Aggressiveness Overcomes Body-Size Effects in Fights Staged between Invasive and Native Fish Species with Overlapping Niches

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Social isolation and aggressiveness in the Amazonian juvenile fish Astronotus ocellatus

Testamos o efeito do isolamento social sobre a agressividade no peixe amazônico, Astronotus ocellatus. Dez peixes juvenis foram transferidos de um aquário de agrupamento (60 x 60 x 40 cm) contendo 15 indivíduos (sem discriminação de sexo) para um aquário de isolamento (50 x 40 x 40 cm). A agressividade foi testada por meio de ataques e exibições direcionadas à imagem do peixe no espelho. O comportamento foi filmado durante 10 min em 4 momentos: 30 min, 1 dia, 5 dias e 15 dias após o isolamento. Nós analisamos a motivação agressiva por meio da latência para início do comportamento agonístico e pela freqüência dos ataques totais e específicos direcionados ao espelho. A latência para o comportamento agonístico reduziu ao longo do isolamento e houve uma tendência de aumento da freqüência de mouth fighting (um ataque de alta intensidade de agressão), mostrando-nos um aumento na motivação agressiva. Os resultados estão de acordo com os encontrados para ciclídeos juvenís de Haplochromis burtoni, mas discordam com os encontrados para Pterophylum scalare (acará bandeira). Sugerimos que o aumento da agressividade em A. ocellatus pode ser mediado pelo efeito de exposição prévia, da residência prévia ou por processos envolvendo reconhecimento de co-específicos.

Aggressiveness of pratylenchus brachyurus to sugarcane, compared with key nematode p. zeae

Pratylenchus zeae, Meloidogyne javanica and M. incognita are considered key species of nematodes in sugarcane in Brazil, but P. brachyurus is also frequently found. This study was conducted to determine the aggressiveness of P. brachyurus compared with P. zeae to sugarcane. Plants were grown in pots (100 L) in an open area with initial inoculation of 10, 100, 1,000, 10,000 and 100,000/plant for P. brachyurus and P. zeae. The nematode inocula were from in vitro, carrot-cylinder cultures. Sampling was performed every 60 days until 300 days after inoculation. At harvest, we evaluated the population dynamics of the nematodes and plant growth characteristics. The population for the initial levels of 10 and 100,000 specimens/plant, for P. brachyurus and P. zeae at 300 days after inoculation were similar. This fact shows that, upon detection of nematodes in a certain place during the planting of sugarcane, the ratoon on this area should be treated so as to control populations of P. brachyurus and/or P. zeae. The damage caused by the initial population of 10 specimens of P. brachyurus was similar to those of 10.000 specimens of P. zeae. The variety CTC 2 was classified as susceptible to P. zeae and intolerant to P. brachyurus. Compared to the control, the losses as measured by the volume and fresh weight of shoots by the nematode species were 29.82% and 40.34%, respectively. Pratylenchus brachyurus was more aggressive than P. zeae to the CTC 2 sugarcane variety.

The role of TMPRSS2:ERG in molecular stratification of PCa and its association with tumor aggressiveness: a study in Brazilian patients

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Gestational protein malnutrition impairs c-myc and p63 protein expression, increases prostatic intraepithelial neoplasia incidence and prostatitis aggressiveness in adult male offspring subjected to hormonal handling

Background: Prostate cancer is the second most common cancer diagnosed in men; however its etiology remains unknown. Previous studies have shown that environmental adverse factors, such as maternal nutritional status during pregnancy, can influence fetal development and predispose people to diseases in adult life. The feeding of low-protein diets to pregnant rats result in fetal growth disturbance, androgen/estrogen unbalance and changes in the expression and sensibility of hormone receptors in male offspring. These alterations can promote permanent changes in androgen dependent organs, such as in the prostate. In this sense, we hypothesized that the hormonal unbalance that occurs during aging can lead to an increase in the susceptibility to prostatic disorders. Aim: To evaluate our hypothesis, malnourished male rat offspring were submitted to simultaneous estrogen and testosterone exposure in adulthood, to drive lesions in the rat ventral prostate gland (VP). Methods: 17 week-old Wistar rats (n=48) that received in utero normal protein diet (NP group, AIN93G=17% protein) or low protein diet (RP group, AIN93G modified=6% protein) were given implants with 17β-estradiol plus testosterone administration (NPH and RPH groups) for 17 weeks. The animals were killed at the age of 34 weeks and the VP were excised, weighted and processed for histopathological, immunohistochemical (Ki67, AR, p63, e-caderin, laminin, c-myc and GSTP), biochemical and ultrastructural analysis. Results: Both absolute and relative VP weight from NPH animals were about 30% higher than RPH. Serological data showed that estradiol levels were similar in both groups, but testosterone levels were lower in the RPH male offspring. The steroid hormone exposure in adult life promoted prostate lesions in both RPH and NPH offspring associated with reactive stroma. VP from RPH group exhibited heightened susceptibility to prostatic intraepithelial neoplasia (mainly cribriform and signet ring-cell patterns) and increased the incidence and aggressiveness of prostatitis. In this group, a higher proportion of basal cells, increased proliferation index, lower expression ofthe androgen receptor and increased focus of collagenous micronodules closely associated to epithelial neoplasias were also observed. Conclusion:These observations suggest that maternal protein restriction alters adult prostate response to androgen/estrogen handling and increases susceptibility to prostate diseases. Ethical protocol:CEEA,476/2013 IBB-UNESP; Funding Support: 2009/50204-6 and 2013/09649-0.

A glycolytic phenotype is associated with prostate cancer progression and aggressiveness: a role for monocarboxylate transporters as metabolic targets for therapy

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

The Role of CEO Statements of Aggressiveness and the Competitive Aggressiveness of Firms: What is the Impact on Performance?

This research examines the impact of a CEO’s statements of aggressiveness on his or her organization’s competitive moves and subsequent performance. Hypotheses were developed based on previous work in Upper Echelon Theory and competitive dynamics. Based on this prior literature, it was hypothesized aggressive statements by CEOs will be associated with more aggressive organizations. It was also hypothesized these more aggressive organizations would display better performance than less aggressive organizations. A content analysis of letters to shareholders and trade publications was performed. This data was analyzed using multiple regression in SPSS 17 to test the hypotheses that aggressive statements by CEOs are associated with aggressive organizations and higher performance. Aggression scores for the content analysis were generated using the software package DICTION. The sample for the study was the organizations with the most revenue in two industries, automobile manufacturing and retailing. Data collection covered a five-year time span from 2003-2007, with performance data lagged one year. Control variables employed included CEO tenure, CEO background, organization size, and organization age. The findings indicate that CEO statements of aggressiveness do not significantly impact the competitive aggressiveness or the performance of their organizations. The implications of these findings are discussed and potential avenues for future research in the area are outlined.

Aggressiveness Overcomes Body-Size Effects in Fights Staged between Invasive and Native Fish Species with Overlapping Niches

Approximately 50 years ago, Nile tilapia were accidentally introduced to Brazil, and the decline of pearl cichlid populations, which has been intensified by habitat degradation, in some locations has been associated with the presence of Nile tilapia. There is, however, little strong empirical evidence for the negative interaction of non-native fish populations with native fish populations; such evidence would indicate a potential behavioural mechanism that could cause the population of the native fish to decline. In this study, we show that in fights staged between pairs of Nile tilapia and pearl cichlids of differing body size, the Nile tilapia were more aggressive than the pearl cichlid. Because this effect prevailed over body-size effects, the pearl cichlids were at a disadvantage. The niche overlap between the Nile tilapia and the pearl cichlid in nature, and the competitive advantage shown by the Nile tilapia in this study potentially represent one of several possible results of the negative interactions imposed by an invasive species. These negative effects may reduce population viability of the native species and cause competitive exclusion.

Matrix metalloproteinases, tissue inhibitors of metalloproteinases, and growth factors regulate the aggressiveness and proliferative activity of keratocystic odontogenic tumors

Objective. The objective of this preliminary study was to evaluate the expression of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs) and growth factors in keratocystic odontogenic tumors (KOTs). Study Design. The expression of MMPs, TIMPs, growth factors, and the extracellular signal-regulated kinase (ERK) 1/2 signaling pathway were assessed by immunohistochemistry in 15 cases of KOT and 4 cases of calcifying cystic odontogenic tumor (CCOT). Results. KOT samples expressed significantly higher amounts of MMPs, TIMPs, growth factors, epidermal growth factor receptor (EGFR), and ERK compared with CCOT samples, with the exception of MMP-2 and TIMP-1. Conclusions. MMP-9, TIMP-2, EGF and transforming growth factor alpha act together and likely regulate the proliferation and aggressiveness of KOT. ERK-1/2 serves as the transducer of signals generated by these proteins, which signal through the common receptor, EGFR. This process may be related to the increased proliferation and aggressiveness observed in KOT. (Oral Surg Oral Med Oral Pathol Oral Radiol 2012;114:487-496)

TAZ AS A REGULATOR OF MESENCHYMAL TRANSFORMATION AND CLINICAL AGGRESSIVENESS IN GLIOMAS

Glioblastoma multiforme (GBM) is an aggressive, high grade brain tumor. Microarray studies have shown a subset of GBMs with a mesenchymal gene signature. This subset is associated with poor clinical outcome and resistance to treatment. To establish the molecular drivers of this mesenchymal transition, we correlated transcription factor expression to the mesenchymal signature and identified transcriptional co-activator with PDZ-binding motif (TAZ) to be highly associated with the mesenchymal shift. High TAZ expression correlated with worse clinical outcome and higher grade. These data led to the hypothesis that TAZ is critical to the mesenchymal transition and aggressive clinical behavior seen in GBM. We investigated the expression of TAZ, its binding partner TEAD, and the mesenchymal marker FN1 in human gliomas. Western analyses demonstrated increased expression of TAZ, TEAD4, and FN1 in GBM relative to lower grade gliomas. We also identified CpG islands in the TAZ promoter that are methylated in most lower grade gliomas, but not in GBMs. TAZ-methylated glioma stem cell (GSC) lines treated with a demethylation agent showed an increase in mRNA and protein TAZ expression; therefore, methylation may be another novel way TAZ is regulated since TAZ is epigenetically silenced in tumors with a better clinical outcome. To further characterize the role of TAZ in gliomagenesis, we stably silenced or over-expressed TAZ in GSCs. Silencing of TAZ decreased invasion, self-renewal, mesenchymal protein expression, and tumor-initiating capacity. Over-expression of TAZ led to an increase in invasion, mesenchymal protein expression, mesenchymal differentiation, and tumor-initiating ability. These actions are dependent on TAZ interacting with TEAD since all these effects were abrogated with TAZ could not bind to TEAD. We also show that TAZ and TEAD directly bind to mesenchymal gene promoters. Thus, TAZ-TEAD interaction is critically important in the mesenchymal shift and in the aggressive clinical behavior of GBM. We identified TAZ as a regulator of the mesenchymal transition in gliomas. TAZ could be used as a biomarker to both estimate prognosis and stratify patients into clinically relevant subgroups. Since mesenchymal transition is correlated to tumor aggressiveness, strategies to target and inhibit TAZ-TEAD and the downstream gene targets may be warranted in alternative treatment.

The aggressiveness of pig slurry to cement mortars

The aim was to measure the behaviour of various mortars employed in livestock media in central Spain and to analyse the aggressiveness of pig slurry to cement blended with fly ash mortars. To achieve this, mortar specimens were immersed in ponds storing pig slurry. Mortar specimens, of 40 ? 40 ? 160 mm, were made from four types of cement commonly used and recommended for rural areas. The types were a sulphate-resistant Portland cement and three cements blended in different proportions with fly ash and limestone filler. After 3, 6, 12, 24, 36, 48 and 60 months of exposure, three or four specimens of each cement type were removed from the pond and washed with water. Their compressive strength and microstructure (X-ray diffraction, mercury intrusion pore-symmetry, thermal analysis and scanning electron microscopy) were then measured. Sulphate-resistant Portland cement (SR-PC), found to be more susceptible to degradation due to its greater proportion of macro-pores and increased total porosity, was found not to be suitable for use with livestock. After 60 months of immersion in the pig slurry medium, CEM II-A (40.3%) mortar retained the greatest compressive strength. Mortars with less than 20% replacement of cement by fly ash were found to be the most durable, with the most suitable mechanical behaviour.

PEG-3, a nontransforming cancer progression gene, is a positive regulator of cancer aggressiveness and angiogenesis

Cancer is a progressive disease culminating in acquisition of metastatic potential by a subset of evolving tumor cells. Generation of an adequate blood supply in tumors by production of new blood vessels, angiogenesis, is a defining element in this process. Although extensively investigated, the precise molecular events underlying tumor development, cancer progression, and angiogenesis remain unclear. Subtraction hybridization identified a genetic element, progression elevated gene-3 (PEG-3), whose expression directly correlates with cancer progression and acquisition of oncogenic potential by transformed rodent cells. We presently demonstrate that forced expression of PEG-3 in tumorigenic rodent cells, and in human cancer cells, increases their oncogenic potential in nude mice as reflected by a shorter tumor latency time and the production of larger tumors with increased vascularization. Moreover, inhibiting endogenous PEG-3 expression in progressed rodent cancer cells by stable expression of an antisense expression vector extinguishes the progressed cancer phenotype. Cancer aggressiveness of PEG-3 expressing rodent cells correlates directly with increased RNA transcription, elevated mRNA levels, and augmented secretion of vascular endothelial growth factor (VEGF). Furthermore, transient ectopic expression of PEG-3 transcriptionally activates VEGF in transformed rodent and human cancer cells. Taken together these data demonstrate that PEG-3 is a positive regulator of cancer aggressiveness, a process regulated by augmented VEGF production. These studies also support an association between expression of a single nontransforming cancer progression-inducing gene, PEG-3, and the processes of cancer aggressiveness and angiogenesis. In these contexts, PEG-3 may represent an important target molecule for developing cancer therapeutics and inhibitors of angiogenesis.

Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities

Brain-derived neurotrophic factor (BDNF) has trophic effects on serotonergic (5-HT) neurons in the central nervous system. However, the role of endogenous BDNF in the development and function of these neurons has not been established in vivo because of the early postnatal lethality of BDNF null mice. In the present study, we use heterozygous BDNF+/− mice that have a normal life span and show that these animals develop enhanced intermale aggressiveness and hyperphagia accompanied by significant weight gain in early adulthood; these behavioral abnormalities are known to correlate with 5-HT dysfunction. Forebrain 5-HT levels and fiber density in BDNF+/− mice are normal at an early age but undergo premature age-associated decrements. However, young adult BDNF+/− mice show a blunted c-fos induction by the specific serotonin releaser-uptake inhibitor dexfenfluramine and alterations in the expression of several 5-HT receptors in the cortex, hippocampus, and hypothalamus. The heightened aggressiveness can be ameliorated by the selective serotonin reuptake inhibitor fluoxetine. Our results indicate that endogenous BDNF is critical for the normal development and function of central 5-HT neurons and for the elaboration of behaviors that depend on these nerve cells. Therefore, BDNF+/− mice may provide a useful model to study human psychiatric disorders attributed to dysfunction of serotonergic neurons.