Background: Shift work, particularly in night shifts, has been linked to adverse health outcomes, including disruptions in circadian rhythms that may contribute to metabolic disorders. However, sexrelated differences in the impact of night shift work on cardiometabolic health remain understudied.This study sought to examine the relationship between night shift work and cardiometabolic health in young adults, identifying potential sex-related differences. Methods: In this prospective cohort study, a total of 3201 participants (mean age: 22.08 years, 59.9% women) were analyzed over a 17-year period. Relative risks (RRs) with 95% confidence intervals (CIs) were calculated to evaluate the impact of night shift work on cardiometabolic health outcomes, including obesity, hyperlipidemia, hypertension, type 2 diabetes, and metabolic syndrome (MetS). Results: At Wave V, 74.7% of participants were diagnosed with overweight/obesity, 51.8% with abdominal obesity, 15.5% with hyperlipidemia, 29.1% with hypertension, 8.3% with type 2 diabetes, and 20.9% with MetS. Night shift work was associated with an increased risk of obesity and abdominal obesity in women (RR = 1.99, 95% CI: 1.08 to 3.65 and RR = 1.60, 95% CI: 1.07 to 2.56, respectively) but not in men. Women also showed an elevated risk of diabetes (RR = 2.69, 95% CI: 1.49 to 4.86), whereas no significant relationship was identified in men. Night shift work was not significantly associated with hypertension and MetS in either men or women. Conclusion Women working night shifts may benefit from targeted interventions for cardiometabolic health, particularly in managing weight and preventing diabetes, while men did not exhibit similar associations.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant global health issue, affecting over 30% of the population worldwide due to the rising prevalence of metabolic risk factors such as obesity and type 2 diabetes mellitus. This spectrum of liver disease ranges from isolated steatosis to more severe forms such as steatohepatitis, fibrosis, and cirrhosis. Recent studies highlight the role of gut microbiota in MASLD pathogenesis, showing that dysbiosis significantly impacts metabolic health and the progression of liver disease. This review critically evaluates current microbiome-centered therapies in MASLD management, including prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and emerging therapies such as engineered bacteria and bacteriophage therapy. We explore the scientific rationale, clinical evidence, and potential mechanisms by which these interventions influence MASLD. The gut-liver axis is crucial in MASLD, with notable changes in microbiome composition linked to disease progression. For instance, specific microbial profiles and reduced alpha diversity are associated with MASLD severity. Therapeutic strategies targeting the microbiome could modulate disease progression by improving gut permeability, reducing endotoxin-producing bacteria, and altering bile acid metabolism. Although promising, these therapies require further research to fully understand their mechanisms and optimize their efficacy. This review integrates findings from clinical trials and experimental studies, providing a comprehensive overview of microbiome-centered therapies’ potential in managing MASLD. Future research should focus on personalized strategies, utilizing microbiome features, blood metabolites, and customized dietary interventions to enhance the effectiveness of these therapies.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant global health issue, affecting over 30% of the population worldwide due to the rising prevalence of metabolic risk factors such as obesity and type 2 diabetes mellitus. This spectrum of liver disease ranges from isolated steatosis to more severe forms such as steatohepatitis, fibrosis, and cirrhosis. Recent studies highlight the role of gut microbiota in MASLD pathogenesis, showing that dysbiosis significantly impacts metabolic health and the progression of liver disease. This review critically evaluates current microbiome-centered therapies in MASLD management, including prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and emerging therapies such as engineered bacteria and bacteriophage therapy. We explore the scientific rationale, clinical evidence, and potential mechanisms by which these interventions influence MASLD. The gut-liver axis is crucial in MASLD, with notable changes in microbiome composition linked to disease progression. For instance, specific microbial profiles and reduced alpha diversity are associated with MASLD severity. Therapeutic strategies targeting the microbiome could modulate disease progression by improving gut permeability, reducing endotoxin-producing bacteria, and altering bile acid metabolism. Although promising, these therapies require further research to fully understand their mechanisms and optimize their efficacy. This review integrates findings from clinical trials and experimental studies, providing a comprehensive overview of microbiome-centered therapies’ potential in managing MASLD. Future research should focus on personalized strategies, utilizing microbiome features, blood metabolites, and customized dietary interventions to enhance the effectiveness of these therapies.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant global health issue, affecting over 30% of the population worldwide due to the rising prevalence of metabolic risk factors such as obesity and type 2 diabetes mellitus. This spectrum of liver disease ranges from isolated steatosis to more severe forms such as steatohepatitis, fibrosis, and cirrhosis. Recent studies highlight the role of gut microbiota in MASLD pathogenesis, showing that dysbiosis significantly impacts metabolic health and the progression of liver disease. This review critically evaluates current microbiome-centered therapies in MASLD management, including prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and emerging therapies such as engineered bacteria and bacteriophage therapy. We explore the scientific rationale, clinical evidence, and potential mechanisms by which these interventions influence MASLD. The gut-liver axis is crucial in MASLD, with notable changes in microbiome composition linked to disease progression. For instance, specific microbial profiles and reduced alpha diversity are associated with MASLD severity. Therapeutic strategies targeting the microbiome could modulate disease progression by improving gut permeability, reducing endotoxin-producing bacteria, and altering bile acid metabolism. Although promising, these therapies require further research to fully understand their mechanisms and optimize their efficacy. This review integrates findings from clinical trials and experimental studies, providing a comprehensive overview of microbiome-centered therapies’ potential in managing MASLD. Future research should focus on personalized strategies, utilizing microbiome features, blood metabolites, and customized dietary interventions to enhance the effectiveness of these therapies.

Killip-Kimball classification has been used for estimating death risk in patients suffering acute myocardial infarction (AMI). Killip-Kimball stage IV corresponds to cardiogenic shock. However, the Society for Cardiovascular Angiography and Interventions (SCAI) classification provides a more precise tool to classify patients according to shock severity. The aim of this study was to apply this classification to a cohort of Killip IV patients and to analyze the differences in death risk estimation between the two classifications. Methods: A single-center retrospective cohort study of 100 consecutive patients hospitalized for “Killip IV AMI” between 2016 and 2023 was performed to reclassify patients according to SCAI stage. Results: Distribution of patients according to SCAI stages was B=4%, C=53%, D=27%, E=16%. Thirty-day mortality increased progressively according to these stages (B=0%, C=11.88%, D=55.56%, E=87.50%; P<0.001). The exclusive use of Killip IV stage overestimated death risk compared to SCAI C (35% vs. 11.88%, P=0.002) and underestimated it compared to SCAI D and E stages (35% vs. 55.56% and 87.50%, P=0.03 and P<0.001, respectively). Age >69 years, creatinine >1.15 mg/dl and advanced SCAI stages (SCAI D and E) were independent predictors of 30-day mortality. Mechanical circulatory support use showed an almost significant benefit in advanced SCAI stages (D and E hazard ratio, 0.45; 95% confidence interval, 0.19–1.06; P=0.058). Conclusions: SCAI classification showed superior death risk estimation compared to Killip IV. Age, creatinine levels and advanced SCAI stages were independent predictors of 30-day mortality. Mechanical circulatory support could play a beneficial role in advanced SCAI stages.

Killip-Kimball classification has been used for estimating death risk in patients suffering acute myocardial infarction (AMI). Killip-Kimball stage IV corresponds to cardiogenic shock. However, the Society for Cardiovascular Angiography and Interventions (SCAI) classification provides a more precise tool to classify patients according to shock severity. The aim of this study was to apply this classification to a cohort of Killip IV patients and to analyze the differences in death risk estimation between the two classifications. Methods: A single-center retrospective cohort study of 100 consecutive patients hospitalized for “Killip IV AMI” between 2016 and 2023 was performed to reclassify patients according to SCAI stage. Results: Distribution of patients according to SCAI stages was B=4%, C=53%, D=27%, E=16%. Thirty-day mortality increased progressively according to these stages (B=0%, C=11.88%, D=55.56%, E=87.50%; P<0.001). The exclusive use of Killip IV stage overestimated death risk compared to SCAI C (35% vs. 11.88%, P=0.002) and underestimated it compared to SCAI D and E stages (35% vs. 55.56% and 87.50%, P=0.03 and P<0.001, respectively). Age >69 years, creatinine >1.15 mg/dl and advanced SCAI stages (SCAI D and E) were independent predictors of 30-day mortality. Mechanical circulatory support use showed an almost significant benefit in advanced SCAI stages (D and E hazard ratio, 0.45; 95% confidence interval, 0.19–1.06; P=0.058). Conclusions: SCAI classification showed superior death risk estimation compared to Killip IV. Age, creatinine levels and advanced SCAI stages were independent predictors of 30-day mortality. Mechanical circulatory support could play a beneficial role in advanced SCAI stages.

Killip-Kimball classification has been used for estimating death risk in patients suffering acute myocardial infarction (AMI). Killip-Kimball stage IV corresponds to cardiogenic shock. However, the Society for Cardiovascular Angiography and Interventions (SCAI) classification provides a more precise tool to classify patients according to shock severity. The aim of this study was to apply this classification to a cohort of Killip IV patients and to analyze the differences in death risk estimation between the two classifications. Methods: A single-center retrospective cohort study of 100 consecutive patients hospitalized for “Killip IV AMI” between 2016 and 2023 was performed to reclassify patients according to SCAI stage. Results: Distribution of patients according to SCAI stages was B=4%, C=53%, D=27%, E=16%. Thirty-day mortality increased progressively according to these stages (B=0%, C=11.88%, D=55.56%, E=87.50%; P<0.001). The exclusive use of Killip IV stage overestimated death risk compared to SCAI C (35% vs. 11.88%, P=0.002) and underestimated it compared to SCAI D and E stages (35% vs. 55.56% and 87.50%, P=0.03 and P<0.001, respectively). Age >69 years, creatinine >1.15 mg/dl and advanced SCAI stages (SCAI D and E) were independent predictors of 30-day mortality. Mechanical circulatory support use showed an almost significant benefit in advanced SCAI stages (D and E hazard ratio, 0.45; 95% confidence interval, 0.19–1.06; P=0.058). Conclusions: SCAI classification showed superior death risk estimation compared to Killip IV. Age, creatinine levels and advanced SCAI stages were independent predictors of 30-day mortality. Mechanical circulatory support could play a beneficial role in advanced SCAI stages.

Killip-Kimball classification has been used for estimating death risk in patients suffering acute myocardial infarction (AMI). Killip-Kimball stage IV corresponds to cardiogenic shock. However, the Society for Cardiovascular Angiography and Interventions (SCAI) classification provides a more precise tool to classify patients according to shock severity. The aim of this study was to apply this classification to a cohort of Killip IV patients and to analyze the differences in death risk estimation between the two classifications. Methods: A single-center retrospective cohort study of 100 consecutive patients hospitalized for “Killip IV AMI” between 2016 and 2023 was performed to reclassify patients according to SCAI stage. Results: Distribution of patients according to SCAI stages was B=4%, C=53%, D=27%, E=16%. Thirty-day mortality increased progressively according to these stages (B=0%, C=11.88%, D=55.56%, E=87.50%; P<0.001). The exclusive use of Killip IV stage overestimated death risk compared to SCAI C (35% vs. 11.88%, P=0.002) and underestimated it compared to SCAI D and E stages (35% vs. 55.56% and 87.50%, P=0.03 and P<0.001, respectively). Age >69 years, creatinine >1.15 mg/dl and advanced SCAI stages (SCAI D and E) were independent predictors of 30-day mortality. Mechanical circulatory support use showed an almost significant benefit in advanced SCAI stages (D and E hazard ratio, 0.45; 95% confidence interval, 0.19–1.06; P=0.058). Conclusions: SCAI classification showed superior death risk estimation compared to Killip IV. Age, creatinine levels and advanced SCAI stages were independent predictors of 30-day mortality. Mechanical circulatory support could play a beneficial role in advanced SCAI stages.

An appendicovesical fistula is defined as an abnormal communication between the appendix and the urinary bladder, with only a few cases reported in the literature. It is very challenging to make an early diagnosis, due to the inability of conventional imaging modalities to detect this unique pathology. The symptoms are often mild, and there are not any specific signs or symptoms that might suggest this type of anomalous communication. We report a case of a 27-year-old male patient who presented difficulty for initiating urination, dysuria, and persistent urinary tract infections. An abdominal x-ray showed a large calculus inside the bladder. A cystoscopy was performed, where the tip of the appendix was seen protruding inside the bladder with a large fecalith adhered to the bladder wall. An appendectomy and partial cystectomy with primary repair were auspiciously achieved. A review of the literature is also presented.

Background: Carnivore protoparvovirus 1, also known as canine parvovirus type 2 (CPV-2), is the main pathogen in hemorrhagic gastroenteritis in dogs, with a high mortality rate. Three subtypes (a, b, c) have been described based on VP2 residue 426, where 2a, 2b, and 2c have asparagine, aspartic acid, and glutamic acid, respectively. Objectives: This study examined the presence of CPV-2 variants in the fecal samples of dogs diagnosed with canine parvovirus in Bogotá. Methods: Fecal samples were collected from 54 puppies and young dogs (< 1 year) that tested positive for the CPV through rapid antigen test detection between 2014–2018. Molecular screening was developed for VP1 because primers 555 for VP2 do not amplify, it was necessary to design a primer set for VP2 amplification of 982 nt. All samples that were amplified were sequenced by Sanger. Phylogenetics and structural analysis was carried out, focusing on residue 426. Results: As a result 47 out of 54 samples tested positive for VP1 screening, and 34/47 samples tested positive for VP2 980 primers as subtype 2a (n = 30) or 2b (n = 4); subtype 2c was not detected. All VP2 sequences had the amino acid, T, at 440, and most Colombian sequences showed an S514A substitution, which in the structural modeling is located in an antigenic region, together with the 426 residue. Conclusions The 2c variant was not detected, and these findings suggest that Colombian strains of CPV-2 might be under an antigenic drift.