Closely related hybridizing species are ideal systems for identifying genomic regions underlying adaptive divergence. Although gene expression plays a central role in determining ecologically-based phenotypic differences, few studies have inferred the role of gene expression for adaptive divergence in Neotropical systems. In this study, we conduct genome-wide expression analysis alongside soil elemental analysis in sympatric and allopatric populations of Epidendrum fulgens and E. puniceoluteum (Orchidaceae), which occur in contrasting adjacent habitats in the Neotropical coastal plains.

These species were highly differentiated by their gene expression profiles, as determined by 18-21% of transcripts. Gene ontology (GO) terms associated with reproductive processes were enriched according to comparisons between species in both allopatric and sympatric populations. Species showed differential expression in genes linked to salt and waterlogging tolerance according to comparisons between species in sympatry, ag ecological differentiation and assortative mating, and suggests candidate genes, such as those encoding catalase and calcium-dependent protein kinase, underling adaptation to harsh edaphic conditions in the Neotropical coastal plains. Moreover, it demonstrates that differential gene expression plays a central role in determining ecologically-based phenotypic differences among co-occurring species and their hybrids.

The degradation of cellulose and hemicellulose molecules into simpler sugars such as glucose is part of the second generation biofuel production process. Hydrolysis of lignocellulosic substrates is usually performed by enzymes produced and secreted by the fungus Trichoderma reesei. Studies identifying transcription factors involved in the regulation of cellulase production have been conducted but no overview of the whole regulation network is available. A transcriptomic approach with mixtures of glucose and lactose, used as a substrate for cellulase induction, was used to help us decipher missing parts in the network of T. reesei Rut-C30.

Experimental results on the Rut-C30 hyperproducing strain confirmed the impact of sugar mixtures on the enzymatic cocktail composition. The transcriptomic study shows a temporal regulation of the main transcription factors and a lactose concentration impact on the transcriptional profile. A gene regulatory network built using BRANE Cut software reveals three sub-networksof the β-glucosidase and a decrease of growth in favor of cellulase production. These conclusions provide us with potential targets for further genetic engineering leading to better cellulase-producing strains in industry-like conditions.

We investigated the association between psychological distress and oral health status/oral health-related quality of life (OHQoL) in Japanese community-dwelling people.

We conducted a cross-sectional study using data from the Nagasaki Islands Study. A total of 1183 (455 men and 728 women) has been analyzed in this study. Psychological distress was measured using the Kessler Psychological Distress Scale (K6). Oral health status was measured by dental examination. The OHQoL was measured using the General Oral Health Assessment Index (GOHAI). We defined the total score of ≥5 points on the K6 as high psychological distress (high-K6 group).

The multiple linear regression analysis to identify the GOHAI showed that gender, K6, the total number of teeth, the number of dental caries, and visiting a dental clinic within the past 6 months significantly associated with the GOHAI. Among all of these variables, high-K6 (≥ 5) was a substantial contributing factor of the GOHAI (β = – 0.23, 95% Cl – 2.31 to -1.41, p < 0.0001).

It is likely that the individual with high psychological distress was strongly related to poor OHQoL even in the general population.

It is likely that the individual with high psychological distress was strongly related to poor OHQoL even in the general population.Transient ischemia is an exacerbation factor of Alzheimer’s disease (AD). We aimed to examine the influence of amyloid β (Aβ) deposition around the cerebral (pial) artery in terms of diameter changes in the cerebral artery during transient ischemia in AD model mice (APPNL-G-F) under urethane anesthesia. TEW-7197 Cerebral vasculature and Aβ deposition were examined using two-photon microscopy. Cerebral ischemia was induced by transient occlusion of the unilateral common carotid artery. The diameter of the pial artery was quantitatively measured. In wild-type mice, the diameter of arteries increased during occlusion and returned to their basal diameter after re-opening. In AD model mice, the artery response during occlusion differed depending on Aβ deposition sites. Arterial diameter changes at non-Aβ deposition site were similar to those in wild-type mice, whereas they were significantly smaller at Aβ deposition site. The results suggest that cerebral artery changes during ischemia are impaired by Aβ deposition.Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. AMI causes a necrosis of cardiac cells and triggers a complex inflammatory response, affecting infarct size, cardiac function and clinical outcomes. This inflammatory response can be divided into 3 phases 1) the pro-inflammatory phase, in which the release of damage-associated molecular patterns from necrotic cells triggers the secretion of pro-inflammatory mediators and attracts immune cells to clean the debris, further damaging viable myocardium, 2) the reparative phase, in which antiinflammatory signals activate immune-modulating cells and trigger the production of a stable scar, 3) the maturation phase, in which inflammatory and fibrotic signals are suppressed, but may persist, leading to left ventricular adverse remodelling. Thus, the inflammatory response is an appealing therapeutic target to improve outcomes of patients AMI. Numerous anti-inflammatory therapies have shown promise in animal models, but translation to human trials exhibited limited benefit. Glucocorticoids and non-steroidal anti-inflammatory drugs showed signals of harm due to their nonspecific effects. Other broad inhibitors, e.g. methotrexate, cyclosporine, or colchicine, did not improve clinical outcomes as acute therapies for MI. Specific inhibitors of the complement cascade, adhesion molecules, or inflammatory mediators were mostly disappointing in humans. However, an interleukin-1 inhibitor (anakinra), and a matrix metalloproteinase inhibitor (doxycycline) improved clinical outcomes in patients with AMI. Promising RNAse1, anti-toll-like receptor 2 antibodies, and inflammasome inhibitors still need to be tested in humans. Finally, positive results should be replicated in large clinical trials before they can be implemented into the standard AMI therapy.