Adding bovine milk-derived oligosaccharides (MOS) enhances the oligosaccharide profile of infant formula. This study aimed to evaluate the safety and efficacy of a MOS-supplemented infant formula.
 
  In this double-blind randomized controlled trial, healthy infants 21-26 days old were either assigned to bovine milk-based, alpha-lactalbumin, and sn-2 palmitate enriched infant formula (control, n = 115) or the same formula with 7.2 gMOS/L (test, n = 115) until aged 6 months. Co-primary endpoints were weight gain through 4 months and stool consistency (validated scale 1 = watery to 5 = hard). Secondary endpoints included parent-reported GI tolerance, health-related quality of life (HRQoL), and adverse events (AEs).
 
  Weight gain was similar (p = 0.695); the difference between test and control (mean; 95% CI 0.29; -1.15, 1.73 g/day) was above the non-inferiority margin (-3 g/day). Test had softer stools than control (mean difference in stool consistency score -0.31; 95% CI -0.42, -0.21; P < 0.0001); fewer pareshows that bovine milk-derived oligosaccharide supplemented infant formula is a safe and effective option for healthy term infants who are formula-fed.
 This is the first study investigating the addition of bovine milk-derived oligosaccharides to an infant formula enriched with alpha-lactalbumin and elevated levels of sn-2 palmitate, providing safety and efficacy data for such a formula. Term infant formula supplemented with 7.2 g bovine milk-derived oligosaccharides per liter supported normal infant growth, was well-tolerated and safe. Addition of bovine milk-derived oligosaccharides to term infant formula promoted softer stooling pattern and reduced difficulties in passing stool. The study shows that bovine milk-derived oligosaccharide supplemented infant formula is a safe and effective option for healthy term infants who are formula-fed.
  Bronchopulmonary dysplasia (BPD) is a major complication in preterm infants <32 weeks. We aimed to assess whether plasma levels of mid-regional pro-atrial natriuretic peptide (MR-proANP) and C-terminal pro-endothelin-1 (CT-proET-1) predict respiratory morbidity.
 
  This was a prospective, two-center, observational cohort study. MR-proANP and CT-proET-1 were measured at day 7 (±2) of life. Associations with duration of supplemental oxygen and the composite outcome of moderate or severe BPD or death (BPD/death) were investigated.
 
  Two hundred and twenty-nine infants <32 weeks were included (median gestational age [GA] 29.6 weeks [interquartile range 29.0-30.7], median birth weight 1150 g [IQR 840-1410]). MR-proANP and CT-proET-1 were associated with the duration of supplemental oxygen in univariable analysis (both p < 0.001) but not after adjusting for co-factors. Infants with BPD/death showed higher plasma levels of MR-proANP (623.50 pmol/L [IQR 458.50-881.38] vs. 308.35 pmol/L [IQR 216.72-538.10]; ET-1, measured on day 7 of life (±2 days) are associated in univariable analyses with duration of supplemental oxygen and the combined outcome of BPD or death in VLGA infants. Associations between both biomarkers and respiratory morbidity do not persist in multivariable models, in particular when gestational age is included. MR-proANP and CT-proET-1 have limited additional value to predict respiratory morbidity in VLGA infants compared to clinical parameters.
  Continuous positive airway pressure (CPAP) in preterm infants is initially beneficial, but animal models suggest longer term detrimental airway effects towards asthma. We used a neonatal CPAP mouse model and human fetal airway smooth muscle (ASM) to investigate the role of extracellular calcium-sensing receptor (CaSR) in these effects.
 
  Newborn wild type and smooth muscle-specific CaSR
  mice were given CPAP for 7 days via a custom device (mimicking CPAP in premature infants), and recovered in normoxia for another 14 days (representing infants at 3-4 years). Airway reactivity was tested using lung slices, and airway CaSR quantified. Role of CaSR was tested using NPS2143 (inhibitor) or siRNA in WT mice. Fetal ASM cells stretched cyclically with/without static stretch mimicking breathing and CPAP were analyzed for intracellular Ca
  ([Ca
  ]
  ) responses, role of CaSR, and signaling cascades.
 
  CPAP increased airway reactivity in WT but not CaSR
  mice, increasing ASM CaSR. NPS2143 or CaSR siRNA reversed CPAPory role for CaSR in stretch effects on the developing airway. These data may impact clinical recognition of the ways that CPAP may contribute to wheezing disorders of former preterm infants.Economic theory predicts that organisations achieve higher levels of productivity when tasks are divided among different subsets of workers. This prediction is based upon the expectation that individuals should perform best when they specialise upon a few tasks. However, in colonies of social insects evidence for a causal link between division of labour and performance is equivocal. To address this issue, we performed a targeted worker removal experiment to disrupt the normal allocation of workers to a cooperative team task - tandem running. During a tandem run a knowledgeable leader communicates the location of a new nest to a follower by physically guiding her there. The targeted removal of prominent leaders significantly reduced tandem performance, whereas removal of prominent followers had no effect. Furthermore, analyses of the experience of both participants in each tandem run revealed that tandem performance was influenced primarily by how consistently the leader acted as a leader when the need arose, but not by the consistency of the follower. Our study shows that performance in ant teams depends largely on whether or not a key role is filled by an experienced individual, and suggests that in animal teams, not all roles are equally important.Hepatocellular carcinoma (HCC) is a global health issue and the fourth leading cause of cancer deaths worldwide.  https://www.selleckchem.com/products/Sunitinib-Malate-(Sutent).html  Large-scale HCC genome sequencing analyses have identified core drivers (TERT, TP53, and CTNNB1/AXIN1) as initial molecular events, and other low-frequent drivers that include therapeutically targetable ones. The recent genetic analysis uncovered a distinctive driver gene landscape in precancerous lesions, arguing a discontinuous process at early HCC development. In advanced tumors, intra-tumoral heterogeneity through clonal evolution processes is common, and it displays clear geographic segregation genetically and epigenetically. Diverse epidemiological risk factors for HCC mirrors heterogeneous mutational processes among patient cohorts with distinctive ethnicity, environmental exposures, and lifestyles. The genetic information of individual tumors has been utilized for optimizing treatments, early diagnosis, and monitoring recurrence. It will expand the opportunity for screening high-risk populations, thereby preventing hepatocarcinogenesis in the near future.