Biomedical subjects
R W McCallum
Publications and source records attributed to R W McCallum.
Non-invasive identification of gastric contractions from surface electrogastrogram using back-propagation neural networks.
Gastric contractions play an important role in the digestive process of the stomach. The established method for the measurement of gastric contractions is invasive and involves the insertion through the nose of a manometric probe into the stomach. A non-invasive method is introduced in this paper for the identification of gastric contractions using the surface electrogastrogram. The electrogastrogram (EGG) was measured by placing surface electrodes on the abdominal skin over the stomach in ten subjects. Gastric contractions were simultaneously monitored using an intraluminal manometric probe. The back-propagation neural network was applied to identify gastric contractions from the EGG. The input of the neural network was composed of spectral data points of the EGG which was computed using the exponential distribution method. Experiments were conducted to optimize network structures and parameters. Using the EGG data in five subjects as the training set and the EGG data in another five subjects as the testing set, an overall accuracy of 92% was achieved in the identification of gastric contractions with an optimized three-layer back-propagation neural network (number of nodes for input:hidden:output layers being 64:10:2).
What is the secretory potential of submucosal mucous glands within the human gullet in health and disease?
Histology of the human esophageal mucosa reveals numerous submucosal mucous glands, scattered along the esophagus and especially accumulated below the upper and above the lower esophageal sphincters. Mucin remains a major organic component of human esophageal secretion, collected using our newly developed esophageal perfusion catheter. Esophageal mucin is accompanied by nonmucin proteins, epidermal growth factor (EGF) and prostaglandin E2 (PGE2). Bicarbonate is the major inorganic component of esophageal secretion in humans. Mucosal exposure to an HC1/pepsin solution, mimicking the natural gastroesophageal scenario, significantly changed the secretory profile of all esophageal secretion components. The rate of secretion of esophageal mucin, EGF and PGE2 under the impact of HC1/pepsin in patients with reflux esophagitis appeared to be significantly impaired, although the basal rate of esophageal PGE2 output remained higher than in controls. These data indicate that a significant impairment in esophageal components of the preepithelial mucosal barrier, paralleling the severity of mucosal inflammation, may have a detrimental impact on the protective potential of the esophageal mucosal barrier, facilitating the development of reflux esophagitis.
What role do salivary inorganic components play in health and disease of the esophageal mucosa?
The integrity of the esophageal mucosa depends upon an equilibrium between aggressive factors and protective mechanisms. Esophageal mucosal protective mechanisms operate at three overlapping levels: (1) preepithelial, (2) epithelial and (3) postepithelial. Since aggressive factors always operate on the luminal side of the esophagus, preepithelial defense remains as the first line in mucosal barrier protection. Salivary secretion quantitatively and qualitatively contributes to the protective potential of the preepithelial barrier. Salivary volume and its buffering capacity are elaborated by lowering intraluminal pH within the esophagus, and are key factors in restoration of physiologic pH within the esophagus. Salivary secretory response to esophageal mechanical (bolus) and chemical (intraluminal pH) stimuli, mediated by the esophagosalivary reflex pathway, is impaired in patients with reflux esophagitis.
Do salivary organic components play a protective role in health and disease of the esophageal mucosa?
Aggressive factors operating within the esophageal lumen during gastroesophageal reflux are balanced by adequately mobilized protective mechanisms. Esophageal mucosal protection operates at three different although complementary dimensions: (1) preepithelial, (2) epithelial and (3) postepithelial. Since aggressive factors predominantly operate within the esophageal lumen, preepithelial defense is pivotal in mucosal protection. The preepithelial barrier is significantly enhanced by the quantity and the quality of salivary organic components such as salivary mucin, nonmucin protein, salivary epidermal growth factor (EGF) and salivary prostaglandin E2. The rate of secretion of salivary mucin, nonmucin protein and EGF under the impact of intraesophageal mechanical (bolus) and chemical (HCl/pepsin) stimulation, mimicking the natural gastroesophageal reflux scenario, is significantly impaired in patients with RE, whereas the rate of salivary PGE2 output remains essentially unchanged. Salivary secretory response to esophageal mechanical and chemical stimuli in terms of organic components, mediated by the esophagosalivary reflex pathway, exhibits a significant impairment in patients with reflux esophagitis.
Modulatory impact of acid and pepsin on esophageal hydrophobicity in humans.
OBJECTIVES: The role of hydrophobicity in the pathophysiology of the gastrointestinal tract is well established as a protective mechanism against the impact of lumenal acid and pepsin. Hydrophobic properties of esophageal secretion in humans remain largely unknown. METHODS: We have studied, therefore, hydrophobicity by using fluorescence probe in human esophageal secretion, elaborated under the impact of saline followed by HCl, HCl/pepsin, and final saline. RESULTS: Basal hydrophobicity of human esophageal secretion, elaborated during mucosal exposure to saline, was 237 +/- 32. This value, however, declined 72% during mucosal exposure to HCl (66 +/- 14 vs 237 +/- 32; p < 0.001) and 87% during mucosal exposure to acid supplemented with pepsin (30 +/- 4 vs 237 +/- 32; p < 0.001). Moreover, hydrophobicity upon perfusion with HCl/pepsin was 55% lower than after perfusion with HCl alone (30 +/- 4 vs 66 +/- 14), although the result was insignificant. Substitution of saline for HCl/pepsin solution during the last perfusion period resulted in a partial recovery of hydrophobicity in esophageal secretion (131 +/- 30 vs 30 +/- 4; p < 0.001), although this value was lower than the basal hydrophobicity value (131 +/- 30 vs 237 +/- 32; p = 0.028). In addition, we continuously observed a significant shift in the fluorescence emission maximum from 508 +/- 6.4 to 486 +/- 0.9 (p < 0.001) during perfusion with starting saline, to 492 +/- 1.6 (p < 0.001) during exposure to HCl, to 493 +/- 1.1 (p < 0.001) during perfusion with HCl/pepsin, and to 488 +/- 0.9 (p < 0.001) during infusion of final saline. The maximum emission wavelength after esophageal exposure to initial saline also was significantly lower than the maximum emission upon perfusion with HCl (492 +/- 1.6 vs 486 +/- 0.9; p < 0.05) and HCl/pepsin (493 +/- 1.1 vs 486 +/- 0.9; p < 0.05). Although basal hydrophobicity in males was similar to corresponding values recorded in females, mucosal exposure to HCl (pH 2.1) resulted in an 84% decline in females but only 60% in males. Therefore, the hydrophobicity value in females during the perfusion period with HCl was 52% lower than in males (p = 0.129). CONCLUSIONS: Esophageal secretion exhibits its hydrophobic nature presumably through the presence of mucus components such as mucin and mucin-associated phospholipids. The inhibitory impact of HCl and HCl/pepsin solutions on esophageal hydrophobicity may play a role in the pathogenesis of mucosal damage by gastroesophagel refluxate.
Doctor's right to refuse to perform abortions. Antiabortion views are not incompatible with gynaecology.
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Declined human esophageal mucin secretion in patients with severe reflux esophagitis.
It has been recently demonstrated that human esophageal submucosal mucous glands exhibit the ability to secrete copious amounts of mucin, well known within the gastrointestinal tract for its protective quality against hydrogen ion and pepsin. Since mucin may also play a protective role within the esophageal compartment, we have studied the rate of secretion of esophageal mucin in patients with RE. Mucin was assessed by periodic acid-Schiff methodology in esophageal secretion collected during continuous perfusion with saline (period I) followed by HCl (period II), HCl/pepsin (period III), and final saline (period IV), mimicking the natural gastroesophageal scenario. The basal rate of the luminal release of mucin in patients with grade II RE was 18% lower as compared with controls. During exposure of the esophageal mucosa to an HCl/pepsin solution, esophageal mucin output in the RE group was 52% lower than in the control group (0.154 +/- 0.027 vs 0.320 +/- 0.049 mg/cm2/min; P = 0.025). Furthermore, the rates of esophageal mucin output in patients with grade III RE during esophageal perfusion with saline and HCl/pepsin were 62% (0.090 +/- 0.021 vs 0.239 +/- 0.036 mg/cm2/min; P = 0.016) and 86% (0.048 +/- 0.010 vs 0.320 +/- 0.049 mg/cm2/min; P = 0.001) lower when compared with corresponding values in controls. After endoscopic healing of RE, the overall impairment in the rate of esophageal mucin secretion in patients with grade II improved from 31% to 17% at the end of therapy, whereas in patients with grade III the impairment in mucin secretion improved only marginally from 71% to 69%.(ABSTRACT TRUNCATED AT 250 WORDS)
Human esophageal secretion: mucosal response to luminal acid and pepsin.
BACKGROUND/AIMS: Although esophageal histology in humans reveals numerous submucosal mucous glands, their secretion has never been explored. Therefore, we have studied the chemical composition and physical characteristics of esophageal secretion under the impact of luminal saline, acid, and acid/pepsin solutions. METHODS: The esophageal lumen in 21 healthy volunteers was continuously perfused with saline, HCI, or HCI/pepsin. Perfusates were assayed for mucin, protein, and viscosity. In addition, analysis of amino acid and sugar composition of purified esophageal mucin was performed. RESULTS: Esophageal perfusion with saline resulted in luminal release of mucin at the rate of 0.23 +/- 0.03 mg.cm-2 x min-1. Acid/pepsin solution significantly enhanced luminal release of mucin (0.32 +/- 0.03 mg.cm-2 x min-1; P < 0.01). HCI/pepsin solution also significantly increased the luminal output of protein (P < 0.01) and significantly impaired the viscosity of the esophageal perfusate (P < 0.05). Threonine, serine, and proline were the major amino acids within the esophageal mucin, whereas galactose was the predominant carbohydrate. CONCLUSIONS: Luminally released esophageal mucin, shown for the first time in humans, contributes significantly to maintaining the high viscosity of esophageal secretions. Significant increase in the luminal release of mucin under the impact of acid and pepsin, with subsequent decline of the perfusate viscosity, may indicate that mucin is the major target for gastric acid and pepsin, absorbing the deleterious impact of the gastroesophageal refluxate.
The effect of esophageal mechanical and chemical stimuli on salivary mucin secretion in healthy individuals.
Because of a newly developed model of esophageal perfusion in humans, the authors could study the role of esophago-salivary reflex in salivary neutral and acidic mucin output. The basal rate of neutral mucin output was 0.24 +/- 0.06 mg per minute. Placement of intraesophageal tubing and inflation of balloons resulted in a highly significant increase in salivary mucin output (2.10 +/- 0.22 mg per minute; p < 0.00001). However, implementation of esophageal perfusion with saline resulted in a significant decline of salivary mucin output (1.28 +/- 0.10 mg/mL NaCl4 versus 2.08 +/- 0.24 mg/mL NaCl1; p < 0.001). Esophageal perfusion with hydrochloric acid prevented the decline of salivary mucin output observed during perfusion with saline, whereas infusion of hydrochloric acid/pepsin resulted in a significant enhancement of salivary mucin output (2.89 +/- 0.31 mg per minute; p < 0.01). Therefore, mechanical and chemical stimulations resulted in an overall 9-fold and 12-fold increase in the rate of salivary mucin output over the basal value, respectively. The basal rate of acidic mucin secretion was 0.26 +/- 0.06 mg per minute. After placement of intraesophageal tubing, inflation of balloons, perfusion hydrochloric acid, or hydrochloric acid-pepsin solution, a significant enhancement in the rate of salivary acidic mucin output, similar to that observed during measurement of neutral mucin, was observed. Therefore, during mechanical and chemical stimulation, the rate of salivary acidic mucin output increased 7.3-fold and 11.1-fold over the basal value, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Serosal and cutaneous recordings of gastric myoelectrical activity in patients with gastroparesis.
The aims of this study were to 1) investigate gastric myoelectrical activity in patients with gastroparesis, 2) validate the cutaneous electrogastrogram (EGG) in tracking the frequency change of the gastric slow wave, and 3) investigate the effect of electrical stimulation on gastric myoelectrical activity. Gastric myoelectrical activity was recorded in 12 patients with documented gastroparesis using serosal electrodes for > 200 min in each subject. All recordings were made at least 4 days after surgery. Each session consisted of a 30-min recording in the fasting state and a 30-min recording after a test meal. The test meal (liquid or mixed) was selected according to patient's tolerance. Electrical stimulation was performed in three subjects via the serosal electrodes at a frequency of 3 cycles/min. Gastric myoelectrical activity was recorded using serosal electrodes in each session. The serosal recording showed slow waves of 2.5 to 4.0 cycles/min in all 12 subjects. Absence of spikes was noted in 11 of the 12 subjects. The simultaneous serosal and cutaneous recording of gastric myoelectrical activity showed that the frequency of the EGG was exactly the same as that of the serosal recording. Liquid meals resulted in a significant decrease in slow-wave frequency (Student's t test, P = 0.006), and the EGG accurately reflected this change. Electrical stimulation had no effect on the frequency of the gastric slow wave and did not induce spikes.(ABSTRACT TRUNCATED AT 250 WORDS)
Occupational exposure to Helicobacter pylori for the endoscopy professional: a sera epidemiological study.
OBJECTIVES: The purpose of this prospective study was to determine if medical and nursing staff in the United States who are regularly involved in endoscopic procedures are at an increased risk of acquiring Helicobacter pylori infection. METHODS: One hundred and twenty-two gastroendoscopists and endoscopy nurses attending an advanced gastroendoscopy course (17 women, 105 men) completed a questionnaire consisting of past medical and professional history. Serum from each subject was collected and tested using a validated ELISA assay (sensitivity 99%, specificity 96%). H. pylori prevalence in the experimental group was compared to that of 510 blood donors. RESULTS: In all age groups, H. pylori positivity was significantly higher among the study subjects compared with controls. Caucasian subjects, when matched to controls for age, race, and level of education, had significantly higher rates of H. pylori positivity. Foreign-born subjects, when compared to US-born subjects, also had higher rates of H. pylori positivity. There was no statistical difference of H. pylori positivity with respect to gender, years involved in endoscopy, or number of endoscopies performed monthly. CONCLUSION: H. pylori infection is more common in gastroendoscopists and endoscopy nurses than the general population and should be viewed as an occupational hazard.
Endoscopy for gastrointestinal bleeding after acute myocardial infarction.
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Diminished luminal release of esophageal epidermal growth factor in patients with reflux esophagitis.
OBJECTIVES: It has recently been demonstrated that human esophageal mucosa, containing numerous submucosal mucous glands, has the ability to elaborate significant amounts of esophageal epidermal growth factor (eEGF). Because of its role in the maintenance of the integrity of the esophageal mucosa, we elected to study the rate of secretion of eEGF in patients with reflux esophagitis (RE), compared with controls, using our newly developed esophageal perfusion model. METHODS: Fourteen healthy asymptomatic volunteers and 14 patients with endoscopically confirmed esophagitis underwent esophageal perfusion with saline, HCl (0.01 M, pH 2.1) HCl/pepsin (0.5 mg/ml of HCl), and ending NaCl solution during four consecutive 8-min perfusion periods. All perfusates were assayed for EGF by RIA (Amersham). Results are expressed as mean +/- SEM. Student's t test was used for statistical analysis. RESULTS: The basal rate of luminal EGF release in patients with RE was 3.78 +/- 0.29 ng/min. This value significantly declined (2.27 +/- 0.27 ng/min; p < 0.001) during mucosal exposure to HCl but was significantly enhanced when the HCl perfusing solution was supplemented with pepsin (4.20 +/- 0.29; p < 0.001 vs. HCl). Introduction of saline during the last perfusion period maintained a rate of luminal EGF release similar to that observed during the initial esophageal perfusion with saline. Luminal release of EGF in patients with RE was significantly lower, compared with corresponding values recorded in controls during perfusion with saline (3.78 +/- 0.29 vs. 14.1 +/- 1.25 ng/min; p < 0.00001), with HCl (2.27 +/- 0.27 vs. 5.95 ng/min; p < 0.0001), with HCl/pepsin solution (4.2 +/- 0.29 vs. 11.7 +/- 1.88 ng/min; p < 0.0001), and during the final perfusion period with saline (3.73 +/- 0.25 vs. 15.1 +/- 1.1 ng/min; p < 0.00001). Therefore, the rate of luminal EGF release in controls was 4-fold, 3-fold, 3-fold, and 4-fold higher than that of patients with RE during perfusion with initial saline, HCl, HCl/pepsin and final saline, respectively. CONCLUSIONS: 1) Decreased esophageal EGF in patients with RE may facilitate the development or delay the healing of mucosal injury. 2) Depletion of EGF from the mucus layer covering the epithelium under the impact of refluxed luminal acid/pepsin may be considered as one of the potential underlying mechanisms leading to damage of the esophageal mucosa during gastroesophageal reflux episodes.
Interrelationship between esophageal challenge with mechanical and chemical stimuli and salivary protective mechanisms.
Using our newly developed model of esophageal perfusion in humans, we were able to study the esophagosalivary reflex in 20 healthy volunteers (12M, 8F; mean age 40 yr). The placement of the intraesophageal catheter resulted in a 6.3-fold increase in the salivation rate over the baseline value (2.27 +/- 0.28 vs. 0.36 +/- 0.06 ml/min; p = 0.02), whereas inflation of the catheter balloons evoked a 6.9-fold increase (2.52 +/- 0.21; p < 0.001) in the rate of salivation. A stepwise and significant decline of salivation (p = 0.02), observed during subsequent perfusion with NaCl was prevented when perfusion with HCl and HCl/pepsin solutions was implemented. The placement of the intraesophageal catheter resulted in a significant increase of salivary pH over its basal value (7.77 +/- 0.05 vs. 6.89 +/- 0.11; p < 0.001). A gradual decline of salivary pH during subsequent perfusion with NaCl was eliminated when saline was replaced with HCl or HCl/pepsin (7.76 +/- 0.04 vs. 7.46 +/- 0.09; p < 0.01). Intraesophageal tubing enormously potentiated the viscosity of saliva (44.50 +/- 9.0 vs. 9.3 +/- 1.0 mPa.s; p < 0.001). A subsequent decline of viscosity during continuous perfusion with saline was also prevented when HCl was substituted for NaCl (29.95 +/- 4.5 vs. 19.50 +/- 3.30; p < 0.05). A significant potentiation of salivary volume, viscosity, and pH during esophageal stimulation of mechano- and chemoreceptors may suggest a contributing role of the esophagosalivary reflex in the maintenance of the esophageal mucosal integrity under the impact gastroesophageal reflux.
Impact of acid and pepsin on human esophageal prostaglandins.
OBJECTIVES: Although the prostaglandin-mediated mucosal protection within the gastric compartment has been well established, its potential role in the maintenance of integrity of the esophageal mucosa in humans has not been explored due to the lack of appropriate methodology. METHODS: We have recently developed an esophageal perfusion catheter, equipped with two balloons, compartmentalizing a 7.5-cm segment of the esophageal lumen. Using this catheter, we studied the impact of the luminal perfusion with saline, HCl (0.01 M, pH 2.1), and HCl/pepsin solutions (0.5 mg/ml) on esophageal luminal release of PGE2 in 21 asymptomatic, presumably healthy volunteers (12 M, 9F; mean age 40 yr). The content of PGE2 in its methyl oximated form was measured by RIA (Amersham, IL), using a novel iodinated label. Results are expressed as mean +/- SEM. Student's t test was used for statistical analysis. RESULTS: Perfusion of the esophageal lumen resulted in continuous release of PGE2 into the perfusate at the rate of 1880 +/- 393 pg/min during the first 8-min perfusion period. During continuation of perfusion with saline, the luminal release of PGE2 was maintained at the rate of 1820 +/- 640 pg/min during the second 8-min perfusion period. This rate declined (although in nonsignificant fashion; p < 0.2) during the third perfusion period, reaching a plateau of 1220 +/- 473 pg/min and maintained during the last (period IV) perfusion period with saline. Introduction of acid during the perfusion period II in the second group of investigated subjects resulted in a rapid and statistically significant decline of the luminal release of PGE2 to the value of 1020 +/- 167 ng/min (p < 0.01). Continuation of esophageal perfusion with acid during the next 8-min perfusion period further diminished the luminal release of PGE2 to the value of 520 +/- 73; p < 0.001. The significant decline in the rate of luminal PGE2 release was still maintained despite the replacement of acid with saline during the ending 8-min perfusion (period IV; 560 +/- 80 ng/min; p < 0.001). Esophageal perfusion with HCl/pepsin solution, in group III subjects, potentiated luminal release of PGE2, reaching the value of 1553 +/- 340 pg/min, which is 3 times higher than the value of PGE2 observed during corresponding perfusion with HCl (period III; p < 0.03). This significant impact of HCl/pepsin solution was still maintained despite the substitution of HCl/pepsin with NaCl during the last perfusion period, and was still significantly higher (1260 +/- 220 pg/min; p < 0.02) than the corresponding value during the ending perfusion with NaCl after HCl (group II). This study for the first time demonstrates that luminal release of PGE2 in humans remains under a significant impact of luminal chemical factors such as acid and pepsin. CONCLUSION: The modulatory effect of acid and pepsin on esophageal mucosal prostaglandin release may play a role in the development of reflux-related mucosal pathology.
Diabetes care.
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Identification of gastric contractions from the cutaneous electrogastrogram.
OBJECTIVE: The objective of this study was to investigate whether gastric contractions in the fasting and fed state can be identified from the cutaneous electrogastrogram. METHODS: Simultaneous measurements of gastric myoelectrical and manometric activities were made in 10 healthy female volunteers from 1:00 AM to 9:45 AM. For manometric recording, a catheter incorporating solid state transducers was used. Cutaneous electrogastrography (EGG) was used for myoelectrical recording. All EGG data from 1:00 AM to 7:30 AM that occurred during motor quiescence, all EGG data that occurred during antral contractions, and 2-h EGG data after breakfast given at 7:30 AM were quantitatively analyzed and compared with each other. The EGG in three specific periods (fasting without antral contractions, fasting with contractions, and postprandial) was characterized by four parameters that include frequency, power, and stabilities of the frequency and power. RESULTS: 1) the peak power of the postprandial EGG was, respectively, 12.5 dB (about 2-fold increase in amplitude) and 6.8 dB (about 1-fold increase in amplitude) higher than that during motor quiescence (p < 0.05) and motor activity in the fasting state; 2) the dominant frequency of the postprandial EGG was, respectively, 6% and 13% higher than that during motor quiescence and motor activity (p < 0.05) in the fasting state; 3) the peak power of the fasting EGG was 48% more unstable during motor activity than motor quiescence (p < 0.05); 4) the stability of the EGG frequency was not significantly different during the three different periods. CONCLUSION: The EGG provides important and useful information for the assessment of gastric motility. An unstable EGG peak power is indicative of gastric contractions in the fasting state. An increase in EGG peak power and/or dominant frequency after a solid test meal suggests a normal postprandial gastric motility.