bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of Ferroptosis-Related Prognostic Models and FDFT1 as a Potential Ferroptosis Driver in Colorectal Cancer
Authors: Duan Lili , Cao Lu , Liu Jinqiang , Wang Zixiang , Liang Jie , Feng Fan , Zhang Jian , Hong Liu , Zheng Jianyong 
Published: February 2025

Aims:
We aimed to develop Ferroptosis-Related Gene (FRG) signatures to predict
overall survival (OS) along with disease-free survival (DFS) in individuals with colorectal
cancer (CRC).

Background:
Prediction of CRC prognosis is challenging. Ferroptosis constitutes a newly
reported kind of cell death, and its association with CRC prognosis remains unexplored.

Objective:
This research endeavored to establish a prognostic risk signature for colorectal
cancer by leveraging ferroptosis-related genes (FRGs), with the objective of refining prognostic
precision in clinical settings.

Methods:
The clinical data and mRNA expression profiles were obtained from The Cancer
Genome Atlas (TCGA) colorectal cancer cohorts. The Lasso algorithm was employed to develop
the overall survival (OS) and disease-free survival (DFS) prediction models. These
models were subsequently validated using independent data from GSE38832.

Results:
Our research unveiled a significant difference in the expression levels of 85% of
ferroptosis-related genes (FRGs) between CRC tissues and paracancer tissues. Out of these,
11 prognostic genes were pinpointed through univariate Cox analysis. By employing two
models, patients were stratified into low- and high-risk groups based on predicted risk
scores, which were subsequently validated as independent prognostic factors via multivariate
Cox analysis. The robustness of these models was further confirmed through Receiver
Operating Characteristic (ROC) curve analysis. Functional enrichment analysis indicated a
predominance of cancer-associated pathways in the high-risk group, including WNT signaling,
along with variations in immune status between the two risk categories. Leveraging the
Connectivity Map (CMap) database, a total of sixteen potential therapeutic drugs were identified.
Additionally, in vitro experiments corroborated that Farnesyl-Diphosphate Farnesyltransferase
1 (FDFT1) was underexpressed in CRC and exhibited tumor suppressive properties.
More specifically, FDFT1 may augment ferroptosis in CRC by modulating the expression
of the Iron-Sulfur Cluster Assembly Enzyme (ISCU).

Conclusion:
Our study highlighted the significance of ferroptosis-related genes in the pathogenesis
of CRC and underscored the potential of ferroptosis-related gene-based risk signatures
as valuable tools for improving prognostic accuracy and tailoring therapeutic strategies.
However, the validity of these predictive models required further validation through real-
world studies to ensure their reliability and applicability.
EGCG Mitigates Apoptosis of Lens Epithelial Cells in Age-Related Cataract via the PAK1/Cleaved Caspase-3 Pathway
Authors: Zhang Yue , Su Dongmei , Sun Zhaoyi , Fu Yanjiang , Chen Xiaoya , Hu Yuzhu , Zhang Xiao , Zheng Shunfei , Ma Xu , Hu Shanshan 
Published: February 2025

Background:
Oxidative damage and apoptosis of lens epithelial cells
(LECs) are the primary factors contributing to the development of age-related cataracts
(ARC). The potential protective effects of epigallocatechin gallate (EGCG) on LECs
remain unclear despite its remarkable antioxidant and anti-apoptotic properties. The
aim of this study was to explore the role of serine/threonine-protein kinase (PAK1) in
EGCG-mediated attenuation of H2O2-induced apoptosis of LECs in vivo and in vitro.

Methods:
PAK1 expression was assessed in the anterior capsule of the lens from
mice and patients with and without ARC using western blotting and immunohistochemistry.
Human lens epithelial B3 (HLE-B3) cells were pre-treated with
EGCG+H2O2 or H2O2 only, and PAK1 expression was determined using qRT-PCR and
western blotting. Apoptosis (following PAK1 overexpression or silencing) and cell
survival were assessed using Hoechst 33342 staining and a cell counting Kit-8 assay,
respectively. Cleaved caspase-3 was measured in transected cells, aged/young mice,
and mice treated with EGCG via western blotting.

Results:
PAK1 expression was significantly lower in ARC LECs than in control LECs.
In HLE-B3 cells, EGCG+H2O2 treatment upregulated PAK1 mRNA and protein
expression when compared with H2O2 alone. PAK1 overexpression alleviated H2O2-
induced apoptosis in LECs, while low expression weakened EGCG’s protective
effects. PAK1 overexpression reduced cleaved caspase-3 expression in H2O2-treated
cells, whereas PAK1 silencing increased its expression in EGCG+H2O2-treated cells.
EGCG decreased cleaved caspase-3 expression in H2O2-treated cells. These results
suggest that PAK1 inhibits cleaved caspase-3 expression, thereby enhancing EGCG’s
attenuation of H2O2-induced LEC apoptosis.

Conclusion:
The PAK1/cleaved caspase-3 pathway plays a key role in EGCG’s
protective effects on the development of ARC. This provides a new therapeutic target
for the use of EGCG in preventing and treating ARC.
Utilization of DNA Replication factor MCM2 by Cancer
Authors: Yuan Yuwei , Zeng Tian , Gao Anbo , Guan Yang , Zhang Qun-feng , Li Yukun , Tan Hui , Zou Juan 
Published: February 2025

Abstract:
MCM2 belongs to the microchromosome maintenance [MCM] family and plays an essential role in initiating DNA replication as well as maintaining normal cellular cycle functions. Recent research indicates that there is the abnormal expression of MCM2 in various cancers, such as breast, cervical, ovarian, lung, hepatocellular carcinoma, nephroblastoma, prostate, and pancreatic cancers, where it shows a strong link to tumorigenesis, growth, invasion, migration, and adverse prognosis. Thus, MCM2 could serve as a significant biomarker for the early identification, diagnosis, and prognostic evaluation of multiple cancers. In addition, targeting MCM2 expression may open new possibilities for a full range of cancer treatments. In this paper, the protein structure, physiological function, and carcinogenic mechanism of MCM2 were reviewed.
Therapeutic Potential of Quercetin in Type 2 Diabetes Based on a Network Pharmacology Study
Authors: Basaldúa-Maciel Viridiana , Guzmán-Flores Juan Manuel , Reyes-Chaparro Andrés , Martínez-Esquivias Fernando 
Published: February 2025

Introduction:
Currently, there are pharmacological treatments for type 2 diabetes
(T2D), but these are ineffective. Quercetin is a flavonoid with antidiabetic properties.

Objective:
This research aimed to identify the molecular mechanism of Quercetin in T2D from
network pharmacology.

Methods:
We obtained T2D-related genes from MalaCards and DisGeNET, while potential targets
for Quercetin were sourced from SwissTargetPrediction and Comparative Toxicogenomics
databases. The overlapping genes were identified and analyzed using ShinyGO 0.77. Subsequently,
we constructed a protein-protein interaction network using Cytoscape, conducted molecular
docking analyses with SwissDock, and validated the results through molecular dynamics
simulation in GROMACS.

Results:
Quercetin is involved in apoptotic processes and in the regulation of insulin activity,
estrogen, prolactin and EGFR receptor. The key driver genes AKT1, GSK3B, SRC, IGF1R, MMP9,
ESR2, PIK3R1, and MMP2 showed high concordance in the molecular docking study, and
molecular dynamics showed stability between Quercetin and ESR2 and PIK3R1.

Conclusions:
Our work helps to identify the molecular mechanism and antidiabetic effect of
quercetin, which needs to be studied experimentally.
Effects of a Rosiridin against Rotenone-induced Rats’ Model of Parkinson's Disease: In-vivo Study and in silico Molecular Modeling
Authors: Rafeeq Misbahuddin , A Al-Abbasi Fahad , Afzal Muhammad , Saad Alharbi Khalid , Moglad Ehssan , D Al-Qahtani Salwa , A Bukhari Hussam , Imam Faisal , Sayyed Nadeem , Kazmi Imran 
Published: February 2025

Aim:
The investigation aimed to study the outcome of rosiridin in Parkinson's disease
(PD) induced by rotenone (ROT) in rodents.

Methods:
Rodents were randomized into IV groups and were induced with ROT followed by treatment
with rosiridin. Group I-IV received saline as a vehicle, II-ROT (0.5 mg/kg S.C) for 28 consecutive
days, III and IV- rosiridin 10 and 20 mg/kg orally with ROT. On completion of the experimental
duration, behavioral investigations were carried out. Biochemical variables such as acetylcholinesterase
(AChE), oxidative stress and antioxidants markers (Malondialdehyde-MDA, glutathione-GSH,
superoxide dismutase-SOD, and catalase-CAT), anti-inflammatory (Interleukin-1 beta-IL-1β, IL-6,
and tumor necrosis factor alpha-TNF-α), alteration in neurotransmitters (Serotonin-5-HT), norepinephrine,
and dopamine-DA, along with metabolites such as 5-hydroxy indole acetic acid-5-
HIAA),), mitochondrial complex I, II, IV, and caspase-3 activity were evaluated at the end of the experiment.
Furthermore, molecular docking and dynamics were performed for target ligands.

Results:
Rosiridin significantly restored the level of AChE, oxidative stress and antioxidants markers
(MDA, GSH, SOD, and CAT), anti-inflammatory (IL-1β, IL-6, and TNF-α), alteration in neurotransmitters,
mitochondrial complex I, II, IV, and caspase-3 activity. Rosiridin has a favorable negative binding
affinity to AChE (-8.99 kcal/mol). The results of the molecular dynamics simulations indicate that
proteins undergo a substantial change in conformational dynamics when binding to rosiridin.

Conclusion:
In this study, rosiridin may exhibit neuroprotective properties against the Parkinson's
model for treating PD.
Transient Receptor Potential Ankyrin 1 (TRPA1) Mediates Hydrogen Sulfide-induced Ca2+ Entry and Nitric Oxide Production in Human Cerebrovascular Endothelium
Authors: Soda Teresa , Brunetti Valentina , De Sarro Giovambattista , Biella Gerardo , Moccia Francesco , Berra-Romani Roberto , Scarpellino Giorgia 
Published: February 2025

Introduction:
The gasotransmitter hydrogen sulfide (H2S) modulates various brain
functions, including neuron excitability, synaptic plasticity, and Ca2+ dynamics. Furthermore, H2S
may stimulate nitric oxide (NO) release from cerebrovascular endothelial cells, thereby regulating
NO-dependent endothelial functions, such as angiogenesis, vasorelaxation, and cerebral blood flow
(CBF). However, the signaling pathway by which H2S induces NO release from cerebrovascular
endothelial cells is still unclear.

Methods:
Herein, we exploited single-cell imaging of intracellular Ca2+, H2S, and NO levels to assess
how H2S induces Ca2+-dependent NO release from the human cerebrovascular endothelial cell
line, hCMEC/D3.

Results:
Administration of the H2S donor, sodium hydrosulfide (NaHS), induced a dose-dependent
increase in (Ca2+)i only in the presence of extracellular Ca2+. NaHS-induced extracellular Ca2+ entry
was mediated by the Ca2+-permeable TRPA1 channel, as shown by pharmacological and genetic manipulation
of the TRPA1 protein. Furthermore, NaHS-dependent TRPA1 activation led to NO release
that was abolished by buffering the concomitant increase in (Ca2+)i and inhibiting eNOS. Furthermore,
the endothelial agonist, adenosine trisphosphate (ATP), caused a long-lasting elevation in
(Ca2+)i that was driven by cystathionine γ-lyase (CSE)-dependent H2S production and by TRPA1 activation.
Consistent with this, ATP-induced NO release was strongly reduced either by blocking CSE
or by inhibiting TRPA1.

Conclusion:
These findings demonstrate for the time that H2S stimulates TRPA1 to induce NO production
in human brain microvascular endothelial cells. Additionally, they show that this signaling
pathway can be recruited by an endothelial agonist to modulate NO-dependent events at the human
neurovascular unit.
The Link between Arterial Atherosclerotic and Venous Thromboembolic Disease
Authors: Poredos Pavel , Poredos Peter , Jezovnik Mateja K. 
Published: February 2025

Abstract:
Traditionally, arterial atherosclerotic (AA) and venous thromboembolic (VTE) diseases
have been separated into two independent entities. However, a body of evidence suggests the link
between arterial and venous disease. In this narrative review, the relationship between these two vascular
diseases is discussed. Different risk factors are common in both diseases, such as dyslipidaemia,
metabolic syndrome, and thrombophilia. Etiopathogenetic mechanisms of both diseases are similar.
Inflammation, as a basic pathogenetic mechanism of atherosclerotic disease, is also involved in the
pathogenesis of VTE. Inflammation as a response to vessel wall injury promotes coagulation and
inhibits endogenic fibrinolytic activity, which results in thromboembolic events in the arterial as well
as in the venous system. A relationship has also been observed between preclinical or clinical atherosclerotic
disease and VTE. These findings indicate that atherosclerosis may induce VTE or that
common risk factors simultaneously stimulate the development of both diseases. The relationship
between arterial and venous disease is also supported by the efficacy of some drugs (antiplatelets,
anticoagulants, statins) in the prevention of both diseases.
In conclusion, arterial and venous diseases share similar pathophysiological mechanisms, often driven
by common risk factors. This overlap suggests that a unified approach to prevention and treatment
may be beneficial for both conditions, potentially improving patient outcomes by addressing the underlying
shared pathways.
Microwave-assisted and Solvent-free Synthesis of Propargylamines via A3-coupling Reaction
Authors: Huong Vuong Thi , Chung Nguyen Thi , Dung Vo Cong , Thao Nguyen Thi Phuong , Xuan Duc Dau 
Published: February 2025

Abstract:
An efficient and green method for the A3- coupling reaction of saliciladehyde, secondary
amines, and terminal alkynes to synthesize propargylamines using a microwave reactor has been
demonstrated. The synthesis showed several salient features, such as high yield of products, rapid
product formation, and environmentally benign reaction conditions. Furthermore, the synthesis could
be performed in gram scale. Nine propargylamine adducts were obtained in high yields and their
structures were confirmed by NMR data. A plausible reaction mechanism was also suggested.
Twins and Necrotizing Enterocolitis: Genetic Relevance
Authors: Bhandari Vineet 
Published: February 2025

Abstract:
In preterm infants, necrotizing enterocolitis (NEC) is one of the most devastating complications
seen in the neonatal intensive care unit (NICU), with both short- and long-term sequelae.
Outcomes reported for mono- (versus di-) chorionic twins suggest an increased incidence in
the monochorionic twins, usually attributed to abnormal placental vascular connections. Same sex
concordance and zygosity data suggest shared genetic and environmental factors as important contributing
factors to the pathogenesis of NEC. This concept is further supported by fecal microbiome
data from preterm twins. However, there is also some uncertainty in these observations because
studies that controlled for gestational age did not show significant differences between singletons
and twins in the occurrence of NEC. This mini-review was undertaken as a critical appraisal
of the published literature in terms of twin studies to establish the genetic relevance vis-àvis
NEC. There is a need for further evaluation of genetic and confounding factors arising from
the environment and the gut microbiome in these infants using cohorts with larger sample sizes.
Circulating Biomarkers as a Window into the Relationship between Sarcopenia and Diabetes: Implications for Effective Management
Authors: Tajik Ali , Mahdavizadeh Vahid , Hadizadeh Farzin , Shakour Neda 
Published: February 2025

Aims:
This study aims to investigate the relationship between sarcopenia and circulating
biomarkers in diabetes, with a focus on early detection and effective management strategies.

Methods:
A literature review was conducted using the ScienceDirect, Scopus, PubMed, and Web
of Science databases up to December 2024. Key search terms included “diabetes,” “sarcopenia,”
“HbA1c”, “glucose,” “insulin,” and specific biomarkers such as inflammatory markers,
adipokines, and myokines.

Results:
Aging is associated with a decline in organ and bodily system functionality, with sarcopenia
being particularly prominent due to its progressive loss of muscle mass and function. This condition
increases health risks and mortality in the elderly. Muscles, as the primary consumers of glucose,
play a crucial role in glucose uptake; reduced mass can exacerbate insulin resistance. Sarcopenia
and diabetes share common pathophysiological mechanisms, including insulin resistance,
inflammation, and vascular complications. Circulating biomarkers, crucial for diabetes management,
may offer insights into the early stages of sarcopenia.

Conclusion:
The complex relationship between sarcopenia and diabetes, influenced by shared
pathophysiological pathways, presents challenges in geriatric healthcare. Circulating biomarkers
hold promise for early detection and monitoring of sarcopenia, potentially enhancing patient outcomes
and quality of life. Further research is necessary to validate these connections and develop
targeted treatments for individuals affected by these conditions.
Photocatalytic Degradation of Binary Dyes, Methyl Orange and Methyl Green, in Aqueous Media Using 2D g-C3N4/Polyaniline/Silver Nanocomposite
Authors: Balu Surendar , Vivek Pranav , Sundramoorthy Ashok K. 
Published: February 2025

Background:
In recent years, azo dyes have become the dominant choice in the textile
industry, accounting for about 60-70% of all dyes used, which has led to growing environmental
concerns.

Aim:
This research focused on the photocatalytic degradation of methyl orange (MO) and methyl
green (MG) dyes using a novel g-C₃N₄ (GCN)/polyaniline (PANI)/Ag composite under
visible light.

Methods:
This composite was synthesized through a straightforward preparation process and
characterized by using various techniques, including UV-visible spectroscopy (UV-Vis), Fourier-
transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), and cyclic
voltammetry (CV).

Results:
Characterization results confirmed the incorporation of PANI and Ag nanoparticles into
the GCN matrix. This composite enhanced the visible light absorption and improved charge
separation, leading to increased photocatalytic efficiency. Photocatalytic experiments were conducted
under visible light irradiation with a catalyst dosage of 10 mg in a 10-ppm solution of the
MO and MG dyes mixture.

Conclusion:
The GCN/PANI/Ag composite achieved significant degradation efficiencies of
70% for MO and 69% for MG within 120 minutes. The degradation process followed first-order
kinetics, with rate constants of 0.0087 min⁻¹ for MO and 0.0086 min⁻¹ for MG, respectively.
Reusability tests showed that the composite retained over 60% of its initial efficiency after five
cycles. These findings highlight the potential of the GCN/PANI/Ag composite as a sustainable
and effective photocatalyst for visible-light-driven dye degradation, offering an eco-friendly
approach to wastewater treatment.
Genotypic Contrasting of Protein and Flavonoid Contributes to Differential Responses of Targeted Metabolites in Soybean Seeds
Authors: Tran Dinh Ha , Tran Trong Dai , Nguyen Tien Dung , Nguyen Xuan Vu , Ngo Xuan Binh , Van Doan Duong , Tran Anh Tuan , Dang Thi Phuong Anh , La Thi Thao , Nguyen Van Tinh , Nguyen Minh , Hoang Van Hung , La Van Hien 
Published: February 2025

Introduction/Objective
Soybean is a major source of various nutrients. Increasing demand for soybeans has created considerable impetus for exploring the nutritional quality of soybeans. We aimed to collect soybean varieties rich in nutrients.

Materials and Methods
Metabolite analysis was carried out for seed compositions, including protein, phenolics, and flavonoids, along with gene expression of protein and phenolic metabolism-related enzymes in 10 soybean accessions collected from different geographical regions.

Results
Total protein content ranged from 29.7% to 35.7%, depending on soybean germplasm accessions. Among them, Vang Ha Giang (VHG) exhibited relatively high protein content, while Cuc Vo Nhai (CVN) had comparatively low protein content. Further analysis of seed compounds indicated that the phenolic compounds were higher in cultivars Dau Tuong Den (DTD) and CVN, with a total phenolic content of 37.7 µg g-1 and total flavonoid of 2.1 mg g-1. These results were reinforced by analysis of gene expression levels of candidate genes β-conglycinin (7S) and glycinin (11S) involving protein storage, phenylalanine ammonia-lyase 1 (GmPAL1) and chalcone synthase 8 (GmCHS8) genes related to phenolic and flavonoid synthesis, which showed similar correlation. We revealed that protein content was correlated with seed weight but not with seed color, even though significant variations were found among soybean genotypes, while flavonoid was affected by seed coat color. Furthermore, the negative correlation of protein with flavonoids demonstrated intricate relationships among seed components.

Conclusion
Protein and flavonoid alteration in seeds is subject to major-effect-genotypes in landrace and breeding cultivar selection, and genotype variants are relevant to geographical regions. Our study provides intricate relationships among seed nutritional components and offers insight into the alteration of soybean quality.
Prediction of the Frictional Power Distribution in the Tire Contact Patch Based on an Empirical Tire Model and an Artificial Neural Network
Authors: Muth Lars , Zharia Raphael , Sahin Hürkan , Sextro Walter 
Published: February 2025

ABSTRACT
To predict and prevent uneven tire wear in addition to a reduction of overall tire wear, it is essential to estimate not only the total amount of wear but also how the wear is distributed across the tire width. This requires knowledge of the frictional power distribution in the tire contact patch, which is the basis for calculating tire wear using a wear law. Usually, only 3D structural tire models can generate such distributed contact results. However, they involve high computational costs and cannot be used for comprehensive optimization of a vehicle’s suspension system with respect to tire wear characteristics. Hence, this contribution presents a methodology on how to accelerate the prediction of the frictional power distribution using two components: The structural tire model is replaced by an empirical tire model that on its own is not able to generate distributed contact results. Therefore, an artificial neural network is trained to predict the desired contact results from the kinematic quantities calculated by the empirical tire model. In the initial training phase, both components are fitted to data generated by the original complex tire model. After training, the empirical tire model can replace the structural tire model in vehicle simulations, resulting in significantly shorter calculation times. The simulation results are fed into the artificial neural network, which predicts the frictional power distributions over the tire width with negligible additional effort. Overall, the methodology reduces calculation time for the prediction of tire wear based on virtual test drives to approximately 25% of the time needed when using structural tire models.