Objective. To investigate the effects of long pulse gastric electrical stimulation (GES) at a tachygastrial frequency on food intake, gastric tone and gastric myoelectrical activity (GMA). Material and methods. Of twelve dogs implanted with electrodes and a gastric cannula, 6 underwent truncal vagotomy. Stimulus consisted of long pulses with a frequency of 9 cycles/min. Experiment one was performed in all dogs to test for food intake with or without GES. Experiment two on six normal dogs consisted of baseline, GES and recovery periods. Gastric volume and GMA were recorded. Results. 1) GES reduced food intake in both normal (398.5±111.7 g versus 573.0±97.9 g; p<0.02) and vagotomized dogs (170.6±100.4 g versus 401.0±97.3 g; p<0.05). 2) Gastric volume was increased with stimulation from 168.4±17.7 ml to 301.1±34.1 ml (p<0.02 ANOVA) and maintained at 271.8±27.6 ml. 3) The percentages of normal slow waves before, during and after GES were 83.3±4.6%, 38.0±3.5% and 61.0±12.5%, respectively (p=0.02 ANOVA). Conclusion. Long-pulse GES at tachygastrial frequency substantially reduces food intake, and is not mediated by the vagal pathway but attributed to relaxation of the stomach and impairment of intrinsic GMA.
Background Vault is the largest nonicosahedral cytosolic nucleoprotein particle, which is widely involved in induction of chemoresistance and lead to failure in long-term chemotherapy. Vault contains three different major vault proteins (MVPs) and four vault RNAs paralogues (vtRNAs, vtRNA1-1, vtRNA1-2, vtRNA1-3 and vtRNA2-1). Disruption of the MVPs do not induce hypersensitivity while expression of vtRNAs contributes to cells' drug resistance, indicates that vtRNAs, but not MVPs play an important role in causing drug resistance. Polypyrimidine tract binding protein associated splicing factor (PSF) contributes to cell sensitivity to chemotherapy by its transcriptional activity, promotes us to figure out its potential association with vtRNAs. Methods We investigate the interaction between PSF and vtRNAs by electrophoretic mobility shift assays (EMSA) and RNA-immunoprecipitation (IP), and showed the binding between PSF and vtRNAs. Chromatin Immunoprecipitation (ChIP) was performed to detect the effects of vtRNAs on the interaction of PSF with GAGE6 promoter. The role of vtRNAs on chemoresistance in MCF-7 was detected by CCK-8 and EdU staining. The independent role of vtRNAs with MVP is detected by MVP or vtRNAs knockdown. Results The complex with vtRNA1-1 releases PSF, allowing transcription of GAGE6 to proceed. Then we showed that induction of GAGE6 caused drug resistance by promoting cell proliferation and colony formation in soft agar. Ectopic expression of shRNA targets to vtRNA1-1 further confirmed the role of vtRNA1-1 in regulating PSF transcriptional activity independent with the expression of MVP. By vtRNA1-1 or MVP knockdown, it is revealed that vtRNA1-1 caused chemoresistance independent of MVP. Furthermore, knockdown of GAGE6 does not cause drug resistance, indicates the GAGE6 is directly involved in cell proliferation, but not the drug resistance. Conclusion These results suggest that vtRNAs regulates cell proliferation, drug resistance, and possibly other physiological processes of humans, by complex formation with PSF.
Abstract Aim: The aim was to investigate the validity of sonometry on the assessment of gastric volumes in comparison with gastric barostat. Method: Six dogs were implanted with gastric serosal electrodes, sonometric sensors, and a gastric cannula. Experiments were performed to assess sensor distance when an intragastric balloon was inflated with different volumes, after a meal with or without a balloon, and with gastric electrical stimulation. Results: (i) The distance measured using sonometry was reproducible and stable, and there was a correlation between sensor distance and the gastric volume measured with barostat. (ii) Simultaneous recordings by sonometry and barostat showed a similar postprandial response, while the postprandial increase of the sensor distance was much smaller without the balloon (3.2 ± 0.2 mm vs 9.7 ± 1.5 mm, P < 0.02). (iii) The sensor distance was increased with gastric electrical stimulation. Conclusions: Sonometry is able to detect gastric volume changes as validated by gastric perturbations with distensions, food ingestion and electrical stimulation. The postprandial increase in gastric volume measured by sonometry with barostat balloon is greater because of the presence of the intragastric balloon.
Objective. Satiation has recently been shown to be associated with gastric volume or gastric tone. Electrical stimulation has been shown to reduce food intake and increase gastric volume, or reduce gastric tone. The aim of this study was to investigate the correlation between gastric or intestinal electrical stimulation (GES/IES)-induced increase in gastric volume and food intake. Material and methods. GES/IES was performed on 14 dogs implanted with electrodes and a gastric cannula. Food intake was measured and gastric volume was assessed using barostat with or without GES/IES. Results. Food intake was correlated to weight (r=0.62, p = 0.02) as well as the fasting gastric volume (r=0.59, p=0.02). GES/IES reduced food intake (240.8 versus 445.0 g, p<0.005) and increased gastric volume in the fasting state (263.4 versus 74.4 ml, p<0.0001). Reduced food intake was correlated to the preprandial gastric volume (r= − 0.58, p=0.02) and postprandial increase in gastric volume with GES/IES (r=0.56, p=0.03). Conclusions. GES/IES reduces food intake and increases gastric volume measured by barostat. The GES/IES-induced increase in gastric volume (or reduced gastric tone) is correlated with reduced food intake during GES/IES.
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