556, P = 0.007). Logarithmically adjusted plasma interleukin-10 levels were negatively correlated with increasing anthocyanin dose (F = 2.738, P = 0.025). Similarly, 8-iso-prostaglandin F2α levels decreased with increasing anthocyanins dose (F = 3.513, P = 0.009). CONCLUSIONS Taken together, our results suggest that anthocyanin supplementation at a dose greater than 80 mg/d is an effective antioxidant and antiinflammatory agent in healthy young adults. OBJECTIVE The aim of this study was to analyze the effect of nighttime energy intake on daily energy and macronutrient distribution and weight gain during pregnancy. METHODS This was a prospective cohort study carried out with 100 pregnant women and the data collection occurred once per trimester. A dietary intake was assessed by three 24-h dietary recalls in each trimester, totaling nine dietary recalls. The distribution of energy and macronutrient intake was evaluated at meals throughout the day in each trimester and overall pregnancy. Women were classified as having "lower" or "higher" nighttime intake (1900 to 0559) if consumption in this period were below or above the median of the population, respectively, for at least two trimesters. Recommendations from the Institute of Medicine were used to assess the adequacy of weight gain. Generalized estimating equation models were used to determine the effects of nighttime intake and gestational trimesters on daily energy distribution and weight gain. RESULTS In overall pregnancy, the higher group consumed a higher percentage of energy and macronutrients in the evening meals, and less energy, proteins, and lipids in morning meals when compared with the lower group. Also, women in the higher group had greater excessive weight gain in the third trimester compared with the lower group. CONCLUSION Pregnant women with a higher energy intake at night had a lower percentage of energy, protein, and lipid intake in morning meals and a higher percentage of energy and macronutrient intake in the evening meals during pregnancy. A worse standard of gestational weight gain in the third trimester was also observed in pregnant women with a higher energy intake at night. Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that is activated downstream of a broad range of receptors particularly interleukin-6 (IL-6) family. STAT3 is the key regulator of cell proliferation, survival and apoptosis and is constitutively activated in most human cancers, indicating that it can be an important potential therapeutic target for cancer treatment. STAT3 also has important roles in lymphocyte biology, regulation of immune responses and autoimmunity. Considering the vital role of STAT3 in tumor progression and autoimmunity, scientists have focused to develop small molecules that suppress STAT3 function. In this review, we firstly discussed the predominant role of STAT3 in cancer and autoimmune diseases. Subsequently, we discussed the efficacy and therapeutic potential of different STAT3 inhibitors in cancer and autoimmune diseases in preclinical studies and clinical trials offering an insight into novel approaches for development of new STAT3 inhibitors. Non-small cell lung cancer (NSCLC) is one of the prevalent and deadly cancers worldwide. Chemotherapy resistance is one of the most challenging problems for NSCLC and other cancer treatment. Recent study suggested that miRNAs are involved in therapeutic functions of chemotherapy during cancer treatment. Our present study established doxorubicin (Dox) resistant NSCLC A549 and H460 cells (named A549Dox/R and H460 Dox/R). We found that miR-199a-5p was significantly down regulated in Dox resistant cells. Over expression of miR-199a-5p can increase the Dox sensitivity of resistant cells. Among various targets of miR-199a-5p, chemoresistance can increase the expression of ABCC1 and HIF-1α. Gain and loss of function studies confirmed that both ABCC1 and HIF-1α were involved in the chemoresistance of NSCLC cells. Collectively, our data showed that miR-199a-5p regulated expression of ABCC1 and HIF-1α were involved in Dox resistance of NSCLC. Obesity is one of the main causes of human cardiovascular and cerebrovascular diseases. Baicalin, a bioactive flavonoid isolated from the herbal medicine Scutellaria baicalensis Georgi, is reported to ameliorate obesity and hyperlipidemia. However, its mechanism remains unclear. Here, we used network pharmacology to explore the potential mechanism of baicalin on a system level. First, we predicted the targets of baicalin and diseases, and then protein-protein interaction (PPI) networks were constructed. Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment was performed via the Database for Annotation, Visualization, and Integrated Discovery (DAVID) server. Lastly, we confirmed the results of the network analysis by palmitic acid (PA) treated human hepatoma cells (HepG2) in vitro. https://www.selleckchem.com/products/pentamidine.html The results indicated that 37 targets related to obesity treated by baicalin were predicted by network pharmacology, and top 10 related pathways were extracted by the KEGG database. Baicalin treatment could reduce triglyceride (TG) contents and lipid droplet accumulation in PA-treated HepG2 cells. The anti-obesity effects of baicalin might be due to the up-regulation of solute carrier family 2 member 1 (SLC2A1) and down-regulation of tumor necrosis factor (TNF), nuclear factor kappa B subunit 1 (NFKB1), sterol regulatory element binding transcription factor 1 (SREBF1), peroxisome proliferator activated receptor gamma and caspase 3 (CASP3). Our results indicated that baicalin may regulate key inflammatory markers, adipogenesis process, and apoptosis for treatment of obesity. It is well demonstrated that antidepressant fluoxetine has significant inhibitory effects on voltage-gated potassium channels. So far, the concise regulation of fluoxetine on Kv2.1, the predominant delayed rectifier potassium channel subtype in the central nervous system, are rarely reported. Here patch-clamp recording was used to investigate the inhibitory effects of fluoxetine on Kv2.1 potassium channels stably expressed in HEK293 cells. The results showed fluoxetine dose-dependently suppressed Kv2.1 currents with an IC50 of 51.3 μM. At the test potential positive to +50 mV, fluoxetine 50 μM voltage-dependently suppressed Kv2.1 currents with an electrical distance δ of 0.28. Moreover, fluoxetine 50 μM did not affect the activation process of Kv2.1, but reduced the decay time constant τinact and obviously accelerated the inactivation process of Kv2.1 and left-shifted the half-maximal inactivation potential of Kv2.1 potassium channel by 9.8 mV. Fluoxetine 50 μM notably delayed the recovery process of Kv2.1 from inactivation with increased time constants.