Objective: Lactate clearance is reportedly associated with the outcomes of various critical illnesses. However, few studies have examined the association between lactate clearance and outcomes in patients with gastrointestinal bleeding (GIB). Methods: A single-center retrospective observational study between 2016 and 2020 was conducted. Consecutive adult patients with GIB symptoms (melena, hematemesis, and hematochezia) presenting to the emergency department were included. Lactate clearance was calculated as ([initial lactate-subsequent lactate]/initial lactate)×100. The association between lactate clearance and outcomes was examined by multivariable logistic regression analysis. The primary outcome was the in-hospital mortality. The area under the curve (AUC) of lactate clearance for in-hospital mortality was calculated. The sensitivity and specificity with optimal cutoff values were computed. The AUC of lactate clearance was compared with the Glasgow-Blatchford score and AIMS65 for predicting in-hospital mortality. Results: Three hundred and fifty-one patients were included in the final analysis, and the in-hospital mortality rate was 12%. Lactate clearance was significantly associated with lower in-hospital mortality (odds ratio, 0.991; P=0.016). The AUC of lactate clearance for in-hospital mortality was 0.64. The AUC of Glasgow-Blatchford score and AIMS65 for inhospital mortality was not significantly different from lactate clearance (P=0.759 and P=0.442, respectively). A cutoff lactate clearance of less than 10% had 45.2% sensitivity, 30.7% specificity, 8.2% positive predictive value, and 80.5% negative predictive value for predicting in-hospital mortality. Conclusion Lactate clearance was independently associated with in-hospital mortality in GIB patients. Further prospective studies will be needed to address the prognostic value of lactate clearance in GIB.

Background/Aims: Although second-look endoscopy (SLE) is frequently performed after gastric endoscopic submucosal dissection (ESD) to prevent bleeding, no studies have reported SLE findings after colorectal ESD. This study aimed to investigate SLE findings and their role in preventing delayed bleeding after colorectal ESD. Methods: Post-ESD ulcer appearances were divided into coagulation (with or without remnant minor vessels) and clip closure groups. SLE findings were categorized according to the Forrest classification (high-risk ulcer stigma [type I and IIa] and low-risk ulcer stigma [type IIb, IIc, III, or clip closure]), and risk factors for high-risk ulcer stigma were analyzed. Results: Among the 375 cases investigated, SLEs were performed in 171 (45.6%) patients. The incidences of high-risk ulcer stigma and low-risk stigma were 5.3% (9/171) and 94.7% (162/171), respectively. During SLE, endoscopic hemostasis was performed more frequently in the high-risk ulcer stigma group than in the lowrisk ulcer stigma group (44.4% [4/9] vs. 1.9% [3/162], respectively; p < 0.001), but most of the endoscopic hemostasis in the high-risk ulcer stigma group (3/4, 75.0%) were prophylactic hemostasis. Post-ESD delayed bleeding occurred in three (0.8%) patients belonging to the SLE group, of which, one patient was from the high-risk stigma group and two were from the low-risk stigma group. Conclusions The incidence of high-risk ulcer stigma during SLE was low, and delayed bleeding occurred in, both, high-risk and low-risk groups of SLE. SLEs performed after colorectal ESD may not be effective in preventing delayed bleeding, and further prospective studies are needed to evaluate the efficacy of SLE in post-colorectal ESD.

KCNQ family constitutes slowly-activating potassium channels among voltage-gated potassium channel superfamily. Recent studies suggested that KCNQ4 and 5 channels are abundantly expressed in smooth muscle cells, especially in lower urinary tract including corpus cavernosum and that both channels can exert membrane stabilizing effect in the tissues. In this article, we examined the electrophysiological characteristics of overexpressed KCNQ4, 5 channels in HEK293 cells with recently developed KCNQ-specific agonist. With submicromolar EC50 , the drug not only increased the open probability of KCNQ4 channel but also increased slope conductance of the channel. The overall effect of the drug in whole-cell configuration was to increase maximal whole-cell conductance, to prolongate the activation process, and left-shift of the activation curve. The agonistic action of the drug, however, was highly attenuated by the co-expression of one of the βancillary subunits of KCNQ family, KCNE4. Strong in vitro interactions between KCNQ4, 5 and KCNE4 were found through Foster Resonance Energy Transfer and co-immunoprecipitation. Although the expression levels of both KCNQ4 and KCNE4 are high in mesenteric arterial smooth muscle cells, we found that 1 μM of the agonist was sufficient to almost completely relax phenylephrine-induced contraction of the muscle strip. Significant expression of KCNQ4 and KCNE4 in corpus cavernosum together with high tonic contractility of the tissue grants highly promising relaxational effect of the KCNQspecific agonist in the tissue.

Background/Aims: Although second-look endoscopy (SLE) is frequently performed after gastric endoscopic submucosal dissection (ESD) to prevent bleeding, no studies have reported SLE findings after colorectal ESD. This study aimed to investigate SLE findings and their role in preventing delayed bleeding after colorectal ESD. Methods: Post-ESD ulcer appearances were divided into coagulation (with or without remnant minor vessels) and clip closure groups. SLE findings were categorized according to the Forrest classification (high-risk ulcer stigma [type I and IIa] and low-risk ulcer stigma [type IIb, IIc, III, or clip closure]), and risk factors for high-risk ulcer stigma were analyzed. Results: Among the 375 cases investigated, SLEs were performed in 171 (45.6%) patients. The incidences of high-risk ulcer stigma and low-risk stigma were 5.3% (9/171) and 94.7% (162/171), respectively. During SLE, endoscopic hemostasis was performed more frequently in the high-risk ulcer stigma group than in the lowrisk ulcer stigma group (44.4% [4/9] vs. 1.9% [3/162], respectively; p < 0.001), but most of the endoscopic hemostasis in the high-risk ulcer stigma group (3/4, 75.0%) were prophylactic hemostasis. Post-ESD delayed bleeding occurred in three (0.8%) patients belonging to the SLE group, of which, one patient was from the high-risk stigma group and two were from the low-risk stigma group. Conclusions The incidence of high-risk ulcer stigma during SLE was low, and delayed bleeding occurred in, both, high-risk and low-risk groups of SLE. SLEs performed after colorectal ESD may not be effective in preventing delayed bleeding, and further prospective studies are needed to evaluate the efficacy of SLE in post-colorectal ESD.

KCNQ family constitutes slowly-activating potassium channels among voltage-gated potassium channel superfamily. Recent studies suggested that KCNQ4 and 5 channels are abundantly expressed in smooth muscle cells, especially in lower urinary tract including corpus cavernosum and that both channels can exert membrane stabilizing effect in the tissues. In this article, we examined the electrophysiological characteristics of overexpressed KCNQ4, 5 channels in HEK293 cells with recently developed KCNQ-specific agonist. With submicromolar EC50 , the drug not only increased the open probability of KCNQ4 channel but also increased slope conductance of the channel. The overall effect of the drug in whole-cell configuration was to increase maximal whole-cell conductance, to prolongate the activation process, and left-shift of the activation curve. The agonistic action of the drug, however, was highly attenuated by the co-expression of one of the βancillary subunits of KCNQ family, KCNE4. Strong in vitro interactions between KCNQ4, 5 and KCNE4 were found through Foster Resonance Energy Transfer and co-immunoprecipitation. Although the expression levels of both KCNQ4 and KCNE4 are high in mesenteric arterial smooth muscle cells, we found that 1 μM of the agonist was sufficient to almost completely relax phenylephrine-induced contraction of the muscle strip. Significant expression of KCNQ4 and KCNE4 in corpus cavernosum together with high tonic contractility of the tissue grants highly promising relaxational effect of the KCNQspecific agonist in the tissue.