The multiple layers of the skin cover and protect our entire body. Among the skin layers, the epidermis is in direct contact with the outer environment and serves as the first line of defense. The epidermis functions as a physical and immunological barrier. To maintain barrier function, the epidermis continually regenerates and repairs itself when injured. Interactions between tissue-resident immune cells and epithelial cells are essential to sustain epidermal regeneration and repair. In this review, we will dissect the crosstalk between epithelial cells and specific immune cell populations located in the epidermis during homeostasis and wound repair. In addition, we will analyze the contribution of dysregulated immune-epithelial interactions in chronic inflammatory diseases.

Reliable preclinical models for assessing drug-induced cardiotoxicity are essential to reduce the high rate of drug withdrawals during development. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have emerged as a promising platform for such assessments due to their expression of cardiacspecific ion channels and electrophysiological properties. In this study, we investigated the effects of eight arrhythmogenic drugs—E4031, nifedipine, mexiletine, JNJ303, flecainide, moxifloxacin, quinidine, and ranolazine—on hiPSC-CMs derived from both healthy individuals and a long QT syndrome (LQTS) patient using multielectrode array systems. The results demonstrated dose-dependent changes in field potential duration and arrhythmogenic risk, with LQTS-derived hiPSC-CMs showing increased sensitivity to hERG channel blockers such as E4031. Furthermore, the study highlights the potential of hiPSC-CMs to model disease-specific cardiac responses, providing insights into genetic predispositions and personalized drug responses.Despite challenges related to the immaturity of hiPSC-CMs, their ability to recapitulate human cardiac electrophysiology makes them a valuable tool for preclinical cardiotoxicity assessments. This study underscores the utility of integrating patientderived hiPSC-CMs with advanced analytical platforms, such as multi-electrode array systems, to evaluate drug-induced electrophysiological changes. These findings reinforce the role of hiPSC-CMs in drug development, facilitating safer and more efficient screening methods while supporting precision medicine applications.

Background/Aims: Buspirone shows promise in treating disorders of gut–brain interaction (DGBIs), particularly functional dyspepsia. However, findings have been mixed. Methods: We systematically searched for prospective studies testing buspirone for any upper gastrointestinal DGBI in 4 databases (Cochrane, PubMed, Scopus, and PsycInfo). The primary outcome was any validated measure of gastrointestinal symptoms. Anxiety, depression and adverse events were secondary outcomes. For randomized controlled trials (RCTs), we performed random-effects meta-analysis of the standardized mean difference (SMD) in post-treatment scores between buspirone and control groups. Risk of bias in RCTs was assessed using the Cochrane Common Mental Disorders Depression Anxiety and Neurosis Group (CCDAN) scale. Results: Ten studies (n = 283) met inclusion criteria, comprising 5 RCTs, 1 N-of-1 trial, 1 cohort, 1 case series, and 2 case reports. Tolerability of buspirone was good. In meta-analysis, buspirone produced a non-significant improvement in functional dyspepsia/gastroparesis symptoms compared to placebo (SMD = –0.14; 95% CI, –0.44 to 0.17; P = 0.39; I 2 = 0%; N studies = 3). Of individual symptoms, buspirone improved bloating severity more than placebo (SMD = –0.41; 95% CI, –0.77 to –0.04; P = 0.03; N studies = 2) but did not improve post-prandial fullness (P = 0.24, N studies = 2) or nausea (P = 0.75, N studies = 2). All RCTs included in the meta-analysis were good quality but most treated for only 4 weeks. Conclusions We found that buspirone did not improve functional dyspepsia symptoms more than placebo, though studies were small. Buspirone showed benefit for bloating severity, albeit based on few studies. Larger and longer trials of buspirone, targeting more defined groups such as patients with bloating, are warranted.

Reliable preclinical models for assessing drug-induced cardiotoxicity are essential to reduce the high rate of drug withdrawals during development. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have emerged as a promising platform for such assessments due to their expression of cardiacspecific ion channels and electrophysiological properties. In this study, we investigated the effects of eight arrhythmogenic drugs—E4031, nifedipine, mexiletine, JNJ303, flecainide, moxifloxacin, quinidine, and ranolazine—on hiPSC-CMs derived from both healthy individuals and a long QT syndrome (LQTS) patient using multielectrode array systems. The results demonstrated dose-dependent changes in field potential duration and arrhythmogenic risk, with LQTS-derived hiPSC-CMs showing increased sensitivity to hERG channel blockers such as E4031. Furthermore, the study highlights the potential of hiPSC-CMs to model disease-specific cardiac responses, providing insights into genetic predispositions and personalized drug responses.Despite challenges related to the immaturity of hiPSC-CMs, their ability to recapitulate human cardiac electrophysiology makes them a valuable tool for preclinical cardiotoxicity assessments. This study underscores the utility of integrating patientderived hiPSC-CMs with advanced analytical platforms, such as multi-electrode array systems, to evaluate drug-induced electrophysiological changes. These findings reinforce the role of hiPSC-CMs in drug development, facilitating safer and more efficient screening methods while supporting precision medicine applications.

Reliable preclinical models for assessing drug-induced cardiotoxicity are essential to reduce the high rate of drug withdrawals during development. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have emerged as a promising platform for such assessments due to their expression of cardiacspecific ion channels and electrophysiological properties. In this study, we investigated the effects of eight arrhythmogenic drugs—E4031, nifedipine, mexiletine, JNJ303, flecainide, moxifloxacin, quinidine, and ranolazine—on hiPSC-CMs derived from both healthy individuals and a long QT syndrome (LQTS) patient using multielectrode array systems. The results demonstrated dose-dependent changes in field potential duration and arrhythmogenic risk, with LQTS-derived hiPSC-CMs showing increased sensitivity to hERG channel blockers such as E4031. Furthermore, the study highlights the potential of hiPSC-CMs to model disease-specific cardiac responses, providing insights into genetic predispositions and personalized drug responses.Despite challenges related to the immaturity of hiPSC-CMs, their ability to recapitulate human cardiac electrophysiology makes them a valuable tool for preclinical cardiotoxicity assessments. This study underscores the utility of integrating patientderived hiPSC-CMs with advanced analytical platforms, such as multi-electrode array systems, to evaluate drug-induced electrophysiological changes. These findings reinforce the role of hiPSC-CMs in drug development, facilitating safer and more efficient screening methods while supporting precision medicine applications.

The multiple layers of the skin cover and protect our entire body. Among the skin layers, the epidermis is in direct contact with the outer environment and serves as the first line of defense. The epidermis functions as a physical and immunological barrier. To maintain barrier function, the epidermis continually regenerates and repairs itself when injured. Interactions between tissue-resident immune cells and epithelial cells are essential to sustain epidermal regeneration and repair. In this review, we will dissect the crosstalk between epithelial cells and specific immune cell populations located in the epidermis during homeostasis and wound repair. In addition, we will analyze the contribution of dysregulated immune-epithelial interactions in chronic inflammatory diseases.

Background/Aims: Buspirone shows promise in treating disorders of gut–brain interaction (DGBIs), particularly functional dyspepsia. However, findings have been mixed. Methods: We systematically searched for prospective studies testing buspirone for any upper gastrointestinal DGBI in 4 databases (Cochrane, PubMed, Scopus, and PsycInfo). The primary outcome was any validated measure of gastrointestinal symptoms. Anxiety, depression and adverse events were secondary outcomes. For randomized controlled trials (RCTs), we performed random-effects meta-analysis of the standardized mean difference (SMD) in post-treatment scores between buspirone and control groups. Risk of bias in RCTs was assessed using the Cochrane Common Mental Disorders Depression Anxiety and Neurosis Group (CCDAN) scale. Results: Ten studies (n = 283) met inclusion criteria, comprising 5 RCTs, 1 N-of-1 trial, 1 cohort, 1 case series, and 2 case reports. Tolerability of buspirone was good. In meta-analysis, buspirone produced a non-significant improvement in functional dyspepsia/gastroparesis symptoms compared to placebo (SMD = –0.14; 95% CI, –0.44 to 0.17; P = 0.39; I 2 = 0%; N studies = 3). Of individual symptoms, buspirone improved bloating severity more than placebo (SMD = –0.41; 95% CI, –0.77 to –0.04; P = 0.03; N studies = 2) but did not improve post-prandial fullness (P = 0.24, N studies = 2) or nausea (P = 0.75, N studies = 2). All RCTs included in the meta-analysis were good quality but most treated for only 4 weeks. Conclusions We found that buspirone did not improve functional dyspepsia symptoms more than placebo, though studies were small. Buspirone showed benefit for bloating severity, albeit based on few studies. Larger and longer trials of buspirone, targeting more defined groups such as patients with bloating, are warranted.

Reliable preclinical models for assessing drug-induced cardiotoxicity are essential to reduce the high rate of drug withdrawals during development. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have emerged as a promising platform for such assessments due to their expression of cardiacspecific ion channels and electrophysiological properties. In this study, we investigated the effects of eight arrhythmogenic drugs—E4031, nifedipine, mexiletine, JNJ303, flecainide, moxifloxacin, quinidine, and ranolazine—on hiPSC-CMs derived from both healthy individuals and a long QT syndrome (LQTS) patient using multielectrode array systems. The results demonstrated dose-dependent changes in field potential duration and arrhythmogenic risk, with LQTS-derived hiPSC-CMs showing increased sensitivity to hERG channel blockers such as E4031. Furthermore, the study highlights the potential of hiPSC-CMs to model disease-specific cardiac responses, providing insights into genetic predispositions and personalized drug responses.Despite challenges related to the immaturity of hiPSC-CMs, their ability to recapitulate human cardiac electrophysiology makes them a valuable tool for preclinical cardiotoxicity assessments. This study underscores the utility of integrating patientderived hiPSC-CMs with advanced analytical platforms, such as multi-electrode array systems, to evaluate drug-induced electrophysiological changes. These findings reinforce the role of hiPSC-CMs in drug development, facilitating safer and more efficient screening methods while supporting precision medicine applications.

The multiple layers of the skin cover and protect our entire body. Among the skin layers, the epidermis is in direct contact with the outer environment and serves as the first line of defense. The epidermis functions as a physical and immunological barrier. To maintain barrier function, the epidermis continually regenerates and repairs itself when injured. Interactions between tissue-resident immune cells and epithelial cells are essential to sustain epidermal regeneration and repair. In this review, we will dissect the crosstalk between epithelial cells and specific immune cell populations located in the epidermis during homeostasis and wound repair. In addition, we will analyze the contribution of dysregulated immune-epithelial interactions in chronic inflammatory diseases.

Background/Aims: Buspirone shows promise in treating disorders of gut–brain interaction (DGBIs), particularly functional dyspepsia. However, findings have been mixed. Methods: We systematically searched for prospective studies testing buspirone for any upper gastrointestinal DGBI in 4 databases (Cochrane, PubMed, Scopus, and PsycInfo). The primary outcome was any validated measure of gastrointestinal symptoms. Anxiety, depression and adverse events were secondary outcomes. For randomized controlled trials (RCTs), we performed random-effects meta-analysis of the standardized mean difference (SMD) in post-treatment scores between buspirone and control groups. Risk of bias in RCTs was assessed using the Cochrane Common Mental Disorders Depression Anxiety and Neurosis Group (CCDAN) scale. Results: Ten studies (n = 283) met inclusion criteria, comprising 5 RCTs, 1 N-of-1 trial, 1 cohort, 1 case series, and 2 case reports. Tolerability of buspirone was good. In meta-analysis, buspirone produced a non-significant improvement in functional dyspepsia/gastroparesis symptoms compared to placebo (SMD = –0.14; 95% CI, –0.44 to 0.17; P = 0.39; I 2 = 0%; N studies = 3). Of individual symptoms, buspirone improved bloating severity more than placebo (SMD = –0.41; 95% CI, –0.77 to –0.04; P = 0.03; N studies = 2) but did not improve post-prandial fullness (P = 0.24, N studies = 2) or nausea (P = 0.75, N studies = 2). All RCTs included in the meta-analysis were good quality but most treated for only 4 weeks. Conclusions We found that buspirone did not improve functional dyspepsia symptoms more than placebo, though studies were small. Buspirone showed benefit for bloating severity, albeit based on few studies. Larger and longer trials of buspirone, targeting more defined groups such as patients with bloating, are warranted.