Objective To compare the effect of treating cricopharyngeal achalasia in stroke survivors using transnasal or transoral balloon dilatation.Methods Thirty stroke survivors with cricopharyngeal achalasia were randomly divided into a transnasal and a transoral balloon dilatation group (group N and group O),each of 15.Both groups were given routine swallowing rehabilitation training as well as the transnasal or transoral balloon dilatation.Their heart rate was monitored during the dilatation.Nasal bleeding,mucous membrane swelling and pain were also observed.Their swallowing function was evaluated using the Fujishima Ichiro swallowing efficacy score (FISE) and videofluoroscopy (VFSS) before and after the intervention.Results After the treatment,the average FISE and VFSS scores of both groups had improved significantly comnpared to before the treatment but there were no significant differences between the groups.During the treatment,the average heart rate of group O increased significantly less than that of group N.The treatment acceptance of group O was 98.2％,significantly higher than that of group N (80.1％).One case of mucosal bleeding was observed in group O,and laryngeal edema occurred significantly less often than in group N (9 cases vs.7).The average pain score was also significantly lower in group O.Conclusions Balloon dilatation facilitates swallowing among stroke survivors with cricopharyngeal achalasia.The transoral approach can help to reduce the occurrence of complications such as mucosal bleeding,laryngeal edema and pain,and has better patient acceptance.

Objective:To evaluate the accuracy of lung recruitment maneuver (LRM) combined with brachial artery peak velocity variation (ΔVp) in predicting fluid responsiveness.Methods:Sixty-four patients of both sexes, aged 18-64 yr, with body mass index 19-26 kg/m 2, of American Society of Anesthesiologists physical status Ⅰor Ⅱ, with New York Heart Association class Ⅰor Ⅱ, scheduled for elective open gastrointestinal surgery under general anesthesia, were enrolled in this study.LRM (positive airway pressure was maintained at 30 cmH 2O for 10 s) and volume loading test were performed in sequence after anesthesia induction.ΔVp was measured by ultrasonography at the beginning of LRM.Mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP) and stroke volume (SV) were recorded before LRM (T 1), during LRM (T 2), before volume expansion (T 3) and after volume expansion (T 4). The changing rate of each index before and after LRM (ΔMAP LRM, ΔHR LRM, ΔCVP LRM, ΔSV LRM) and before and after volume expansion (ΔMAP VE, ΔHR VE, ΔCVP VE, ΔSV VE) were calculated.ΔSV VE≥15% was considered to be a positive response after volume expansion, and patients were divided into response group (≥ 15%, R group) and non-response group (< 15%, NR group). Results:There were 34 cases in R group and 30 cases in NR group.Compared with NR group, MAP at T 2 and SV at T 1, 2 were significantly decreased, ΔMAP LRM, ΔMAP VE, ΔSV LRM and ΔSV VE were increased, and ΔVp was increased in group R ( P<0.05). There was a positive correlation between ΔVp and ΔSV VE ( r=0.829, P<0.05), a negative correlation between ΔSV LRM and ΔSV VE ( r=-0.876, P<0.05), and a negative correlation between ΔVp and ΔSV LRM ( r=-0.819, P<0.05). The area under the receiver operating characteristic curve of LRM combined with ΔVp was 0.808, and the cut-off value was 32.3%, the sensitivity 75.3%, and the specificity 88.2%. Conclusion:LRM combined with ΔVp (≥32.3%) can accurately predict the intraoperative fluid responsiveness in patients.

Background Arsenic is a toxicant that can affect the expressions of the cellular anti-apoptotic gene BCL-2 and its protein, but the effects of arsenic on BCL-2α and BCL-2\begin{document}$\beta $\end{document} transcripts have not been reported. Objective To investigate the potential effects of arsenic and its metabolites, methylarsonic acid (MMA) and dimethylarsonic acid (DMA), on BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T (total of α and \begin{document}$\beta $\end{document} transcripts) in human bronchial epithelial cells (16HBE) and human lung adenocarcinoma cells (A549). Methods 16HBE cells and A549 cells were randomly divided into three categories of exposure after in vitro culture: single-selected arsenic compound exposure groups with isoconcentration (16HBE cells were treated with 4.5 μmol·L⁻¹ of MMA, DMA, and sodium arsenite, respectively, while A549 cells were treated with 60 μmol·L⁻¹ of MMA, DMA, and sodium arsenite, respectively), sodium arsenite exposure groups with different concentrations (16HBE cells were treated with 1.5, 3.0, and 4.5 μmol·L⁻¹ of sodium arsenite respectively, while A549 cells were treated with 20, 40, and 60 μmol·L⁻¹ of sodium arsenite respectively), and combined exposure groups (i.e. MMA+sodium arsenite, and DMA+sodium arsenite; the exposure concentrations of 16HBE cells were both 1.5 μmol·L⁻¹ and both 4.5 μmol·L⁻¹ respectively, and those of A549 cells were both 20 μmol·L⁻¹ and both 60 μmol·L⁻¹ respectively). Meanwhile, a blank control group was also set up in each exposure category. After 48 h of continuous exposure, the relative expressions of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T in both cells were detected by real-time PCR. Results Regarding the single-selected arsenic compound exposure, in 16HBE cells, the expression levels of BCL-2α and BCL-2T under 4.5 μmol·L⁻¹ MMA treatment were lower than those in their control groups (q=3.27, 2.93, both P<0.05), and the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T under 4.5 μmol·L⁻¹ sodium arsenite were lower than those in their respective control groups (q=11.06, 3.65, 10.70, all P<0.05). In A549 cells, the expression level of BCL-2T treated with 60 μmol·L⁻¹ DMA was lower than that in the control group (q=3.12, P<0.05), and the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T treated with 60 μmol·L⁻¹ sodium arsenite were lower than those in their respective control groups (q=7.59, 7.27, 8.06, all P<0.05). Regarding the sodium arsenite exposure: 16HBE cells treated with 1.5 μmol·L⁻¹ sodium arsenite had a lower expression level of BCL-2α and a higher expression level of BCL-2\begin{document}$\beta $\end{document} than those in their respective control groups (q=6.06, 11.92, both P<0.05); the expression level of BCL-2α under 3.0 μmol·L⁻¹ sodium arsenite was lower than that in the control group (q=12.72, P<0.05); and under 4.5 μmol·L⁻¹ sodium arsenite treatment, the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T were lower than those in their respective control groups (q=15.72, 6.79, 6.62, all P<0.05). The expression levels of BCL-2α gradually decreased with increasing concentrations of sodium arsenite (F_{α trend}=144.80, P<0.001), while BCL-2\begin{document}$\beta $\end{document} and BCL-2T decreased in a dose-dependent manner in the range of 1.5-4.5 μmol·L⁻¹ (F\begin{document}${}_{\beta } $\end{document} _trend=135.40, F_{T trend}=38.24, both P<0.001). In A549 cells, the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T under each concentration of sodium arsenite treatments were lower than those in their respective control groups (all P<0.05); the results of further trend tests showed that their expression levels gradually decreased with increasing concentrations of sodium arsenite (F_{α trend} =31.97, F\begin{document}${}_{\beta} $\end{document} _trend=549.50, F_{T trend}=252.40, all P<0.001). Regarding the combined exposure, under MMA+sodium arsenite treatment at both 60 μmol·L⁻¹, the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T in A549 cells were higher than those in their respective control groups (q=6.37, 14.91, 5.33, all P<0.05); under DMA+sodium arsenite treatment at both 60 μmol·L⁻¹, their expression levels in A549 cells were also higher than those in their respective control group (q=8.60, 17.29, 6.91, all P<0.05). Conclusion Exposure to a high concentration (16HBE: 4.5 μmol·L⁻¹, A549: 60 μmol·L⁻¹) of a single arsenic metabolite has no effect on BCL-2 transcripts in 16HBE cells and A549 cells. Exposure to a low concentration (1.5 μmol·L⁻¹) of sodium arsenite alone would decrease the expression level of BCL-2α and increase the expression level of BCL-2\begin{document}$\beta $\end{document} in 16HBE cells, and exposure to all designed concentrations of sodium arsenite alone would decrease the expressions of all transcripts in A549 cells. The combined exposure to high concentrations (both 60 μmol·L⁻¹) of MMA plus sodium arsenite or high concentrations (both 60 μmol·L⁻¹) of DMA plus sodium arsenite would increase the expressions of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T in A549 cells, which are different from the effects presented by single exposure.