This study aimed to determine how antibiotic-driven intestinal dysbiosis impairs the development and differentiation of the digestive tract and immune organs of host animals. BALB/C neonatal mice were orally administered ceftriaxone or vancomycin from postnatal day 1 to day 21 and sacrificed on day 21. The diversity and abundance of the intestinal bacteria, morphological changes and barrier function of intestinal tract, and the splenic CD4+CD25+Foxp3+ T cells were investigated. The gut microbiota and intestinal tissue were damaged, and the numbers of Ki67-, Muc2- and ZO-1-positive cells were significantly decreased in the antibiotic treatment groups. Furthermore, the administration of ceftriaxone, but not vancomycin, led to a significant reduction in the abundance of splenic CD4+CD25+Foxp3+ T cells. Each antibiotic caused intestinal dysbiosis and characteristically influenced the regeneration of intestinal epithelial cells, formation of the intestinal mucus layer and tight junctions, and differentiation of splenic Foxp3+ Treg cells of the neonatal mice before any clinical side effects were observed. The potent ability of each antibiotic to affect the makeup of intestinal commensal microbiota may be a key determinant of the spectrum of antibiotics and influence the health of the host animal, at least partly.

BackgroundLittle is known about the effect of meteorological conditions and geographical location on bacterial colonization rates particularly of antibiotic-resistant Gram-positive bacteria. We aimed to evaluate the effect of season, meteorological factors, and geographic location on methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE) colonization.MethodsThe prospective cohort included all adults admitted to 20 geographically-dispersed ICUs across the US from September 1, 2011 to October 4, 2012. Nasal and perianal swabs were collected at admission and tested for MRSA and VRE colonization respectively. Poisson regression models using monthly aggregated colonization counts as the outcome and mean temperature, relative humidity, total precipitation, season, and/or latitude as predictors were constructed for each pathogen.ResultsA total of 24,704 ICU-admitted patients were tested for MRSA and 24,468 for VRE. On admission, 10% of patients were colonized with MRSA and 12% with VRE. For MRSA and VRE, a 10% increase in relative humidity was associated with approximately a 9% increase in prevalence rate. Southerly latitudes in the US were associated with higher MRSA colonization, while northerly latitudes were associated with higher VRE colonization. In contrast to MRSA, the association between VRE colonization and latitude was observed only after adjusting for relative humidity, which demonstrates how this effect is highly driven by this meteorological factor.ConclusionsTo our knowledge, we are the first to study the effect of meteorological factors and geographical location/latitude on MRSA and VRE colonization in adults. Increasing humidity was associated with greater MRSA and VRE colonization. Southerly latitudes in the US were associated with greater MRSA and less VRE. The effect of these factors on MRSA and VRE rates has the potential not only to inform patient management and treatment, but also infection prevention interventions.

X-ray powder diffraction data, unit-cell parameters, and space group for meloxicam, C14H13N3O4S2, are reported [a = 6.997(2) Å, b = 8.113(2) Å, c = 13.604(4) Å, α = 85.774(2)°, β = 88.311(1)°, γ = 74.994(1)°, unit-cell volume V = 743.821 Å3, Z = 2, and space group P-1]. All measured lines were indexed, and no detectable impurity was observed.

Alcohol-associated liver disease (ALD) is caused by alcohol metabolism's effects on the liver. The underlying mechanisms from a metabolic view in the development of alcohol-associated liver cirrhosis (ALC) are still elusive. We performed an untargeted serum metabolomic analysis in 14 controls, 16 patients with ALD without cirrhosis (NC), 27 patients with compensated cirrhosis, and 79 patients with decompensated ALC. We identified two metabolic fingerprints associated with ALC development (38 metabolites) and those associated with hepatic decompensation (64 metabolites) in ALC. The cirrhosis-associated fingerprint (eigenmetabolite) showed a better capability to differentiate ALC from NC than the aspartate aminotransferase-to-platelet ratio index score. The eigenmetabolite associated with hepatic decompensation showed an increasing trend during the disease progression and was positively correlated with the Model for End-Stage Liver Disease score. These metabolic fingerprints belong to the metabolites in lipid metabolism, amino acid pathway, and intermediary metabolites in the tricarboxylic acid cycle. Conclusion: The metabolomic fingerprints suggest the disturbance of the metabolites associated with cellular energy supply as an underlying mechanism in the development and progression of alcoholic cirrhosis. (Hepatology Communications 2021;0:1-15). T he prevalence of alcohol-associated liver disease (ALD) is on the rise, and ALD has become one of the common noninfectious liver diseases worldwide. (1-3) ALD represents a spectrum of histopathological changes ranging from alcoholic steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Alcoholic steatosis, a reversible process following abstinence, occurs in most if not all heavy drinkers. However, only 20% of these patients develop alcoholic hepatitis and cirrhosis. (4) Alcohol-associated liver cirrhosis (ALC) is the leading cause of mortality in patients with ALD. (4,5) It accounts for 1% of all deaths worldwide and 50% of cirrhosis-related deaths. (6) The prognosis is poor with 5-year mortality around 85%, especially in those with complications from portal hypertension, such as variceal bleeding, hepatic encephalopathy, and ascites. (7) Once ingested, alcohol is primarily metabolized by the liver with by-products such as acetaldehyde and reactive oxygen species (ROS), leading to liver