Introdução - O receptor de vitamina D (VDR) é expresso em vários tecidos e quando este se encontra na sua forma ativada, modula a expressão de diversos genes. Esses incluem variações dos níveis circulantes de 1,25(OH) 2 D , variações na densidade mineral óssea, secreção e sensibilidade à insulina em resposta à glicose, suscetibilidade à diabetes tipo 1 e 2, obesidade, dislipidemias e hipertensão arterial. Atualmente, evidências têm sugerido o envolvimento da vitamina D com a síndrome metabólica. Objetivo - Investigar a concentração sérica da vitamina D e sua relação com a síndrome metabólica e avaliar a potencial associação entre estes fatores com a presença de polimorfismos no gene do receptor de vitamina D (VDR) em indivíduos adultos. Métodos - Trata-se de um estudo transversal, onde foram avaliados 372 indivíduos adultos. Foram coletadas amostras sanguíneas para dosagens laboratoriais da 25(OH)D 3 , PTH e exames bioquímicos relacionados à SM, além disso foram realizadas avaliações antropométricas (peso, altura, IMC). A síndrome metabólica (SM) foi classificada usando o critério proposto pelo National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III). A resistência a insulina foi estimada pelo cálculo de HOMA IR e a função da célula pelo cálculo de HOMA . A 25(OH)D foi dosada por HPLC e a insuficiência foi determinada pelo ponto de corte da curva Roc (52,6nmol/l). Foram avaliados também PTH intacto e cálcio sérico. Os polimorfismos BsmI e FokI foram detectados através da digestão das enzimas de restrições específicas para cada polimorfismo e confirmados através da técnica PCR alelo específico (ASPCR) ou amplificação de mutação refratária (ARMs) nos indivíduos com e sem SM (52 por cento vs. 48 por cento , respectivamente). A análise estatística inclui construção da curva ROC, teste T de Student, testes de correlação, teste de equilíbrio de Hardy-Weinberg, ANOVA, regressão logística binária (Odds Ratio). Estas análises foram conduzidas no software SPSS para Windows, versão 18 e p < 0,05 foi considerado significante. Resultados - A idade média dos participantes foi 51(15) anos, o IMC médio 29(6) kg/m 3 2 e 48 por cento apresentaram SM. Como esperado, os 3 indivíduos com SM apresentaram maiores valores de idade 57(12) anos, IMC 32(6) Kg/m , circunferência de cintura 103(13) cm, pressão sistólica 138(17) mmHg e diastólica 83(10) mmHg, glicemia de jejum 98(12) mg/dl, triglicérides 165(76) mg/dl, índices HOMA-IR 2.2(1.7) e 116(95), e menores valores de colesterol HDL colesterol 41(11) mg/dl. Com relação às concentrações séricas de 25(OH)D propostas pela análise da curva ROC, 43 por cento dos indivíduos com SM e 57 por cento dos indivíduos sem SM apresentam insuficiência desta vitamina. Correlações entre 25(OH)D 3 3 com PTH (r = -0.153; p = 0.005) e com circunferência da cintura (r = -0.106; p = 0.05) foram observada em todos os participantes. Considerando os polimorfismos do gene VDR, nos pacientes com SM, não houve associação entre o polimorfismo BsmI e os componentes da SM, HOMA e IR, 25(OH)D e PTH. No entanto, indivíduos sem SM, mas com homozigose para polimorfismo BsmI (genótipo recessivo bb ), apresentaram concentrações mais baixas de 25(OH)D 3 3 do que aqueles com o genótipo BB normal. Além disso, os indivíduos com SM e heterozigose para o polimorfismo FokI (genótipo Ff) têm maiores concentrações de PTH e HOMA do que aqueles com genótipo normal FF. Nesse mesmo grupo, os indivíduos com o genótipo recessivo ff têm maior resistência à insulina do que aqueles com genótipo Ff. Por outro lado, os pacientes sem SM, mas carregando o genótipo Ff, apresentaram maiores concentrações de triglicerídeos e baixos níveis de HDL do que aqueles com genótipo FF. A presença de um alelo f no genótipo (Ff ou ff) é, aparentemente, o suficiente para aumentar os níveis de triglicérides e resistência à insulina, quando comparados ao genótipo normal FF. Conclusão - Os resultados demonstram que o polimorfismo FokI no gene VDR associa-se a resistência à insulina e maiores concentrações de PTH em pacientes que apresentam SM. Além disso, o polimorfismo BsmI associa-se a menores concentrações de 25(OH)D em indivíduos sem SM. Portanto, esses novos dados indicam que polimorfismos no gene do VDR estão associados a diferentes fenótipos dos componentes da SM / Introduction - The vitamin D receptor (VDR) is expressed in many tissues and when it is in its activated form modulates the expression of several genes. These include changes in circulating levels of 1,25(OH)2D3, variations in bone mineral density, sensitivity and secretion of insulin in response to glucose, susceptibility to type 1 and 2 diabetes mellitus, obesity, dyslipidemia and hypertension. Currently, evidences have suggested the involvement of vitamin D with the metabolic syndrome. Objective - To investigate the serum concentrations of vitamin D and its relationship with metabolic syndrome (MS) and to evaluate the potential association between these factors with the presence of polymorphisms in vitamin D receptor gene in individuals adults. Methods - This is a cross-sectional study, which evaluated 243 adults and elderly. We collected blood samples for measurements of 25(OH)D3, iPTH, biochemical tests related to MS, and anthropometric evaluation (weight, height, BMI) were also assessed. MS was classified using the criteria proposed by the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III). Insulin resistance and cell secretion were estimated by calculating HOMA IR and HOMA , respectively. The 25(OH)D3 was measured by HPLC and insufficiency was determined by the Roc curve cut-off (52.6 nmol/L). Intact PTH and serum calcium were also evaluated. The BsmI and FokI polymorphisms were detected by enzymatic digestion with specific enzymes and confirmed by allele specific PCR (ASPCR) or amplification of refractory mutation (ARM) in individuals with or without MS (52 per cent vs. 48 per cent , respectively). Statistical analyses include construction of Roc curves, Student T test, correlation tests, Hardy-Weinberg test, ANOVA, binary logistic regression (odds ratio), and TwoStep Cluster. These analyses were conducted with SPSS for Windows, version 18 and p < 0.05 was considered significant. Results - The mean age of participants was 51(15) years, mean BMI was 29(6) kg/m2, and 48 per cent of individuals presented MS. As expected, subjects with MS showed higher values of age (57(12) years), BMI was 32(6) kg/m2, waist circumference was 103(13) cm, systolic blood pressure was 138(17) mmHg, diastolic was 83(10) mmHg, fasting glucose was 98(12) mg/dl, triglycerides was 165(76) mg/dl, HOMA-IR was 2.2(1.7), HOMA was 116(95), and lower levels of HDL cholesterol was observed (41 mg/dl(11)). With respect to serum 25(OH)D3 proposed by ROC curve analysis, 43 per cent of individuals with MS and 57 per cent of individuals without MS presented insufficiency of this vitamin. Correlations between 25(OH)D3, iPTH (r = -0,153, p = 0.005), and waist circumference (r = -0,106, p = 0.05) were observed in all participants. Considering the VDR gene polymorphisms, in patients with MetSyn, there is no association among BsmI polymorphism and components of MetSyn, HOMA IR and , 25(OH)D3, and PTH. However, subjects without MetSyn, but with homozygosis for BsmI polymorphism (recessive bb genotype), presented lower levels of 25(OH)D3 than those with normal BB genotype. In addition, individuals with MetSyn and heterozygosis for FokI polymorphism (Ff genotype) have higher concentrations of PTH and HOMA than those with normal FF genotype. In this same group, subjects with the recessive ff genotype have higher insulin resistance than those with Ff genotype. On the other hand, patients without MetSyn, but carrying the Ff genotype, have higher concentration of triglycerides and lower levels of HDL than those with FF genotype. Interestingly, the presence of one allele f in the (Ff or ff) genotype is apparently enough to increase triglycerides levels and insulin resistance, when compared to the normal FF genotype. Conclusion - The results show that FokI polymorphism in the VDR gene is associated to insulin resistance and higher concentrations of PTH in patients with MetSyn. Moreover, BsmI polymorphism is related to a lower concentration of 25(OH)D3 in individuals without MetSyn. Therefore, the results indicated that VDR gene polymorphisms are associated to different phenotypes of MetSyn components

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Made available in DSpace on 2019-03-30T00:18:44Z (GMT). No. of bitstreams: 0 Previous issue date: 2018-01-26 / Introduction: Hypovitaminosis D is already considered a global public health problem in several populations and age groups. A serum vitamin D insufficiency status has been proposed as a risk factor for several diseases, being associated with the incidence, progression and severity of these diseases, including asthma. Over the years, the incidence of asthma has been increasing markedly throughout the world, affecting more than 300 million people. Although increasing, there is still little research with direct evaluation of the role of vitamin D in asthma, especially in the pediatric range. Objective: To analyze the relationship between serum levels of vitamin D and asthma in childhood and adolescence. Methodology: Case-control study, carried out in an outpatient clinic for infantile pneumology and general surgery of a pediatric tertiary hospital. Results: A total of 159 children and adolescents were evaluated, of which 92 had asthma and 67 healthy children (control group). There is an appreciable occurrence of hypovitaminosis D in asthmatic and non-asthmatic children and adolescents, with a slight predominance in the asthmatic group, but without a statistically significant difference (p = 0.6626). It was observed that asthmatic subjects with allergic rhinitis were 4 times more likely to have hypovitaminosis D (OR = 4.12) when compared to asthmatic individuals without reports of allergic rhinitis (p = 0.027). There was also an association in obese asthmatic children and in use of inhaled corticosteroid therapy with hypovitaminosis D, but without statistical significance (OR = 2.87 and 1.05, respectively). The occurrence of hypovitaminosis D in children and adolescents in general is relatively high, but no difference in the asthmatic group. The main risk factor for asthmatics with hypovitaminosis D was the association with allergic rhinitis. Conclusion: To know better this disease is important to reduce the gaps in its relationship with chronic diseases in childhood, such as asthma, and thus develop effective strategies for control and treatment. Keynotes: Vitamin D; Asthma; Children; Adolescents. / Introdução: A hipovitaminose D já é considerada um problema de saúde pública mundial, em diversas populações e faixas etárias. Um status sérico de insuficiência de vitamina D vem sendo proposto como um fator de risco para diversas doenças, sendo associado com a incidência, progressão e gravidade destas, incluindo a asma. A incidência de asma, ao longo dos anos, vem aumentando acentuadamente, e, hoje, estima-se que afete mais de 300 milhões de pessoas em todo o mundo. Apesar de crescentes, ainda existem poucas pesquisas com avaliação direta do papel da vitamina D na asma, principalmente na faixa pediátrica. Objetivo: Analisar a relação entre os níveis séricos da vitamina D e asma, na infância e adolescência. Metodologia: Estudo caso-controle, realizado em ambulatório de pneumologia infantil e de cirurgia geral de um hospital terciário pediátrico. Resultados: Foram avaliados 159 crianças e adolescentes, sendo 92 com asma e 67 crianças saudáveis (grupo controle). Há uma apreciável ocorrência de hipovitaminose D em crianças e adolescentes asmáticos e não-asmáticos, com leve predomínio no grupo composto de asmáticos, mas sem diferença estatisticamente significativa (p= 0,6626). Observou-se que indivíduos asmáticos com rinite alérgica tinham 4 vezes mais chances de ter hipovitaminose D (OR=4,12) quando comparados com indivíduos asmáticos sem relato de rinite alérgica (p=0,027). Houve ainda uma associação em crianças asmáticas obesas e em uso de corticoterapia inalada com hipovitaminose D, porém sem significância estatística (OR=2,87 e 1,05, respectivamente). A ocorrência de hipovitaminose D em crianças e adolescentes em geral é relativamente alta, mas sem diferença do grupo de asmático. O principal fator de risco encontrado para asmáticos com hipovitaminose D foi a associação com rinite alérgica. Conclusão: Conhecer melhor essa enfermidade é importante para diminuir as lacunas sobre a sua relação com as doenças crônicas na infância, como asma, e assim desenvolver estratégias efetivas de controle e tratamento. Palavras-chave: Vitamina D; Asma; Crianças; Adolescentes.

Given the strong evidence for a beneficial role of vitamin D in diabetes and CVD pathogenesis, and the prevalence of vitamin D deficiency, vitamin D supplementation has been advocated for the prevention of cardiometabolic disease. To provide information on the effects of 5,000IU (125µg) vitamin D3 on cardiometabolic risk, a double blind, RCT in a cohort of overweight and obese UK adult males with plasma 25(OH)D concentration < 75nmol/L for a duration of 8 weeks was conducted. To the best of my knowledge, this is the first RCT to investigate the effect of 5,000IU (125µg) vitamin D3 on cardiometabolic markers in vitamin D insufficient, non-hypertensive and non-diabetic overweight and obese adult males.

Colorectal cancer (CRC) is common, with >1 million annual incidence worldwide and is associated with significant morbidity and mortality. Prevention is a particularly appealing strategy to combat CRC, but there is a paucity of well-founded mechanistic research in the area. CRC is a complex disorder, with both genetic and environmental factors influencing incidence. The heritable component of CRC variance is estimated to be ~35%, with ~5% due to highly penetrant mutations. Common genetic variance likely makes up the majority of the heritable component, yet a large proportion of heritability remains unexplained. One possible explanation is gene-environment interactions (GxE) where-by both genetic and environmental factors interact to influence risk. Observational data implicate vitamin D as an environmental risk factor in CRC aetiology and in-house data indicates that genotype at the GWAS identified CRC risk locus rs9929218 influences this association, i.e. a GxE. The rs9929218 locus is intronic within CDH1, a tumour suppressor gene, and present evidence suggests a gene-environment interaction model of vitamin D-induced CDH1 transcription dependent on genotype at the rs9929218 locus and mediated by VDR and FOXO transcription factors and SIRT1, a FOXO regulator. To test this model, two broad approaches were employed - an observational approach to assess the association between human plasma vitamin D status, rs9929218 genotype and normal colorectal mucosa CDH1 expression and an interventional approach treating cell lines, organoids and human subjects with vitamin D to assess genotype-specific effects. Observational analysis of vitamin D level (25OHD) in CRC cases identified a significant influence of age, gender, BMI and selected vitamin D pathway genetic variation, while analysis of 424 normal colorectal mucosa samples from CRC cases and cancer-free subjects demonstrated strong sampling, gender, age and site differences in gene expression. 25OHD was not significantly associated with mucosa gene expression at individual gene level. However, association with a number of pathways relevant to tumourigenesis, including 'cell adhesion', 'migration' and 'cell death' was seen, providing possible mechanism to the published observational data. Circulating 25OHD level was not associated with mucosa CDH1 expression, yet crucially, analysis demonstrated a strong additive gene-environment interaction effect between plasma 25OHD, the rs9929218 genotype and NM expression of VDR, FOXO and SIRT1 explaining ~70% of the variance of mucosal CDH1 expression. The interventional approach first investigated vitamin D effects on CRC cell lines and human colorectal mucosa organoids. Calcitriol, the active form of vitamin D, induced CDH1 expression in 4 CRC cell lines, with interaction effects explaining 66% of the variance of CDH1 expression. CDH1 induction was replicated in human colorectal epithelial organoids, a non-aberrant tissue model, while gene enrichment analysis from both cells and organoids implicate vitamin D in a number of processes relevant to CRC tumourigenesis including regulation of cell proliferation, differentiation, migration and apoptosis, consistent with the pleiotropic effects of vitamin D reported in the published literature. Finally, a novel human intervention study was undertaken to investigate the impact of vitamin D supplementation in human blood and rectal mucosa. Short-term high-dose supplementation of 50 participants significantly induced CDH1 expression in rectal mucosa, with significant gene interaction effects between 25OHD, rs992818 genotype and CDH1, VDR and FOXO expression, thus independently replicating the same gene interaction effects seen in the human observational study. Meanwhile, transcriptome profiling identified numerous pathways relevant to tumourigenesis significantly enriched after supplementation, validating several pathways also associated with vitamin D status in the observational study. In summary, the research presented in this thesis demonstrates that vitamin D treatment of cells, epithelial organoids and human subjects induces CDH1 expression, and that strong gene interaction effects involving the colorectal cancer risk locus rs9929218 modulate this effect. FOXO transcription factors influence the gene interaction effect, consistent with the proposed model of ligand dependent regulation of FOXO by VDR and transcription activation of the CDH1 gene by the FOXO complex dependent on rs9929218 genotype. These data provide support for rectal CDH1 expression as an intermediate biomarker for vitamin D chemopreventive studies and suggest that gene environment interactions underlie some of the missing heritability of CRC.

Adaptation to alterations in nutrient availability ensures the survival of organisms. In vertebrates, adipocytes play a decisive role in this process due to their ability to store large amounts of excess nutrients and release them in times of food deprivation. In todays western world, a rather unlimited excess of nutrients leads to high-caloric food consumption in humans. Nutrient overload together with a decreased energy dissipation result in obesity as well as associated diseases such as insulin resistance, diabetes, and liver steatosis. Obesity causes a hormonal imbalance, which in combination with altered nutrient levels can aberrantly activate G-protein coupled receptors utilizing diacylglycerol (DAG) as secondary messenger. Protein kinase D (PKD) 1 is a DAG effector integrating multiple hormonal and nutritional inputs. Nevertheless, its physiological role in adipocytes has not been investigated so far. In this thesis, evidence is provided that the deletion of PKD1 in adipocytes suppresses lipogenesis as well as the accumulation of triglycerides. Furthermore, PKD1 depletion results in increased mitochondrial biogenesis as well as decoupling activity. Moreover, PKD1 deletion promotes the expression of the β3-adrenergic receptor (ADRB3) in a CCAAT/enhancer-binding protein (C/EBP)-α and δ-dependent manner. This results in elevated expression levels of beige markers in adipocytes in the presence of a β-agonist. Contrarily, adipocytes expressing a constitutive active form of PKD1 present a reversed phenotype. Additionally, PKD1 regulates adipocyte metabolism in an AMP-activated protein kinase (AMPK)-dependent manner by suppressing its activity through phosphorylation of AMPK α1/α2 subunits. Thus, PKD1 deletion results in an enhanced activity of the AMPK complex. Consistent with the in vitro findings, mice lacking PKD1 in adipocytes demonstrate a resistance to high-fat diet-induced obesity due to an elevated energy expenditure caused by trans-differentiation of white into beige adipocytes. Moreover, deletion of PKD1 in murine adipocytes improves systemic insulin sensitivity and ameliorates liver steatosis. Finally, PKD1 levels positively correlate with HOMA-IR as well as insulin levels in human subjects. Furthermore, inhibition of PKD1 in human adipocytes leads to metabolic alterations, which are comparable to the alterations seen in their murine counterparts. Taken together, these data demonstrate that PKD1 suppresses energy dissipation, drives lipogenesis, and adiposity. Therefore, increased energy dissipation induced by several complementary mechanisms upon PKD1 deletion might represent an attractive strategy to treat obesity and its related complications. / Die Anpassung an veränderte Nährstoffverfügbarkeiten sichert das Überleben eines jeden Organismus. Dabei spielen in Vertebraten vorallem Adipozyten eine entscheidende Rolle. Sie haben die Fähigkeit, große Mengen überschüssiger Nährstoffe zu speichern und diese in Zeiten des Mangels wieder freizusetzen. Heutzutage herrscht jedoch besonders in Industrieländern ein ausreichendes Angebot an Nahrungsmitteln, was zu einer übermäßigen Kalorienzufuhr einzelner Individuen führt. Durch überschüssige Energiezufuhr in Verbindung mit einem verringerten Energieverbrauch kommt es zu Fettleibigkeit und damit verbundenen Erkrankungen wie Insulinresistenz, Diabetes und nichtalkoholischer Fettleber. Übergewicht führt zu einem hormonellen Ungleichgewicht, das im Zusammenhang mit veränderten Nährstoffgehalten, unter Verwendung von Diacylglycerol (DAG) als sekundären Botenstoff, G-Protein-gekoppelte Rezeptoren unkontrollierten aktiviert. Protein Kinase D (PKD) 1 ist ein DAG Effektor, der an unterschiedlichsten hormonellen und ernährungsphysiologischen Vorgängen beteiligt ist. Die zugrunde liegende physiologische Rolle von PKD1 in Adipozyten ist jedoch weitgehend unverstanden. In dieser Doktorarbeit wird gezeigt, dass eine Adipozyten spezifische PKD1 Defizienz sowohl Lipogenese als auch die Akkumulation von Triglyceriden unterdrückt. Darüber hinaus wird durch die Deletion von PKD1 sowohl der Mitochondriengehalt als auch die Dynamik erhöht und die Entkopplungsaktivität gesteigert. Zudem wird die Expression des β3-adrenergen Rezeptors (ADRB3) durch die PKD1 Defizienz in einer CCAAT/Enhancer-Bindungsprotein (C/EBP) -α und δ-abhängigen Weise gefördert. In Gegenwart eines β-Agonisten kommt es dadurch zu einer erhöhten Expression von Genen, die auf beige Fettzellen hindeuten. Im Gegensatz dazu weisen Adipozyten, die eine konstitutiv aktive Form von PKD1 exprimieren, einen umgekehrten Phänotyp auf. Zusätzlich reguliert PKD1 den Adipozytenmetabolismus abhängig von AMP-aktivierter Proteinkinase (AMPK). PKD1 unterdrückt die AMPK-Aktivität durch Phosphorylierung von AMPK-α1/α2-Untereinheiten. Daher steigert die PKD1-Deletion die Tätigkeit des AMPK-Komplexes. In Übereinstimmung mit den In-vitro-Daten zeigen Mäuse, denen PKD1 in Adipozyten fehlt, eine Resistenz gegen nahrungsinduzierte Fettleibigkeit. Dies lässt sich durch eine gesteigerte Transdifferenzierung von weißen zu beigen Fettzellen erklären, die einen erhöhten Energieumsatz aufweisen. Weiterhin verbessert die Deletion von PKD1 in Adipozyten der Maus die systemische Insulinsensitivität und schützt vor einer Lebersteatose. In humanen Fettzellen zeigen sich ähnliche Veränderungen im Metabolismus, wie bereits in den Adipozyten der Maus beobachtet wurden. Des Weiteren korreliert die Expression von PKD1 in humanem Fettgewebe positiv mit HOMA-IR, einem Marker für Insulin-Resistenz sowie den Insulinwerten beim Menschen. Zusammengefasst weisen die Daten dieser Thesis auf, dass PKD1 den Energieverbrauch unterdrückt und sowohl Lipogenese als auch Adipositas fördert. Adipozyten, denen PKD1 fehlt, zeigen demnach einen erhöhten Energieumsatz, der durch unterschiedliche komplementäre Mechanismen verursacht wird. Dadurch könnte sich eine attraktive Strategie zur Behandlung von Fettleibigkeit und den damit verbundenen Komplikationen ergeben.

There are numerous physical and mental health implications associated with burnout and Type D personality (TDP). TDP is defined by the presence of specific levels of both negative affectivity and social inhibition. The purpose of this research was to examine the severity and prevalence of burnout in working adults with TDP in comparison to those without TDP. Social cognitive theory was the theoretical foundation for this study. Online surveys were used to gather responses to the Type D Scale-14 (DS14), the standard for measure for assessing TDP, and the Burnout Measure, Short Version (BMS) from 333 participants. Quantitative analyses included the use of t tests, chi square tests, correlation, and regression analysis to determine (a) if there is a disparity in the severity and prevalence of burnout in individuals with and without TDP; (b) if levels of burnout correlate with levels of TDP; and (c) whether age, gender, or both moderate the relationship between burnout and TDP. According to study results, there was a difference in the prevalence of burnout between groups, as 25.5% of the 143 participants with TDP had burnout compared to 9.3% of the 190 participants without TDP. Mean scores on the BMS were also higher, indicating a significantly greater level of burnout severity for participants with TDP. A positive correlation was found between severity of TDP and severity of burnout. Age was found to moderate the relationship between burnout severity and TDP, but did not affect the relationship between burnout prevalence and TDP. Gender did not have any impact on burnout in individuals with TDP. Neither age nor gender affected the prevalence or severity of burnout in individuals without TDP. These results can be beneficial in healthcare environments for the development of treatments and preventative measures for patients, as well as used by businesses, which have increased expenditures associated with employee burnout.

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<p>The paper is an extensive review of inter organizational relation. Every organization wants to attain the competitive position in the Global market. The organization is effectively utilizing the R&D, production and marketing units, to develop the innovative products to accomplish the consumer needs.  The need for innovation is growing every day. The innovation success depends on the vital link between R&D, production and Marketing. In this paper concentrated on R&D and Marketing units at Ericsson Telecom Company, because these two units are combined and work together to discover new innovative products according to the customer requirements and to improve their operational excellence. The paper analyzed the relation between the R&D and Marketing departments of Ericsson is Strong or weak by using the factors like communication, decision making, formal and informal mechanism between the two units and also identified the relationship between these two units has it improved during last three years (2006- 2008).</p><p>Research Methodology: In this dissertation work the authors were taken the interpretative research. The researchers used Primary data and secondary data. The primary data collected by E mail questions to Ericsson's employees and secondary data collected by Journals, Ericsson home page, magazines and library online database etc.</p><p>Findings: The researchers analyzed the current relationship between R&D and Marketing units at Ericsson Organization. We scrutinized communication, decision making, and formal and informal mechanism are giving positive support and build the strong relationship between two units. The researchers also found few gaps between two units, but the overall relationship between two units were strong. It positively contributes to Ericsson's operational excellence.</p>

Synthèse générale des noyaux spiranniques Au cours de ce travail, nous avons développé une méthode générale permettant d'assembler rapidement les noyaux spiro[4,4+n]alcanones (5) et spiro[5,4+n]alcanones (6). Durant l'étape de condensation, les ß-cétocétals (4) et (7) ont été obtenus avec de bons rendements grâce à l'emploi de dichlorure de zinc comme acide de Lewis. Différentes bases ont été testées dans l'étape de spiroannélation. Les meilleurs résultats ont été obtenus en utilisant du tert-butanolate de potassium dans le THF en présence d'un équivalent d'eau. La sélectivité de notre méthodologie a également été examinée lors de la génération des composés spiranniques substitués (10), (11), (13) et (15). Durant cette étude, nous avons notamment montré que la condensation et la cyclisation sont complètement diastéréosélectives au départ des éthers d'énols silylés (12) et des orthoesters (2) et (3). Applications En utilisant notre séquence réactionnelle, nous avons synthétisé la spirocétone (18). La fonctionnalisation de ce dérivé spirannique (18), nous a conduit à l'intermédiaire (19) qui pourrait être ultérieurement utilisé pour la synthèse de produits naturels tel que (20), appartenant à la classe des spirovétivanes La spirodicétone (23) a été employée dans la synthèse total de l'Erythrodiène (24) et du Spirojatamol (25) par Fukumoto. Notre méthodologie nous a permis de générer cet intermédiaire clef (23) en seulement trois étapes.