Miracle-dz/UniFAR-FTUs huggingface dataset:
Predicting implementation of an empirically supported treatment for cancer patients using the theory of planned behavior.

BACKGROUND There is a continuing gap between the availability of cancer control empirically supported treatments (ESTs) to address psychological needs of cancer patients and their dissemination to and implementation by providers in the community. The Theory of Planned Behavior (TPB), with constructs of attitudes, subjective norms, perceived behavioral control, and intentions, is used to understand the pathways to and prediction of providers' behavior, that is, implementation of a cancer control EST and its provision to patients. PURPOSE The purpose of the study was to prospectively test the TPB in predicting providers' usage of a cancer-specific EST, the biobehavioral intervention (BBI). METHOD Providers (N = 166) were trained. At training's end, providers completed measures of attitudes, perceived behavioral control, and intentions to use the BBI, and their supervisors completed measures of attitudes operationalized as subjective norms. Providers were followed up and 4 months later reported their usage of the BBI with patients in the last 2 months. Regression-based path analyses tested attitudes, perceived behavioral control, subjective norms, and intentions as predictors of BBI usage and for the possible effect of intentions as a mediator. RESULTS Provider's BBI usage was high, delivered to 65.6% of patients. Providers' attitudes toward the BBI (b = .006; 95% confidence interval [CI: .002, .010]) and subjective norms (supervisors' attitudes toward providers' EST usage; b = .021; 95% CI [.007, .034]) predicted usage. Intentions predicted usage in univariate analyses but was not a mediator for usage. CONCLUSIONS Use of theory in implementation science can test and identify variables key to implementation success. Here the TPB identified providers' and supervisors' attitudes as predictors of EST usage. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
Microglial Pro-Inflammatory and Anti-Inflammatory Phenotypes Are Modulated by Translocator Protein Activation

A key role of the mitochondrial Translocator Protein 18 KDa (TSPO) in neuroinflammation has been recently proposed. However, little is known about TSPO-activated pathways underlying the modulation of reactive microglia. In the present work, the TSPO activation was explored in an in vitro human primary microglia model (immortalized C20 cells) under inflammatory stimulus. Two different approaches were used with the aim to (i) pharmacologically amplify or (ii) silence, by the lentiviral short hairpin RNA, the TSPO physiological function. In the TSPO pharmacological stimulation model, the synthetic steroidogenic selective ligand XBD-173 attenuated the activation of microglia. Indeed, it reduces and increases the release of pro-inflammatory and anti-inflammatory cytokines, respectively. Such ligand-induced effects were abolished when C20 cells were treated with the steroidogenesis inhibitor aminoglutethimide. This suggests a role for neurosteroids in modulating the interleukin production. The highly steroidogenic ligand XBD-173 attenuated the neuroinflammatory response more effectively than the poorly steroidogenic ones, which suggests that the observed modulation on the cytokine release may be influenced by the levels of produced neurosteroids. In the TSPO silencing model, the reduction of TSPO caused a more inflamed phenotype with respect to scrambled cells. Similarly, during the inflammatory response, the TSPO silencing increased and reduced the release of pro-inflammatory and anti-inflammatory cytokines, respectively. In conclusion, the obtained results are in favor of a homeostatic role for TSPO in the context of dynamic balance between anti-inflammatory and pro-inflammatory mediators in the human microglia-mediated inflammatory response. Interestingly, our preliminary results propose that the TSPO expression could be stimulated by NF-κB during activation of the inflammatory response.
Advances and Innovations in Aphasia Treatment Trials.

Aphasia is a common complication of stroke with a prevalence of ≈1 million in the United States alone. Poststroke aphasia (PSA) can be devastating, impacting an individual’s ability to express or comprehend language, often disrupting communication, socialization, and work. Intervention is often necessary to improve language, independence, and quality of life. This article summarizes advances in clinical trials of PSA treatment in the past 5 years. We completed a search of Pubmed to identify clinical trials completed within the past 5 years using the following terms: stroke, aphasia, treatment, speech therapy, speech-language pathology, transcranial direct current stimulation (tDCS), and transcranial magnetic stimulation (TMS). We included the 40 most relevant studies found in our search. Research trends include noninvasive brain stimulation (NIBS), novel Speech-Language Therapy (SLT), pharmacological treatments, and alternative treatments.
Comparison of vascular–function and structure–function correlations in glaucomatous eyes with high myopia

Background/aims To determine the usefulness of peripapillary retinal vessel density (VD) measured using optical coherence tomography (OCT) angiography (OCTA) in the evaluation of glaucomatous visual field damage in highly myopic eyes with primary open-angle glaucoma (POAG). Methods This cross-sectional observational study enrolled a total of 124 myopic POAG eyes consisting of 40 eyes showing a segmentation error (SE) in OCT scans and 84 eyes without an SE. The peripapillary retinal VD, circumpapillary retinal nerve fibre layer thickness (RNFLT) and visual field sensitivity loss (VFSL) were assessed using OCTA, spectral-domain OCT and standard automated perimetry, respectively. The topographical correlations between the VD and VFSL, and between the RNFLT and VFSL were determined in subgroups divided according to the presence of an SE. Results The peripapillary retinal VD showed significant topographical correlation with VFSL both in the highly myopic POAG eyes without an SE globally (R=0.527, p<0.001), and in temporal (R=0.593), temporal-superior (R=0.543), nasal-inferior (R=0.422) and temporal-inferior sectors (R=0.600, all p<0.001), and in those with an SE globally (R=0.343, p=0.030), and in temporal (R=0.494, p=0.001), temporal-superior (R=0.598, p<0.001), and temporal-inferior sectors (R=0.424, p=0.006). The correlation with VFSL did not differ between the VD and RNFLT in the eyes without an SE Conclusion Peripapillary VD as measured with OCTA showed a topographical correlation with VFSL in highly myopic POAG eyes regardless of the presence of an OCT SE OCTA may be a useful adjunct for evaluating glaucomatous visual field damage in high myopia, where the OCT results are frequently confounding.
The cellular prion protein and its derived fragments in human prion diseases and their role as potential biomarkers

ABSTRACT Introduction: Human prion diseases are a heterogeneous group of incurable and debilitating conditions characterized by a progressive degeneration of the central nervous system. The conformational changes of the cellular prion protein and its formation into an abnormal isoform, spongiform degeneration, neuronal loss, and neuroinflammation are central to prion disease pathogenesis. It has been postulated that truncated variants of aggregation-prone proteins are implicated in neurodegenerative mechanisms. An increasing body of evidence indicates that proteolytic fragments and truncated variants of the prion protein are formed and accumulated in the brain of prion disease patients. These prion protein variants provide a high degree of relevance to disease pathology and diagnosis. Areas covered: In the present review, we summarize the current knowledge on the occurrence of truncated prion protein species and their potential roles in pathophysiological states during prion diseases progression. In addition, we discuss their usability as a diagnostic biomarker in prion diseases. Expert opinion: Either as a primary factor in the formation of prion diseases or as a consequence from neuropathological affection, abnormal prion protein variants and fragments may provide independent information about mechanisms of prion conversion, pathological states, or disease progression.
Decreased Blood Asprosin in Hyperglycemic Menopausal Women as a Result of Whole-Body Cryotherapy Regardless of Metabolic Syndrome

Endocrine dysfunction often occurs in metabolic syndrome (MetS), resulting in hyperglycemia and atherogenic blood lipid profile disorders. Asprosin is a newly discovered glucose-regulating hormone. The study aim was to determine whether the application of whole-body cryotherapy (WBC) affects asprosin and selected adipocytokines as well as insulin resistance in menopausal women with metabolic disorders. A total of 37 menopausal women were exposed to 20 WBC (−130 °C, 3 min). Blood glucose, asprosin, irisin, leptin, adiponectin, and insulin were measured before and after 20 WBC treatments, after which a homeostasis model assessment of insulin resistance (HOMA-IR) and atherogenic index of plasma (AIP) were calculated. The results were analyzed in the MetS group compared to the controls (CON) without MetS, and in the hyperglycemic (HG) group compared to the normoglycemic group (NG). After 20 WBC, a significant reduction (p < 0.05) in asprosin concentration was found in the MetS, HG, and CON groups, and a significant decrease (p < 0.05) in glucose concentration was noted in the HG group. Changes in asprosin concentration positively correlated with changes in glucose concentration. Asprosin concentration before WBC correlated positively with metabolic disorder risk factor levels, and the change in asprosin concentration after 20 WBC correlated negatively with metabolic disorder risk factor levels: fasting glucose, AIP, and the leptin/adiponectin index. Research indicates the possibility of using WBC in supporting metabolic disorders, type 2 diabetes (T2DM), and insulin resistance.
Development of a diet quality index to assess adherence to Canadian dietary recommendations in 3-year-old children

Abstract Objective: Little is known about the diet quality of preschool children in Canada. We adapted an established diet quality index for European preschool children to align with the Canadian context and applied the index to dietary data of 3-year-old children to assess patterns of diet quality. Design: Our diet quality index (DQI-C) consists of four components that align with Canada’s Food Guide (Vegetables and Fruit, Grain Products, Milk and Alternatives and Meat and Alternatives) and two components that account for less healthy intakes (Candy/Snacks, and Sugar-Sweetened Beverages (SSB)). The ratio between consumption v. recommended intakes is calculated for each component and summed to give a total score from 0 to 6. Setting: Alberta, Canada. Participants: The DQI-C was applied to FFQ data from 1260 3-year-old children. Results: Mean DQI-C was 3·69 (sd 0·6). Most children met recommendations for Vegetables and Fruit (73 %) and Meat and Alternatives (70 %); however, fewer met recommendations for Milk and Alternatives (38 %) and Grain Products (13 %). Children in the lowest quartile for DQI-C score consumed a mean of 82 g of Candy/Snacks and 193 g of SSB daily, whereas those in the highest quartile consumed 45 g/d and 17 g/d of Candy and Snacks and SSB, respectively. Conclusion: This DQI-C score is useful for ranking Canadian preschool children according to their overall diet quality. There is room for improvement for consumptions of Grain Products, Meat and Alternatives, Candy/Snacks and SSB, which could be a target for initiatives to improve diet quality of preschool children in Canada.
Quercetin reduces atherosclerotic lesions by altering the gut microbiota and reducing atherogenic lipid metabolites

Epidemiological studies have correlated cardiovascular disease and atherosclerosis with lifestyle factors such as sedentary behaviour and a high‐calorie diet. Recent studies of pathogenesis have highlighted the significance of the intestinal microbiota and chronic inflammation with respect to both the onset and development of atherosclerosis. This study examined the hypothesis that the oral administration of quercetin to low‐density lipoprotein receptor‐null (Ldlr−/−) mice would improve gut health by altering the gut microbiota and controlling the levels of atherogenic lipid metabolites and proinflammatory mediators in the intestine and serum.
Predicting gene expression in the human malaria parasite Plasmodium falciparum using histone modification, nucleosome positioning, and 3D localization features

Empirical evidence suggests that the malaria parasite Plasmodium falciparum employs a broad range of mechanisms to regulate gene transcription throughout the organism’s complex life cycle. To better understand this regulatory machinery, we assembled a rich collection of genomic and epigenomic data sets, including information about transcription factor (TF) binding motifs, patterns of covalent histone modifications, nucleosome occupancy, GC content, and global 3D genome architecture. We used these data to train machine learning models to discriminate between high-expression and low-expression genes, focusing on three distinct stages of the red blood cell phase of the Plasmodium life cycle. Our results highlight the importance of histone modifications and 3D chromatin architecture in Plasmodium transcriptional regulation and suggest that AP2 transcription factors may play a limited regulatory role, perhaps operating in conjunction with epigenetic factors.
E-cadherin Downregulation and microRNAs in Sporadic Intestinal-Type Gastric Cancer

CDH1 gene, encoding E-cadherin, is a tumor suppressor gene frequently altered in gastric cancers (GCs) of both diffuse (DGC) and intestinal (IGC) histotypes, albeit through different mechanisms. The study aimed to characterize CDH1 expression in sporadic IGC and to investigate whether microRNAs (miRs) are involved in its transcriptional control. We evaluated CDH1 expression by quantitative real-time PCR (RT-qPCR) in 33 IGC patients and found a significant downregulation in tumor tissues compared to normal counterparts (p-value = 0.025). Moreover, 14 miRs, predicted to be involved in CDH1 regulation in both a direct and indirect manner, were selected and analyzed by RT-qPCR in an independent case series of 17 IGCs and matched normal tissues. miR-101, miR-26b, and miR-200c emerged as significantly downregulated and were confirmed in the case series of 33 patients (p-value < 0.001). Finally, we evaluated EZH2 expression, a target of both miR-101 and miR-26b, which showed significant upregulation in IGCs (p-value = 0.005). A significant inverse correlation was observed between EZH2 overexpression and CDH1, miR-101, and miR-26b levels (p-value < 0.001). Our results reinforce the link between CDH1 and IGC, highlighting the role of miRs in its transcriptional control and improving our understanding of GC subtypes and biomarkers.
Behavioral and Emotional Disorders and Transportation Noise among Children and Adolescents: A Systematic Review and Meta-Analysis

Children and adolescents may be particularly vulnerable to environmental influences such as noise which can affect mental well-being. The aim of this systematic review was to evaluate the effect of transportation noise on behavioral and emotional disorders in children and adolescents using a meta-analytic approach. Therefore, we searched four databases (Pubmed, Embase, PsychINFO, and PSYNDEX) and grey literature until February of 2019. We identified 14 articles from 10 studies examining the effect of transportation noise exposure on the mental health of children. These studies predominately used the Strength and Difficulties Questionnaire (SDQ) and mainly focused on schoolchildren and adolescents aged 9–10 years and 15–17 years in Europe. Three studies could be included in the meta-analysis. In sum, the odds for hyperactivity/inattention and total difficulties was significantly increased by 11% (Odds Ratio, OR = 1.11 (95% Confidence Interval, CI 1.04–1.19), respectively 9% (95% CI 1.02–1.16) per 10 dB road traffic noise. Thus, we obtained evidence for an effect of road traffic noise on hyperactivity/inattention and total difficulties, although we could consider few studies. Future studies are needed that use similar techniques to assess outcomes and exposures at schools and in homes. This would make it possible to conduct an individual participant data pooled analysis of the data.
Elektra prosthesis versus resection-suspension arthroplasty for thumb carpometacarpal osteoarthritis: a long-term cohort study

The present study compares 34 patients with thumb carpometacarpal osteoarthritis (37 thumbs) treated with the Elektra® prosthesis, with 18 patients (18 thumbs) treated with resection-suspension arthroplasty, with an overall mean follow-up period of 13.3 years. Evaluation with disability of arm and shoulder scores, pain via visual analogue scale and range of motion (radial and palmar abduction, and opposition) indicated no significant difference. However, the cohort with a surviving prosthesis showed significantly better subjective grip strength (p = 0.04). Complications occurred in 23 of the 37 thumbs in the prosthesis group compared with two in the resection-suspension arthroplasty patients. Seventeen prostheses required revision. At revision operations, we observed local signs of metallosis in 15 of 17 cases. The patients receiving resection-suspension arthroplasty were more satisfied with their treatment (p = 0.003). Therefore, we cannot recommend the implantation of Elektra® prosthesis and we speculate that the key problem of aseptic cup loosening is a result of the metal-on-metal bearing. Level of evidence: III
Neural stem cell temporal patterning and brain tumour growth rely on oxidative phosphorylation

Translating advances in cancer research to clinical applications requires better insight into the metabolism of normal cells and tumour cells in vivo. Much effort has focused on understanding how glycolysis and oxidative phosphorylation (OxPhos) support proliferation, while their impact on other aspects of development and tumourigenesis remain largely unexplored. We found that inhibition of OxPhos in neural stem cells (NSCs) or tumours in the Drosophila brain not only decreases proliferation, but also affects many different aspects of stem cell behaviour. In NSCs, OxPhos dysfunction leads to a protracted G1/S-phase and results in delayed temporal patterning and reduced neuronal diversity. As a consequence, NSCs fail to undergo terminal differentiation, leading to prolonged neurogenesis into adulthood. Similarly, in brain tumours inhibition of OxPhos slows proliferation and prevents differentiation, resulting in reduced tumour heterogeneity. Thus, in vivo, highly proliferative stem cells and tumour cells require OxPhos for efficient growth and generation of diversity.
JAK2 mutant hematopoietic cells display metabolic alterations that can be targeted to treat myeloproliferative neoplasms.

Increased energy requirement and metabolic reprograming are hallmarks of cancer cells. We show that metabolic alterations in hematopoietic cells are fundamental to the pathogenesis of mutant JAK2 driven myeloproliferative neoplasms (MPNs). We found that expression of mutant JAK2 augmented and subverted metabolic activity of MPN cells resulting in systemic metabolic changes in vivo, including hypoglycemia, adipose tissue atrophy and early mortality. Hypoglycemia in MPN mouse models correlated with hyperactive erythropoiesis and was due to a combination of elevated glycolysis and increased oxidative phosphorylation. Modulating nutrient supply through high fat diet improved survival, while high glucose diet augmented the MPN phenotype. Transcriptomic and metabolomic analyses identified numerous metabolic nodes in JAK2 mutant hematopoietic stem and progenitor cells that were altered in comparison with wildtype controls. We studied the consequences of elevated levels of Pfkfb3, a key regulatory enzyme of glycolysis, and found that pharmacological inhibition of Pfkfb3 with the small molecule 3PO reversed hypoglycemia and reduced hematopoietic manifestations of MPN. These effects were additive with the JAK1/2 inhibitor, Ruxolitinib, in vivo and in vitro. Inhibition of glycolysis by 3PO altered the redox homeostasis, leading to accumulation of reactive oxygen species and augmented apoptosis rate. Our findings reveal the contribution of metabolic alterations to the pathogenesis of MPN and suggest that metabolic dependencies of mutant cells represent vulnerabilities that can be targeted for treating MPN.
POT1 and Damage Response Malfunction Trigger Acquisition of Somatic Activating Mutations in the VEGF Pathway in Cardiac Angiosarcomas

Background Mutations in the POT1 gene explain abnormally long telomeres and multiple tumors including cardiac angiosarcomas (CAS). However, the link between long telomeres and tumorigenesis is poorly understood. Methods and Results Here, we have studied the somatic landscape of 3 different angiosarcoma patients with mutations in the POT1 gene to further investigate this tumorigenesis process. In addition, the genetic landscape of 7 CAS patients without mutations in the POT1 gene has been studied. Patients with CAS and nonfunctional POT1 did not repress ATR (ataxia telangiectasia RAD3‐related)–dependent DNA damage signaling and showed a constitutive increase of cell cycle arrest and somatic activating mutations in the VEGF (vascular endothelial growth factor)/angiogenesis pathway (KDR gene). The same observation was made in POT1 mutation carriers with tumors different from CAS and also in CAS patients without mutations in the POT1 gene but with mutations in other genes involved in DNA damage signaling. Conclusions Inhibition of POT1 function and damage‐response malfunction activated DNA damage signaling and increased cell cycle arrest as well as interfered with apoptosis, which would permit acquisition of somatic mutations in the VEGF/angiogenesis pathway that drives tumor formation. Therapies based on the inhibition of damage signaling in asymptomatic carriers may diminish defects on cell cycle arrest and thus prevent the apoptosis deregulation that leads to the acquisition of driver mutations.
Fractional exhaled nitric oxide measurement: Comparison between the Sunvou-CA2122 analyzer and the NIOX VERO analyzer

Abstract Background and objectives Fractional exhaled nitric oxide (FeNO) has been developed as a useful marker for eosinophilic airway inflammation and is widely used in clinical practice due to its convenience and noninvasiveness. There are two NO analyzers commonly used in China: the Sunvou-CA2122 Analyzer (NOS) and the NIOX VERO Analyzer (NOV). However, the relationships between the two devices have not yet been reported. The aim of our study was to determine the correlation and differences in the FeNO levels measured by the two devices. Methods FeNO levels were measured by both NOS and NOV in 107 adult patients with asthma. The asthma control test (ACT) score and lung function were also evaluated. This study was registered in the Chinese Clinical Trial Registry (http://www.chictr.org.cn). Results NOS yielded generally higher FeNO values than NOV [median (range): 87.0 (16 ∼ 276) vs 58.0 (9 ∼ 228); p < . 001], and the difference increased with increasing FeNO levels. There was a high degree of correlation between FeNO values obtained with both devices (r s = 0.878, p < .001). However, the Bland–Altman plot showed a low degree of agreement, with a mean difference of –0.16 between logFeNONOS and logFeNONOV (95% CI: –0.45 ∼ 0.14). The conversion equation was calculated as follows: logFeNONOS= 0.027 + 0.904× logFeNONOV. Conclusion This was the first report to compare FeNO levels measured by NOS and NOV, showing a strongly positive correlation and a low degree of consistency between the two devices. Further prospective studies are required to verify our conclusions and determine the validity of the equation.