em túbulo distal final (segmento conector e duto coletor cortical) através da técnica de microperfusão estacionária in vivo e mensuração da atividade catiônica por meio de microeletrodos contendo resina de troca iônica sensível a K+. A perfusão luminal com ANG II reduziu o fluxo secretório de potássio (JK+) observado no grupo controle de 0.900.19 nmol/cm2.s, n=12, para 0.51±0.05, n=9, (ANG II 10-12M), 0.700.22, n=27 (ANG II 10-11M) e 0.630.08 nmol/cm2.s, n=12 (ANG II 10-9M); (p<0.05 teste t pareado). Entretanto, na presença de dose elevada de ANG II (10-6M) não observamos efeito significante sobre o JK+. A presença de Losartan (10-6M), um bloqueador não peptídico do receptor AT1 reverteu o efeito inibitório da ANG II. No intuito de se avaliar a possibilidade da via PLA2/ácido araquidônico/PGE2 participar deste processo de regulação celular, uma vez que tais agentes participam da inibição de outros mecanismos de transporte que envolve a ativação da sinalização celular mediada por Angiotensina II, perfundimos luminalmente PGE2 o qual inibiu o fluxo secretório de K+ em ambas doses utilizadas no presente trabalho; Jk+ controle = 0.930.08 nmol/cm2.s, n=12 para 0.550.05 nmol/cm2.s, n=12 (PGE2 10-9M) e 0.470.04 nmol/cm2.s, (PGE2 10-6M), n=12, (p<0.01). A perfusão com Indometacina (10-5M), bloqueador inespecífico da via PLA2/Ácido Araquidônico/PGE2 associado a Angiotensina II (10-9M) aumentou o JK+ (0.95±0.12 nmol.cm-2.s-1, n = 13) quando comparado a perfusão isolada de ANG II (10-9M) (Jk+ = 0.630.05 nmol/cm2.s, n = 10); (p<0.05). Concluímos que a ANG II inibiu luminalmente a secreção distal de K+ provavelmente acoplado ao receptor AT1 e este efeito pode ser mediado pela via PLA2/Acido Araquidônico/ /PGE2 / Abstract: The effect of luminal ANGII on K+ secretion by late distal tubule (connecting segment and initial cortical collecting duct) was studied using "in vivo" stationary microperfusion and K-sensitive microelectrode techniques. Luminal perfusion of ANG II reduced Jk+ from a control value of 0.900.19 (n=12) nmol/cm2.s to 0.51±0.05, n=9, (10-12M), 0.700.22, n=27 (10-11M) and 0.630.08, n=12 (10-9M) nmol/cm2.s (p<0.05 by paired t-test). However, high doses of ANGII (10-6M) had no significant effect on Jk+. Losartan 10-6M, a non-peptide AT1 receptor blocker, reverted the inhibitory effect of ANGII. To test the possibility that the PLA2/arachidonic acid/PGE2 pathway, which had been shown to inhibit other transport mechanisms, is involved in ANGII-mediated cellular signaling cascades, PGE2 was perfused luminally (Jk+ control = 0.930.08, n=12 nmol/cm2.s; 10-9M PGE2, Jk+ = 0.550.05, n-12; 10-6M PGE2, Jk+ = 0.470.04), n=12; both doses reduced K+ secretion significantly (p<0.01). Perfusing with Indomethacin, an unspecific blocker of the PLA2/arachidonic acid/PGE2 path, (10-5M), plus ANG II (10-9M), JK+ increased to 0.95±0.12 (n=13) nmol.cm-2.s-1 compared to ANG II alone (Jk+ = 0.630.05, (n=13) nmol/cm2.s, p<0.05). During luminal perfusion with Indomethacin alone, no significant effect on K+ secretion was seen (Jk+ control = 0.730.05 (n=10) nmol/cm2.s, 10-6M INDO Jk+ = 0.630.07 (n=10), P>0.19. In conclusion, ANG II is able to regulate distal K+ secretion when applied to the tubule lumen, probably via AT1 receptors; it is suggested that the signalling path of the inhibitory effect of ANG II may involve PLA2/arachidonic acid/PGE2

No description available.

[by] Joseph T. Eisinger [and] Benjamin Bederson. / Portion of a thesis. "January 28, 1952." / Bibliography: p. 32. / Army Signal Corps Contract No. DA 36-039 sc-100. Project No. 8-102B-0. Dept. of the Army Project No. 3-99-10-022.