scholarly journals Wing Design in Flies: Properties and Aerodynamic Function

Insects ◽  
2020 ◽  
Vol 11 (8) ◽  
pp. 466
Author(s):  
Swathi Krishna ◽  
Moonsung Cho ◽  
Henja-Niniane Wehmann ◽  
Thomas Engels ◽  
Fritz-Olaf Lehmann

The shape and function of insect wings tremendously vary between insect species. This review is engaged in how wing design determines the aerodynamic mechanisms with which wings produce an air momentum for body weight support and flight control. We work out the tradeoffs associated with aerodynamic key parameters such as vortex development and lift production, and link the various components of wing structure to flight power requirements and propulsion efficiency. A comparison between rectangular, ideal-shaped and natural-shaped wings shows the benefits and detriments of various wing shapes for gliding and flapping flight. The review expands on the function of three-dimensional wing structure, on the specific role of wing corrugation for vortex trapping and lift enhancement, and on the aerodynamic significance of wing flexibility for flight and body posture control. The presented comparison is mainly concerned with wings of flies because these animals serve as model systems for both sensorimotor integration and aerial propulsion in several areas of biology and engineering.

2006 ◽  
Vol 74 (11) ◽  
pp. 6252-6263 ◽  
Author(s):  
Jodie S. Haring ◽  
John T. Harty

ABSTRACT Several lines of evidence from different model systems suggest that gamma interferon (IFN-γ) is an important regulator of T-cell contraction after antigen (Ag)-driven expansion. To specifically investigate the role of IFN-γ in regulating the contraction of Ag-specific CD4 T cells, we infected IFN-γ−/− and IFN-γR1−/− mice with attenuated Listeria monocytogenes and monitored the numbers of Ag-specific CD4 T cells during the expansion, contraction, and memory phases of the immune response to infection. In the absence of IFN-γ or the ligand-binding portion of its receptor, Ag-specific CD4 T cells exhibited normal expansion in numbers, but in both strains of deficient mice there was very little decrease in the number of Ag-specific CD4 T cells even at time points later than day 90 after infection. This significant delay in contraction was not due to prolonged infection, since mice treated with antibiotics to conclusively eliminate infection exhibited the same defect in contraction. In addition to altering the number of Ag-specific CD4 T cells, the absence of IFN-γ signaling also changed the phenotype of cells generated after infection. IFN-γR1−/− Ag-specific CD4 T cells reacquired expression of CD127 more quickly than wild-type cells, and more IFN-γR1−/− CD4 T cells were capable of producing both IFN-γ and interleukin 2 following Ag stimulation. From these data we conclude that IFN-γ regulates the contraction, phenotype, and function of Ag-specific CD4 T cells generated after infection.


1999 ◽  
Vol 26 (7) ◽  
pp. 671 ◽  
Author(s):  
Conrad W. Mullineaux

In recent years there has been remarkable progress in determining the three-dimensional structures of photosynthetic complexes. A new challenge is emerging: can we understand the organisation and interaction of those complexes in the intact photosynthetic membrane? Intact membranes are complex, dynamic systems. If we are to understand the function of the intact membrane, we will need to understand the organisation of the complexes, how they can diffuse and interact in the membrane, how they are assembled, repaired and broken down, and how their function is regulated. Cyanobacteria have some crucial advantages as model systems. The complete sequencing of the Synechocystis 6803 genome, coupled with the ease of genetic manipulation of Synechocystis (and certain other cyanobacteria) have given us a unique tool for studying a photosynthetic organism. Furthermore, some cyanobacteria have a very simple, regular thylakoid membrane structure. The unique geometry of photosynthetic membranes of these cyanobacteria will greatly facilitate biophysical studies of membrane function. This review summarises recent progress in understanding the structure, function and dynamics of cyanobacterial thylakoid membranes, highlights the questions that remain to be answered and suggests some possible approaches towards solving those questions.


2012 ◽  
Vol 693 ◽  
pp. 473-499 ◽  
Author(s):  
Hu Dai ◽  
Haoxiang Luo ◽  
James F. Doyle

AbstractIn order to study the role of the passive deformation in the aerodynamics of insect wings, we computationally model the three-dimensional fluid–structure interaction of an elastic rectangular wing at a low aspect ratio during hovering flight. The code couples a viscous incompressible flow solver based on the immersed-boundary method and a nonlinear finite-element solver for thin-walled structures. During a flapping stroke, the wing surface is dominated by non-uniform chordwise deformations. The effects of the wing stiffness, mass ratio, phase angle of active pitching, and Reynolds number are investigated. The results show that both the phase and the rate of passive pitching due to the wing flexibility can significantly modify the aerodynamics of the wing. The dynamic pitching depends not only on the specified kinematics at the wing root and the stiffness of the wing, but also greatly on the mass ratio, which represents the relative importance of the wing inertia and aerodynamic forces in the wing deformation. We use the ratio between the flapping frequency, $\omega $, and natural frequency of the wing, ${\omega }_{n} $, as the non-dimensional stiffness. In general, when $\omega / {\omega }_{n} \leq 0. 3$, the deformation significantly enhances the lift and also improves the lift efficiency despite a disadvantageous camber. In particular, when the inertial pitching torque is assisted by an aerodynamic torque of comparable magnitude, the lift efficiency can be markedly improved.


2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Benoy Nalin Shah

Echocardiography remains the most frequently performed cardiac imaging investigation and is an invaluable tool for detailed and accurate evaluation of cardiac structure and function. Echocardiography, nuclear cardiology, cardiac magnetic resonance imaging, and cardiovascular-computed tomography comprise the subspeciality of cardiovascular imaging, and these techniques are often used together for a multimodality, comprehensive assessment of a number of cardiac diseases. This paper provides the general cardiologist and physician with an overview of state-of-the-art modern echocardiography, summarising established indications as well as highlighting advances in stress echocardiography, three-dimensional echocardiography, deformation imaging, and contrast echocardiography. Strengths and limitations of echocardiography are discussed as well as the growing role of real-time three-dimensional echocardiography in the guidance of structural heart interventions in the cardiac catheter laboratory.


2015 ◽  
Vol 26 (2) ◽  
pp. 294-304 ◽  
Author(s):  
Toshiyuki Oda ◽  
Haruaki Yanagisawa ◽  
Masahide Kikkawa

The nexin-dynein regulatory complex (N-DRC) forms a cross-bridge between the outer doublet microtubules of the axoneme and regulates dynein motor activity in cilia/flagella. Although the molecular composition and the three-dimensional structure of N-DRC have been studied using mutant strains lacking N-DRC subunits, more accurate approaches are necessary to characterize the structure and function of N-DRC. In this study, we precisely localized DRC1, DRC2, and DRC4 using cryo–electron tomography and structural labeling. All three N-DRC subunits had elongated conformations and spanned the length of N-DRC. Furthermore, we purified N-DRC and characterized its microtubule-binding properties. Purified N-DRC bound to the microtubule and partially inhibited microtubule sliding driven by the outer dynein arms (ODAs). Of interest, microtubule sliding was observed even in the presence of fourfold molar excess of N-DRC relative to ODA. These results provide insights into the role of N-DRC in generating the beating motions of cilia/flagella.


Membranes ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 24
Author(s):  
Catarina Pereira-Leite ◽  
Marina Figueiredo ◽  
Kinga Burdach ◽  
Cláudia Nunes ◽  
Salette Reis

Cardiovascular (CV) toxicity is nowadays recognized as a class effect of non-aspirin nonsteroidal anti-inflammatory drugs (NSAIDs). However, their mechanisms of cardiotoxicity are not yet well understood, since different compounds with similar action mechanisms exhibit distinct cardiotoxicity. For instance, diclofenac (DIC) is among the most cardiotoxic compounds, while naproxen (NAP) is associated with low CV risk. In this sense, this study aimed to unravel the role of drug-lipid interactions in NSAIDs-induced cardiotoxicity. For that, DIC and NAP interactions with lipid bilayers as model systems of cell and mitochondrial membranes were characterized by derivative spectrophotometry, fluorometric leakage assays, and synchrotron X-ray scattering. Both DIC and NAP were found to have the ability to permeabilize the membrane models, as well as to alter the bilayers’ structure. The NSAIDs-induced modifications were dependent on the lipid composition of the membrane model, the three-dimensional structure of the drug, as well as the drug:lipid molar ratio tested. Altogether, this work supports the hypothesis that NSAIDs-lipid interactions, in particular at the mitochondrial level, may be another key step among the mechanisms underlying NSAIDs-induced cardiotoxicity.


Author(s):  
Kenya Bonitto ◽  
Kirthana Sarathy ◽  
Kaiser Atai ◽  
Mithun Mitra ◽  
Hilary A. Coller

Many of the cells in our bodies are quiescent, that is, temporarily not dividing. Under certain physiological conditions such as during tissue repair and maintenance, quiescent cells receive the appropriate stimulus and are induced to enter the cell cycle. The ability of cells to successfully transition into and out of a quiescent state is crucial for many biological processes including wound healing, stem cell maintenance, and immunological responses. Across species and tissues, transcriptional, epigenetic, and chromosomal changes associated with the transition between proliferation and quiescence have been analyzed, and some consistent changes associated with quiescence have been identified. Histone modifications have been shown to play a role in chromatin packing and accessibility, nucleosome mobility, gene expression, and chromosome arrangement. In this review, we critically evaluate the role of different histone marks in these processes during quiescence entry and exit. We consider different model systems for quiescence, each of the most frequently monitored candidate histone marks, and the role of their writers, erasers and readers. We highlight data that support these marks contributing to the changes observed with quiescence. We specifically ask whether there is a quiescence histone “code,” a mechanism whereby the language encoded by specific combinations of histone marks is read and relayed downstream to modulate cell state and function. We conclude by highlighting emerging technologies that can be applied to gain greater insight into the role of a histone code for quiescence.


RNA ◽  
2021 ◽  
pp. rna.079001.121
Author(s):  
Natalia B. Nedelsky ◽  
J. Paul Taylor

The genetics of human disease serves as a robust and unbiased source of insight into human biology, both revealing fundamental cellular processes and exposing the vulnerabilities associated with their dysfunction. Over the last decade, the genetics of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) have epitomized this concept, as studies of ALS-FTD-causing mutations have yielded fundamental discoveries regarding the role of biomolecular condensation in organizing cellular contents while implicating disturbances in condensate dynamics as central drivers of neurodegeneration. Here we review this genetic evidence, highlight its intersection with patient pathology, and discuss how studies in model systems have revealed a role for aberrant condensation in neuronal dysfunction and death. We detail how multiple, distinct types of disease-causing mutations promote pathological phase transitions that disturb the dynamics and function of ribonucleoprotein (RNP) granules. Dysfunction of RNP granules causes pleiotropic defects in RNA metabolism and can drive evolution of these structures to end-stage pathological inclusions characteristic of ALS-FTD. We propose that aberrant phase transitions of these complex condensates in cells provide a parsimonious explanation for the widespread cellular abnormalities observed in ALS as well as certain histopathological features that characterize late-stage disease.


2017 ◽  
Vol 284 (1859) ◽  
pp. 20171124 ◽  
Author(s):  
Jonas O. Wolff ◽  
Arie van der Meijden ◽  
Marie E. Herberstein

Building behaviour in animals extends biological functions beyond bodies. Many studies have emphasized the role of behavioural programmes, physiology and extrinsic factors for the structure and function of buildings. Structure attachments associated with animal constructions offer yet unrealized research opportunities. Spiders build a variety of one- to three-dimensional structures from silk fibres. The evolution of economic web shapes as a key for ecological success in spiders has been related to the emergence of high performance silks and thread coating glues. However, the role of thread anchorages has been widely neglected in those models. Here, we show that orb-web (Araneidae) and hunting spiders (Sparassidae) use different silk application patterns that determine the structure and robustness of the joint in silk thread anchorages. Silk anchorages of orb-web spiders show a greater robustness against different loading situations, whereas the silk anchorages of hunting spiders have their highest pull-off resistance when loaded parallel to the substrate along the direction of dragline spinning. This suggests that the behavioural ‘printing' of silk into attachment discs along with spinneret morphology was a prerequisite for the evolution of extended silk use in a three-dimensional space. This highlights the ecological role of attachments in the evolution of animal architectures.


2020 ◽  
Vol 48 (1) ◽  
pp. 137-146 ◽  
Author(s):  
Michael M. Kessels ◽  
Britta Qualmann

The formation of caveolae, bulb-shaped plasma membrane invaginations, requires the coordinated action of distinct lipid-interacting and -shaping proteins. The interdependence of caveolar structure and function has evoked substantial scientific interest given the association of human diseases with caveolar dysfunction. Model systems deficient of core components of caveolae, caveolins or cavins, did not allow for an explicit attribution of observed functional defects to the requirement of caveolar invagination as they lack both invaginated caveolae and caveolin proteins. Knockdown studies in cultured cells and recent knockout studies in mice identified an additional family of membrane-shaping proteins crucial for caveolar formation, syndapins (PACSINs) — BAR domain superfamily proteins characterized by crescent-shaped membrane binding interfaces recognizing and inducing distinct curved membrane topologies. Importantly, syndapin loss-of-function resulted exclusively in impairment of caveolar invagination without a reduction in caveolin or cavin at the plasma membrane, thereby allowing the specific role of the caveolar invagination to be unveiled. Muscle cells of syndapin III KO mice showed severe reductions of caveolae reminiscent of human caveolinopathies and were more vulnerable to membrane damage upon changes in membrane tensions. Consistent with the lack of syndapin III-dependent invaginated caveolae providing mechanoprotection by releasing membrane reservoirs through caveolar flattening, physical exercise of syndapin III KO mice resulted in pathological defects reminiscent of the clinical symptoms of human myopathies associated with caveolin 3 mutation suggesting that the ability of muscular caveolae to respond to mechanical forces is a key physiological process.


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