No description available.

The purpose of this thesis is to determine what effects a dietary magnesium deficiency has on the discriminative avoidance behavior of rats. Three experiments were conducted. Experiment I compared two groups to determine the effects of magnesium deficiency on bar-press discriminative avoidance behavior. The results of Experiment l clearly illustrated that rats fed n diet deficient in magnesium began to lose their discriminative avoidance behavior after approximately five days with a steady decrease in performance over the remaining five days. Experiment II used a single subject design in an attempt to replicate Experiment I and to determine whether or not the magnesium deficiency effect could be reversed. Blood samples of serum magnesium for each rat were taken daily. The results confirmed Experiment I. A magnesium deficiency did cause a decrease in the performance of discriminative bar-press avoidance. Two of the four rats responded to the rehabilitation treatment with a corresponding increase in avoidance behavior with an increase in serum magnesium levels. The other two rats did not recover avoidance performance with rehabilitation, but did improve with regard to other behavioral measurements. Experiment III again employed two groups of rats in an attempt to determine the effects of a magnesium deficiency upon acquisition of a discriminative shuttle box avoidance performance. A pilot study to Experiment III showed a clear effect with normal controls displaying statistically more avoidance responses than the experimentals who received subnormal levels of magnesium. The results from Experiment III however showed no statistically significant difference between the controls and experimentals even though there was a statistical difference in serum magnesium concentration.

The effect of Mg status on the behavior of rats, as determined by nonspecific excitability level and audio genic seizure susceptibility, was investigated. Also, selected biochemical and neurological mechanisms mediating the chain of events from dietary magnesium deficit to the hyper excitability symptoms were examined. Weanling rats fed a low magnesium (10 ppm) diet for 14 days had reduced serum, cerebrospinal fluid and brain magnesium concentrations, and increased brain (Na+ K+)-ATPase activity. They exhibited increased NEL and became highly susceptible to audio genic seizures. Through dietary manipulation and intraperitoneal and cerebral intraventricular injections, it was possible selectively to alter either serum or cerebrospinal fluid magnesium concentrations. Both nonspecific excitability level and audio genic seizure susceptibility responded inversely to cerebrospinal fluid magnesium concentration, but not to serum magnesium, unless the latter was very high. In this instance, nonspecific excitability level but not seizure activity was depressed. Brain serotonin concentration was elevated in 150- 200 g rats fed a low magnesium diet for 21 days, compared with rats fed a control diet (0.73 μg/g fresh brain cf. 0.56 μg/g) . The magnesium deficient rat may serve as an excellent model for epilepsy research. The animal can often be revived following seizure, thus enabling the study of drug interactions while using a small number of subjects. Preliminary findings indicate that the most promising subjects are female rats between 3 and 5 weeks old at the start of feeding and who are fed a low magnesium diet 17 to 21 days. A procedure for determining (Na+ K+)-ATPase activity in rat brain homogenates, without requiring isolation or purification, is described. Computer modeling techniques have yielded expressions for equating enzyme activity to sodium, potassium, magnesium or calcium concentrations in the reaction media. A thorough statistical treatment of the data is presented.

Resumo: Introdução: O magnésio (Mg+2) é essencial para a vida, sendo importante em reações enzimáticas de vários tipos celulares, além de ter um papel importante no tecido ósseo e na homeostase mineral, podendo afetar diretamente a função das células ósseas e a formação da hidroxiapatita. O entendimento de fatores associados à modificação do metabolismo ósseo é de extremo interesse na reabilitação oral com implantes osseointegrados. O contato íntimo entre o metal do implante e o tecido ósseo é fundamental para o sucesso desta forma de tratamento. Diversas alterações sistêmicas, dentre elas a deficiência de Mg, podem representar um risco à osseointegração, podendo afetar a remodelação e diminuir o contato osso-implante. Objetivo: Avaliar, em animais com diferentes idades, o efeito da deficiência de magnésio na dieta sobre o metabolismo ósseo ao redor de implantes de Ticp (titânio comercialmente puro) com osseointegração estabelecida Material e Método: Foram utilizados 90 ratos machos, divididos em 2 grupos de acordo com a idade, sendo constituídos por animais jovens (60 dias) e adultos (150 dias). Após adaptação ao ambiente do biotério, todos os animais foram submetidos à cirurgia de instalação dos implantes nas tíbias direita e esquerda (dia 0). Decorrido um período de 60 dias, necessário à osseointegração dos implantes, os animais de cada grupo foram então subdivididos em 3 subgrupos conforme a dieta que iriam receber (dieta padrão, dieta com redução de 75% do magnésio necessário diariamente e dieta com redução de 90% do magnésio necessário diariamente), a qual foi administrada por mais 90 dias para instalação da deficiência mineral. No período de 24 horas antes do sacrifício foram coletadas amostras de urina. Após o sacrifício, foram coletadas amostras de soro para determinação da concentração de magnésio (Mg) e cálcio (Ca). / Abstract: Introduction: Magnesium (Mg+2) is essential for life, it is important for many enzymatic reactions of several kinds of cells. Magnesium is very important for bone and mineral homeostasis; it can directly affect bone cell functions and crystal formation (hydroxyapatite). The factors associated to the modification of bone metabolism are extremely important in oral rehabilitation of osseointegrated implants. The intimate bone to implant contact is fundamental for the success of this kind of treatment. Several systemic alterations, like magnesium deficiency, can represent a risk factor to implants osseointegration, it could affect bone remodeling and reduce the bone-implants contact. Objective: This study evaluated, in animals with different ages, the effect of magnesium deficiency in diet on bone metabolism around integrated implants. Methods: Ninety male Holtzman rats were divided in 2 groups by the age, young animals were 60 days years old and adult animals were 150 days years old. After acclimation to the vivarium, all the animals were submitted to a titanium implant at right and left tibias (day 0). After a healing period of 60 days the animals were ramdonly divided into 3 subgroups: rats were fed either normal control magnesium diet (CTL), a reduction of 75% of magnesium diet (Mg1) and a reduction of 90% of magnesium diet (Mg2). After 90 days on the experimental diet the animals were sacrificed. In order to confirm the systemic deficiency of magnesium the serum and urine were colleted for determination of magnesium and calcium concentration. In order to confirm the systemic osteopenia, a dual-energy X-ray absorptiometry (DEXA) was performed in lombar vertebra and femur. For evaluation of bone density around integrated implants, radiographs were taken. And for evaluation of magnesium deficiency in osseous metabolism, mRNA levels of RANKL and OPG were quantified. / Orientador: Silvana Regina Perez Orrico / Coorientador: Elcio Marcantonio Junior / Banca: Maria Lúcia Rubo de Menezes / Banca: Luis Antônio Borelli Barros / Mestre

Made available in DSpace on 2014-06-11T19:28:02Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-03-30Bitstream added on 2014-06-13T18:32:30Z : No. of bitstreams: 1 belluci_mm_me_arafo.pdf: 440178 bytes, checksum: 35317c8e4b52e9365849659880e3c237 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Introdução: O magnésio (Mg+2) é essencial para a vida, sendo importante em reações enzimáticas de vários tipos celulares, além de ter um papel importante no tecido ósseo e na homeostase mineral, podendo afetar diretamente a função das células ósseas e a formação da hidroxiapatita. O entendimento de fatores associados à modificação do metabolismo ósseo é de extremo interesse na reabilitação oral com implantes osseointegrados. O contato íntimo entre o metal do implante e o tecido ósseo é fundamental para o sucesso desta forma de tratamento. Diversas alterações sistêmicas, dentre elas a deficiência de Mg, podem representar um risco à osseointegração, podendo afetar a remodelação e diminuir o contato osso-implante. Objetivo: Avaliar, em animais com diferentes idades, o efeito da deficiência de magnésio na dieta sobre o metabolismo ósseo ao redor de implantes de Ticp (titânio comercialmente puro) com osseointegração estabelecida Material e Método: Foram utilizados 90 ratos machos, divididos em 2 grupos de acordo com a idade, sendo constituídos por animais jovens (60 dias) e adultos (150 dias). Após adaptação ao ambiente do biotério, todos os animais foram submetidos à cirurgia de instalação dos implantes nas tíbias direita e esquerda (dia 0). Decorrido um período de 60 dias, necessário à osseointegração dos implantes, os animais de cada grupo foram então subdivididos em 3 subgrupos conforme a dieta que iriam receber (dieta padrão, dieta com redução de 75% do magnésio necessário diariamente e dieta com redução de 90% do magnésio necessário diariamente), a qual foi administrada por mais 90 dias para instalação da deficiência mineral. No período de 24 horas antes do sacrifício foram coletadas amostras de urina. Após o sacrifício, foram coletadas amostras de soro para determinação da concentração de magnésio (Mg) e cálcio (Ca). / Introduction: Magnesium (Mg+2) is essential for life, it is important for many enzymatic reactions of several kinds of cells. Magnesium is very important for bone and mineral homeostasis; it can directly affect bone cell functions and crystal formation (hydroxyapatite). The factors associated to the modification of bone metabolism are extremely important in oral rehabilitation of osseointegrated implants. The intimate bone to implant contact is fundamental for the success of this kind of treatment. Several systemic alterations, like magnesium deficiency, can represent a risk factor to implants osseointegration, it could affect bone remodeling and reduce the bone-implants contact. Objective: This study evaluated, in animals with different ages, the effect of magnesium deficiency in diet on bone metabolism around integrated implants. Methods: Ninety male Holtzman rats were divided in 2 groups by the age, young animals were 60 days years old and adult animals were 150 days years old. After acclimation to the vivarium, all the animals were submitted to a titanium implant at right and left tibias (day 0). After a healing period of 60 days the animals were ramdonly divided into 3 subgroups: rats were fed either normal control magnesium diet (CTL), a reduction of 75% of magnesium diet (Mg1) and a reduction of 90% of magnesium diet (Mg2). After 90 days on the experimental diet the animals were sacrificed. In order to confirm the systemic deficiency of magnesium the serum and urine were colleted for determination of magnesium and calcium concentration. In order to confirm the systemic osteopenia, a dual-energy X-ray absorptiometry (DEXA) was performed in lombar vertebra and femur. For evaluation of bone density around integrated implants, radiographs were taken. And for evaluation of magnesium deficiency in osseous metabolism, mRNA levels of RANKL and OPG were quantified.

A series of four experiments was undertaken to determine both the quantitative and qualitative effects of magnesium deprivation on the urinary glycoproteins of adult and grow.ing rats. The glycoproteins were to be isolated in 0.58 M Na.Cl, the isolation technique for Tamm-Horsfall glycoprotein. Quantitative excretion was measured as ɣ hexose/rat/day. Qualitative analyses were reported as percent of dry weight of material isolated. A glycoprotein-containing material precipitated spontaneously from the urine before addition of NaCl. The dry weight ratio of spontaneously precipitating material (Fraction I) to salt-precipitable material (Fraction II) was 16 to one in normal animals, 3.4 to one in depleted animals. The hexose to amino acid to uronic acids ratio was the same for both fractions in both groups. No hexosamines were found in either fraction. The ash content was lower in Fraction I for deficient animals, but higher in Fraction II for deficient animals, when compared to control animals. Increased phosphate binding by Fraction II from deficient animals was indicated. A slight rise in total glycoprotein excreted daily was shown in animals fed a magnesium deficient diet, but not until after the first week, when irreversible kidney damage is initiated. Control animals whose weight ga:m was restricted to 32% 0£ normal excreted less of Fraction I per day. Amino acid patterns of both fractions from all groups were similar, but differed from those reported for human and sheep Tamm-Horsfall glycoprotein. All depleted animals showed a significant (p> 0.01} increase in kidney calcium content, and one group showed a significant (p> 0.01) decrease in kidney magnesium content at five weeks. / M.S.

Feeding growing rats a diet deficient in magnesium results in a deficiency condition whose major characteristic, that of kidney calcification, exhibits a mechanism very similar to that of urolithiasis in humans. Work done with lysosomal stabilizers and rats fed this deficient diet shows a reduction in calcification with the administration of these drugs. Accordingly, a study was undertaken to examine the mechanism of this process more closely with regards to a possible involvement of kidney lysosomes or the vacuolar apparatus. Lysosomal enzyme levels in the kidneys of rats fed either a low magnesium or a control diet were examined and an attempt made to determine if there were any differences due to treatments. While biochemical evidence suggests no differences, histochemically we see what appears to be a shift in activity to the area where calcification occurs. At the same time, while there is no effect from treatment, there appears to be a time effect, enzyme activity decreasing or increasing significantly with day. This seems to appear histochemically in the form of increased PAS sustainability in sections from rats on either low magnesium or control diet compared to rats on a rat pellet diet. / Master of Science

A deficiência dietética de magnésio (Mg), muitas vezes observada na população, em obesos, é condição que pode contribuir para a inflamação que, por sua vez, influencia o metabolismo do ferro. Com essa perspectiva, o objetivo deste trabalho foi avaliar a influência da deficiência de magnésio no processo inflamatório do tecido adiposo de ratos alimentados com rações hiperlipídicas e a repercussão desses efeitos na homeostase de ferro (Fe). Dois ensaios, com duração de 8 semanas, foram conduzidos, com ratos Wistar, machos, com peso inicial entre 180 e 200 g. No primeiro ensaio (Ensaio 1), os animais consumiram ad libitum rações normolipídicas com diferentes concentrações de Mg (500, 300 e 150 mg de Mg/kg; 100, 60 e 30% das recomendações para roedores, respectivamente). No segundo ensaio (Ensaio 2), os animais foram distribuídos em 3 grupos, que receberam, ad libitum, rações controle (normolipídica, 7% de lipídios; 16% do valor calórico total - VCT) e hiperlipídicas (32% de lipídios, uma mistura de óleo de soja e banha suína; 60% do VCT), sendo estas últimas adequadas ou restritas em Mg (500 e 150 mg de Mg/kg). A restrição dietética de Mg resultou em alterações tanto na composição corporal (diminuição da gordura e aumento da massa magra) como na distribuição compartimental de Mg (diminuição da excreção urinaria), sem alterar o status em Fe, estes efeitos foram mais exacerbados nos animais do grupo Mg-150 (Ensaio 1). Quando associada à dieta hiperlipídica (Ensaio 2), a restrição dietética de Mg levou a redução em sua excreção urinaria e fecal. Aumento do percentual de gordura corporal, hipertrofia do adipócito e alteração histopatológica indicativa de processo inflamatório no tecido adiposo visceral, além de menores concentrações de Fe no baço e menor saturação da transferrina, foram observados nos animais alimentados com as rações hiperlipídicas, independentemente da concentração dietética de Mg. Entretanto, nos animais que receberam ração hiperlipídica e restrita em Mg foi observado aumento da fragilidade osmótica do eritrócito, sugerindo maior atividade eritropoetica, apesar de a contagem de eritrócitos e reticul6citos não se alterar. É possível que a associação entre sobrecarga lipídica e restrição dietética de Mg resulte em aumento da demanda de Fe para eritropoese, antes de ocorrerem modificações nos parâmetros hematológicos. / The dietary deficiency of magnesium (Mg) often observed in obese is a condition that can contribute to the inflammatory process which, in turn, is a factor which influences the metabolism of iron. Thus, this study aimed lo assess the effect of magnesium deficiency on the inflammatory process of adipose tissue of rats fed high-fat diets and the impact of such effects on the homeostasis of iron (Fe). Two experiments with duration 8 weeks, were conducted with male Wistar rats, initial weight between 180-200 g. In the first test (Test 1), the animals consumed ad libitum normolipidic diets with different concentrations of Mg (500, 300, and 150 mg Mg / kg; 100, 60 and 30% of recommendations for rodents, respectively). In the second test (Test 2), the animals were divided into 3 groups, which received ad libitum control diets (nrmolipidic, 7% fat, 16% of the total caloric value - VCT) and hyperlipidemic (32% lipids, one mixture of soybean oil and lard, 60% of TAC), the latter being suitable or limited for mg (500 mg and 1S0 mg / kg). The dietary restriction of Mg resulted in changes in body composition (decreased fat and increased lean mass) and compartmental distribution of Mg (decreased urine output), without changing the status of Fe, these effects were exacerbated in group mg-150 (test 1). When combined with high-fat diet (trial 2), dietary restriction of Mg led to reduction in urinary and fecal excretion. Increase the percentage of body fat, adipocyte hypertrophy and histopathological changes indicative of inflammation in visceral adipose tissue, and lower concentrations of Fe in the spleen and lower transferrin saturation were observed in animals fed hyperlipidemic diets, independent of dietary concentration Mg. However, the animals fed high fat and restricted diet in Mg had increased osmotic fragility of erythrocytes, suggesting greater erythropoietic activity, despite the number of erythrocytes and reliculocy1es have not changed. It is possible that the association between lipid overload and dietary restriction of Mg result in increased demand for Fe for erythropoiesis occurred before changes in hematological parameters.

A resistência dos tecidos à ação da insulina é uma das principais complicações do excesso de peso. O aumento da gordura corporal, decorrente do consumo excessivo de nutrientes, é acompanhado por um quadro de inflamação crônica de baixa intensidade que está relacionado com a fisiopatologia da resistência à insulina. O magnésio (Mg) é um mineral envolvido com diversos processos fisiológicos e bioquímicos, especialmente aqueles relacionados ao metabolismo energético e ao controle glicêmico. Apesar de a deficiência deste mineral estar relacionada com condições pré-diabéticas, não está claro se a inadequação dietética promove alterações na sensibilidade à insulina e/ou se condições de resistência à insulina causam distúrbios na homeostase de Mg. O objetivo deste trabalho foi investigar os efeitos da restrição dietética de Mg e sua associação com o excesso de lipídios sobre a homeostase do mineral e a sensibilidade à insulina. Ratos Wistar, machos, com peso entre 97-123 g, permaneceram em gaiolas individuais por 24 semanas. Os animais receberam rações normolipídicas (CON, 7% de lipídios) ou hiperlipídicas (HL, 32% de lipídios), adequadas (CON e HL Mg; 500 mg de Mg/kg de ração; n = 6 para cada grupo) ou com restrição de Mg (Mg[50] e HL Mg[50]; 50 mg de Mg/kg de ração; n = 6 para cada grupo). O consumo da dieta HL promoveu maior acúmulo de tecido adiposo e maior ganho de peso corporal (p < 0,05). Os animais que consumiram rações com restrição de Mg apresentaram hipomagnesemia (p<0,01), menor excreção urinária (p < 0,01) e fecal (p < 0,001) de Mg e menor concentração óssea desse mineral (p < 0,001). No entanto, não foram observadas alterações no Mg muscular (p > 0,05). O grupo HL Mg[50] apresentou maior concentração de Mg no eritrócito quando comparado aos outros grupos. A restrição dietética de Mg, isoladamente, não promoveu alterações na sensibilidade à insulina (avaliada pelo teste de tolerância à insulina). Quando associada à dieta hiperlipídica, resultou em aumento da glicemia de jejum e em redução da sensibilidade à insulina, após 16 semanas (p < 0,01). Em nível molecular, a fosforilação da proteína quinase B (Akt) no músculo e no fígado foi significantemente menor no grupo HL Mg[50] (p < 0,05). A restrição dietética de Mg induziu ao aumento do conteúdo proteico dos canais TRPM6 e TRPM7 no rim, independentemente da sensibilidade à insulina. Os resultados deste estudo apontam que a deficiência de Mg tende a agravar as repercussões metabólicas do consumo de dietas hiperlipídicas na sensibilidade à insulina e que a resistência à insulina altera a compartimentalização do Mg. / Insulin resistance is one of the main complications of overweight. Increase body fat, due to excessive consumption of nutrients is accompanied by a chronic low-grade inflammation related to insulin resistance pathophysiology. Magnesium (Mg) is a mineral involved in many physiological and biochemical processes, especially those related to energy metabolism and glycemic control. Although Mg deficiency is related to pre-diabetic conditions, it is unclear whether dietary inadequacy promotes changes in insulin sensitivity and/or if conditions of insulin resistance cause disturbances in Mg homeostasis. This work aimed to investigate the effects of dietary Mg restriction and its association with high-fat diet on mineral homeostasis and insulin sensitivity. Male Wistar rat (97-123 g) remained in individual cages for 24 weeks. Animals received normolipid diet (CON, 7% lipid) or high-fat diet (HF, 32% lipid), adequate (CON and HF, 500 mg Mg / kg diet, n = 6 for each group) or Mg restricted (Mg[50] and HF Mg[50], 50 mg of Mg / kg of diet, n = 6 for each group). High-fat diet promoted a greater adipose tissue excess and body weight gain (p<0.05). Animals with Mg restricted diet had hypomagnesemia (p<0.01), lower Mg urinary (p<0.01) and faecal loss (p<0.001) and lower bone Mg concentration (p<0.001). However, no changes were observed in muscle Mg (p>0.05). HF Mg[50] group presented higher concentration of erythrocyte Mg when compared to the other groups. Singly, dietary Mg restriction did not induce changes in insulin sensitivity (as assessed by the insulin tolerance test). When associated with high-fat diet, dietary Mg restriction resulted in higher fasting glycemia and lower insulin sensitivity after 16 weeks (p<0.01). At the molecular level, protein kinase B (Akt) phosphorylation in muscle and liver was significantly lower in HFMg [50] group (p<0.05). Dietary Mg restriction induced increased protein content of renal TRPM6 and TRPM7 channels, regardless of insulin sensitivity. The results of this study indicate that Mg deficiency worsens metabolic effects of high-fat diet on insulin sensitivity. In addition, insulin resistance changes Mg compartmentalization.

by Xiao Gang. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 91-99). / Abstract also in Chinese. / ACKNOWLEDGEMENTS --- p.i / SUMMARY --- p.1 / Chapter 1 --- LITERATURE REVIEW / Chapter 1.1 --- MAGNESIUM --- p.3 / Chapter 1.1.1 --- GENERAL FUNCTION OF MAGNESIUM --- p.3 / Chapter 1.1.2 --- ABSORPTION AND METABOLISM OF MAGNESIUM --- p.6 / Chapter 1.1.3 --- CLINICAL ASPECTS --- p.8 / Chapter 1.1.4 --- METHODS OF DETERMINATION OF MAGNESIUM --- p.11 / Chapter 1.2 --- ZINC --- p.13 / Chapter 1.2.1 --- GENERAL FUNCTION OF ZINC --- p.13 / Chapter 1.2.2 --- ABSORPTION AND METABOLISM OF ZINC --- p.14 / Chapter 1.2.3 --- CLINICAL ASPECTS --- p.16 / Chapter 1.2.4 --- ASSESSMENT OF THE BODY ZINC STATUS --- p.19 / Chapter 1.2.5 --- METHODS OF DETERMINATION OF ZINC --- p.20 / Chapter 1.3 --- COPPER --- p.21 / Chapter 1.3.1 --- GENERAL FUNCTION OF COPPER --- p.21 / Chapter 1.3.2 --- ABSORPTION AND METABOLISM OF COPPER --- p.21 / Chapter 1.3.3 --- CLINICAL ASPECT --- p.25 / Chapter 1.3.4 --- LABORATORY ASSESSMENT OF COPPER STATUS --- p.28 / Chapter 1.3.5 --- METHODS FOR THE DETERMINATION OF COPPER --- p.29 / Chapter 1.4 --- SELENIUM --- p.31 / Chapter 1.4.1 --- GENERAL FUNCTION OF SELENIUM --- p.31 / Chapter 1.4.2 --- ABSORPTION AND METABOLISM OF SELENIUM --- p.31 / Chapter 1.4.3 --- CLINICAL ASPECTS --- p.34 / Chapter 1.4.4 --- ASSESSMENT --- p.36 / Chapter 1.4.5 --- METHODS OF DETERMINATION OF SELENIUM --- p.37 / Chapter 1.5 --- INTRODUCTION TO ATOMIC ABSORPTION SPECTROPHOTOMETRY --- p.38 / Chapter 1.5.1 --- PRINCIPLE OF AAS --- p.38 / Chapter 1.5.2 --- INSTRUMENTATION --- p.39 / Chapter 2 --- INTRODUCTION --- p.43 / Chapter 2.1 --- TRACE ELEMENT DEFICIENCY IN HOSPITAL PATIENT --- p.43 / Chapter 2.2 --- MICRONUTRIENT DEFICIENCY AMONG PATIENTS WITH ACUTE MYOCARDIAL INFARCTION --- p.44 / Chapter 2.2.1 --- MAGNESIUM DEFICIENCY --- p.44 / Chapter 2.2.2 --- CHANGE OF ZINC AND COPPER IN AMI --- p.47 / Chapter 2.2.3 --- SELENIUM DEFICIENCY --- p.50 / Chapter 2.3 --- OBJECTIVES OF THIS PROJECT --- p.52 / Chapter 3 --- MATERIALS AND METHODS / Chapter 3.1 --- PATIENTS SELECTION --- p.53 / Chapter 3.1.1 --- CONTROL GROUP --- p.53 / Chapter 3.1.2 --- AMI GROUP --- p.53 / Chapter 3.1.3 --- DIGOXIN TREATMENT GROUP --- p.54 / Chapter 3.2 --- ANALYTIC METHODS --- p.55 / Chapter 3.2.1 --- DETERMINATION OF SERUM Magnesium --- p.55 / Chapter 3.2.2 --- DETERMINATION OF SERUM ZINC --- p.57 / Chapter 3.2.3 --- DETERMINATION OF SERUM COPPER --- p.60 / Chapter 3.2.4 --- DETERMINATION OF SERUM SELENIUM --- p.63 / Chapter 4 --- RESULTS --- p.68 / Chapter 4.1 --- RESULTS OF EVALUATION OF ANALYTICAL --- p.68 / Chapter 4.1.1 --- RESULTS OF METHODS EVALUATION OF SERUM ZINC ASSAY --- p.68 / Chapter 4.1.2 --- RESULTS OF METHODS EVALUATION OF SERUM COPPER ASSAY --- p.71 / Chapter 4.1.3 --- RESULTS OF METHODS EVALUATION OF SERUM SELENIUM ASSAY --- p.73 / Chapter 4.2 --- RESULTS OF PATIENTS STUDY --- p.76 / Chapter 4.2.1 --- CONTROL GROUP --- p.76 / Chapter 4.2.2 --- PATIENTS WITH ACUTE MYOCARDIAL INFARCTION I DEMOGRAPHIC DATA --- p.77 / Chapter 4.2.3 --- DIGOXIN GROUP --- p.83 / Chapter 5 --- DISCUSSION --- p.85 / Chapter 5.1 --- AMI PATIENTS AND TRACE ELEMENT STATUS --- p.85 / Chapter 5.2 --- MAGNESIUM AND ZINC STATUS IN PATIENTS RECEIVING DIGOXIN TREATMENT --- p.88 / REFERENCE --- p.91 / LIST OF TABLES --- p.99 / LIST OF TABLES --- p.102 / TABLES & FIGURES