Transient Relaxation Research Articles

Investigation of transient responses of nanoscale transistors by deterministic solution of the time-dependent BTE

In this work, the transient characteristics of nanoscale field-effect transistors (FETs) have been investigated using a deterministic solver based on the time-dependent multi-subband Boltzmann transport equation (BTE). The response to a step signal superimposed on the gate or drain electrode is simulated. The transient process can be understood as a combination of electrostatic and transport relaxation. The extracted transient relaxation time for the drain current, which is unrelated to the direct-current (DC) shift, is important for transient device modeling.

FFA3 activation inhibits nicotine‐induced secretion and motility in rat proximal colon

Short‐chain fatty acids (SCFA) are microbial fermentation products that are absorbed from the colon. Although luminal SCFA stimulate colonic secretion and motility, we have recently reported that activation of a SCFA receptor termed FFA3, expressed in cholinergic nerves, suppresses cholinergic‐mediated transepithelial anion secretion. Since myenteric neurons are FFA3‐positive, we further investigated how activation of neurally‐expressed FFA3 affects colonic motility.We used the selective FFA3 agonists (N‐[2‐methylphenyl]‐[4‐furan‐3‐yl]‐2‐methyl‐5‐oxo‐1,4,5,6,7,8‐hexahydro‐quinoline‐3‐carboxamide; MQC) and AR420626 to activate neural FFA3. Short‐circuit current (Isc) was measured to determine anion secretion in Ussing‐chamber. Circular muscle contractions were measured with isolated muscle strips without mucosa and submucosa. Muscle contractions were analyzed by wave analysis according to the parameters: basal tone, peak frequency, peak force, and half‐width (HW) of peak. The effect of FFA3 agonists on defecation in vivo was investigated with an established exogenous serotonin‐induced defecation model.In Ussing chambered mucosa‐submucosa preparations, pretreatment with MQC (100 μM) or AR420626 (10 μM) suppressed the Isc increase induced by carbachol (CCh, 10 μM) or nicotine (100 μM) by 65%, but did not affect the response to bethanechol (100 μM). The inhibitory effect of FFA3 activation on CCh‐evoked Isc was reversed by pretreatment with the Gi/o inhibitor pertussis toxin (500 ng/mL).Circular muscle strips exhibited periodic spontaneous contractions that were not altered by the application of MQC or AR420626. The addition of nicotine (10 μM) into the organ bath transiently relaxed the muscle, inhibited by the NO synthase inhibitor L‐NAME. In the presence of L‐NAME and the cyclooxygenase inhibitor indomethacin, nicotine (100 μM) induced large amplitude contractions. Pretreatment with FFA3 agonists inhibited nicotine‐induced transient relaxation and contraction, but had no effect on bethanechol‐induced contractions, suggesting that FFA3 agonists had no direct effect on smooth muscle contraction. Pretreatment with tetrodotoxin did not alter the nicotine‐evoked contraction or the inhibitory effect of FFA3 agonists, whereas atropine or hexamethonium inhibited nicotine‐evoked contractions as did FFA3 agonists. The effect of AR420626 was more potent than the effect of MQC. Nicotine‐evoked contraction was abolished by AR420626 (10 μM) and reversed by pretreatment with pertussis toxin, suggesting that FFA3 activation suppresses nicotinic neural activity in the myenteric neurons, consistent with a FFA3‐mediated secretory pathway.In conscious rats, serotonin (10 mg/kg, i.p.) treatment significantly increased the volume of fecal output, compared with the non‐treated group, although frank diarrhea was not present. Pretreatment with AR420626 (0.1 mg/kg, i.p.) significantly suppressed serotonin‐induced fecal output. These results are suggesting that FFA3 agonists may be useful therapeutically for diarrheal disorders due to their highly targeted and localized anti‐cholinergic effects.Support or Funding InformationSupported by VA Merit Review and NIH R01 DK54221

USING TAILORED TRANQUILIZER COMBINATIONS TO REDUCE STRESS ASSOCIATED WITH LARGE UNGULATE CAPTURE AND TRANSLOCATION.

Capture and translocation are important tools for managing and studying large ungulates. Although widely used, many established field practices cause fear and stress in subject animals that can hamper overall effectiveness and safety. Over the last 10 years we have been exploring uses of tranquilizer combinations as adjuncts to wild ungulate capture and translocation work in Colorado, USA. Our approaches have been tailored to various field applications to reduce fear and stress, facilitate handling, and improve the overall success of capture and translocation for research or management purposes. For physical capture (drop net or helicopter-net gunning) with local release, combinations of midazolam and azaperone administered immediately upon capture provide transient tranquilization and muscle relaxation during manual restraint and handling to prevent hyperthermia and capture myopathy. For extended tranquilization (during transport and overnight holding), adding a sustained-release haloperidol formulation provides calming effects for at least 24-48 h. In our assessment, appropriate and adaptive use of these tranquilizer combinations benefits captured animals without impeding management or research goals.

Su1072 Air Swallowed During Meals Increases Frequency of Transient LES Relaxations and Trans-Sphincteric Pressure Gradient in NERD Patients and Healthy Controls

Su1072 Air Swallowed During Meals Increases Frequency of Transient LES Relaxations and Trans-Sphincteric Pressure Gradient in NERD Patients and Healthy Controls

Su1105 Extent of Esophageal Shortening Is Greater in Incomplete Transient LES Relaxations Than Swallows in NERD Patients and Healthy Controls

Su1105 Extent of Esophageal Shortening Is Greater in Incomplete Transient LES Relaxations Than Swallows in NERD Patients and Healthy Controls

Su1083 Effect of a Carbonated Beverage on Transient Lower Esophageal Sphincter Relaxations (TLESR). A Study in Healthy Volunteers

Su1083 Effect of a Carbonated Beverage on Transient Lower Esophageal Sphincter Relaxations (TLESR). A Study in Healthy Volunteers

P2Y receptor-mediated transient relaxation of rat longitudinal ileum preparations involves phospholipase C activation, intracellular Ca(2+) release and SK channel activation.

Purinergic signaling plays a major role in the enteric nervous system, where it governs gut motility through a number of P2X and P2Y receptors. The aim of this study was to investigate the P2Y receptor-mediated motility in rat longitudinal ileum preparations. Ileum smooth muscle strips were prepared from rats, and fixed in an organ bath. Isometric contraction and relaxation responses of the muscle strips were measured with force transducers. Drugs were applied by adding of stock solutions to the organ bath to yield the individual final concentrations. Application of the non-hydrolyzable P2 receptor agonists α,β-Me-ATP or 2-Me-S-ADP (10, 100 μmol/L) dose-dependently elicited a transient relaxation response followed by a sustained contraction. The relaxation response was largely blocked by SK channel blockers apamin (500 nmol/L) and UCL1684 (10 μmol/L), PLC inhibitor U73122 (100 μmol/L), IP3 receptor blocker 2-APB (100 μmol/L) or sarcoendoplasmic Ca(2+) ATPase inhibitor thapsigargin (1 μmol/L), but not affected by atropine, NO synthase blocker L-NAME or tetrodotoxin. Furthermore, α,β-Me-ATP-induced relaxation was suppressed by P2Y1 receptor antagonist MRS2179 (50 μmol/L) or P2Y13 receptor antagonist MRS2211 (100 μmol/L), and was abolished by co-application of the two antagonists, whereas 2-Me-S-ADP-induced relaxation was abolished by P2Y6 receptor antagonist MRS2578 (50 μmol/L). In addition, P2Y1 receptor antagonist MRS2500 (1 μmol/L) not only abolished α,β-Me-ATP-induced relaxation, but also suppressed 2-Me-S-ADP-induced relaxation. P2Y receptor agonist-induced transient relaxation of rat ileum smooth muscle strips is mediated predominantly by P2Y1 receptor, but also by P2Y6 and P2Y13 receptors, and involves PLC, IP3, Ca(2+) release and SK channel activation, but is independent of acetylcholine and NO release.

Laparoscopic management of reflux after Roux-en-Y gastric bypass using the LINX system and repair of hiatal hernia: a case report

idesu Roux-en-Y gastric bypass (RYGB) has been advocated for the treatment of gastroesophageal reflux in obese and nonobese patients [1,2]. Its effect in the resolution of reflux symptoms has been shown to be independent of weight loss [3,4]. The mechanism of its action in controlling reflux is reducing parietal cells in the stomach pouch as well as diverting bile via the jejuno–jejunal anastomoses. Unfortunately, this mechanism does not address the role of a weak lower esophageal sphincter (LES) and transient LES relaxation (TLESR) as contributing factors in reflux symptoms [5,6]. Managing patients who present with reflux after RYGB can be challenging. Revision of the gastric pouch has been described along with other procedures to treat this problem. We present a case of laparoscopic augmentation of the LES using the LINX system (Torax Medical, Inc., Shoreview, Minnesota) and repair of hiatal hernia to control reflux after RYGB.

Tohoku rupture reloaded?

correspondence Tohoku rupture reloaded? To the Editor — Tormann et al. 1 evaluate changes in the b-value, a measure of the relative abundance of small and large earthquakes, as a function of space and time in northeast Japan. Near the high-slip zone of the 2011 magnitude 9 Tohoku-oki rupture, they document a sudden increase in the b-value at the time of the earthquake and its return to about 77% of its average 1998–2003 value within about two years. Assuming that the b-value is negatively correlated with differential stress 2 , they infer that the stress relieved by the earthquake has very rapidly recovered to levels found before the earthquake. Consequently, the authors propose that megathrust earthquake occurrences follow a Poisson process and are effectively random in time. However, we argue that the hazard of a great tsunami-producing earthquake in this section of the Japan megathrust zone is unlikely to already be almost as high as it was just before the 2011 event. Instead, many centuries of stress accumulation are required to rebuild stress and produce another great event. Prior to the earthquake, the seismicity in northeast Japan was predominantly contractional and involved reverse faults (Fig. 1a,c). Since the Tohoku-oki earthquake, there have been few reverse events near the high-slip zone of the rupture (Fig. 1b,d) and aftershocks primarily occurred as extensional (normal faulting) events in both the overriding and down- going plates of the subduction zone. The dominance of normal faulting suggests that the stress drop during the mainshock was large enough, relative to the background stress, to reverse the style of faulting near the high-slip zone 3,4 . Because events with different faulting types in northeast Japan have different b-values (Supplementary Information), we suggest that the observed coseismic rise and postseismic decay of b-values (Fig. 1f) partly reflect the fact that Tormann and colleagues sampled event populations with different mechanisms and from different source volumes in the subduction zone (Fig. 1e). Tormann and colleagues argue that reloading of stress caused by rapid postseismic deformation processes, complemented by fault healing processes and stress-field homogenization, may quickly re-establish compressional stress levels to those found just before the earthquake. However, although reloading of a megathrust rupture is indeed most rapid during the early period of postseismic relaxation, our models of stress recovery constrained by geodetic and seismicity data suggest that only a very small fraction of the approximately 10 MPa coseismic stress drop in the high-slip zone could have been recovered in the first three postseismic years. Even when considering the contributions from multiple sources of postseismic deformation 5 , the average shear-stress changes near the high-slip zone only amount to less than 0.5 MPa within three years and approach 1 MPa after relaxation of coseismic stress perturbations more than two decades later (Fig. 1g). Completion of the transient relaxation together with loading from steady plate convergence allow for full shear-stress recovery within several hundred years (Supplementary Information). In summary, we suggest that the temporal changes of b-values near the high- slip zone of the Tohoku-oki earthquake may reflect sampling of earthquakes from different volumes and fault populations in the subduction zone. Furthermore, postseismic relaxation processes are not capable of rapidly reloading the fault. Although the spatial and temporal variations of b-values are intriguing, it appears premature to assume b-values as a direct proxy for stress on the Japan subduction thrust and to argue for general randomness of megathrust earthquakes based on this observation.

Na(+) /Ca(2+) exchanger-heterozygote knockout mice display increased relaxation in gastric fundus and accelerated gastric transit in vivo.

For the contraction and relaxation of gastric smooth muscles to occur, the intracellular Ca(2+) concentration must be increased and decreased, respectively. The Na(+) /Ca(2+) exchanger (NCX) is a plasma membrane transporter that is involved in regulating intracellular Ca(2+) concentrations. To determine the role of NCX in gastrointestinal tissues, we examined electric field stimulation (EFS)-induced relaxations in the circular muscles of the gastric fundus in NCX1 and NCX2 heterozygote knockout mice (HET). The myenteric plexus layers and the longitudinal and circular muscle layers in the gastric fundus of wild-type mice (WT) were strongly immunoreactive to NCX1 and NCX2. EFS induced a transient relaxation that was apparent during the stimulus and a sustained relaxation that persisted after the end of the stimulus. The amplitudes of EFS-induced transient relaxation and sustained relaxation were greater in NCX1 HET and NCX2 HET than in WT. When an inhibitor of nitric oxide synthase was added following the EFS, neither NCX1 HET nor NCX2 HET exhibited transient relaxation, similar to WT. Furthermore, when a PACAP antagonist was added following the EFS, sustained relaxation in NCX1 HET and NCX2 HET was not observed, similar to WT. Next, we examined the effect of NCX heterozygous deficiency on relaxation in response to NO and PACAP in smooth muscles. The magnitude of NOR-1- and PACAP-induced relaxations in NCX1 HET and NCX2 HET was similar to that of WT. In this study, we demonstrate that NCX1 and NCX2 expressed in neurons regulate the motility in the gastric fundus.

Inhibitory Effect of Nasal Intermittent Positive Pressure Ventilation on Gastroesophageal Reflux.

Non-invasive intermittent positive pressure ventilation can lead to esophageal insufflations and in turn to gastric distension. The fact that the latter induces transient relaxation of the lower esophageal sphincter implies that it may increase gastroesophageal refluxes. We previously reported that nasal Pressure Support Ventilation (nPSV), contrary to nasal Neurally-Adjusted Ventilatory Assist (nNAVA), triggers active inspiratory laryngeal closure. This suggests that esophageal insufflations are more frequent in nPSV than in nNAVA. The objectives of the present study were to test the hypotheses that: i) gastroesophageal refluxes are increased during nPSV compared to both control condition and nNAVA; ii) esophageal insufflations occur more frequently during nPSV than nNAVA. Polysomnographic recordings and esophageal multichannel intraluminal impedance pHmetry were performed in nine chronically instrumented newborn lambs to study gastroesophageal refluxes, esophageal insufflations, states of alertness, laryngeal closure and respiration. Recordings were repeated without sedation in control condition, nPSV (15/4 cmH2O) and nNAVA (~ 15/4 cmH2O). The number of gastroesophageal refluxes recorded over six hours, expressed as median (interquartile range), decreased during both nPSV (1 (0, 3)) and nNAVA [1 (0, 3)] compared to control condition (5 (3, 10)), (p < 0.05). Meanwhile, the esophageal insufflation index did not differ between nPSV (40 (11, 61) h-1) and nNAVA (10 (9, 56) h-1) (p = 0.8). In conclusion, nPSV and nNAVA similarly inhibit gastroesophageal refluxes in healthy newborn lambs at pressures that do not lead to gastric distension. In addition, the occurrence of esophageal insufflations is not significantly different between nPSV and nNAVA. The strong inhibitory effect of nIPPV on gastroesophageal refluxes appears identical to that reported with nasal continuous positive airway pressure.

Esophageal testing: What we have so far.

Gastroesophageal reflux disease (GERD) is a common disorder of the gastrointestinal tract. In the last few decades, new technologies have evolved and have been applied to the functional study of the esophagus, allowing for the improvement of our knowledge of the pathophysiology of GERD. High-resolution manometry (HRM) permits greater understanding of the function of the esophagogastric junction and the risks associated with hiatal hernia. Moreover, HRM has been found to be more reproducible and sensitive than conventional water-perfused manometry to detect the presence of transient lower esophageal sphincter relaxation. Esophageal 24-h pH-metry with or without combined impedance is usually performed in patients with negative endoscopy and reflux symptoms who have a poor response to anti-reflux medical therapy to assess esophageal acid exposure and symptom-reflux correlations. In particular, esophageal 24-h impedance and pH monitoring can detect acid and non-acid reflux events. EndoFLIP is a recent technique poorly applied in clinical practice, although it provides a large amount of information about the esophagogastric junction. In the coming years, laryngopharyngeal symptoms could be evaluated with up and coming non-invasive or minimally invasive techniques, such as pepsin detection in saliva or pharyngeal pH-metry. Future studies are required of these techniques to evaluate their diagnostic accuracy and usefulness, although the available data are promising.

Enfermedad por reflujo gastroesofágico

IntroductionGastro-oesophageal reflux disease (GERD) arises as complication of sustained nonphysiological reflux, with a balance between protective and aggressive factors that favours the latter. AetiopathogenesisThe main mechanism consists of transient relaxations of the lower oesophageal sphincter (LES), although a hiatal hernia or an LES with sustained hypotension can contribute. Clinical manifestationsThis imbalance leads to a series of manifestations including heartburn and the sensation of reflux, although many other symptoms can occur such as dysphagia, sore throat and even extraoesophageal manifestations. DiagnosisThe diagnosis of GERD can be established by clinical improvement after several weeks of medical treatment. However, in certain scenarios, endoscopy or other additional tests might be necessary to rule out various processes. TreatmentThe medical treatment of GERD is based on the use of proton pump inhibitors (PPI), although surgery might be required in certain cases.

The Physiology of Eructation.

Eructation is composed of three independent phases: gas escape, upper barrier elimination, and gas transport phases. The gas escape phase is the gastro-LES inhibitory reflex that causes transient relaxation of the lower esophageal sphincter, which is activated by distension of stretch receptors of the proximal stomach. The upper barrier elimination phase is the transient relaxation of the upper esophageal sphincter along with airway protection. This phase is activated by stimulation of rapidly adapting mechanoreceptors of the esophageal mucosa. The gas transport phase is esophageal reverse peristalsis mediated by elementary reflexes, and it is theorized that this phase is activated by serosal rapidly adapting tension receptors. Alteration of the receptors which activate the upper barrier elimination phase of eructation by gastro-esophageal reflux of acid may in part contribute to the development of supra-esophageal reflux disease.

Investigation on transient electrically-assisted stress relaxation of QP980 advanced high strength steel

Advanced high strength steels have been increasingly used in auto body manufacturing industry to reduce weight and increase safety. However springback often occurs after stamping and seriously affects the forming accuracy, which is one of the bottle necks of its application. Targeting to control the springback, a novel method which employs the electric pulses to promote the relaxation of residual stress is investigated. In order to achieve this goal, electrically-assisted stress relaxation tests were carried out which shows that at a relative lower temperature, 373 K, the residual stress decreases with increasing electric parameters, and the athermal effect of the electric pulses is observed. A model of electrically-assisted stress relaxation is proposed. By combining the proposed stress relaxation model and the perfect plastic material model, a springback angle prediction model considering electric pulses is also proposed. The proposed models are verified with experimental results.

Transient mode competition in directly modulated DFB semiconductor laser

A new effect of transient mode competition in directly modulated DFB laser based on equivalent phase-shift (EPS) technique is presented and studied. Since there are multi-order reflections in EPS structure and if the 0th order subgrating is properly designed, the transient lasing of 0th order will occur during the rising time of the injection current. As a result, transient mode competition between -1st order (main mode) and 0th order will occur accordingly. This can consume redundant carrier and suppress the transient relaxation oscillation, which may be applied in some areas like on-off switching modulation of DFB semiconductor lasers. As an example, an equivalent π phase shift (π-EPS) is carefully designed to realize the effect. In such a laser the 0th order wavelength is in the margin of the material gain region and the -1st order wavelength is around the gain peak, while the stable single longitudinal mode (SLM) operation of the -1st order is guaranteed. The simulation investigation is performed. Good results with suppressed relaxation oscillation and 1.25 Gb/s directly on-off modulation (32 dB extinction ratio) are demonstrated. We believe it provides a new kind of method for on-off switching with high extinction ratio and weak relaxation oscillation.

Intra-bolus pressure and esophagogastric gradient, assessed with high-resolution manometry, are associated with acid exposure and proximal migration of refluxate

Trans-sphincteric pressure gradient (TSPG) seems to play a relevant role in eliciting refluxes during transient lower esophageal sphincter relaxations (TLESRs). Intra-bolus pressure (IBP) is considered to be correlated to esophageal wall tone. We aimed to evaluate the relationship between IBP, TSPG during TLESRs and the dynamic properties of refluxate in gastroesophageal reflux disease. Sixteen non-erosive reflux disease (NERD), 10 erosive disease (ERD) patients and 12 healthy volunteers (HVs), underwent 24-hour impedance-pH monitoring and combined high-resolution manometry-impedance before and 60 minutes. After a meal, ERD patients presented a significantly lower mean IBP (4.7 ± 1.6 mmHg) respect to NERD patients (8.9 ± 2.8 mmHg) and HVs (9.2 ± 3.2 mmHg). NERD patients with physiological abnormal acid exposure time showed a mean IBP (10.4 ± 3.1 mmHg) significantly higher than that in NERD with pathological abnormal acid exposure time (5.1 ± 1.5 mmHg). The TSPG value was significantly higher during TLESRs accompanied by reflux than during TLESRs not associated with reflux, both in patients and in HVs. A significant direct correlation was found between IBP, TSPG and proximal spread of refluxes in patients and in HVs. Gastroesophageal reflux disease patients display different degrees of esophageal distension. An increased compliance of the distal esophagus may accommodate larger volumes of refluxate and likely facilitates the injuries development. Higher TSPG values appear to facilitate the occurrence of refluxes during TLESRs. In patients with NERD, higher TSPG and IBP values favor proximal spread of refluxate and hence may play a relevant role in symptom generation.

Effect of baclofen on gastric acid pocket in subjects with gastroesophageal reflux disease symptoms.

Postprandial gastroesophageal reflux (PGER) in the distal esophagus (DE) is associated with a gastric juice 'acid pocket' (AP). Baclofen reduces AP extension into the DE in healthy volunteers, in part through increased lower esophageal sphincter (LES) pressure. We aimed to verify whether baclofen also affects postprandial AP location and extent in gastroesophageal reflux disease (GERD) patients. Thirteen treatment-naive heartburn-prevalent GERD patients underwent two AP studies, after pretreatment with baclofen 40 mg or placebo 30 minutes preprandially. We performed pH-probe stepwise pull-throughs (PT) (1 cm/min, LES -10 to +5 cm) before and every 30 minutes from 30 minutes before up to 150 minutes after a test meal. After the meal, both after placebo and baclofen, gastric pH significantly dropped at 30, 60, 90 minutes postprandially (P: nadir pHs of 3.9 ± 0.6, 2.3 ± 0.6, 2.1 ± 0.4; B: nadir pHs of 2.5 ± 0.4, 2.8 ± 0.4, 2.5 ± 0.3; all P < 0.05). After placebo, LES pressure decreased at 60, 90 and 120 minutes postprandially (32.7 ± 6.1 vs. 24.5 ± 3.1, 27.3 ± 5.9, 27.3 ± 6.0 mmHg; analysis of variance [ANOVA], P = 0.037), but this was prevented by baclofen (25.4 ± 3.4 vs. 29.4 ± 2, 32.2 ± 1.4, 35.5 ± 1.7 mmHg, ANOVA, P = not significant (NS)). Baclofen did not significantly decrease the postprandial AP extent above the LES but prevented the postprandial increase in transient lower esophageal sphincter relaxations (TLESRs) (preprandial vs. postprandial, placebo: 1.1 ± 0.3 vs. 3.7 ± 0.7, P < 0.05; baclofen: 1.4 ± 0.4 vs. 2 ± 0.5, P = NS). In GERD patients, baclofen significantly increases postprandial LES pressure, prevents the increase TLESRs but, unlike in healthy volunteers, does not affect AP extension into the DE.

Numerical Modelling of Prestresssing Steel Tendons under Fire and Post-Fire Conditions

The behaviour of prestressing steel tendons under fire and post-fire conditions is investigated numerically employing the ABAQUS package and its user-defined material subroutine UMAT which allows comprehensive constitutive relationships to be implemented. Based on an existing thermal creep model, a new set of parameters are proposed and calibrated against available test results in the literature. The proposed numerical model is versatile in predicting thermal creep, isothermal response and transient thermal relaxation of prestressing steel tendons. Moreover, parametric studies are conducted to investigate the effects of heating rate, heated length ratio, initial stress and various boundary conditions on the thermal relaxation of prestressing steel tendons. Besides, transient state analyses are carried out with constant heating rate and initial stress to investigate the rupture properties of prestressing steel tendons.

OP‐14 EFFECT OF TUBE‐FEEDING ON BOLUS CLEARANCE TIME IN NEUROLOGICALLY IMPAIRED CHILDREN VERSUS NORMAL CHILDREN

Aim:Neurologically impaired children are at increased risk of gastro‐esophageal reflux disease (GERD). Pathogenic factors that can lead to GERD include transient lower oesophageal sphincter relaxation and impaired oesophageal clearance. Previous studies had suggested that neurologically impaired children have increased bolus clearance time (BCT). The aim of our study is to determine the effect of (naso‐gastric) tube‐feeding on BCT in these children.Methods: Retrospective review of the multi‐channel intra‐luminal impedance‐pH (MII‐pH) results of the paediatric population performed from January 2012 to December 2014.Results:A total of 71 studies were performed. 7 studies were excluded from data analysis as these children had previous fundoplication which is known to alter oesophageal peristalsis. Of the 64 analysed, 33 were in neurologically impaired children and 32 were male. The median (range) age was 1.35 (0.03–18.58) years. 60 (93.75%) children were less than 5 years old at the time of the study.In our cohort, all the neurologically impaired children were tube‐fed. 41 (68.75%) of the children were tube‐fed; bolus fed (n = 30), continuous naso‐gastric (n = 7) or naso‐jejunal (n = 4). Based on the MII‐pH results, 16 children (25%) were diagnosed to have GERD. 9 of the neurologically‐impaired children had GERD while 7 of the neurologically normal children had GERD. There was no difference in the means of the “median BCT” in neurologically impaired versus normal children (10.42 (SD 4.27) vs 9.18 (SD 2.12) seconds, p = 0.144), or in those with or without GERD based on MII‐pH, regardless of underlying neurological status.Conclusions:Our data suggest that BCT in neurologically abnormal children who are tube‐fed do not appear to be longer than neurologically normal children, or associated with an increased risk of GERD. This suggests that other mechanisms have a greater role in conferring the increased risk of GERD in this population. Of note, “median BCT” values were also shorter in our population of predominantly young children of age less than 5.