bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comunicación Terapéutica y Satisfacción del Usuario en la atención de Enfermería en un Establecimiento de Salud
Authors: Alfonso Sanchez Jose Rodrigo , Cholán Cabanillas Johana Jhoselyn , Velásquez Porras Paul Cesar , Aguayo Cabana Anabel 
Published: January 2025

Objetivo: Determinar la relación entre la comunicación terapéutica y la satisfacción del usuario en la atención de Enfermería en un Establecimiento de Salud, Lima -2024. Materiales y métodos: Investigación tipo básico, diseño no experimental de enfoque cuantitativo, realizado en 2024. Se contó con una población de 120 pacientes de un establecimiento de salud. Se aplicó 2 cuestionarios, un cuestionario para comunicación terapéutica la cual logró un V-Aiken de 0.96 y la confiabilidad de 0.70 con el estadístico KR-20 de Kunder- Richardson. Asimismo, un cuestionario para satisfacción del usuario con una validez V-Aiken de 0.94 y la confiabilidad de 0.892 con el estadístico alfa de Cronbach. Resultados: Tras los análisis obtenidos, estadísticamente se evidencia que existe relación estadística (p=.847) entre ambas variables. Conclusión: Existe una relación estadística directa (p=.847) entre las variables comunicación terapéutica y satisfacción del usuario en la atención de Enfermería en un Establecimiento de Salud, debido a que los niveles de comunicación terapéutica influyen significativamente en la percepción de satisfacción del usuario.
Dampak Penerapan Ekonomi Syariah terhadap Kinerja Keuangan Bank Syariah di Indonesia
Authors: Wafi Inngamul , Akhmadi Fauzan , Ngasifudin Muhammad , Nurfauzi Yogi 
Published: January 2025

Implementasi prinsip-prinsip ekonomi syariah telah mengubah secara signifikan lanskap keuangan perbankan syariah di Indonesia, menghadirkan pemeriksaan kritis terhadap dampaknya pada kinerja keuangan. Penelitian kualitatif deskriptif dengan metodologi library research ini mengeksplorasi hubungan antara prinsip ekonomi Syariah dan kinerja keuangan bank syariah. Dengan menggunakan Teori Kelembagaan yang dikembangkan oleh Neil Fligstein, studi ini menyelidiki bagaimana kerangka kelembagaan dan struktur normatif memengaruhi strategi operasional dan keuangan lembaga keuangan syariah. Penelitian ini mensintesis literatur ekstensif dari jurnal akademik, laporan keuangan, dokumen regulasi, dan publikasi ilmiah untuk menganalisis dimensi multifaset kinerja perbankan syariah. Dengan menguji integrasi prinsip-prinsip Syariah ke dalam operasi perbankan, studi ini mengungkapkan tantangan dan peluang unik yang ditawarkan oleh model ekonomi syariah. Temuan menunjukkan bahwa penerapan prinsip-prinsip ekonomi Syariah secara signifikan meningkatkan transparansi keuangan, manajemen risiko, dan praktik keuangan etis di antara bank syariah di Indonesia. Dimensi analitis utama mencakup efisiensi keuangan, mekanisme tata kelola, tanggung jawab sosial, dan kepatuhan terhadap standar keuangan Islam. Penelitian ini berkontribusi pada badan pengetahuan yang ada dengan memberikan pemahaman komprehensif tentang bagaimana prinsip-prinsip ekonomi syariah berdampak pada kinerja perbankan, menawarkan wawasan bagi pembuat kebijakan, praktisi keuangan, dan peneliti akademik. Studi ini menyoroti potensi perbankan syariah sebagai sistem keuangan alternatif yang kuat yang menyeimbangkan pertumbuhan ekonomi dengan pertimbangan etis dan sosial.Implikasi penelitian ini melampaui Indonesia, menawarkan perspektif kritis tentang perkembangan global lembaga keuangan Islam dan potensinya untuk menciptakan ekosistem perbankan yang lebih inklusif dan bertanggung jawab secara sosial.
Single-nucleotide polymorphisms in genes associated with the vitamin D pathway related to clinical and therapeutic outcomes of American tegumentary leishmaniasis
Authors: Oliveira Iara Barreto Neves , Nunes Ramon Vieira , Leite Vanessa Rafaela Milhomem Cruz , Araújo Camila Freire , Silveira Murilo Barros , Pinto Sebastião Alves , Lamounier Lorena Andrade , Borges Clayton Luiz , Martins Edésio , Porto Iane de Oliveira Pires , Gomes Rodrigo Saar , Ribeiro-Dias Fátima 
Published: January 2025

BackgroundThe vitamin D pathway contributes to the microbicidal activity of macrophages against Leishmania infection. In addition to induction of this pathway, interferon-gamma (IFNγ), interleukin (IL)-15, and IL32γ are part of a network of pro-inflammatory cytokines. The aim of this study was to evaluate single-nucleotide polymorphisms (SNPs) in the components of the vitamin D pathway and associated cytokine genes that could be related to resistance or susceptibility to American tegumentary leishmaniasis (ATL).MethodsThe expressions of IFNG, IL15, IL32, CYP27B1, VDR, and other pro-inflammatory cytokines TNF, IL6, and IL17 genes were evaluated using real-time polymerase chain reaction (qPCR) in lesions of patients with localized cutaneous leishmaniasis (LCL) or mucosal leishmaniasis (ML). SNP genotypes/alleles (in IL15, IL32, CYP27B1, and VDR) were evaluated by TaqMan PCR assays using DNA from the blood of patients and healthy individuals. Serum vitamin D levels were determined by chemiluminescence.ResultsVitamin D pathway-associated genes were expressed in cutaneous as well as mucosal lesions. IFNG, IL6, and IL17 were more highly expressed in ML than in LCL. In contrast, IL32γ/CYP27B1/VDR mRNAs were mainly correlated in LCL, and IL32γ in ML makes strong connections with all cytokines. The SNP IL32 rs1555001 was less frequent in patients with ML. In addition, some SNPs appear to influence the VDR and CYP27B1 (IL15 rs10519613 and IL15 rs3775597) and IL6 (VDR rs7975232) expressions in LCL and the IL17 expression in ML (IL15 rs3775597). Gene expression was also correlated with clinical parameters, such as number of lesions (CYP27B1 mRNA) and treatment failure (VDR mRNA). In addition, one SNP was associated with treatment failure in ML (VDR rs7975232).ConclusionsOur findings suggested that some SNPs in the vitamin D pathway-associated genes can be related to resistance and therapeutic outcomes of ATL. They are promising candidates that need to be further evaluated to understand their biological effects in the control or immunopathogenesis of ATL.
Case Report: Painful left bundle branch block syndrome complicated with vasovagal syncope
Authors: Luo Jiangying , Xue Yajun , Liu Fang , Yang Jing , Zhou Boda , Zhang Ping 
Published: January 2025

BackgroundPainful left bundle branch block (LBBB) syndrome is an uncommon disease that is defined as intermittent episodes of angina associated with simultaneous LBBB changes on an electrocardiogram (ECG) with the absence of flow-limiting coronary artery disease or ischemia on functional testing. Vasovagal syncope (VVS) is the most common cause of syncope and can be provoked by sublingual nitroglycerin (NTG). Herein, we report a case of painful LBBB syndrome complicated with VVS, which was misdiagnosed as acute coronary syndrome and cardiogenic shock.Case summaryA 62-year-old woman presented with intermittent exertional chest pain for 3 years and deteriorated for 2 weeks. An ECG, transthoracic echocardiography, and laboratory test results were all normal. Exercise treadmill testing induced chest pain, accompanied by new-onset LBBB. She fainted after finishing the test and receiving sublingual NTG, with a rapid decline in heart rate and blood pressure, which was relieved by 0.5 mg of atropine administered intravenously. Coronary angiography showed no evidence of obstructive lesions. Isoprenaline stress echocardiography induced chest pain and rate-dependent LBBB and showed interventricular/intraventricular desynchrony simultaneously. A head-up tilt test verified mixed VVS in the provocative phase. A diagnosis of painful LBBB syndrome complicated with VVS induced by sublingual NTG was made. The patient received an extended-release metoprolol succinate tablet and had no symptoms at a 1-year follow-up.ConclusionPainful LBBB syndrome is an uncommon cause of chest pain and is often overlooked by physicians. Misdiagnosis and mistreatment of painful LBBB syndrome may even cause secondary damage, such as VVS induced by sublingual NTG, which is usually used to alleviate angina.
Elucidating the causal relationship between gut microbiota, metabolites, and diabetic nephropathy in European patients: Revelations from genome-wide bidirectional mendelian randomization analysis
Authors: Song Siyuan , Ning Li , Yu Jiangyi 
Published: January 2025

ObjectivePrevious observational studies suggest a potential link between gut microbiota, metabolites, and diabetic nephropathy. However, the exact causal relationship among these factors remains unclear.MethodWe conducted a two-sample bidirectional Mendelian randomization study using summary statistics from the IEU OpenGWAS Project database to investigate gut microbiota, metabolites, and diabetic nephropathy. A range of methods, including inverse variance weighting, MR-Egger, weighted median, and simple median, were applied to examine causal associations. Sensitivity analyses were performed to assess the robustness of the results. Additionally, reverse Mendelian randomization analysis was conducted, treating significant gut microbiota as the outcome, to evaluate effects and perform sensitivity testing. This comprehensive approach provided an in-depth assessment of the interactions among gut microbiota, metabolites, and diabetic nephropathy.ResultThe Inverse Variance Weighted estimates revealed that the abundance of Lachnospiraceae, Parasutterella, and Eubacterium exhibited negative causal effects on diabetic nephropathy, while Coprococcus, Sutterella, Faecalibacterium prausnitzii, and Bacteroides vulgatus showed protective causal effects against the condition. However, reverse Mendelian randomization analysis did not identify any significant associations between diabetic nephropathy and the identified gut microbiota. Furthermore, the estimates indicated that Cholesterol, Pyridoxate, Hexanoylcarnitine, X-12007, Octanoylcarnitine, 10-nonadecenoate (19:1n9), X-12734, and the average number of double bonds in a fatty acid chain had negative causal effects on diabetic nephropathy. In contrast, Methionine, Glycodeoxycholate, X-06351, 1-stearoylglycerol (1-monostearin), 5-dodecenoate (12:1n7), X-13859, 2-hydroxyglutarate, Glycoproteins, Phospholipids in IDL, and the concentration of small HDL particles demonstrated protective causal effects. Notably, sensitivity analyses did not detect any heterogeneity or horizontal pleiotropy, ensuring the robustness of the findings.ConclusionModulating gut microbiota diversity and composition offers a promising strategy for improving the incidence and prognosis of diabetic nephropathy. This highlights the need for future clinical trials focusing on microbiome-based interventions, potentially utilizing microbiome-dependent metabolites. Such approaches could transform the treatment and management of diabetic nephropathy and its associated risk factors, paving the way for more effective therapeutic strategies to combat this debilitating condition.
Comprehensive bioinformatics analysis identifies metabolic and immune-related diagnostic biomarkers shared between diabetes and COPD using multi-omics and machine learning
Authors: Liang Qianqian , Wang Yide , Li Zheng 
Published: January 2025

BackgroundDiabetes and chronic obstructive pulmonary disease (COPD) are prominent global health challenges, each imposing significant burdens on affected individuals, healthcare systems, and society. However, the specific molecular mechanisms supporting their interrelationship have not been fully defined.MethodsWe identified the differentially expressed genes (DEGs) of COPD and diabetes from multi-center patient cohorts, respectively. Through cross-analysis, we identified the shared DEGs of COPD and diabetes, and investigated alterations of signaling pathways using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA). By using weighted gene correlation network analysis (WGCNA), key gene modules for COPD and diabetes were identified, and various machine learning algorithms were employed to identify shared biomarkers. Using xCell, we investigated the relationship between shared biomarkers and immune infiltration in diabetes and COPD. Single-cell sequencing, clinical samples, and animal models were used to confirm the robustness of shared biomarkers.ResultsCross-analysis identified 186 shared DEGs between diabetes and COPD patients. Functional enrichment results demonstrate that metabolic and immune-related pathways are common features altered in both diabetes and COPD patients. WGCNA identified 526 genes from key gene modules in COPD and diabetes. Multiple machine learning algorithms identified 4 shared biomarkers for COPD and diabetes, including CADPS, EDNRB, THBS4 and TMEM27. Finally, the 4 shared biomarkers were validated in single-cell sequencing data, clinical samples, and animal models, and their expression changes were consistent with the results of bioinformatic analysis.ConclusionsThrough comprehensive bioinformatics analysis, we revealed the potential connection between diabetes and COPD, providing a theoretical basis for exploring the common regulatory genes.
Case report: Looking for relationship between type 1 diabetes and chronic recurrent osteomyelitis: short literature review and case presentation
Authors: Snipaitiene Ausra , Radzeviciute Laura , Aleknaviciene Kristina , Dobrovolskiene Rimante , Stankute Ingrida 
Published: January 2025

BackgroundChildhood autoimmune disorders involve the immune system attacking its own tissues, leading to varied symptoms, while autoinflammatory disorders result from innate immune system dysregulation, both requiring extensive diagnosis and multidisciplinary management due to their complexity.Case presentationWe present a unique clinical case of a teenager with a combination of autoimmune and autoinflammatory disorders. The initial manifestation of hip pain, coupled with progressive symptoms over several years and findings in multiple magnetic resonance imaging (MRI) scans, culminated in the diagnosis of chronic recurrent multifocal osteomyelitis (CRMO). Subsequently, the patient was diagnosed with type 1 diabetes (T1D), celiac disease, and juvenile idiopathic arthritis.The therapeutic course proved challenging, marked by unsuccessful attempts with nonsteroidal anti-inflammatory drugs (NSAIDs), and biphosphonates. However, a stable clinical status was ultimately achieved upon the introduction of methotrexate, concomitant with insulin therapy for diabetes and the implementation of a gluten-free diet for celiac disease.ConclusionsOur case showed that the combination of autoimmune and autoinflammatory diseases, brought not only a challenging diagnostic process, but also complicated treatment.
Downregulation of MerTK in circulating T cells of patients with non-proliferative diabetic retinopathy
Authors: Bu Shimiao , Ling Jiang-Yue , Wu Xiaojun , Zhang Liting , Shi Xiangyu , Huang Lang , Zhao Zheng , Yang Ying , Xiang Zongqin , Liu Yong U. , Liu Yufeng , Zhang Yuehong 
Published: January 2025

ObjectiveTo explore the differential gene expression in peripheral blood immune cells of individuals with type 2 diabetes mellitus (DM), comparing those with and without non-proliferative diabetic retinopathy (NPDR).MethodsFrom a pool of 126 potential participants, 60 were selected for detailed analysis. This group included 12 healthy donors (HDs), 22 individuals with DM, and 26 with NPDR. We analyzed peripheral blood mononuclear cells (PBMCs) using RNA sequencing and quantitative PCR (qPCR) to pinpoint differentially expressed genes (DEGs). Western blot and flow cytometry were also employed to evaluate the protein expression of specific genes.ResultsIn patients with NPDR compared to those with DM alone, MerTK—a gene implicated in inherited retinal dystrophies due to its mutations—was notably downregulated in PBMCs. Through flow cytometry, we assessed the protein levels and cellular distribution of MerTK, finding a predominant expression in monocytes and myeloid-derived suppressor cells (MDSCs), with a marked reduction in CD4+ and CD8+ T cells, as well as in natural killer T (NKT) cells. Patients with DM demonstrated a significant deviation in the PBMCs composition, particularly in B cells, CD4+ T cells, and NK cells, when compared to HDs. ConclusionsThe study indicates that MerTK expression in T cells within PBMCs could act as a viable blood biomarker for NPDR risk in patients with DM. Furthermore, the regulation of T cells by MerTK might represent a critical pathway through which DM evolves into NPDR.
Maternal-fetal cytokine profiles in acute SARS-CoV-2 “breakthrough” infection after COVID-19 vaccination
Authors: Packer Claire H. , Jasset Olyvia , Hanniford Nikolina , Brigida Sara , Demidkin Stepan , Perlis Roy H. , Edlow Andrea G. , Shook Lydia L. 
Published: January 2025

ObjectiveVaccination is protective against severe COVID-19 disease, yet whether vaccination reduces COVID-19-associated inflammation in pregnancy has not been established. The objective of this study is to characterize maternal and cord cytokine profiles of acute SARS-CoV-2 “breakthrough” infection (BTI) after vaccination, compared with unvaccinated infection and uninfected controls.Study design66 pregnant individuals enrolled in the MGH COVID-19 biorepository (March 2020-April 2022) were included. Maternal sera were collected from 26 unvaccinated and 21 vaccinated individuals with acute SARS-CoV-2 infection. Cord sera were collected at delivery. Maternal and cord sera from 19 term dyads without current or prior SARS-CoV-2 infection were analyzed as controls. Cytokines were quantified using the Human Inflammation 20-Plex ProcartaPlex assay.ResultsThere was a significantly higher incidence of severe/critical maternal illness in unvaccinated pregnant individuals with SARS-CoV-2 compared to vaccinated (10/26 (38%) vs. 0/21 (0%), p&lt;0.01). Significantly higher maternal levels of TNFα and CD62P were observed in vaccinated individuals with SARS-CoV-2 BTI compared with unvaccinated individuals with infection (p&lt;0.05). Network correlation analyses revealed a distinct maternal cytokine response to SARS-CoV-2 in vaccinated vs unvaccinated individuals. Neither unvaccinated nor vaccinated SARS-CoV-2 infection resulted in elevated cord cytokines compared to controls. Multivariate analyses demonstrate distinct maternal and cord cytokine profiles in the setting of maternal SARS-CoV-2 at delivery.ConclusionVaccination was associated with higher maternal cytokine levels during acute SARS-CoV-2 infection compared to unvaccinated infection, which may reflect vaccine-mediated priming of the immune system. A fetal inflammatory response specific to maternal SARS-CoV-2 infection was not observed.
Comparison of autologous hematopoietic cell transplantation, matched sibling donor hematopoietic cell transplantation, and chemotherapy in patients with favorable- and intermediate-risk acute myeloid leukemia
Authors: Wang Mingyang , Chen Shulian , Zhang Qiuqiu , Yuan Linyu , Wang Xue , Zhang Junshi , Zhang Xiaoyu , Cao Yigeng , Li Dongmei , Lu Xinxiao , Wang Meijiao , Jiang Xiaosi , Zhang Rongli , Chen Xin , Ma Qiaoling , Wei Jialin , Yang Donglin , He Yi , Pang Aiming , Feng Sizhou , Han Mingzhe , Zhai Weihua , Zhao Xingli , Jiang Erlie 
Published: January 2025

IntroductionHematopoietic stem cell transplantation (HSCT) and chemotherapy are considered potentially curative options for post-remission therapy in acute myeloid leukemia (AML). However, the comparative effectiveness of these approaches in favorable- and intermediate-risk AML remains unclear and requires further investigation.MethodsIn this retrospective study, 111 patients diagnosed with de novo favorable- and intermediate-risk AML, categorized according to the ELN 2022 guidelines, were investigated to compare outcomes following autologous HSCT (auto-HSCT), matched sibling donor HSCT (MSD-HSCT), and chemotherapy. Through propensity score matching for disease status before HSCT, 42 cases in first complete remission were selected for each of the auto-HSCT group and the MSD-HSCT group. Additionally, 27 cases in the chemotherapy group, excluding patients with early relapse or death, were included for comparison.ResultsIn the overall population, the 3-year overall survival (OS) rates were 85.7%, 83.1%, and 70.4% (p = 0.043), while the disease-free survival (DFS) rates were 78.6%, 83.2%, and 57.1% (p = 0.002) in the auto-HSCT, MSD-HSCT, and chemotherapy groups, respectively. Notably, both auto-HSCT and MSD-HSCT demonstrated significantly improved DFS compared to chemotherapy in patients with favorable-risk AML. Multivariate analysis further revealed that chemotherapy was significantly associated with inferior DFS compared to auto-HSCT (HR=2.82; 95% CI, 1.26–6.32, p=0.012), while DFS was similar between the MSD-HSCT and auto-HSCT groups (HR=0.80; 95% CI, 0.31–2.09, p=0.645).DiscussionThe findings suggested the advantages of both MSD-HSCT and auto-HSCT over chemotherapy as post-remission therapy for AML patients with favorable and intermediate risk. Further research is needed to support these conclusions.
Deciphering hub genes and immune landscapes related to neutrophil extracellular traps in rheumatoid arthritis: insights from integrated bioinformatics analyses and experiments
Authors: Li Yang , Liu Jian , Sun Yue , Hu Yuedi , Zhou Qiao , Cong Chengzhi , Chen Yiming 
Published: January 2025

BackgroundRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and progressive joint destruction. Neutrophil extracellular traps (NETs), a microreticular structure formed after neutrophil death, have recently been implicated in RA pathogenesis and pathological mechanisms. However, the underlying molecular mechanisms and key genes involved in NET formation in RA remain largely unknown.MethodsWe obtained single-cell RNA sequencing data of synovial tissues from the Gene Expression Omnibus (GEO) database and performed cellular annotation and intercellular communication analyses. Subsequently, three microarray datasets were collected for a training cohort and correlated with a bulk RNA-seq dataset associated with NETs. Differentially expressed genes were identified, and weighted gene correlation network analysis was used to characterize gene association. Using three machine learning techniques, we identified the most important hub genes to develop and evaluate a nomogram diagnostic model. CIBERSORT was used to elucidate the relationship between hub genes and immune cells. An external validation dataset was used to verify pivotal gene expression and to construct co-regulatory networks using the NetworkAnalyst platform. We further investigated hub gene expression using immunohistochemistry (IHC) in an adjuvant-induced arthritis rat model and real-time quantitative polymerase chain reaction (RT-qPCR) in a clinical cohort.ResultsSeven cellular subpopulations were identified through downscaling and clustering, with neutrophils likely the most crucial cell clusters in RA. Intercellular communication analysis highlighted the network between neutrophils and fibroblasts. In this context, 4 key hub genes (CRYBG1, RMM2, MMP1, and SLC19A2) associated with NETs were identified. A nomogram model with a diagnostic value was developed and evaluated. Immune cell infiltration analysis indicated associations between the hub genes and the immune landscape in NETs and RA. IHC and RT-qPCR findings showed high expression of CRYBG1, RMM2, and MMP1 in synovial and neutrophilic cells, with lower expression of SLC19A2. Correlation analysis further emphasized close associations between hub genes and laboratory markers in patients with RA.ConclusionThis study first elucidated neutrophil heterogeneity in the RA synovial microenvironment and mechanisms of communication with fibroblasts. CRYBG1, RMM2, MMP1, and SLC19A2 were identified and validated as potential NET-associated biomarkers, offering insights for diagnostic tools and immunotherapeutic strategies in RA.