Numerous previous studies have demonstrated that ghrelin promotes gastric motility when administered peripherally. This effect appears to be regulatory but not directly stimulatory, and therefore may involve a number of complex mechanisms. In the periphery, ghrelin may affect gastric motility through intercellular networks among interstitial cells of Cajal, myenteric nerve cells and smooth muscle cells. The aim of the present study was to investigate the effects and possible mechanisms underlying this hypothesis. The effects of ghrelin on the contraction force of gastric antrum smooth muscle strips of rats were studied in the presence or absence of carbachol (CCh), [D‑Lys3]‑GHRP‑6, atropine, tetrodotoxin (TTX) and nimodipine in vitro. The expression of ghrelin receptors (GHS‑Rs) on different cell types in gastric muscle layers was observed by means of immunofluorescence. Ghrelin enhanced smooth muscle strip contraction induced by CCh, but when CCh was absent, this effect was eliminated. Atropine and nimodipine eradicated the muscle strip contraction enhanced by ghrelin, while [D‑Lys3]‑GHRP‑6 was only able to partly block this effect and TTX had no effect on muscle strip contraction. It was identified that ghrelin had no effect on the contractive rhythm of the strips. GHS‑R1s were located differentially depending on the cell type, including myenteric nerve cells, interstitial cells of Cajal and smooth muscle cells. In conclusion the present study demonstrated that ghrelin may act as an adjuvant to regulate gastric smooth muscle contraction induced by CCh through GHS‑R1s, which are expressed on myenteric nerve cells, Cajal cells and smooth muscle cells. Ghrelin may exert its effects by influencing the functional status of different cell types in the gastric muscle layer to subsequently enhance the contractive effect of cholinergic neurotransmitters and enhance gastric motility.
Background Gallbladder carcinoma (GBC) is relatively rare but highly aggressive and it has poor prognosis, especially for metastatic GBC. We aimed to determine the prognostic significance of primary tumor resection on patients with metastatic GBC. Material/Methods The records of patients with GBC with distant metastasis from 2010 to 2015 were extracted from the Surveillance, Epidemiology, and End Results (SEER) database. Kaplan-Meier methods were used to compare overall survival (OS) and carcinoma-specific survival (CSS) between patients receiving primary tumor resection and those without surgery. Cox regression analysis was conducted to identity independent factors significantly associated with survival. In addition, a propensity score-matched analysis was performed to adjust for the heterogeneity between the groups. Results Of the 1337 patients included, 496 patients underwent primary tumor resection and 841 patients did not. Multivariate Cox regression analysis showed that OS (hazard ratio [HR]: 0.56, 95% confidence interval [CI]: 0.48–0.66, P <0.001) and CSS (HR: 0.57, 95% CI: 0.48–0.66, P <0.001) were significantly improved in patients receiving surgical resection of the primary tumor lesion in the unmatched cohort. Additionally, in the matched cohort, univariate Cox regression analysis similarly indicated that performing surgery at the primary site was associated with better OS (HR: 0.62, 95% CI: 0.50–0.77, P <0.001) and CSS (HR: 0.61, 95% CI: 0.50–0.762, P <0.001). Conclusions This study indicated that primary tumor resection might prolong survival in patients with metastatic GBC.
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