Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Escap”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

Convergent evolution of the head retraction escape response in elongate fishes and amphibians.

Aquatic escape responses have typically been described as C-starts. However, another aquatic escape response, head retraction, occurs in several elongate species, but has never been studied in detail. The goals of this study are to describe the head retraction escape response in a phylogenetically diverse sample of species, to trace the evolution of head retraction in anamniote vertebrates, and to correlate key morphological traits with escape response behavior. In analyzing the evolution of escape behavior, we found that the head retraction escape response has evolved at least six times in anamniote vertebrates. Using independent contrast analysis, the head retraction escape response was found to be correlated with an increase in the total number of vertebrae and an increase in the elongation of an animal. Results from this study indicate a correlation between head retraction as an escape response, elongation of the axial skeleton, and living in structured habitats.

Journal Article↗

Promoter clearance and escape in prokaryotes.

Promoter escape is the last stage of transcription initiation when RNA polymerase, having initiated de novo phosphodiester bond synthesis, must begin to relinquish its hold on promoter DNA and advance to downstream regions (DSRs) of the template. In vitro, this process is marked by the release of high levels of abortive transcripts at most promoters, reflecting the high instability of initial transcribing complexes (ITCs) and indicative of the existence of barriers to the escape process. The high abortive initiation level is the result of the existence of unproductive ITCs that carry out repeated initiation and abortive release without escaping the promoter. The formation of unproductive ITCs is a widespread phenomenon, but it occurs to different extent on different promoters. Quantitative analysis of promoter mutations suggests that the extent and pattern of abortive initiation and promoter escape is determined by the sequence of promoter elements, both in the promoter recognition region (PRR) and the initial transcribed sequence (ITS). A general correlation has been found that the stronger the promoter DNA-polymerase interaction, the poorer the ability of RNA polymerase to escape the promoter. In gene regulation, promoter escape can be the rate-limiting step for transcription initiation. An increasing number of regulatory proteins are known to exert their control at this step. Examples are discussed with an emphasis on the diverse mechanisms involved. At the molecular level, the X-ray crystal structures of RNA polymerase and its various transcription complexes provide the framework for understanding the functional data on abortive initiation and promoter escape. Based on structural and biochemical evidence, a mechanism for abortive initiation and promoter escape is described.

Bacteria↗

[Validation of ESCAP-CD as an instrument of measure for the evaluation of the quality of life in prostatic cancer. Part 2a].

UNLABELLED: In order to make a measure of quality of life related to health (QLRH) useful in the investigation, it must fulfill the psychometric properties (validity, reliability and sensibility). The selection of an instrument is a job for the clinic that must choose the most effective for each proposed objective. We set out the objectives to validate the ESCAP-CDV in a multicentric study in Andalusia. We studied 88 patients who were submitted to the instrument presented to validation and two more tests recognized already: the QLQ-C30 from EORTC gold standard in Europe in the valuation of the neoplastic patients' quality of life and the KARNOFSKY the most clinic utility index in neoplastic patients, used to correlate the items. RESULTS: Questionnaire acceptance analysis: The difficulty of understanding was greater for QLQ C30 items (6.81%) than ESCAP items (1.98%). The lapse of time needed to carry out the test was shorter in the ESCAP test (9.84 min) than in the QLQ C30 (13.13), test. Structural analysis or internal validity analysis: The homogeneity index of the items is high (alfa of Cronbach = 0.93). The dimensionality proposed is not accepted, due to the existence of some modifications pund in the factorial analysis. Finally, the established dimensions: Physical and Emotional Capacity (PEC), 5 items; General Symptoms (GS), 4 items; Pain (P), 3 items; Ligh Functional Capcity (LFC), 4 items; Serious Functional Capacity (SFC), 2 items; Economic State (ES), 3 items; Social and Family State (SFE), 5 items; Capacity Sexual (CSX), 2 items; Isolated Variables (IV), 2 items; and Specific Questionnaire (P), 6 items. The ESCAP is a scale with a normal distribution. Approach or external validity analysis: The ESCAP test is well correlated with the other two scales. Reliability test retest: The interclass correlation coefficient is 0.94 in the ESCAP, not so in the KARNOFSKY that is 0.77. CONCLUSIONS: The ESCAP-CDV is a new instrument of valuation of the QLRH composed of a general questionnaire and other specific test of prostate cancer. It has turned out to be a very homogeneous scale due to its internal consistence (alfa of Cronbach of 0.93), showing that it has a normal distribution, that correlates correctly with the scales compared and it is a valid scale to measure the prostate cancer patients' quality of life. The ESCAP-CDV has shown to be a scale with a high reliability (0.94), setting up as an instrument not only useful for investigation, but to clinical use, as well.

Humans↗

The escape process of carbon monoxide from myoglobin to solution at physiological temperature.

The carbon monoxide (CO) docking sites involved in the ligand escape process from the iron atom in hem of myoglobin (Mb) to solution at physiological temperature were studied on the basis of the effect of xenon (Xe) on the ligand escape rate by the transient grating (TG) technique. The TG method provides a direct measurement of the changes in molecular volume. The apparent CO escaping rate and the volume contraction increase with increasing Xe pressure. The pressure dependence of the rate is consistent with that of the Xe population at the Xe(1) site. This result clearly shows that CO is trapped at the Xe(1) site before escaping to solvent in a Xe-free solution at room temperature. It is shown that only CO but not the trapped Xe is released by the photoexcitation of the Xe-trapped MbCO. A dissociation scheme is proposed to explain the enhancement of the escaping rate by the presence of Xe(1). There are two branches for the CO escaping pathway. The dominant part of the dissociated CO escapes to the solvent through the Xe(1) trapping site under the Xe-free condition, and there are at least three intermediate states along this pathway. When a Xe atom blocks the Xe(1) site, the CO escapes through another route.

Animals↗

Determinants of human immunodeficiency virus type 1 escape from the primary CD8+ cytotoxic T lymphocyte response.

CD8+ cytotoxic T lymphocytes (CTLs) play an important role in containment of virus replication in primary human immunodeficiency virus (HIV) infection. HIV's ability to mutate to escape from CTL pressure is increasingly recognized; but comprehensive studies of escape from the CD8 T cell response in primary HIV infection are currently lacking. Here, we have fully characterized the primary CTL response to autologous virus Env, Gag, and Tat proteins in three patients, and investigated the extent, kinetics, and mechanisms of viral escape from epitope-specific components of the response. In all three individuals, we observed variation beginning within weeks of infection at epitope-containing sites in the viral quasispecies, which conferred escape by mechanisms including altered peptide presentation/recognition and altered antigen processing. The number of epitope-containing regions exhibiting evidence of early CTL escape ranged from 1 out of 21 in a subject who controlled viral replication effectively to 5 out of 7 in a subject who did not. Evaluation of the extent and kinetics of HIV-1 escape from >40 different epitope-specific CD8 T cell responses enabled analysis of factors determining escape and suggested that escape is restricted by costs to intrinsic viral fitness and by broad, codominant distribution of CTL-mediated pressure on viral replication.

Amino Acid Sequence↗

Factors affecting the escape of Francisella tularensis from the phagolysosome.

The highly virulent bacterium Francisella tularensis is well adapted to the intracellular habitat but the mechanisms behind its intracellular survival have been elusive. Recently, it was shown that the bacterium is capable of escaping from the phagosome of human and mouse monocytic cells. Here it is shown that this escape is affected by gamma interferon (IFN-gamma) treatment of mouse peritoneal exudate cells since in treated cells the proportion that escaped was significantly lower (80%) than in untreated cells (97%) as determined by transmission electron microscopy. By contrast, < 1% of mutant bacteria lacking expression of a 23 kDa protein denoted IglC were able to escape from the phagosome. Infection with the DeltaiglC strain complemented with the iglC gene resulted in 60% of the bacteria escaping from the phagosome. Whereas IFN-gamma treatment conferred a static effect on intracellular wild-type bacteria, the treatment had a bactericidal effect on the DeltaiglC strain. The results show that the activation status of infected cells affects the escape of F. tularensis from the phagosome. An even more profound effect on this escape is related to expression of IglC by F. tularensis. Its absence rendered the mutant bacteria incapable of escaping from the phagosome and of multiplying intracellularly.

Animals↗

Comparison between patients with and without reliable ventricular escape rhythm in the presence of long standing complete atrioventricular block.

The underlying heart rhythm was evaluated in 74 patients with complete atrioventricular block and had a permanent pacemaker implantation. The pacing was inhibited for 10 seconds or until the patient developed symptoms of presyncope or syncope. Fifty-six patients (74%) had a reliable escape with a mean cycle length of 2010 +/- 596 msec and a mean escape interval of 2335 +/- 971 msec. In 93% of these patients the escape interval was < 4 seconds. The patients without reliable escape (24%), developed symptoms only after a mean of 7153 +/- 1875 msec. The duration of the conduction disorder was longer in the patients without escape and the intraventricular conduction was slower. More patients without escape were treated and antiarrhythmic agents. Forty-eight patients were followed for 1 year and underwent at least two different studies and 13% had different results at different tests. In conclusion, patients without reliable escape have a longer history of conduction disorder, a slower intraventricular conduction, and are frequently treated with antiarrhythmic agents. Even patients with reliable escape occasionally may show a greater pacemaker dependence; therefore, they should also be considered as pacemaker dependent.

Aged↗

Initial and long-term evaluation of escape rhythm after radiofrequency ablation of the AV junction in 50 patients.

Between 1986 and 1994, 50 patients (mean age 63 +/- 13 years), 25 of whom had organic heart disease and presenting with atrial arrhythmias refractory to 5.6 +/- 1.6 antiarrhythmic drugs, underwent radiofrequency ablation (5 +/- 3 pulses by procedure; duration of pulses 50.5 +/- 32 s) of the proximal AV junction to create complete and permanent AV block. The escape rhythm was studied immediately after the procedure and during long-term follow-up. Immediately after the procedure, an escape rhythm was observed in 80% of the patients (junctional in 92%). Over a mean follow-up of 36 +/- 16 months in 47 patients (2 patients died before assessment of escape rhythm and 1 was lost to follow-up), an escape rhythm was present in 39 patients (83%) and absent in the remaining 8 (17%). The only significant difference between the two groups was the initial presence of an escape rhythm (P = 0.008). However, three patients with an initial escape rhythm had none during long-term follow-up. The initial presence of an escape rhythm as a predictive factor of its presence during follow-up had a sensitivity of 87%, specificity of 63%, positive predictive value of 92%, and negative predictive value of 50%. Thus, the absence of an escape rhythm during long-term follow-up causing pacemaker dependency was noted in 1 of 6 patients. This represents a limitation to this palliative treatment, which should be reserved for patients suffering from supraventricular tachycardias refractory to other treatments.

Adult↗

Fitness cost of escape mutations in p24 Gag in association with control of human immunodeficiency virus type 1.

Mutational escape by human immunodeficiency virus (HIV) from cytotoxic T-lymphocyte (CTL) recognition is a major challenge for vaccine design. However, recent studies suggest that CTL escape may carry a sufficient cost to viral replicative capacity to facilitate subsequent immune control of a now attenuated virus. In order to examine how limitations can be imposed on viral escape, the epitope TSTLQEQIGW (TW10 [Gag residues 240 to 249]), presented by two HLA alleles associated with effective control of HIV, HLA-B*57 and -B*5801, was investigated. The in vitro experiments described here demonstrate that the dominant TW10 escape mutation, T242N, reduces viral replicative capacity. Structural analysis reveals that T242 plays a critical role in defining the start point and in stabilizing helix 6 within p24 Gag, ensuring that escape occurs at a significant cost. A very similar role is played by Thr-180, which is also an escape residue, but within a second p24 Gag epitope associated with immune control. Analysis of HIV type 1 gag in 206 B*57/5801-positive subjects reveals three principle alternative TW10-associated variants, and each is strongly linked to concomitant additional variants within p24 Gag, suggesting that functional constraints operate against their occurrence alone. The extreme conservation of p24 Gag and the predictable nature of escape variation resulting from these tight functional constraints indicate that p24 Gag may be a critical immunogen in vaccine design and suggest novel vaccination strategies to limit viral escape options from such epitopes.

Alleles↗

Premature escape beats induced by overdrive pacing in canine Purkinje fibers. Evidence for the role of normal automaticity as an underlying cellular mechanism.

Premature escape beats induced in conscious dogs with chronic complete atrioventricular block have been defined as escape beats occurring on cessation of overdrive pacing and having a coupling interval to the last paced beat shorter than the coupling interval between the premature escape beat and the second postpacing beat. Triggered activity has been proposed as the primary underlying mechanism. We used standard microelectrode techniques to study the effects of overdrive pacing on normal automatic canine Purkinje fibers to determine if premature escape beats could be induced and if so, to define the underlying cellular mechanism(s). For this purpose, we overdrive-paced Purkinje fibers for 10 and 50 seconds and for 10 and 50 beats at a pacing cycle length (PCL) of 1,000-200 msec. In addition, to help distinguish among major arrhythmogenic mechanisms, we used a matrix of drugs consisting of propranolol, nadolol, lidocaine, ethmozin, and doxorubicin. Fifty-second stimulation trains induced "classic" overdrive suppression of the first three postpacing impulses, whereas 10-second overdrive pacing induced significant overdrive suppression only at a PCL of 200 msec. With 50-beat overdrive pacing and a PCL of 1,000-600 msec, there was overdrive suppression of postpacing impulses, whereas reduced overdrive suppression was observed at a PCL of 400-200 msec. Ten-beat stimulation trains induced a "flat response" of postpacing impulses. Ten- and 50-beat overdrive pacing provoked premature escape beats in 66% of the fibers, with the higher incidence at a PCL of 200 msec for 50-beat stimulation trains. No shortening of the coupling interval of premature escape beats was observed at faster pacing rates. Only lidocaine (which suppresses normal automaticity) abolished premature escape beats. We conclude that normal automaticity is the most likely mechanism underlying premature escape beats in Purkinje fibers with high levels of membrane potential.

Animals↗

Mechanics of the fast-start: muscle function and the role of intramuscular pressure in the escape behavior of amia calva and polypterus palmas

The fast-start escape response is a rapid, powerful body motion used to generate high accelerations of the body in virtually all fishes. Although the neurobiology and behavior of the fast-start are often studied, the patterns of muscle activity and muscle force production during escape are less well understood. We studied the fast-starts of two basal actinopterygian fishes (Amia calva and Polypterus palmas) to investigate the functional morphology of the fast-start and the role of intramuscular pressure (IMP) in escape behavior. Our goals were to determine whether IMP increases during fast starts, to look for associations between muscle activity and elevated IMP, and to determine the functional role of IMP in the mechanics of the escape response. We simultaneously recorded the kinematics, muscle activity patterns and IMP of four A. calva and three P. palmas during the escape response. Both species generated high IMPs of up to 90 kPa (nearly 1 atmosphere) above ambient during the fast-start. The two species showed similar pressure magnitudes but had significantly different motor patterns and escape performance. Stage 1 of the fast-start was generated by simultaneous contraction of locomotor muscle on both sides of the body, although electromyogram amplitudes on the contralateral (convex) side of the fish were significantly lower than on the ipsilateral (concave) side. Simultaneous recordings of IMP, escape motion and muscle activity suggest that pressure change is caused by the contraction and radial swelling of cone-shaped myomeres. We develop a model of IMP production that incorporates myomere geometry, the concept of constant-volume muscular hydrostats, the relationship between fiber angle and muscle force, and the forces that muscle fibers produce. The timing profile of pressure change, behavior and muscle action indicates that elevated muscle pressure is a mechanism of stiffening the body and functions in force transmission during the escape response.

Journal Article↗

[Examination of the escape phenomenon in disease modifying antirheumatic drugs].

Although disease-modifying antirheumatic drugs (DMARDs) are used in the treatment of rheumatoid arthritis (RA), the selection of agents in the case of relapse (escape phenomenon) lacks clear-cut standards. Therefore we investigated the rate and conditions of escape as well as the agents used after escapes had occurred. Outpatients of the Matsubara Mayflower Hospital with a history of DMARD administration during the 4 years prior to May 2003 were studied. Those receiving salazosulfapyridine (SASP) had a high escape rate and those receiving methotrexate (MTX) and bucillamine (BC) had a low rate. The continuous duration of administration was long for MTX and BC, but short for sodium aurothiomalate (GST). BC and Actarit (AR) gradually elevated C-reactive protein (CRP) levels and the erythrocyte sedimentation rate (ESR). In patients receiving SASP and MTX, a high level of CRP and high ESR was seen 2 months prior to the occurrence of escape and remained unchanged after escape. With respect to the agents used after escape, SASP and BC were substituted with other DMARDs. A combination with other DMARDs was usually administered to patients who had been receiving MTX. Taken together, the present results clarified the characteristics of DMARD escape and will contribute to the appropriate pharmacotherapy for RA.

Aged↗

Schedule-induced escape from fixed-interval reinforcement.

Pigeons trained to peck one of two keys for food were exposed to an ascending and descending series of fixed-interval values. A response on the second key produced an escape period consisting of a visual stimulus change. During escape periods, the fixed-interval timer continued to operate and even if it timed out, a response on the food key would not operate the feeder unless preceded by an escape-key response that terminated the escape condition. As the fixed-interval schedule was increased logarithmically through six values from 30 to 960 sec, the percentage of session time spent in escape as well as the frequency, duration, and rate of escape increased to a maximum and then decreased. One subject did not develop escape behavior to any significant degree. For all pigeons, escapes usually occurred after, rather than before, reinforcement.

Journal Article↗

The effect of breathing hyperoxic gas during simulated submarine escape on venous gas emboli and decompression illness.

Raised internal pressure in a distressed submarine rapidly increases the risk of decompression sickness (DCS) following submarine escape. The hypothesis that breathing a hyperoxic gas during escape may reduce the risk of DCS was tested using goats. Shallow air saturation and simulated submarine escape dives were carried out either singularly or in combination (saturation, escape, or saturation followed by escape) using air or 60% / 40% oxygen (O2) / nitrogen (N2) mixture as breathing gas during the escapes. Post-surfacing, animals were observed for signs of DCI and O2 toxicity. Precordial Doppler ultrasound was used to score venous gas emboli (VGE) using the Kisman Masurel (KM) scale. Following escape from 2.5 MPa, the rate at which VGE disappeared in the hyperoxic group (n = 8) was significantly faster(p < 0.05) than the air group (n = 7). One case of pulmonary barotrauma with arterial gas embolism occurred in the air group, but no cases of DCS were observed. After saturation at 0.18 MPa followed by escape from 2.5 MPa, DCS occurred in four of 15 animals in the air group and in two of 16 animals in the hyperoxic group. The rate of disappearance of VGE was significantly faster (p < 0.01) in the hyperoxic group. O2 toxicity was not discernible in any of the animals.

Air↗

[Mid-term outcome of escape rhythm after radiofrequency ablation of the atrioventricular junction].

UNLABELLED: Mid-term outcome of the underlying escape rhythm developed after radiofrequency ablation of the atrio-ventricular junction was studied in 50 consecutive patients (28 women and 22 men with a mean age of 66.2 +/- 9.6 years). The escape rhythm was assessed immediately after ablation and after 13.7 +/- 8 months. At the end of ablation: an escape rhythm was present in 38 patients (76%), with a mean rate of 40.7 +/- 9.7 beats/min and a QRS morphology identical to the preablation QRS morphology in 22 patients (58%). At follow-up: an escape rhythm was present in 37 patients (74%), with a slower mean rate of 36.4 +/- 6.8 beats/min (p < 0.05) and an unchanged QRS morphology in 87.5% of the patients. Patients presenting with an escape rhythm at follow-up were more frequently found to have a postablation escape rhythm (p < 0.01). Escape rhythm presence at follow-up was not influenced by age, presence of a cardiac disease, continuation of an antiarrhythmic treatment after ablation, use of a bilateral approach for ablation or number of radiofrequency applications. CONCLUSION: after abrupt inhibition of the stimulation, an escape rhythm was present only in 74% of the patients 13.7 +/- 8 months after atrio-ventricular junction radiofrequency ablation. QRS morphology was identical to the preablation morphology in 57% of the patients.

Aged↗

Failure of rats to escape from a potentially lethal microwave field.

Ocularly pigmented rats, all mature females of the Long-Evans strain, were repeatedly presented an opportunity to escape from an intense 918-MHz field (whole-body dose rate = 60 mW/g) to a field of lower intensity (40, 30, 20, or 2 mW/g) by performing a simple locomotor response. Other rats could escape 800-microamperemeter faradic shock to the feet and tail by performing the same response in the same milieu, a multimode cavity. None of 20 irradiated rats learned to associate entry into a visually well-demarcated area of the cavity with immediate reduction of dose rate, in spite of field-induced elevations of body temperature to levels that exceeded 41 degrees C and would have been lethal but for a limit on durations of irradiation. In contrast, all of ten rats motivated by faradic shock rapidly learned to escape. The failure of escape learning by irradiated animals probably arose from deficiencies of motivation and, especially, sensory feedback. Whole-body hyperthermia induced by a multipath field may lack the painful or directional sensory properties that optimally promote the motive to escape. Moreover, a decline of body temperature after an escape-response-contingent reduction of field strength will be relatively slow because of the large thermal time constants of mammalian tissues. Without timely sensory feedback, which is an essential element of negative reinforcement, stimulus-response associability would be imparied, which could retard or preclude learning of an escape response.

Animals↗

Maturation of escape circuit function during the early adulthood of cockroaches Periplaneta americana.

During postembryonic development of insects, sensorimotor pathways, which generate specific behaviors, undergo maturational changes. It is less clear whether such pathways are typically stable, or undergo further maturation, during the adult stage. In the present study, we have examined this issue by multilevel analysis of a simple model system, the escape behavior of the cockroach, from identified synapses to behavior. We show that the escape system is highly responsive immediately after the molt to adulthood, but that the latency of escape responses was not at its typical value immediately after the molt to adult. The latency of escape behavior increased over the first 30 days of adult life, perhaps indicating maturational adjustments of the escape sensorimotor pathway. The first station in the escape circuitry is the synaptic connections between the cercal wind receptors and the giant interneurons. We measured unitary excitatory synaptic potentials between single sensory neurons and an identified giant interneuron (GI(2)). We found a decrease in the synaptic strength between identified cercal hairs from a single column and GI(2) over the first month after the adult molt. Consequently, the latency and the number of action potentials of GI(2) in response to natural stimuli increased and decreased respectively during this time. Thus, we show that both behavioral performance and the wind sensitivity of GI(2) decreased over the first month after molt. We conclude that the cockroach escape system undergoes further sensorimotor maturation over a period of 1 month, and that cellular changes correlate with, or predict, some changes in behavioral performance.

Action Potentials↗

Cholinergic influences on escape deficits produced by uncontrollable stress.

A series of experiments assessed the potential role of acetylcholine (ACh) in the escape interference produced by inescapable shock. Treatment with the anticholinesterase, physostigmine, successfully mimicked the effects of inescapable shock. That is, the drug disrupted performance when escape was prevented for 6 s on any given trial, thereby necessitating sustained active responding. When escape was possible upon shock onset, the drug treatment did not influence performance. The centrally acting anticholinergic scopolamine hydrobromide antagonized the effects of physostigmine, and when administered prior to escape testing antagonized the disruptive effects of previously administered inescapable shock. In contrast, the peripherally acting agent scopolamine methylbromide did not influence the effects of these treatments, suggesting that the effects of physostigmine and inescapable shock involved central ACh changes. Scopolamine hydrobromide administered prior to inescapable shock did not prevent the escape interference from subsequently appearing, but this effect could not be attributed to state dependence. It was argued that the interference of escape following uncontrollable stress was due to non-associative motor deficits. Alterations of the escape deficits by scopolamine were due to elimination of the motor disruption.

Acetylcholine↗