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H Fischer

Publications and source records attributed to H Fischer.

At least 127 records · Page 7Linked to original sources
PubMed1999

Contrast-enhanced MR imaging of two superparamagnetic RES-contrast agents: functional assessment of experimental radiation-induced liver injury.

The purpose of this study was to compare liver contrast-enhancing characteristics of two superparamagnetic reticuloendothelial system (RES)-directed agents with different particle sizes, polycrystalline iron oxide nanocompounds (PION) and carboxydextran-coated maghemite (DDM128N/389, later referred to as DDM128), in an experimental model of focal radiation-induced hepatitis. PION, for the small particle size (31 nm), and DDM128, for the large particle size (59 nm), RES-directed agents were compared for liver enhancement after radiation-induced liver injury. A single x-irradiation exposure varying from 10 to 60 Gy was delivered to one side of the liver. T2-weighted spinecho magnetic resonance imaging was performed 3 days after x-irradiation at 30 minutes post-contrast. Using the RES-directed PION, the normal, non-irradiated portion of the liver decreased in signal intensity with a maximum negative enhancement of -66%, while the irradiated portion of the liver decreased in signal intensity by -24% (60 Gy). The signal intensity decline of irradiated liver tissue using PION was dose dependent, but was found at all radiation dose levels (10-60 Gy). The difference in signal intensity between irradiated (-63%) and non-irradiated (-82%) portions was also statistically different using DDM128 at 60 Gy. However, lower irradiation doses (10 and 30 Gy) failed to produce a statistically significantly different enhancement in the irradiated and non-irradiated portion of the liver. Sensitivity of liver enhancement with RES-directed agents is size dependent. The smaller particle (PION) is more sensitive for detection of radiation-induced hepatitis than the larger particle (DDM128). The relative insensitivity of DDM128 enhancement for diffuse liver injury will be clinically advantageous for detecting focal lesions in the presence of diffuse hepatic injury.

Animals↗
PubMed1999

Neural network-based analysis of MR time series.

Clustering has been introduced to analyze fMRI data by means of partitioning data into time series of similar temporal behavior. It is hoped that one of these clusters represents a dynamic effect of interest, like functional activation. Using self-organizing maps for clustering, additional information can be obtained by ordering cluster centers on a two-dimensional projection plane. The map's capability of data visualization is used to summarize all dynamic effects of an experiment by means of data partitioning. The map does allow differently sized and populated clusters in the data by forming "superclusters" on the map. The method is introduced as a conceptual extension to clustering. Applications to fMRI and to MR mammography are discussed.

Artifacts↗
PubMed1999

Histaminergic neurons modulate acetylcholine release in the ventral striatum: role of H3 histamine receptors.

To investigate whether histaminergic neurons influence the activity of cholinergic neurons, the ventral striatum was superfused through a push-pull cannula and the release of endogenous acetylcholine was determined in the superfusate. Local inhibition of histamine synthesis by superfusion with alpha-fluoromethylhistidine (FMH) gradually decreased the release rate of acetylcholine. Superfusion with histamine increased the release of acetylcholine. The releasing effect of histamine was greatly inhibited when the striatum was simultaneously superfused with the D2/D3 agonist quinpirole and the D1 antagonist (+/-)-7-bromo-1-(fluoresceinylthioureido)phenyl-8-hydroxy-3-methyl -2,3,4,5-tetrahydro-1H-3-benzapine (SKF 83566). The effect of histamine on acetylcholine release was abolished by the GABA(A) receptor antagonist bicuculline. Superfusion with the H3 receptor agonists imetit or immepip increased acetylcholine release rate in the striatum. The releasing effects of the two H3 agonists were FMH resistant, while superfusion with quinpirole and SKF 83566 abolished the H3 receptor agonist-induced acetylcholine release. Superfusion with the H3 receptor antagonist thioperamide enhanced acetylcholine release rate. The releasing effect of thioperamide was abolished after inhibition of histamine synthesis by FMH. The release of acetylcholine by thioperamide was also abolished on simultaneous superfusion with quinpirole and SKF 83566. The findings show that, in the striatum, the activity of cholinergic neurons is permanently modulated by neighbouring histaminergic nerve terminals and axons. The release of acetylcholine is also permanently inhibited by neighbouring GABAergic neurons. The enhanced release of acetylcholine by the H3 receptor agonists imetit and immepip is due to stimulation of H3 heteroreceptors, while the increase of acetylcholine release by the H3 receptor antagonist thioperamide is elicited via blockade of H3 autoreceptors. Histamine released from histaminergic nerve terminals increases the release of acetylcholine in part by inhibition of dopamine release which, in turn, decreases GABAergic transmission. A dopamine-independent way seems also to be involved in the histamine-evoked acetylcholine release.

Acetylcholine↗
PubMed1999

Histaminergic neurons modulate acetylcholine release in the ventral striatum: role of H1 and H2 histamine receptors.

To investigate whether H1 and H2 histamine receptors are implicated in the modulation of acetylcholine release by endogenous histamine, the ventral striatum of the conscious, freely moving rat was superfused by the push-pull superfusion technique with drugs and the release of acetylcholine was determined in the superfusate. Superfusion with the H1 receptor agonist 2-thiazolylethylamine (TEA, 50 micromol/l) enhanced the release of acetylcholine, while the H1 receptor antagonist triprolidine (50 micromol/l) reduced acetylcholine outflow and abolished the TEA-evoked release of the neurotransmitter. The inhibitory effect of triprolidine was not influenced either on simultaneous superfusion with 10 micromol/l (+/-)-7-bromo-1-(fluoresceinylthioureido)phenyl-8-hydroxy-3-methyl -2,3,4,5-tetrahydro-1H-benzazepine (SKF-83566, D1 dopamine receptor antagonist) and 50 micromol/l quinpirole (D2/D3 dopamine receptor agonist) or on superfusion with the GABAA receptor antagonist bicuculline (50 micromol/l). The H2 receptor antagonists ranitidine or famotidine (50 micromol/l each) greatly enhanced acetylcholine release rate in the ventral striatum. Presuperfusion with alpha-fluoromethylhistidine (FMH, 1 mmol/l), which inhibits neuronal synthesis of histamine, abolished the famotidine-induced release of acetylcholine. The releasing effect of famotidine was also abolished on simultaneous superfusion with 10 micromol/l SKF-83566 and 50 micromol/l quinpirole. The release of acetylcholine elicited by famotidine was reversed to a decreased acetylcholine outflow when the striatum was superfused with the GABA(A) receptor antagonist bicuculline (50 micromol/l) prior to famotidine. Superfusion with the H2 receptor agonist impromidine (1 micromol/l) decreased acetylcholine outflow, while the H2 agonist dimaprit (50 micromol/l) exerted the opposite effect. The releasing effect of dimaprit was not influenced by FMH (1 mmol/l), but it was abolished in the presence of SKF-83566 (10 micromol/l) and quinpirole (50 micromol/l). In the presence of bicuculline the release of acetylcholine by dimaprit was enhanced and prolonged. It seems possible that dimaprit and impromidine stimulate different subtypes of H2 receptors. The findings suggest that the release of acetylcholine in the striatum is modulated by neighbouring histaminergic neurons in a complex way. Stimulation of H1 histamine receptors, probably located on cholinergic neurons, enhances acetylcholine release. Stimulation by histamine of H2 receptors located on cholinergic or GABAergic neurons enhances the release of acetylcholine, while stimulation of H2 receptors located on dopaminergic neurons exerts the opposite effect.

Acetylcholine↗
PubMed1999

Introducing fluorine-18 fluoromisonidazole positron emission tomography for the localisation and quantification of pig liver hypoxia.

Fluorine-18 labelled fluoromisonidazole ([18F]FMISO) has been shown to accumulate in hypoxic tissue in inverse proportion to tissue oxygenation. In order to evaluate the potential of [18F]FMISO as a possible positron emission tomography (PET) tracer for imaging of liver tissue hypoxia, we measured the [18F]FMISO uptake in 13 domestic pigs using dynamic PET scanning. Hypoxia was induced by segmental arterial hepatic occlusion. During the experimental procedure the fractional concentration of inspired oxygen (FiO2) was set to 0.67 in group A (n=6) and to 0.21 in group B (n=7) animals. Before and after arterial occlusion, the partial pressure of O2 in tissue (TPO2) and the arterial blood flow were determined in normal flow and flow-impaired liver segments. Standardised uptake values [SUV=kBq tissue (in g) / body weight (in kg) x injected dose (in kBq)] for [18F]FMISO were calculated from PET images obtained 3 hours after injection of about 10 MBq/kg body weight [18F]FMISO. Immediately before PET scanning, the mean arterial blood flow was significantly decreased in arterially occluded segments [group A: 0. 41 (0.32-0.52); group B: 0.24 (0.16-0.33) ml min-1 g-1] compared with normal flow segments [group A: 1.05 (0.76-1.46); group B: 1.14 (0.83-1.57) ml min-1 g-1; geometric mean (95% confidence limits); P<0.001 for both groups]. After PET scanning, the TPO2 of occluded segments (group A: 5.1 (4.1-6.4); group B: 3.5 (2.6-4.9) mmHg] was significantly decreased compared with normal flow segments [group A: 26.4 (21.2-33.0); group B: 18.2 (13.3-25.1) mmHg; P<0.001 for both groups]. During the 3-h PET scan, the mean [18F]FMISO SUV determined in occluded segments increased significantly to 3.84 (3.12-4.72) in group A and 5.7 (4.71-6.9) in group B, while the SUV remained unchanged in corresponding normal liver tissue [group A: 1.4 (1.14-1. 71); group B: 1.31 (1.09-1.57); P<0.001 for both groups]. Regardless of ventilation conditions, a significant inverse exponential relationship was found between the TPO2 and the [18F]FMISO SUV (r2=0. 88, P<0.001). Our results suggest that because tracer delivery to hypoxic tissues was maintained by the portal circulation, the [18F]FMISO accumulation in the liver was found to be directly related to the severity of tissue hypoxia. Thus, [18F]FMISO PET allows in vivo quantification of pig liver hypoxia using simple SUV analysis as long as tracer delivery is not critically reduced.

Animals↗
PubMed1999

Anion selectivity of apical membrane conductance of Calu 3 human airway epithelium.

Anion selectivity of the cystic fibrosis conductance transmembrane conductance regulator (CFTR) and other channels and parallel pathways expressed endogenously in apical membranes of polarized Calu-3 epithelial monolayers was studied under control conditions and during cAMP stimulation. Basolateral membranes were eliminated using alpha-toxin. The cAMP-stimulated, gradient-driven currents had the sequence Br>/=Cl>/=NO3>SCN> I>/=F>formate>HCO3>acetate>propionate=butyrate=ATP= PPi=PO4=SO4=0. Selectivity of parallel cAMP-independent pathway(s) was Br>Cl=SCN=NO3>I>formate=F >HCO3>acetate>propionate. SCN, I, F or formate blocked cAMP-stimulated, but not control, Cl currents. Anions >0.53 nm in diameter were impermeant, suggesting that the apical CFTR channel has a limiting diameter of 0.53 nm. The selectivity, blocking patterns and pore size of the cAMP-stimulated conductance pathway were very similar to those in previous reports in which CFTR was heterologously expressed in non-epithelial cells. Thus, CFTR appears to be the major apical anion conductance pathway in Calu-3 cells, and its conduction properties are independent of the expression system. CFTR in Calu-3 cells also conducts physiologically relevant anions, but not ATP, PO4 or SO4. A pathway parallel (probably a tight junction) showed a different selectivity than CFTR.

Adenocarcinoma↗
PubMed1999

Purification and spectroscopic studies on catechol oxidases from Lycopus europaeus and Populus nigra: evidence for a dinuclear copper center of type 3 and spectroscopic similarities to tyrosinase and hemocyanin.

We purified two catechol oxidases from Lycopus europaeus and Populus nigra which only catalyze the oxidation of catechols to quinones without hydroxylating tyrosine. The molecular mass of the Lycopus enzyme was determined to 39,800 Da and the mass of the Populus enzyme was determined to 56,050 Da. Both catechol oxidases are inhibited by thiourea, N-phenylthiourea, dithiocarbamate, and cyanide, but show different pH behavior using catechol as substrate. Atomic absorption spectrosopic analysis found 1.5 copper atoms per protein molecule. Using EPR spectroscopy we determined 1.8 Cu per molecule catechol oxidase. Furthermore, EPR spectroscopy demonstrated that catechol oxidase is a copper enzyme of type 3. The lack of an EPR signal is due to strong antiferromagnetic coupling that requires a bridging ligand between the two copper ions in the met preparation. Addition to H2O2 to both enzymes leads to oxy catechol oxidase. In the UV/Vis spectrum two new absorption bands occur at 345 nm and 580 nm. In accordance with the oxy forms of hemocyanin and tyrosinase the absorption band at 345 nm is due to an O2(2-) (pi sigma *)-->Cu(II) (dx2 - y2) charge transfer (CT) transition. The absorption band at 580 nm corresponds to the second O2(2)- (pi v*)-->Cu(II) (dx2 - y2) CT transition. The UV/Vis bands in combination with the resonance Raman spectra of oxy catechol oxidase indicate a mu-eta 2:eta 2 binding mode for dioxygen. The intense resonance Raman peak at 277 cm-1, belonging to a Cu-N (axial His) stretching mode, suggests that catechol oxidase has six terminal His ligands, as known for molluscan and arthropodan hemocyanin.

Binding Sites↗
PubMed1999

Microsatellite instability in sporadic colorectal cancer is not an independent prognostic factor.

Hereditary non-polyposis colorectal cancer (HNPCC) is linked to an inherited defect in the DNA mismatch repair system. DNA from HNPCC tumours shows microsatellite instability (MSI). It has been reported that HNPCC patients have a better prognosis than patients with sporadic colorectal cancer. We examined whether the presence of MSI in a series of unselected colorectal tumours carries prognostic information. In a series of 181 unselected colorectal tumours, 22 tumours (12%) showed MSI. Survival analysis at 5-10 years follow-up showed no statistically significant difference in prognosis between MSI-positive and -negative tumours. Our results suggest that the MSI phenotype as such is not an independent prognostic factor.

Aged↗
PubMed1999

Tacrolimus and minidose methotrexate for prevention of acute graft-versus-host disease after HLA-mismatched marrow or blood stem cell transplantation.

Thirty adults with leukemia or lymphoma transplanted with marrow or blood stem cells from 1-antigen mismatched related donors received tacrolimus and minidose methotrexate to prevent acute graft-versus-host disease (GVHD). The group had a median age of 42 years (range 18-56 years). Twenty-seven patients had advanced disease, and 13 were resistant to conventional therapy. Tacrolimus was administered at 0.03 mg/kg/day i.v. by continuous infusion from day -2, converted to oral at four times the i.v. dose following engraftment, and continued to day 180 post-transplant. Methotrexate 5 mg/m2 was given i.v. on days 1, 3, 6 and 11. Mild nephrotoxicity was common before day 100; 69% of patients had a doubling of creatinine, 56% had a peak creatinine greater than 2 mg/dl, and two patients were dialyzed. Other toxicities prior to day 100 thought to be related to tacrolimus included hypertension (45%), hyperkalemia (17%), hyperglycemia (14%), seizures (13%), headache (3%) and hemolytic uremic syndrome (3%). Grades 2-4 GVHD occurred in 59% (95% CI, 38-70%), and grades 3-4 GVHD in 17% (95% CI, 1-32%). Overall survival at 1 year was 29% (95% CI, 12-45%). We conclude that tacrolimus and minidose methotrexate is active post-transplant immunosuppression for patients with 1-antigen mismatched donors.

Acute Disease↗
PubMed1999

Efficient CFTR expression from AAV vectors packaged with promoters--the second generation.

Gene therapy studies of cystic fibrosis (CF) have shown that AAV-based vector was efficient in transferring but not in expressing the CFTR cDNA in the target cells. The levels of CFTR gene expression were limited by the small packaging capacity of AAV because it had been difficult to package the CFTR cDNA with an efficient promoter. In the present study we have developed a new generation of AAV/CFTR vectors which contain efficient short promoters to express the CFTR gene in target cells. To do so, we reduced the size of the CFTR cDNA by determining the minimal untranslated regions required for expression of CFTR cDNA. We also identified short and efficient promoters that could be packaged with the down-sized CFTR cDNA into a novel AAV vector that had a maximal packaging capacity. Functional analyses showed that the new vectors were packaged efficiently and expressed higher levels of CFTR than a vector in which the CFTR gene was driven by the ITR sequence of AAV. Transduction of airway epithelial cells containing [symbol: see text] 508 mutation with the new vectors demonstrated efficient expression of the wild-type CFTR and correction of the CF phenotype. In contrast, no significant CFTR expression was detected in cells infected with the vector that express the CFTR gene from the ITR. These findings support the notion that the AAV can be developed into an efficient vector to transduce the CFTR gene and vectors expressing higher levels of CFTR from an efficient promoter should provide better efficacy for gene therapy of cystic fibrosis.

Cystic Fibrosis↗
PubMed1999

Expression of endothelial cell-derived nitric oxide synthase (eNOS) is increased during gastric adaptation to chronic aspirin intake in humans.

BACKGROUND: Gastric adaptation to aspirin is well-documented. However, the mechanisms underlying the reduction of aspirin-induced mucosal damage despite continued ingestion of the drug remain poorly understood. METHODS: Eight healthy volunteers who received aspirin 1 g b.d. for 14 days were compared with eight placebo-dosed controls. Gastroscopy with mucosal biopsy was performed, and gastric mucosal blood flow was measured before and following 3, 7 and 14 days of aspirin treatment. At the same time points, tissue concentration and the content of prostaglandin E2 in the gastric juice were determined and expression of endothelial cell-derived nitric oxide synthase (eNOS) in mucosal biopsies was measured using Western blot analysis. RESULTS: Aspirin-induced mucosal damage that reached a maximum on day 3, declining significantly by day 14. Concomitantly, mucosal blood flow significantly increased on day 3 and returned to initial values on day 14. Aspirin intake led to a significant decrease in prostaglandin E2 concentration in the gastric mucosa and in gastric juice during the whole period of aspirin consumption. eNOS expression started to increase on day 7 in oxyntic mucosa and on day 3 in antral mucosa, reaching its highest values at the end of the consumption of aspirin. CONCLUSIONS: The human gastric mucosa adapts to prolonged aspirin intake, and this is accompanied by an increase in mucosal blood flow and reduced prostaglandin synthesis. Increase of mucosal eNOS expression might compensate for reduced prostaglandin synthesis and be responsible for gastric adaptation to chronic aspirin intake in humans.

Adult↗
PubMed1999

Endogenous nitric oxide in the regulation of gastric secretory and motor activity in humans.

BACKGROUND: Studies in animals have shown that nitric oxide (NO) affects gastric secretory and motor functions. However, little information is available about the involvement of this substance in the control of gastric secretory and motor activity in man. METHODS: This study, performed on 18 healthy, Helicobacter pylori-negative volunteers, was designed to evaluate the role of NO in the control of gastric acid secretion and of gastrin and somatostatin release in response to ordinary feeding (group A) and on gastric motor and electrical activity (group B). Gastric acid secretion was determined by means of intragastric pH-metry before and after feeding with a semi-liquid meal. Plasma levels of gastrin and somatostatin were measured using specific radioimmunoassays. Gastric emptying rate was measured using the 13C-acetate breath test, antral motor activity using a manometric catheter and myoelectric activity using cutaneous electrogastrography. Studies were repeated following pre-treatment with NG-monomethyl-L-Arginine (L-NMMA), L-Arginine (L-Arg) or their combination. RESULTS: L-NMMA delayed the recovery of intragastric pH to the pre-meal value, and suppressed postprandial gastrin release while increasing the plasma somatostatin level. L-Arg did not affect postprandial pH and plasma hormones, but reversed L-NMMA-induced alterations in intragastric pH and in plasma gastrin and somatostatin levels. Both postprandial antral motor activity (motility index) and gastric emptying significantly increased in tests with L-NMMA, but this was not observed when L-NMMA was given in combination with L-Arg or when L-Arg alone was used. The gastric electrical pattern, as measured by cutaneous electrogastrography, was not affected by L-NMMA, L-Arg or their combination. CONCLUSIONS: (1) Endogenous NO appears to be involved in the regulation of postprandial gastric acid secretion. This effect may be mediated by the changes in release of gastrin and somatostatin. (2) Endogenous NO delays gastric emptying and antral motor activity without affecting gastric myoelectrical activity.

Acetates↗
PubMed1999

Functional anatomy of hypnotic analgesia: a PET study of patients with fibromyalgia.

Hypnosis is a powerful tool in pain therapy. Attempting to elucidate cerebral mechanisms behind hypnotic analgesia, we measured regional cerebral blood flow with positron emission tomography in patients with fibromyalgia, during hypnotically-induced analgesia and resting wakefulness. The patients experienced less pain during hypnosis than at rest. The cerebral blood-flow was bilaterally increased in the orbitofrontal and subcallosial cingulate cortices, the right thalamus, and the left inferior parietal cortex, and was decreased bilaterally in the cingulate cortex. The observed blood-flow pattern supports notions of a multifactorial nature of hypnotic analgesia, with an interplay between cortical and subcortical brain dynamics. Copyright 1999 European Federation of Chapters of the International Association for the Study of Pain.

Journal Article↗
PubMed1999

Use of the [(14)C]leucine incorporation technique to measure bacterial production in river sediments and the epiphyton.

Bacterial production is a key parameter for the understanding of carbon cycling in aquatic ecosystems, yet it remains difficult to measure in many aquatic habitats. We therefore tested the applicability of the [(14)C]leucine incorporation technique for the measurement of bulk bacterial production in various habitats of a lowland river ecosystem. To evaluate the method, we determined (i) extraction efficiencies of bacterial protein from the sediments, (ii) substrate saturation of leucine in sediments, the biofilms on aquatic plants (epiphyton), and the pelagic zone, (iii) bacterial activities at different leucine concentrations, (iv) specificity of leucine uptake by bacteria, and (v) the effect of the incubation technique (perfused-core incubation versus slurry incubation) on leucine incorporation into protein. Bacterial protein was best extracted from sediments and precipitated by hot trichloroacetic acid treatment following ultrasonication. For epiphyton, an alkaline-extraction procedure was most efficient. Leucine incorporation saturation occurred at 1 microM in epiphyton and 100 nM in the pelagic zone. Saturation curves in sediments were difficult to model but showed the first level of leucine saturation at 50 microM. Increased uptake at higher leucine concentrations could be partly attributed to eukaryotes. Addition of micromolar concentrations of leucine did not enhance bacterial electron transport activity or DNA replication activity. Similar rates of leucine incorporation into protein calculated for whole sediment cores were observed after slurry and perfused-core incubations, but the rates exhibited strong vertical gradients after the core incubation. We conclude that the leucine incorporation method can measure bacterial production in a wide range of aquatic habitats, including fluvial sediments, if substrate saturation and isotope dilution are determined.

Bacteria↗
PubMed1999

Defective function of the cystic fibrosis-causing missense mutation G551D is recovered by genistein.

The patch-clamp technique was used to investigate the effects of the isoflavone genistein on disease-causing mutations (G551D and DeltaF508) of the cystic fibrosis transmembrane conductance regulator (CFTR). In HeLa cells recombinantly expressing the trafficking-competent G551D-CFTR, the forskolin-stimulated Cl currents were small, and average open probability of G551D-CFTR was P(o) = 0.047 +/- 0.019. Addition of genistein activated Cl currents approximately 10-fold, and the P(o) of G551D-CFTR increased to 0.49 +/- 0.12, which is a P(o) similar to wild-type CFTR. In cystic fibrosis (CF) epithelial cells homozygous for the trafficking-impaired DeltaF508 mutation, forskolin and genistein activated Cl currents only after 4-phenylbutyrate treatment. These data suggested that genistein activated CFTR mutants that were present in the cell membrane. Therefore, we tested the effects of genistein in CF patients with the G551D mutation in nasal potential difference (PD) measurements in vivo. The perfusion of the nasal mucosa of G551D CF patients with isoproterenol had no effect; however, genistein stimulated Cl-dependent nasal PD by, on average, -2.4 +/- 0.6 mV, which corresponds to 16.9% of the responses (to beta-adrenergic stimulation) found in healthy subjects.

Biological Transport↗
PubMed1999

Timing of elevator muscle activity during climbing in free locust flight

Despite detailed knowledge of the sensory-motor interactions during elevator muscle timing for the generation of a 'functional' flight motor pattern in flying locusts, there is little information about how a possible shift in the onset of elevator activity is correlated with changes in flight variables under closed-loop conditions (i.e. during free flight). Free-flight variables were investigated with respect to ascent angle during climbing flight in locusts Schistocerca gregaria. The motor pattern during free flight was examined by telemetric electromyography of particular antagonistic flight muscles in both ipsilateral hemisegments of the pterothorax while flight variables were recorded simultaneously on video. In the majority of the animals tested, the onset of elevator muscle activity within the wingbeat cycle is delayed when animals increase their ascent angle during climbing flight. In accordance with the motor pattern, the downstroke phase and the stroke amplitude of the wings increased with increasing the ascent angle. This suggests that the relative elevator timing during the wingbeat cycle may be related to the generation of the additional aerodynamic lift required for ascending flight and may, therefore, play a role in the regulation of ascent angle during free flight in the locust.

Journal Article↗
PubMed1999

Tegula function during free locust flight in relation to motor pattern, flight speed and aerodynamic output

Tegulae are complex proprioceptors at the wing base of locusts. Deafferentation of the tegulae causes a lack of specific phasic information related to the wing downstroke and the timing of the upstroke. Employing telemetry during free flight of the locust Schistocerca gregaria, we investigated the consequences of tegula ablation on free flight parameters including motor patterns (wingbeat frequency and the relationship between the activation of flight muscle antagonists), free flight speed and aerodynamic output. We investigated the role of the tegula pairs of both wings on the motor pattern generated in free-flying locusts. We show that the tegula organs are not essential for generating the motor patterns necessary for free flight. However, they are required for increasing the motor output to give additional effective lifting power during adaptive behaviour. We also investigated long-term changes in the free flight parameters after tegula ablation. The recovery of the adult flight system revealed in the present study suggests that there is adaptation to the loss of proprioceptive information; this argues for a full functional and behavioural recovery of the flight system of the locust under closed-loop conditions.

Journal Article↗