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Incorporation of complementary and provocative test swallows to the high-resolution manometry (HRM) protocol offers potential to address limitations posed by HRM protocols that involve only a single swallow type. The aim of this study is to describe normal findings of a comprehensive HRM testing protocol performed on healthy asymptomatic volunteers.

Thirty healthy asymptomatic volunteers completed HRM with 5-mL liquid swallows in the supine position. They also completed 5-mL liquid swallows in the upright position, viscous swallows, solid test swallows, multiple rapid swallows, and a rapid drink challenge. HRM studies were analyzed via Chicago classification version 3.0.

The median (5th-95th percentiles) for integrated relaxation pressure (IRP) on supine swallows was 11 (4-16) mmHg; IRP was lower than supine on upright liquid 9 (0-17) mmHg, viscous 6 (0-15) mmHg, solid 9 (1-19) mmHg, multiple rapid swallows 3 (0-12) mmHg, and rapid drink challenge 5 (-3-12) mmHg;

< 0.005. While an “elevated” IRP vdividual metrics.

Esophageal high-resolution manometry (HRM) enables the comprehensive evaluation of the esophageal motor function. However, protocols are not uniform and clinical practices vary widely among institutions. This study aims to understand the current HRM practice in Korea.

The survey was sent via email through the Korean Society of Neurogastroenterology and Motility. The questions covered descriptive information, preparation, techniques, analysis, and reporting of esophageal HRM.

The survey was completed in 32 (74.4%) out of 43 centers, including 24 tertiary and 8 secondary referral centers. Of the 32 centers, 25 (78.1%) performed HRM in a sitting position, while 7 centers (21.9%) reported performing HRM in a supine position. All the centers utilized single wet swallows as a standard, but the volume, frequency, and interval between swallows varied widely. Sixteen centers (50.0%) applied adjunctive tests, including multiple rapid swallows (n = 16) and rapid drink challenges (n = 9). Parameters assessed and documented in the report were similar. In addition to the assessment of the esophagogastric junction and esophageal body, 27 centers (84.8%) and 18 centers (56.3%) included measurements for the upper esophageal sphincter and the pharynx, respectively, in the HRM protocol.

We found a variation in the available HRM practice among centers, even though they broadly agreed in the data analysis. Efforts are needed to develop a standardized protocol for HRM measurement.

We found a variation in the available HRM practice among centers, even though they broadly agreed in the data analysis. Efforts are needed to develop a standardized protocol for HRM measurement.Functional dyspepsia (FD) is considered to be a heterogeneous disorder with different pathophysiological mechanisms or pathogenetic factors. In addition to traditional mechanisms, novel concepts regarding pathophysiologic mechanisms of FD have been proposed. Candidates of therapeutic agents based on novel concepts have also been suggested. FD is a symptom complex and currently diagnosed by symptom-based Rome criteria. In the Rome criteria, symptom-based subtypes of FD including postprandial distress syndrome and epigastric pain syndrome are recommended to be used, based on the assumption that each subtype is more homogenous in terms of underlying pathophysiologic mechanisms than FD as a whole. In this review, the usefulness of symptombased subtypes of FD for predicting underlying pathophysiologic mechanisms and choosing appropriate therapeutic agents was evaluated. Although several classic pathophysiologic mechanisms are suggested to be associated with individual dyspeptic symptoms, symptom-based subtypes of FD are not specific for a certain pathogenetic factor or pathophysiologic mechanism, and may be frequently associated with multiple pathophysiologic abnormalities. Novel concepts on the pathophysiology of FD show complex interactions between pathophysiologic mechanisms and pathogenetic factors, and prediction of underlying mechanisms of individual patients simply by the symptom pattern or symptom-based subtypes may not be accurate in a considerable proportion of cases. Therefore, subtyping by the Rome criteria appears to have limited value to guide therapeutic strategy, suggesting that the addition of objective parameters or subclassification reflecting physiologic or pathologic tests may be necessary for the targeted therapeutic approaches, particularly when therapeutic agents targeting novel mechanisms are available.An active compound, triterpene saponin, astersaponin I (AKNS-2) was isolated from Aster koraiensis Nakai (AKNS) and the autophagy activation and neuroprotective effect was investigated on in vitro and in vivo Parkinson’s disease (PD) models. The autophagy-regulating effect of AKNS-2 was monitored by analyzing the expression of autophagy-related protein markers in SHSY5Y cells using Western blot and fluorescent protein quenching assays. The neuroprotection of AKNS-2 was tested by using a 1-methyl-4-phenyl-2,3-dihydropyridium ion (MPP+)-induced in vitro PD model in SH-SY5Y cells and an MPTP-induced in vivo PD model in mice. selleck The compound-treated SH-SY5Y cells not only showed enhanced microtubule-associated protein 1A/1B-light chain 3-II (LC3-II) and decreased sequestosome 1 (p62) expression but also showed increased phosphorylated extracellular signal-regulated kinases (p-Erk), phosphorylated AMP-activated protein kinase (p-AMPK) and phosphorylated unc-51-like kinase (p-ULK) and decreased phosphorylated mammalian target of rapamycin (p-mTOR) expression. AKNS-2-activated autophagy could be inhibited by the Erk inhibitor U0126 and by AMPK siRNA. In the MPP+-induced in vitro PD model, AKNS-2 reversed the reduced cell viability and tyrosine hydroxylase (TH) levels and reduced the induced α-synuclein level. In an MPTP-induced in vivo PD model, AKNS-2 improved mice behavioral performance, and it restored dopamine synthesis and TH and α-synuclein expression in mouse brain tissues. Consistently, AKNS-2 also modulated the expressions of autophagy related markers in mouse brain tissue. Thus, AKNS-2 upregulates autophagy by activating the Erk/mTOR and AMPK/mTOR pathways. AKNS-2 exerts its neuroprotective effect through autophagy activation and may serve as a potential candidate for PD therapy.