Miracle-dz/UniFAR-FTUs huggingface dataset:
Twelve‐month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States

Estimates of 12‐month and lifetime prevalence and of lifetime morbid risk (LMR) of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM‐IV‐TR) anxiety and mood disorders are presented based on US epidemiological surveys among people aged 13+. The presentation is designed for use in the upcoming DSM‐5 manual to provide more coherent estimates than would otherwise be available. Prevalence estimates are presented for the age groups proposed by DSM‐5 workgroups as the most useful to consider for policy planning purposes. The LMR/12‐month prevalence estimates ranked by frequency are as follows: major depressive episode: 29.9%/8.6%; specific phobia: 18.4/12.1%; social phobia: 13.0/7.4%; post‐traumatic stress disorder: 10.1/3.7%; generalized anxiety disorder: 9.0/2.0%; separation anxiety disorder: 8.7/1.2%; panic disorder: 6.8%/2.4%; bipolar disorder: 4.1/1.8%; agoraphobia: 3.7/1.7%; obsessive‐compulsive disorder: 2.7/1.2. Four broad patterns of results are most noteworthy: first, that the most common (lifetime prevalence/morbid risk) lifetime anxiety‐mood disorders in the United States are major depression (16.6/29.9%), specific phobia (15.6/18.4%), and social phobia (10.7/13.0%) and the least common are agoraphobia (2.5/3.7%) and obsessive‐compulsive disorder (2.3/2.7%); second, that the anxiety‐mood disorders with the earlier median ages‐of‐onset are phobias and separation anxiety disorder (ages 15–17) and those with the latest are panic disorder, major depression, and generalized anxiety disorder (ages 23–30); third, that LMR is considerably higher than lifetime prevalence for most anxiety‐mood disorders, although the magnitude of this difference is much higher for disorders with later than earlier ages‐of‐onset; and fourth, that the ratio of 12‐month to lifetime prevalence, roughly characterizing persistence, varies meaningfully in ways consistent with independent evidence about differential persistence of these disorders. Copyright © 2012 John Wiley & Sons, Ltd.
Richtmyer-meshkov and rayleigh-taylor fractal mixing

Turbulence affects molecular mixing in a large variety of physical processes both in the environment, in astrophysics and in industrial situations. In some events it is interesting to enhance the transport of mass, heat, humidity and pollutants, while sometimes it is interesting to reduce mixing. Here we analyse some turbulent descriptors which reflect the mixing processes in the compressible induced instabilities that take place in shocks, such as Richtmyer-Meshkov and Rayleigh-Taylor (RM and RT). We present results related to both instabilities and discuss their spatial and temporal variability during the advance of a mixing front, and also their relationships with other scaling arguments. Two types of experiments were used in this study: Mixing generated by gravitational acceleration in low Atwood number incompressible experiments using fluids; and the full compressible shocktube experiments using interfaces between different density gases. The role of local turbulence has mostly relied on advanced visualization measurements through multifractal methods. Comparisons with numerical experiments of shock driven fronts occurring at density interfaces are also relevant. The global advance of the fronts is also measured and fractal descriptors are calculated in both Large Eddy Simulation (LES) and Kinematic Simulation KS models.
Haliotis discus discus Sialic Acid-Binding Lectin Reduces the Oncolytic Vaccinia Virus Induced Toxicity in a Glioblastoma Mouse Model

Although oncolytic viruses provide attractive vehicles for cancer treatment, their adverse effects are largely ignored. In this work, rat C6 glioblastoma cells were subcutaneously xenografted into mice, and a thymidine kinase-deficient oncolytic vaccinia virus (oncoVV) induced severe toxicity in this model. However, oncoVV-HddSBL, in which a gene encoding Haliotis discus discus sialic acid-binding lectin (HddSBL) was inserted into oncoVV, significantly prolonged the survival of mice as compared to the control virus. HddSBL reduced the tumor secreted serum rat IL-2 level upregulated by oncoVV, promoted viral replication, as well as inhibited the expression of antiviral factors in C6 glioblastoma cell line. Furthermore, HddSBL downregulated the expression levels of histone H3 and H4, and upregulated histone H3R8 and H4R3 asymmetric dimethylation, confirming the effect of HddSBL on chromatin structure suggested by the transcriptome data. Our results might provide insights into the utilization of HddSBL in counteracting the adverse effects of oncolytic vaccinia virus.
Identification of apoB‐100 Peptide‐Specific CD8+ T Cells in Atherosclerosis

Background T cells are found in atherosclerotic plaques, with evidence supporting a potential role for CD8+ T cells in atherogenesis. Prior studies provide evidence of low‐density lipoprotein and apoB‐100 reactive T cells, yet specific epitopes relevant to the disease remain to be defined. The current study was undertaken to identify and characterize endogenous, antigen‐specific CD8+ T cells in atherosclerosis. Methods and Results A peptide fragment of apoB‐100 that tested positive for binding to the mouse MHC‐I allele H2Kb was used to generate a fluorescent‐labeled H2Kb pentamer and tested in apoE−/− mice. H2Kb pentamer(+)CD8+ T cells were higher in apoE−/− mice fed an atherogenic diet compared with those fed a normal chow. H2Kb pentamer (+)CD8+ T cells in atherogenic diet–fed mice had significantly increased effector memory phenotype with a shift in Vβ profile. H2Kb pentamer blocked lytic activity of CD8+ T cells from atherogenic diet–fed mice. Immunization of age‐matched apoE−/− mice with the apoB‐100 peptide altered the immune‐dominant epitope of CD8+ T cells and reduced atherosclerosis. Conclusions Our study provides evidence of a self‐reactive, antigen‐specific CD8+ T‐cell population in apoE−/− mice. Immune modulation using the peptide antigen reduced atherosclerosis in apoE−/− mice.
Helios Controls a Limited Subset of Regulatory T Cell Functions

A subpopulation (60–70%) of Foxp3+ regulatory T cells (Tregs) in both mouse and man expresses the transcription factor Helios, but its role in Treg function is still unknown. We generated Treg-specific Helios-deficient mice to examine the function of Helios in Tregs. We show that the selective deletion of Helios in Tregs leads to slow, progressive systemic immune activation, hypergammaglobulinemia, and enhanced germinal center formation in the absence of organ-specific autoimmunity. Helios-deficient Treg suppressor function was normal in vitro, as well as in an in vivo inflammatory bowel disease model. However, Helios-deficient Tregs failed to control the expansion of pathogenic T cells derived from scurfy mice, failed to mediate T follicular regulatory cell function, and failed to control both T follicular helper cell and Th1 effector cell responses. In competitive settings, Helios-deficient Tregs, particularly effector Tregs, were at a disadvantage, indicating that Helios regulates effector Treg fitness. Thus, we demonstrate that Helios controls certain aspects of Treg-suppressive function, differentiation, and survival.
Specific and Non-specific Effects of Educational Intervention for Families Living with Schizophrenia

Three methods of delivering an educational intervention to families living with a schizophrenic relative were compared in terms of their efficacy in improving understanding and promoting family and patient well-being. Relatives receiving education in a group acquired more information than relatives receiving information by post or on video, but these differences were not maintained at six-month follow-up. The inclusion of homework assignments did not significantly affect gains in knowledge or any of the non-specific effects observed. The intervention overall led to considerable gains in knowledge, increased optimism concerning the family's role in treatment, and reductions in relatives' stress, which were maintained at follow-up. Fear was reduced in the short-term. Significant improvements in social function were observed at follow-up. The results suggest that the delivery of information, rather than the mode of delivery, is the crucial element in the intervention; however, the additional contextual factors operating in a group may be important if the full potential of education is to be realised.
Postoperative Atrial Fibrillation After Coronary Artery Bypass Grafting Surgery.

INTRODUCTION Postoperative atrial fibrillation (PoAF) is the most common arrhythmia following cardiac surgery, which increase the patient's morbidity and mortality. PURPOSE The aim of this study was to evaluate new onset of atrial fibrillation (AF) after isolated coronary artery bypass grafting (CABG) surgery, its clinical and surgical predictors, and its impact in immediate and long-term outcomes. METHODS Retrospective study including all CABG surgeries performed in a tertiary centre, between 2004 and 2011. Patients with documented episodes of AF or pacing rhythm before cardiac surgery were excluded. Preoperative, surgical and postoperative data were collected through clinical files and informatics databases. Qui-square tests and independent t-tests were used to compare categorical and continuous data, respectively, between patients with and without PoAF. A multivariate logistic regression model was used to identify independent risk factors of PoAF. To determine the effect of PoAF in long-term survival, we used Kaplan-Meier curves, Log Rank test and multivariate Cox regression (maximum follow-up time: 13 years). RESULTS We included 2511 patients, mean age of 63±10 years, 78.7% being male. PoAF occurred in 450 patients (18.0%), 3±3 days after surgery, the majority pharmacologically cardioverted with amiodarone (96.2%). These patients were older (67±9 vs. 62±10 years, p<0.001), more frequently obese (27.8% vs. 22.9%, p=0.026), hypertensive (76.7% vs. 69.7%, p=0.003) and had lower preoperative creatinine clearance (CC) values (73.2±27.4 vs. 81.4±28.3 ml/min, p<0.001), longer cardiopulmonary bypass time (60.0% vs. 54.8%, p=0.043) compared with patients without PoAF. In multivariate analysis, older age (OR: 1.035, 95% CI: 1.015-1.056, p=0.001), lower preoperative CC values (OR: 0.992, 95% CI: 0.985-0.999, p=0.032) and larger left atrial diameter (OR: 1.058, 95% CI: 1.024-1.093, p=0.001) were determined as independent predictors of PoAF. These patients also revealed longer hospitalization time (8 [4 to 193] vs. 6 [4 to 114] days, p<0.001) and higher hospital mortality (2.9% vs. 0.8%, p<0.001). Regarding long-term survival, patients with PoAF showed lower cumulative survival than patients without AF events (52% vs. 66%, p<0.001). PoAF was also found as an independent predictor of mortality in multivariate Cox regression (HR: 1.394, 95% CI: 1.147- 1.695, p=0.001). CONCLUSION PoAF incidence after CABG surgery was 18%. Older age, lower CC values and larger left atrial diameter were settled as PoAF independent predictors. Additionally, the occurrence of this arrhythmia was independently associated with lower long-term survival, after CABG surgery.
Cutting Edge: NK Cell Licensing Modulates Adhesion to Target Cells

Binding of NK cell inhibitory receptors to MHC class I (MHC-I) confers increased responsiveness to NK cells by a process known as NK cell licensing/education. Reduced MHC-I expression or a lack of inhibitory receptors for MHC-I results in diminished NK cell responsiveness. In this study, we evaluated the effect of human and mouse NK cell licensing on early stages of natural cytotoxicity. Unlicensed NK cells did not form as many stable conjugates with target cells. The reduction of NK cell conjugation to target cells was not attributed to altered β2 integrin LFA-1 properties but was instead due to reduced inside-out signaling to LFA-1 by activating receptors. For those unlicensed NK cells that did form conjugates, LFA-1–dependent granule polarization was similar to that in licensed NK cells. Thus, licensing controls signals as proximal as inside-out signaling by activating receptors but not integrin outside-in signaling for granule polarization.
Recruitment methods employed in the prostate, lung, colorectal, and ovarian cancer screening trial

Background The Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO) is a US National Cancer Institute (NCI)-funded randomized controlled trial designed to evaluate whether certain screening tests reduce mortality from prostate, lung, colorectal, and ovarian cancer. To obtain adequate statistical power, it was necessary to enroll over 150,000 healthy volunteers. Recruitment began in 1993 and ended in 2001. Purpose Our goal is to evaluate the success of recruitment methods employed by the 10 PLCO screening centers. We also provide estimates of recruitment yield and cost for our most successful strategy, direct mail. Methods Each screening center selected its own methods of recruitment. Methods changed throughout the recruitment period as needed. For this manuscript, representatives from each screening center provided information on methods utilized and their success. Results In the United States between 1993 and 2001, ten screening centers enrolled 154,934 study participants. Based on participant self-report, an estimated 95% of individuals were recruited by direct mail. Overall, enrollment yield for direct mail was 1.0%. Individual center enrollment yield ranged from 0.7% to 3.8%. Cost per enrolled participant was $9.64—35.38 for direct mail, excluding personnel costs. Limitations Numeric data on recruitment processes were not kept consistently at individual screening centers. Numeric data in this manuscript are based on the experiences of 5 of the 10 centers. Conclusions Direct mail, using rosters of names and addresses from profit and not-for-profit (including government) organizations, was the most successful and most often used recruitment method. Other recruitment strategies, such as community outreach and use of mass media, can be an important adjunct to direct mail in recruiting minority populations. Clinical Trials 2009; 6: 52—59. http://ctj.sagepub. com
The trajectory of depressive symptoms across the adult life span.

IMPORTANCE Long-term longitudinal studies are needed to delineate the trajectory of depressive symptoms across adulthood and to individuate factors that may contribute to increases in depressive symptoms in older adulthood. OBJECTIVES To estimate the trajectory of depressive symptoms across the adult life span; to test whether this trajectory varies by demographic factors (sex, ethnicity, and educational level) and antidepressant medication use; and to test whether disease burden, functional limitations, and proximity to death explain the increase in depressive symptoms in old age. DESIGN Longitudinal study. SETTING Community. PARTICIPANTS The study included 2320 participants (47.0% female; mean [SD] age at baseline, 58.1 [17.0] years; range, 19-95 years) from the Baltimore Longitudinal Study of Aging. MAIN OUTCOMES AND MEASURES Estimated trajectory of depressive symptoms modeled from 10, 982 assessments (mean [SD] assessments per participant, 4.7 [3.6]; range, 1-21) based on the Center for Epidemiologic Studies Depression scale and 3 subscales (depressed affect, somatic complaints, and interpersonal problems). RESULTS The linear (γ10 = 0.52; P < .01) and quadratic (γ20 = 0.43; P < .01) terms were significant, which indicated that depressive symptoms were highest in young adulthood, decreased across middle adulthood, and increased again in older adulthood. The subscales followed a similar pattern. Women reported more depressed affect at younger ages, but an interaction with age suggested that this gap disappeared in old age. Accounting for comorbidity, functional limitations, and impending death slightly reduced but did not eliminate the uptick in depressive symptoms in old age. CONCLUSIONS AND RELEVANCE Symptoms of depression follow a U-shaped pattern across adulthood. Older adults experience an increase in distress that is not due solely to declines in physical health or approaching death.
Mechanisms of Enhanced &bgr;-Adrenergic Reserve From Cardiac Resynchronization Therapy

Background— Cardiac resynchronization therapy (CRT) is the first clinical heart failure treatment that improves chamber systolic function in both the short-term and long-term yet also reduces mortality. The mechanical impact of CRT is immediate and well documented, yet its long-term influences on myocyte function and adrenergic modulation that may contribute to its sustained benefits are largely unknown. Methods and Results— We used a canine model of dyssynchronous heart failure (DHF; left bundle ablation, atrial tachypacing for 6 weeks) and CRT (DHF for 3 weeks, biventricular tachypacing for subsequent 3 weeks), contrasting both to nonfailing controls. CRT restored contractile synchrony and improved systolic function compared with DHF. Myocyte sarcomere shortening and calcium transients were markedly depressed at rest and after isoproterenol stimulation in DHF (both anterior and lateral walls), and CRT substantially improved both. In addition, &bgr;1 and &bgr;2 stimulation was enhanced, coupled to increased &bgr;1 receptor abundance but no change in binding affinity. CRT also augmented adenylate cyclase activity over DHF. Inhibitory G-protein (G&agr;i) suppression of &bgr;-adrenergic stimulation was greater in DHF and reversed by CRT. G&agr;i expression itself was unaltered; however, expression of negative regulators of G&agr;i signaling (particularly RGS3) rose uniquely with CRT over DHF and controls. CRT blunted elevated myocardial catecholamines in DHF, restoring levels toward control. Conclusions— CRT improves rest and &bgr;-adrenergic-stimulated myocyte function and calcium handling, upregulating &bgr;1 receptors and adenylate cyclase activity and suppressing Gi-coupled signaling associated with novel RGS upregulation. The result is greater rest and sympathetic reserve despite reduced myocardial neurostimulation as components underlying its net benefit.
Integrative genomics reveals mechanisms of copy number alterations responsible for transcriptional deregulation in colorectal cancer

To evaluate the mechanisms and consequences of chromosomal aberrations in colorectal cancer (CRC), we used a combination of spectral karyotyping, array comparative genomic hybridization (aCGH), and array‐based global gene expression profiling on 31 primary carcinomas and 15 established cell lines. Importantly, aCGH showed that the genomic profiles of primary tumors are recapitulated in the cell lines. We revealed a preponderance of chromosome breakpoints at sites of copy number variants (CNVs) in the CRC cell lines, a novel mechanism of DNA breakage in cancer. The integration of gene expression and aCGH led to the identification of 157 genes localized within high‐level copy number changes whose transcriptional deregulation was significantly affected across all of the samples, thereby suggesting that these genes play a functional role in CRC. Genomic amplification at 8q24 was the most recurrent event and led to the overexpression of MYC and FAM84B. Copy number dependent gene expression resulted in deregulation of known cancer genes such as APC, FGFR2, and ERBB2. The identification of only 36 genes whose localization near a breakpoint could account for their observed deregulated expression demonstrates that the major mechanism for transcriptional deregulation in CRC is genomic copy number changes resulting from chromosomal aberrations. © 2009 Wiley‐Liss, Inc.
Decursin attenuates the amyloid‐β‐induced inflammatory response in PC12 cells via MAPK and nuclear factor‐κB pathway

Decursin, the major bioactive component of Angelica gigas Nakai, exhibited neuroprotective properties. Our previous studies showed that decursin conferred neuroprotective effects in PC12 cells induced by Amyloid‐β (Aβ)25–35 via antiapoptosis and antioxidant. In this study, the antiinflammatory effects of decursin against PC12 cells injury stimulated by Aβ25–35 were assessed. Our results demonstrated that decursin suppressed the expression of cyclooxygenase‐2 protein and prostaglandin E2 content which was stimulated by Aβ25–35 in PC12 cells. Meanwhile, the nuclear translocation of nuclear factor‐κB in Aβ25–35‐treated PC12 cells was also inhibited by decursin. In addition, decursin suppressed phosphorylation of the two upstream pathway kinases, p38 and c‐Jun N‐terminal kinase. Overall, our findings indicate that decursin exerts protective effects against neuroinflammation stimulated by Aβ25–35 in PC12 cells by abolishing cyclooxygenase‐2 protein expression through inactivation of nuclear factor‐κB via the upstream kinases including p38 and c‐Jun N‐terminal kinase. This work provides a new insight into the pharmacological mode of decursin and should facilitate its therapeutic application in treatment of inflammatory disorders.
Recent trends in the incidence of testicular germ cell tumors in the United States

Testicular germ cell tumors (TGCT), which comprise 98% of all testicular malignancies, are the most commonly occurring cancers among men between the ages of 15 and 44 years in the United States (US). A prior report from our group found that while TGCT incidence among all US men increased between 1973 and 2003, the rate of increase among black men was more pronounced starting in 1989–1993 than was the rate of increase among other men. In addition, TGCT incidence increased among Hispanic white men between 1992 and 2003. To determine whether these patterns have continued, in the current study, we examined temporal trends in incidence through 2011. Between 1992 and 2011, 21 271 TGCTs (12 419 seminomas; 8715 non‐seminomas; 137 spermatocytic seminomas) were diagnosed among residents of the Surveillance, Epidemiology, and End Results 13 registry areas. The incidence of TGCT was highest among non‐Hispanic white men (6.97 per 100 000 man‐years) followed by American Indian/Alaska Native (AI/AN; 4.66), Hispanic white (4.11), Asian/Pacific Islander (A/PI; 1.95), and black (1.20) men. Non‐Hispanic white men were more likely to present with smaller tumors (3.5 cm) and localized disease (72.6%) than were men of other races/ethnicities. Between 1992 and 2011, TGCT incidence increased significantly among Hispanic white [annual percent change (APC) = 2.94, p < 0.0001], black (APC = 1.67, p = 0.03), non‐Hispanic white (APC = 1.23, p < 0.0001), and A/PI (APC = 1.04, p = 0.05) men. Incidence rates also increased, although not significantly, among AI/AN men (APC = 2.96, p = 0.06). The increases were greater for non‐seminoma than seminoma. In summary, while non‐Hispanic white men in the US continue to have the highest incidence of TGCT, they present at more favorable stages of disease and with smaller tumors than do other men. The increasing rates among non‐white men, in conjunction with the larger proportion of non‐localized stage disease, suggest an area where future research is warranted.
VOCATIONAL DISCERNMENT AND ACTION : AN EXPLORATORY STUDY OF MALE AND FEMALE UNIVERSITY PROFESSORS

The current study examined 158 university faculty members' discernment and living out of vocation using both quantitative and qualitative data assessing concepts of vocation definition, personal experiences of discerning vocation, personal bridges, and barriers experienced while pursuing one's vocation, as well as differences in living out one's vocation that are experienced by men versus women. The implications of this research are discussed in terms of enhancing faculty members'abilities to integrate their faith and vocation with their ongoing work as teachers, writers, and academic leaders.