Background/Aims: Distal mean nocturnal baseline impedance (MNBI) measuring via pH-impedance may be valuable in diagnosing patients with suspected laryngopharyngeal reflux (LPR). However, its wide adoption is hindered by cost and invasiveness. This study investigates whether baseline impedance measured during high-resolution impedance manometry (HRIM-BI) can predict pathological MNBI. Methods: A cross-sectional study in Taiwan included 74 subjects suspected of LPR, who underwent HRIM (MMS) and pH-impedance testing (Diversatek), after stopping proton pump inhibitors for more than 7 days. Subjects with grade C or D esophagitis or Barrett’s esophagus were excluded. The cohort was divided into 2 groups: those with concomitant typical reflux symptoms (CTRS, n = 28) and those with isolated LPR symptoms (ILPRS, n = 46). HRIM-BI measurements focused on both distal and proximal esophagi. Pathological MNBI was identified as values below 2065 Ω, measured 3 cm above the lower esophageal sphincter. Results: In all subjects, distal HRIM-BI values correlated weakly with distal MNBI(r = 0.34-0.39, P < 0.005). However, in patients with ILPRS, distal HRIM-BI corelated moderately with distal MNBI(r = 0.43-0.48, P < 0.005). The areas under the receiver operating characteristic curve was 0.78 (P = 0.001) with a sensitivity of 0.83 and a specificity of 0.68. No correlation exists between distal HRIM-BI and distal MNBI in patients with CTRS, and between proximal HRIM-BI and proximal MNBI in both groups. Conclusions Distal HRIM-BI from HRIM may potentially predict pathological MNBI in patients with ILPRS, but not in those with CTRS. Future outcome studies linked to the metric are warranted.

Background/Aims: Distal mean nocturnal baseline impedance (MNBI) measuring via pH-impedance may be valuable in diagnosing patients with suspected laryngopharyngeal reflux (LPR). However, its wide adoption is hindered by cost and invasiveness. This study investigates whether baseline impedance measured during high-resolution impedance manometry (HRIM-BI) can predict pathological MNBI. Methods: A cross-sectional study in Taiwan included 74 subjects suspected of LPR, who underwent HRIM (MMS) and pH-impedance testing (Diversatek), after stopping proton pump inhibitors for more than 7 days. Subjects with grade C or D esophagitis or Barrett’s esophagus were excluded. The cohort was divided into 2 groups: those with concomitant typical reflux symptoms (CTRS, n = 28) and those with isolated LPR symptoms (ILPRS, n = 46). HRIM-BI measurements focused on both distal and proximal esophagi. Pathological MNBI was identified as values below 2065 Ω, measured 3 cm above the lower esophageal sphincter. Results: In all subjects, distal HRIM-BI values correlated weakly with distal MNBI(r = 0.34-0.39, P < 0.005). However, in patients with ILPRS, distal HRIM-BI corelated moderately with distal MNBI(r = 0.43-0.48, P < 0.005). The areas under the receiver operating characteristic curve was 0.78 (P = 0.001) with a sensitivity of 0.83 and a specificity of 0.68. No correlation exists between distal HRIM-BI and distal MNBI in patients with CTRS, and between proximal HRIM-BI and proximal MNBI in both groups. Conclusions Distal HRIM-BI from HRIM may potentially predict pathological MNBI in patients with ILPRS, but not in those with CTRS. Future outcome studies linked to the metric are warranted.

Background/Aims: Distal mean nocturnal baseline impedance (MNBI) measuring via pH-impedance may be valuable in diagnosing patients with suspected laryngopharyngeal reflux (LPR). However, its wide adoption is hindered by cost and invasiveness. This study investigates whether baseline impedance measured during high-resolution impedance manometry (HRIM-BI) can predict pathological MNBI. Methods: A cross-sectional study in Taiwan included 74 subjects suspected of LPR, who underwent HRIM (MMS) and pH-impedance testing (Diversatek), after stopping proton pump inhibitors for more than 7 days. Subjects with grade C or D esophagitis or Barrett’s esophagus were excluded. The cohort was divided into 2 groups: those with concomitant typical reflux symptoms (CTRS, n = 28) and those with isolated LPR symptoms (ILPRS, n = 46). HRIM-BI measurements focused on both distal and proximal esophagi. Pathological MNBI was identified as values below 2065 Ω, measured 3 cm above the lower esophageal sphincter. Results: In all subjects, distal HRIM-BI values correlated weakly with distal MNBI(r = 0.34-0.39, P < 0.005). However, in patients with ILPRS, distal HRIM-BI corelated moderately with distal MNBI(r = 0.43-0.48, P < 0.005). The areas under the receiver operating characteristic curve was 0.78 (P = 0.001) with a sensitivity of 0.83 and a specificity of 0.68. No correlation exists between distal HRIM-BI and distal MNBI in patients with CTRS, and between proximal HRIM-BI and proximal MNBI in both groups. Conclusions Distal HRIM-BI from HRIM may potentially predict pathological MNBI in patients with ILPRS, but not in those with CTRS. Future outcome studies linked to the metric are warranted.

The aim of this study was to investigate whether β-hydroxybutyric acid(BHB)inhibits the phagocytic function of CD14+monocytes in dairy cows through the ROS(reactive oxygen spe-cies)-NLRP3(NOD-like receptor thermal protein domain associated protein 3)pathway.CD14+monocytes in the blood of postpartum healthy cows were extracted,and 3 mmol/L BHB was added after transfection of small interfering RNA targeting NLRP3(si-NLRP3).Monocytes were pre-treated with 10 nmol/L NLRP3 inhibitor MCC950(CP-456773)or 10 mmol/L ROS scavenger N-acetyl cysteine(NAC),and then was treated with 3 mmol/L BHB for 24 h.The protein abundance of NLRP3 was detected by Western blot and the phagocytosis of monocytes was determined by flow cytometry and immunofluorescence.The results showed that compared with the si-Control+BHB group,the phagocytic function of monocytes in the si-NLRP3+BHB treatment group was significantly increased,while the protein abundance of NLRP3 was significantly decreased.Com-pared with DMSO+BHB group,the phagocytic function of monocytes in MCC950+BHB group was significantly increased.In addition,compared with DMSO+BHB group,the protein abundance of NLRP3 in monocytes was significantly decreased in MCC950+BHB group.Compared with the PBS+BHB group,the phagocytosis of monocytes was significantly increased after the addition of ROS scavenger NAC,while the protein abundance of NLRP3 was significantly decreased.These results indicated that BHB inhibited the phagocytosis of CD14+monocytes in cows via the ROS-NLRP3 pathway.Therefore,regulating the activation of NLRP3 inflammasome may be an effective method to improve the decrease of monocyte phagocytosis in perinatal dairy cows.

The aim of this study was to investigate whether β-hydroxybutyric acid(BHB)inhibits the phagocytic function of CD14+monocytes in dairy cows through the ROS(reactive oxygen spe-cies)-NLRP3(NOD-like receptor thermal protein domain associated protein 3)pathway.CD14+monocytes in the blood of postpartum healthy cows were extracted,and 3 mmol/L BHB was added after transfection of small interfering RNA targeting NLRP3(si-NLRP3).Monocytes were pre-treated with 10 nmol/L NLRP3 inhibitor MCC950(CP-456773)or 10 mmol/L ROS scavenger N-acetyl cysteine(NAC),and then was treated with 3 mmol/L BHB for 24 h.The protein abundance of NLRP3 was detected by Western blot and the phagocytosis of monocytes was determined by flow cytometry and immunofluorescence.The results showed that compared with the si-Control+BHB group,the phagocytic function of monocytes in the si-NLRP3+BHB treatment group was significantly increased,while the protein abundance of NLRP3 was significantly decreased.Com-pared with DMSO+BHB group,the phagocytic function of monocytes in MCC950+BHB group was significantly increased.In addition,compared with DMSO+BHB group,the protein abundance of NLRP3 in monocytes was significantly decreased in MCC950+BHB group.Compared with the PBS+BHB group,the phagocytosis of monocytes was significantly increased after the addition of ROS scavenger NAC,while the protein abundance of NLRP3 was significantly decreased.These results indicated that BHB inhibited the phagocytosis of CD14+monocytes in cows via the ROS-NLRP3 pathway.Therefore,regulating the activation of NLRP3 inflammasome may be an effective method to improve the decrease of monocyte phagocytosis in perinatal dairy cows.

The aim of this study is to investigate whether β-hydroxybutyrate(BHB)impaired the mitochondrial function of dairy cow monocytes through the peroxisome proliferator-activated re-ceptor γ coactivator 1 alpha(PGC-1α)signaling pathway.According to the clinical symptoms and the concentration of BHB in whole blood,the tail vein blood of 12 healthy cows(BHB＜1.2 mmol/L)and 12 clinical ketotic cows(CK,BHB＞3.0 mmol/L)was collected.In vivo,after isolation and purification of CD14+monocytes,the intracellular mitochondrial membrane potential was detected by flow cytometry.The protein abundance of oxidative phosphorylation complex cytochrome c oxi-dase subunit Ⅰ(CO Ⅰ),CO Ⅱ,CO Ⅲ,COⅣ,CO Ⅴ,PGC-1 α,mitochondrial transcription factor A(TFAM)and nuclear respiratory factor 1(NFR1)were determined by Western blot.In vitro,CD14+monocytes were co-cultured with 3.0 mmol/L BHB for 0,6,12,24 h.Flow cytometry was applied for intracellular mitochondrial membrane potential detection,and determination the protein abundance of PGC-1α,TFAM and NFR1 by Western blot.The results showed that compared with control group,the mitochondrial membrane potential in CD14+monocytes of ketotic cows was sig-nificantly increased,and the protein abundance of CO Ⅰ,CO Ⅱ,CO Ⅲ,CO Ⅳ,CO Ⅴ PGC-1α,TFAM,and NRF1 in CD14+monocytes of ketotic cows were significantly decreased.Compared with 0 h,the mitochondrial membrane potential of CD14+monocytes was significantly increased after BHB treatment for 6,12,24 h,and the protein abundance of PGC-1α,TFAM and NRF1 were significantly decreased.The results indicated that BHB induced mitochondrial dysfunction in CD14+monocytes of ketotic cows by inhibiting PGC-1α signaling pathway.Therefore,the PGC-1αsignaling pathway may be a preventive and therapeutic target to the mitochondrial dysfunction of monocytes in ketotic cows caused by BHB.

The aim of this study is to investigate whether β-hydroxybutyrate(BHB)impaired the mitochondrial function of dairy cow monocytes through the peroxisome proliferator-activated re-ceptor γ coactivator 1 alpha(PGC-1α)signaling pathway.According to the clinical symptoms and the concentration of BHB in whole blood,the tail vein blood of 12 healthy cows(BHB＜1.2 mmol/L)and 12 clinical ketotic cows(CK,BHB＞3.0 mmol/L)was collected.In vivo,after isolation and purification of CD14+monocytes,the intracellular mitochondrial membrane potential was detected by flow cytometry.The protein abundance of oxidative phosphorylation complex cytochrome c oxi-dase subunit Ⅰ(CO Ⅰ),CO Ⅱ,CO Ⅲ,COⅣ,CO Ⅴ,PGC-1 α,mitochondrial transcription factor A(TFAM)and nuclear respiratory factor 1(NFR1)were determined by Western blot.In vitro,CD14+monocytes were co-cultured with 3.0 mmol/L BHB for 0,6,12,24 h.Flow cytometry was applied for intracellular mitochondrial membrane potential detection,and determination the protein abundance of PGC-1α,TFAM and NFR1 by Western blot.The results showed that compared with control group,the mitochondrial membrane potential in CD14+monocytes of ketotic cows was sig-nificantly increased,and the protein abundance of CO Ⅰ,CO Ⅱ,CO Ⅲ,CO Ⅳ,CO Ⅴ PGC-1α,TFAM,and NRF1 in CD14+monocytes of ketotic cows were significantly decreased.Compared with 0 h,the mitochondrial membrane potential of CD14+monocytes was significantly increased after BHB treatment for 6,12,24 h,and the protein abundance of PGC-1α,TFAM and NRF1 were significantly decreased.The results indicated that BHB induced mitochondrial dysfunction in CD14+monocytes of ketotic cows by inhibiting PGC-1α signaling pathway.Therefore,the PGC-1αsignaling pathway may be a preventive and therapeutic target to the mitochondrial dysfunction of monocytes in ketotic cows caused by BHB.

Purpose: This study was conducted to evaluate the efficacy of bladder outlet surgery in patients with detrusor underactivity (DU) and to identify factors associated with successful outcomes. Methods: We conducted a retrospective review of men diagnosed with DU in urodynamic studies who underwent bladder outlet surgery for lower urinary tract symptoms between May 2018 and April 2023. The International Prostate Symptom Score (IPSS) questionnaire, uroflowmetry (UFM), and multichannel urodynamic studies were administered. Successful treatment outcomes were defined as either an IPSS improvement of at least 50% or the regaining of spontaneous voiding in patients urethral catheterization prior to surgery. Results: The study included 93 male patients. Men diagnosed with significant or equivocal bladder outlet obstruction (BOO) experienced significant postoperative improvements in IPSS (from 20.6 to 6.0 and from 17.4 to 6.5, respectively), maximum urine flow rate (from 5.0 mL/sec to 14.4 mL/sec and from 8.8 mL/sec to 12.2 mL/sec, respectively) and voiding efficiency (from 48.8% to 86.0% and from 61.2% to 85.1%, respectively). However, in the group without obstruction, the improvements in IPSS and UFM results were not significant. The presence of detrusor overactivity (odds ratio [OR], 3.152; P=0.025) and preoperative urinary catheterization (OR, 2.756; P=0.040) were associated with favorable treatment outcomes. Conversely, an unobstructed bladder outlet was identified as a negative prognostic factor. Conclusions In men with DU accompanied by equivocal or significant BOO, surgical intervention to alleviate the obstruction may enhance the IPSS, quality of life, and UFM results. However, those with DU and an unobstructed bladder outlet face a comparatively high risk of treatment failure. Preoperative detrusor overactivity and urinary catheterization are associated with more favorable surgical outcomes. Consequently, active deobstructive surgery should be considered for patients with DU who are experiencing urinary retention.

Ulcerative colitis (UC) is a chronic inflammation of the gastrointestinal tract and is characterized by alternating periods of inflammation and remission. Although UC incidence is lower in Taiwan than in Western countries, its impact remains considerable, demanding updated guidelines for addressing local healthcare challenges and patient needs. The revised guidelines employ international standards and recent research, emphasizing practical implementation within the Taiwanese healthcare system. Since the inception of the guidelines in 2017, the Taiwan Society of Inflammatory Bowel Disease has acknowledged the need for ongoing revisions to incorporate emerging therapeutic options and evolving disease management practices. This updated guideline aims to align UC management with local contexts, ensuring comprehensive and context-specific recommendations, thereby raising the standard of care for UC patients in Taiwan. By adapting and optimizing international protocols for local relevance, these efforts seek to enhance health outcomes for patients with UC.

Crohn’s disease (CD) is a chronic, fluctuating inflammatory condition that primarily affects the gastrointestinal tract. Although the incidence of CD in Taiwan is lower than that in Western countries, the severity of CD presentation appears to be similar between Asia and the West. This observation indicates the urgency for devising revised guidelines tailored to the unique reimbursement system, and patient requirements in Taiwan. The core objectives of these updated guidelines include the updated treatment choices and the integration of the treat-to-target strategy into CD management, promoting the achievement of deep remission to mitigate complications and enhance the overall quality of life. Given the diversity in disease prevalence, severity, insurance policies, and access to medical treatments in Taiwan, a customized approach is imperative for formulating these guidelines. Such tailored strategies ensure that international standards are not only adapted but also optimized to local contexts. Since the inception of its initial guidelines in 2017, the Taiwan Society of Inflammatory Bowel Disease (TSIBD) has acknowledged the importance of continuous revisions for incorporating new therapeutic options and evolving disease management practices. The latest update leverages international standards and recent research findings focused on practical implementation within the Taiwanese healthcare system.