Flow reversals in thermally driven turbulence

We analyze the reversals of the large scale flow in Rayleigh-B\'enard convection both through particle image velocimetry flow visualization and direct numerical simulations (DNS) of the underlying Boussinesq equations in a (quasi) two-dimensional, rectangular geometry of aspect ratio 1. For medium Prandtl number there is a diagonal large scale convection roll and two smaller secondary rolls in the two remaining corners diagonally opposing each other. These corner flow rolls play a crucial role for the large scale wind reversal: They grow in kinetic energy and thus also in size thanks to plume detachments from the boundary layers up to the time that they take over the main, large scale diagonal flow, thus leading to reversal. Based on this mechanism we identify a typical time scale for the reversals. We map out the Rayleigh number vs Prandtl number phase space and find that the occurrence of reversals very sensitively depends on these parameters.Comment: 4 pages, 4 figure

Phase transition in bulk single crystals and thin films of VO2 by nanoscale infrared spectroscopy and imaging

We have systematically studied a variety of vanadium dioxide (VO2) crystalline forms, including bulk single crystals and oriented thin films, using infrared (IR) near-field spectroscopic imaging techniques. By measuring the IR spectroscopic responses of electrons and phonons in VO2 with sub-grain-size spatial resolution (∼20nm), we show that epitaxial strain in VO2 thin films not only triggers spontaneous local phase separations, but also leads to intermediate electronic and lattice states that are intrinsically different from those found in bulk. Generalized rules of strain- and symmetry-dependent mesoscopic phase inhomogeneity are also discussed. These results set the stage for a comprehensive understanding of complex energy landscapes that may not be readily determined by macroscopic approaches

2-HG通过上调RIP3启动子的甲基化水平抑制细胞坏死

文章简介在异柠檬酸脱氢酶1/2(IDH1/2)突变的细胞中,高浓度的2-羟基戊二酸(2-HG)通过抑制TET2的活性增强了DNA的甲基化。在本研究中,课题组发现2-HG可通过直接激活DNA甲基转移酶DNMT1的作用而促进RIP3启动子的国家基础研究计划基金(973 Program;2015CB553800,2013CB944903,2014CB541804);;国家自然科学基金项目(91029304,31420103910,31330047,81630042,81372702,81402285,31571473);;中央高校基本科研专项资金(20720140552,10120100002);;国家基础科学人才培养基金(Grant No.J1310027)的资

Food habits and risk of cardiovascular disease in schoolchildren from Ouro Preto, Minas Gerais

OBJECTIVE: To investigate the relationship between food habits and risk factors for cardiovascular disease in schoolchildren of the city Ouro Preto, Minas Gerais. METHODS: A cross-sectional study was conducted in a population-based sample of 738 schoolchildren aged 6-14 years. A semi-structured questionnaire was used for collecting demographic, socioeconomic, biochemical, clinical, and anthropometric data. Food intake was determined by a food-frequency questionnaire. Food habits were evaluated according to the adapted Recommended Food Score. Multiple linear regression models were constructed to assess how food consumption was associated with cardiovascular risk factors. RESULTS: The schoolchildren presented a dietary pattern characterized by low consumption of healthy foods. Association of cardiovascular risk factors showed that the consumption of foods according to the adapted Recommended Food Score was negatively and significantly associated with tetrapolar percentage of body fat (p=0.030) and systolic blood pressure (p=0.049) in children aged 6-9 years. CONCLUSION: Children's dietary patterns proved to be an important determinant of some of the cardiovascular risk factors studied. Thus, food intake assessment is a primary tool for the prevention and early intervention on cardiovascular risk factors during childhood

Serine residue 115 of MAPK-activated protein kinase MK5 is crucial for its PKA-regulated nuclear export and biological function

The mitogen-activated protein kinase-activated protein kinase-5 (MK5) resides predominantly in the nucleus of resting cells, but p38MAPK, extracellular signal-regulated kinases-3 and -4 (ERK3 and ERK4), and protein kinase A (PKA) induce nucleocytoplasmic redistribution of MK5. The mechanism by which PKA causes nuclear export remains unsolved. In the study reported here we demonstrated that Ser-115 is an in vitro PKA phosphoacceptor site, and that PKA, but not p38MAPK, ERK3 or ERK4, is unable to redistribute MK5 S115A to the cytoplasm. However, the phosphomimicking MK5 S115D mutant resides in the cytoplasm in untreated cells. While p38MAPK, ERK3 and ERK4 fail to trigger nuclear export of the kinase dead T182A and K51E MK5 mutants, S115D/T182A and K51E/S115D mutants were able to enter the cytoplasm of resting cells. Finally, we demonstrated that mutations in Ser-115 affect the biological properties of MK5. Taken together, our results suggest that Ser-115 plays an essential role in PKA-regulated nuclear export of MK5, and that it also may regulate the biological functions of MK5

For whom and under what circumstances do school-based energy balance behavior interventions work? Systematic review on moderators

The aim of this review was to systematically review the results and quality of studies investigating the moderators of school-based interventions aimed at energy balance-related behaviors. We systematically searched the electronic databases of Pubmed, EMBASE, Cochrane, PsycInfo, ERIC and Sportdiscus. In total 61 articles were included. Gender, ethnicity, age, baseline values of outcomes, initial weight status and socioeconomic status were the most frequently studied potential moderators. The moderator with the most convincing evidence was gender. School-based interventions appear to work better for girls than for boys. Due to the inconsistent results, many studies reporting non-significant moderating effects, and the moderate methodological quality of most studies, no further consistent results were found. Consequently, there is lack of insight into what interventions work for whom. Future studies should apply stronger methodology to test moderating effects of important potential target group segmentations

EGCG Enhances the Therapeutic Potential of Gemcitabine and CP690550 by Inhibiting STAT3 Signaling Pathway in Human Pancreatic Cancer

Background: Signal Transducer and Activator of Transcription 3 (STAT3) is an oncogene, which promotes cell survival, proliferation, motility and progression in cancer cells. Targeting STAT3 signaling may lead to the development of novel therapeutic approaches for human cancers. Here, we examined the effects of epigallocathechin gallate (EGCG) on STAT3 signaling in pancreatic cancer cells, and assessed the therapeutic potential of EGCG with gemcitabine or JAK3 inhibitor CP690550 (Tasocitinib) for the treatment and/or prevention of pancreatic cancer. Methodology/Principal Findings: Cell viability and apoptosis were measured by XTT assay and TUNEL staining, respectively. Gene and protein expressions were measured by qRT-PCR and Western blot analysis, respectively. The results revealed that EGCG inhibited the expression of phospho and total JAK3 and STAT3, STAT3 transcription and activation, and the expression of STAT3-regulated genes, resulting in the inhibition of cell motility, migration and invasion, and the induction of caspase-3 and PARP cleavage. The inhibition of STAT3 enhanced the inhibitory effects of EGCG on cell motility and viability. Additionally, gemcitabine and CP690550 alone inhibited STAT3 target genes and synergized with EGCG to inhibit cell viability and induce apoptosis in pancreatic cancer cells. Conclusions/Significance: Overall, these results suggest that EGCG suppresses the growth, invasion and migration of pancreatic cancer cells, and induces apoptosis by interfering with the STAT3 signaling pathway. Moreover, EGCG furthe

The diterpenoid alkaloid noroxoaconitine is a Mapkap kinase 5 (MK5/PRAK) inhibitor

The mitogen-activated protein kinase-activated protein kinase MK5 is ubiquitously expressed in vertebrates and is implicated in cell proliferation, cytoskeletal remodeling, and anxiety behavior. This makes MK5 an attractive drug target. We tested several diterpenoid alkaloids for their ability to suppress MK5 kinase activity. We identified noroxoaconitine as an ATP competitor that inhibited the catalytic activity of MK5 in vitro (IC50 = 37.5 μM; Ki = 0.675 μM) and prevented PKA-induced nuclear export of MK5, a process that depends on kinase active MK5. MK5 is closely related to MK2 and MK3, and noroxoaconitine inhibited MK3- and MK5- but not MK2-mediated phosphorylation of the common substrate Hsp27. Molecular docking of noroxoaconitine into the ATP binding sites indicated that noroxoaconitine binds more strongly to MK5 than to MK3. Noroxoaconitine and derivatives may help in elucidating the precise biological functions of MK5 and may prove to have therapeutic values