Unsteady Aerodynamic Performance of Model Wings at Low Reynolds Numbers

The synthesis of a comprehensive theory of force production in insect flight is hindered in part by the lack of precise knowledge of unsteady forces produced by wings. Data are especially sparse in the intermediate Reynolds number regime (10<Re<1000) appropriate for the flight of small insects. This paper attempts to fill this deficit by quantifying the time-dependence of aerodynamic forces for a simple yet important motion, rapid acceleration from rest to a constant velocity at a fixed angle of attack. The study couples the measurement of lift and drag on a two-dimensional model with simultaneous flow visualization. The results of these experiments are summarized below. 1. At angles of attack below 13.5°, there was virtually no evidence of a delay in the generation of lift, in contrast to similar studies made at higher Reynolds numbers. 2. At angles of attack above 13.5°, impulsive movement resulted in the production of a leading edge vortex that stayed attached to the wing for the first 2 chord lengths of travel, resulting in an 80 % increase in lift compared to the performance measured 5 chord lengths later. It is argued that this increase is due to the process of detached vortex lift, analogous to the method of force production in delta-wing aircraft. 3. As the initial leading edge vortex is shed from the wing, a second vortex of opposite vorticity develops from the trailing edge of the wing, correlating with a decrease in lift production. This pattern of alternating leading and trailing edge vortices generates a von Karman street, which is stable for at least 7.5 chord lengths of travel. 4. Throughout the first 7.5 chords of travel the model wing exhibits a broad lift plateau at angles of attack up to 54°, which is not significantly altered by the addition of wing camber or surface projections. 5. Taken together, these results indicate how the unsteady process of vortex generation at large angles of attack might contribute to the production of aerodynamic forces in insect flight. Because the fly wing typically moves only 2–4 chord lengths each half-stroke, the complex dynamic behavior of impulsively started wing profiles is more appropriate for models of insect flight than are steady-state approximations

The wake dynamics and flight forces of the fruit fly Drosophila melanogaster

We have used flow visualizations and instantaneous force measurements of tethered fruit flies (Drosophila melanogaster) to study the dynamics of force generation during flight. During each complete stroke cycle, the flies generate one single vortex loop consisting of vorticity shed during the downstroke and ventral flip. This gross pattern of wake structure in Drosophila is similar to those described for hovering birds and some other insects. The wake structure differed from those previously described, however, in that the vortex filaments shed during ventral stroke reversal did not fuse to complete a circular ring, but rather attached temporarily to the body to complete an inverted heart-shaped vortex loop. The attached ventral filaments of the loop subsequently slide along the length of the body and eventually fuse at the tip of the abdomen. We found no evidence for the shedding of wing-tip vorticity during the upstroke, and argue that this is due to an extreme form of the Wagner effect acting at that time. The flow visualizations predicted that maximum flight forces would be generated during the downstroke and ventral reversal, with little or no force generated during the upstroke. The instantaneous force measurements using laser-interferometry verified the periodic nature of force generation. Within each stroke cycle, there was one plateau of high force generation followed by a period of low force, which roughly correlated with the upstroke and downstroke periods. However, the fluctuations in force lagged behind their expected occurrence within the wing-stroke cycle by approximately 1 ms or one-fifth of the complete stroke cycle. This temporal discrepancy exceeds the range of expected inaccuracies and artifacts in the measurements, and we tentatively discuss the potential retarding effects within the underlying fluid mechanics

The active control of wing rotation by Drosophila

This paper investigates the temporal control of a fast wing rotation in flies, the ventral flip, which occurs during the transition from downstroke to upstroke. Tethered flying Drosophila actively modulate the timing of these rapid supinations during yaw responses evoked by an oscillating visual stimulus. The time difference between the two wings is controlled such that the wing on the outside of a fictive turn rotates in advance of its contralateral partner. This modulation of ventral-flip timing between the two wings is strongly coupled with changes in wing-stroke amplitude. Typically, an increase in the stroke amplitude of one wing is correlated with an advance in the timing of the ventral flip of the same wing. However, flies do display a limited ability to control these two behaviors independently, as shown by flight records in which the correlation between ventral-flip timing and stroke amplitude transiently reverses. The control of ventral-flip timing may be part of an unsteady aerodynamic mechanism that enables the fly to alter the magnitude and direction of flight forces during turning maneuvers

Animal models for pah and increased pulmonary blood flow

Pulmonary arterial hypertension (PAH), a progressive pulmonary vasoproliferative disorder, is characterized by the development of unique neointimal lesions including concentric laminar intimal fibrosis and plexiform lesions.In PAH associated with congenital heart disease, increased pulmonary blood flow (i.e., systemic-to-pulmonary shunt) is an essential trigger for the occurrence of neointimal lesions and disease development. Although neointimal development is well described histopathologically, the pathogenesis of flow-induced PAH and its typical vascular lesions is largely unknown.Animal models play a crucial part in giving insight in new pathobiological processes in PAH and possible new therapeutic targets. However, as for any preclinical model, the pathophysiological mechanism and clinical course have to be comparable to the human disease that it is supposed to mimic. This means that animal models mimicking human PAH ideally are characterized by (1) a hit resembling the human disease, (2) specific vascular remodeling that resembles neointimal development in human PAH, and (3) progressive disease development that leads to right ventricular (RV) dysfunction and eventually death.Therefore, this chapter will discuss currently used animal models for pulmonary hypertension that are of interest for PAH in the pediatric population, specifically PAH associated with congenital heart disease. Since increased pulmonary blood flow is known to be a trigger for PAH development in this population, particular emphasis will be put on models with increased pulmonary blood flow.</p

Animal models for pah and increased pulmonary blood flow

Pulmonary arterial hypertension (PAH), a progressive pulmonary vasoproliferative disorder, is characterized by the development of unique neointimal lesions including concentric laminar intimal fibrosis and plexiform lesions.In PAH associated with congenital heart disease, increased pulmonary blood flow (i.e., systemic-to-pulmonary shunt) is an essential trigger for the occurrence of neointimal lesions and disease development. Although neointimal development is well described histopathologically, the pathogenesis of flow-induced PAH and its typical vascular lesions is largely unknown.Animal models play a crucial part in giving insight in new pathobiological processes in PAH and possible new therapeutic targets. However, as for any preclinical model, the pathophysiological mechanism and clinical course have to be comparable to the human disease that it is supposed to mimic. This means that animal models mimicking human PAH ideally are characterized by (1) a hit resembling the human disease, (2) specific vascular remodeling that resembles neointimal development in human PAH, and (3) progressive disease development that leads to right ventricular (RV) dysfunction and eventually death.Therefore, this chapter will discuss currently used animal models for pulmonary hypertension that are of interest for PAH in the pediatric population, specifically PAH associated with congenital heart disease. Since increased pulmonary blood flow is known to be a trigger for PAH development in this population, particular emphasis will be put on models with increased pulmonary blood flow.</p

Animal models for pah and increased pulmonary blood flow

Pulmonary arterial hypertension (PAH), a progressive pulmonary vasoproliferative disorder, is characterized by the development of unique neointimal lesions including concentric laminar intimal fibrosis and plexiform lesions.In PAH associated with congenital heart disease, increased pulmonary blood flow (i.e., systemic-to-pulmonary shunt) is an essential trigger for the occurrence of neointimal lesions and disease development. Although neointimal development is well described histopathologically, the pathogenesis of flow-induced PAH and its typical vascular lesions is largely unknown.Animal models play a crucial part in giving insight in new pathobiological processes in PAH and possible new therapeutic targets. However, as for any preclinical model, the pathophysiological mechanism and clinical course have to be comparable to the human disease that it is supposed to mimic. This means that animal models mimicking human PAH ideally are characterized by (1) a hit resembling the human disease, (2) specific vascular remodeling that resembles neointimal development in human PAH, and (3) progressive disease development that leads to right ventricular (RV) dysfunction and eventually death.Therefore, this chapter will discuss currently used animal models for pulmonary hypertension that are of interest for PAH in the pediatric population, specifically PAH associated with congenital heart disease. Since increased pulmonary blood flow is known to be a trigger for PAH development in this population, particular emphasis will be put on models with increased pulmonary blood flow.</p

Animal models for pah and increased pulmonary blood flow

Pulmonary arterial hypertension (PAH), a progressive pulmonary vasoproliferative disorder, is characterized by the development of unique neointimal lesions including concentric laminar intimal fibrosis and plexiform lesions.In PAH associated with congenital heart disease, increased pulmonary blood flow (i.e., systemic-to-pulmonary shunt) is an essential trigger for the occurrence of neointimal lesions and disease development. Although neointimal development is well described histopathologically, the pathogenesis of flow-induced PAH and its typical vascular lesions is largely unknown.Animal models play a crucial part in giving insight in new pathobiological processes in PAH and possible new therapeutic targets. However, as for any preclinical model, the pathophysiological mechanism and clinical course have to be comparable to the human disease that it is supposed to mimic. This means that animal models mimicking human PAH ideally are characterized by (1) a hit resembling the human disease, (2) specific vascular remodeling that resembles neointimal development in human PAH, and (3) progressive disease development that leads to right ventricular (RV) dysfunction and eventually death.Therefore, this chapter will discuss currently used animal models for pulmonary hypertension that are of interest for PAH in the pediatric population, specifically PAH associated with congenital heart disease. Since increased pulmonary blood flow is known to be a trigger for PAH development in this population, particular emphasis will be put on models with increased pulmonary blood flow.</p

Animal models for pah and increased pulmonary blood flow

Pulmonary arterial hypertension (PAH), a progressive pulmonary vasoproliferative disorder, is characterized by the development of unique neointimal lesions including concentric laminar intimal fibrosis and plexiform lesions.In PAH associated with congenital heart disease, increased pulmonary blood flow (i.e., systemic-to-pulmonary shunt) is an essential trigger for the occurrence of neointimal lesions and disease development. Although neointimal development is well described histopathologically, the pathogenesis of flow-induced PAH and its typical vascular lesions is largely unknown.Animal models play a crucial part in giving insight in new pathobiological processes in PAH and possible new therapeutic targets. However, as for any preclinical model, the pathophysiological mechanism and clinical course have to be comparable to the human disease that it is supposed to mimic. This means that animal models mimicking human PAH ideally are characterized by (1) a hit resembling the human disease, (2) specific vascular remodeling that resembles neointimal development in human PAH, and (3) progressive disease development that leads to right ventricular (RV) dysfunction and eventually death.Therefore, this chapter will discuss currently used animal models for pulmonary hypertension that are of interest for PAH in the pediatric population, specifically PAH associated with congenital heart disease. Since increased pulmonary blood flow is known to be a trigger for PAH development in this population, particular emphasis will be put on models with increased pulmonary blood flow.</p

Animal models for pah and increased pulmonary blood flow

Pulmonary arterial hypertension (PAH), a progressive pulmonary vasoproliferative disorder, is characterized by the development of unique neointimal lesions including concentric laminar intimal fibrosis and plexiform lesions.In PAH associated with congenital heart disease, increased pulmonary blood flow (i.e., systemic-to-pulmonary shunt) is an essential trigger for the occurrence of neointimal lesions and disease development. Although neointimal development is well described histopathologically, the pathogenesis of flow-induced PAH and its typical vascular lesions is largely unknown.Animal models play a crucial part in giving insight in new pathobiological processes in PAH and possible new therapeutic targets. However, as for any preclinical model, the pathophysiological mechanism and clinical course have to be comparable to the human disease that it is supposed to mimic. This means that animal models mimicking human PAH ideally are characterized by (1) a hit resembling the human disease, (2) specific vascular remodeling that resembles neointimal development in human PAH, and (3) progressive disease development that leads to right ventricular (RV) dysfunction and eventually death.Therefore, this chapter will discuss currently used animal models for pulmonary hypertension that are of interest for PAH in the pediatric population, specifically PAH associated with congenital heart disease. Since increased pulmonary blood flow is known to be a trigger for PAH development in this population, particular emphasis will be put on models with increased pulmonary blood flow.</p