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Overall, earlier acquisition was predicted by features representing frames that select for nouns and verbs, and by thematic content related to food and face-to-face play topics; later acquisition was predicted by features representing frames that select for pronouns and question words, and by content related to narratives and object play.Epidermal growth factor receptor (EGFR) induces peroxisome-proliferator-activated receptor-δ (PPARδ)-Y108 phosphorylation, while it is unclear the effect of phosphorylation of PPARδ on cancer cell metabolism. Here we found that EGF treatment increased its protein stability by inhibiting its lysosomal dependent degradation, which was reduced by gefitinib (EGFR inhibitor) treatment. PPARδ-Y108 phosphorylation in response to EGF recruited HSP90 (heat shock protein 90) to PPARδ resulting in increased PPARδ stability. In addition, PPARδ-Y108 phosphorylation promoted cancer cell metabolism, proliferation, and chemoresistance. Therefore, this study revealed a novel molecular mechanism of EGFR/HSP90/PPARδ pathway-mediated cancer cell metabolism, proliferation, and chemoresistance, which provides a strategy for cancer treatment.The aberrant expression of long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) has been previously associated with myocardial ischemia-reperfusion injury (MIRI), but the underlying molecular mechanisms remain elusive. The current study aimed to clarify the functional role of TUG1/microRNA (miR)-340/histone deacetylase 4 (HDAC4)/β-catenin/glucose transporter type 1 (GLUT1) axes in MIRI. The database-based analyses performed predicted the downstream factors of lncRNA TUG1. In the MIRI mouse models and hypoxia/reoxygenation (H/R)-induced cardiomyocyte models, the expression of TUG1/miR-340/HDAC4/β-catenin/GLUT1 was manipulated to examine their effects on the infarction area, cardiomyocyte viability and apoptosis employing the Evans blue/TTC double staining, CCK-8 and TUNEL assays. Furthermore, the dual luciferase reporter and RIP assays verified the binding affinity of miR-340 to TUG1 and HDAC4. Subsequently, a negative correlation between miR-340 and TUG1 or HDAC4 expression was identified in myocardial tissues of MIRI mice and H/R-induced cardiomyocyte models, along with a positive correlation between TUG1 and HDAC4. Additionally, it was established that TUG1 bound to miR-340, and miR-340 targeted HDAC4. TUG1 upregulated HDAC4 expression, thereby promoting MIRI in the mouse models. HDAC4 was proven to repress the expression of β-catenin and its target gene GLUT1. Moreover, the in vivo experiments validated that the inhibition of TUG1/miR-340/HDAC4/β-catenin/GLUT1 axes alleviated MIRI in mice. Collectively, the current study uncovered the role of TUG1/miR-340/HDAC4/β-catenin/GLUT1 axes in MIRI mouse models and H/R-induced cardiomyocyte models which may be a potential therapeutic target for MIRI treatment.The authors conducted a subanalysis of the ReHOT (Resistant Hypertension Optimal Treatment) study to evaluate the association between endothelial dysfunction and resistant hypertension in a population of patients treated in a staged fashion for hypertension. One hundred and three hypertensive patients were followed for 6 months and participated in seven visits (V0-V6) 28 days apart. selleck There was a first phase (V0-V3) of antihypertensive adjustment with three drugs and determination of resistant hypertension and a second randomized phase (V3-V6) of treatment with a fourth drug (clonidine or spironolactone) in the hypertensive patients characterized as resistant. Of the 103 patients included, 86 (83.5%) underwent the randomization visit (V3), 71 were characterized as non-resistant hypertensives (82.5%), and 15 as resistant hypertensives (17.5%). Serum asymmetric dimethylarginine (ADMA) was shown to be an independent predictor of resistant hypertension after adjustment for multiple variables (OR 11.42, 95% CI 1.02-127.71, P = .048), and in addition, there was a reduction in blood pressure levels and ADMA values during follow-up with a positive correlation in both groups and a greater reduction in the group of resistant hypertensives. We demonstrated that ADMA was an independent predictor of resistant hypertension, and we observed that the improvement in blood pressure levels obtained with the treatment was proportional to the reduction in ADMA values, suggesting a complementary role of ADMA not only as a stratification tool for the occurrence of resistant hypertension, but also as a possible therapeutic target in this population.

To systematically review and evaluate the effects of different types of attachments, implant numbers and loading protocols on the peri-implant mucosa of implant-supported overdentures (ISODs).

The impact of peri-implant tissue health on the ISOD treatment outcome is unclear, and current evidence is inadequate on this aspect.

A systematic literature search for randomised controlled trials or prospective studies was conducted in indexed databases from 1995 to April 2020. The focused question was as follows How does the peri-implant mucosa respond to implant-supported or implant-tissue-supported complete overdentures based on different types of attachments, implant numbers, and loading protocols, in terms of clinical outcomes achieved [plaque index (PI), gingival index (GI), probing pocket depth (PD) and bleeding index (BI)]? A random- or fixed-effects model was applied to measure the significance of standardised mean differences (SMD) of PD between the groups.

Seventeen studies met the eligibility criteria. The SMD for PD between splinted/bar and unsplinted/stud attachments was 0.10mm (95% CI -0.27 to 0.47; P=.60) and between 2- and 4-implant groups was 0.15mm (95% CI -0.16 to 0.45; P=.34), which were not statistically significant. Significant difference (P=.003) was observed between immediate/early loading and delayed loading (SMD=0.46mm [95% CI 0.16 to 0.75]).

Probing depth for the immediate loaded implants was significantly higher than for the delayed loading group. No attachment type, implant number or loading protocol seemed to have a clear advantage over the other, in terms of other peri-implant mucosal outcome measures.

Probing depth for the immediate loaded implants was significantly higher than for the delayed loading group. No attachment type, implant number or loading protocol seemed to have a clear advantage over the other, in terms of other peri-implant mucosal outcome measures.