bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of depression and anxiety symptoms and their determinant factors among patients with cancer in southern Ethiopia: a cross-sectional study
Authors: Ayalew Mohammed , Deribe Bedilu , Duko Bereket , Geleta Dereje , Bogale Netsanet , Gemechu Lalisa , Gebretsadik Achamyelesh , Bedaso Asres 
Published: January 2022

ObjectiveThe study was aimed to assess the prevalence of depression and anxiety symptoms and their determinant factors among patients with cancer attending follow-up at Hawassa University Comprehensive Specialized Hospital cancer treatment centre, Ethiopia.DesignInstitution-based cross-sectional study design was implemented.SettingPatients with cancer at Hawassa University Comprehensive Specialized Hospital cancer treatment centre from October 2019 to December 2019.ParticipantsRandomly selected 415 patients with cancer who had follow-up at cancer treatment centre.Main outcome measuresAnxiety and depression symptoms were assessed using Hospital Anxiety and Depression Scale.ResultThe prevalence rates of depression and anxiety symptoms were found to be 244 (58.8%) and 249 (60.0%), respectively. Older age (>50 years) (AOR (adjusted OR)=2.24, 95% CI=1.14 to 4.40), being unemployed (AOR=1.96, 95% CI=1.08 to 3.56), advanced stage of cancer such as stage III (AOR=5.37, 95% CI=1.34 to 21.45) and stage IV (AOR=4.55, 95% CI=1.12 to 18.44), comorbid psychotic symptoms (AOR=1.67, 95% CI=1.07 to 2.61) and eating problem in the past 2 weeks (AOR=6.16, 95% CI=1.98 to 19.11) were independent factors significantly associated with depressive symptoms. In addition, cancer stage such as stage II (AOR=3.92, 95% CI=1.07 to 14.36) and stage IV (AOR=5.04, 95% CI=1.44 to 17.59) and comorbid psychotic symptoms (AOR=1.73, 95% CI=1.12 to 2.66) were significantly associated with anxiety symptoms.ConclusionDepression and anxiety symptoms among patients with cancer were considerably high. Age, occupation, cancer stage, comorbid psychotic symptoms and eating problem were determinant factors of depressive symptoms among patients with cancer. Moreover, cancer stage and comorbid psychosis were determinants of anxiety symptoms. Healthcare professionals working in the oncology unity need to conduct routine screening and treatment of depression and anxiety symptoms for patients with cancer.
Persistent SOMAtic symptoms ACROSS diseases — from risk factors to modification: scientific framework and overarching protocol of the interdisciplinary SOMACROSS research unit (RU 5211)
Authors: Löwe Bernd , Andresen Viola , Van den Bergh Omer , Huber Tobias B , von dem Knesebeck Olaf , Lohse Ansgar W , Nestoriuc Yvonne , Schneider Gudrun , Schneider Stefan W , Schramm Christoph , Ständer Sonja , Vettorazzi Eik , Zapf Antonia , Shedden-Mora Meike , Toussaint Anne 
Published: January 2022

IntroductionPersistent somatic symptoms (PSS) are highly prevalent in all areas of medicine; they are disabling for patients and costly for society. The subjective symptom burden often correlates poorly with the underlying disease severity, and patients’ needs for effective treatment are far from being met. Initial evidence indicates that, in addition to disease-specific pathophysiological processes, psychological factors such as expectations, somatosensory amplification and prior illness experiences contribute to symptom persistence in functional as well as in somatic diseases. However, prospective studies investigating the transition from acute to chronic somatic symptoms, integrating pathophysiological, psychological and social factors, are scarce. A better understanding of the multifactorial mechanisms of symptom persistence is crucial for developing targeted mechanism-based interventions for effective prevention and treatment of PSS. Thus, the overall aim of the interdisciplinary SOMACROSS research unit is to identify generic and disease-specific risk factors and aetiological mechanisms of symptom persistence across a range of diseases.Methods and analysisSeven projects will investigate risk factors and mechanisms of symptom persistence in a total of 3916 patients across 10 medical conditions. All study designs are prospective and share common assessment points, core instruments and outcome variables to allow comparison and validation of results across projects and conditions. Research will focus on the identification of generic and disease-specific mechanisms associated with unfavourable symptom course. The development of a multivariate prediction model will facilitate the understanding of the course of PSS across diseases.Ethics and disseminationAll individual SOMACROSS studies were approved by the ethics committees of the Medical Chambers Hamburg and Münster, Germany. Findings will be disseminated through peer-reviewed publications, scientific conferences and the involvement of relevant stakeholders, patients and the lay public. This interdisciplinary research unit will fundamentally contribute to earlier recognition of patients at risk, and to the development of prevention and tailored treatment concepts for PSS.
Indwelling pleural catheters: evidence for and management
Authors: Davidson Richard , Carling Michael , Jackson Karl , Aujayeb Avinash 
Published: January 2022

Abstract
The incidence of pleural disease is increasing, and pleural medicine is increasingly recognised as a subspecialty within respiratory medicine. This often requires additional training time. Once underresearched, the last decade has seen an explosion in evidence related to the management of pleural disease. One of the cornerstones of pleural effusion management is the insertion of an indwelling pleural catheter. This allows patient-centred outpatient management and now has a robust evidence base. This article summarises evidence as well serves as a practical guide to the management of any complications related to an indwelling pleural catheter that might present on an acute take.
Neural ventilatory drive decline as a predominant mechanism of obstructive sleep apnoea events
Authors: Gell Laura K , Vena Daniel , Alex Raichel M , Azarbarzin Ali , Calianese Nicole , Hess Lauren B , Taranto-Montemurro Luigi , White David P , Wellman Andrew , Sands Scott A 
Published: January 2022

BackgroundIn the classic model of obstructive sleep apnoea (OSA), respiratory events occur with sleep-related dilator muscle hypotonia, precipitating increased neural ventilatory ‘drive’. By contrast, a drive-dependent model has been proposed, wherebyfallingdrive promotes dilator muscle hypotonia to precipitate respiratory events. Here we determine the extent to which the classic versus drive-dependent models of OSA are best supported by direct physiological measurements.MethodsIn 50 OSA patients (5–91 events/hour), we recorded ventilation (‘flow’, oronasal mask and pneumotach) and ventilatory drive (calibrated intraoesophageal diaphragm electromyography, EMG) overnight. Flow and drive during events were ensemble averaged; patients were classified asdrive dependentif flow fell/rose simultaneously with drive. Overnight effects of lower drive on flow, genioglossus muscle activity (EMGgg) and event risk were quantified (mixed models).ResultsOn average, ventilatory drive fell (rather than rose) during events (−20 (−42 to 3)%baseline, median (IQR)) and was strongly correlated with flow (R=0.78 (0.24 to 0.94)). Most patients (30/50, 60%) were classified as exhibitingdrive-dependentevent pathophysiology. Lower drive during sleep was associated with lower flow (−17 (−20 to –14)%/drive) and EMGgg (−3.5 (−3.8 to –3.3)%max/drive) and greater event risk (OR: 2.2 (1.8 to 2.5) per drive reduction of 100%eupnoea); associations were concentrated in patients with drive-dependent OSA (ie, flow: −37 (−40 to –34)%/drive, OR: 6.8 (5.3 to 8.7)). Oesophageal pressure—without tidal volume correction—falsely suggested rising drive during events (classicmodel).ConclusionsIn contrast to the prevailing view, patients with OSA predominantly exhibitdrive-dependentevent pathophysiology, whereby flow is lowest at nadir drive, and lower drive raises event risk. Preventing ventilatory drive decline is therefore considered a target for OSA intervention.
Validation of an automated self-administered 24-hour dietary recall web application against urinary recovery biomarkers in a sample of French-speaking adults of the province of Québec, Canada
Authors: Paradis Frédérique , Lamarche Benoît , Robitaille Julie , Couillard Charles , Lafrenière Jacynthe , Tremblay André J. , Corneau Louise , Lemieux Simone 
Published: January 2022

The objective of this study was to validate an automated self-administered 24-hour dietary recall web application (R24W) against recovery biomarkers for sodium, potassium and protein intakes and to identify individual characteristics associated with misreporting in a sample of 61 men and 69 women aged 20–65 years from Québec City, Canada. Each participant completed 3 dietary recalls using the R24W, provided two 24-hour urinary samples and completed questionnaires to document psychosocial factors. Mean reported intakes were 2.2%, 2.1% and 5.0% lower than the urinary reference values, respectively, for sodium, potassium and proteins (significant difference for proteins only (p = 0.04)). Deattenuated correlations between the self-reported intake and biomarkers were significant for sodium (r = 0.48), potassium (r = 0.56) and proteins (r = 0.68). Cross-classification showed that 39.7% (sodium), 42.9% (potassium) and 42.1% (proteins) of participants were ranked into the same quartile with both methods and only 4.8% (sodium), 3.2% (potassium) and 0.8% (proteins) were ranked in opposite quartiles. Lower body esteem related to appearance was associated with sodium underreporting in women (r = 0.33, p = 0.006). No other individual factor was found to be associated with misreporting. These results suggest that the R24W has a good validity for the assessment of sodium, potassium and protein intakes in a sample of French-speaking adults. Novelty: The validity of an automated self-administered 24-hour dietary recall web application named the R24W was tested using urinary biomarkers. According to 7 criteria, the R24W was found to have a good validity to assess self-reported intakes of sodium, potassium and proteins.
Redox Metabolism-Associated Molecular Classification of Clear Cell Renal Cell Carcinoma
Authors: Wei Xiangling , Deng Weiming , Dong Zhanwen , Luo You , Hu Xiao , Zhang Jinhua , Xie Zhenwei , Zheng Tong , Tan Yuqin , Tang Zuofu , Li Heng , Na Ning 
Published: January 2022

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cell carcinoma. Redox metabolism has been recognized as the hallmark of cancer. But the concrete role of redox-related genes in patient stratification of ccRCC remains unknown. Herein, we aimed to characterize the molecular features of ccRCC based on the redox gene expression profiles from The Cancer Genome Atlas. Differentially expressed redox genes (DERGs) and vital genes in metabolism regulation were identified and analyzed in the ccRCC. Consensus clustering was performed to divide patients into three clusters (C1, C2, and C3) based on 139 redox genes with median

FPKM

value
>
1

. We analyzed the correlation of clusters with clinicopathological characteristics, immune infiltration, gene mutation, and response to immunotherapy. Subclass C1 was metabolic active with moderate prognosis and associated with glucose, lipid, and protein metabolism. C2 had intermediate metabolic activity with worse prognosis and correlated with more tumor mutation burden, neoantigen, and aneuploidy, indicating possible drug sensitivities towards immune checkpoint inhibitors. Metabolic exhausted subtype C3 showed high cytolytic activity score, suggesting better prognosis than C1 and C2. Moreover, the qRT-PCR was performed to verify the expression of downregulated DERGs including ALDH6A1, ALDH1L1, GLRX5, ALDH1A3, and GSTM3, and upregulated SHMT1 in ccRCC. Overall, our study provides an insight into the characteristics of molecular classification of ccRCC patients based on redox genes, thereby deepening the understanding of heterogeneity of ccRCC and allowing prediction of prognosis of ccRCC patients.
EBV Infection in Epithelial Malignancies Induces Resistance to Antitumor Natural Killer Cells via F3-Mediated Platelet Aggregation
Authors: Duan Xiaobing , Chen Haiwen , Zhou Xiang , Liu Pingjuan , Zhang Xiao , Zhu Qian , Zhong Ling , Zhang Wanlin , Zhang Shanshan , Zhang Xinyu , Chen Yanhong , Zhou Yan , Yang Chaopin , Feng Qisheng , Zeng Yi-Xin , Xu Miao , Xiang Tong 
Published: January 2022

Abstract

Nasopharyngeal carcinoma (NPC) and Epstein–Barr virus (EBV)–associated gastric carcinoma (EBVaGC) are two major EBV-associated epithelial malignancies, both of which are characterized by the infiltration of a large number of lymphocytes, including natural killer (NK) cells. Although NK cells can prevent the development of EBV-associated epithelial malignancies, EBV-infected tumor cells often develop resistance to surveillance by NK cells. Elucidating the interactions between NK cells and EBV-infected tumor cells will facilitate the development of more effective NK-mediated therapies for treating EBV-associated malignancies. Here we investigated the cytotoxic function of NK cells in EBV-associated epithelial malignancies and discovered that EBV infection-induced upregulation of F3 expression correlates with NK-cell dysfunction in NPC and EBVaGC. The subsequent inhibitory effect of F3-mediated platelet aggregation on NK-cell function was verified in vitro and in vivo. Mechanistically, EBV latent membrane protein 2A (LMP2A) mediated upregulation of F3 through the PI3K/AKT signaling pathway. In an NPC xenograft mouse model, inhibition of F3 restored the antitumor function of NK cells and showed therapeutic efficacy when administered with NK-cell transfer. On the basis of these findings, EBV infection induces F3-mediated platelet aggregation that inhibits the antitumor function of NK cells, providing a rationale for developing and combining NK-cell–based therapies with F3 inhibitors to treat EBV-associated epithelial malignancies.

Significance:
This study reveals a mechanism by which EBV-associated epithelial malignancies escape NK-cell–mediated immune surveillance, providing a new target for improving NK-cell immunotherapy.
Development of Novel Aptamer-Based Targeted Chemotherapy for Bladder Cancer
Authors: Wang Yao , Zhang Yang , Li Peng-Chao , Guo Jiajie , Huo Fan , Yang Jintao , Jia Ru , Wang Juan , Huang Qiju , Theodorescu Dan , Yu Hanyang , Yan Chao 
Published: January 2022

Abstract

Bladder cancer is common worldwide, with most patients presenting with nonmuscle invasive disease. Multiple intravesical recurrences lead to reduced quality of life and high costs for patients with this form of bladder cancer. Intravesical chemotherapy aimed at reducing recurrence is the standard-of-care but has significant side effects from nonspecific cytotoxicity to normal urothelium. Importantly, toxicity limits doses that can be administered. Thus, tumor-specific drug targeting could reduce toxicity and enhance effectiveness by allowing higher doses. Here, using cell internalization systematic evolution of ligands by exponential enrichment (SELEX), we identify a novel bladder cancer-specific, chemically modified nucleic acid aptamer that can be preferentially internalized into tumor cells but not normal urothelial cells. The 35-nucleotide B1 aptamer is internalized into bladder cancer cells through clathrin-mediated endocytosis and macropinocytosis. As proof of principle, a B1-guided DNA nanotrain delivery vehicle for epirubicin was constructed as a targeted intravesical chemotherapy. The B1-nanotrain-epirubicin construct exhibited selective cytotoxicity towards bladder cancer cells and outperformed epirubicin in murine orthotopic xenograft models of human bladder cancer. This aptamer-based delivery system makes targeted chemotherapy possible for bladder cancer, providing a compelling rationale for clinical development.

Significance:
These findings identify a bladder cancer–specific aptamer that can be used for targeted delivery of chemotherapy, potentially reducing toxicity and enhancing therapeutic efficacy.
Financial Hardship by Age at Diagnosis Including in Young Adulthood among African American Cancer Survivors
Authors: Hastert Theresa A. , Ruterbusch Julie J. , Abrams Judith , Nair Mrudula , Wenzlaff Angie S. , Beebe-Dimmer Jennifer L. , Pandolfi Stephanie S. , Schwartz Ann G. 
Published: January 2022

Abstract

Background:
Financial hardship is most common among cancer survivors with the fewest financial resources at diagnosis; however, little is known about the financial outcomes of young adult (YA) survivors (ages 20–39 at diagnosis), despite their having fewer financial reserves than older adults.

Methods:
We utilized data from 3,888 participants in the population-based Detroit Research on Cancer Survivors cohort. Participants self-reported several forms of material and behavioral financial hardship (MFH and BFH, respectively). Psychological financial hardship (PFH) was measured using the Comprehensive Score for financial Toxicity (COST) score. Modified Poisson models estimated prevalence ratios (PR) and 95% confidence intervals (CI) for financial hardship by age at diagnosis controlling for demographic, socioeconomic, and cancer-related factors.

Results:
MFH prevalence was inversely associated with age such that 72% of YA survivors reported MFH, 62% ages 40 to 54, 49% ages 55 to 64, and 33% ages 65 to 79 (PRadjusted YA vs. 65+: 1.75; 95% CI, 1.49–2.04; Ptrend &lt; 0.001). BFH was also more common among YA survivors (26%) than those ages 65 to 79 (20%; PRadjusted: 1.50; 95% CI, 1.08–2.08; Ptrend = 0.019). Age was positively associated with financial wellbeing. COST scores ranged from 20.7 (95% CI, 19.0–22.4) among YA survivors to 27.2 (95% CI, 26.1–28.2) among adults 65 to 79 years old (Ptrend &lt; 0.001).

Conclusions:
In this population of African American cancer survivors, MFH and BFH were more common, and PFH was more severe, in YA survivors compared with those diagnosed as older adults.

Impact:
Young adulthood at diagnosis should be considered a risk factor for cancer-related financial hardship and addressed in work designed to reduce the adverse financial impacts of cancer.
AHRR (cg05575921) Methylation Safely Improves Specificity of Lung Cancer Screening Eligibility Criteria: A Cohort Study
Authors: Jacobsen Katja Kemp , Schnohr Peter , Jensen Gorm Boje , Bojesen Stig E. 
Published: January 2022

Abstract

Background:
Screening reduces lung cancer mortality, but specificities of eligibility criteria are low. We tested if leukocyte AHRR(cg05575921) methylation improves specificity of lung cancer screening eligibility criteria.

Methods:
A total of 9,206 and 5,370 individuals of the 1991 to 1994 and 2001 to 2003 examinations of the Copenhagen City Heart Study, Denmark, were followed for lung cancer within 5 years after examination and mortality. Screening eligibility criteria (DANTE, DLCST, ITALUNG, LUSI, NELSON, NLST, and PLCOM2012) were evaluated, and AHRR (cg05575921) methylation extent at different methylation cut points was added. The model with the lowest number of eligible individuals per 5-year lung cancer was validated within the 2001 to 2003 examination.

Results:
Eligibility criteria identified risk-groups ranging from 3,182 (DANTE) to 1,641 (ITALUNG) individuals. The positive predictive value was highest for PLCOM2012 (3.2%), while DANTE showed the highest negative predictive value (99.7%). Adding AHRR (cg05575921) methylation led to higher specificities for all criteria. Number of eligible individuals per 5-year lung cancer varied from 38 (NELSON) to 27 (NLST) with AHRR (cg05575921) methylation &lt;55%. This last model led to a 21.9% lower screening burden and increased (P &lt; 0.05) specificity of 84.0%. Findings were reproduced among the 5,334 individuals of the 2001 to 2003 examination.

Conclusions:
Adding AHRR (cg05575921) methylation on top of current eligibility criteria for lung cancer screening improves specificity by excluding those individuals with the lowest risk.

Impact:
The results point toward a potential clinical use of AHRR (cg05575921) methylation, which is a cost-effective measurement compared with lung CT scanning, to provide additional predictive risk information to identify eligible smokers for lung cancer screening.
See related commentary by Hung, p. 698
Transient Cell Cycle Induction in Cardiomyocytes to Treat Subacute Ischemic Heart Failure
Authors: Abouleisa Riham R.E. , Salama Abou Bakr M. , Ou Qinghui , Tang Xian-Liang , Solanki Mitesh , Guo Yiru , Nong Yibing , McNally Lindsey , Lorkiewicz Pawel K. , Kassem Kamal M. , Ahern Brooke M. , Choudhary Krishna , Thomas Reuben , Huang Yu , Juhardeen Hamzah R. , Siddique Aisha , Ifthikar Zainab , Hammad Sally K. , Elbaz Ayman S. , Ivey Kathryn N. , Conklin Daniel J. , Satin Jonathan , Hill Bradford G. , Srivastava Deepak , Bolli Roberto , Mohamed Tamer M.A. 
Published: January 2022

Background:
The regenerative capacity of the heart after myocardial infarction is limited. Our previous study showed that ectopic introduction of 4 cell cycle factors (4F; CDK1 [cyclin-dependent kinase 1], CDK4 [cyclin-dependent kinase 4], CCNB [cyclin B1], and CCND [cyclin D1]) promotes cardiomyocyte proliferation in 15% to 20% of infected cardiomyocytes in vitro and in vivo and improves cardiac function after myocardial infarction in mice.

Methods:
Using temporal single-cell RNA sequencing, we aimed to identify the necessary reprogramming stages during the forced cardiomyocyte proliferation with 4F on a single cell basis. Using rat and pig models of ischemic heart failure, we aimed to start the first preclinical testing to introduce 4F gene therapy as a candidate for the treatment of ischemia-induced heart failure.

Results:
Temporal bulk and single-cell RNA sequencing and further biochemical validations of mature human induced pluripotent stem cell–derived cardiomyocytes treated with either LacZ or 4F adenoviruses revealed full cell cycle reprogramming in 15% of the cardiomyocyte population at 48 hours after infection with 4F, which was associated mainly with sarcomere disassembly and metabolic reprogramming (n=3/time point/group). Transient overexpression of 4F, specifically in cardiomyocytes, was achieved using a polycistronic nonintegrating lentivirus (NIL) encoding 4F; each is driven by a TNNT2 (cardiac troponin T isoform 2) promoter (TNNT2-4Fpolycistronic-NIL). TNNT2-4Fpolycistronic-NIL or control virus was injected intramyocardially 1 week after myocardial infarction in rats (n=10/group) or pigs (n=6–7/group). Four weeks after injection, TNNT2-4Fpolycistronic-NIL–treated animals showed significant improvement in left ventricular ejection fraction and scar size compared with the control virus–treated animals. At 4 months after treatment, rats that received TNNT2-4Fpolycistronic-NIL still showed a sustained improvement in cardiac function and no obvious development of cardiac arrhythmias or systemic tumorigenesis (n=10/group).

Conclusions:
This study provides mechanistic insights into the process of forced cardiomyocyte proliferation and advances the clinical feasibility of this approach by minimizing the oncogenic potential of the cell cycle factors owing to the use of a novel transient and cardiomyocyte-specific viral construct.