996 resultados para Structural Defects
Resumo:
The objective of this work was to analyze the floristic variation and phytosociological structure of weeds as influenced by relief and time of year in eucalyptus plantations in Santana do Paraíso and Guanhães - MG. The total area sampled for each locality was approximately 10 ± 3 hectares, comprising three types of relief: lowland, slope, and upper area. In each type of relief, 10 plots of 1 m² were sampled, corresponding to 30 plots per locality, where they were randomly allocated in a zigzag. The taxonomic identification was performed in four assessments, corresponding to the months of November and March, comprising two ratings each season, always at the same points, and geo-referenced using the Global Positioning System (GPS). A total of 3,893 individuals, 18 families and 61 species, were identified in Santana do Paraiso and a total of 1,166 individuals, 13 families and 58 species, in Guanhães. In both localities, the most representative families in terms of wealth were: Poaceae, Asteraceae, and Fabaceae. Galinsoga parviflora was the most abundant species. The Vernonia polyantes was identified only in the lowlands, while Arrabida florida was identified in the slope and upper area. On the other hand, Emilia coccinea, Sida rhombifolia, S. paniculatum and Spermacoce latifolia were common to all three environments. Commelina benghalensis was present only in the month of March, while G. parviflora was present only in the month of November. It was concluded that the floristic and phytosociological variation of weeds in eucalyptus plantations is influenced by the type of relief and time of year, which should guide the management practices used in the culture.
Resumo:
Echinolaena inflexa (Poir.) Chase is a native C3 grass species with high biomass production and abundance in the cerrado comparable to Melinis minutiflora Beauv., a C4 forage grass of African origin, widespread in the cerrado, displacing some native herbaceous species. These species accumulate mainly starch, differently of Lolium multiflorum Lam. ssp. italicum Beck cv. Lema (ryegrass), a C3 temperate forage grass that accumulates fructans as the major storage carbohydrate in the vegetative tissues. In the present study, we analyzed diurnal variations in the content and composition of non-structural carbohydrates (NSC) in the aerial vegetative parts of the three species. Results showed similarity in water-soluble carbohydrates (WSC) and starch contents between Melinis minutiflora and Echinolaena inflexa, with the exotic grass accumulating higher amounts of NSC. However, the levels of sucrose, glucose and fructose were 10 fold higher in Lolium multiflorum, that accumulates fructan as the main storage carbohydrate. Although the contents of WSC and starch were similar in the tropical species E. inflexa and M. minutiflora, their diurnal variations were different and could be related to starch metabolism, especially in M. minutiflora.
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Granitic rock outcrops of the Brazilian southeast are either coastal or inland. The latter can often have high altitudes, such as in the summits of "Serra do Mar" and "Serra da Mantiqueira", where they are known as "Campos de Altitude". The landscape on these high altitude plateaux is often a mosaic of shrubs and treelets within a bunchgrass matrix, with sparse pteridophytes and other herbs, interspersed with variable extensions of rock outcrops. Despite the pervasiveness of rock outcrops in the Brazilian landscape, studies on the structural analysis of the vegetation on such formations are scarce. This study aimed to analyze the structure of the vegetation on a highland granitic rock outcrop in "Parque Estadual da Serra do Brigadeiro", state of Minas Gerais, Southeast Brazil (42°20' - 42°40' S and 20°20' - 21°00' W, 1,722 m of elevation ). Quantitative parameters of absolute and relative frequency and dominance (cover) were estimated. The group analysis used the Jaccard similarity index. Trilepis lhotzkiana, Panicum sp. 1, and Vellozia variegata presented the highest relative frequencies, relative dominances and importance values. These three species, along with Dyckia bracteata, Rhynchospora emaciate, and Tibouchina cf. manicata, represented 98.3% of the relative dominance. The remaining 1.7% referred to 22 remaining species. The distinction among quadrats within formed groups by cluster analysis was due to the great number of low frequency species.
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Lipoprotein Lp(a) is a major and independent genetic risk factor for atherosclerosis and cardiovascular disease. The essential difference between Lp(a) and low density lipoproteins (LDL) is apolipoprotein apo(a), a glycoprotein structurally similar to plasminogen, the precursor of plasmin, the fibrinolytic enzyme. This structural homology endows Lp(a) with the capacity to bind to fibrin and to membrane proteins of endothelial cells and monocytes, and thereby to inhibit plasminogen binding and plasmin generation. The inhibition of plasmin generation and the accumulation of Lp(a) on the surface of fibrin and cell membranes favor fibrin and cholesterol deposition at sites of vascular injury. Moreover, insufficient activation of TGF-ß due to low plasmin activity may result in migration and proliferation of smooth muscle cells into the vascular intima. These mechanisms may constitute the basis of the athero-thrombogenic mode of action of Lp(a). It is currently accepted that this effect of Lp(a) is linked to its concentration in plasma. An inverse relationship between Lp(a) concentration and apo(a) isoform size, which is under genetic control, has been documented. Recently, it has been shown that inhibition of plasminogen binding to fibrin by apo(a) is also inversely associated with isoform size. Specific point mutations may also affect the lysine-binding function of apo(a). These results support the existence of functional heterogeneity in apolipoprotein(a) isoforms and suggest that the predictive value of Lp(a) as a risk factor for vascular occlusive disease would depend on the relative concentration of the isoform with the highest affinity for fibrin
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Rolling element bearings are essential components of rotating machinery. The spherical roller bearing (SRB) is one variant seeing increasing use, because it is self-aligning and can support high loads. It is becoming increasingly important to understand how the SRB responds dynamically under a variety of conditions. This doctoral dissertation introduces a computationally efficient, three-degree-of-freedom, SRB model that was developed to predict the transient dynamic behaviors of a rotor-SRB system. In the model, bearing forces and deflections were calculated as a function of contact deformation and bearing geometry parameters according to nonlinear Hertzian contact theory. The results reveal how some of the more important parameters; such as diametral clearance, the number of rollers, and osculation number; influence ultimate bearing performance. Distributed defects, such as the waviness of the inner and outer ring, and localized defects, such as inner and outer ring defects, are taken into consideration in the proposed model. Simulation results were verified with results obtained by applying the formula for the spherical roller bearing radial deflection and the commercial bearing analysis software. Following model verification, a numerical simulation was carried out successfully for a full rotor-bearing system to demonstrate the application of this newly developed SRB model in a typical real world analysis. Accuracy of the model was verified by comparing measured to predicted behaviors for equivalent systems.
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The characterization of proteins from Brucella spp, the causative agent of brucellosis, has been the subject of intensive research. We have described an 18-kDa cytoplasmic protein of Brucella abortus and shown the potential usefulness of this protein as an antigen for the serologic diagnosis of brucellosis. The amino acid sequence of the protein showed a low but significant homology with that of lumazine synthases. Lumazine is an intermediate product in bacterial riboflavin biosynthesis. The recombinant form of the 18-kDa protein (expressed in E. coli) folds like the native Brucella protein and has lumazine-synthase enzymatic activity. Three-dimensional analysis by X-ray crystallography of the homolog Bacillus subtilis lumazine synthase has revealed that the enzyme forms an icosahedral capsid. Recombinant lumazine synthase from B. abortus was crystallized, diffracted X rays to 2.7-Å resolution at room temperature, and the structure successfully solved by molecular replacement procedures. The macromolecular assembly of the enzyme differs from that of the enzyme from B. subtilis. The Brucella enzyme remains pentameric (90 kDa) in its crystallographic form. Nonetheless, the active sites of the two enzymes are virtually identical at the structural level, indicating that inhibitors of these enzymes could be viable pharmaceuticals across a broad species range. We describe the structural reasons for the differences in their quaternary arrangement and also discuss the potential use of this protein as a target for the development of acellular vaccines.
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Seven unrelated patients with hemoglobin (Hb) H disease and 27 individuals with alpha-chain structural alterations were studied to identify the alpha-globin gene mutations present in the population of Southeast Brazil. The -alpha3.7, --MED and -(alpha)20.5 deletions were investigated by PCR, whereas non-deletional alpha-thalassemia (alphaHphalpha, alphaNcoIalpha, aaNcoI, alphaIcalpha and alphaTSaudialpha) was screened with restriction enzymes and by nested PCR. Structural alterations were identified by direct DNA sequencing. Of the seven patients with Hb H disease, all of Italian descent, two had the -(alpha)20.5/-alpha3.7 genotype, one had the --MED/-alpha3.7 genotype, one had the --MED/alphaHphalpha genotype and three showed interaction of the -alpha3.7 deletion with an unusual, unidentified form of non-deletional alpha-thalassemia [-alpha3.7/(aa)T]. Among the 27 patients with structural alterations, 15 (of Italian descent) had Hb Hasharon (alpha47Asp->His) associated with the -alpha3.7 deletion, 4 (of Italian descent) were heterozygous for Hb J-Rovigo (alpha53Ala->Asp), 4 (3 Blacks and 1 Caucasian) were heterozygous for Hb Stanleyville-II (alpha78Asn->Lys) associated with the alpha+-thalassemia, 1 (Black) was heterozygous for Hb G-Pest (alpha74Asp->Asn), 1 (Caucasian) was heterozygous for Hb Kurosaki (alpha7Lys->Glu), 1 (Caucasian) was heterozygous for Hb Westmead (alpha122His->Gln), and 1 (Caucasian) was the carrier of a novel silent variant (Hb Campinas, alpha26Ala->Val). Most of the mutations found reflected the Mediterranean and African origins of the population. Hbs G-Pest and Kurosaki, very rare, and Hb Westmead, common in southern China, were initially described in individuals of ethnic origin differing from those of the carriers reported in the present study and are the first cases to be reported in the Brazilian population.
Resumo:
The recently cloned extracellular calcium-sensing receptor (CaR) is a G protein-coupled receptor that plays an essential role in the regulation of extracellular calcium homeostasis. This receptor is expressed in all tissues related to this control (parathyroid glands, thyroid C-cells, kidneys, intestine and bones) and also in tissues with apparently no role in the maintenance of extracellular calcium levels, such as brain, skin and pancreas. The CaR amino acid sequence is compatible with three major domains: a long and hydrophilic aminoterminal extracellular domain, where most of the activating and inactivating mutations described to date are located and where the dimerization process occurs, and the agonist-binding site is located, a hydrophobic transmembrane domain involved in the signal transduction mechanism from the extracellular domain to its respective G protein, and a carboxyterminal intracellular tail, with a well-established role for cell surface CaR expression and for signal transduction. CaR cloning was immediately followed by the association of genetic human diseases with inactivating and activating CaR mutations: familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism are caused by CaR-inactivating mutations, whereas autosomal dominant hypoparathyroidism is secondary to CaR-activating mutations. Finally, we will comment on the development of drugs that modulate CaR function by either activating (calcimimetic drugs) or antagonizing it (calcilytic drugs), and on their potential therapeutic implications, such as medical control of specific cases of primary and uremic hyperparathyroidism with calcimimetic drugs and a potential treatment for osteoporosis with a calcilytic drug.
Resumo:
The aim of the present study was to investigate the expression of alpha-smooth muscle actin (alpha-SM-actin) and proliferating cell nuclear antigen (PCNA) in renal cortex from patients with focal segmental glomerulosclerosis (FSGS) and their correlations with parameters of renal disease progression. We analyzed renal biopsies from 41 patients with idiopathic FSGS and from 14 control individuals. The alpha-SM-actin immunoreaction was evaluated using a score that reflected the changes in the extent and intensity of staining in the glomerular or cortical area. The PCNA reaction was quantified by counting the labeled cells of the glomeruli or renal cortex. The results, reported as median ± percentile (25th; 75th), showed that the alpha-SM-actin scores in the glomeruli and tubulointerstitium from the renal cortex were 2.0 (2.0; 4.0) and 3.0 (3.0; 4.0), respectively, in patients with FSGS, and 0.5 (0.0; 1.0) and 0.0 (0.0; 0.5) in the controls. The number of PCNA-positive cells per glomerulus and graded field of tubulointerstitium from the renal cortex was 0.2 (0.0; 0.4) and 1.1 (0.3; 2.2), respectively, for patients with FSGS, and 0.0 (0.0; 0.5) and 0.0 (0.0; 0.0) for controls. The present data showed an increase of alpha-SM-actin and PCNA expression in glomeruli and renal cortex from FSGS patients. The extent of immunoreaction for alpha-SM-actin in the tubulointerstitial area was correlated with the intensity of proteinuria. However, there was no correlation between the kidney expression of these proteins and the reciprocal of plasma creatinine level or renal fibrosis. These findings suggest that the immunohistochemical alterations may be reversible.
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Reconstitution of membrane proteins into lipid bilayers is a powerful tool to analyze functional as well as structural areas of membrane protein research. First, the proper incorporation of a purified membrane protein into closed lipid vesicles, to produce proteoliposomes, allows the investigation of transport and/or catalytic properties of any membrane protein without interference by other membrane components. Second, the incorporation of a large amount of membrane proteins into lipid bilayers to grow crystals confined to two dimensions has recently opened a new way to solve their structure at high resolution using electron crystallography. However, reconstitution of membrane proteins into functional proteoliposomes or 2-D crystallization has been an empirical domain, which has been viewed for a long time more like "black magic" than science. Nevertheless, in the last ten years, important progress has been made in acquiring knowledge of lipid-protein-detergent interactions and has permitted to build upon a set of basic principles that has limited the empirical approach of reconstitution experiments. Reconstitution strategies have been improved and new strategies have been developed, facilitating the success rate of proteoliposome formation and 2-D crystallization. This review deals with the various strategies available to obtain proteoliposomes and 2-D crystals from detergent-solubilized proteins. It gives an overview of the methods that have been applied, which may be of help for reconstituting more proteins into lipid bilayers in a form suitable for functional studies at the molecular level and for high-resolution structural analysis.
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The aim of this study was to determine the relationship between urinary albumin excretion (UAE), cardiac structural changes upon echocardiography and 24-h ambulatory blood pressure (ABPM) levels. Twenty mild hypertensive patients (mean age 56.8 ± 9.6 years) were evaluated. After 2 weeks of a washout period of all antihypertensive drugs, all patients underwent an echocardiographic evaluation, a 24-h ABPM and an overnight urine collection. Systolic and diastolic blood pressure during 24-h ABPM was 145 ± 14/91 ± 10 mmHg (daytime) and 130 ± 14/76 ± 8 mmHg (nighttime), respectively. Seven (35%) patients presented UAE > or = 15 µg/min, and for the whole group, the geometric mean value for UAE was 10.2 x/÷ 3.86 µg/min. Cardiac measurements showed mean values of interventricular septum thickness (IVS) of 11 ± 2.3 mm, left ventricular posterior wall thickness (PWT) of 10 ± 2.0 mm, left ventricular mass (LVM) of 165 ± 52 g, and left ventricular mass index (LVMI) of 99 ± 31 g/m². A forward stepwise regression model indicated that blood pressure levels did not influence UAE. Significant correlations were observed between UAE and cardiac structural parameters such as IVS (r = 0.71, P<0.001), PWT (r = 0.64, P<0.005), LVM (r = 0.65, P<0.005) and LVMI (r = 0.57, P<0.01). Compared with normoalbuminuric patients, those who had microalbuminuria presented higher values of all cardiac parameters measured. The predictive positive and negative values of UAE > or = 15 µg/min for the presence of geometric cardiac abnormalities were 75 and 91.6%. These data indicate that microalbuminuria in essential hypertension represents an early marker of cardiac structural damage.
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Muscular dystrophies are a heterogeneous group of genetically determined progressive disorders of the muscle with a primary or predominant involvement of the pelvic or shoulder girdle musculature. The clinical course is highly variable, ranging from severe congenital forms with rapid progression to milder forms with later onset and a slower course. In recent years, several proteins from the sarcolemmal muscle membrane (dystrophin, sarcoglycans, dysferlin, caveolin-3), from the extracellular matrix (alpha2-laminin, collagen VI), from the sarcomere (telethonin, myotilin, titin, nebulin), from the muscle cytosol (calpain 3, TRIM32), from the nucleus (emerin, lamin A/C, survival motor neuron protein), and from the glycosylation pathway (fukutin, fukutin-related protein) have been identified. Mutations in their respective genes are responsible for different forms of neuromuscular diseases. Protein analysis using Western blotting or immunohistochemistry with specific antibodies is of the utmost importance for the differential diagnosis and elucidation of the physiopathology of each genetic disorder involved. Recent molecular studies have shown clinical inter- and intra-familial variability in several genetic disorders highlighting the importance of other factors in determining phenotypic expression and the role of possible modifying genes and protein interactions. Developmental studies can help elucidate the mechanism of normal muscle formation and thus muscle regeneration. In the last fifteen years, our research has focused on muscle protein expression, localization and possible interactions in patients affected by different forms of muscular dystrophies. The main objective of this review is to summarize the most recent findings in the field and our own contribution.
Resumo:
Background: Interest in limb defects has grown after the thalidomide tragedy in the 1960s. As a result, congenital malformation registries, monitoring changes in birthprevalence and defect patterns, have been established in several countries. However, there are only a few true population based studies on birth prevalence of upper limb defects. The burden of hospital care among these children, specifically in terms of the number of admissions and total time spent in hospital, is also unknown. Aims and Methods: This study is based on information gathered from the Finnish Register of Congenital malformations (FRM) and the Finnish Hospital Discharge Register (FHDR). A total of 417 children born between 1993 and 2005 with an upper limb defect were gathered from the FRM. The upper limb defects were classified using the International Federation of Societies for Surgery of the Hand -classification that enables comparison with previous and future studies. Birth and live birth prevalence, sex and side distribution, frequency of associated anomalies as well as the proportion of perinatal and infant deaths according to the different subtypes were calculated. The number of hospital admissions, days spent in hospital, number and type of surgical operations were collected from the FHDR. Special features of two subgroups, radial ray defects (RRD) and constriction band syndrome (CBS), were explored. Results: Upper limb defects were observed in 417 of 753 342 consecutive births and in 392 of 750 461 live births. Birth prevalence was 5.5 per 10 000 births and 5.2 per 10 000 live births. Multiple anomalies or a known syndrome was found in 250 cases (60%). Perinatal mortality was 139 per 1000 births and infant mortality 135 per 1000 live births (overall Finnish perinatal mortality <5 per 1000 births and infant mortality 3.7 per 1000 live births). Altogether, 138 infants had RRD and 120 (87%) of these had either a known syndrome or multiple major anomalies. The proportion of perinatal deaths in RRD group was 29% (40/138) and infant deaths 35% (43/123). Fifty-one children had CBS in upper limbs. Fifteen of these (29%) had other major anomalies associated with constriction rings. The number of hospital admissions per year of children with congenital upper limb defects was 11-fold and the time spent in hospital 13-fold as compared with the general paediatric population. Conclusions: Birth prevalence of congenital upper limb defects was 5.5 per 10 000 births and 5.2 per 10 000 live births. RRD was especially associated with other major anomalies and high mortality. Nearly one third of the children with CBS also had other major anomalies suggesting different aetiologies inside the group. The annual burden of hospital care of children with congenital upper limb defects was at least 11-fold as compared with the general paediatric population.
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The bedrock of old crystalline cratons is characteristically saturated with brittle structures formed during successive superimposed episodes of deformation and under varying stress regimes. As a result, the crust effectively deforms through the reactivation of pre-existing structures rather than by through the activation, or generation, of new ones, and is said to be in a state of 'structural maturity'. By combining data from Olkiluoto Island, southwestern Finland, which has been investigated as the potential site of a deep geological repository for high-level nuclear waste, with observations from southern Sweden, it can be concluded that the southern part of the Svecofennian shield had already attained structural maturity during the Mesoproterozoic era. This indicates that the phase of activation of the crust, i.e. the time interval during which new fractures were generated, was brief in comparison to the subsequent reactivation phase. Structural maturity of the bedrock was also attained relatively rapidly in Namaqualand, western South Africa, after the formation of first brittle structures during Neoproterozoic time. Subsequent brittle deformation in Namaqualand was controlled by the reactivation of pre-existing strike-slip faults.In such settings, seismic events are likely to occur through reactivation of pre-existing zones that are favourably oriented with respect to prevailing stresses. In Namaqualand, this is shown for present day seismicity by slip tendency analysis, and at Olkiluoto, for a Neoproterozoic earthquake reactivating a Mesoproterozoic fault. By combining detailed field observations with the results of paleostress inversions and relative and absolute time constraints, seven distinctm superimposed paleostress regimes have been recognized in the Olkiluoto region. From oldest to youngest these are: (1) NW-SE to NNW-SSE transpression, which prevailed soon after 1.75 Ga, when the crust had sufficiently cooled down to allow brittle deformation to occur. During this phase conjugate NNW-SSE and NE-SW striking strike-slip faults were active simultaneous with reactivation of SE-dipping low-angle shear zones and foliation planes. This was followed by (2) N-S to NE-SW transpression, which caused partial reactivation of structures formed in the first event; (3) NW-SE extension during the Gothian orogeny and at the time of rapakivi magmatism and intrusion of diabase dikes; (4) NE-SW transtension that occurred between 1.60 and 1.30 Ga and which also formed the NW-SE-trending Satakunta graben located some 20 km north of Olkiluoto. Greisen-type veins also formed during this phase. (5) NE-SW compression that postdates both the formation of the 1.56 Ga rapakivi granites and 1.27 Ga olivine diabases of the region; (6) E-W transpression during the early stages of the Mesoproterozoic Sveconorwegian orogeny and which also predated (7) almost coaxial E-W extension attributed to the collapse of the Sveconorwegian orogeny. The kinematic analysis of fracture systems in crystalline bedrock also provides a robust framework for evaluating fluid-rock interaction in the brittle regime; this is essential in assessment of bedrock integrity for numerous geo-engineering applications, including groundwater management, transient or permanent CO2 storage and site investigations for permanent waste disposal. Investigations at Olkiluoto revealed that fluid flow along fractures is coupled with low normal tractions due to in-situ stresses and thus deviates from the generally accepted critically stressed fracture concept, where fluid flow is concentrated on fractures on the verge of failure. The difference is linked to the shallow conditions of Olkiluoto - due to the low differential stresses inherent at shallow depths, fracture activation and fluid flow is controlled by dilation due to low normal tractions. At deeper settings, however, fluid flow is controlled by fracture criticality caused by large differential stress, which drives shear deformation instead of dilation.