Miracle-dz/UniFAR-FTUs huggingface dataset:
Detecting Signs of Depression in Tweets in Spanish: Behavioral and Linguistic Analysis

Background Mental disorders have become a major concern in public health, and they are one of the main causes of the overall disease burden worldwide. Social media platforms allow us to observe the activities, thoughts, and feelings of people’s daily lives, including those of patients suffering from mental disorders. There are studies that have analyzed the influence of mental disorders, including depression, in the behavior of social media users, but they have been usually focused on messages written in English. Objective The study aimed to identify the linguistic features of tweets in Spanish and the behavioral patterns of Twitter users who generate them, which could suggest signs of depression. Methods This study was developed in 2 steps. In the first step, the selection of users and the compilation of tweets were performed. A total of 3 datasets of tweets were created, a depressive users dataset (made up of the timeline of 90 users who explicitly mentioned that they suffer from depression), a depressive tweets dataset (a manual selection of tweets from the previous users, which included expressions indicative of depression), and a control dataset (made up of the timeline of 450 randomly selected users). In the second step, the comparison and analysis of the 3 datasets of tweets were carried out. Results In comparison with the control dataset, the depressive users are less active in posting tweets, doing it more frequently between 23:00 and 6:00 (P<.001). The percentage of nouns used by the control dataset almost doubles that of the depressive users (P<.001). By contrast, the use of verbs is more common in the depressive users dataset (P<.001). The first-person singular pronoun was by far the most used in the depressive users dataset (80%), and the first- and the second-person plural pronouns were the least frequent (0.4% in both cases), this distribution being different from that of the control dataset (P<.001). Emotions related to sadness, anger, and disgust were more common in the depressive users and depressive tweets datasets, with significant differences when comparing these datasets with the control dataset (P<.001). As for negation words, they were detected in 34% and 46% of tweets in among depressive users and in depressive tweets, respectively, which are significantly different from the control dataset (P<.001). Negative polarity was more frequent in the depressive users (54%) and depressive tweets (65%) datasets than in the control dataset (43.5%; P<.001). Conclusions Twitter users who are potentially suffering from depression modify the general characteristics of their language and the way they interact on social media. On the basis of these changes, these users can be monitored and supported, thus introducing new opportunities for studying depression and providing additional health care services to people with this disorder.
The Metabolic Cytokine Adiponectin Inhibits Inflammatory Lung Pathology in Invasive Aspergillosis

Key Points Adiponectin KO mice show increased pathology in a mouse model of IA. KO mice show increased inflammatory and decreased anti-inflammatory phenotypes. Increased lung inflammation in KO mice is independent of invasive fungal growth. Systemic immunity and metabolism are coregulated by soluble factors, including the insulin-regulating adipose tissue cytokine adiponectin. How these factors impact detrimental inflammatory responses during fungal infection remains unknown. In this study, we observed that mortality, fungal burden, and tissue histopathology were increased in adiponectin-deficient mice in a neutropenic model of invasive aspergillosis. Lung RNA sequencing, quantitative RT-PCR, and subsequent pathway analysis demonstrated activation of inflammatory cytokine pathways with upstream regulation by IL-1 and TNF in adiponectin-deficient mice with decreased/inhibited anti-inflammatory genes/pathways, suggesting broad cytokine-mediated pathology along with ineffective fungal clearance. Quantitative RT-PCR analysis confirmed increased transcription of IL-1a, IL-6, IL-12b, IL-17A/F, and TNF in adiponectin-deficient mice at early time points postinfection, with a specific increase in intracellular TNF in alveolar macrophages. Although eosinophil recruitment and activation were increased in adiponectin-deficient mice, mortality was delayed, but not decreased, in mice deficient in both adiponectin and eosinophils. Interestingly, neutrophil depletion was required for increased inflammation in adiponectin-deficient mice in response to swollen/fixed conidia, suggesting that immune suppression enhances detrimental inflammation, whereas invasive fungal growth is dispensable. Our results suggest that adiponectin inhibits excessive lung inflammation in invasive aspergillosis. Our study has therefore identified the adiponectin pathway as a potential source for novel therapeutics in immune-compromised patients with detrimental immunity to invasive fungal infection.
An integrative approach to detect epigenetic mechanisms that putatively mediate the influence of lifestyle exposures on disease susceptibility

Abstract Background There is mounting evidence that our environment and lifestyle has an impact on epigenetic regulatory mechanisms, such as DNA methylation. It has been suggested that these molecular processes may mediate the effect of risk factors on disease susceptibility, although evidence in this regard has been challenging to uncover. Using genetic variants as surrogate variables, we have used two-sample Mendelian randomization (2SMR) to investigate the potential implications of putative changes to DNA methylation levels on disease susceptibility. Methods To illustrate our approach, we identified 412 CpG sites where DNA methylation was associated with prenatal smoking. We then applied 2SMR to investigate potential downstream effects of these putative changes on 643 complex traits using findings from large-scale genome-wide association studies. To strengthen evidence of mediatory mechanisms, we used multiple-trait colocalization to assess whether DNA methylation, nearby gene expression and complex trait variation were all influenced by the same causal genetic variant. Results We identified 22 associations that survived multiple testing (P < 1.89 × 10–7). In-depth follow-up analyses of particular note suggested that the associations between DNA methylation at the ASPSCR1 and REST/POL2RB gene regions, both linked with reduced lung function, may be mediated by changes in gene expression. We validated associations between DNA methylation and traits using independent samples from different stages across the life course. Conclusion Our approach should prove valuable in prioritizing CpG sites that may mediate the effect of causal risk factors on disease. In-depth evaluations of findings are necessary to robustly disentangle causality from alternative explanations such as horizontal pleiotropy.
Synthesis of either C2- or C4'-alkylated derivatives of honokiol and their biological evaluation for anti-inflammatory activity.

Honokiol, a biphenolic neolignan isolated from Magnolia officinalis, was reported to have a promising anti-inflammatory activity for the treatment of various diseases. There are many efforts on the synthesis and structure-activity relationship of honokiol derivatives. However, regioselective O-alkylation of honokiol remains a challenge and serves as a tool to provide not only some derivatives but also chemical probes for target identification and mode of action. In this study, we examined the reaction condition for regioselective O-alkylation, in which C2 and C4'-alkylated analogs of honokiol were synthesized and evaluated for inhibitory activity on nitric oxide production and cyclooxygenase-2 expression. Furthermore, we successfully synthesized a potential photoaffinity probe consisting of biotin and benzophenone based on a C4'-alkylated derivative.
S. cerevisiae Strain Lacking Mitochondrial IF3 Shows Increased Levels of Tma19p during Adaptation to Respiratory Growth

After billions of years of evolution, mitochondrion retains its own genome, which gets expressed in mitochondrial matrix. Mitochondrial translation machinery rather differs from modern bacterial and eukaryotic cytosolic systems. Any disturbance in mitochondrial translation drastically impairs mitochondrial function. In budding yeast Saccharomyces cerevisiae, deletion of the gene coding for mitochondrial translation initiation factor 3—AIM23, leads to an imbalance in mitochondrial protein synthesis and significantly delays growth after shifting from fermentable to non-fermentable carbon sources. Molecular mechanism underlying this adaptation to respiratory growth was unknown. Here, we demonstrate that slow adaptation from glycolysis to respiration in the absence of Aim23p is accompanied by a gradual increase of cytochrome c oxidase activity and by increased levels of Tma19p protein, which protects mitochondria from oxidative stress.
SGEF forms a complex with Scribble and Dlg1 and regulates epithelial junctions and contractility

Awadia et al. show that SGEF, a RhoG-specific GEF, forms a ternary complex with two members of the Scribble polarity complex, Scribble and Dlg1, and regulates junction formation, apical contractility, E-cadherin stability, and lumen formation in epithelial cells.
The Effect of Hypnosis on Intraoperative Hemorrhage and Postoperative Pain in Rhinoplasty

Abstract This prospective, randomized study investigated the effects of preoperative hypnosis on hemorrhage and pain in open septorhinoplasty (SRP). Twenty-two patients undergoing SRP under general anesthesia were included and equally divided into two groups. Patients in the hypnosis group (HG) received a total of three sessions of hypnotic induction. The first two sessions occurred 3 days and 1 day prior to surgery, respectively, and the last session was in the hospital the day of surgery. The other 11 patients constituted the control group (CG). Compared with the CG, the HG’s intraoperative use of total remifentanil and the visual analog scale scores at the 2nd and 3rd postoperative hours were significantly lower (p < .05). Hypnosis did not affect the quality of the surgical field. However, preoperative use of hypnosis decreased intraoperative remifentanil requirements and postoperative pain.
Norepinephrine Inhibits Synovial Adipose Stem Cell Chondrogenesis via α2a-Adrenoceptor-Mediated ERK1/2 Activation

In recent years, first evidences emerged that sympathetic neurotransmitters influence osteoarthritis (OA) manifestation. Joint-resident stem cells might contribute to cartilage repair, however, their chondrogenic function is reduced. The neurotransmitter norepinephrine (NE) was detected in the synovial fluid of trauma and OA patients. Therefore, the aim of this study was to analyse how NE influences the chondrogenesis of synovial adipose tissue-derived stem cells (sASCs). sASCs were isolated from knee-OA patients synovia. After adrenoceptor (AR) expression analysis, proliferation and chondrogenic differentiation in presence of NE and/or α- and β-AR antagonist were investigated. Cell count, viability, chondrogenic and hypertophic gene expression, sulfated glycosaminoglycan (sGAG) and type II collagen content were determined. Key AR-dependent signaling (ERK1/2, PKA) was analyzed via western blot. sASC expressed α1A-, α1B-, α2A-, α2B-, α2C-, and β2-AR in monolayer and pellet culture. NE did not affect proliferation and viability, but 10−7 and 10−6 M NE significantly reduced sGAG and type II collagen content as well as ERK1/2 phosphorylation. These effects were fully reversed by yohimbine (α2-AR antagonist). Our study confirms the important role of NE in sASC chondrogenic function and provides new insights in OA pathophysiology. Future studies might help to develop novel therapeutic options targeting neuroendocrine pathways for OA treatment.
Creatine supplementation (3 g/day) and bone health in older women: a 2-year, randomized, placebo-controlled trial.

BACKGROUND Creatine supplementation could be a non-expensive, safe and effective dietary intervention to counteract bone loss. The aim of this study was to investigate whether long-term creatine supplementation can improve bone health in older, postmenopausal women. METHODS A double-blind, placebo-controlled, parallel-group, randomized trial was conducted between November 2011 and December 2017 in Sao Paulo, Brazil. Two hundred postmenopausal women with osteopenia were randomly allocated to receive either creatine monohydrate (3 g/day) or placebo over 2 years. At baseline and after 12 and 24 months, we assessed areal bone mineral density (aBMD; primary outcome), lean and fat mass (through dual X-ray absorptiometry), volumetric BMD and bone microarchitecture parameters, biochemical bone markers, physical function and strength, and the number of falls and fractures. Possible adverse effects were self-reported. RESULTS Lumbar spine (p<0.001), femoral neck (p<0.001) and total femur aBMD (p=0.032) decreased across time; however, no interaction effect was observed (all p>0.050). Bone markers, microarchitecture parameters, and the number of falls/fractures were not changed with creatine (all p>0.050). Lean mass and appendicular skeletal muscle mass increased throughout the intervention (p<0.001), with no additive effect of creatine (p=0.731 and p=0.397, respectively). Creatine did not affect health-related laboratory parameters. CONCLUSION Creatine supplementation over 2 years did not improve bone health in older, postmenopausal women with osteopenia, nor did it affect lean mass or muscle function in this population. This refutes the long-lasting notion that this dietary supplement alone has osteogenic or anabolic properties in the long run.
Coronary Artery Disease Risk and Lipidomic Profiles Are Similar in Hyperlipidemias With Family History and Population‐Ascertained Hyperlipidemias

Background We asked whether, after excluding familial hypercholesterolemia, individuals with high low‐density lipoprotein cholesterol (LDL‐C) or triacylglyceride levels and a family history of the same hyperlipidemia have greater coronary artery disease risk or different lipidomic profiles compared with population‐based hyperlipidemias. Methods and Results We determined incident coronary artery disease risk for 755 members of 66 hyperlipidemic families (≥2 first‐degree relatives with similar hyperlipidemia) and 19 644 Finnish FINRISK population study participants. We quantified 151 circulating lipid species from 550 members of 73 hyperlipidemic families and 897 FINRISK participants using mass spectrometric shotgun lipidomics. Familial hypercholesterolemia was excluded using functional LDL receptor testing and genotyping. Hyperlipidemias (LDL‐C or triacylglycerides >90th population percentile) associated with increased coronary artery disease risk in meta‐analysis of the hyperlipidemic families and the population cohort (high LDL‐C: hazard ratio, 1.74 [95% CI, 1.48–2.04]; high triacylglycerides: hazard ratio, 1.38 [95% CI, 1.09–1.74]). Risk estimates were similar in the family and population cohorts also after adjusting for lipid‐lowering medication. In lipidomic profiling, high LDL‐C associated with 108 lipid species, and high triacylglycerides associated with 131 lipid species in either cohort (at 5% false discovery rate; P‐value range 0.038–2.3×10−56). Lipidomic profiles were highly similar for hyperlipidemic individuals in the families and the population (LDL‐C: r=0.80; triacylglycerides: r=0.96; no lipid species deviated between the cohorts). Conclusions Hyperlipidemias with family history conferred similar coronary artery disease risk as population‐based hyperlipidemias. We identified distinct lipidomic profiles associated with high LDL‐C and triacylglycerides. Lipidomic profiles were similar between hyperlipidemias with family history and population‐ascertained hyperlipidemias, providing evidence of similar and overlapping underlying mechanisms.
Fibrillin‐1 in the Vasculature: In Vivo Accumulation of eGFP‐Tagged Fibrillin‐1 in a Knockin Mouse Model

Immunolocalization studies have shown that fibrillin‐1 is distributed ubiquitously in the connective tissue space from early embryonic times through old age. When mutated, the gene for fibrillin‐1 (FBN1) causes the Marfan syndrome, a common inherited disorder of connective tissue. The multiple manifestations of the Marfan syndrome reflect the known distribution of fibrillin‐1 in cardiovascular, musculoskeletal, ocular, and dermal tissues. In this study, a mouse model of Marfan syndrome in which fibrillin‐1 is truncated and tagged with green fluorescence was used to estimate the relative abundance of fibrillin‐1 in developing tissues. In embryonic tissues, the aorta was the only tissue in which fibrillin‐1 green fluorescence was detectable. Other arteries gained detectable fibrillin‐1 green fluorescence just after birth. Fibrillin‐1 fluorescence was observed at later postnatal times in the lung, skin, perichondrium, tendon, and ocular tissues, while other tissues remained negative. These results indicated that tissues most affected in the Marfan syndrome are the tissues in which fibrillin‐1 is most abundant. Focus was placed on the aorta, since aortic disease is life threatening in the Marfan syndrome and fibrillin‐1 green fluorescence was most abundant in this tissue. Fibrillin‐1 green fluorescence and immunostaining showed that fibrillin‐1 is within aortic medial elastic lamellae. Endothelial‐specific compared to smooth muscle‐specific fibrillin‐1 green fluorescence, together with light microscopic analyses of fragmentation of aortic elastic lamellae, demonstrated that smooth muscle cell mutated fibrillin‐1 contributed most to progressive aortic fragmentation. However, these studies also indicated that other cells, possibly endothelial cells, also contribute to this aortic pathology. Anat Rec, 2019. © 2019 Wiley Periodicals, Inc.
Long Noncoding RNA NEAT1 Aggravates Aβ-Induced Neuronal Damage by Targeting miR-107 in Alzheimer's Disease

Purpose Alzheimer's disease (AD) is the most common neurodegenerative disease, with a rising prevalence worldwide. Long noncoding RNAs (lncRNAs) have been found to play important roles in the development and treatment of AD. However, the exact role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in neuronal damage in AD is largely unknown. Materials and Methods The AD model was established in SH-SY5Y and SK-N-SH cells via treatment with amyloid β1−42 (Aβ). The expression of NEAT1 and microRNA-107 (miR-107) was measured by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were detected by MTT assay, immunocytochemistry, and flow cytometry. The expression of phosphorylated tau protein (p-Tau) was measured by Western blot. The interaction between NEAT1 and miR-107 was explored by bioinformatics analysis, luciferase activity, and RNA immunoprecipitation assays. Results NEAT1 expression was enhanced in Aβ-treated SH-SY5Y and SK-N-SH cells, and its knockdown attenuated Aβ-induced inhibition of viability and promotion of apoptosis and p-Tau levels. NEAT1 was indicated as a decoy of miR-107. miR-107 abundance was reduced in Aβ-treated cells, and its overexpression reversed Aβ-induced injury. Moreover, interference of miR-107 abated silencing of NEAT1-mediated inhibition of neuronal damage in Aβ-treated SH-SY5Y and SK-N-SH cells. Conclusion LncRNA NEAT1 aggravated Aβ-induced neuronal damage by sponging miR-107, indicating a novel avenue for treatment of AD.
Relationship between Helicobacter pylori infection and osteoporosis: a systematic review and meta-analysis

Objectives Many studies have explored the association between Helicobacter pylori infection and osteoporosis. However, the results remain controversial. Therefore, we performed this systematic review and meta-analysis to evaluate the association between H. pylori infection and osteoporosis. Design Systematic review and meta-analysis of case–control studies. Data sources Databases, including PubMed, Embase, Web of Science and Chinese Biomedical Literature Database, were screened from inception to 30 April 2018. Eligibility criteria Case–control studies aimed at assessing the association between H. pylori infection and osteoporosis. Data extraction and analysis Study characteristics and study quality sections were reviewed. Studies were selected, and data were extracted by two reviewers. Pooled ORs and 95% CIs were calculated using random effects model if heterogeneity existed; otherwise, fixed effects model was used. Subgroup analyses were performed to explore the source of heterogeneity. Publication bias and sensitivity analyses were also tested. Results A total of 21 studies with 9655 participants were included in our analyses. Taking together, we found that H. pylori infection was associated with increased odds of osteoporosis (OR (95% CI): 1.39 (1.13 to 1.71)); there was no significant difference between osteoporosis and osteopaenia; the association between osteoporosis and H. pylori infection was relatively higher in men than women but did not reach significant level. However, the decrease of bone mineral density in H. pylori-positive patients was not significant when compared with H. pylori negative controls, which may due to the sample size. Conclusions Our meta-analysis suggests an association between osteoporosis and H. pylori infection. The clinicians should pay more attention to the patients infected with H. pylori. Further studies were still needed to exploring the confounding factors among studies and to elucidate the underlying biological mechanisms.
Prevention of parastomal hernia using mesh in patients undergoing rectum extirpation.

INTRODUCTION Developing a parastomal hernia can lead to emergency surgery and cause discomfort. Placing a pro-phylactic mesh around the ostomy may potentially prevent hernias from developing. Randomised clinical trials and reviews have reported contradictory results from this prophylactic procedure with different rates of hernias and success. This descriptive cohort study aimed to investigate the rate of parastomal hernia after applying prophylactic mesh in patients undergoing surgery for rectal cancer. METHODS In the period from 2010 to 2016, we included 133 patients who had a permanent colostomy with prophylactic mesh placement due to rectal cancer. The patients were seen in the ostomy ambulatory at least three times annually, and bulges and hernias were registered by a trained nurse. Computed tomography was used for verification of parastomal hernia. Data were registered retrospectively from patient files. RESULTS After a median follow-up of 22 months, 24% of patients developed a parastomal hernia. Development of parastomal bulge without a subsequent hernia diagnosis was seen in 21%. The one-year rate of parastomal hernia was 9.7%. CONCLUSIONS This cohort study supports the thesis of a low short-time rate of parastomal hernia in patients who had a prophylactic mesh placed during the ostomy formation and indicates that the rate of hernia increases over time after the first post-operative year. FUNDING none. TRIAL REGISTRATION not relevant.