Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Purpose: Nutritional support for adult critically ill patients is essential due to the high risk of malnutrition, which can lead to severe complications. This paper aims to develop evidence-based guidelines to optimize nutritional support in intensive care units (ICUs). Methods: The Grading Recommendations, Assessment, Development and Evaluation process was used to develop and summarize the evidence on which the recommendations were based. Clinical outcomes were assessed for seven key questions. Results: We recommend the following: (1) initiate enteral nutrition (EN) within 48 hours after treatment as it is associated with improved outcomes, including reduced infection rates and shorter ICU stays; (2) early EN is preferred over early parenteral nutrition due to better clinical outcomes; (3) the use of supplementary parenteral nutrition to meet energy targets during the first week of ICU admission in patients receiving early EN is conditionally recommended based on patient-specific needs; (4) limited caloric support should be supplied to prevent overfeeding and related complications, particularly in the early phase of critical illness; (5) higher protein intake is suggested to improve clinical outcomes, such as muscle preservation and overall recovery; (6) additional enteral or parenteral glutamine is conditionally recommended against due to the lack of significant benefit and potential harm; and (7) fish oil-containing lipid emulsions is conditionally recommended due to their potential to enhance clinical outcomes, including reduced infection rates and shorter ICU stays. Conclusion These evidence-based recommendations can improve clinical outcomes and support healthcare providers in making informed decisions about nutritional interventions in the ICU.

Purpose: Nutritional support for adult critically ill patients is essential due to the high risk of malnutrition, which can lead to severe complications. This paper aims to develop evidence-based guidelines to optimize nutritional support in intensive care units (ICUs). Methods: The Grading Recommendations, Assessment, Development and Evaluation process was used to develop and summarize the evidence on which the recommendations were based. Clinical outcomes were assessed for seven key questions. Results: We recommend the following: (1) initiate enteral nutrition (EN) within 48 hours after treatment as it is associated with improved outcomes, including reduced infection rates and shorter ICU stays; (2) early EN is preferred over early parenteral nutrition due to better clinical outcomes; (3) the use of supplementary parenteral nutrition to meet energy targets during the first week of ICU admission in patients receiving early EN is conditionally recommended based on patient-specific needs; (4) limited caloric support should be supplied to prevent overfeeding and related complications, particularly in the early phase of critical illness; (5) higher protein intake is suggested to improve clinical outcomes, such as muscle preservation and overall recovery; (6) additional enteral or parenteral glutamine is conditionally recommended against due to the lack of significant benefit and potential harm; and (7) fish oil-containing lipid emulsions is conditionally recommended due to their potential to enhance clinical outcomes, including reduced infection rates and shorter ICU stays. Conclusion These evidence-based recommendations can improve clinical outcomes and support healthcare providers in making informed decisions about nutritional interventions in the ICU.

Purpose: Nutritional support for adult critically ill patients is essential due to the high risk of malnutrition, which can lead to severe complications. This paper aims to develop evidence-based guidelines to optimize nutritional support in intensive care units (ICUs). Methods: The Grading Recommendations, Assessment, Development and Evaluation process was used to develop and summarize the evidence on which the recommendations were based. Clinical outcomes were assessed for seven key questions. Results: We recommend the following: (1) initiate enteral nutrition (EN) within 48 hours after treatment as it is associated with improved outcomes, including reduced infection rates and shorter ICU stays; (2) early EN is preferred over early parenteral nutrition due to better clinical outcomes; (3) the use of supplementary parenteral nutrition to meet energy targets during the first week of ICU admission in patients receiving early EN is conditionally recommended based on patient-specific needs; (4) limited caloric support should be supplied to prevent overfeeding and related complications, particularly in the early phase of critical illness; (5) higher protein intake is suggested to improve clinical outcomes, such as muscle preservation and overall recovery; (6) additional enteral or parenteral glutamine is conditionally recommended against due to the lack of significant benefit and potential harm; and (7) fish oil-containing lipid emulsions is conditionally recommended due to their potential to enhance clinical outcomes, including reduced infection rates and shorter ICU stays. Conclusion These evidence-based recommendations can improve clinical outcomes and support healthcare providers in making informed decisions about nutritional interventions in the ICU.

Purpose: Nutritional support for adult critically ill patients is essential due to the high risk of malnutrition, which can lead to severe complications. This paper aims to develop evidence-based guidelines to optimize nutritional support in intensive care units (ICUs). Methods: The Grading Recommendations, Assessment, Development and Evaluation process was used to develop and summarize the evidence on which the recommendations were based. Clinical outcomes were assessed for seven key questions. Results: We recommend the following: (1) initiate enteral nutrition (EN) within 48 hours after treatment as it is associated with improved outcomes, including reduced infection rates and shorter ICU stays; (2) early EN is preferred over early parenteral nutrition due to better clinical outcomes; (3) the use of supplementary parenteral nutrition to meet energy targets during the first week of ICU admission in patients receiving early EN is conditionally recommended based on patient-specific needs; (4) limited caloric support should be supplied to prevent overfeeding and related complications, particularly in the early phase of critical illness; (5) higher protein intake is suggested to improve clinical outcomes, such as muscle preservation and overall recovery; (6) additional enteral or parenteral glutamine is conditionally recommended against due to the lack of significant benefit and potential harm; and (7) fish oil-containing lipid emulsions is conditionally recommended due to their potential to enhance clinical outcomes, including reduced infection rates and shorter ICU stays. Conclusion These evidence-based recommendations can improve clinical outcomes and support healthcare providers in making informed decisions about nutritional interventions in the ICU.

Purpose: Nutritional support for adult critically ill patients is essential due to the high risk of malnutrition, which can lead to severe complications. This paper aims to develop evidence-based guidelines to optimize nutritional support in intensive care units (ICUs). Methods: The Grading Recommendations, Assessment, Development and Evaluation process was used to develop and summarize the evidence on which the recommendations were based. Clinical outcomes were assessed for seven key questions. Results: We recommend the following: (1) initiate enteral nutrition (EN) within 48 hours after treatment as it is associated with improved outcomes, including reduced infection rates and shorter ICU stays; (2) early EN is preferred over early parenteral nutrition due to better clinical outcomes; (3) the use of supplementary parenteral nutrition to meet energy targets during the first week of ICU admission in patients receiving early EN is conditionally recommended based on patient-specific needs; (4) limited caloric support should be supplied to prevent overfeeding and related complications, particularly in the early phase of critical illness; (5) higher protein intake is suggested to improve clinical outcomes, such as muscle preservation and overall recovery; (6) additional enteral or parenteral glutamine is conditionally recommended against due to the lack of significant benefit and potential harm; and (7) fish oil-containing lipid emulsions is conditionally recommended due to their potential to enhance clinical outcomes, including reduced infection rates and shorter ICU stays. Conclusion These evidence-based recommendations can improve clinical outcomes and support healthcare providers in making informed decisions about nutritional interventions in the ICU.

Differentiated thyroid cancer demonstrates a wide range of clinical presentations, from very indolent cases to those with an aggressive prognosis. Therefore, diagnosing and treating each cancer appropriately based on its risk status is important. The Korean Thyroid Association (KTA) has provided and amended the clinical guidelines for thyroid cancer management since 2007. The main changes in this revised 2024 guideline include 1) individualization of surgical extent according to pathological tests and clinical findings, 2) application of active surveillance in low-risk papillary thyroid microcarcinoma, 3) indications for minimally invasive surgery, 4) adoption of World Health Organization pathological diagnostic criteria and definition of terminology in Korean, 5) update on literature evidence of recurrence risk for initial risk stratification, 6) addition of the role of molecular testing, 7) addition of definition of initial risk stratification and targeting thyroid stimulating hormone (TSH) concentrations according to ongoing risk stratification (ORS), 8) addition of treatment of perioperative hypoparathyroidism, 9) update on systemic chemotherapy, and 10) addition of treatment for pediatric patients with thyroid cancer.