ObjectiveThe objective of this experiment was to investigate the effects of heat stress on milk protein and blood amino acid profile in dairy cows.MethodsTwelve dairy cows with the similar parity, days in milk and milk yield were randomly divided into two groups with six cows raised in summer and others in autumn, respectively. Constant managerial conditions and diets were maintained during the experiment. Measurements and samples for heat stress and no heat stress were obtained according to the physical alterations of the temperature-humidity index.ResultsResults showed that heat stress significantly reduced the milk protein content (p<0.05). Heat stress tended to decrease milk yield (p = 0.09). Furthermore, heat stress decreased dry matter intake, the concentration of blood glucose and insulin, and glutathione peroxidase activity, while increased levels of non-esterified fatty acid and malondialdehyde (p<0.05). Additionally, the concentrations of blood Thr involved in immune response were increased under heat stress (p<0.05). The concentration of blood Ala, Glu, Asp, and Gly, associated with gluconeogenesis, were also increased under heat stress (p<0.05). However, the concentration of blood Lys that promotes milk protein synthesis was decreased under heat stress (p<0.05).ConclusionIn conclusion, this study revealed that more amino acids were required for maintenance but not for milk protein synthesis under heat stress, and the decreased availability of amino acids for milk protein synthesis may be attributed to competition of immune response and gluconeogenesis.

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We reported two Au clusters with precisely controlled molecular size (AuPeptide and AuPeptide) showing different antitumor effects. In vitro, both AuPeptide and AuPeptide were well taken up by human nasopharyngeal cancer cells (CNE1 cells). However, only AuPeptide significantly induced CNE1 cell apoptosis. Further studies showed that CNE1 cells took up AuPeptide (1.98 × 10 mol/cell), and 9% of them entered mitochondria (0.186 × 10 mol/cell). As a comparison, the uptake of AuPeptide was only half the amount of AuPeptide (1.11 × 10 mol/cell), and only 1% of them entered mitochondria (0.016 × 10 mol/cell). That gave 11.6-fold more AuPeptide in mitochondria of CNE1 cells than AuPeptide. Further cell studies revealed that the antitumor effect may be due to the enrichment of AuPeptide in mitochondria. AuPeptide slightly decreased the Mcl-1 (antiapoptotic protein of mitochondria) and significantly increased the Puma (pro-apoptotic protein of mitochondria) expression level in CNE1 cells, which resulted in mitochondrial transmembrane potential change and triggered the caspase 9-caspase 3-PARP pathway to induce CNE1 cell apoptosis. In vivo, CNE1 tumor growth was significantly suppressed by AuPeptide in the xenograft model after 3 weeks of intraperitoneal injection. The TUNEL and immuno-histochemical studies of tumor tissue verified that CNE1 cell apoptosis was mainly via the Puma and Mcl-1 apoptosis pathway in the xenograft model, which matched the aforementioned CNE1 cell studies in vitro. The discovery of Au but not Au suppressing tumor growth via the mitochondria target was a breakthrough in the nanomedical field, as this provided a robust approach to turn on/off the nanoparticles' medical properties via atomically controlling their sizes.

A macrocyclic aromatic pyridone pentamer was shown to catalyze highly efficient transition-metal-free arylations of unactivated aromatic C-H bonds with aryl iodides and bromides in the presence of potassium tert-butoxide.