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The beam transport process plays a crucial role in the design and realization of negative-ion-based neutral beam injection (N-NBI) systems for thermonuclear fusion. In particular, space charge compensation (SCC), where positive ions generated by collisions between negative ions and background gas mitigate space charge effects, serves as a critical mechanism influencing beam divergence and envelope evolution. In this work, the SCC process in N-NBI systems and its impact on beam transport are investigated using a 3D simulation model based on a Vlasov beam-tracing algorithm. Systematic simulations show that SCC evolution and downstream beam optics are jointly controlled by background gas pressure and beam energy, with higher pressure and higher energy strengthening SCC and mitigating divergence and envelope growth downstream of the extraction system. A key physical observation is that collisionless phase mixing drives the transverse velocity distribution of secondary ions toward a Maxwellian distribution, enabling an effective transverse ion temperature that quantitatively correlates with SCC degree. The residual electric field leaking downstream of the extraction system locally weakens SCC over a finite extent, producing negligible beam optics impact for the ITER-relevant 1 MeV case at pressures of 5 × 10 − 3 Pa and 1 × 10 − 2 Pa , but non-negligible transport sensitivity at 200 keV under the same pressure range. These results provide new insight into the interplay between SCC, secondary-ion dynamics, and beam transport, with direct relevance to the modeling and optimization of high-energy NBI beamlines.

Introduction Postoperative ileus (POI) is a heavy burden for healthcare industries and reduces the postoperative quality of life. The aim of this study was to investigate the effects and mechanisms of the intraoperative vagus nerve stimulation (iVNS) on gastrointestinal motility in a rodent model of POI. Methods For control group (control, n  = 8), electrodes were placed on the chest wall for recording the electrocardiogram and on the stomach and small intestine for measuring gastric slow waves (GSWs) and small intestinal slow waves (SSWs). For sham group (sham, n  = 8) and iVNS group (VNS, n  = 8), after the same surgery as the control, intestinal manipulation (IM) was performed to induce POI. iVNS was performed during the surgery for the iVNS group. Small intestinal transit (SIT), gastric emptying (GE), postoperative pain, and plasma TNF-α were evaluated after operation. Results IM delayed GE that was normalized by iVNS ( P  < 0.05). iVNS reduced plasma TNF-α increased by IM ( P  = 0.04). iVNS prevents the injury of ileum mucosa induced by IM ( P  < 0.05). iVNS reduced the postoperative pain ( P  < 0.05). iVNS prevented the IM-induced decrease in vagal activity (sham 0–30 min vs. 150–180 min, P  = 0.03, VNS 0–30 min vs. 150–180 min, P  = 0.58) and increase in sympathovagal balance (sham 0–30 min vs. 150–180 min, P  = 0.04, VNS 0–30 min vs. 150–180 min, P  = 0.72). Conclusions iVNS accelerates postoperative recovery by improving GE, reducing postoperative pain, and preventing the injury of ileum mucosa mediated via the autonomic mechanisms.

Patients with ulcerative colitis are typically suspected of an inflammatory flare based on suggestive symptoms of inflammation. The aim of this study was to evaluate the impact of inflammation on colonic motility and rectal sensitivity from active to recovery of inflammation. Male rats were given drinking water with 5% dextran sulfate sodium for 7 days. Inflammation, intestinal motor and sensory functions were investigated weekly for 6 weeks. (1) The disease activity index score, fecal calprotectin and tumor necrosis factor alpha were increased from Day 0 to Day 7 (active inflammation) and then decreased gradually until recovery. (2) Distal colon transit was accelerated on Day 7, and then remained unchanged. Whole gut transit was delayed on Day 7 but accelerated from Day 14 to Day 42. (3) Rectal compliance was unaffected from Day 0 to Day 7, but decreased afterwards. (4) Rectal hypersensitivity was noted on Day 7 and persistent. (5) Plasma acetylcholine was decreased on Day 7 but increased from Day 14 to Day 42. Nerve growth factor was increased from Day 7 to Day 42. DSS-induced inflammation leads to visceral hypersensitivity that is sustained until the resolution of inflammation, probably mediated by NGF. Rectal compliance is reduced one week after the DSS-induced inflammation and the reduction is sustained until the resolution of inflammation. Gastrointestinal transit is also altered during and after active colonic inflammation.

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 Constipation Quality of Life (PAC-QOL), and anorectal motility were 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 = 0.0 1 ) . (2) TN improved PAC-SYM and PAC-QOL scores ( P < 0.00 1 , resp.). (3) TN significantly decreased the threshold volume to elicit RAIR ( P < 0.05 ) , ameliorated rectal sensory threshold ( P = 0.04 ) , and maximum tolerance ( 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.

This study summarizes our current research in using different types of nanographene platelets (NGPs) to create polymer–graphene nanocomposites for selective laser sintering manufacturing application. This article describes five NGPs that were available to our research group. Morphological characterization of their microstructures was examined using scanning electron microscopy. Thermal characterization of these NGPs was conducted using thermogravimetric analysis. Kinetics of these NGPs was calculated using the isoconversion technique. Similarities and differences of these NGPs were drawn from the above measurements and calculations. Two NGPs were selected for further studies.

•  Subtypes and functions of ICC in the gut ‐  Subtypes of ICC ‐  ICC along the gut ‐  Functions of ICC •  Mutant animal models used in in vitro and in vivo studies •  Roles of ICC in generating slow waves ‐  Gastrointestinal slow waves and their clinical ‐  significance ‐  In vitro studies ‐  In vivo studies •  Roles of ICC in regulating gastrointestinal motility ‐  Gastrointestinal motility and roles of slow waves ‐  Roles of ICC in regulating peristaltic contractions •  Roles of ICC in mediating neural transmission ‐  In vitro studies ‐  LOS and pylorus sphincter ‐  Stomach ‐  Small intestine ‐  Colon ‐  In vivo studies ‐  Lower oesophageal sphincter ‐  Stomach ‐  Colon ‐  Anal sphincter •  Roles of ICC as mechanoreceptors •  Conclusions The aim of this article is to provide a better understanding of the roles of interstitial cells of Cajal (ICC) in regulating gastrointestinal motility by reviewing in vitro and in vivo physiological motility studies. Based on the in vitro studies, ICC are proposed to have the following functions: to generate slow waves, to mediate neurotransmission between the enteric nerves and the gastrointestinal muscles and to act as mechanoreceptors. However, there is limited evidence available for these hypotheses from the in vivo motility studies. In this review, we first introduce the major subtypes of ICC and their established functions. Three Kit mutant mouse and rodent models are presented and the loss of ICC subtypes in these mutants is reviewed. The physiological motility findings from various in vitroand in vivo experiments are discussed to give a critical review on the roles of ICC in generating slow waves, regulating gastrointestinal motility, mediating neural transmission and serving as mechanoreceptors. It is concluded that the role of ICC as pacemakers may be well established, but other cells may also be involved in the generation of slow waves; the theory that ICC are mediators of neurotransmission is challenged by the majority of the in vivo motility studies; the hypothesis that ICC are mechanoreceptors has not found supportive evidence from the in vivo studies yet. More studies are needed to explain discrepancies in motility findings between the in vitro and in vivo experiments.

Neuromodulation based on the vagal anti‐inflammatory reflex has emerged as an exciting therapeutic approach for chronic inflammatory diseases. However, it is unclear whether direct stimulation of the vagus or of pelvic nerves coming from sacral roots, providing the bulk of colonic parasympathetic innervation, is the best approach. We hypothesized that sacral nerve stimulation (SNS) would be an effective treatment for colitis. Age and sex‐matched Sprague‐Dawley rats were administered 5% dextran sulphate sodium (DSS) in drinking water ad libitum for 7 days. A group of rats was sacrificed after DSS treatment, and the remaining rats were randomized to either sham‐SNS or SNS groups, which were performed for 1 hr daily for 10 days. Stimulations were delivered via chronically implanted electrodes using an 8‐channel universal pulse generator. Sacral nerve stimulation promoted recovery of colitis demonstrated by decreased disease activity index, myeloperoxidase activity, tissue TNF‐alpha, and histological scores as well as an increased colonic M2 macrophage population. Heart rate variability analysis demonstrated a decrease in low frequency and increase in high frequency with SNS, corresponding to increased vagal tone. Additionally, plasma pancreatic peptide was increased and norepinephrine was decreased after SNS in colitis while colon tissue acetylcholine was increased with SNS. This is the first study to the best of our knowledge that demonstrates the benefit of SNS with autonomic mediation. SNS alters the expression of inflammatory cytokines and macrophages as well as modulates neurotransmitters involved in systemic inflammation. Sacral nerve stimulation has shown clinical promise in other GI conditions such as fecal incontinence; however, the mechanism of sacral nerve stimulation has not been fully elucidated. In a DSS rodent model, we show that sacral nerve stimulation ameliorates colitis, and is associated with increased vagal expression. These results indicate that sacral nerve stimulation may signal via an autonomic mechanism to potentially attenuate inflammatory bowel disease in humans.

This study aims to investigate the role of transcutaneous neuromodulation (TN) on the regulation of gastrointestinal hormones and bile acids in patients with functional constipation (FC). Twenty FC patients were treated with TN for four weeks. The effects of TN on symptoms were evaluated by questionnaires. Plasma levels of serotonin (5-HT), motilin, somatostatin, and vasoactive intestinal peptide (VIP) were measured by ELISA and 12 individual bile acids assayed by liquid chromatography tandem mass spectrometry. Results were as follows. (1) TN treatment increased the frequency of spontaneous bowel movement, improved the Bristol Stool Score, and reduced Patient Assessment of Constipation Symptom score and Patient Assessment of Constipation Quality of Life score. (2) FC patients showed decreased plasma levels of 5-HT, motilin, and VIP and an increased plasma level of somatostatin (P<0.05). Four-week TN treatment increased plasma levels of 5-HT and motilin and decreased the plasma level of somatostatin in the FC patients (P<0.05). (3) Taurocholic deoxycholate, taurocholic acid, and taurocholic lithocholic acid were increased in the FC patients (P<0.005) but reduced by TN treatment (P<0.05). This study has suggested that the therapy may improve the symptoms of FC by alleviating the disorders of gastrointestinal hormones and bile acids.

Objective. To investigate effects and possible mechanisms of transcutaneous electrical acustimulation (TEA) performed by a wearable watch-size stimulator for refractory gastroesophageal reflux disease (RGERD). Methods. Twenty patients diagnosed as RGERD were enrolled in the study and randomly divided into four groups: esomeprazole group (Group A), esomeprazole combined with TEA group (Group B), esomeprazole combined with sham-TEA group (Group C), and esomeprazole combined with domperidone group (Group D). HRM and 24 h pH-impedance monitoring and GerdQ score were used to measure related indexes before and after treatment. Results. (1) TEA significantly increased LESP, compared with PPI treatment only or PPI plus sham-TEA. After pairwise comparison, LESP of Group B was increased more than Group A ( P = 0.008 ) or Group C ( P = 0.021 ). (2) PPI plus TEA decreased not only the number of acid reflux episodes but also the number of weak acid reflux episodes ( P = 0.005 ). (3) Heartburn and reflux symptoms were improved more with PPI + TEA than with PPI treatment only or PPI plus sham-TEA (GerdQ scores, P = 0.001 ). Conclusion. TEA can improve symptoms in RGERD patients by increasing LESP and decreasing events of weak acid reflux and acid reflux; addition of TEA to esomeprazole significantly enhances the effect of TEA.