Relevant bibliographies by topics / Ants – Physiology

Academic literature on the topic 'Ants – Physiology'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Ants – Physiology"

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Angilletta, Michael J., Robbie S. Wilson, Amanda C. Niehaus, Michael W. Sears, Carlos A. Navas, and Pedro L. Ribeiro. "Urban Physiology: City Ants Possess High Heat Tolerance." PLoS ONE 2, no. 2 (February 28, 2007): e258. http://dx.doi.org/10.1371/journal.pone.0000258.

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Paul, Jürgen. "Mandible movements in ants." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 131, no. 1 (December 2001): 7–20. http://dx.doi.org/10.1016/s1095-6433(01)00458-5.

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Diamond, S. E., C. A. Penick, S. L. Pelini, A. M. Ellison, N. J. Gotelli, N. J. Sanders, and R. R. Dunn. "Using Physiology to Predict the Responses of Ants to Climatic Warming." Integrative and Comparative Biology 53, no. 6 (July 26, 2013): 965–74. http://dx.doi.org/10.1093/icb/ict085.

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Graham, Paul, and Thomas S. Collett. "View-based navigation in insects: how wood ants (Formica rufaL.) look at and are guided by extended landmarks." Journal of Experimental Biology 205, no. 16 (August 15, 2002): 2499–509. http://dx.doi.org/10.1242/jeb.205.16.2499.

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SUMMARYBees, wasps and ants learn landmarks as views from particular vantage points, storing the retinal positions of landmark edges. By moving so as to minimise the difference between their stored and current view, they can return to the vantage point from which a view was taken. We have examined what wood ants learn about a laterally placed, extended landmark, a wall, while walking parallel to it to reach a feeder and how they use this stored information to guide their path. Manipulation of the height of the wall and the ant's starting distance from it reveals that ants maintain a desired distance from the wall by keeping the image of the top of the wall at a particular retinal elevation. Ants can thus employ image matching both for returning to a place and for following a fixed route.Unlike many flying insects, an ant's direction of motion while walking is always along its longitudinal body axis and, perhaps for this reason, it favours its frontal retina for viewing discrete landmarks. We find that ants also use their frontal retina for viewing a laterally placed wall. On a coarse scale, the ant's path along the wall is straight, but on a finer scale it is roughly sinusoidal, allowing the ant to scan the surrounding landscape with its frontal retina. The ant's side-to-side scanning means that the wall is viewed with its frontal retina for phases of the scanning cycle throughout its trajectory. Details of the scanning pattern depend on the scene. Ants scan further to the side that is empty of the wall than to the side containing the wall, and they scan further into the wall side when the wall is of a lower apparent height. We conclude that frontal retina is employed for image storage and for path control.
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Poulsen, Michael, and Cameron R. Currie. "On ants, plants and fungi." New Phytologist 182, no. 4 (May 8, 2009): 785–88. http://dx.doi.org/10.1111/j.1469-8137.2009.02863.x.

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Freas, Cody A., Jenna V. Congdon, Nicola J. R. Plowes, and Marcia L. Spetch. "Same but different: Socially foraging ants backtrack like individually foraging ants but use different mechanisms." Journal of Insect Physiology 118 (October 2019): 103944. http://dx.doi.org/10.1016/j.jinsphys.2019.103944.

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Federle, W., T. Endlein, and T. Bruening. "Locomotion and adhesion in arboreal ants." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 146, no. 4 (April 2007): S145. http://dx.doi.org/10.1016/j.cbpa.2007.01.291.

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DAVID MORGAN, E. "Trail pheromones of ants." Physiological Entomology 34, no. 1 (December 2, 2008): 1–17. http://dx.doi.org/10.1111/j.1365-3032.2008.00658.x.

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Wheeler, Diana, Jürgen Liebig, and Bert Hölldobler. "Atypical vitellins in ponerine ants (Formicidae: Hymenoptera)." Journal of Insect Physiology 45, no. 3 (March 1999): 287–93. http://dx.doi.org/10.1016/s0022-1910(98)00124-3.

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Heinze, J., and B. Holldobler. "Fighting for a harem of queens: physiology of reproduction in Cardiocondyla male ants." Proceedings of the National Academy of Sciences 90, no. 18 (September 15, 1993): 8412–14. http://dx.doi.org/10.1073/pnas.90.18.8412.

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Dissertations / Theses on the topic "Ants – Physiology"

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Nguyen, Andrew D. "Evolutionary Innovations In Ants To Thermally Stressful Environments." ScholarWorks @ UVM, 2017. http://scholarworks.uvm.edu/graddis/739.

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Temperature is a fundamental environmental force shaping species abundance and distributions through its effects on biochemical reaction rates, metabolism, activity, and reproduction. In light of future climate shifts, mainly driven by temperature increases, how will organisms persist in warmer environments? One molecular mechanism that may play an important role in coping with heat stress is the heat shock response (HSR), which protects against molecular damage. To prevent and repair protein damage specifically, Hsps activate and become up-regulated. However, the functional diversity and relevance of heat shock proteins (Hsps) in extending upper thermal limits in taxonomic groups outside marine and model systems is poorly understood. Ants are a good system to understand the physiological mechanisms for coping with heat stress because they have successfully diversified into thermally stressful environments. To identify and characterize the functional diversity of Hsps in ants, I surveyed Hsp orthologues from published ant genomes to test for signatures of positive selection and to reconstruct their evolutionary history. Within Hymenoptera, ants utilize unique sets of Hsps for the HSR. Stabilizing selection was the prevailing force among Hsp orthologues, suggesting that protein activity is conserved. At the same time, regulatory regions (promoters) governing transcriptional up-regulation diversified: species differ in the number and location of heat shock elements (HSEs). Therefore, Hsp expression patterns may be a target for selection in warm environments. I tested whether Hsp expression corresponded with variation in upper thermal limits in forest ant species within the genus Aphaenogaster. Whole colonies were collected throughout the eastern United States and were lab acclimated. There was a positive relationship between upper thermal limits (Critical Thermal maxima, CTmax) and local temperature extremes. Upper thermal limits were also higher in ant species that lived in open habitats (shrub-oak and long-leaf pine savannah) than species occupying closed habitats (deciduous forest). Ant species with higher CTmax expressed Hsps more slowly, at higher temperatures, and at higher maximum levels than those with low CTmax. Because Hsps sense and repair molecular damage, these results suggest the proteomes of open relative to closed canopy forests are more stable. Although deciduous forest ant species may be buffered from temperature stress, it is likely that temperature interacts with other environmental stressors such as water and nutrient availability that may impact upper thermal limits. I measured the influence of dehydration and nutrition stress on upper thermal limits of forest ants from a single population. Ants that were initially starved were much less thermally tolerant than controls and ants that were initially desiccated. Because ants are likely to experience similar combination of stressors in the wild, upper thermal limits may be severely overestimated in single factor experiments. Therefore, realistic forecasting models need to consider multiple environmental stressors. Overall, adaptive tuning of Hsp expression that reflects better protection and tolerance of protein unfolding may have facilitated ant diversification into warm environments. However, additional stressors and mechanisms may constrain the evolution of upper thermal limits.
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Muncy, Nathan McKay. "A Semi-Automated Algorithm for Segmenting the Hippocampus in Patient and Control Populations." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6421.

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Calculating hippocampal volume from Magnetic Resonance (MR) images is an essential task in many studies of neurocognition in healthy and diseased populations. The `gold standard' method involves hand tracing, which is accurate but laborious, requiring expertly trained researchers and significant amounts of time. As such, segmenting large datasets with the standard method is impractical. Current automated pipelines are inaccurate at hippocampal demarcation and volumetry. We developed a semi-automated hippocampal segmentation pipeline based on the Advanced Normalization Tools (ANTs) suite of programs to segment the hippocampus. We applied the semi-automated segmentation pipeline to 70 participant scans (26 female) from groups that included participants diagnosed with autism spectrum disorder, healthy older adults (mean age 74) and healthy younger controls. We found that hippocampal segmentations obtained with the semi-automated pipeline more closely matched the segmentations of an expert rater than those obtained using FreeSurfer or the segmentations of novice raters. Further, we found that the pipeline performed best when including manually- placed landmarks and when using a template generated from a heterogeneous sample (that included the full variability of group assignments) than a template generated from more homogeneous samples (using only individuals within a given age or with a specific neuropsychiatric diagnosis). Additionally, the semi-automated pipeline required much less time (5 minutes per brain) than manual segmentation (30-60 minutes per brain) or FreeSurfer (8 hours per brain).
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Geerdes, Bastiaan Petrus. "Dynamic graciloplasty (patho)physiology of failure and success /." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=6789.

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Bhavaraju, Kamala. "MOLECULAR PHYSIOLOGY OF THROMBOXANE A2 GENERATION IN PLATELETS." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/92746.

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Molecular and Cellular Physiology
Ph.D.
Cardiovascular diseases are a major cause of mortality and morbidity in the developed countries. Anti-platelet therapy is a cornerstone treatment for patients with cardiovascular diseases. Patients are routinely managed with a combination therapy consisting of aspirin and clopidogrel. Aspirin inhibits cyclooxygenase 1 (COX 1) a crucial intermediate enzyme involved in thromboxane biosynthesis. Clopidogrel on the other hand antagonizes ADP receptor P2Y12. ADP is a weak platelet agonist stored in platelet dense granules and is released upon platelet activation. ADP activates platelets through two purinergic receptors namely P2Y1 and P2Y12 these receptors couple to Gq and Gi class of G-proteins, respectively. P2Y1 causes calcium mobilization through activation of PLC-β. P2Y12 inhibits adenylyl cyclase, causes activation of Rap1B and Akt. Signaling from both the receptors is required for complete integrin activation, thromboxane generation and Erk activation. Previous studies have shown that P2Y12 potentiates fibrinogen receptor activation, secretion, thrombi stabilization, thrombin generation, platelet leukocyte aggregation formation. ThromboxaneA2 (TXA2) is a potent platelet agonist generated through arachidonic acid metabolism in platelets. TXA2 thus, generated after platelet activation acts as a positive feedback mediator along with ADP. Under physiological conditions, platelet activation leads to thrombin generation through coagulation cascades. Generated thrombin activates PAR receptors and ADP is released from dense granules, which further potentiates thromboxane generation downstream of PARs. Current anti-platelet therapy regimens often include P2Y12 antagonists and aspirin in management of patients with acute coronary syndrome (ACS) and in those undergoing percutaneous coronary intervention (PCI) with stent implantation. However, there still exists a need for improved treatment strategies as not all patients benefit from this dual combination therapy. Reasons include, poor responders either to P2Y12 antagonists or to aspirin, or if aspirin is contraindicated in these patient populations. In the current study we evaluated the role of P2Y12 in thromboxane generation under physiological conditions. We studied serum thromboxane generation in a model system wherein P2Y12 was antagonized or deficient. Using pharmacological approaches we show that dosing mice with 30mg/Kg/body weight clopidogrel or 3mg/Kg/body weight prasugrel decreased serum thromboxane levels when compared to the control mice. Pre-treatment of human blood ex vivo with active metabolites of clopidogrel (R361015) or prasugrel (R138727) also led to reduction in thromboxane levels. We also evaluated serum thromboxane levels in P2Y receptor null mice, serum thromboxane levels in P2Y1 null mice were similar to those in wild type littermates, and were inhibited in P2Y12 null mice. Furthermore, serum thromboxane levels in P2Y12 deficient patients, previously described in France and Japan, were also evaluated and these patients had lower serum thromboxane levels compared to normal controls. In a pilot study, serum thromboxane levels were radically reduced in healthy human volunteers upon dosing with clopidogrel, compared to the levels before dosing. In conclusion, P2Y12 antagonism alone can decrease physiological thromboxane levels. Thus P2Y12 regulates physiological thromboxane levels. Further it is known that ADP-induced thromboxane generation is integrin-dependent. However it is not clear if other potent platelet agonists like thrombin require outside-in signaling for thromboxane generation. Our results show that thrombin-induced thromboxane generation was independent of integrins i.e. when platelets were stimulated with PAR agonists in presence of fibrinogen receptor antagonist thromboxane generation was not affected. Since PAR agonists, unlike ADP, activate G12/13 signaling pathways. Hence, we hypothesized that these pathways might play a role in TXA2 generation. Our results show, that inhibition of ADP-induced thromboxane generation by fibrinogen receptor antagonist SC57101 was rescued by costimulation of G12/13 pathways with YFLLRNP. This observation suggested an existence of a common signaling effector downstream of integrins and G12/13 pathways. Next, we evaluated role of three potential tyrosine kinases; c-Src, Syk and FAK (Focal Adhesion Kinase) that are known to be activated by integrins. Our results showed that c-Src and Syk kinase did not play a role in ADP-induced functional responses in platelets. We observed differential activation of FAK downstream of integrins and G12/13 pathways. ADP-induced activation of FAK was integrindependent and SFK-independent. On the other hand selective activation of G12/13 pathway lead to FAK activation, in SFK and Rho dependent manner. We also evaluated specificity of new FAK inhibitor TAE-226 to understand the role of FAK in TXA2 generation. Our results showed that TAE-226 exhibited non-specific effects at higher concentrations. Furthermore, in comparison to WT mice, FAK null mice did not show any difference in TXA2 generation. Therefore, we concluded that differential activation of FAK occurs downstream of Integrins and G12/13 pathways. However, the common effector molecule downstream of integrins and G12/ 13 pathways contributing to TXA2 generation in platelets remains elusive.
Temple University--Theses
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Ronca, Rich Daniel. "The Cannabinoid-2 Receptor Agonist O-1966 Reverses Postischemic Learning and Memory Deficits Through Anti-Inflammatory Processes." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/253154.

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Pharmacology
Ph.D.
Ischemic stroke is the third leading cause of death and the leading cause of morbidity in the United States. Cognitive deficits, specifically with respect to learning and memory, are a significant contributor to morbidity in stroke patients. Unfortunately, current treatment options must be administered within a thin therapeutic window of the initial infarct. This requirement results in less than 10% of stroke patients being eligible for treatment. There are currently no treatment options that are effective in the subacute phase of the disease and no treatments that are effective in reversing postischemic learning and memory deficits. We sought to examine the potential efficacy of the anti-inflammatory Cannabinoid-2 Receptor Agonist, O-1966, in attenuating infarct expansion and reversing cognitive deficits in the subacute phase of the disease using a photothrombosis model of stroke. Additionally, we sought to characterize the inflammatory response in photothrombosis. Mice were treated with repeated doses of O-1966 or vehicle and were sacrificed at 24 hours and 7 days to study the acute and subacute phase of the disease respectively. Learning and memory testing, immunohistochemistry, and polymerase chain reaction were used to measure the effect of O-1966 on infarct expansion, inflammatory gene expression, and cognitive function. In addition to PCR, flow cytometry was used to characterize the temporal dynamics of inflammation following photothrombosis. Our studies show that O-1966 is effective in the subacute phase in attenuating infarct expansion and proinflammatory gene expression and reversing learning and memory deficits.
Temple University--Theses
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Washington, N. "In vitro and in vivo evaluation of antacid and anti-reflux formulations." Thesis, University of Nottingham, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376161.

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Shimizu, Manabu. "Acid-base balance in arterial plasma of white Pekin duck (Anas platyrhynchos) during forced submergence and recovery." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25044.

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Acid-base balance in plasma was studied in forcibly submerged Pekin ducks (Anas platyrhynchos). All important variables determining acid-base balance (arterial CO₂ tension (PαCO₂) strong ion difference ([SID]) and total protein content which approximates total weak acid concentration in plasma) were measured. During forced submergence PαCO₂ increased and pHa steadily decreased with time. There was also an increase in [lactate⁻], which was accompanied by an increase of equal magnitude in [Na⁺]. There were no significant changes in the concentrations of other strong ions (K⁺, Ca²⁺, Mg²⁺ and Cl⁻). Strong ion difference did not change during the first two minutes of submergence, but there was about a 4 mequiv/L increase by the end of the four-minute dive. Theoretically an increase in [SID] should cause plasma to be alkaline, but since plasma became progressively acidic, this condition can only be due to the increase in PαCO₂. During recovery from dives, the plasma remained as acidic one minute after emersion as at the end of the dives. On the other hand, arterial pH slowly increased towards the pre-dive level during recovery. Arterial CO₂ tension decreased much more rapidly and was already at or below the pre-dive level one minute after emersion. Therefore, PαCO₂ could no longer affect plasma pH. There was, however, a great increase in [lactate-] in the first minute of recovery. Although [Na⁺] and [K⁺] were elevated, from pre-dive values after the four minute dive, the increase in [lactate⁻] resulted in a marked reduction in [SID]. Since there was no change in the total plasma protein content, the acidic condition observed in recovery could only be due to decreased [SID]. Breathing 0₂ before diving prevented circulatory adjustments and pH returned to pre-dive levels one minute after emersion, confirming that the acidic condition observed in recovery is a consequence of the lactate produced in the hypoperfused tissues during submergence.
Science, Faculty of
Zoology, Department of
Graduate
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Lopez, Tapia Francisco Javier. "A general approach to the total synthesis of yeuhchukene and its analogues : a novel anti-implantation agent." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29013.

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This thesis concerns a general approach to the total synthesis of yuehchukene 2 and its analogues. Yuehchukene has a potent anti-implantation activity. It also lacks the estrogenic side effect of most compounds with similar biological activity. However, it is somewhat unstable and this could bring some problems when administered to humans. Development of a versatile synthesis of yuehchukene capable of producing a variety of analogous structures in order to fully exploit the pharmacological properties of this novel molecular system and/or to make a more stable product without losing its biological properties was the central objective of this project. Specifically, the total synthesis of yuehchukene 2 and its analogue 6a-ep/-yuehchukene 25 are described. After some preliminary studies, it was found that a kinetic carboxylation (lithium 2,6-di-tert-butyl-4-methylphenoxide, CO₂) of isophorone 26 followed by a reduction (NaBH₄) produced stereoselectively cis-hydroxyacid 46 in good yield. The latter was transformed into indoleacid 48 by dibenzoylation (PhCOCI, DMAP) and treatment with indolylmagnesium iodide. The key intermediate trans-ketone 60 was obtained by treatment of 48 with oxalyl chloride followed by indolylmagnesium iodide. Epimerization of 60 to the more stable cis-ketone 24 was accomplished quantitatively under basic conditions (MeONa/MeOH, reflux). Reduction (LiAlH₄) and dibenzoylation (PhCOCI, DMAP, Et₃N) of 24 furnished the benzoate 68 which was subjected to a nucleophilic substitution with indolylmagnesium iodide to give N-benzoylyuehchukene 69. The latter transformation also gave the interesting compound 75 which was submitted to an X-Ray diffraction analysis. The total synthesis of yuehchukene 2 was then achieved by methanolysis (NaOMe/MeOH) of 69. As far as the synthesis of 6a-epi-yuehchukene 25 is concerned, it was found that, after a thorough study, it was best to transform trans-ketone 60 into its SEM-derivative 85 (SEM-CI,NaH). The latter was reduced (DIBAL) and acetylated (Ac₂O, DMAP, Et₃N) to produce stereoselectively the acetate 87 which, by treatment with indolylmagnesium iodide, furnished SEM-trans-yuehchukene 88. The newly incorporated indole group bears a 1,3-diaxial-like interaction with the β-methyl group at C-7. Unlike 88, tosylacetate 82 gave the compound 84. Finally, the total synthesis of 6a-epi-yuehchukene was accomplished by deprotection of the indole system. Various compounds from this study are now under investigation at WHO and in Hong Kong but, unfortunately, biological results are unavailable at present. [Formula Omitted]
Science, Faculty of
Chemistry, Department of
Graduate
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Hoggatt, April Marie. "Mab anti-type I and Mab anti-zebrin II labelling in two siluriform fishes : the role of shared lineage versus shared function in polypeptide co-distributions." Virtual Press, 1994. http://liblink.bsu.edu/uhtbin/catkey/902481.

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Two monoclonal antibodies (mabs), the newly generated mab anti-type I and the previously documented mab anti-zebrin II, were reacted with brainstem sections of two ostariophysan siluriforms, the gymnotoid Rhamphichthys rostratus and the siluroid Ictalurus punctatus. Mab anti-type I recognizes a 47 kD polypeptide present in the dendrites and soma of projection neurons. Mab anti-zebrin II recognizes a 36 kD polypeptide present throughout the neuronal cytoplasm, including the axon. Strongly type I immunopositive cells include all cerebellar Purkinje cells, pyramidal cells of the nucleus medialis, electrosensory lateral line lobe, and tectum, pacemaker relay cells, Mauthner neurons, lateral line ganglion cells, and cells of the reticular formation, lateral reticular nucleus, and inferior olive. Weakly reactive type I cells include neurons in the torus semicircularis, medial and efferent octavolateralis nuclei, magnocellular and lateral tegmentum, and motor neurons of the Vth, V I Ith, and Xth cranial nerves. All type I positive cells are projection neurons. Zebrin II expression is restricted to subsets of two cell types which also express the type I antigen -- Purkinje cells and developing acousticolateralis pyramidal cells. Both of these neurons develop from the region of the rhombic lip. Thus, the mutual expression of the type I antigen can be explained by the shared function of projection neurons, while the common expression of the zebrin II antigen may be due to a shared embryological lineage.
Department of Physiology and Health Science
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Totton, Rebecca. "Examining Anti-Transgender Prejudice: Identity-Confusion and Deception as Aspects ofDistrust." Ohio University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1597060574652936.

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Books on the topic "Ants – Physiology"

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Clark, Christopher. Oxford activity books for children. Oxford: OUP, 1987.

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1943-, Eng Kenneth, and Coppa Gene Francis, eds. Anorectal, presacral, and sacral tumors: Anatomy, physiology, pathogenesis, and management. Philadelphia: Saunders, 1987.

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Velvet glove, iron fist: A history of anti-smoking. Ripon, England: Little Dice, 2009.

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N, Losso Jack, Shahidi Fereidoon 1951-, and Bagchi Debasis, eds. Anti-angiogenic functional and medicinal foods. Boca Raton: CRC Press, 2007.

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Antimicrobial drug resistance. [Totowa, N.J.]: Humana Press, 2009.

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Kronhausen, Eberhard. Formula for life: The anti-oxidant, free-radical, detoxification program. New York: Morrow, 1989.

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D, Catto Graeme R., ed. Drugs and the kidney. Dordrecht: Kluwer Academic Publishers, 1990.

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1946-, Feuerstein Giora Z., ed. Inflammation and stroke. Basel: Birkhäuser, 2001.

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Antiarrhythmic drugs: A practical guide. 2nd ed. Malden, Mass: Blackwell Pub., 2007.

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Antiarrhythmic drugs: A practical guide. Cambridge, Mass., USA: Blackwell Science, 1997.

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Book chapters on the topic "Ants – Physiology"

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Roces, Flavio. "Vibrational Communication Outside and Inside the Nest in Leaf-Cutting Ants." In Biotremology: Physiology, Ecology, and Evolution, 411–35. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-97419-0_17.

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Gosling, Jonathan, and Anton Emmanuel. "Anorectal Physiology." In Anus, 13–33. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-84882-091-3_2.

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Abdel-Halim, Mostafa. "Incontinence Assessment: Physiology and Imaging." In Anus, 115–32. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-84882-091-3_11.

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Guillemain, Matthieu, Pär Söderquist, Jocelyn Champagnon, and Johan Elmberg. "Mallard (Anas platyrhynchos Linnaeus, 1758)." In Invasive birds: global trends and impacts, 194–99. Wallingford: CABI, 2020. http://dx.doi.org/10.1079/9781789242065.0194.

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Abstract This chapter describes the common terminologies, taxonomy, morphology, geographical distribution, physiology, diet, behaviour, reproduction, habitats, ecology, invasion pathways, environmental impact, control and human use of the mallard (Anas platyrhynchos).
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Felt-Bersma, Richelle J. F. "Physiology of the Rectum and Anus." In Colon, Rectum and Anus: Anatomic, Physiologic and Diagnostic Bases for Disease Management, 55–69. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-09807-4_8.

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Felt-Bersma, Richelle J. F. "Physiology of the Rectum and Anus." In Coloproctology, 1–15. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-10154-5_8-1.

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Krogh, Klaus, and Soeren Laurberg. "Physiology of Colon, Rectum, and Anus." In Coloproctology, 23–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-53210-2_3.

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Bassotti, Gabrio, and Edda Battaglia. "Physiology of the Colon." In Colon, Rectum and Anus: Anatomic, Physiologic and Diagnostic Bases for Disease Management, 43–53. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-09807-4_7.

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Krogh, Klaus, and Janne Fassov. "Factors Affecting the Intestinal Physiology." In Colon, Rectum and Anus: Anatomic, Physiologic and Diagnostic Bases for Disease Management, 71–77. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-09807-4_9.

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Chadwick, Mike. "Anatomy and Physiology of the Rectum and Anus." In Modern Management of Cancer of the Rectum, 21–34. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6609-2_3.

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Conference papers on the topic "Ants – Physiology"

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Fernandez, Joaquin R., A. Mendioroz, and Rolindes Balda. "Anti-Stokes laser cooling in Yb3+-doped KPb 2 Cl 5 crystal." In Medical Imaging 2003 Physiology and Function: Methods, Systems, and Applications, edited by Alexis Carabelas, Giuseppe Baldacchini, Paolo Di Lazzaro, and Dimitrios Zevgolis. SPIE, 2003. http://dx.doi.org/10.1117/12.513507.

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Nayak, Siddharth, Saikat Sahoo, Biswajeet Champaty, and Kunal Pal. "Effect of horror clips on the physiology of ANS & heart using ECG signal classification." In 2014 International Conference on Control, Instrumentation, Communication and Computational Technologies (ICCICCT). IEEE, 2014. http://dx.doi.org/10.1109/iccicct.2014.6993010.

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Chen, W. J., Z. Chen, and C. X. Bao. "HIP2: A NEW MONOCLONAL ANTI-HUMAN PLATELET ANTIBODY WITH STIMULANT FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643505.

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A monoclonal anti-human platelet antibody(MoAb), HIP2 (IgG3) which induced irrevesible aggregation of platelet in association with the release of serotonin and thromboxane B2 formation is described. Indirect immunofluorescence assay (IFS) showed that the antibody binded to platelets and megakryocytes, and gave a weak reaction with aortic, liver and capillary endothelial cells. Electrophoresis of radiolabelled antigen showed that HIP2 recognized platelet membrane glycoprotein lib (130KD). The purified HIP2 MoAb induced aggregation with normal PRP, not with thrombasthenia platelets, formalin-fixed platelets, washed platelets and EDTA-PRP. Washed platelet aggregation with HIP2 could be restored by adding normal plasma or serum into medium, but not by inactivated serum at 56°C for 30 minutes and fibrinogen, The results suggested that the aggregation induced by HIP2 needed Ca++ and complement in medium. HIP2-induced aggregation was completely inhibited by calmodulin inhibitor, compound 48/80, and partially inhibited by aspirin, apyrase, ATP, antimycin A and phentolamine. Anti-glycoprotein Ilia MoAb(SZ-21) inhibited HIP2-induced platelet aggregation, did not block HIP2 binding on platelet surface in IFS. HIP2 no affected platelet adhision on glass. HIP2 prolonged koalin cephalin clotting time in PRP and interruped whole blood retraction. Under electron microscopy, the fibrin formation of clots in the presence of HIP2 was much less than the control. Recently, we found that the platelets from patients with myelo-proligerative diseases had decreased response to HIP2 aggregation. So that, HIP2 MoAb may be a very useful tool not only for study of the platelet membrane structure associated with function of platelet and platelet physiology, but also of the pathogenesis of some platelet diseases.
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Grishina, T. V., T. S. Leonova, E. V. Kissel, D. P. Gorbach, N. Y. Rogovskaya, E. V. Romanovskaya, V. N. Babakov, L. Vessjohann, and A. A. Frolov. "The study of the neuroprotective and anti-inflammatory effects of natural compounds in cell culture." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-138.

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Mokashi, Chinmay, Suraj K. Nayak, Ashirbad Pradhan, Sunil K. Rout, Kunal Pal, Biswajeet Champaty, and Arfat Anis. "Effect of sound in a horror movie clip on the physiology of the ANS and the conduction pathway of the heart." In 2016 IEEE Annual India Conference (INDICON). IEEE, 2016. http://dx.doi.org/10.1109/indicon.2016.7839020.

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Timmins, Lucas H., Clark A. Meyer, Michael R. Moreno, and James E. Moore. "Stented Artery Biomechanics in the Presence of Stenoses and Tapering." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176143.

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The implantation of a balloon expandable stent induces chronic stent-induced stresses on the artery wall. These highly non-physiologic stresses can provoke inflammation and smooth muscle cell proliferation. Ultimately, this cascade of events leads to restenosis, or the development of a new blockage in the stented artery. Since the initial human implantation of balloon expandable stents, technological advances in stent design, material properties, and deliverability have expanded the application and success rate of the procedure. More recently, anti-restenotic strategies such as drug-eluting stents have aimed to counteract the restenosis process. While clinical trials have demonstrated the success of drug eluting stents in coronary arteries [1], risk of late thrombosis [2] and failure to prevent restenosis in peripheral arteries [3] has limited this technology. A further investigation into the artery wall stresses induced by stent implantation, and the pursuit of strategies to minimize them could reduce the restenosis rates for both bare metal and drug-eluting stents.
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Piotrowicz, Randolph S., Kenneth M. Yamada, and Kunicki J. Kunicki. "HUMAN PLATELET GLYCOPROTEIN Ic-IIa IS AN ACTIVATION-INDEPENDENT FIBRONECTIN RECEPTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643911.

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Human platelets express the membrane glycoprotein (GP) heterodimer GPIIb-IIIa, which functions as an activation-dependent fibronectin (Fn) receptor. We have immunopurified the components of an activation-independent Fn receptor (FR) from human platelets employing a well-characterized rabbit polyclonal antibody raised against the beta chain of the chicken embryo fibroblast (CEF) FR (anti-band 3). This antibody crossreacts with antigen(s) expressed on both chicken thrombocytes and human platelets and inhibits the binding of both normal and thrombasthenic platelets (lacking GPIIb-IIIa) to Fn-coated surfaces in the absence of platelet activation.A monoclonal antibody directed against GPIIb-IIIa (AP2) partially inhibits the adhesion of normal platelets to Fn, but the combination of AP2 and anti-band 3 results in a level of inhibition greater than that obtained with either antibody alone. Thus, the presence of the FR alone is sufficient for the observed normal to enhanced binding of thrombasthenic platelets to Fn, whereas adhesion of normal platelets involves the synergistic action of the FR and GPIIb-IIIa. The adhesion of platelets to Fn mediated by the FR is inhibited by the tetrapeptide RGDS.Immunopurified FR appears to be a complex of two proteins: an alpha chain with an apparent molecular weight of 155/130 KD (nonreduced/reduced) and a beta chain with an apparent molecular weight of 125/147 KD. The alpha chain is composed of two subunits, dissociated by reduction, with electrophoretic mobilities identical to platelet glycoproteins previously designated lea and IcB. The beta chain comigrates with that platelet glycoprotein known as GPIIa. In an immunoblot assay, anti-band 3 binds to GPIIa but not to GPIc. The fact that anti-band 3 iramunoprecipitates both GP therefore suggests that they exist in a complex.Our findings establish GPIc-IIa as yet another platelet glycoprotein receptor complex and pave the way for future studies of the relative role of GPIIb-IIIa and GPIc-IIa in the adhesion of platelets to physiologic surfaces.
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Van der Heiden, K., H. C. Groen, P. C. Evans, L. Speelman, F. Gijsen, M. de Jong, A. F. W. van der Steen, and J. J. Wentzel. "Non-Invasive Molecular Imaging of Shear Stress-Induced Endothelial Activation and Atherosclerotic Plaque Vulnerability." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80515.

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Atherosclerosis is a lipid- and inflammation driven disease of the larger arteries and is found at specific locations in the arterial tree, i.e. at branches and bends where endothelial cells are exposed to low and low, oscillatory shear stress. Shear stress, the frictional force acting on the endothelial cells as a result of the blood flow, affects endothelial physiology. It determines the location of atherosclerotic lesion development as low and low, oscillatory shear stress induce pro-inflammatory transcription factors but reduce expression and/or activity of anti-inflammatory transcription factors in endothelial cells, rendering the vascular wall vulnerable for inflammation. Consequently, in the presence of atherosclerotic risk factors, such as hypercholesterolemia and diabetes, atherosclerotic lesion development can occur. Although the relationship between low and low, oscillatory shear stress and the prevalence of atherosclerosis has been recognized for several decades, insight into the mechanisms underlying this relationship is still incomplete. The correlation between shear stress and endothelial inflammation was demonstrated by in vitro experiments, in which cultured endothelial cells were exposed to specific flow profiles, and confirmed in vivo by gene expression pattern studies at atherosclerosis-susceptible sites. However, the relationship was not substantiated by direct causal in vivo evidence. Therefore, we developed a method to change the local shear stress field in mice in vivo and studied its effect on the endothelial molecular pathways and resulting atherosclerotic plaque formation. Moreover it allowed us to develop non-invasive molecular imaging strategies to detect vulnerable plaques.
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Nayak, Suraj K., Karan Pande, Pratyush K. Patnaik, Shikshya Nayak, Shankar J. Patel, Arfat Anis, Anilesh Dey, and Kunal Pal. "Understanding the effect of cannabis abuse on the ANS and cardiac physiology of the Indian women paddy-field workers using RR interval and ECG signal analyses." In 2017 Asia-Pacific Signal and Information Processing Association Annual Summit and Conference (APSIPA ASC). IEEE, 2017. http://dx.doi.org/10.1109/apsipa.2017.8282047.

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Mukhlova Montiel, M., and H. Bussey. "RESPONSE OF PROTEIN C AND PROTEIN S INHIBITORS IN LONG-TERM ORAL ANTICOAGULANT THERAPY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643877.

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Protein C (PC) and its coenzyme Protein S (PS) are physiologic inhibitors of activated factors Va and Villa. Deficiency of either one of these inhibitors has been associated with venous thrombosis. Their activity is dependent on vitamin K for hepatic gamma carboxylation and it is depressed during oral anticoagulant therapy. Because rebound thrombosis complicates cessation of anticoagulant therapy, we investigated the response of PC and PS during long term oral anti coagulation. The study encompassed 30 patients ranging between 26 and 76 years of age, who have received therapeutic doses of coumadin from 15 days to more than 8 years. The conditions for which treatment was initiated were deep vein thrombosis, cerebral vascular accidents and cardiac valve replacements.Factor VII and X activity was assayed by one step routine clotting assays. PC antigen (ag), total PSag and free PSag were assayed by Laurel 1 Rocket electroimmunodiffusion method. The measurement of the free PS was carried out after precipitation of C4b-binding protein with polyethylene glycol. PC activity was measured by clotting assay using PC deficient plasma to which was added patient plasma as a source of PC. Control group of 30 individuals in similar age group were assayed parallel with the patient samples. Compared with the control group the coumadin-treated patients showed substantial decrease of all factors studied. Statistical regression analysis of the coumadin group showed a significant increase in PS free (p = 0.014)during long term anti coagulation, while all of the other variables did not change significantly.PCag and total PSag were decreased and their activities, as expected, were more severely affected. The ratio of PC activity to PCag averages 0.39 (normal >0.80) and free PS represented only 27% of the total PSag (normal about 40%). The inhibitors' persistent activity parallels that of the depression of Factors VII and X and there appears to be a balanced coagulation-inhibi-tion system. If PC and PS play a role in rebound thrombosis after a prolonged anticoagulation therapy, the changes may occur after discontinuation of medication.
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Reports on the topic "Ants – Physiology"

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Glaser, Roger M., Betram Ezenna, and Stephen E. Popper. Physiologic Evaluation of the L1/M1 Anti-G Straining Maneuver. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada251257.

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Chamovitz, A. Daniel, and Georg Jander. Genetic and biochemical analysis of glucosinolate breakdown: The effects of indole-3-carbinol on plant physiology and development. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597917.bard.

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Genetic and biochemical analysis of glucosinolate breakdown: The effects of indole-3-carbinol on plant physiology and development Glucosinolates are a class of defense-related secondary metabolites found in all crucifers, including important oilseed and vegetable crops in the Brassica genus and the well-studied model plant Arabidopsis thaliana. Upon tissue damage, such as that provided by insect feeding, glucosinolates are subjected to catalysis and spontaneous degradation to form a variety of breakdown products. These breakdown products typically have a deterrent effect on generalist herbivores. Glucosinolate breakdown products also contribute to the anti-carcinogenic effects of eating cabbage, broccoli and related cruciferous vegetables. Indole-3-carbinol, a breakdown product of indol-3-ylmethylglucosinolate, forms conjugates with several other plant metabolites. Although some indole-3-carbinol conjugates have known functions in defense against herbivores and pathogens, most play as yet unidentified roles in plant metabolism, and possibly also plant development. At the outset, our proposal had three main hypotheses: (1) There is a specific detoxification pathway for indole-3-carbinol; (2) Metabolites derived from indole-3-carbinol are phloem-mobile and serve as signaling molecules; and (3) Indole-3-carbinol affects plant cell cycle and cell-differentiation pathways. The experiments were designed to enable us to elucidate how indole-3-carbinol and related metabolites affect plants and their interactions with herbivorous insects. We discovered that indole-3- carbinol rapidly and reversibly inhibits root elongation in a dose-dependent manner, and that this inhibition is accompanied by a loss of auxin activity in the root meristem. A direct interaction between indole-3-carbinol and the auxin perception machinery was suggested, as application of indole-3-carbinol rescued auxin-induced root phenotypes. In vitro and yeast-based protein interaction studies showed that indole-3-carbinol perturbs the auxin-dependent interaction of TIR1 with Aux/IAA proteins, supporting the notion that indole-3-carbinol acts as an auxin antagonist. Furthermore, transcript profiling experiments revealed the influence of indole-3-carbinol on auxin signaling in root tips, and indole-3-carbinol also affected auxin transporters. Brief treatment with indole-3-carbinol led to a reduction in the amount of PIN1 and to mislocalization of PIN2. The results indicate that chemicals induced by herbivory, such as indole-3-carbinol, function not only to repel herbivores, but also as signaling molecules that directly compete with auxin to fine tune plant growth and development, which implies transport of indole-3- carbinol that we are as yet unsuccessful in detecting. Our results indicate that plant defensive metabolites also have secondary functions in regulating aspects of plant metabolism, thereby providing diversity in defense-related plant signaling pathways. Such diversity of of signaling by defensive metabolites would be beneficial for the plant, as herbivores and pathogens would be less likely to mount effective countermeasures. We propose that growth arrest can be mediated directly by the herbivory-induced chemicals, in our case, indole-3-carbinol. Thus, glucosinolate breakdown to I3C following herbivory would have two outcomes: (1) Indole-3-carbinaol would inhibit the herbivore, while (2) at the same time inducing growth arrest within the plant. Thus, our results indicate that I3C is a defensive phytohormone that modulates auxin signaling, leading to growth arrest.
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