Johns Hopkins Center for Neurogastroenterology

Baltimore, MD, United States

Johns Hopkins Center for Neurogastroenterology

Baltimore, MD, United States
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Song G.-Q.,Oklahoma Medical Research Foundation | Song G.-Q.,Texas Tech University Health Sciences Center | Zhu H.,Oklahoma Medical Research Foundation | Lei Y.,Oklahoma Medical Research Foundation | And 7 more authors.
Obesity Surgery | Year: 2015

Aims: The aim of this study was to test the hypothesis that that a method of gastric electrical stimulation (GES) optimized to inhibit gastric motility was effective in reducing food intake in dogs. Methods: Female dogs with a gastric cannula and gastric serosal electrodes were studied in three experiments: (1) to determine the best parameters and locations of GES in inhibiting gastric tone, slow waves, and contractions in dogs;(2) to investigate the reproducibility of the inhibitory effects of GES; and (3) to study the effect of the GES method on food intake in dogs. Results: (1) For GES to exert significant effects on gastric motility, a pulse width of ≥2 ms was required, and with other appropriate inhibitory parameters, GES was able to increase gastric volume by 190.4 %, reduce antral contractions by 39.7 %, and decrease the percentage of normal slow waves by 47.6 %. In addition, the inhibitory effect of GES was more potent with the stimulation electrodes placed along the lesser or greater curvature than placed in the middle, and more potent with the electrodes placed in the distal stomach than in the proximal stomach; (2) the inhibitory effects of GES on gastric motility were reproducible; (3) the GES method optimized to inhibit gastric motility produced a 20 % reduction in food intakes in non-obese dogs. Conclusion: GES with appropriate parameters inhibits gastric motility, and the effects are reproducible. The GES method optimized to inhibit gastric motility reduces food intake in healthy dogs and may have a therapeutic potential for treating obesity. © 2014, Springer Science+Business Media New York.


Jin H.,Oklahoma Medical Research Foundation | Jin H.,The University of Oklahoma Health Sciences Center | Jin H.,Zhejiang University | Liu J.,Oklahoma Medical Research Foundation | And 8 more authors.
American Journal of Physiology - Gastrointestinal and Liver Physiology | Year: 2015

Electroacupuncture (EA) has been shown to improve impaired gastric motility and slow waves in both humans and animals. However, its effects on colonic motility have rarely been investigated. The aim of this study was to investigate the effects and underlying mechanisms of EA on impaired colonic mo-tility induced by rectal distension (RD)in dogs. Colon contractions and transit were measured in various sessions with and without EA in hound dogs chronically placed with a colonic cannula. Colonic contractile activity was assessed by motility index (MI). Autonomic functions were determined by the spectral analysis of the heart rate variability derived from the electrocardiogram. It was found 1)RD suppressed colonic motility by 40.5% (10.8 ± 0.9 with RD vs. 6.4 ± 0.8 at baseline, P < 0.002). EA at ST36 normalized colonic contractions suppressed by RD (12.9 ± 2.8, P < 0.002 vs. RD and P = 0.1 vs. control). 2) Administration of atropine blocked the ameliorating effect of EA on colon motility. 3) RD also delayed colonic transit (65.0 ± 2.0% with RD vs. 86.0 ± 1.9% without RD, P < 0.001) that was restored with EA (84.0 ± 1.9%, P = 0.178 vs. control). 4)EA increased vagal activity suppressed by RD (0.37 ± 0.07 with RD + EA vs. 0.09 ± 0.03 with RD without EA, P < 0.001). In conclusion, RD inhibits colonic contractions and delays colonic transit in dogs; EA at ST36 restores the RD-induced impairment in both colonic contraction and transit by enhancing vagal activity and mediated via the cholinergic pathway. © 2015 the American Physiological Society.


Zhang N.,Ningbo Pace Translational Medical Research Center | Zhang N.,Nanjing Medical University | Huang Z.,Ningbo Pace Translational Medical Research Center | Huang Z.,Zhejiang University | And 7 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2014

The aims of this study were to investigate the effects and possible mechanisms of transcutaneous neuromodulation (TN) in patients with chronic constipation. Twelve patients were recruited. The treatment consisted of 2-week TN and 2-week sham-TN which was performed in a crossover design. Bowel habit diary, Patient Assessment of Constipation Symptom (PAC-SYM), Patient Assessment of ConstipationQuality of Life (PAC-QOL), and anorectalmotilitywere evaluated. Electrocardiogram was recorded for the assessment of autonomic function during acute TN therapy. It was found that (1) TN improved the frequency of spontaneous defecation. After 2-week TN therapy, 83% patients had more than 3 times bowel movements per week which was significantly different from sham-TN (P = 0.01). (2) TN improved PAC-SYM and PAC-QOL scores (P < 0.001, resp.). (3) TN significantly decreased the threshold volume to elicit RAIR (P < 0.05), ameliorated rectal sensory threshold (P = 0.04), and maximumtolerance (P = 0.04). (4) TN, but not sham-TN, increased the vagal activity (P = 0.01 versus baseline) and decreased the sympathetic activity (P = 0.01, versus baseline). It was concluded that needleless TN at posterior tibial nerve and ST36 using a watch-size stimulator is effective in chronic constipation, and the effect was possibly mediated via the autonomic mechanism. Copyright © 2014 Nina Zhang et al.


Pasricha P.J.,Johns Hopkins Center for Neurogastroenterology | Parkman H.P.,Temple University
Gastroenterology Clinics of North America | Year: 2015

Gastroparesis is a chronic symptomatic disorder of the stomach characterized by delayed emptying without evidence of mechanical obstruction. Symptoms of gastroparesis include nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain. The 3 main causes are diabetic, postsurgical, and idiopathic. Diagnosis is confirmed by demonstrating delayed gastric emptying. Gastric emptying rates measured by gastric motor testing generally correlate poorly with symptoms and quality of life in patients with gastroparesis. It may be appropriate to reconsider the definition of gastroparesis, recognizing it as a broader spectrum of gastric neuromuscular dysfunction. © 2015 Elsevier Inc.


PubMed | Johns Hopkins Center for Neurogastroenterology and Temple University
Type: Journal Article | Journal: Gastroenterology clinics of North America | Year: 2015

Gastroparesis is a chronic symptomatic disorder of the stomach characterized by delayed emptying without evidence of mechanical obstruction. Symptoms of gastroparesis include nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain. The 3 main causes are diabetic, postsurgical, and idiopathic. Diagnosis is confirmed by demonstrating delayed gastric emptying. Gastric emptying rates measured by gastric motor testing generally correlate poorly with symptoms and quality of life in patients with gastroparesis. It may be appropriate to reconsider the definition of gastroparesis, recognizing it as a broader spectrum of gastric neuromuscular dysfunction.


Zhu Y.,Johns Hopkins Center for Neurogastroenterology | Colak T.,Stanford University | Shenoy M.,Stanford University | Liu L.,Johns Hopkins Center for Neurogastroenterology | And 6 more authors.
Molecular Pain | Year: 2012

Background: Transforming growth factor beta (TGFβ) is upregulated in chronic inflammation, where it plays a key role in wound healing and promoting fibrosis. However, little is known about the peripheral effects of TGFβ on nociception.Methods: We tested the in vitro effects of TGFβ1 on the excitability of dorsal root ganglia (DRG) neurons and the function of potassium (K) channels. We also studied the effects of TGFβ1 infusion on pain responses to noxious electrical stimulation in healthy rats as well as the effects of neutralization of TGFβ1 on evoked pain behaviors in a rat model of chronic pancreatitis.Results: Exposure to TGFβ1 in vitro increased sensory neuronal excitability, decreased voltage-gated A-type K+ currents (IA) and downregulated expression of the Kv1.4 (KCNA4) gene. Further TGFβ1 infusion into the naïve rat pancreas in vivo induces hyperalgesia and conversely, neutralization of TGFβ1 attenuates hyperalgesia only in rats with experimental chronic pancreatitis. Paradoxically, TGFβ1 neutralization in naïve rats results in pancreatic hyperalgesia.Conclusions: TGFβ1 is an important and complex modulator of sensory neuronal function in chronic inflammation, providing a link between fibrosis and nociception and is a potentially novel target for the treatment of persistent pain associated with chronic pancreatitis. © 2012 Zhu et al.; licensee BioMed Central Ltd.


Moran R.A.,Johns Hopkins Center for Neurogastroenterology | James T.,Johns Hopkins Center for Neurogastroenterology | Pasricha P.J.,Johns Hopkins Center for Neurogastroenterology
Current Opinion in Gastroenterology | Year: 2015

Purpose of review Pain is the most common symptom of chronic pancreatitis, with a profound socioeconomic impact. Historical management paradigms failed, as they did not adequately address the fundamental underlying mechanisms. The present article describes the neurobiology of pain and sensitization in this condition, in an effort to explain prior failings and provide future directions for managing pain in chronic pancreatitis. Recent findings A number of recent advances have been made in understanding the neurobiology of pain for this condition. This has been coupled with clinical advances in assessing sensitization to pain in these patients, which has been shown to predict response to medical and surgical therapy. Summary Pain in chronic pancreatitis is complex. Addressing the mechanical and morphological findings in chronic pancreatitis without addressing the underlying neurobiological mechanisms is destined to fail. New advances in our understanding of the neurobiology of pain in chronic pancreatitis helps to explain prior failings and provides future direction for managing pain in patients afflicted by this disease. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.


Pasricha P.J.,Johns Hopkins Center for Neurogastroenterology
Gastroenterology Clinics of North America | Year: 2015

Understanding of gastroparesis is evolving, in part because of systematic studies on the pathology, pathophysiology, and outcomes. It is clear that simply accelerating gastric emptying may not effectively control symptoms in this syndrome and more creative approaches are required that address aberrant sensation (vagal and spinal) as well as regional disturbances in motility. Further, with the growing recognition of a possible inflammatory basis, the prospects of disease modifying now seem realistic. © 2015 Elsevier Inc.


PubMed | Johns Hopkins Center for Neurogastroenterology
Type: Journal Article | Journal: Gastroenterology clinics of North America | Year: 2015

Understanding of gastroparesis is evolving, in part because of systematic studies on the pathology, pathophysiology, and outcomes. It is clear that simply accelerating gastric emptying may not effectively control symptoms in this syndrome and more creative approaches are required that address aberrant sensation (vagal and spinal) as well as regional disturbances in motility. Further, with the growing recognition of a possible inflammatory basis, the prospects of disease modifying now seem realistic.


Transforming growth factor beta (TGF) is upregulated in chronic inflammation, where it plays a key role in wound healing and promoting fibrosis. However, little is known about the peripheral effects of TGF on nociception.We tested the in vitro effects of TGF1 on the excitability of dorsal root ganglia (DRG) neurons and the function of potassium (K) channels. We also studied the effects of TGF1 infusion on pain responses to noxious electrical stimulation in healthy rats as well as the effects of neutralization of TGF1 on evoked pain behaviors in a rat model of chronic pancreatitis.Exposure to TGF1 in vitro increased sensory neuronal excitability, decreased voltage-gated A-type K(+) currents (IA) and downregulated expression of the Kv1.4 (KCNA4) gene. Further TGF1 infusion into the nave rat pancreas in vivo induces hyperalgesia and conversely, neutralization of TGF1 attenuates hyperalgesia only in rats with experimental chronic pancreatitis. Paradoxically, TGF1 neutralization in nave rats results in pancreatic hyperalgesia.TGF1 is an important and complex modulator of sensory neuronal function in chronic inflammation, providing a link between fibrosis and nociception and is a potentially novel target for the treatment of persistent pain associated with chronic pancreatitis.

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