Purpose: Feeding intolerance (FI) is a prevalent clinically sequential condition in preterm infants. To clarify its relationship with the gut microbiota, we compared microbial diversity and taxonomic composition at 2 and 4 weeks of age in infants born before 32 weeks of gestation. Methods: Between August 2021 and December 2022, we prospectively enrolled infants who delivered before 32 weeks of gestation and were admitted to the neonatal intensive care unit at CHA Bundang Medical Center. Forty-four preterm infants were grouped based on the presence (n=16) or absence (n=28) of FI. Fecal samples were obtained at 2 and 4 weeks after birth and analyzed using 16S rRNA gene sequencing to determine microbial profiles. Results: Microbial α-diversity and β-diversity did not differ significantly between groups at either time point. At the genus level, Staphylococcus was significantly more abundant in the FI group than in the feeding tolerance group at 2 weeks postnatal age (P=0.016). Linear discriminant analysis effect size revealed that Staphylococcus, Pseudomonas, and Escherichia were markedly enriched in the FI group at all time points. Conclusion Early colonization by potentially pathogenic genera, particularly Staphylococcus, may precede the development of FI in preterm infants. These findings highlight the potential microbial composition associated with FI and may provide preliminary insights for future microbiome-targeted research in neonatal care.

Purpose: Feeding intolerance (FI) is a prevalent clinically sequential condition in preterm infants. To clarify its relationship with the gut microbiota, we compared microbial diversity and taxonomic composition at 2 and 4 weeks of age in infants born before 32 weeks of gestation. Methods: Between August 2021 and December 2022, we prospectively enrolled infants who delivered before 32 weeks of gestation and were admitted to the neonatal intensive care unit at CHA Bundang Medical Center. Forty-four preterm infants were grouped based on the presence (n=16) or absence (n=28) of FI. Fecal samples were obtained at 2 and 4 weeks after birth and analyzed using 16S rRNA gene sequencing to determine microbial profiles. Results: Microbial α-diversity and β-diversity did not differ significantly between groups at either time point. At the genus level, Staphylococcus was significantly more abundant in the FI group than in the feeding tolerance group at 2 weeks postnatal age (P=0.016). Linear discriminant analysis effect size revealed that Staphylococcus, Pseudomonas, and Escherichia were markedly enriched in the FI group at all time points. Conclusion Early colonization by potentially pathogenic genera, particularly Staphylococcus, may precede the development of FI in preterm infants. These findings highlight the potential microbial composition associated with FI and may provide preliminary insights for future microbiome-targeted research in neonatal care.

Purpose: Feeding intolerance (FI) is a prevalent clinically sequential condition in preterm infants. To clarify its relationship with the gut microbiota, we compared microbial diversity and taxonomic composition at 2 and 4 weeks of age in infants born before 32 weeks of gestation. Methods: Between August 2021 and December 2022, we prospectively enrolled infants who delivered before 32 weeks of gestation and were admitted to the neonatal intensive care unit at CHA Bundang Medical Center. Forty-four preterm infants were grouped based on the presence (n=16) or absence (n=28) of FI. Fecal samples were obtained at 2 and 4 weeks after birth and analyzed using 16S rRNA gene sequencing to determine microbial profiles. Results: Microbial α-diversity and β-diversity did not differ significantly between groups at either time point. At the genus level, Staphylococcus was significantly more abundant in the FI group than in the feeding tolerance group at 2 weeks postnatal age (P=0.016). Linear discriminant analysis effect size revealed that Staphylococcus, Pseudomonas, and Escherichia were markedly enriched in the FI group at all time points. Conclusion Early colonization by potentially pathogenic genera, particularly Staphylococcus, may precede the development of FI in preterm infants. These findings highlight the potential microbial composition associated with FI and may provide preliminary insights for future microbiome-targeted research in neonatal care.

Purpose: Feeding intolerance (FI) is a prevalent clinically sequential condition in preterm infants. To clarify its relationship with the gut microbiota, we compared microbial diversity and taxonomic composition at 2 and 4 weeks of age in infants born before 32 weeks of gestation. Methods: Between August 2021 and December 2022, we prospectively enrolled infants who delivered before 32 weeks of gestation and were admitted to the neonatal intensive care unit at CHA Bundang Medical Center. Forty-four preterm infants were grouped based on the presence (n=16) or absence (n=28) of FI. Fecal samples were obtained at 2 and 4 weeks after birth and analyzed using 16S rRNA gene sequencing to determine microbial profiles. Results: Microbial α-diversity and β-diversity did not differ significantly between groups at either time point. At the genus level, Staphylococcus was significantly more abundant in the FI group than in the feeding tolerance group at 2 weeks postnatal age (P=0.016). Linear discriminant analysis effect size revealed that Staphylococcus, Pseudomonas, and Escherichia were markedly enriched in the FI group at all time points. Conclusion Early colonization by potentially pathogenic genera, particularly Staphylococcus, may precede the development of FI in preterm infants. These findings highlight the potential microbial composition associated with FI and may provide preliminary insights for future microbiome-targeted research in neonatal care.

Purpose: Feeding intolerance (FI) is a prevalent clinically sequential condition in preterm infants. To clarify its relationship with the gut microbiota, we compared microbial diversity and taxonomic composition at 2 and 4 weeks of age in infants born before 32 weeks of gestation. Methods: Between August 2021 and December 2022, we prospectively enrolled infants who delivered before 32 weeks of gestation and were admitted to the neonatal intensive care unit at CHA Bundang Medical Center. Forty-four preterm infants were grouped based on the presence (n=16) or absence (n=28) of FI. Fecal samples were obtained at 2 and 4 weeks after birth and analyzed using 16S rRNA gene sequencing to determine microbial profiles. Results: Microbial α-diversity and β-diversity did not differ significantly between groups at either time point. At the genus level, Staphylococcus was significantly more abundant in the FI group than in the feeding tolerance group at 2 weeks postnatal age (P=0.016). Linear discriminant analysis effect size revealed that Staphylococcus, Pseudomonas, and Escherichia were markedly enriched in the FI group at all time points. Conclusion Early colonization by potentially pathogenic genera, particularly Staphylococcus, may precede the development of FI in preterm infants. These findings highlight the potential microbial composition associated with FI and may provide preliminary insights for future microbiome-targeted research in neonatal care.

Background and Objectives: Air pollution, particularly particulate matter (PM), has a variety of adverse effects on human health. PM is known to induce cell death through various pathways, including pyroptosis. Despite its significance, research on PM-induced pyroptosis in nasal epithelial cells remains limited. This study aimed to explore PM-induced pyroptosis in cultured human nasal epithelial cells. Methods: For the in vitro experiments, human nasal epithelial cells were cultured. Cell viability was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while cell death was evaluated through propidium iodide (PI) staining and lactate dehydrogenase (LDH) release measurement. Protein expression levels related to pyroptosis were examined via western blot using antibodies against NOD-like receptor family, pyrin domain containing 3 (NLRP3), cleaved caspase-1 (CASP1 P20), gasdermin D (GSDMD)-N, and glyceraldehyde phosphate dehydrogenase. Immunofluorescent staining with a CASP1 P20 antibody was conducted to visualize cellular localization. Enzyme-linked immunosorbent assay was utilized to quantify interleukin (IL)-1β and IL-18 protein levels. Results: Treatment with PM resulted in decreased cell viability, elevated LDH release, and intensified PI staining, indicating cell death. Pyroptosis was confirmed by the elevated expression of NLRP3, CASP1 P20, and GSDMD-N, along with increased levels of IL-1β and IL-18. Inhibiting the NLRP3 inflammasome with MCC950 reduced the PM-induced effects on protein expression and cytokine release, highlighting the role of the NLRP3 inflammasome in PM-triggered pyroptosis in human nasal epithelial cells. Conclusion We showed that PM triggers pyroptosis in human nasal epithelial cells, driven by NLRP3 inflammasome-dependent signaling pathways.

Background: The scuticociliate Miamiensis avidus is a major pathogenic agent that causes significant economic losses in the flounder aquaculture industry. Many different types of drugs are being tested to control this disease, including mebendazole, which is a broad-spectrum antiprotozoal agent. The purpose of this study was to determine whether mebendazole worked in vitro against M. avidus and to explore its mechanism of action. Methods: Transcriptome and gene ontology analyses were conducted to investigate the specifically expressed gene profile. We confirmed the cytotoxic effect of mebendazole against M. avidus when it was applied intermittently for a total of three times. We also identified differentially expressed genes using transcriptome analysis. Results: Most of the upregulated genes were membrane transport-related genes, including Na+/K+-ATPase. Most of the downregulated genes were categorized into three groups: tubulin-related, metabolism-related, and transport-related genes. The expression levels of glucose uptake-related genes decreased due to the inhibition of tubulin polymerization, but this was not statistically significant. Conclusions Our results demonstrate that intermittent treatment with mebendazole has a significant cytotoxic effect on M. avidus. Furthermore, mebendazole induces downregulation of the tubulin-alpha chain and metabolism-related genes. It is presumed that this leads to a glucose shortage and the death of M. avidus. Transcriptome analysis will provide useful clues for further studies on mebendazole applications for scutica control.

Purpose: The standard care for patients with ipsilateral breast tumor recurrence (IBTR) after breast-conserving surgery (BCS) is a total mastectomy (TM); however, there is growing interest in repeating BCS for IBTR. Methods: We retrospectively analyzed patients with IBTR who underwent initial BCS for breast cancer at our institution between January 2000 and December 2018. The Kaplan-Meier method was used to compare survival rates between the standard BCS-TM treatment group and the repeat-BCS group. Results: We enrolled 209 IBTR patients with a median follow-up of 102.3 months. No significant differences were observed in overall survival (10 years: 87.3% vs. 78.8%; hazard ratio [HR], 1.11; 95% confidence interval [CI], 0.44-2.81; p=0.821), distant metastasis free survival (10 years: 73.9% vs. 77.7%; HR, 0.80; 95% CI, 0.37-1.72; p=0.727) and disease-free survival (10 years: 57.1% vs. 65.2%; HR, 0.63; 95% CI, 0.35-1.12; p=0.115) between two groups. Repeat-BCS group showed significantly poorer locoregional recurrence free survival rate than did the TM group (HR, 2.44; 95% CI, 1.06-5.56; p=0.029) but the significance was not shown after excluding ipsilateral breast tumor recurrence events. Conclusion No significant differences were observed in survival outcomes and recurrence rates between patients with IBTR who underwent mastectomy or repeat BCS regardless of molecular subtype, except secondary IBTR rates.

Major depressive disorder (MDD) and anxiety disorder (AD) are mental disorders with a high social burden. Since the discovery of neurogenesis, one effect of anti-depressant was revealed as increasing the neurogenesis of the dentate gyrus (DG). Thus, many researchers have speculated that neurogenesis may correlate with the pathogenesis of depression and anxiety disorders. It was reasonable to hypothesize that neurogenesis would be essential for the therapeutic mechanism. We call this new hypothesis the neurogenic theory. In this review, we investigated the validity and evidence of neurogenic theory through post-mortem studies and animal models. As a result, it seems to be a lack of strong evidence to claim that the defect of neurogenesis itself causes MDD and AD. However, neurogenesis seems to be essential, at least for improving depressive or anxiety behaviors. From the algorithmic perspective, we also discussed the pattern separation, suggested function of neurogenesis of the DG, in the relationship with the symptoms of mental disorder. We tried to show that it is appropriate to interpret the relationship between neurogenesis and mental disorder using the term “overgeneralization” rather than the theoretical term “pattern separation”.Overgeneralization was especially beneficial for interpreting the relationship between the defect of neurogenesis and post-traumatic stress syndrome (PTSD) among AD. It is necessary to further investigate the effect of neurogenesis in the treatment of mental illnesses such as MDD and AD including PTSD, and in the prognosis of patients.

Major depressive disorder (MDD) and anxiety disorder (AD) are mental disorders with a high social burden. Since the discovery of neurogenesis, one effect of anti-depressant was revealed as increasing the neurogenesis of the dentate gyrus (DG). Thus, many researchers have speculated that neurogenesis may correlate with the pathogenesis of depression and anxiety disorders. It was reasonable to hypothesize that neurogenesis would be essential for the therapeutic mechanism. We call this new hypothesis the neurogenic theory. In this review, we investigated the validity and evidence of neurogenic theory through post-mortem studies and animal models. As a result, it seems to be a lack of strong evidence to claim that the defect of neurogenesis itself causes MDD and AD. However, neurogenesis seems to be essential, at least for improving depressive or anxiety behaviors. From the algorithmic perspective, we also discussed the pattern separation, suggested function of neurogenesis of the DG, in the relationship with the symptoms of mental disorder. We tried to show that it is appropriate to interpret the relationship between neurogenesis and mental disorder using the term “overgeneralization” rather than the theoretical term “pattern separation”.Overgeneralization was especially beneficial for interpreting the relationship between the defect of neurogenesis and post-traumatic stress syndrome (PTSD) among AD. It is necessary to further investigate the effect of neurogenesis in the treatment of mental illnesses such as MDD and AD including PTSD, and in the prognosis of patients.