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We found that GATA6-AS1 expression was low-expressed in LUAD tissues and cells. Furthermore, the upregulation of GATA6-AS1 suppressed the proliferative, migration and invasion abilities, as well as promoted apoptotic rate of A549 and H1975 cells. Moreover, the mechanistic investigations revealed that GATA6-AS1 upregulated the expression of its cognate sense gene GATA6 by binding with miR-4530, thereby modulating the malignant progression of LUAD cells.

GATA6-AS1 repressed LUAD cell proliferation, migration and invasion, and promoted cell apoptosis via regulation of the miR-4530/GATA6 axis, indicating GATA6-AS1 as a new prognostic biomarker for LUAD.
GATA6-AS1 repressed LUAD cell proliferation, migration and invasion, and promoted cell apoptosis via regulation of the miR-4530/GATA6 axis, indicating GATA6-AS1 as a new prognostic biomarker for LUAD.
The refractive surgeries induce corneal higher order aberrations (C-HOAs). In this study, change of C-HOAs after small-incision lenticule extraction (SMILE) compared to femtosecond assisted laser in situ keratomileusis (femto-LASIK), and to photorefractive keratectomy with mitomycin-C (PRK) under photopic and mesopic conditions.

In this prospective study, age, gender, and apical corneal thickness (ACT) matched cases with moderate myopia [spherical equivalent (SE) 3.00 to 6.00D) to high myopia (SE > 6.00D)] were enrolled. In addition to visual acuity and refraction, total C-HOA, coma, spherical aberration (SA), and trefoil in the 3- and 6-mm zones were measured before and 3 and 6 months after surgery.

Overall, 372 moderate myopia cases (124 eyes of 124 individuals in each surgical group) and 171 high myopia cases (57 eyes of 57 individuals in each surgical group) were enrolled. At baseline, the differences in age, gender, ACT, uncorrected and corrected visual acuity, and SE were not statistically significant between subgroups of surgical methods within each myopia group (all P > 0.05). At 12 months, in the moderate myopia group, there was less increase in 6-mm zone total C-HOA, coma, and SA with SMILE compared to the other groups (all P < 0.05). In the high myopia group, there was greater increase in photopic total C-HOA and trefoil and less increase in mesopic SA with SMILE (all P < 0.05).

In correction of moderate myopia, SMILE has better results in mesopic condition. In high myopia correction, femto-LASIK and PRK have better results in photopic and SMILE in mesopic condition.
In correction of moderate myopia, SMILE has better results in mesopic condition. In high myopia correction, femto-LASIK and PRK have better results in photopic and SMILE in mesopic condition.
Nintedanib is effective for treating idiopathic pulmonary fibrosis (IPF), but some patients may exhibit a suboptimal response and develop on-treatment acute exacerbation (AE-IPF), hepatic injury, or mortality. It remains unclear which patients are at risk for these adverse outcomes.

We analysed the demographic and clinical data, baseline plasma levels of Krebs von den Lungen-6 (KL-6) and surfactant protein A (SPA), and longitudinal clinical courses of a real-world cohort of IPF patients who received nintedanib ≥ 14days between March 2017 and December 2020. Cox proportional-hazards regression, subdistribution hazards regression, and sensitivity analyses were performed to investigate the association between baseline predictors and AE-IPF, mortality, and nintedanib-related hepatic injury. The relationship between baseline predictors and pulmonary function decline was determined.

Fifty-seven patients were included, of whom 24 (42%) developed hepatic injury, 20 (35%) had AE-IPF, and 16 (28%) died on-treatmenthe risk of adverse outcomes. Patients with these predictors may require close monitoring for unfavourable responses during treatment. Our findings also support the prognostic role of molecular markers like KL-6 and may contribute to future formulation of more individualized therapeutic strategies for IPF.
For patients with IPF who are receiving nintedanib, we have identified baseline predictors, in particular plasma KL-6 levels, for the risk of adverse outcomes. Patients with these predictors may require close monitoring for unfavourable responses during treatment. Our findings also support the prognostic role of molecular markers like KL-6 and may contribute to future formulation of more individualized therapeutic strategies for IPF.
Anxiety disorders are highly prevalent mental health conditions and are managed predominantly in primary care. We conducted a systematic review and meta-analysis of psychological and pharmacological treatments in countries with universal healthcare, and investigated the influence of treatment provider on the efficacy of psychological treatment.

PubMed, Cochrane, PsycINFO, CINAHL, and Scopus were searched in April 2017 for controlled studies of evidence-based anxiety treatment in adults in primary care, published in English since 1997. Searches were repeated in April 2020. find more We synthesised results using a combination of meta-analysis and narrative methods. Meta-analysis was conducted using a random-effects multi-level model to account for intercorrelation between effects contributed different treatment arms of the same study. Moderator variables were explored using meta-regression analyses.

In total, 19 articles (from an initial 2,247) reporting 18 studies were included. Meta-analysis including ten studiesvide effective treatment compared with no care at all. Limited research into the efficacy of pharmacological treatments in primary care needs to be considered carefully by prescribers TRIAL REGISTRATION PROSPERO registration number CRD42018050659.
Psychological treatments for anxiety are effective in primary care and are more effective when provided by a specialist (psychologist or clinical psychologist) than a non-specialist (GP, nurse, trainee). However, non-specialists provide effective treatment compared with no care at all. Limited research into the efficacy of pharmacological treatments in primary care needs to be considered carefully by prescribers TRIAL REGISTRATION PROSPERO registration number CRD42018050659.
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