16 resultados para biological changes


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Variations in environmental parameters (e. g. temperature) that form part of global climate change have been associated with shifts in the timing of seasonal events for a broad range of organisms. Most studies evaluating such phenological shifts of individual taxa have focused on a limited number of locations, making it difficult to assess how such shifts vary regionally across a species range. Here, by using 1445 records of the date of first nesting for loggerhead sea turtles (Caretta caretta) at different breeding sites, on different continents and in different years across a broad latitudinal range (25-39 degrees ' N), we demonstrate that the gradient of the relationship between temperature and the date of first breeding is steeper at higher latitudes, i.e. the phenological responses to temperature appear strongest at the poleward range limit. These findings support the hypothesis that biological changes in response to climate change will be most acute at the poleward range limits and are in accordance with the predictions of MacArthur's hypothesis that poleward range limit for species range is environmentally limited. Our findings imply that the poleward populations of loggerheads are more sensitive to climate variations and thus they might display the impacts of climate change sooner and more prominently.

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Accumulating data have led to a re-conceptualization of depression that emphasizes the role of immuneinflammatory processes, coupled to oxidative and nitrosative stress (O&NS). These in turn drive the production of neuroregulatory tryptophan catabolites (TRYCATs), driving tryptophan away from serotonin, melatonin, and Nacetylserotonin production, and contributing to central dysregulation. This revised perspective better encompasses the diverse range of biological changes occurring in depression and in doing so provides novel and readily attainable treatment targets, as well as potential screening investigations prior to treatment initiation. We briefly review the role that immune-inflammatory, O&NS, and TRYCAT pathways play in the etiology, course, and treatment of depression. We then discuss the pharmacological treatment implications arising from this, including the potentiation of currently available antidepressants by the adjunctive use of immune- and O&NS- targeted therapies. The use of such a frame of reference and the treatment benefits attained are likely to have wider implications and utility for depression-associated conditions, including the neuroinflammatory and (neuro)degenerative disorders.

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BACKGROUND: Bipolar disorder (BD) is commonly comorbid with many medical disorders including atopy, and appears characterized by progressive social, neurobiological, and functional impairment associated with increasing number of episodes and illness duration. Early and late stages of BD may present different biological features and may therefore require different treatment strategies. Consequently, the aim of this study was to evaluate serum levels of eotaxin/CCL11, eotaxin-2/CCL24, IL-2, IL-4, IL-6, IL-10, IL-17, TNF-α, IFNγ, BDNF, TBARS, carbonyl, and GPx in a sample of euthymic patients with BD at early and late stages compared to controls. METHODS: Early-stage BD patients, 12 late-stage patients, and 25 controls matched for sex and age were selected. 10mL of peripheral blood was drawn from all subjects by venipuncture. Serum levels of BDNF, TBARS, carbonyl content, glutathione-peroxidase activity (GPx), cytokines (IL-2, IL-4, IL-6, IL-10, IL-17, TNF-α and IFNγ), and chemokines (eotaxin/CCL11 and eotaxin-2/CCL24) were measured. RESULTS: There were no demographic differences between patients and controls. No significant differences were found for any of the biomarkers, except chemokine eotaxin/CCL11, whose serum levels were higher in late-stage patients with BD when compared to controls (p=0.022; Mann-Whitney U test). LIMITATIONS: Small number of subjects and use of medication may have influenced in our results. CONCLUSION: The present study suggests a link between biomarkers of atopy and eosinophil function and bipolar disorder. These findings are also in line with progressive biological changes partially mediated by inflammatory imbalance, a process referred to as neuroprogression.

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Background
Our understanding of the importance of transcriptional regulation for biological function is continuously improving. We still know, however, comparatively little about how environmentally induced stress affects gene expression in vertebrates, and the consistency of transcriptional stress responses to different types of environmental stress. In this study, we used a multi-stressor approach to identify components of a common stress response as well as components unique to different types of environmental stress. We exposed individuals of the coral reef fish Pomacentrus moluccensis to hypoxic, hyposmotic, cold and heat shock and measured the responses of approximately 16,000 genes in liver. We also compared winter and summer responses to heat shock to examine the capacity for such responses to vary with acclimation to different ambient temperatures.
Results
We identified a series of gene functions that were involved in all stress responses examined here, suggesting some common effects of stress on biological function. These common responses were achieved by the regulation of largely independent sets of genes; the responses of individual genes varied greatly across different stress types. In response to heat exposure over five days, a total of 324 gene loci were differentially expressed. Many heat-responsive genes had functions associated with protein turnover, metabolism, and the response to oxidative stress. We were also able to identify groups of co-regulated genes, the genes within which shared similar functions.
Conclusion
This is the first environmental genomic study to measure gene regulation in response to different environmental stressors in a natural population of a warm-adapted ectothermic vertebrate. We have shown that different types of environmental stress induce expression changes in genes with similar gene functions, but that the responses of individual genes vary between stress types. The functions of heat-responsive genes suggest that prolonged heat exposure leads to oxidative stress and protein damage, a challenge of the immune system, and the re-allocation of energy sources. This study hence offers insight into the effects of environmental stress on biological function and sheds light on the expected sensitivity of coral reef fishes to elevated temperatures in the future.

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The research successfully showed how biological communities change in wetlands that are affected by salinity and altered water regimes as a result of irrigation and river regulation. As an outcome of the study, recommendations have been made for the future management of wetlands in the Kerang region in northern Victoria.

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The effective management of our marine ecosystems requires the capability to identify, characterise and predict the distribution of benthic biological communities within the overall seascape architecture. The rapid expansion of seabed mapping studies has seen an increase in the application of automated classification techniques to efficiently map benthic habitats, and the need of techniques to assess confidence of model outputs. We use towed video observations and 11 seafloor complexity variables derived from multibeam echosounder (MBES) bathymetry and backscatter to predict the distribution of 8 dominant benthic biological communities in a 54 km2 site, off the central coast of Victoria, Australia. The same training and evaluation datasets were used to compare the accuracies of a Maximum Likelihood Classifier (MLC) and two new generation decision tree methods, QUEST (Quick Unbiased Efficient Statistical Tree) and CRUISE (Classification Rule with Unbiased Interaction Selection and Estimation), for predicting dominant biological communities. The QUEST classifier produced significantly better results than CRUISE and MLC model runs, with an overall accuracy of 80% (Kappa 0.75). We found that the level of accuracy with the size of training set varies for different algorithms. The QUEST results generally increased in a linear fashion, CRUISE performed well with smaller training data sets, and MLC performed least favourably overall, generating anomalous results with changes to training size. We also demonstrate how predicted habitat maps can provide insights into habitat spatial complexity on the continental shelf. Significant variation between patch-size and habitat types and significant correlations between patch size and depth were also observed.

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The marine and estuarine ecosystems of South Australia are likely to alter significantly in response to a changing climate, but also in response to managerial decisions we make. The allocation of fishing effort is an example of one such decision. We summarise some projections on a state-wide basis for how different components of these ecosystems may be expected to change. We anticipate that tropical elements will expand in range but cold-temperate communities will contract or disappear from South Australia. As a specific example, we have modelled the ecosystem states of the Coorong and the Murray Mouth. We combined biological and physico-chemical components of an ecosystem into co-occurring units (termed ecosystem states) with well-defined thresholds between them. Predictions were then made using time series of inputs from modelled water flows and other predictors. Using this model, we will discuss the likely implication of a range of climate change and management scenarios, highlighting the potential impact on the commercial fishing opportunities. Specifically we will discuss the potential sensitivity of the fishery to climate changes versus various management options. Understanding these possible future changes should allow the industry to adapt before climate change reduces the sustainability of the industry.

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The hypothesis that heavy fishing pressure has led to changes in the biological characteristics of the estuary cobbler (Cnidoglanis macrocephalus) was tested in a large seasonally open estuary in southwestern Australia, where this species completes its life cycle and is the most valuable commercial fish species. Comparisons were made between seasonal data collected for this plotosid (eeltail catfish) in Wilson Inlet during 2005-08 and those recorded with the same fishery-independent sampling regime during 1987-89. These comparisons show that the proportions of larger and older individuals and the catch rates in the more recent period were far lower, i.e., they constituted reductions of 40% for fish ≥430 mm total length, 62% for fish ≥4 years of age, and 80% for catch rate. In addition, total mortality and fishing-induced mortality estimates increased by factors of ~2 and 2.5, respectively. The indications that the abundance and proportion of older C. macrocephalus declined between the two periods are consistent with the perception of long-term commercial fishermen and their shift toward using a smaller maximum gill net mesh to target this species. The sustained heavy fishing pressure on C. macrocephalus between 1987-89 and 2005-08 was accompanied by a marked reduction in length and age at maturity of this species. The shift in probabilistic maturation reaction norms toward smaller fish in 2005-08 and the lack of a conspicuous change in growth between the two periods indicate that the maturity changes were related to fishery-induced evolution rather than to compensatory responses to reduced fish densities.

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The ability to quantify change in marine benthic habitats must be considered a key goal of marine habitat mapping activities. Changes in distribution of distinct suites of benthic biological species may occur as a result of natural or human induced processes and these processes may operate at a range of temporal and spatial scales. It is important to understand natural small scale inter-annual patterns of change in order to separate these signals from potential patterns of longer term change. Work to describe these processes of change from an acoustic remote sensing stand point has thus far been limited due to the relatively recent availability of full coverage swath acoustic datasets and cost pressures associated with multiple surveys of the same area. This paper describes the use of landscape transition analysis as a means to differentiate seemingly random patterns of habitat change from systematic signals of habitat transition at a shallow (10–50 m depth) 18 km2 study area on the temperate Australian continental shelf between the years 2006 and 2007. Supervised classifications for each year were accomplished using independently collected high resolution (3 m cell-size) multibeam echosounder (MBES) and video-derived reference data. Of the 4 representative biotic classes considered, signals of directional systematic changes were observed to occur between a shallow kelp dominated class, a deep sessile invertebrate dominated class and a mixed class of kelp and sessile invertebrates. These signals of change are interpreted as inter-annual variation in the density and depth related extent of canopy forming kelp species at the site, a phenomenon reported in smaller scale temporal studies of the same species. The methods applied in this study provide a detailed analysis of the various components of the traditional change detection cross tabulation matrix allowing identification of the strongest signals of systematic habitat transitions across broad geographical regions. Identifying clear patterns of habitat change is an important first step in linking these patterns to the processes that drive them.

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Multiple studies have demonstrated an association between cigarette smoking and increased anxiety symptoms or disorders, with early life exposures potentially predisposing to enhanced anxiety responses in later life. Explanatory models support a potential role for neurotransmitter systems, inflammation, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophins and neurogenesis, and epigenetic effects, in anxiety pathogenesis. All of these pathways are affected by exposure to cigarette smoke components, including nicotine and free radicals. This review critically examines and summarizes the literature exploring the role of these systems in increased anxiety and how exposure to cigarette smoke may contribute to this pathology at a biological level. Further, this review explores the effects of cigarette smoke on normal neurodevelopment and anxiety control, suggesting how exposure in early life (prenatal, infancy, and adolescence) may predispose to higher anxiety in later life. A large heterogenous literature was reviewed that detailed the association between cigarette smoking and anxiety symptoms and disorders with structural brain changes, inflammation, and cell-mediated immune markers, markers of oxidative and nitrosative stress, mitochondrial function, neurotransmitter systems, neurotrophins and neurogenesis. Some preliminary data were found for potential epigenetic effects. The literature provides some support for a potential interaction between cigarette smoking, anxiety symptoms and disorders, and the above pathways; however, limitations exist particularly in delineating causative effects. The literature also provides insight into potential effects of cigarette smoke, in particular nicotine, on neurodevelopment. The potential treatment implications of these findings are discussed in regards to future therapeutic targets for anxiety. The aforementioned pathways may help mediate increased anxiety seen in people who smoke. Further research into the specific actions of nicotine and other cigarette components on these pathways, and how these pathways interact, may provide insights that lead to new treatment for anxiety and a greater understanding of anxiety pathogenesis.

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Anodization of titanium and its alloys, under controlled conditions, generates a nanotubular architecture on the material surface. The biological consequences of such changes are poorly understood, and therefore, we have analyzed the cellular and molecular responses of osteoblasts that were plated on nanotubular anodized surface of a titanium-zirconium (TiZr) alloy. Upon comparing these results with those obtained on acid etched and polished surfaces of the same alloy, we observed a significant increase in adhesion and proliferation of cells on anodized surfaces as compared to acid etched or polished surface. The expression of genes related to cell adhesion was high only on anodized TiZr, but that of genes related to osteoblast differentiation and osteocalcin protein and extracellular matrix secretion were higher on both anodized and acid etched surfaces. Examination of surface morphology, topography, roughness, surface area and wettability using scanning electron microscopy, atomic force microscopy, and contact angle goniometry, showed that higher surface area, hydrophilicity, and nanoscale roughness of nanotubular TiZr surfaces, which were generated specifically by the anodization process, could strongly enhance the adhesion and proliferation of osteoblasts. We propose that biological properties of known bioactive titanium alloys can be further enhanced by generating nanotubular surfaces using anodization.

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Marine diatoms and dinoflagellates play a variety of key ecosystem roles as important primary producers (diatoms and some dinoflagellates) and grazers (some dinoflagellates). Additionally some are harmful algal bloom (HAB) species and there is widespread concern that HAB species may be increasing accompanied by major negative socio-economic impacts, including threats to human health and marine harvesting1, 2. Using 92,263 samples from the Continuous Plankton Recorder survey, we generated a 50-year (1960–2009) time series of diatom and dinoflagellate occurrence in the northeast Atlantic and North Sea. Dinoflagellates, including both HAB taxa (for example, Prorocentrum spp.) and non-HAB taxa (for example, Ceratium furca), have declined in abundance, particularly since 2006. In contrast, diatom abundance has not shown this decline with some common diatoms, including both HAB (for example, Pseudo-nitzschia spp.) and non-HAB (for example, Thalassiosira spp.) taxa, increasing in abundance. Overall these changes have led to a marked increase in the relative abundance of diatoms versus dinoflagellates. Our analyses, including Granger tests to identify criteria of causality, indicate that this switch is driven by an interaction effect of both increasing sea surface temperatures combined with increasingly windy conditions in summer.

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Objective
Somatization is a symptom cluster characterized by ‘psychosomatic’ symptoms, that is, medically unexplained symptoms, and is a common component of other conditions, including depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This article reviews the data regarding the pathophysiological foundations of ‘psychosomatic’ symptoms and the implications that this has for conceptualization of what may more appropriately be termed physio-somatic symptoms.

Method
This narrative review used papers published in PubMed, Scopus, and Google Scholar electronic databases using the keywords: depression and chronic fatigue, depression and somatization, somatization and chronic fatigue syndrome, each combined with inflammation, inflammatory, tryptophan, and cell-mediated immune (CMI).

Results

The physio-somatic symptoms of depression, ME/CFS, and somatization are associated with specific biomarkers of inflammation and CMI activation, which are correlated with, and causally linked to, changes in the tryptophan catabolite (TRYCAT) pathway. Oxidative and nitrosative stress induces damage that increases neoepitopes and autoimmunity that contribute to the immuno-inflammatory processes. These pathways are all known to cause physio-somatic symptoms, including fatigue, malaise, autonomic symptoms, hyperalgesia, intestinal hypermotility, peripheral neuropathy, etc.

Conclusion

Biological underpinnings, such as immune-inflammatory pathways, may explain, at least in part, the occurrence of physio-somatic symptoms in depression, somatization, or myalgic encephalomyelitis/chronic fatigue syndrome and thus the clinical overlap among these disorders.

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Children of obese mothers have increased risk of metabolic syndrome as adults. Here we report the effects of a high-fat diet in the absence of maternal obesity at conception on skeletal muscle metabolic and transcriptional profiles of adult male offspring. Female Sprague Dawley rats were fed a diet rich in saturated fat and sucrose [high-fat diet (HFD): 23.5% total fat, 9.83% saturated fat, 20% sucrose wt:wt] or a normal control diet [(CD) 7% total fat, 0.5% saturated fat, 10% sucrose wt:wt] for the 3 wk prior to mating and throughout pregnancy and lactation. Maternal weights were not different at conception; however, HFD-fed dams were 22% heavier than controls during pregnancy. On a normal diet, the male offspring of HFD-fed dams were not heavier than controls but demonstrated features of insulin resistance, including elevated plasma insulin concentration [40.1 ± 2.5 (CD) vs 56.2 ± 6.1 (HFD) mU/L; P = 0.023]. Next-generation mRNA sequencing was used to identify differentially expressed genes in the offspring soleus muscle, and gene set enrichment analysis (GSEA) was used to detect coordinated changes that are characteristic of a biological function. GSEA identified 15 upregulated pathways, including cytokine signaling (P < 0.005), starch and sucrose metabolism (P < 0.017), inflammatory response (P < 0.024), and cytokine-cytokine receptor interaction (P < 0.037). A further 8 pathways were downregulated, including oxidative phosphorylation (P < 0.004), mitochondrial matrix (P < 0.006), and electron transport/uncoupling (P < 0.022). Phosphorylation of the insulin signaling protein kinase B was reduced [2.86 ± 0.63 (CD) vs 1.02 ± 0.27 (HFD); P = 0.027] and mitochondrial complexes I, II, and V protein were downregulated by 50-68% (P < 0.005). On a normal diet, the male offspring of HFD-fed dams did not become obese adults but developed insulin resistance, with transcriptional evidence of muscle cytokine activation, inflammation, and mitochondrial dysfunction. These data indicate that maternal overnutrition, even in the absence of prepregnancy obesity, can promote metabolic dysregulation and predispose offspring to type 2 diabetes.