bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is Blockchain a Panacea for Guarding PDO Supply Chains? Exploring Vulnerabilities, Critical Control Points, and Blockchain feasibility in Greece
Authors: Vasileiou Marios , Kyrgiakos Leonidas Sotirios , Kleisiari Christina , Prosperi Paolo , Kleftodimos Georgios , Ragkos Athanasios , Tsinopoulos Christos , Abou Nader Elie , Moulogianni Christina , Vlontzos George 
Published: June 2024

AbstractWithin food Supply Chains (SCs), food products labeled through Geographical Indications (GIs) hold paramount importance as distinctive and culturally significant entities, ensuring the integrity and distinctiveness of regional specialties. By strictly regulating the geographic origin and production methods, the Protected Designation of Origin (PDO) not only guarantees the preservation of traditional practices but also safeguards the cultural legacy and identity of the regions where genuine PDO products are produced. However, the very mechanisms safeguarding PDO authenticity can be exploited within globalized food systems, creating opportunities for fraudulent activities and intentional or unintentional adulteration. This study specifically delves into the overarching realm of PDO SCs, using PDO Feta cheese as a prominent case study. Through an assessment of Feta cheese SC in Greece, encompassing the Delphi Technique with the amalgamation of the design stages of Hazard Analysis and Critical Control Points (HACCP), Vulnerabilities Assessment and Critical Control Point (VACCP), and Threat Assessment and Critical Control Point (TACCP) methodologies, the operations, vulnerabilities, and critical control points are scrutinized. The results indicate multifaceted vulnerabilities and Critical Control Points (CCPs) in the Feta cheese SC that need to be addressed and constitute a precursor for augmenting PDO SCs. Moreover, the utilization of Blockchain Technology (BT) exhibits intrinsic potential for enhancing the administration of supply chains with the potential to fundamentally transform data management practices and foster increased levels of trust among stakeholders.
Minor Spliceosomal 65K/RNPC3 Interacts with ANKRD11 and Mediates HDAC3‐Regulated Histone Deacetylation and Transcription
Authors: Li Chen‐Hui , Liang Shao‐Bo , Huang Qi‐Wei , Zhou Zhen‐Zhen , Ding Zhan , Long Ni , Wi Kwang‐Chon , Li Liang , Jiang Xi‐Ping , Fan Yu‐Jie , Xu Yong‐Zhen 
Published: June 2024

AbstractRNA splicing is crucial in the multilayer regulatory networks for gene expression, making functional interactions with DNA‐ and other RNA‐processing machineries in the nucleus. However, these established couplings are all major spliceosome‐related; whether the minor spliceosome is involved remains unclear. Here, through affinity purification using Drosophila lysates, an interaction is identified between the minor spliceosomal 65K/RNPC3 and ANKRD11, a cofactor of histone deacetylase 3 (HDAC3). Using a CRISPR/Cas9 system, Deletion strains are constructed and found that both Dm65KΔ/Δ and Dmankrd11Δ/Δ mutants have reduced histone deacetylation at Lys9 of histone H3 (H3K9) and Lys5 of histone H4 (H4K5) in their heads, exhibiting various neural‐related defects. The 65K‐ANKRD11 interaction is also conserved in human cells, and the HsANKRD11 middle‐uncharacterized domain mediates Hs65K association with HDAC3. Cleavage under targets and tagmentation (CUT&Tag) assays revealed that HsANKRD11 is a bridging factor, which facilitates the synergistic common chromatin‐binding of HDAC3 and Hs65K. Knockdown (KD) of HsANKRD11 simultaneously decreased their common binding, resulting in reduced deacetylation of nearby H3K9. Ultimately, this study demonstrates that expression changes of many genes caused by HsANKRD11‐KD are due to the decreased common chromatin‐binding of HDAC3 and Hs65K and subsequently reduced deacetylation of H3K9, illustrating a novel and conserved coupling mechanism that links the histone deacetylation with minor spliceosome for the regulation of gene expression.
Single‐Cell Spatial Transcriptomics Unveils Platelet‐Fueled Cycling Macrophages for Kidney Fibrosis
Authors: Liu Jun , Zheng Bo , Cui Qingya , Zhu Yu , Chu Likai , Geng Zhi , Mao Yiming , Wan Lin , Cao Xu , Xiong Qianwei , Guo Fujia , Yang David C , Hsu Ssu‐Wei , Chen Ching‐Hsien , Yan Xiangming 
Published: June 2024

AbstractWith the increasing incidence of kidney diseases, there is an urgent need to develop therapeutic strategies to combat post‐injury fibrosis. Immune cells, including platelets, play a pivotal role in this repair process, primarily through their released cytokines. However, the specific role of platelets in kidney injury and subsequent repair remains underexplored. Here, the detrimental role of platelets in renal recovery following ischemia/reperfusion injury and its contribution to acute kidney injury to chronic kidney disease transition is aimed to investigated. In this study, it is shown that depleting platelets accelerates injury resolution and significantly reduces fibrosis. Employing advanced single‐cell and spatial transcriptomic techniques, macrophages as the primary mediators modulated by platelet signals is identified. A novel subset of macrophages, termed “cycling M2”, which exhibit an M2 phenotype combined with enhanced proliferative activity is uncovered. This subset emerges in the injured kidney during the resolution phase and is modulated by platelet‐derived thrombospondin 1 (THBS1) signaling, acquiring profibrotic characteristics. Conversely, targeted inhibition of THBS1 markedly downregulates the cycling M2 macrophage, thereby mitigating fibrotic progression. Overall, this findings highlight the adverse role of platelet THBS1‐boosted cycling M2 macrophages in renal injury repair and suggest platelet THBS1 as a promising therapeutic target for alleviating inflammation and kidney fibrosis.
Red Blood Cell Membrane‐Coated Nanoparticles Enable Incompatible Blood Transfusions
Authors: Yang Xuewei , Chen Mengchun , Weng Cuiye , Zhuge Deli , Jin Fangsi , Xiao Yingnan , Tian Dongyan , Yin Qingqing , Li Li , Zhang Xufei , Shi Genghe , Lu Xiaosheng , Yan Linzhi , Wang Ledan , Wen Bin , Zhao Yingzheng , Lin Jiajin , Wang Fang , Zhang Weixi , Chen Yijie 
Published: June 2024

AbstractBlood transfusions save lives and improve health every day. Despite the matching of blood types being stricter than it ever has been, emergency transfusions among incompatible blood types are still inevitable in the clinic when there is a lack of acceptable blood types for recipients. Here to overcome this, a counter measure nanoplatform consisting of a polymeric core coated by a red blood cell (RBC) membrane is developed. With A‐type or B‐type RBC membrane camouflaging, the nanoplatform is capable of specifically capturing anti‐A or anti‐B IgM antibodies within B‐type or A‐type whole blood, thereby decreasing the corresponding IgM antibody levels and then allowing the incompatible blood transfusions. In addition to IgM, the anti‐RBC IgG antibody in a passive immunization murine model can likewise be neutralized by this nanoplatform, leading to prolonged circulation time of incompatible donor RBCs. Noteworthily, nanoplatform made by expired RBCs (>42 days stored hypothermically) and then subjected to lyophilization does not impair their effect on antibody neutralization. Most importantly, antibody‐captured RBC‐NP do not exacerbate the risk of inflammation, complement activation, and coagulopathy in an acute hemorrhagic shock murine model. Overall, this biomimetic nanoplatform can safely neutralize the antibody to enable incompatible blood transfusion.
CD9 Counteracts Liver Steatosis and Mediates GCGR Agonist Hepatic Effects
Authors: Zheng Yi , Wang Yuren , Xiong Xin , Zhang Linlin , Zhu Jiaran , Huang Bangliang , Liu Xiufei , Liu Jinbo , Zhu Zhiming , Yang Gangyi , Qu Hua , Zheng Hongting 
Published: June 2024

AbstractGlucagon receptor (GCGR) agonism offers potentially greater effects on the mitigation of hepatic steatosis. However, its underlying mechanism is not fully understood. Here, it screened tetraspanin CD9 might medicate hepatic effects of GCGR agonist. CD9 is decreased in the fatty livers of patients and upregulated upon GCGR activation. Deficiency of CD9 in the liver exacerbated diet‐induced hepatic steatosis via complement factor D (CFD) regulated fatty acid metabolism. Specifically, CD9 modulated hepatic fatty acid synthesis and oxidation genes through regulating CFD expression via the ubiquitination‐proteasomal degradation of FLI1. In addition, CD9 influenced body weight by modulating lipogenesis and thermogenesis of adipose tissue through CFD. Moreover, CD9 reinforcement in the liver alleviated hepatic steatosis, and blockage of CD9 abolished the remission of hepatic steatosis induced by cotadutide treatment. Thus, CD9 medicates the hepatic beneficial effects of GCGR signaling, and may server as a promising therapeutic target for hepatic steatosis.
SIRT5‐Mediated Desuccinylation of RAB7A Protects Against Cadmium‐Induced Alzheimer's Disease‐Like Pathology by Restoring Autophagic Flux
Authors: Deng Ping , Fan Tengfei , Gao Peng , Peng Yongchun , Li Min , Li Jingdian , Qin Mingke , Hao Rongrong , Wang Liting , Li Min , Zhang Lei , Chen Chunhai , He Mindi , Lu Yonghui , Ma Qinlong , Luo Yan , Tian Li , Xie Jia , Chen Mengyan , Xu Shangcheng , Zhou Zhou , Yu Zhengping , Pi Huifeng 
Published: June 2024

AbstractCadmium (Cd) is a neurotoxic contaminant that induces cognitive decline similar to that observed in Alzheimer's disease (AD). Autophagic flux dysfunction is attributed to the pathogenesis of AD, and this study aimed to investigate the effect of autophagy on environmental Cd‐induced AD progression and the underlying mechanism. Here, Cd exposure inhibited autophagosome‐lysosome fusion and impaired lysosomal function, leading to defects in autophagic clearance and then to APP accumulation and nerve cell death. Proteomic analysis coupled with Ingenuity Pathway Analysis (IPA) identified SIRT5 as an essential molecular target in Cd‐impaired autophagic flux. Mechanistically, Cd exposure hampered the expression of SIRT5, thus increasing the succinylation of RAB7A at lysine 31 and inhibiting RAB7A activity, which contributed to autophagic flux blockade. Importantly, SIRT5 overexpression led to the restoration of autophagic flux blockade, the alleviation of Aβ deposition and memory deficits, and the desuccinylation of RAB7A in Cd‐exposed FAD4T mice. Additionally, SIRT5 levels decrease mainly in neurons but not in other cell clusters in the brains of AD patients according to single‐nucleus RNA sequencing data from the public dataset GSE188545. This study reveals that SIRT5‐catalysed RAB7A desuccinylation is an essential adaptive mechanism for the amelioration of Cd‐induced autophagic flux blockade and AD‐like pathogenesis.
Vacancy Mediated Electrooxidation of 5‐Hydroxymethyl Furfuryl Using Defect Engineered Layered Double Hydroxide Electrocatalysts
Authors: Zubair Muhammad , Usov Pavel M. , Ohtsu Hiroyoshi , Yuwono Jodie A. , Gerke Carter S. , Foley Gregory D. Y. , Hackbarth Haira , Webster Richard F. , Yang Yuwei , Lie William Hadinata , Ma Zhipeng , Thomsen Lars , Kawano Masaki , Bedford Nicholas M. 
Published: June 2024

AbstractElectrochemical biomass oxidation coupled with hydrogen evolution offers a promising route to generate value‐added chemicals and clean energy. The complex adsorption behavior of 5‐hydroxymethyl furfural (HMF) and hydroxyl ions (OH−) on the electrocatalyst surface during HMF electrooxidation reaction (HMFOR) necessitates an in‐depth understanding of active sites available for adsorption. Herein, oxygen vacancy (VO) defects are introduced in NiFe layered double hydroxide (LDH) using Ce dopants to manipulate electronic structure. Synchrotron‐based HE‐XRD and XAS indicate negligible VO in La‐doped NiFe while Ce doping leads to VO defects due to flexible Ce redox (Ce3+↔ Ce4+). The VO‐rich Ce‐NiFe exhibits higher Faradic efficiency of ≈90% to produce 2,5‐furan dicarboxylic acid (FDCA), far greater than ≈60% for NiFe VO in Ce‐NiFe act as alternative active sites for OH− adsorption, hence reducing adsorption competition for the same metal sites. DFT calculation results corroborate experimental findings by showcasing that the presence of VO in Ce‐NiFe manipulates the adsorption energies and facilitates the chemical adsorption OH− in VO to improve HMFOR. In situ HE‐XRD derived pair distribution function coupled to RMC simulations confirm OH− trapping in VO and HMF adsorption on metal centers as evident by interlayer distance evolution. Taken together, this work showcases routes for dual‐site electrocatalyst design for improved biomass electrooxidation.
Why Perovskite Thermal Stress is Unaffected by Thin Contact Layers
Authors: McAndrews Gabriel R. , Ahmad Muneeza , Guo Boyu , Kaczaral Samantha C. , Amassian Aram , Rolston Nicholas , McGehee Michael D. 
Published: June 2024

AbstractMetal halide perovskite photovoltaics have emerged as a high efficiency, low‐cost alternative that can potentially rival or enhance conventional silicon technology. Despite exceptional initial power conversion efficiencies, achieving compliance with international standards and widespread adoption requires further enhancements to their operational stability. Notably, addressing mechanical strain and stress in brittle perovskites has emerged as a pivotal approach to mitigate chemical degradation and improve reliability during thermal cycling. In this study, a popularized strain engineering strategy is investigated in which a high coefficient of thermal expansion (CTE) hole transport layer (i.e., PDCBT) is cast onto inorganic perovskite (CsPbI2Br) at 100 °C. Contrary to previously published results, the X‐ray diffraction (XRD):Sin2ψ and substrate curvature measurement techniques show that the hole transport layer has no discernible impact on perovskite strain. The accuracy of the XRD:Sin2ψ method for measuring strain is highlighted in contrast to an analysis based on shifts of single XRD peaks which can be influenced by multiple artifacts. The findings in this study are in accordance with mechanics theory: thin layers are unable to induce significant strain changes in perovskite thin films as the force they apply is negligible compared to that applied by a thick and stiff substrate.
Multifunctional Nanodiamond Interfacial Layer for Ultra‐Stable Zinc‐Metal Anodes
Authors: Liu Kai , Sun Mingzi , Yang Shuo , Gan Guoqiang , Bu Shuyu , Zhu Anquan , Lin Dewu , Zhang Tian , Luan Chuhao , Zhi Chunyi , Wang Pengfei , Huang Bolong , Hong Guo , Zhang Wenjun 
Published: June 2024

AbstractAchieving reversible plating/stripping of zinc (Zn) anodes is crucial in aqueous Zn‐ion batteries (AZIBs). However, undesired dendrite growth and parasitic side reactions severely deteriorate battery lifespan. The construction of stable protective coating is an effective strategy to enhance anode stability. In this study, a multifunctional nanodiamond (ND) inorganic layer is designed and constructed on both Zn and Cu electrodes that can both effectively inhibit dendrite growth and suppress Zn anode corrosion. Experimental results and theoretical calculations demonstrate that this artificial protective layer, with ultra‐high surface energy, enables the controlled creation of abundant nucleation sites (in the order of 1012 cm−2) for the homogenization of ion flux and electric field on the anode. It is found that zinc ions preferentially adhere to the diamond surfaces with lower diffusion barriers, leading to uniform zinc deposition. A symmetric cell with the ND‐protected Zn (Zn‐ND) anode exhibits reversible plating/stripping behavior for an impressive duration of over 3600 h at 1 mA cm−2. Furthermore, the MnO2||Zn full battery retains 90% of its initial capacity after 3500 cycles at 2 A g−1, and assembled hybrid capacitor operates smoothly over 65 000 cycles at 10 A g−1. These results underscore the potential of this coating as a promising solution for achieving highly stable Zn anodes for aqueous batteries.
Abdominal aortic calcification among gastroenterological and transplant surgery
Authors: Imaoka Yuki , Ohira Masahiro , Akabane Miho , Sasaki Kazunari , Ohdan Hideki 
Published: June 2024

AbstractThis review discusses the increasing global trend towards an aging population, which has resulted in a growing number of surgeries being performed on elderly patients, particularly those living with cancer. The focus was on the implications of abdominal aortic calcification (AAC), an indicator of systemic atherosclerosis, in these patients. This comprehensive review provided evidence detailing the complex processes of atherosclerosis and vascular calcification and various approaches to assess this condition. The prevalence of AAC is related to multiple factors, including cardiovascular disease, inflammation, frailty in various types of gastroenterological surgery. Additionally, notable links were found between AAC, postoperative complications, and patient survival following gastroenterological surgery. This study highlights how AAC could negatively impact the health status of elderly patients and undermine treatment efficacy, stressing the need for more research in this domain to improve patient outcomes.
fNIRS as a biomarker for individuals with subjective memory complaints and MCI
Authors: Lee Tsz‐lok , Guo Lizhi , Chan Agnes S. 
Published: June 2024

AbstractINTRODUCTIONIdentifying individuals at risk of developing dementia is crucial for early intervention. Mild cognitive impairment (MCI) and subjective memory complaints (SMCs) are considered its preceding stages. This study aimed to assess the utility of functional near‐infrared spectroscopy (fNIRS) in identifying individuals with MCI and SMC.METHODSOne hundred fifty‐one participants were categorized into normal cognition (NC); amnestic MCI (aMCI); non‐amnestic MCI (naMCI); and mild, moderate, and severe SMC groups. Task‐related prefrontal hemodynamics were measured using fNIRS during a visual memory span task.RESULTSResults showed significantly lower oxyhemoglobin (HbO) levels in aMCI, but not in naMCI, compared to the NC. In addition, severe SMC had lower HbO levels than the NC, mild, and moderate SMC. Receiver operating characteristic analysis demonstrated 69.23% and 69.70% accuracy in differentiating aMCI and severe SMC from NC, respectively.DISCUSSIONFNIRS may serve as a potential non‐invasive biomarker for early detection of dementia.Highlights
Only amnestic mild cognitive impairment (aMCI), but not non‐amnestic MCI, showed lower oxyhemoglobin (HbO) than normal individuals.
Reduced HbO was observed in those with severe subjective memory complaints (SMCs) compared to normal cognition (NC), mild, and moderate SMCs.
Functional near‐infrared spectroscopy measures were associated with performance in memory assessments.
Prefrontal hemodynamics could distinguish aMCI and severe SMC from NC.
Social determinants of health but not global genetic ancestry predict dementia prevalence in Latin America
Authors: Llibre‐Guerra Jorge J. , Jiang Miao , Acosta Isaac , Sosa Ana Luisa , Acosta Daisy , Jimenez‐Velasquez Ivonne Z. , Guerra Mariella , Salas Aquiles , Rodriguez Salgado Ana M. , Llibre‐Guerra Juan C. , Sánchez Nedelys Díaz , Prina Matthew , Renton Alan , Albanese Emiliano , Yokoyama Jennifer S. , Llibre Rodriguez Juan J. 
Published: June 2024

AbstractINTRODUCTIONLeveraging the nonmonolithic structure of Latin America, which represents a large variability in social determinants of health (SDoH) and high levels of genetic admixture, we aim to evaluate the relative contributions of SDoH and genetic ancestry in predicting dementia prevalence in Latin American populations.METHODSCommunity‐dwelling participants aged 65 and older (N = 3808) from Cuba, Dominican Republic, Mexico, and Peru completed the 10/66 protocol assessments. Dementia was diagnosed using the cross‐culturally validated 10/66 algorithm. Multivariate linear regression models adjusted for SDoH were used in the main analysis. This study used cross‐sectional data from the 1066 population‐based study.RESULTSIndividuals with higher proportions of Native American (>70%) and African American (>70%) ancestry were more likely to exhibit factors contributing to worse SDoH, such as lower educational levels (p < 0.001), lower socioeconomic status (p < 0.001), and higher frequency of vascular risk factors (p < 0.001). After adjusting for measures of SDoH, there was no association between ancestry proportion and dementia probability, and ancestry proportions no longer significantly accounted for the variance in cognitive performance (African predominant p = 0.31 [‐0.19, 0.59] and Native predominant p = 0.74 [‐0.24, 0.33]).DISCUSSIONThe findings suggest that social and environmental factors play a more crucial role than genetic ancestry in predicting dementia prevalence in Latin American populations. This underscores the need for public health strategies and policies that address these social determinants to effectively reduce dementia risk in these communities.Highlights
Countries in Latin America express a large variability in social determinants of health and levels of admixture.
After adjustment for downstream societal factors linked to SDoH, genetic ancestry shows no link to dementia.
Population ancestry profiles alone do not influence cognitive performance.
SDoH are key drivers of racial disparities in dementia and cognitive performance.
Progress in experimental models to investigate the in vivo and in vitro antidiabetic activity of drugs
Authors: Janapati Yasodha Krishna , Junapudi Sunil 
Published: June 2024

AbstractDiabetes mellitus is one of the world's most prevalent and complex metabolic disorders, and it is a rapidly growing global public health issue. It is characterized by hyperglycemia, a condition involving a high blood glucose level brought on by deficiencies in insulin secretion, decreased activity of insulin, or both. Prolonged effects of diabetes include cardiovascular problems, retinopathy, neuropathy, nephropathy, and vascular alterations in both macro‐ and micro‐blood vessels. In vivo and in vitro models have always been important for investigating and characterizing disease pathogenesis, identifying targets, and reviewing novel treatment options and medications. Fully understanding these models is crucial for the researchers so this review summarizes the different experimental in vivo and in vitro model options used to study diabetes and its consequences. The most popular in vivo studies involves the small animal models, such as rodent models, chemically induced diabetogens like streptozotocin and alloxan, and the possibility of deleting or overexpressing a specific gene by knockout and transgenic technologies on these animals. Other models include virally induced models, diet/nutrition induced diabetic animals, surgically induced models or pancreatectomy models, and non‐obese models. Large animals or non‐rodent models like porcine (pig), canine (dog), nonhuman primate, and Zebrafish models are also outlined. The in vitro models discussed are murine and human beta‐cell lines and pancreatic islets, human stem cells, and organoid cultures. The other enzymatic in vitro tests to assess diabetes include assay of amylase inhibition and inhibition of α‐glucosidase activity.