[Show abstract][Hide abstract] ABSTRACT: This article presents a model for efficiency evaluation applied to associated companies with the Minas Gerais Software Foundation - FUMSOFT. The appropriate model in the measurement was the Variable Return to Scale (VRS) - (Banker, Charnes & Cooper, 1984) output oriented. The methodology focused on production metrics of innovation in firms. The inputs chosen based on literature were number of employees in general and employees with education in stricto sensu master or PhD; and the outputs were billing amount, number of innovation projects developed with success and participation of new products or services in the billing. The measures of results were based on the construction and analysis of a relative technical efficiency frontier through which companies are classified as efficient or non efficient. Data was collected from 28 organizations. Non-parametric method Data Envelopment Analysis (DEA) - (Charnes, Cooper & Rhodes, 1978) was used in order to evaluate efficiency degrees. In conclusion, eleven organizations operated efficiently, nine have opportunity for improvement in a total of twenty-five companies analyzed. Five were excluded as outliers.
Revista de Administração e Inovação. 07/2014; 11(2):220.
[Show abstract][Hide abstract] ABSTRACT: Benzo[a]pyrene (BaP) is an environmental contaminant produced during incomplete combustion of organic material that is well known as a mutagenic and carcinogenic toxin. There are few studies addressing the molecular and cellular basis of behavioural alterations related to BaP exposure. The aim of this study was to evaluate the effect of subchronic oral administration of BaP on behavioral and neurochemical parameters. Wistar male rats received BaP (2 mg/kg) or corn oil (control), once a day for 28 days (n = 12/group). Spontaneous locomotor activity and short- and long-term memories were evaluated. Glial fibrillary acid protein and S100B content in the hippocampus, serum and CSF were measured using ELISA and total and phosphorylated forms of mitogen activated protein kinases (MAPKs) named extracellular signal-regulated kinases 1 and 2, p38(MAPK) and c-Jun amino-terminal kinases 1 and 2, in the hippocampus, were evaluated by western blotting. BaP induced a significant increase on locomotor activity and a decrease in short-term memory. S100B content was increased significantly in cerebrospinal fluid. BaP induced a decrease on ERK2 phosphorylation in the hippocampus. Thus, BaP subchronic treatment induces an astroglial response and impairs both motor and cognitive behavior, with parallel inhibition of ERK2, a signaling enzyme involved in the hippocampal neuroplasticity. All these effects suggest that BaP neurotoxicity is a concern for environmental pollution.
Neurochemical Research 03/2014; · 2.13 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Lectins are proteins capable of reversible binding to the carbohydrates in glycoconjugates that can regulate many physiological and pathological events. Galectin-1, a β-galactoside-binding lectin, is expressed in the central nervous system (CNS) and exhibits neuroprotective functions. Additionally, lectins isolated from plants have demonstrated beneficial action in the CNS. One example is a lectin with mannose-glucose affinity purified from Canavalia brasiliensis seeds, ConBr, which displays neuroprotective and antidepressant activity. On the other hand, the effects of the galactose-binding lectin isolated from Vatairea macrocarpa seeds (VML) on the CNS are largely unknown. The aim of this study was to verify if VML is able to alter neural function by evaluating signaling enzymes, glial and inflammatory proteins in adult mice hippocampus, as well as behavioral parameters. VML administered by intracerebroventricular (i.c.v) route increased the immobility time in the forced swimming test (FST) 60 min after its injection through a carbohydrate recognition domain-dependent mechanism. Furthermore, under the same conditions, VML caused an enhancement of COX-2, GFAP and S100B levels in mouse hippocampus. However, phosphorylation of Akt, GSK-3β and mitogen-activated protein kinases named ERK1/2, JNK1/2/3 and p38(MAPK), was not changed by VML. The results reported here suggest that VML may trigger neuroinflammatory response in mouse hippocampus and exhibit a depressive-like activity. Taken together, our findings indicate a dual role for galactose binding lectins in the modulation of CNS function.
Neurochemical Research 09/2013; · 2.13 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The influence of the strategic management research rooted conception of firm performance as resulting from the structure–agency duality is clear in the academic spin-off (ASO) literature. However, the interplay of structuration aspects during ASO emergence is still under-researched—though potentially relevant to explain spin-offs’ heterogeneity. Thus, this paper presents a roadmap-based investigation of structure and agency patterns in the emergence of a Brazilian high-tech ASO focused on developing products from carbon nanotubes to industrial applications. Causal cognitive mapping was used to construct seven emergence roadmaps from entrepreneurs' retrospective narratives and the qualitative comparative analysis (QCA) was applied to formally analyze the maps. As a result, the main generative mechanisms of the structuration aspects were identified, leading to evidence-based propositions about the distinctive explanatory capability of: R&D-oriented agency, internal structures and environment–resources combinations. Moreover, the study identified subsets of the original roadmap layers able to consistently limit, in a logically parsimonious way, the empirical diversity of various phenomena considered theoretically relevant aspects of academic spin-off emergence. Hence, the paper illustrates the value, from a scholarly perspective, of incorporating formal techniques to roadmap analyses and identifies complex patterns of structure and agency to be further explored by future investigations.
Technological Forecasting and Social Change 07/2013; 80(6):1162–1178. · 1.71 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Congenital hypothyroidism is associated with delay in cell migration and proliferation in brain tissue, impairment of synapse formation, misregulation of neurotransmitters, hypomyelination and mental retardation. However, the mechanisms underlying the neuropsychological deficits observed in congenital hypothyroidism are not completely understood. In the present study we proposed a mechanism by which hypothyroidism leads to hippocampal neurotoxicity. Congenital hypothyroidism induces c-Jun-N-terminal kinase (JNK) pathway activation leading to hyperphosphorylation of the glial fibrillary acidic protein (GFAP), vimentin and neurofilament subunits from hippocampal astrocytes and neurons, respectively. Moreover, hyperphosphorylation of the cytoskeletal proteins was not reversed by T3 and poorly reversed by T4. In addition, congenital hypothyroidism is associated with downregulation of astrocyte glutamate transporters (GLAST and GLT-1) leading to decreased glutamate uptake and subsequent influx of Ca(2)(+)through N-methyl-D-aspartate (NMDA) receptors. The Na(+)-coupled (14)C-α-methyl-amino-isobutyric acid ((14)C-MeAIB) accumulation into hippocampal cells also might cause an increase in the intracellular Ca(2+) concentration by opening voltage-dependent calcium channels (VDCC). The excessive influx of Ca(2)(+)through NMDA receptors and VDCCs might lead to an overload of Ca(2)(+)within the cells, which set off glutamate excitotoxicity and oxidative stress. The inhibited acetylcholinesterase (AChE) activity might also induce Ca(2)(+) influx. The inhibited glucose-6-phosphate dehydrogenase (G6PD) and gamma-glutamyl transferase (GGT) activities, associated with altered glutamate and neutral amino acids uptake could somehow affect the GSH turnover, the antioxidant defense system, as well as the glutamate-glutamine cycle. Reduced levels of S100B and glial fibrillary acidic protein (GFAP) take part of the hypothyroid condition, suggesting a compromised astroglial/neuronal neurometabolic coupling which is probably related to the neurotoxic damage in hypothyroid brain.
Molecular and Cellular Endocrinology 05/2013; · 4.04 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This article examines the practices of knowledge management and innovation in a franchise of a major multinational company in the fast-food industry of Minas Gerais: Subway. As a research strategy, we used a descriptive case study and data were collected through a in-depth interview conducted with the owner of four stores in that franchise located in strategic areas of the city of Belo Horizonte. The results showed that the processes of creation, development and sharing of knowledge between the administrative and operational staff are encouraged and have achieved significant results, the franchise stores, as the theory claims. However, perhaps because of this business model (franchise), this knowledge produced and shared among such employees are not applied in its entirety on product innovation and operational processes on the sales, because most of the innovations developed in the environment and the franchisor, which restricts the space for innovation in franchised stores, in spite of satisfactory results in some innovation management processes.
Perspectivas em Ciência da Informação 03/2013; 18(1):86-105.
[Show abstract][Hide abstract] ABSTRACT: A novel series of tacrine-lophine hybrids was synthesized and tested for their ability to inhibit acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) with IC(50) in the nanomolar concentration scale. The key step is the one-pot four component condensation reaction of 9-aminoalkylamino-1,2,3,4-tetrahydroacridines, benzil, different substituted aromatic aldehydes and NH(4)OAc, using InCl(3) as the best catalyst. Tacrine-lophine hybrids were found to be potent and selective inhibitors of cholinesterases. As an extension of the four component approach to tetrasubstituted imidazoles, a new series of bis-(2,4,5-triphenyl-1H-imidazoles) or bis(n)-lophines was tested against AChE and BuChE.
European Journal of Medicinal Chemistry 02/2013; 62C:556-563. · 3.43 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Physical exercise effects on brain health and cognitive performance have been described. Synaptic remodeling in hippocampus induced by physical exercise has been described in animal models, but the underlying mechanisms remain poorly understood. Changes in astrocytes, the glial cells involved in synaptic remodeling, need more characterization. We investigated the effect of moderate treadmill exercise (20 min/day) for 4 weeks on some parameters of astrocytic activity in rat hippocampal slices, namely, glial fibrillary acidic protein (GFAP), glutamate uptake and glutamine synthetase (GS) activities, glutathione content, and S100B protein content and secretion, as well as brain-derived neurotrophic factor (BDNF) levels and glucose uptake activity in this tissue. Results show that moderate treadmill exercise was able to induce a decrease in GFAP content (evaluated by ELISA and immunohistochemistry) and an increase in GS activity. These changes could be mediated by corticosterone, whose levels were elevated in serum. BDNF, another putative mediator, was not altered in hippocampal tissue. Moreover, treadmill exercise caused a decrease in NO content. Our data indicate specific changes in astrocyte markers induced by physical exercise, the importance of studying astrocytes for understanding brain plasticity, as well as reinforce the relevance of physical exercise as a neuroprotective strategy.
[Show abstract][Hide abstract] ABSTRACT: This paper was designed to identify and discuss the function of Industry level performance, in the relations between corporate strategic factors and performance, following the classic and modern prospects of Industrial organization theory, applied to the Brazilian industrial activities. Objects of this study are Brazilian enterprises, in activity between 1997 and 2006. The results obtained by the study of the proposed models show that this research intend was successfully reached, helping the understanding of the industrial environment role in the relations between corporate strategy and performance, under the vision of the industrial organization economy; Insignificance of the strategy role. A relation between industrial environment and organization performance was also found. Although no moderator role is played by environment, as former proposed in this study, the influence of the corporate strategies appears directly in the interlocking strategies, and indirectly in strategies in terms of size and diversification, through the length of time variations, which in turn influence positively variations in the capital market performance, this way suggesting adoption of an evolutionary perspective, when doing new researches on the theme.
African journal of business management 10/2012; 6(39):10477-10485. · 1.11 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A dysfunctional glutamatergic system is thought to be central to the negative symptoms and cognitive deficits recognized as determinant to the poor quality of life of people with schizophrenia. Modulating glutamate uptake has, thus, been suggested as a novel target for antipsychotics. Alstonine is an indole alkaloid sharing with atypical antipsychotics the profile in animal models relevant to schizophrenia, though divergent in its mechanism of action. The aim of this study was to evaluate the effects of alstonine on glutamate uptake. Additionally, the effects on glutathione content and extracellular S100B levels were assessed. Acute hippocampal slices were incubated with haloperidol (10μM), clozapine (10 and 100μM) or alstonine (1-100μM), alone or in combination with apomorphine (100μM), and 5-HT(2) receptor antagonists (0.01μM altanserin and 0.1μM SB 242084). A reduction in glutamate uptake was observed with alstonine and clozapine, but not haloperidol. Apomorphine abolished the effect of clozapine, whereas 5-HT(2A) and 5-HT(2C) antagonists abolished the effects of alstonine. Increased levels of glutathione were observed only with alstonine, also the only compound that failed to decrease the release of S100B. This study shows that alstonine decreases glutamate uptake, which may be beneficial to the glutamatergic deficit observed in schizophrenia. Noteworthily, the decrease in glutamate uptake is compatible with the reversal of MK-801-induced social interaction and working memory deficits. An additional potential benefit of alstonine as an antipsychotic is its ability to increase glutathione, a key cellular antioxidant reported to be decreased in the brain of patients with schizophrenia. Adding to the characterization of the novel mechanism of action of alstonine, the lack of effect of apomorphine in alstonine-induced changes in glutamate uptake reinforces that D(2) receptors are not primarily implicated. Though clearly mediated by 5-HT(2A) and 5-HT(2C) serotonin receptors, the precise mechanisms that result in the effects of alstonine on glutamate uptake warrant elucidation.
Neurochemistry International 08/2012; · 2.66 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Methylmercury (MeHg) is an environmental pollutant that biomagnifies throughout the aquatic food chain thus representing a toxicological concern for humans subsiding on fish for their dietary intake. Although the developing brain is considered the critical target organ of MeHg toxicity, recent evidence indicates that the cardiovascular system may be the most sensitive in adults. However, data on the mechanisms mediating MeHg-induced cardiovascular toxicity is scarce. Based on the close relationship between cardiovascular disease and dyslipidemia, this study was designed to investigate the effects of long-term MeHg exposure on plasma lipid levels in mice, as well as their underlying mechanisms and potential relationships to MeHg-induced neurotoxicity. Our major finding was that long-term MeHg exposure induced dyslipidemia in rodents. Specifically, Swiss and C57BL/6 mice treated for 21 days with a drinking solution of MeHg (40 mg/L, ad libitum) diluted in tap water showed increased total and non-HDL plasma cholesterol levels. MeHg-induced hypercholesterolemia was also observed in low-density lipoprotein receptor knockout (LDLr(-/-)) mice, indicating that this effect was not related to decreased LDLr-mediated cholesterol transport from blood to others tissues. Although the hepatic synthesis of cholesterol was unchanged, significant signs of nephrotoxicity (glomerular shrinkage, tubular vacuolization and changed urea levels) were observed in MeHg-exposed mice, indicating that the involvement of nephropathy in MeHg-induced lipid dyshomeostasis may not be ruled out. Notably, Probucol (a lipid-lowering drug) prevented the development of hypercholesterolemia when co-administered with MeHg. Finally, hypercholesterolemic LDLr(-/-) mice were more susceptible to MeHg-induced cerebellar glial activation, suggesting that hypercholesterolemia in itself may pose a risk factor in MeHg-induced neurotoxicity. Overall, based on the strong and graded positive association between total as well as LDL cholesterol and risk of cardiovascular diseases our data support the concept of MeHg-induced cardiovascular toxicity.
[Show abstract][Hide abstract] ABSTRACT: In the present report 15day-old Wistar rats were injected with 0.3μmol of diphenyl ditelluride (PhTe)(2)/kg body weight and parameters of neurodegeneration were analyzed in slices from striatum 6days afterwards. We found hyperphosphorylation of intermediate filament (IF) proteins from astrocyte (glial fibrillary acidic protein-GFAP and vimentin) and from neuron (low-, medium- and high molecular weight neurofilament subunits: NF-L, NF-M and NF-H, respectively) and increased MAPK (Erk, JNK and p38MAPK) as well as PKA activities. The treatment induced reactive astrogliosis in the striatum, evidenced by increased GFAP and vimentin immunocontent as well as their mRNA overexpression. Also, (PhTe)(2) significantly increased the propidium iodide (PI) positive cells in NeuN positive population without altering PI incorporation into GFAP positive cells, indicating that in vivo exposure to (PhTe)(2) provoked neuronal damage. Immunohistochemistry showed a dramatic increase of GFAP staining characteristic of reactive astrogliosis. Moreover, increased caspase 3 in (PhTe)(2) treated striatal slices suggested apoptotic cell death. (PhTe)(2) exposure decreased Akt immunoreactivity, however phospho-GSK-3-β (Ser9) was unaltered, suggesting that this kinase is not directly implicated in the neurotoxicity of this compound. Therefore, the present results shed light into the mechanisms of (PhTe)(2)-induced neurodegeneration in rat striatum, evidencing a critical role for the MAPK and Akt signaling pathways and disruption of cytoskeletal homeostasis, which could be related with apoptotic neuronal death and astrogliosis.
Toxicology and Applied Pharmacology 08/2012; 264(2):143-52. · 3.98 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: In this study, 12 healthy men aging 22.8 ± 2.2 years old were submitted to a protocol of isometric resistance to fatigue contemplating elbow flexion on three different angles: 45°, 90° and 135°. The objective was to study electromyographic median frequency (MDF) in the following muscles: i) Biceps Brachialis Long Head (BBL), Brachioradialis (BRD), Flexor Digitorum Superficialis (FDS), Triceps Brachialis Long Head (TBL), and Extensor Digitorum (ED). It was verified that, for all muscles, including the muscles that act in opposition to the contraction, fatigue presence was verified by the decrease of MDF value.
Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 08/2012; 2012:3592-5.
[Show abstract][Hide abstract] ABSTRACT: Methylglyoxal is a dicarbonyl compound that is physiologically produced by enzymatic and non-enzymatic reactions. It can lead to cytotoxicity, which is mainly related to Advanced Glycation End Products (AGEs) formation. Methylglyoxal and AGEs are involved in the pathogenesis of Neurodegenerative Diseases (ND) and, in these situations, can cause the impairment of energetic metabolism. Astroglial cells play critical roles in brain metabolism and the appropriate functioning of astrocytes is essential for the survival and function of neurons. However, there are only a few studies evaluating the effect of methylglyoxal on astroglial cells. The aim of this study was to evaluate the effect of methylglyoxal exposure, over short (1 and 3 h) and long term (24 h) periods, on glucose, glycine and lactate metabolism in C6 glioma cells, as well as investigate the glyoxalase system and AGEs formation. Glucose uptake and glucose oxidation to CO(2) increased in 1 h and the conversion of glucose to lipids increased at 3 h. In addition, glycine oxidation to CO(2) and conversion of glycine to lipids increased at 1 h, whereas the incorporation of glycine in proteins decreased at 1 and 3 h. Methylglyoxal decreased glyoxalase I and II activities and increased AGEs content within 24 h. Lactate oxidation and lactate levels were not modified by methylglyoxal exposure. These data provide evidence that methylglyoxal may impair glucose metabolism and can affect glyoxalase activity. In periods of increased methylglyoxal exposure, such alterations could be exacerbated, leading to further increases in intracellular methylglyoxal and AGEs, and therefore triggering and/or worsening ND.
[Show abstract][Hide abstract] ABSTRACT: In this study we investigated the anti-inflammatory effects of chronic ethanol (EtOH) treatment on lipopolysaccharide (LPS)-stimulated C6 glioma cells. The cells were chronically treated with 200mM EtOH; coincubation with LPS and EtOH was obtained upon addition of 2μg/ml LPS to the incubation medium in the last 24h of EtOH exposure. We found that EtOH prevented the LPS-induced production of tumor necrosis factor α (TNFα) without decreasing cell viability. Either LPS treated or EtOH plus LPS treated cells presented upregulated glial fibrillary acidic protein (GFAP) and downregulated vimentin levels characterizing a program of reactive astrogliosis. Also, EtOH plus LPS stimulation greatly increased the oxidative stress generation evaluated by DCF-DA measurement, while either EtOH alone or LPS alone was unable to induce oxidative stress. Western blot analysis indicated that either EtOH, LPS or EtOH plus LPS treatments are unable to affect Akt/GSK3β signaling pathway. However, LPS alone and EtOH plus LPS co-treatment inhibited Erk phosphorylation. A dramatic loss of stress fibers was found in EtOH exposed cells, evaluated by cytochemistry using phalloidin-fluorescein. However, LPS alone was not able to disrupt actin organization. Furthermore, cells co-incubated with LPS and EtOH presented reversion of the disrupted stress fibers provoked by EtOH. Supporting this action, RhoA and vinculin immunocontent were upregulated in response to EtOH plus LPS. Interestingly, EtOH suppresses the inflammatory cascade (TNFα production) in response to LPS. Concomitantly it sustains Erk inhibition, increases oxidative stress generation and induces reactive astrogliosis in the presence of LPS, conditions associated with neurotoxicity. The effects observed were not supported by actin reorganization. Altogether, these findings suggest that Erk signaling inhibition could play a role in both suppressing TNFα production and inducing oxidative stress generation and astrogliosis, therefore modulating a dual action of EtOH plus LPS in glial cells.
Journal of neuroimmunology 05/2012; 249(1-2):8-15. · 2.84 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Adverse early life events, such as periodic maternal separation, may alter the normal pattern of brain development and subsequently the vulnerability to a variety of mental disorders in adulthood. Patients with a history of early adversities show higher frequency of post-traumatic stress disorder (PTSD). This study was undertaken to verify if repeated long-term separation of pups from dams would affect memory and oxidative stress parameters after exposure to an animal model of PTSD. Nests of Wistar rats were divided into intact and subjected to maternal separation (incubator at 32°C, 3 h/day) during post-natal days 1-10. When adults, the animals were subdivided into exposed or not to a PTSD model consisting of exposure to inescapable footshock, followed by situational reminders. One month after exposure to the shock, the animals were exposed to a memory task (Morris water maze) and another month later animals were sacrificed and DNA breaks and antioxidant enzymes activities were measured in the hippocampus. Rats exposed to shock or maternal separation plus shock showed long-lasting effects on spatial memory, spending more time in the opposite quadrant of the water maze. This effect was higher in animals subjected to both maternal separation and shock. Both shock and maternal separation induced a higher score of DNA breaks in the hippocampus. No differences were observed on antioxidant enzymes activities. In conclusion, periodic maternal separation may increase the susceptibility to the effects of a stressor applied in adulthood on performance in the water maze. Increased DNA breaks in hippocampus was induced by both, maternal separation and exposure to shock.
Neurochemical Research 11/2011; 37(4):700-7. · 2.13 Impact Factor