BackgroundA major protein component of cow’s milk is β-casein. The most frequent variants in dairy herds are A1 and A2. Recent studies showed that milk containing A1 β-casein promoted intestinal inflammation and exacerbated gastrointestinal symptoms. However, the acute gastrointestinal effects of A1 β-casein have not been investigated. This study compared the gastrointestinal effects of milk containing A1 and A2 β-casein versus A2 β-casein alone in Chinese adults with self-reported lactose intolerance.MethodsIn this randomised, crossover, double-blind trial, with a 3-day dairy washout period at baseline, subjects were randomised to consume 300 mL of milk containing A1 and A2 β-casein (ratio 58:42; conventional milk) or A2 β-casein alone; subjects consumed the alternative product after a 7-day washout period. Urine galactose was measured at baseline after a 15 g lactose load. Subjects completed 9-point visual analogue scales for gastrointestinal symptoms (borborygmus, flatulence, bloating, abdominal pain, stool frequency, and stool consistency) at baseline and at 1, 3, and 12 h after milk consumption.ResultsA total of 600 subjects were included. All six symptom scores at 1 and 3 h were significantly lower after consuming A2 β-casein versus conventional milk (all P<0.0001). At 12 h, significant differences remained for bloating, abdominal pain, stool frequency, and stool consistency (all P<0.0001). Symptom scores were consistently lower with A2 β-casein in both lactose absorbers (urinary galactose ≥0.27 mmol/L) and lactose malabsorbers (urinary galactose <0.27 mmol/L).ConclusionMilk containing A2 β-casein attenuated acute gastrointestinal symptoms of milk intolerance, while conventional milk containing A1 β-casein reduced lactase activity and increased gastrointestinal symptoms compared with milk containing A2 β-casein. Thus, milk-related gastrointestinal symptoms may result from the ingestion of A1 β-casein rather than lactose in some individuals.Trial registration NCT02878876, registered August 16, 2016. Retrospectively registered.Electronic supplementary materialThe online version of this article (10.1186/s12937-017-0275-0) contains supplementary material, which is available to authorized users.

Background Dexmedetomidine (DEX) had organ protection effects and could decrease mortality in animal models, but its association with mortality and length of stay (LOS) in ICU and hospital in critically ill patients was conflicting. Whether acute kidney injury (AKI) subgroup of critically ill patients could benefit from DEX was unknown. The present study aimed to evaluate the effects of DEX on clinical outcomes of critically ill patients with AKI. Methods Data were extracted from the Medical Information Mart for Intensive Care Ⅲ database (MIMIC Ⅲ). Propensity score matching (PSM) analysis (1:3), cox proportional hazards model, linear regression and logistic regression model were used to assess the effect of DEX on clinical outcomes. Results After PSM, 324 pairs of patients were matched between the patients with DEX administration and those without. DEX administration was associated with decreased in-hospital mortality [hazard ratio (HR) 0.287; 95% CI 0.151–0.542; P < 0.001] and 90-day mortality [HR 0.344; 95% CI 0.221–0.534; P < 0.001], and it was also associated with reduced length of stay (LOS) in ICU [4.54(3.13,7.72) versus 5.24(3.15,10.91), P < 0.001] and LOS in hospital [11.63(8.02,16.79) versus 12.09(7.83,20.44), P = 0.002]. Subgroup analysis showed the above associations existed only in mild and moderate AKI subgroups, but not in severe AKI subgroup. Nevertheless, DEX administration was not associated with the recovery of renal function [HR 1.199; 95% CI 0.851–1.688; P = 0.300]. Conclusions DEX administration improved outcomes in critically ill patients with mild and moderate AKI and could be a good choice of sedation.