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      Effects of pacifier and taste on swallowing, esophageal motility, transit, and respiratory rhythm in human neonates

      1 , 1 , 1 , 2
      Neurogastroenterology & Motility
      Wiley

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          Abstract

          <div class="section"> <a class="named-anchor" id="S1"> <!-- named anchor --> </a> <h5 class="section-title" id="d5289654e133">Background</h5> <p id="P1">Pacifier use is widely prevalent globally despite hygienic concerns and uncertain mechanistic effects on swallowing or airway safety. </p> </div><div class="section"> <a class="named-anchor" id="S2"> <!-- named anchor --> </a> <h5 class="section-title" id="d5289654e138">Aims</h5> <p id="P2">The effects of pacifier and taste interventions on pharyngo-esophageal motility, bolus transit and respiratory rhythms were investigated by determining the upper esophageal sphincter (UES), esophageal body, esophagogastric junction (EGJ) motor patterns as well as deglutition apnea, respiratory rhythm disturbances and esophageal bolus clearance. </p> </div><div class="section"> <a class="named-anchor" id="S3"> <!-- named anchor --> </a> <h5 class="section-title" id="d5289654e143">Methods</h5> <p id="P3">Fifteen infants (6 males; median gestation 31 wks and birth weight 1.4 kg) underwent high resolution impedance manometry at 43 (41-44) weeks post-menstrual age. Manometric, respiratory, and impedance characteristics of spontaneous swallows, pacifier associated dry swallowing and taste (pacifier dipped in 3% sucrose) associated swallowing were analyzed. Linear mixed and generalized estimating equation models were used. Data are presented as mean ± SEM, %, or median (IQR). </p> </div><div class="section"> <a class="named-anchor" id="S4"> <!-- named anchor --> </a> <h5 class="section-title" id="d5289654e148">Key Results</h5> <p id="P4">Pharyngo-esophageal motility, respiratory, and impedance characteristics of 209 swallows were analyzed (85 spontaneous swallows, 63 pacifier associated dry swallows, 61 taste associated swallows). Basal UES and EGJ pressures decreased upon pacifier (P&lt;0.05) and taste interventions (P&lt;0.05); however, esophageal motility, respiratory rhythm, and impedance transit characteristics were similar with both interventions. </p> </div><div class="section"> <a class="named-anchor" id="S5"> <!-- named anchor --> </a> <h5 class="section-title" id="d5289654e153">Conclusions and Inferences</h5> <p id="P5">Oral stimulus with pacifier or taste interventions decreases UES and EGJ basal pressure, but has no effects on pharyngo-esophageal motility, airway interactions, or esophageal bolus transit. A decrease in central parasympathetic-cholinergic excitatory drive is likely responsible for the basal effects. </p> </div>

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          Most cited references41

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          Regulation of salivary gland function by autonomic nerves.

          Oral homeostasis is dependent upon saliva and its content of proteins. Reflex salivary flow occurs at a low 'resting' rate and for short periods of the day more intense taste or chewing stimuli evoke up to ten fold increases in salivation. The secretion of salivary fluid and proteins is controlled by autonomic nerves. All salivary glands are supplied by cholinergic parasympathetic nerves which release acetylcholine that binds to M3 and (to a lesser extent) M1 muscarinic receptors, evoking the secretion of saliva by acinar cells in the endpieces of the salivary gland ductal tree. Most salivary glands also receive a variable innervation from sympathetic nerves which released noradrenaline from which tends to evoke greater release of stored proteins, mostly from acinar cells but also ductal cells. There is some 'cross-talk' between the calcium and cyclic AMP intracellular pathways coupling autonomic stimulation to secretion and salivary protein secretion is augmented during combined stimulation. Other non-adrenergic, non-cholinergic neuropeptides released from autonomic nerves evoke salivary gland secretion and parasympathetically derived vasointestinal peptide, acting through endothelial cell derived nitric oxide, plays a role in the reflex vasodilatation that accompanies secretion. Neuronal type, calcium-activated, soluble nitric oxide within salivary cells appears to play a role in mediating salivary protein secretion in response to autonomimetics. Fluid secretion by salivary glands involves aquaporin 5 and the extent to which the expression of aquaporin 5 on apical acinar cell membranes is upregulated by cholinomimetics remains uncertain. Extended periods of autonomic denervation, liquid diet feeding (reduced reflex stimulation) or duct ligation cause salivary gland atrophy. The latter two are reversible, demonstrating that glands can regenerate provided that the autonomic innervation remains intact. The mechanisms by which nerves integrate with salivary cells during regeneration or during salivary gland development remain to be elucidated.
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            Chicago classification criteria of esophageal motility disorders defined in high resolution esophageal pressure topography.

            The Chicago Classification of esophageal motility was developed to facilitate the interpretation of clinical high resolution esophageal pressure topography (EPT) studies, concurrent with the widespread adoption of this technology into clinical practice. The Chicago Classification has been an evolutionary process, molded first by published evidence pertinent to the clinical interpretation of high resolution manometry (HRM) studies and secondarily by group experience when suitable evidence is lacking. This publication summarizes the state of our knowledge as of the most recent meeting of the International High Resolution Manometry Working Group in Ascona, Switzerland in April 2011. The prior iteration of the Chicago Classification was updated through a process of literature analysis and discussion. The major changes in this document from the prior iteration are largely attributable to research studies published since the prior iteration, in many cases research conducted in response to prior deliberations of the International High Resolution Manometry Working Group. The classification now includes criteria for subtyping achalasia, EGJ outflow obstruction, motility disorders not observed in normal subjects (Distal esophageal spasm, Hypercontractile esophagus, and Absent peristalsis), and statistically defined peristaltic abnormalities (Weak peristalsis, Frequent failed peristalsis, Rapid contractions with normal latency, and Hypertensive peristalsis). The Chicago Classification is an algorithmic scheme for diagnosis of esophageal motility disorders from clinical EPT studies. Moving forward, we anticipate continuing this process with increased emphasis placed on natural history studies and outcome data based on the classification. © 2012 Blackwell Publishing Ltd.
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              Does breastfeeding reduce the risk of sudden infant death syndrome?

              In the last 20 years, the prevention campaigns to reduce the risk of sudden infant death syndrome were very successful. In some countries the advice to breastfeed is included in the campaigns' messages, but in other countries it is not. To examine the association between type of infant feeding and sudden infant death syndrome. The German Study of Sudden Infant Death is a case-control study of 333 infants who died of sudden infant death syndrome and 998 age-matched controls. A total of 49.6% of cases and 82.9% of controls were breastfed at 2 weeks of age. Exclusive breastfeeding at 1 month of age halved the risk, partial breastfeeding at the age of 1 month also reduced the risk of sudden infant death syndrome, but after adjustment this risk was not significant. Being exclusively breastfed in the last month of life/before the interview reduced the risk, as did being partially breastfed. Breastfeeding survival curves showed that both partial breastfeeding and exclusive breastfeeding were associated with a reduced risk of sudden infant death syndrome. This study shows that breastfeeding reduced the risk of sudden infant death syndrome by approximately 50% at all ages throughout infancy. We recommend including the advice to breastfeed through 6 months of age in sudden infant death syndrome risk-reduction messages.
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                Author and article information

                Journal
                Neurogastroenterology & Motility
                Neurogastroenterol. Motil.
                Wiley
                13501925
                April 2016
                April 2016
                January 04 2016
                : 28
                : 4
                : 532-542
                Affiliations
                [1 ]Neonatal and Infant Feeding Disorders Program; Center for Perinatal Research; Nationwide Children's Hospital; Columbus OH USA
                [2 ]Division of Pediatric Gastroenterology and Nutrition; Nationwide Children's Hospital; The Ohio State University; Columbus OH USA
                Article
                10.1111/nmo.12748
                4808369
                26727930
                5d0cacf9-8bd2-4535-a0cd-026e772ef2bd
                © 2016

                http://doi.wiley.com/10.1002/tdm_license_1.1

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