bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multicentre Cross-Sectional Study Describing Postoperative Wound Care Practice in Northeast Ethiopia
Authors: Fasil Tegegn Lidiya , Andualem Fantahun , Derbie Begashaw Tesfaye , Seid Jemal , Temesgen Kibir 
Published: December 2023

Background Postoperative care is the management of a patient after surgery that includes care given during the immediate postoperative period. Postoperative complications are continuing to be a major source of morbidity following operative procedures. Postoperative wound infection delays the patient’s recovery, increases discomfort, and prolongs the hospital stay. Objective The study aimed to assess among nurses working in governmental hospitals in the south Wollo zone and Oromia special zone, northeast Ethiopia, 2020. Methods Institution-based cross-sectional study design was conducted on governmental hospitals in the south Wollo zone and Oromia special zone. Variables in multivariable logistic regression, p-value < 0.05 was used to declare statistical significance. Result From a total of 411 samples, 402 nurses responded to the questionnaire, with a response rate of 97.81%. This study showed that 49.8% of participants had good practice. The availability of a wound management tool was 1.6 times more likely to promote good practice than the lack of a wound assessment tool. Nurses who had documented their wound assessment and management activities were 2.1 times more likely to have good practice than those who hadn’t documented. Conclusion This study showed that half of the participants had poor wound care practices. Regarding associated factors, the availability of wound management tools and documentation of wound assessment and management had a significant association with the nurse's poor wound care practice. On the basis of these results, health policymakers and hospital administrators should develop a program to train nurses in wound care practice, and it helps as a reference for the researchers to further study.
ALDH2 mitigates LPS-induced cardiac dysfunction, inflammation, and apoptosis through the cGAS/STING pathway
Authors: Liu Haoran , Hu Qin , Ren Ke , Wu Pengxin , Wang Yang , Lv Chuanzhu 
Published: December 2023

Abstract
Background
Sepsis is a severe syndrome of organ dysfunction that often leads to cardiac dysfunction and endangers life. The role of mitochondrial aldehyde dehydrogenase 2 (ALDH2) in LPS-induced myocardial injury is unclear. The purpose of this study was to assess the role of ALDH2 in lipopolysaccharide (LPS)-induced myocardial injury and the regulatory mechanism and to identify potential therapeutic strategies for treating this condition.

Methods
An in vivo model was established by 12 h of LPS (10 mg/kg, intraperitoneal injection) stimulation, and an in vitro model was generated by stimulating H9C2 cells with LPS (10 μg/ml) for 12 h. We then used the ALDH2 activator Alda-1 and the ALDH2 inhibitor daidzin to assess their effects on LPS-induced cardiac injury. Cardiac function in mice was evaluated by using cardiac ultrasound. We used various methods to evaluate inflammation, apoptosis, and oxidative stress, including ELISA, flow cytometry, JC-1 staining, Western blotting, and DCFH-DA staining. Additionally, we used a small interfering RNA (siRNA) to knock down cyclic GMP-AMP synthase (cGAS) to further investigate the relationship between ALDH2 and cGAS in LPS-induced cardiac injury.

Results
LPS-induced cardiac dysfunction and increased the levels of the cardiac injury markers creatine kinase-MB (CKMB) and lactate dehydrogenase (LDH) in vivo. This change was accompanied by an increase in reactive oxygen species (ROS) levels, which exacerbated the oxidative stress response and regulated apoptosis through cleaved caspase-3, BAX, BCL-2. The expression of inflammatory cytokines such as IL-6/IL-1β/TNF-α was also upregulated. However, these effects were reversed by pretreatment with Alda-1 via the inhibition of cGAS/stimulator of interferon genes (STING) signaling pathway. Interestingly, LPS, Alda-1 and daidzin altered the activity of ALDH2 but did not regulate its protein expression. Knocking down cGAS in H9C2 cardiomyocytes alleviated LPS-induced cardiac inflammation, apoptosis, and ROS production and weakened the synergistic effect of daidzin.

Conclusion
We demonstrated that ALDH2 alleviated LPS-induced cardiac dysfunction, inflammation, and apoptosis through the cGAS/STING signaling pathway, thereby protecting against LPS-induced cardiac injury. This study identifies a novel therapeutic approach for treating sepsis-induced cardiomyopathy (SIC).
Do sociodemographic factors influence the levels of health and oral literacy? A cross-sectional study
Authors: Veladas Francisco Manuel Veigas , De la Torre Canales Giancarlo , de Souza Nobre Bryanne Brissian , Escoval Ana , Pedro Ana Rita , de Almeida André Mariz , Assunção Victor Abreu , Manso Ana Cristina 
Published: December 2023

Abstract
Background
Oral health literacy has gained importance in dental literature, and its relationship with oral health status and association with health status (HL) has been reported. Then, an association between the levels of HL and OHL could be expected. This study aimed to assess the levels of HL and OHL according to sociodemographic factors and to explore a possible association between HL and OHL.

Methods
The European Health Literacy Survey and Oral Health Literacy Adults Questionnaire were applied to a convenience sample from Portuguese individuals. Also, sociodemographic factors such as sex, age, schooling level of the participants and their parents, and if the participants were professionals or students of the health field were assessed. To analyze the data, the Kruskal–Wallis and Mann–Whitney U tests were used to compared sociodemographic variables and the levels of literacy in general and oral health. The Spearman correlation test assessed the correlation between the levels of HL and OHL.

Results
HL results showed that 45.1% of the volunteers were considered in a “problematic level” and 10.3% in “excellent level”. However, 75% presented an adequate level of OHL. Regarding the levels of HL in each sociodemographic variable, significant higher levels of “excellent level” were found in health professionals and students when compared with participants not related to health area (p < 0.001). Comparisons between the levels of OHL in each sociodemographic variable showed, significant differences regarding sex (p < 0.05), age (p < 0.001), levels of schooling of the participants and their parents (p < 0.009 and p < 0.001) and relationship with health field. (p < 0.001). A significant positive – weak correlation was found between HL and OHL (p < 0.001).

Conclusions
HL and OHL levels are associated and could be influenced by sociodemographic factors.
Faecal microbiota and fatty acids in feline chronic enteropathy
Authors: Miller Julia , Żebrowska-Różańska Paulina , Czajkowska Aleksandra , Szponar Bogumiła , Kumala-Ćwikła Aleksandra , Chmielarz Magdalena , Łaczmański Łukasz 
Published: December 2023

Abstract
Background
Feline chronic enteropathy is a set of disorders defined as the presence of clinical signs of gastrointestinal disease for at least three weeks. The most common final diagnoses are inflammatory bowel disease and alimentary small cell lymphoma. The etiopathogenesis of these diseases is incompletely understood; however, it is hypothesised that they involve a combination of factors, including altered composition and/or functionality of the intestinal microbiome. An important factor in the interplay of the microbiome and host is the production of short- and branched-chain fatty acids.
The aim of this study was to evaluate the possible differences in faecal microbiota diversity, composition and fatty acid production between cats suffering from chronic enteropathy and healthy cats. Sixteen cats suffering from chronic enteropathy and fourteen healthy control cats were enrolled in the study. The microbiota compositions of faecal samples were analysed by using next-generation amplicon sequencing of the V3V4 fragment of the 16S rRNA gene. Fatty acids were evaluated by high-performance liquid chromatography.

Results
Both the alpha and beta diversities were significantly lower in samples obtained from cats with chronic enteropathy. The relative abundance of the phylum Proteobacteria, orders Lactobacillales and Enterobacterales, family Enteriobacteriaceae and genus Escherichia Shigella were higher in diseased cats, whereas the abundance of the phylum Bacteroidota and order Peptococcales were higher in control cats. The faecal concentrations of short-chain fatty acids were higher in cats with chronic enteropathy, with lower propionate proportions and higher butyrate proportions.

Conclusion
The study revealed alterations in microbiota compositions and short-chain fatty acid concentration in cats suffering from chronic enteropathy, which is an important finding both for research on the pathogenesis of the disease and for potential therapeutic interventions in the form of faecal microbiota transplantation and/or probiotic supplementation.
Quinolinic acid impairs mitophagy promoting microglia senescence and poor healthspan in C. elegans: a mechanism of impaired aging process
Authors: Dongol Anjila , Chen Xi , Zheng Peng , Seyhan Zehra Boz , Huang Xu-Feng 
Published: December 2023

AbstractSenescent microglia are a distinct microglial phenotype present in aging brain that have been implicated in the progression of aging and age-related neurodegenerative diseases. However, the specific mechanisms that trigger microglial senescence are largely unknown. Quinolinic acid (QA) is a cytotoxic metabolite produced upon abnormal activation of microglia. Brain aging and age-related neurodegenerative diseases have an elevated concentration of QA. In the present study, we investigated whether QA promotes aging and aging-related phenotypes in microglia and C. elegans. Here, we demonstrate for the first time that QA, secreted by abnormal microglial stimulation, induces impaired mitophagy by inhibiting mitolysosome formation and consequently promotes the accumulation of damaged mitochondria due to reduced mitochondrial turnover in microglial cells. Defective mitophagy caused by QA drives microglial senescence and poor healthspan in C. elegans. Moreover, oxidative stress can mediate QA-induced mitophagy impairment and senescence in microglial cells. Importantly, we found that restoration of mitophagy by mitophagy inducer, urolithin A, prevents microglial senescence and improves healthspan in C. elegans by promoting mitolysosome formation and rescuing mitochondrial turnover inhibited by QA. Thus, our study indicates that mitolysosome formation impaired by QA is a significant aetiology underlying aging-associated changes. QA-induced mitophagy impairment plays a critical role in neuroinflammation and age-related diseases. Further, our study suggests that mitophagy inducers such as urolithin A may offer a promising anti-aging strategy for the prevention and treatment of neuroinflammation-associated brain aging diseases.
RETRACTED ARTICLE: csi-miR-96-5p delivered by Clonorchis sinensis extracellular vesicles promotes intrahepatic cholangiocarcinoma proliferation and migration via the ferroptosis-related PTEN/SLC7A11/GPX4 axis
Authors: Wen Li-Jia , Yin Ji-Gang , Wang Yong-Xin , Liu Kai , Zhao Ji-Xue 
Published: December 2023

Abstract
Background
Clonorchis sinensis (CS) is classified as a group 1 carcinogen and can cause intrahepatic cholangiocarcinoma (ICC). CS extracellular vesicles (CsEVs) play important roles in mediating communication between parasitic helminths and humans. Ferroptosis is a novel cell death mechanism that is mainly induced by lipid peroxidation and iron overload. However, the role of CsEVs in the regulation of ferroptosis in ICC remains unclear. This study aimed to explore the role of CS-secreted miR-96-5p (csi-miR-96-5p) delivered by CsEVs in ICC progression and ferroptosis.

Methods
Tissue samples were collected from ICC patients with CS infection (CS-ICC) or without CS infection (NC-ICC). The levels of csi-miR-96-5p and PTEN gene were determined by quantitative polymerase chain reaction (qPCR) and western blotting, and survival analysis was performed. CsEVs were isolated and identified by ultracentrifugation and transmission electron microscopy. Lentiviruses were used to establish stable cell lines with csi-miR-96-5p mimic expression, PTEN overexpression (PTEN-EXO) and PTEN CRISPR/Cas9-based knockout (PTEN-KO) and their respective negative controls. Cell proliferation was assessed by performing Cell Counting Kit-8 assays in vitro and in a tumor xenograft model in vivo, and cell migration was assessed by performing Transwell assays. Erastin is used to induce ferroptosis. Ferroptosis levels were evaluated using biomarkers.

Results
High csi-miR-96-5p and low PTEN expression was observed in CS-ICC tissues and was associated with poor overall survival. csi-miR-96-5p was highly enriched in CsEVs and was taken up by ICC cells. csi-miR-96-5p mimics or PTEN-KO significantly promoted the growth and migration of ICC cells in vitro and in vivo, whereas PTEN-EXO exerted the opposite effect. Mechanistically, csi-miR-96-5p mimics or PTEN-KO inhibited erastin-induced ferroptosis, including reducing the accumulation of Fe2+, lipid reactive oxygen species, and malondialdehyde, increasing the GSH/GSSG ratio and levels of SLC7A11 and GPX4, whereas PTEN-EXOs exerted the opposite effect.

Conclusions
csi-miR-96-5p delivered by CsEVs reduced ferroptosis by regulating the expression of the PTEN/SLC7A11/GPX4 axis, thereby promoting ICC proliferation and migration. For the first time to our knowledge, we found that CS miRNAs could promote tumor development through ferroptosis.

Graphical Abstract
Association between serum PCSK9 and coronary heart disease in patients with type 2 diabetes mellitus
Authors: Huang Juan , Gu Jun-Xu , Wang Kun , Zhang Ai-Min , Hong Ting-Ting , Li Shan-Shan , Yao Xiao-Qin , Yang Ming , Yin Yue , Zhang Na , Su Ming , Hu Jia-Jia , Zhang Xue-Zhi , Jia Mei 
Published: December 2023

Abstract
Background and aims
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is considered a new biomarker for atherosclerosis, but its ability to predict cardiovascular outcomes has been controversial. This study aimed to address the lack of data on PCSK9, coronary heart disease (CHD) severity, and major cardiovascular events (MACEs) in patients with type 2 diabetes mellitus (T2DM).

Methods
A total of 2984 T2DM patients underwent selective coronary angiography, and their serum PCSK9 levels were measured using enzyme-linked immunosorbent assay. Correlation and logistic regression analyses were performed to investigate the association between PCSK9 expression and CHD severity. This study used Cox regression analysis to assess the association between circulating PCSK9 levels and the risk of MACEs.

Results
Circulating PCSK9 levels were significantly higher in the CHD group than in the non-CHD group [554.62 (265.11) ng/mL vs. 496.86 (129.05) ng/mL, p < 0.001]. Circulating PCSK9 levels positively correlated with CHD severity (diseased vessels: r = 0.35, p < 0.001; Gensini score: r = 0.46, p < 0.001). Elevated PCSK9 levels are an independent risk factor for CHD risk and severity (CHD group vs. non–CHD group: OR = 2.829, 95% CI: 1.771–4.520, p < 0.001; three vessel disease group vs. one vessel disease group: OR = 4.800, 95% CI: 2.387–9.652, p < 0.001; high GS group vs. low GS group: OR = 5.534, 95% CI: 2.733–11.208, p < 0.001). Through a six-year follow-up and multivariate Cox regression analysis, elevated circulating PCSK9 levels were found to be independently associated with MACEs in all participants (HR: 3.416, 5% CI: 2.485–4.697, p < 0.001; adjusted HR: 2.780, 95% CI: 1.930–4.004, p < 0.001).

Conclusions
Serum PCSK9 levels were positively correlated with multi-vessel CHD and Gensini score. Elevated circulating PCSK9 levels are an independent risk factor for CHD and increased incidence of MACEs in T2DM.
A comprehensive characterisation of phaeochromocytoma and paraganglioma tumours through histone protein profiling, DNA methylation and transcriptomic analysis genome wide
Authors: Chatzikyriakou Prodromos , Brempou Dimitria , Quinn Mark , Fishbein Lauren , Noberini Roberta , Anastopoulos Ioannis N. , Tufton Nicola , Lim Eugenie S. , Obholzer Rupert , Hubbard Johnathan G. , Moonim Mufaddal , Bonaldi Tiziana , Nathanson Katherine L. , Izatt Louise , Oakey Rebecca J. 
Published: December 2023

Abstract
Background
Phaeochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumours. Pathogenic variants have been identified in more than 15 susceptibility genes; associated tumours are grouped into three Clusters, reinforced by their transcriptional profiles. Cluster 1A PPGLs have pathogenic variants affecting enzymes of the tricarboxylic acid cycle, including succinate dehydrogenase. Within inherited PPGLs, these are the most common. PPGL tumours are known to undergo epigenetic reprograming, and here, we report on global histone post-translational modifications and DNA methylation levels, alongside clinical phenotypes.

Results
Out of the 25 histone post-translational modifications examined, Cluster 1A PPGLs were distinguished from other tumours by a decrease in hyper-acetylated peptides and an increase in H3K4me2. DNA methylation was compared between tumours from individuals who developed metastatic disease versus those that did not. The majority of differentially methylated sites identified tended to be completely methylated or unmethylated in non-metastatic tumours, with low inter-sample variance. Metastatic tumours by contrast consistently had an intermediate DNA methylation state, including the ephrin receptor EPHA4 and its ligand EFNA3. Gene expression analyses performed to identify genes involved in metastatic tumour behaviour pin-pointed a number of genes previously described as mis-regulated in Cluster 1A tumours, as well as highlighting the tumour suppressor RGS22 and the pituitary tumour-transforming gene PTTG1.

Conclusions
Combined transcriptomic and DNA methylation analyses revealed aberrant pathways, including ones that could be implicated in metastatic phenotypes and, for the first time, we report a decrease in hyper-acetylated histone marks in Cluster 1 PPGLs.
Statins and cognitive decline in patients with Alzheimer’s and mixed dementia: a longitudinal registry-based cohort study
Authors: Petek Bojana , Häbel Henrike , Xu Hong , Villa-Lopez Marta , Kalar Irena , Hoang Minh Tuan , Maioli Silvia , Pereira Joana B. , Mostafaei Shayan , Winblad Bengt , Gregoric Kramberger Milica , Eriksdotter Maria , Garcia-Ptacek Sara 
Published: December 2023

Abstract
Background
Disturbances in brain cholesterol homeostasis may be involved in the pathogenesis of Alzheimer’s disease (AD). Lipid-lowering medications could interfere with neurodegenerative processes in AD through cholesterol metabolism or other mechanisms.

Objective
To explore the association between the use of lipid-lowering medications and cognitive decline over time in a cohort of patients with AD or mixed dementia with indication for lipid-lowering treatment.

Methods
A longitudinal cohort study using the Swedish Registry for Cognitive/Dementia Disorders, linked with other Swedish national registries. Cognitive trajectories evaluated with mini-mental state examination (MMSE) were compared between statin users and non-users, individual statin users, groups of statins and non-statin lipid-lowering medications using mixed-effect regression models with inverse probability of drop out weighting. A dose-response analysis included statin users compared to non-users.

Results
Our cohort consisted of 15,586 patients with mean age of 79.5 years at diagnosis and a majority of women (59.2 %). A dose-response effect was demonstrated: taking one defined daily dose of statins on average was associated with 0.63 more MMSE points after 3 years compared to no use of statins (95% CI: 0.33;0.94). Simvastatin users showed 1.01 more MMSE points (95% CI: 0.06;1.97) after 3 years compared to atorvastatin users. Younger (< 79.5 years at index date) simvastatin users had 0.80 more MMSE points compared to younger atorvastatin users (95% CI: 0.05;1.55) after 3 years. Simvastatin users had 1.03 more MMSE points (95% CI: 0.26;1.80) compared to rosuvastatin users after 3 years. No differences regarding statin lipophilicity were observed. The results of sensitivity analysis restricted to incident users were not consistent.

Conclusions
Some patients with AD or mixed dementia with indication for lipid-lowering medication may benefit cognitively from statin treatment; however, further research is needed to clarify the findings of sensitivity analyses.
Development of a thick and functional human adipose-derived stem cell tissue sheet for myocardial infarction repair in rat hearts
Authors: Zhang Jingbo , Li Junjun , Qu Xiang , Liu Yuting , Harada Akima , Hua Ying , Yoshida Noriko , Ishida Masako , Tabata Akiko , Sun Lifu , Liu Li , Miyagawa Shigeru 
Published: December 2023

Abstract
Background
Heart failure (HF) is a major cause of death worldwide. The most effective treatment for HF is heart transplantation, but its use is limited by the scarcity of donor hearts. Recently, stem cell-based therapy has emerged as a promising approach for treating myocardial infarction. Our research group has been investigating the use of human induced pluripotent stem cell-derived cardiomyocyte patches as a potential therapeutic candidate. We have successfully conducted eight cases of clinical trials and demonstrated the safety and effectiveness of this approach. However, further advancements are necessary to overcome immune rejection and enhance therapeutic efficacy. In this study, we propose a novel and efficient technique for constructing mesenchymal stem cell (MSC) tissue sheets, which can be transplanted effectively for treating myocardial infarction repair.

Methods
We applied a one-step method to construct the human adipose-derived mesenchymal stem cell (hADSC) tissue sheet on a poly(lactic-co-glycolic acid) fiber scaffold. Histology, immunofluorescence, and paracrine profile assessment were used to determine the organization and function of the hADSC tissue sheet. Echocardiography and pathological analyses of heart sections were performed to evaluate cardiac function, fibrosis area, angiogenesis, and left ventricular remodeling.

Results
In vitro, the hADSC tissue sheet showed great organization, abundant ECM expression, and increased paracrine secretion than single cells. In vivo, the hADSC tissue sheet group demonstrated improved cardiac functional recovery, less ventricular remodeling, decreased fibrosis, and enhanced angiogenesis than the MI group.

Conclusions
We developed thick and functional hADSC tissue sheets via the one-step strategy. The hADSC tissue sheet showed excellent performance in treating myocardial infarction in the rat model.

Graphical Abstract