scholarly journals Warmer temperatures interact with salinity to weaken physiological facilitation to stress in freshwater fishes

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Richard H Walker ◽  
Geoffrey D Smith ◽  
Spencer B Hudson ◽  
Susannah S French ◽  
Annika W Walters
Keyword(s):  
Stress Reactivity ◽  
Multiple Stressors ◽  
Cutthroat Trout ◽  
Freshwater Fishes ◽  
Freshwater Ecosystems ◽  
Negative Effects ◽  
Temperature Dependent ◽  
Glucose Levels ◽  
Baseline Concentrations ◽  
Underlying Mechanisms

Abstract Management of stressors requires an understanding of how multiple stressors interact, how different species respond to those interactions and the underlying mechanisms driving observed patterns in species’ responses. Salinization and rising temperatures are two pertinent stressors predicted to intensify in freshwater ecosystems, posing concern for how susceptible organisms achieve and maintain homeostasis (i.e. allostasis). Here, glucocorticoid hormones (e.g. cortisol), responsible for mobilizing energy (e.g. glucose) to relevant physiological processes for the duration of stressors, are liable to vary in response to the duration and severity of salinization and temperature rises. With field and laboratory studies, we evaluated how both salinity and temperature influence basal and stress-reactive cortisol and glucose levels in age 1+ mottled sculpin (Cottus bairdii), mountain sucker (Catostomus platyrhynchus) and Colorado River cutthroat trout (Oncorhynchus clarki pleuriticus). We found that temperature generally had the greatest effect on cortisol and glucose concentrations and the effect of salinity was often temperature dependent. We also found that when individuals were chronically exposed to higher salinities, baseline concentrations of cortisol and glucose usually declined as salinity increased. Reductions in baseline concentrations facilitated stronger stress reactivity for cortisol and glucose when exposed to additional stressors, which weakened as temperatures increased. Controlled temperatures near the species’ thermal maxima became the overriding factor regulating fish physiology, resulting in inhibitory responses. With projected increases in freshwater salinization and temperatures, efforts to reduce the negative effects of increasing temperatures (i.e. increased refuge habitats and riparian cover) could moderate the inhibitory effects of temperature-dependent effects of salinization for freshwater fishes.

Temperature and parasite life-history are important modulators of the outcome of Trypanosoma rangeli–Rhodnius prolixus interactions

Parasitology ◽  
2016 ◽  
Vol 143 (11) ◽  
pp. 1459-1468 ◽  
Author(s):  
JULIANA DE O. RODRIGUES ◽  
MARCELO G. LORENZO ◽  
OLINDO A. MARTINS-FILHO ◽  
SIMON L. ELLIOT ◽  
ALESSANDRA A. GUARNERI
Keyword(s):  
Life Histories ◽  
Protozoan Parasite ◽  
Infection Rates ◽  
Trypanosoma Rangeli ◽  
Negative Effects ◽  
Temperature Dependent ◽  
Liver Infusion Tryptose ◽  
Insect Fitness ◽  
Different Levels

SUMMARYTrypanosoma rangeli is a protozoan parasite, which does not cause disease in humans, although it can produce different levels of pathogenicity to triatomines, their invertebrate hosts. We tested whether infection imposed a temperature-dependent cost on triatomine fitness using T. rangeli with different life histories. Parasites cultured only in liver infusion tryptose medium (cultured) and parasites exposed to cyclical passages through mice and triatomines (passaged) were used. We held infected insects at four temperatures between 21 and 30 °C and measured T. rangeli growth in vitro at the same temperatures in parallel. Overall, T. rangeli infection induced negative effects on insect fitness. In the case of cultured infection, parasite effects were temperature-dependent. Intermoult period, mortality rates and ecdysis success were affected in those insects exposed to lower temperatures (21 and 24 °C). For passaged-infected insects, the effects were independent of temperature, intermoult period being prolonged in all infected groups. Trypanosoma rangeli seem to be less tolerant to higher temperatures since cultured-infected insects showed a reduction in the infection rates and passaged-infected insects decreased the salivary gland infection rates in those insects submitted to 30 °C. In vitro growth of T. rangeli was consistent with these results.

scholarly journals Nitrogen enrichment offsets direct negative effects of ocean acidification on a reef-building crustose coralline alga

2018 ◽  
Vol 14 (7) ◽  
pp. 20180371 ◽  
Author(s):  
Maggie D. Johnson ◽  
Robert C. Carpenter
Keyword(s):  
Ocean Acidification ◽  
Nutrient Enrichment ◽  
Multiple Stressors ◽  
Crustose Coralline Alga ◽  
Nitrogen Enrichment ◽  
Coralline Alga ◽  
Ambient Conditions ◽  
Negative Effects ◽  
Near Shore ◽  
Near Future

Ocean acidification (OA) and nutrient enrichment threaten the persistence of near shore ecosystems, yet little is known about their combined effects on marine organisms. Here, we show that a threefold increase in nitrogen concentrations, simulating enrichment due to coastal eutrophication or consumer excretions, offset the direct negative effects of near-future OA on calcification and photophysiology of the reef-building crustose coralline alga, Porolithon onkodes . Projected near-future pCO 2 levels (approx. 850 µatm) decreased calcification by 30% relative to ambient conditions. Conversely, nitrogen enrichment (nitrate + nitrite and ammonium) increased calcification by 90–130% in ambient and high pCO 2 treatments, respectively. pCO 2 and nitrogen enrichment interactively affected instantaneous photophysiology, with highest relative electron transport rates under high pCO 2 and high nitrogen. Nitrogen enrichment alone increased concentrations of the photosynthetic pigments chlorophyll a , phycocyanin and phycoerythrin by approximately 80–450%, regardless of pCO 2 . These results demonstrate that nutrient enrichment can mediate direct organismal responses to OA. In natural systems, however, such direct benefits may be counteracted by simultaneous increases in negative indirect effects, such as heightened competition. Experiments exploring the effects of multiple stressors are increasingly becoming important for improving our ability to understand the ramifications of local and global change stressors in near shore ecosystems.

scholarly journals Glucose stimulates somatostatin secretion in pancreatic δ-cells by cAMP-dependent intracellular Ca2+ release

2019 ◽  
Vol 151 (9) ◽  
Author(s):  
Geoffrey Denwood ◽  
Andrei Tarasov ◽  
Albert Salehi ◽  
Elisa Vergari ◽  
Reshma Ramracheya ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Secretory Vesicles ◽  
Glucose Levels ◽  
Somatostatin Secretion ◽  
Elevated Glucose ◽  
Mouse Islets ◽  
Underlying Mechanisms ◽  
Fold Stimulation ◽  
Cyclase Activator ◽  
Stimulation Of

Somatostatin secretion from pancreatic islet δ-cells is stimulated by elevated glucose levels, but the underlying mechanisms have only partially been elucidated. Here we show that glucose-induced somatostatin secretion (GISS) involves both membrane potential-dependent and -independent pathways. Although glucose-induced electrical activity triggers somatostatin release, the sugar also stimulates GISS via a cAMP-dependent stimulation of CICR and exocytosis of somatostatin. The latter effect is more quantitatively important and in mouse islets depolarized by 70 mM extracellular K+, increasing glucose from 1 mM to 20 mM produced an ∼3.5-fold stimulation of somatostatin secretion, an effect that was mimicked by the application of the adenylyl cyclase activator forskolin. Inhibiting cAMP-dependent pathways with PKI or ESI-05, which inhibit PKA and exchange protein directly activated by cAMP 2 (Epac2), respectively, reduced glucose/forskolin-induced somatostatin secretion. Ryanodine produced a similar effect that was not additive to that of the PKA or Epac2 inhibitors. Intracellular application of cAMP produced a concentration-dependent stimulation of somatostatin exocytosis and elevation of cytoplasmic Ca2+ ([Ca2+]i). Both effects were inhibited by ESI-05 and thapsigargin (an inhibitor of SERCA). By contrast, inhibition of PKA suppressed δ-cell exocytosis without affecting [Ca2+]i. Simultaneous recordings of electrical activity and [Ca2+]i in δ-cells expressing the genetically encoded Ca2+ indicator GCaMP3 revealed that the majority of glucose-induced [Ca2+]i spikes did not correlate with δ-cell electrical activity but instead reflected Ca2+ release from the ER. These spontaneous [Ca2+]i spikes are resistant to PKI but sensitive to ESI-05 or thapsigargin. We propose that cAMP links an increase in plasma glucose to stimulation of somatostatin secretion by promoting CICR, thus evoking exocytosis of somatostatin-containing secretory vesicles in the δ-cell.

scholarly journals Gut Microbial Metabolites and Biochemical Pathways Involved in Irritable Bowel Syndrome: Effects of Diet and Nutrition on the Microbiome

2019 ◽  
Vol 150 (5) ◽  
pp. 1012-1021 ◽  
Author(s):  
Shanalee C James ◽  
Karl Fraser ◽  
Wayne Young ◽  
Warren C McNabb ◽  
Nicole C Roy
Keyword(s):  
Irritable Bowel Syndrome ◽  
Metabolic Pathways ◽  
Critical Discussion ◽  
Microbial Metabolites ◽  
Dietary Interventions ◽  
Negative Effects ◽  
Gut Function ◽  
Underlying Mechanisms ◽  
Irritable Bowel ◽  
The Impact

ABSTRACT The food we consume and its interactions with the host and their gut microbiota affect normal gut function and health. Functional gut disorders (FGDs), including irritable bowel syndrome (IBS), can result from negative effects of these interactions, leading to a reduced quality of life. Certain foods exacerbate or reduce the severity and prevalence of FGD symptoms. IBS can be used as a model of perturbation from normal gut function with which to study the impact of foods and diets on the severity and symptoms of FGDs and understand how critical processes and biochemical mechanisms contribute to this impact. Analyzing the complex interactions between food, host, and microbial metabolites gives insights into the pathways and processes occurring in the gut which contribute to FGDs. The following review is a critical discussion of the literature regarding metabolic pathways and dietary interventions relevant to FGDs. Many metabolites, for example bile acids, SCFAs, vitamins, amino acids, and neurotransmitters, can be altered by dietary intake, and could be valuable for identifying perturbations in metabolic pathways that distinguish a “normal, healthy” gut from a “dysfunctional, unhealthy” gut. Dietary interventions for reducing symptoms of FGDs are becoming more prevalent, but studies investigating the underlying mechanisms linked to host, microbiome, and metabolite interactions are less common. Therefore, we aim to evaluate the recent literature to assist with further progression of research in this field.

scholarly journals Bexarotene normalizes chemotherapy-induced myelin decompaction and reverses cognitive and sensorimotor deficits in mice

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Angie C. A. Chiang ◽  
Alexandre V. Seua ◽  
Pooja Singhmar ◽  
Luis D. Arroyo ◽  
Rajasekaran Mahalingam ◽  
...  
Keyword(s):  
Sensorimotor Cortex ◽  
Ultrastructural Level ◽  
Term Treatment ◽  
Synaptic Function ◽  
Axonal Guidance ◽  
Sensorimotor Function ◽  
Negative Effects ◽  
Short Term Treatment ◽  
Canonical Pathways ◽  
Underlying Mechanisms

AbstractFrequently reported neurotoxic sequelae of cancer treatment include cognitive deficits and sensorimotor abnormalities that have long-lasting negative effects on the quality of life of an increasing number of cancer survivors. The underlying mechanisms are not fully understood and there is no effective treatment. We show here that cisplatin treatment of mice not only caused cognitive dysfunction but also impaired sensorimotor function. These functional deficits are associated with reduced myelin density and complexity in the cingulate and sensorimotor cortex. At the ultrastructural level, myelin abnormalities were characterized by decompaction. We used this model to examine the effect of bexarotene, an agonist of the RXR-family of nuclear receptors. Administration of only five daily doses of bexarotene after completion of cisplatin treatment was sufficient to normalize myelin density and fiber coherency and to restore myelin compaction in cingulate and sensorimotor cortex. Functionally, bexarotene normalized performance of cisplatin-treated mice in tests for cognitive and sensorimotor function. RNAseq analysis identified the TR/RXR pathway as one of the top canonical pathways activated by administration of bexarotene to cisplatin-treated mice. Bexarotene also activated neuregulin and netrin pathways that are implicated in myelin formation/maintenance, synaptic function and axonal guidance. In conclusion, short term treatment with bexarotene is sufficient to reverse the adverse effects of cisplatin on white matter structure, cognitive function, and sensorimotor performance. These encouraging findings warrant further studies into potential clinical translation and the underlying mechanisms of bexarotene for chemobrain.

scholarly journals Multiple Stressors Determine Community Structure and Estimated Function of River Biofilm Bacteria

2020 ◽  
Vol 86 (12) ◽  
Author(s):  
Ferran Romero ◽  
Vicenç Acuña ◽  
Sergi Sabater
Keyword(s):  
Bacterial Community ◽  
Community Composition ◽  
Bacterial Communities ◽  
Pesticide Exposure ◽  
Multiple Stressors ◽  
Bacterial Community Composition ◽  
Freshwater Ecosystems ◽  
Low Flow ◽  
Hydrological Stress ◽  
The Individual

ABSTRACT Freshwater ecosystems are exposed to multiple stressors, but their individual and combined effects remain largely unexplored. Here, we investigated the response of stream biofilm bacterial communities to warming, hydrological stress, and pesticide exposure. We used 24 artificial streams on which epilithic (growing on coarse sediments) and epipsammic (growing on fine sediments) stream biofilms were maintained. Bacterial community composition and estimated function of biofilms exposed during 30 days to individual and combined stressors were assessed using 16S rRNA gene metabarcoding. Among the individual effects by stressors, hydrological stress (i.e., a simulated low-flow situation) was the most relevant, since it significantly altered 57% of the most abundant bacterial taxa (n = 28), followed by warming (21%) and pesticide exposure (11%). Regarding the combined effects, 16% of all stressor combinations resulted in significant interactions on bacterial community composition and estimated function. Antagonistic responses prevailed (57 to 89% of all significant interactions), followed by synergisms (11 to 43%), on specific bacterial taxa, indicating that multiple-stressor scenarios could lead to unexpected shifts in the community composition and associated functions of riverine bacterial communities. IMPORTANCE Freshwater ecosystems such as rivers are of crucial importance for human well-being. However, human activities result in many stressors (e.g., toxic chemicals, increased water temperatures, and hydrological alterations) cooccurring in rivers and streams worldwide. Among the many organisms inhabiting rivers and streams, bacteria are ecologically crucial; they are placed at the base of virtually all food webs and they recycle the organic matter needed for bigger organisms. Most of these bacteria are in close contact with river substratum, where they form the biofilms. There is an urgent need to evaluate the effects of these stressors on river biofilms, so we can anticipate future environmental problems. In this study, we experimentally exposed river biofilms to a pesticide mixture, an increase in water temperature and a simulated low-flow condition, in order to evaluate the individual and joint effects of these stressors on the bacterial community composition and estimated function.

Multiple stressors in freshwater ecosystems

2010 ◽  
Vol 55 ◽  
pp. 1-4 ◽  
Author(s):  
S. J. ORMEROD ◽  
M. DOBSON ◽  
A. G. HILDREW ◽  
C. R. TOWNSEND
Keyword(s):  
Multiple Stressors ◽  
Freshwater Ecosystems

scholarly journals Gastrin induces ductal cell dedifferentiation and β-cell neogenesis after 90% pancreatectomy

2014 ◽  
Vol 223 (1) ◽  
pp. 67-78 ◽  
Author(s):  
Noèlia Téllez ◽  
Eduard Montanya
Keyword(s):  
Cell Mass ◽  
Β Cell ◽  
Neurogenin 3 ◽  
Glucose Levels ◽  
Ductal Cells ◽  
Blood Glucose Levels ◽  
Morphometric Analyses ◽  
Underlying Mechanisms ◽  
Mass Expansion

Induction of β-cell mass regeneration is a potentially curative treatment for diabetes. We have recently found that long-term gastrin treatment results in improved metabolic control and β-cell mass expansion in 95% pancreatectomised (Px) rats. In this study, we investigated the underlying mechanisms of gastrin-induced β-cell mass expansion after Px. After 90%-Px, rats were treated with gastrin (Px+G) or vehicle (Px+V), pancreatic remnants were harvested on days 1, 3, 5, 7, and 14 and used for gene expression, protein immunolocalisation and morphometric analyses. Gastrin- and vehicle-treated Px rats showed similar blood glucose levels throughout the study. Initially, after Px, focal areas of regeneration, showing mesenchymal cells surrounding ductal structures that expressed the cholecystokinin B receptor, were identified. These focal areas of regeneration were similar in size and cell composition in the Px+G and Px+V groups. However, in the Px+G group, the ductal structures showed lower levels of keratin 20 and β-catenin (indicative of duct dedifferentiation) and higher levels of expression of neurogenin 3 and NKX6-1 (indicative of endocrine progenitor phenotype), as compared with Px+V rats. In Px+G rats, β-cell mass and the number of scattered β-cells were significantly increased compared with Px+V rats, whereas β-cell replication and apoptosis were similar in the two groups. These results indicate that gastrin treatment-enhanced dedifferentiation and reprogramming of regenerative ductal cells in Px rats, increased β-cell neogenesis and fostered β-cell mass expansion.

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