The recent momentum in energy research has simplified converting solar to electrical energy through photoelectrochemical (PEC) cells. There are numerous benefits to these PEC cells, such as the inexpensive fabrication of thin film, reduction in absorption loss (due to transparent electrolyte), and a substantial increase in the energy conversion efficiency. Alpha-hematite ([U+F061]-Fe2O3) has received considerable attention as a photoanode for water-splitting applications in photoelectrochemical (PEC) devices. The alpha-hematite ([U+F061]-Fe2O3) nanomaterial is attractive due to its bandgap of 2.1eV allowing it to absorb visible light. Other benefits of [U+F061]-Fe2O3 include low cost, chemical stability and availability in nature, and excellent photoelectrochemical (PEC) properties to split water into hydrogen and oxygen. However, [U+F061]-Fe2O3 suffers from low conductivity, slow surface kinetics, and low carrier diffusion that causes degradation of PEC device performance. The low carrier diffusion of [U+F061]-hematite is related to higher resistivity, slow surface kinetics, low electron mobility, and higher electro-hole combinations. All the drawbacks of [U+F061]-Fe2O3, such as low carrier mobility and electronic diffusion properties, can be enhanced by doping, which forms the nanocomposite and nanostructure films. In this study, all nanomaterials were synthesized utilizing the sol-gel technique and investigated using Scanning Electron Microscopy (SEM), X-ray Diffractometer (XRD), UV-Visible Spectrophotometer (UV-Vis), Fourier Transform Infrared Spectroscopy (FTIR), Raman techniques, Particle Analyzer, Cyclic Voltammetry (CV), and Chronoamperometry, respectively. The surface morphology is studied by SEM. X-Ray diffractometer (XRD) is used to identify the crystalline phase and to estimate the crystalline size. FTIR is used to identify the chemical bonds as well as functional groups in the compound. A UV-Vis absorption spectral study may assist in understanding electronic structure of the optical band gap of the material. Cyclic voltammetry and chronoamperometry were used to estimate the diffusion coefficient and study electrochemical activities at the electrode/electrolyte interface. In this investigation, the [U+F061]-Fe2O3 was doped with various materials such as metal oxide (aluminum, Al), dichalcogenide (molybdenum disulfide, MoS2), and co-catalyst (titanium dioxide, TiO2). By doping or composite formation with different percentage ratios (0.5, 10, 20, 30) of aluminum (Al) containing [U+F061]-Fe2O3, the mobility and carrier diffusion properties of [U+F061]-hematite ([U+F061]-Fe2O3) can be enhanced. The new composite, Al-[U+F061]-Fe2O3, improved charge transport properties through strain introduction in the lattice structure, thus increasing light absorption. The increase of Al contents in [U+F061]-Fe2O3 shows clustering due to the denser formation of the Al-[U+F061]-Fe2O3 particle. The presence of aluminum causes the change in structural and optical and morphological properties of Al-[U+F061]-Fe2O3 more than the properties of the [U+F061]-Fe2O3 photocatalyst. There is a marked variation in the bandgap from 2.1 to 2.4 eV. The structure of the composite formation Al-[U+F061]-Fe2O3, due to a high percentage of Al, shows a rhombohedra structure. The photocurrent (35 A/cm2) clearly distinguishes the enhanced hydrogen production of the Al-[U+F061]-Fe2O3 based photocatalyst. This work has been conducted with several percentages (0.1, 0.2, 0.5, 1, 2, 5) of molybdenum disulfide (MoS2) that has shown enhanced photocatalytic activity due to its bonding, chemical composition, and nanoparticle growth on the graphene films. The MoS2 material has a bandgap of 1.8 eV that works in visible light, responding as a photocatalyst. The photocurrent and electrode/electrolyte interface of MoS2-[U+F061]-Fe2O3 nanocomposite films were investigated using electrochemical techniques. The MoS2 material could help to play a central role in charge transfer with its slow recombination of electron-hole pairs created due to photo-energy with the charge transfer rate between surface and electrons. The bandgap of the MoS2 doped [U+F061]-Fe2O3 nanocomposite has been estimated to be vary from 1.94 to 2.17 eV. The nanocomposite MoS2-[U+F061]-Fe2O3 films confirmed to be rhombohedral structure with a lower band gap than Al-[U+F061]-Fe2O3 nanomaterial. The nanocomposite MoS2-[U+F061]-Fe2O3 films revealed a more enhanced photocurrent (180 μA/cm2) than pristine [U+F061]-Fe2O3 and other transition metal doped Al-[U+F061]-Fe2O3 nanostructured films. The p-n configuration has been used because MoS2 can remove the holes from the n-type semiconductor by making a p-n configuration. The photoelectrochemical properties of the p-n configuration of MoS2-α-Fe2O3 as the n-type and ND-RRPHTh as the p-type deposited on both n-type silicon and FTO-coated glass plates. The p-n photoelectrochemical cell is stable and allows for eliminating the photo-corrosion process. Nanomaterial-based electrodes [U+F061]-Fe2O3-MoS2 and ND-RRPHTh have shown an improved hydrogen release compared to [U+F061]-Fe2O3, Al-[U+F061]-Fe2O3 and MoS2-[U+F061]-Fe2O3 nanostructured films in PEC cells. By using p-n configuration, the chronoamperometry results showed that 1% MoS2 in MoS2-[U+F061]-Fe2O3 nanocomposite can be a suitable structure to obtain a higher photocurrent density. The photoelectrochemical properties of the p-n configuration of MoS2-α-Fe2O3 as n-type and ND-RRPHTh as p-type showed 3-4 times higher (450 A/cm2) in current density and energy conversion efficiencies than parent electrode materials in an electrolyte of 1M of NaOH in PEC cells. Titanium dioxide (TiO2) is known as one of the most explored electrode materials due to its physical and chemical stability in aqueous materials and its non-toxicity. TiO2 has been investigated because of the low cost for the fabrication of photoelectrochemical stability and inexpensive material. Incorporation of various percentages (2.5, 5, 16, 25, 50) of TiO2 in Fe2O3 could achieve better efficiencies as the photoanode by enhancing the electron concentration and low combination rate, and both materials can have a wide range of wavelength which could absorb light in both UV and visible spectrum ranges. TiO2 doped with [U+F061]-Fe2O3 film was shown as increasing contacting area with the electrolyte, reducing e-h recombination and shift light absorption along with visible region. The [U+F061]-Fe2O3-TiO2 nanomaterial has shown a more enhanced photocurrent (800 μA/cm2) than metal doped [U+F061]-Fe2O3 photoelectrochemical devices.

No description available.

I present a study done to determine the characteristics of the LHIRES III spectrograph on the 20 inch RC Optics telescope at Hard Labor Creek Observatory. I describe the settings of three different diffraction gratings, collimation and focus issues, and practical aspects of use. The spectrograph was used with a SBIG ST-8XME camera for all studies. Data collection was accomplished with the Maxim DL software package and analysis was completed with IRAF. Solutions for the dispersion relation with all three diffraction gratings were found. Several projects are underway with this instrument. I present time series spectra of α Vir to demonstrate the practical applications of the spectrograph. This non-radially pulsating star shows Doppler shifts that were recorded in the Si III 4552, 4568, 4574 Å triplet over the course of a night. The observed profile variations showed the spectrograph capable of exacting scientific work.

The overall objective of this research was to investigate the status of tumor necrosis factor-α (TNF-α), and molecules associated with its signaling, in the pathological state of hepatic steatosis. The effect of NSAID piroxicam, a cancer preventive agent also known to affect TNF-α signaling on hepatic steatosis, was also investigated. The biological state of the tissue was assessed by examining the expression of TNF-α signaling molecule in whole tissue, as well as in hepatic lipid raft. Lipid rafts are dynamic assemblies of cholesterol and sphingolipids, microdomains that form in the exoplasmic leaflet of the biological membranes shown to play a role in compartmentalization, modulation and integration of the cell signaling. In the present research, Zucker obese rats were used as a model of human obesity and insulin resistant state. These rats exhibit hepatic steatosis in adulthood similar to those noted in obese individuals. Female Zucker obese and lean rats (5 weeks old) were fed a semisynthetic diet with or without piroxicam (150 ppm). Zucker lean counterparts served as control. After 8 weeks of feeding, rats were euthanized and liver from each animal was collected. Liver tissue from each animal was processed for histology and biochemical analysis which included lipids and proteins (COX-1 and 2, TNF-α, TNF-RI and RII, IKK-β, IκB-α and NF-κB). Liver histology and the level of total lipids confirmed that Zucker obese rats had hepatic steatosis, which was further augmented by piroxicam treatment. Whole tissue protein expression, using western blot, showed that the steatotic liver differed from non-steatotic livers by having lower levels of TNF-RII. TNF-RII showed a trend which was inversely proportional to the pathological state of the tissue. The obese-piroxicam liver had the lowest level of TNF-RII and lean livers had the highest (p<0.05). The total NF-κB level was higher in the obese and obese-piroxicam groups compared to the lean or lean-piroxicam groups (p<0.05). Piroxicam treatment lowered the level of NF-κB in obese and lean livers. IκB-α was higher in obese livers than in lean livers. The nuclear level of NF-κB by western blot analysis showed the same pattern as noted in the whole tissue homogenate. However, the difference in the level between obese and lean was marked. The obese nuclei contained two to three fold higher levels of NF-κB protein than the lean liver nuclei. IκB-α level was significantly higher in the obese liver tissues and nuclei than their lean counterparts. While transcriptionally active NF-κB was higher (p<0.05) in the obese livers than in the lean livers, the difference between obese and lean groups was not as significant as that noted for the level of NF-κB assessed by western blot. This suggests that the proportion of active NF-κB present in the nuclear fraction is much higher in the lean than in the obese nuclei. Lipid raft was extracted and identified successfully from obese and lean livers. The total caveolin and flotillin levels were significantly higher in the liver lipid rafts of the obese-piroxicam than that of the other groups. This is the group that also exhibited higher steatosis. Piroxicam treatment significantly decreased the level of caveolin in the lean liver and significantly increased the level of flotillin in the obese liver. While COX-1 was not detectable, however, the level of COX-2 and TNF-RII in lipid raft was opposite to the level noted in the whole tissue homogenate. TNFRII was highest in the obese-piroxicam lipid raft and lowest in the lean-piroxicam lipid raft. TNF-RII, COX-2, IκB-α and NF-κB proteins were the molecules profoundly affected by the pathological state of the tissue and piroxicam treatment. This research is the first to report the presence of IκB-α in the nuclear compartment with a higher level in the nuclei and whole tissue in the obese liver than in the lean liver. This research demonstrates that TNF-α to NF-κB axis is altered in steatotic liver, and analysis of lipid rafts in steatotic and non-steatotic liver demonstrates that lipid rafts play a distinct role in modifying the biological availability of key proteins in the pathological state of liver steatosis.

Two types of fuzzy linear programming i.e. fuzzy number linear programming and interval number linear programming are used for optimization problems. In interval form of linear programming we convert the inequalities from the feasible region, containing intervals as coefficients, to two groups of inequalities characterized by real, exact coefficients values. Then classical programming has been used to achieve an optimal solution in the feasible region. In fuzzy number linear programming, α‐cuts and LR forms of fuzzy numbers as coefficients have been used to find optimal solution in the feasible region. Finally the numerical examples and their solutions are attached to provide explanations of procedures.

No description available.

Skeletal muscle injury results in functional deficits that can take several weeks to fully recover. Ultimate recovery of function is dependent on the muscle’s ability to regenerate, a highly coordinated process that involves transient muscle inflammation and the replacement of damaged myofibers. Instrumental in the inflammatory response, is the pro-inflammatory cytokine TNF-α. Expression of TNF-α is thought to be regulated, in part, by the stress sensing 70 kDa heat shock protein (Hsp70). However, it remains unclear how Hsp70 alters TNF-α following injury, and if so, how these changes affect skeletal muscle repair. Therefore, we up-regulated Hsp70 expression using 17-allylamino-17-demethoxygeldanamycin (17-AAG) prior to and following BaCl2-induced injury, and assessed TNF-α and myogenin content. Regenerating fiber cross-sectional area (CSA) and in vivo isometric torque were also analyzed in the weeks following the injury. Treatment of 17-AAG resulted in a ~5 fold increase in Hsp70 of the uninjured muscle, but did not affect any other biochemical, morphological or functional variables compared to controls. In the days following the injury, TNF-α and myogenin were elevated and directly correlated. At these earlier time points (≤7 days), treatment of 17-AAG increased TNF-α above that of the injured controls and resulted in a sustained increase in myogenin. However, no differences were observed in regenerating fiber CSA or in vivo torque production between the groups. Together, these data suggest that Hsp70 induction increases TNF-α and myogenin content following BaCl2-induced injury, but does not appear to alter skeletal muscle regeneration or attenuate functional deficits in otherwise healthy young mice.

Sleep fragmentation induces acute inflammation and increases glucocorticosteroids in vertebrates. Obesity and sleep fragmentation are often concurrent pro-inflammatory conditions in patients with obstructive sleep apnea. Despite the association between the two, their simultaneous effects on immune and endocrine profiles have not been explored. In the first experiment, we investigated changes in proinflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokine gene expression in the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) in mice exposed to various intervals of sleep fragmentation. Serum corticosterone concentration was also assessed. Sleep was disrupted in male C57BL/6J mice using an automated sleep fragmentation chamber (Lafayette Industries), which involved movement of a sweeping bar at specified intervals. Mice were exposed to bar sweeps every 20 sec (high sleep fragmentation; HSF), 120 sec (low sleep fragmentation; LSF), or the bar remained stationary (control). Trunk blood and tissue samples were collected after 24 h of SF. It was found that HSF is a potent inducer of inflammation in the periphery (IL-1β: adipose, heart, and hypothalamus), but leads to upregulation of antiinflammatory cytokines in the brain (TGF-β1: hypothalamus and hippocampus), despite elevated serum corticosterone. Due to the association between obesity and SF, this experiment was replicated in male C57BL/6J mice (lean) and ob/ob KO mice (obese) using the previously described methods. We predicted the acute inflammatory response resulting from HSF would be different for the lean and the obese mice, with the greatest cytokine gene expression levels in the OB HSF group, due to a summative effect of the pro-inflammatory conditions. Obesity was the factor that most affected cytokine gene expression profiles. Additionally, the pro- vs anti-inflammatory gene expression profile varied with tissue type. While obesity resulted in neuroinflammation (hypothalamus, prefrontal cortex, hippocampus), it led to decreases in pro-inflammatory cytokine gene expression in the periphery (spleen, fat, heart). Serum corticosterone concentration was significantly elevated due to SF, but was not affected by obesity. As a result, the obese mice likely had neuroendocrine adaptations to combat the pre-existing pro-inflammatory condition of obesity, which impacted the acute inflammatory response to sleep loss.

Oxidative and nitrosative stress are deleterious physiological processes caused by an imbalance between reactants such as reactive oxygen and nitrogen species and antioxidants. Due to the links between oxidative and nitrosative stress and disease, there is much interest in accurately quantifying these in biological and physiological samples. There are numerous methods to quantify the in vivo oxidative and nitrosative damage to lipids, DNA and proteins however they are generally time-consuming, expensive and difficult. Furthermore, due to the complex nature of oxidative and nitrosative stress it would be appropriate to measure a number of different biomarkers, however this is rarely done. The first section of this thesis contains research aimed at developing a bioassay to simultaneously detect markers of oxidative and nitrosative stress. This includes; 1) a review of the studies investigating the ability of these biomarkers to predict the onset of disease, 2) a description of the attempts to develop the bioassay, 3) a study designed to test the sensitivity of the bioassay to detect changes in oxidative stress. Unfortunately, the attempts to develop the bioassay were not as successful as hoped and, in the interests of completing the PhD in the time allowed, the PhD changed focus to look at the effects of oxidant:antioxidant balance on mitochondrial biogenesis. The second section of the thesis contains a review of the literature on this topic and two original investigations. It is well documented that oxidative and nitrosative stress contributes to the progression of many diseases including; cardiovascular disease, type 2 diabetes, Alzheimer’s disease, kidney disease and cancer. To determine which biomarkers would have the greatest efficacy in the bioassay, a comprehensive review was undertaken. The aim of the review was to investigate studies which have measured oxidative and nitrosative biomarkers to determine whether they are independent predictors of cardiovascular events (Chapter two). From the review, fifty-one studies were identified with twenty-six of these measuring oxidised (Ox)-LDL, fifteen assessing myeloperoxidase (MPO), seven using lipid peroxidation measures and three quantifying protein oxidation in plasma/serum. The recommendation of the review was that all areas require further investigation, however, it was determined that Ox-LDL and MPO would be beneficial for inclusion in the bio-assay. Other biomarkers considered for the bio-assay were nitrotyrosine, superoxide dismutase and glutathione peroxidase. Chapter three outlines method development used to measure the oxidative and nitrosative markers simultaneously. Recent technology allows multiple analytes to be detected simultaneously from the one sample. The Mulit-plex system is used to detect analytes that have been sandwiched between primary capture and secondary biotinylated detection antibodies. The secondary antibody attaches to streptavidin-phycoerythrin and is used by the Mulit-plex analyser to quantify the analyte. During development of the bio-assay, clumping of microspheres, high background, no detection of standard curve or samples, matrix effects, mislabeling of antibodies by manufacturers and lack of commercial available antibodies were obstacles that limited the success of this method. MPO was the only biomarker that was successful. Chapter four contains a study that investigated the sensitivity of the MPO mulitplex bio-assay. Nine highly trained cyclists underwent an extensive exercise protocol designed to induce dehydration by 4 % body mass, rehydration of 150 % fluid loss and a performance time-trial. Plasma samples were taken at five time points; baseline, post dehydration, post rehydration, pre time-trial and post time-trial and analysed using the mulitplex bio-assay. The results showed that there was a significant increase in MPO post dehydration and post time-trial compared with all other time points (P<0.05), thereby demonstrating that the mulitplex bio-assay is sensitive to detect changes in exercise and appropriate rehydration reduces oxidative stress. The MPO mulitplex bio-assay requires further testing on patients with diseases to further validate its future applications. As mentioned above, due to time constraints it was decided to stop the attempts to create a multi-analyte bioassay and focus on another important area of cellular oxidative stress. Currently, there is much interest in the involvement of oxidant:antioxidant balance in mitochondrial biogenesis. The increase of mitochondrial content within the skeletal muscle, termed mitochondrial biogenesis, provides an increased capacity to generate ATP during exercise and is recognized as one of major cellular adaptations to exercise. Reactive oxygen species are produced during exercise and have been shown to induce mitochondrial biogenesis. One of the key instigators of mitochondrial biogenesis is peroxisome proliferator activated receptor gamma coactivator-1α (PGC-1α). PGC-1α is central to the transcription of mitochondrial and nuclear encoded genes, which regulate downstream pathways such as oxidative phosphorylation and fatty acid oxidation. Antioxidant supplementation is common among athletes and healthy individuals; however, antioxidant supplements suppress reactive oxygen species and could therefore could hinder mitochondrial biogenesis and the positive adaptations associated with exercise. To establish whether antioxidant supplementation reduced mitochondrial biogenesis in skeletal muscle, male Wistar rats were supplemented with α-tocopherol and α-lipoic acid for fourteen weeks (Chapter six). Animals were separated into four groups: 1) sedentary control diet, 2) sedentary antioxidant diet, 3) exercise control diet and 4) exercise antioxidant diet. The exercise animals were trained 5 days/week for 14 weeks. Consistent with increased mitochondrial biogenesis and antioxidant defences following training, there were significant increases in PGC-1α mRNA and protein, COX IV and Cyt C protein abundance, citrate synthase activity, Nfe2l2 and SOD2 protein (P<0.05). Antioxidant supplementation reduced PGC-1α mRNA, PGC-1α and COX IV protein, and citrate synthase enzyme activity (P<0.05) in both sedentary and exercise-trained rats. In summary, antioxidants α-tocopherol and -lipoic acid supplementation suppresses beneficial adaptations in skeletal muscle such as markers of mitochondrial biogenesis and mitochondrial proteins, regardless of training status. The reduction in mitochondrial biogenesis may affect exercise training adaptations and reduce the ability of healthy individuals to attain optimal exercise adaptations. The last investigation (Chapter seven) studied the effect of reduced glutathione, through diethyl maleate (DEM) administration, on upstream regulators of mitochondrial biogenesis, markers of mitochondrial biogenesis and downstream signalling. Glutathione is a key antioxidant that reduces the amount of hydrogen peroxide. Male Wistar rats were divided into six groups 1) sedentary control, 2) sedentary DEM, 3) post-exercise control, 4) post-exercise DEM, 5) exercise-recovery and 6) exercise-recovery DEM. After an exercise bout to fatigue, animals were euthanized directly after exercise (post-exercise) or four hours post exercise (exercise-recovery). Exercising animals given DEM had significantly (P<0.05) decreased glutathione in skeletal muscle and had a significantly (P<0.05) greater increase in PGC-1α gene expression. There were also main interaction effects between exercise and DEM administration on SOD2 activity. Exercise altered the gene expression of GPx and the phosphorylation of p38 MAPK. Glutathione depletion decreased GPX activity and oxidised glutathione levels. These novel findings represent important in vivo evidence of the involvement of glutathione and oxidant:antioxidant balance in mitochondrial biogenisis. Overall this thesis has provided 1) the first comprehensive review on the prognostic ability of oxidative stress biomarkers to predict the onset of cardiovascular disease, 2) detailed information to assist in the further development of a multi-analyte bioassay to quantify oxidative and nitrosative stress, 3) data indicating that the MPO Mulit-plex bioassay is sensitive to detect physiological perturbations to oxidative stress, 4) evidence that antioxidant supplementation suppresses mitochondrial biogenesis and 5) proof that glutathione is important in the regulation of exercise-induced mitochondrial biogenesis.

Dissertação (mestrado)—Universidade de Brasília, Faculdade de Ciências da Saúde, 2008. / Submitted by Jaqueline Oliveira (jaqueoliveiram@gmail.com) on 2008-11-20T18:39:27Z No. of bitstreams: 1 DISSERTACAO_2008_ EvertonMacedoSilva.pdf: 1736502 bytes, checksum: 0be5a2d852e64d2c266dca5f1edb4431 (MD5) / Approved for entry into archive by Georgia Fernandes(georgia@bce.unb.br) on 2009-02-05T17:17:27Z (GMT) No. of bitstreams: 1 DISSERTACAO_2008_ EvertonMacedoSilva.pdf: 1736502 bytes, checksum: 0be5a2d852e64d2c266dca5f1edb4431 (MD5) / Made available in DSpace on 2009-02-05T17:17:28Z (GMT). No. of bitstreams: 1 DISSERTACAO_2008_ EvertonMacedoSilva.pdf: 1736502 bytes, checksum: 0be5a2d852e64d2c266dca5f1edb4431 (MD5) / As α-amilases são enzimas digestivas amplamente distribuídas em microrganimos, plantas e animais, que catalisam a hidrólise de ligações glicosídicas α-1,4 e atuam no metabolismo de carboidratos. A inibição de α-amilases pode ser aplicada no controle de insetos-praga dependentes de dieta rica em amido para obtenção de energia, reduzindo a quantidade de nutrientes para evitar seu desenvolvimento. Essa ação permite o uso desses inibidores como bioinseticidas. A inibição da captação de carboidratos na saúde humana pode ser uma alternativa terapêutica no controle glicêmico, reduzindo picos de glicose pós-prandial no tratamento de doenças crônicas, tais como diabetes, obesidade e hiperlipidemia. Este projeto propõe a prospecção de moléculas ativas sobre as α- amilases. Nesse contexto, as plantas são fontes ricas em compostos que possam ser estudados. Assim, o potencial biológico do Banco de Extratos de Plantas do Bioma Cerrado, do Laboratório de Farmacognosia da Universidade de Brasília, foi avaliado sobre α-amilases de Acanthoscelides obtectus, Zabrotes subfasciatus e α-amilase salivar humana. Foram testados cento e oitenta e cinco extratos vegetais hexânicos, diclorometânicos, etanólicos e hidroetanólicos pertencentes a vinte e quatro espécies de dez famílias. O extrato hidroetanólico da casca do caule de Kielmeyera coriacea foi selecionado para estudo químico-biológico devido ao seu forte perfil inibitório, com IC50 110,00 µg.mL-1 e 272,12 µg.mL-1 sobre α-amilases de Z. subfasciatus e de A. obtectus, respectivamente. O extrato apresentou 97,09% de inibição sobre a isoforma humana a 125 µg.mL-1. A parttição líquido-líquido forneceu duas fazses com alto potencial inibitório, a fase 1, precipitado metanol/hexano, que inibiu 96,35%, e a fase 5, metanol/água, que apresentou 99,35% de inibição a 125 µg.mL-1. O fracionamento químico da fase 1 em coluna cromatográfica aberta de sephadex LH-20 permitiu a obtenção de 11 grupos. Dentre esses, os mais ativos sobre α-amilase humana foram o grupo 10 (95,24%) e o grupo 11 (99,00%). O conteúdo de fenóis totais e taninos foi analisado para o extrato bruto, fases e grupos ativos. A fase 1 demonstrou um forte teor de compostos fenólicos, com 1 mg.mL-1, sendo 53,56% de taninos e a fase 5 apresentou 0,95 mg.mL-1 de polifenóis, dos quais 35,96% são taninos. O grupo 11 mostrou 81,03% de constituintes taninos e inibiu 82% da α-amilase salivar humana a apenas 50 µg.mL-1. A avaliação de extratos e taninos sobre α-amilases demonstraram atividade promissora na inibição de captação de carboidratos, representando uma alternativa para o controle do diabetes e obesidade, assim como um potencial bem interessante na inibição de α- amilases de insetos. ______________________________________________________________________________________ ABSTRACT / α-amylases are digestive enzymes widely distributed in microrganims, plants and animals, that catalyze hidrolysis of α-1,4 glicosidic bonds and act in carbohydrate metabolism. The inhibition of α-amylases can be applied on control of insect pests that depends on starch-rich diet to energy production, reducing the amount of nutrients to avoid its development. This action allow the use of these inhibitors like bio-insecticides. The inhibition of carbohydrate uptake in human health could be an alternative therapeutic on glicemic control, reducing post-prandial glucose peaks in chronic diseases treatment, such as diabetes, obesity an hyperlipidaemia. This project purposes the prospection of active molecules. In this context, plants are rich sources of compounds that could be studied. Then, the biologic potential of Cerrado Biome Plant Extract Bank, of University of Brasilia Pharmacognosy Laboratory, was evaluated on Acanthoscelides obtectus α-amylases, Zabrotes subfasciatus α-amylases and human saliva α-amylase. One hundred eighty-five hexanic, dichlorometanic, ethanolic and hidro-ethanolic extracts belonging to twenty-four species from ten families. The hidroethanolic bark stem extract of Kielmeyera coriacea was selected to chemical-biological study because of its strong inhibitory profile, with IC50 110,00 µg.mL-1 and 272,12 µg.mL-1 towards Z. subfasciatus and A. obtectus α-amylases, respectively. The extract presented 97,09% of inhibition of human isoform at 125 µg.mL-1. The liquid-liquid partition yielded two phases with a great inhibitory potential, phase 1, methanol/hexan precipitated, that inhibited 96,35%, and phase 5, methanol/water, that presented 99,35% of inhibition at 125 µg.mL-1. The chemical frationation of fase 1 in open chromatographic sephadex LH-20 column alowed the separation of 11 groups. Among them, the most active on human α-amylase were group 10 (95,24%) and group 11 (99,00%). The content of total phenols and tannins was analysed to crude extract, phases and active groups. Phase 1 demonstrated a high teor of phenolic compounds, with 1 mg.mL-1, including 53,56% of tannins and phase 5 showed 0,95 mg.mL-1 of polyphenols content, in wich 35,96% are tannins. Group 11 showed 81,03% of tannins content which inhibited 82% of human saliva α-amylase at only 50 µg.mL-1. The evaluation of extracts and tannins on α-amylases demonstrated a promising activity in carbohydrate uptake inhibition, representing a alternative to control diabetes and obesity, as well as a really interesting potential to insects α-amylases inhibition.</p>