RESUMO
Aggressive behaviour can ensure animal access to local resources. To reduce constant costs in the defence of territories, species could save energy with conflicts avoiding aggression with neighbour or in situations with abundance of resources. In the present study, we analysed the effect of distance among colonies and resource availability on the aggression level and responses to chemical cues of Nasutitermes aff. coxipoensis (Holmgren) (Termitidae: Nasutitermitinae). Manipulation of resource offer was conducted in the field, where nests with different distances were kept without addition of baits (control), with addition of three or 16 sugarcane baits/nest. After 3 months, aggressiveness, linear and Y-shaped trail-following bioassays were carried out with all pairwise combinations of colonies in each treatment. Our results showed that aggressive index of N. aff. coxipoensis was affected by the resource availability. However, individuals from colonies with 0 and 3 baits/nest showed a higher number of fighting with neighbours than those from non-neighbours colonies. Termite workers from colonies without baits (control) followed shorter distance in the linear trails compared to those from colonies with addition of baits. In all treatments, there was no preference of workers in relation to the choice of chemical cues from own or other colonies. The response of intercolonial aggressiveness in N. aff. coxipoensis seems to be resource-dependent. These results may contribute to the comprehension of the use of space by N. aff. coxipoensis and could be useful to explain patterns of termite co-occurrence at different spatial scales, from local (inside the nest-e.g. cohabitation of nests by inquilines) to regional (e.g. around the nest).
Assuntos
Agressão , Isópteros/química , Isópteros/fisiologia , Animais , Sinais (Psicologia) , Ecossistema , Comportamento de NidaçãoRESUMO
Symbiosis between plants and ants include examples in which the plant provides shelter and/or food for ants that, in turn, act in the defense or in the dispersion of seeds from the host plant. Although traditionally referred as mutualistic, the results of these interactions may vary with the ecological context in which patterns are involved. A range of species have facultative association with Turnera subulata (Turneraceae). Here, using behavioral bioassays, we investigated the effects of the most frequent ant species associated with T. subulata (Brachymyrmex sp.1, Camponotus blandus (Smith), Dorymyrmex sp.1, Crematogaster obscurata Emery, and Solenopsis invicta Buren) in the dispersion of plant host seeds and in the number of seedlings around the associated ant nests. We also evaluated the effects of these ant species in the germination of T. subulata seeds, in the consumption of elaiosome, and in the attractiveness to elaiosome odor. Our results showed that the ant species associated with T. subulata presented variation in the attraction by the odor and in the rate of consumption of the elaiosomes. However, none of the ant species studied contributed significantly to the increase of seed germination and seedling growth. Our results suggest that the consumption of the elaiosome by ant species is not a determinant factor to the success of germination of T. subulata. However, such species could contribute indirectly to seed germination by carrying seeds to sites more fertile to germination. In general, our results help to elucidate the results of ecological interactions involving ants and plants.
Assuntos
Formigas/fisiologia , Germinação , Dispersão de Sementes , Turnera/fisiologia , Animais , SimbioseRESUMO
Breast cancer is the most common cancer among women and its metastatic potential is responsible for numerous deaths. Thus, the need to find new targets for improving treatment, and even finding the cure, becomes increasingly greater. Ion channels are known to participate in several physiological functions, such as muscle contraction, cell volume regulation, immune response and cell proliferation. In breast cancer, different types of ion channels have been associated with tumorigenesis. Recently, voltage-gated Na+ channels (VGSC) have been implicated in the processes that lead to increased tumor aggressiveness. To explain this relationship, different theories, associated with pH changes, gene expression and intracellular Ca2+, have been proposed in an attempt to better understand the role of these ion channels in breast cancer. However, these theories are having difficulty being accepted because most of the findings are contrary to the present scientific knowledge. Several studies have shown that VGSC are related to different types of cancer, making them a promising pharmacological target against this debilitating disease. Molecular biology and cell electrophysiology have been used to look for new forms of treatment aiming to reduce aggressiveness and the disease progress.
Assuntos
Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Regulação Neoplásica da Expressão Gênica , Canais de Sódio Disparados por Voltagem/metabolismo , Feminino , Humanos , Invasividade Neoplásica , Metástase NeoplásicaRESUMO
Nanodiamonds (NDs), multiwalled carbon nanotubes (MWCNTs) and gold nanorods (NRs) can be functionalized to promote gene delivery to hard-to-transfect cells with higher transfection efficiency than cationic lipids, and inducing less cell death.
Assuntos
Nanoestruturas/química , Transfecção/métodos , Animais , Linhagem Celular , Camundongos , Nanoestruturas/ultraestruturaRESUMO
In cardiomyocytes, calcium (Ca2+) release units comprise clusters of intracellular Ca2+ release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca2+ sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca2+ sparks (HC=7.61±0.26 vs NC=4.79±0.19 per 100 µm/s) and decreased its amplitude (HC=0.260±0.08 vs NC=0.324±0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05±0.08 vs NC=1.26±0.01 µm), total duration (HC=11.51±0.12 vs NC=14.97±0.24 ms), time to peak (HC=4.84±0.06 vs NC=6.31±0.14 ms), and time constant of decay (HC=8.68±0.12 vs NC=10.21±0.22 ms). These changes were partially reversed in HT rats (frequency of Ca2+ sparks=6.26±0.19 µm/s, amplitude=0.282±0.10 ΔF/F0, full width at half-maximum amplitude=1.14±0.01 µm, total duration=13.34±0.17 ms, time to peak=5.43±0.08 ms, and time constant of decay=9.43±0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.
Assuntos
Animais , Masculino , Cálcio/fisiologia , Ventrículos do Coração/metabolismo , Hipertensão/terapia , Atividade Motora/fisiologia , Miócitos Cardíacos/metabolismo , Condicionamento Físico Animal/métodos , Sinalização do Cálcio/fisiologia , Teste de Esforço/métodos , Ventrículos do Coração/citologia , Hipertensão/metabolismo , Ratos Endogâmicos SHR , Ratos Wistar , Canal de Liberação de Cálcio do Receptor de Rianodina/genética , Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo , Proteínas de Ligação a Tacrolimo/genética , Proteínas de Ligação a Tacrolimo/metabolismoRESUMO
In cardiomyocytes, calcium (Ca²âº) release units comprise clusters of intracellular Ca²âº release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca²âº sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca²âº sparks (HC=7.61 ± 0.26 vs NC=4.79 ± 0.19 per 100 µm/s) and decreased its amplitude (HC=0.260 ± 0.08 vs NC=0.324 ± 0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05 ± 0.08 vs NC=1.26 ± 0.01 µm), total duration (HC=11.51 ± 0.12 vs NC=14.97 ± 0.24 ms), time to peak (HC=4.84 ± 0.06 vs NC=6.31 ± 0.14 ms), and time constant of decay (HC=8.68 ± 0.12 vs NC=10.21 ± 0.22 ms). These changes were partially reversed in HT rats (frequency of Ca²âº sparks=6.26 ± 0.19 µm/s, amplitude=0.282 ± 0.10 ΔF/F0, full width at half-maximum amplitude=1.14 ± 0.01 µm, total duration=13.34 ± 0.17 ms, time to peak=5.43 ± 0.08 ms, and time constant of decay=9.43 ± 0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.
Assuntos
Cálcio/fisiologia , Ventrículos do Coração/metabolismo , Hipertensão/terapia , Atividade Motora/fisiologia , Miócitos Cardíacos/metabolismo , Condicionamento Físico Animal/métodos , Animais , Sinalização do Cálcio/fisiologia , Teste de Esforço/métodos , Ventrículos do Coração/citologia , Hipertensão/metabolismo , Masculino , Ratos Endogâmicos SHR , Ratos Wistar , Canal de Liberação de Cálcio do Receptor de Rianodina/genética , Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo , Proteínas de Ligação a Tacrolimo/genética , Proteínas de Ligação a Tacrolimo/metabolismoRESUMO
BACKGROUND AND AIMS: Thiamine deficiency is a condition that is known to cause damage to the nervous and cardiovascular systems because it interferes with cellular metabolism. It is well known that the control of vascular function is highly dependent on the production of nitric oxide (NO) by NO synthases. Studies exploring the physiological relevance of NO signaling under conditions of thiamine deficiency are scarce. The present study sought to investigate whether chronic metabolic changes would cause alterations in vascular responsiveness. METHODS AND RESULTS: By removing thiamine from the diet, we observed a reduced acetylcholine-mediated relaxation and an increased phenylephrine-mediated vasoconstriction in the aortas containing functional endothelium. Removal of the endothelium or the pre-treatment of vessels with l-NAME restored the contractile responses to the level of controls. Conversely, indomethacin did not modify phenylephrine-mediated contractions. We also used carbon microsensors to continually measure NO production in situ while simultaneously measuring the vascular tone. The results revealed a significant decrease in NO production. Western blot analysis showed a decreased expression of the total eNOS in the thiamine-deficient aorta compared to the control. Concentration-response curves for phenylephrine indicated no difference between the control and deficient groups in the presence and absence of SOD or Tyron. The NO donor DEA-NONOate produced a concentration-dependent relaxation response in the endothelium-denuded vessels that did not differ between the control and thiamine-deficient rats. CONCLUSION: Thiamine deficiency modulates eNOS-dependent NO production, leading to a decreased vasorelaxation and an increased contractile response in the rat aorta.
Assuntos
Óxido Nítrico/metabolismo , Deficiência de Tiamina/patologia , Doenças Vasculares/patologia , Acetilcolina/farmacologia , Animais , Aorta/efeitos dos fármacos , Aorta/metabolismo , Hidrazinas/farmacologia , Indometacina/farmacologia , Masculino , Contração Muscular/efeitos dos fármacos , NG-Nitroarginina Metil Éster/metabolismo , Óxido Nítrico Sintase/metabolismo , Óxido Nítrico Sintase Tipo III/genética , Óxido Nítrico Sintase Tipo III/metabolismo , Fenilefrina/farmacologia , Ratos , Ratos Wistar , Deficiência de Tiamina/complicações , Doenças Vasculares/etiologia , Vasoconstrição/efeitos dos fármacos , Vasodilatação/efeitos dos fármacosRESUMO
Thiamine deficiency during embryonic or early postnatal development causes deficits in cerebellum-dependent activities including motor control and procedural memory. Here, we give a detailed description of the changes to A-type current in cultured cerebellar granule neurons exposed to thiamine deficiency in vitro. A-type current in treated neurons was reduced to 51% of that in controls. The remaining A-type current in treated neurons exhibited normal activation kinetics and voltage dependence whereas inactivation was markedly faster. These effects were selective because the delayed-rectifier potassium current density and kinetics were unchanged in thiamine-deficient neurons. A computational model of the cerebellar granule neuron was used to test the impact of these alterations and predicts an increase in excitability that is especially pronounced for synaptic activation. Our results suggest that the loss of A-type potassium conductance leads to hyperactivity in cerebellar granule neurons and may contribute to cell death observed in the granule layer of cerebellum during thiamine-deficiency in vivo.
Assuntos
Fenômenos Biofísicos/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Canais de Potássio/fisiologia , Tiamina/metabolismo , Tiamina/farmacologia , Animais , Animais Recém-Nascidos , Biofísica , Cerebelo/citologia , Simulação por Computador , Estimulação Elétrica , Potenciais da Membrana/efeitos dos fármacos , Potenciais da Membrana/fisiologia , Modelos Neurológicos , Inibição Neural/efeitos dos fármacos , Inibição Neural/fisiologia , Técnicas de Patch-Clamp , Canais de Potássio/efeitos dos fármacos , Ratos , Ratos WistarRESUMO
Our objective was to determine lipid peroxidation and nuclear factor-κB (NF-κB) activation in skeletal muscle and the plasma cytokine profile following maximum progressive swimming. Adult male Swiss mice (N = 15) adapted to the aquatic environment were randomly divided into three groups: immediately after exercise (EX1), 3 h after exercise (EX2) and control. Animals from the exercising groups swam until exhaustion, with an initial workload of 2 percent of body mass attached to the tail. Control mice did not perform any exercise but were kept immersed in water for 20 min. Maximum swimming led to reactive oxygen species (ROS) generation in skeletal muscle, as indicated by increased thiobarbituric acid reactive species (TBARS) levels (4062.67 ± 1487.10 vs 19,072.48 ± 8738.16 nmol malondialdehyde (MDA)/mg protein, control vs EX1). Exercise also promoted NF-κB activation in soleus muscle. Cytokine secretion following exercise was marked by increased plasma interleukin-6 (IL-6) levels 3 h post-exercise (P < 0.05). Interleukin-10 (IL-10) levels were reduced following exercise and remained reduced 3 h post-exercise (P < 0.05). Plasma levels of other cytokines investigated, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin-12 (IL-12), were not altered by exercise. The present findings showed that maximum swimming, as well as other exercise models, led to lipid peroxidation and NF-κB activation in skeletal muscle and increased plasma IL-6 levels. The plasma cytokine response was also marked by reduced IL-10 levels. These results were attributed to exercise type and intensity.
Assuntos
Animais , Masculino , Camundongos , Citocinas/sangue , Peroxidação de Lipídeos/fisiologia , Músculo Esquelético/metabolismo , NF-kappa B/metabolismo , Natação/fisiologia , Índice de Massa Corporal , /sangue , /sangue , /sangue , Malondialdeído/metabolismo , Condicionamento Físico Animal/fisiologia , Distribuição Aleatória , Espécies Reativas de Oxigênio/metabolismo , Fatores de Tempo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
Our objective was to determine lipid peroxidation and nuclear factor-κB (NF-κB) activation in skeletal muscle and the plasma cytokine profile following maximum progressive swimming. Adult male Swiss mice (N = 15) adapted to the aquatic environment were randomly divided into three groups: immediately after exercise (EX1), 3 h after exercise (EX2) and control. Animals from the exercising groups swam until exhaustion, with an initial workload of 2% of body mass attached to the tail. Control mice did not perform any exercise but were kept immersed in water for 20 min. Maximum swimming led to reactive oxygen species (ROS) generation in skeletal muscle, as indicated by increased thiobarbituric acid reactive species (TBARS) levels (4062.67 ± 1487.10 vs 19,072.48 ± 8738.16 nmol malondialdehyde (MDA)/mg protein, control vs EX1). Exercise also promoted NF-κB activation in soleus muscle. Cytokine secretion following exercise was marked by increased plasma interleukin-6 (IL-6) levels 3 h post-exercise (P < 0.05). Interleukin-10 (IL-10) levels were reduced following exercise and remained reduced 3 h post-exercise (P < 0.05). Plasma levels of other cytokines investigated, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin-12 (IL-12), were not altered by exercise. The present findings showed that maximum swimming, as well as other exercise models, led to lipid peroxidation and NF-κB activation in skeletal muscle and increased plasma IL-6 levels. The plasma cytokine response was also marked by reduced IL-10 levels. These results were attributed to exercise type and intensity.