83; 95% CI 0.71, 0.96; p-trend = 0.03) and significantly higher BUA (Q5-Q1 1.4 dB/MHz 95% CI 0.5, 2.3; p-trend less then 0.01) and FFMBMI (Q5-Q1 0.03 kg/(kg/m2) 95% CI 0.01, 0.04; p-trend less then 0.01). This evidence supports the need to develop interventions to enhance MD adherence, particularly in women, where evidence for associations was stronger.Aluminum (Al) is well known as a potent inhibitor of plant growth and development. It is notably present in soils in the soluble and bioavailable form Al3+ when the soil pH drops below 5. This situation is frequent, especially in softwood forests when litter decomposition is slow. In the present work, we studied the effects of Al3+ on the growth and development of Douglas fir plantlets. Somatic plantlets, regenerated via somatic embryogenesis, were grown in vitro on media supplemented with different concentrations of aluminum chloride (AlCl3) 0 µM, 200 µM, 500 µM. and 1 mM. We show that a concentration of 500 µM AlCl3 in medium significantly reduced root elongation (-21.8%), as well as stem growth (-14.6%). Also, a 25% reduction in dry mass of the plantlets was observed in presence of a concentration of 200 µM of AlCl3. Histological analysis of root tissues revealed significant damage, especially in conducting vessels. In addition, mineral cation content of plantlets was disturbed under Al exposure. More particularly, the Mg and K contents of needles and the Ca content of stems and needles were significantly reduced in presence of a concentration of 500 µM AlCl3 in the culture medium (-35.6%, -33.5%, -24%, and -34% respectively). However, all these damages appeared at relatively high Al concentrations when compared with other herbaceous species. This study shed light on the ability of Douglas fir in vitro plantlets to cope with the acid-driven toxicity of Al.Gastric cancer (GC) is turning out today to be one of the most important welfare issues for both Asian and European countries. Indeed, while the vast majority of the disease burden is located in China and in Pacific and East Asia, GC in European countries still account for about 100,000 deaths per year. With this review article, we aim to focus the attention on one of the most complex cellular pathways involved in GC proliferation, invasion, migration, and metastasis the MAP kinases. Such large kinases family is to date constantly studied, since their discovery more than 30 years ago, due to the important role that it plays in the regulation of physiological and pathological processes. Interactions with other cellular proteins as well as miRNAs and lncRNAs may modulate their expression influencing the cellular biological features. Here, we summarize the most important and recent studies involving MAPK in GC. At the same time, we need to underly that, differently from cancers arising from other tissues, where MAPK pathways seems to be a gold target for anticancer therapies, GC seems to be unique in any aspect. Our aim is to review the current knowledge in MAPK pathways alterations leading to GC, including H. pylori MAPK-triggering to derail from gastric normal epithelium to GC and to encourage researches involved in MAPK signal transduction, that seems to definitely sustain GC development.Peer networks at school and students’ position in these networks can influence their academic well-being. We study here individual students’ network position (isolation, popularity, social activity) and peer network structures at the school level (centralization, density, clustering, school connectedness) and their relations to students’ academic well-being (school burnout, SB; schoolwork engagement, SE). Classroom surveys for 14-16-year-olds (N = 11,015) were conducted in six European cities (SILNE survey). Students were asked to nominate up to five schoolmates with whom they preferred to do schoolwork. SP600125negativecontrol SB and SE correlated negatively (-0.32; p less then 0.0001). Students had on average 3.4 incoming (popularity; range 0-5) and 3.4 outgoing (social activity; 0-5) social ties. Percentage of isolated students was 1.4. Students’ network position was associated weakly with academic well-being-popular students had less SB and higher SE, and socially active students had higher SE. School-level peer networks showed high clustering and school connectedness, but low density and low centralization. Clustering was associated with higher SB. Low centralization and high school connectedness protected from SB. Dense networks supported SE as did high average school connectedness. Correlations between these network indicators and academic well-being were, however, low. Our study showed that both students’ network position and network characteristics at the school level can influence adolescents’ academic well-being.Cystic fibrosis (CF), caused by biallelic inactivating mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, has recently been categorized as a familial colorectal cancer (CRC) syndrome. CF patients are highly susceptible to early, aggressive colorectal tumor development. Endoscopic screening studies have revealed that by the age of forty 50% of CF patients will develop adenomas, with 25% developing aggressive advanced adenomas, some of which will have already advanced to adenocarcinomas. This enhanced risk has led to new CF colorectal cancer screening recommendations, lowering the initiation of endoscopic screening to age forty in CF patients, and to age thirty in organ transplant recipients. The enhanced risk for CRC also extends to the millions of people (more than 10 million in the US) who are heterozygous carriers of CFTR gene mutations. Further, lowered expression of CFTR is reported in sporadic CRC, where downregulation of CFTR is associated with poor survival. Mechanisms underlying the actions of CFTR as a tumor suppressor are not clearly understood. Dysregulation of Wnt/β-catenin signaling and disruption of intestinal stem cell homeostasis and intestinal barrier integrity, as well as intestinal dysbiosis, immune cell infiltration, stress responses, and intestinal inflammation have all been reported in human CF patients and in animal models. Notably, the development of new drug modalities to treat non-gastrointestinal pathologies in CF patients, especially pulmonary disease, offers hope that these drugs could be repurposed for gastrointestinal cancers.