bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevention of malnutrition after one anastomosis gastric bypass: value of the common channel limb length
Authors: Mostafapour Elyas , Shahsavan Masoumeh , Shahmiri Shahab Shahabi , Jawhar Noura , Ghanem Omar M. , Kermansaravi Mohammad 
Published: May 2024

Abstract
Purpose
Hypoalbuminemia and anemia are commonly observed indications for one anastomosis gastric bypass (OAGB) reversal and remain significant concerns following the procedure. Sufficient common channel limb length (CCLL) is crucial to minimize nutritional complications. However, limited literature exists regarding the impact of CCLL on OAGB outcomes. This study aimed to assess the effect of CCLL on weight loss and nutritional status in patients who underwent OAGB.

Methods
A prospective cohort study was conducted from August 2021 to July 2022, involving 64 patients with a body mass index of 40–50 kg/m2. The standardized length of the biliopancreatic limb (BPLL) for all patients in this study was set at 175 cm. Additionally, the measurement of the common channel limb length (CCLL) was performed consistently by the same surgeon for all included patients.

Results
The mean age and BMI of the patients were 39.91 ± 10.03 years and 43.13 ± 2.43 kg/m2, respectively, at the time of surgery. There was a statistically significant negative correlation between CCLL and percent total weight loss (%TWL) at the 12-month mark after OAGB (P = 0.02). Hypoalbuminemia was observed in one patient (1.6%), while anemia was present in 17 patients (26.6%) at the one-year follow-up. Statistical analysis revealed no significant difference in the incidence of anemia and hypoalbuminemia between patients with CCLL < 4 m and those with CCLL ≥ 4 m.

Conclusion
A CCLL of 4 m does not appear to completely prevent nutritional complications following OAGB. However, maintaining a CCLL of at least 4 m may be associated with a reduced risk of postoperative nutritional deficiencies.
Generalist, specialist, or expert in palliative care? A cross-sectional open survey on healthcare professionals’ self-description
Authors: van Zuilekom Ingrid , Metselaar Suzanne , Godrie Fleur , Onwuteaka-Philipsen Bregje , van Os-Medendorp Harmieke 
Published: May 2024

Abstract
Background
In the Netherlands, palliative care is provided by generalist healthcare professionals (HCPs) if possible and by palliative care specialists if necessary. However, it still needs to be clarified what specialist expertise entails, what specialized care consists of, and which training or work experience is needed to become a palliative care specialist. In addition to generalists and specialists, ‘experts’ in palliative care are recognized within the nursing and medical professions, but it is unclear how these three roles relate. This study aims to explore how HCPs working in palliative care describe themselves in terms of generalist, specialist, and expert and how this self-description is related to their work experience and education.

Methods
A cross-sectional open online survey with both pre-structured and open-ended questions among HCPs who provide palliative care. Analyses were done using descriptive statistics and by deductive thematic coding of open-ended questions.

Results
Eight hundred fifty-four HCPs filled out the survey; 74% received additional training, and 79% had more than five years of working experience in palliative care. Based on working experience, 17% describe themselves as a generalist, 34% as a specialist, and 44% as an expert. Almost three out of four HCPs attributed their level of expertise on both their education and their working experience. Self-described specialists/experts had more working experience in palliative care, often had additional training, attended to more patients with palliative care needs, and were more often physicians as compared to generalists. A deductive analysis of the open questions revealed the similarities and distinctions between the roles of a specialist and an expert. Seventy-six percent of the respondents mentioned the importance of having both specialists and experts and wished more clarity about what defines a specialist or an expert, how to become one, and when you need them. In practice, both roles were used interchangeably. Competencies for the specialist/expert role consist of consulting, leadership, and understanding the importance of collaboration.

Conclusions
Although the grounds on which HCPs describe themselves as generalist, specialist, or experts differ, HCPs who describe themselves as specialists or experts mostly do so based on both their post-graduate education and their work experience. HCPs find it important to have specialists and experts in palliative care in addition to generalists and indicate more clarity about (the requirements for) these three roles is needed.
Luteolin attenuates CCl4-induced hepatic injury by inhibiting ferroptosis via SLC7A11
Authors: Han Zhiqiang , Batudeligen  , Chen Hongmei , Narisu  , Anda  , Xu Yanhua , Xue Lan 
Published: May 2024

Abstract
Background
Luteolin (3,4,5,7-tetrahydroxy flavone) is reported to strongly protect from acute carbon tetrachloride (CCl4) -induced liver injury or fibrosis. Ferroptosis can be induced by hepatic injury, and contributes to liver fibrosis development. The exact functional mechanism underlying luteolin inhibition of hepatic injury and whether ferroptosis is involved are unclear.

Methods
Mice model and cell model of liver injury were constructed or induced to explore the effect and molecular mechanisms of Luteolin in the treatment of hepatic injury using CCl4. Cell Counting Kit-8 (CCK-8) and flow cytometry were used to evaluate HepG2 cell viability and apoptosis. The differential expressed genes involved in liver injury were scanned using RNA-seq and confirmed using functional study. Western blot was used to detect the indicators related to ferroptosis.

Results
Luteolin attenuated hepatic injury by alleviating cell morphology and decreasing serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) levels in vivo mice models, and increasing cell viability, downregulating arachidonate 12-lipoxygenase (ALOX12), cyclooxygenase-2 (COX-2) and P21 protein expression, suppressing apoptosis in vitro cell models. Luteolin also inhibited ferroptosis by stimulating glutathione peroxidase 4 (GPX4) and mitochondrial ferritin (FTMT) protein expression, increasing glutathione (GSH) content, and minimizing Fe2+ and malondialdehyde (MDA) levels. Solute carrier family 7a member 11 (SLC7A11) was identified to be a key regulatory gene that participated in luteolin attenuation of CCl4-induced hepatic injuries in HepG2 cells using Microarray assay. Functional study showed that SLC7A11 can alleviate hepatic injury and ferroptosis.

Conclusion
Luteolin attenuated CCl4-induced hepatic injury by inhibiting ferroptosis via SLC7A11. SLC7A11 may serve as a novel alternative therapeutic target for hepatic injury.
Comparison of barriers to effective nurse-patient communication in COVID-19 and non-COVID-19 wards
Authors: Bakhshi Hamed , Shariati Mohammad Javad , Basirinezhad Mohammad Hasan , Ebrahimi Hossein 
Published: May 2024

Abstract
Background
Communication is a basic need of humans. Identifying factors that prevent effective nurse-patient communication allows for the better implementation of necessary measures to modify barriers. This study aims to compare the barriers to effective nurse-patient communication from the perspectives of nurses and patients in COVID-19 and non-COVID-19 wards.

Materials and methods
This cross-sectional descriptive study was conducted in 2022. The participants included 200 nurses (by stratified sampling method) and 200 patients (by systematic random sampling) referred to two conveniently selected hospitals in Shahroud, Iran. The inclusion criteria for nurses were considered having at least a bachelor’s degree and a minimum literacy level for patients to complete the questionnaires. Data were collected by the demographic information form and questionnaire with 30 and 15 questions for nurses and patients, which contained similar questions to those for nurses, based on a 5-point Likert scale. Data were analysis using descriptive indices and inferential statistics (Linear regression) in SPSS software version 18.

Results
The high workload of nursing, excessive expectations of patients, and the difficulty of nursing work were identified by nurses as the main communication barriers. From the patients’ viewpoints, the aggressiveness of nurses, the lack of facilities (welfare treatment), and the unsanitary conditions of their rooms were the main communication barriers. The regression model revealed that the mean score of barriers to communication among nurses would decrease to 0.48 for each unit of age increase. Additionally, the patient’s residence explained 2.3% of the nurses’ barriers to communication, meaning that native participants obtained a mean score of 2.83 units less than non-native nurses, and there was no statistically significant difference between the COVID and non-COVID wards.

Conclusion
In this study, the domain of job characteristics was identified by nurses as the major barrier, and patients emphasized factors that were in the domain of individual/social factors. There is a pressing need to pay attention to these barriers to eliminate them through necessary measures by nursing administrators.
GPS2 ameliorates cigarette smoking-induced pulmonary vascular remodeling by modulating the ras-Raf-ERK axis
Authors: Hu Ting , Mu Chaohui , Li Yanmiao , Hao Wanming , Yu Xinjuan , Wang Yixuan , Han Wei , Li Qinghai 
Published: May 2024

Abstract
Background
Mitogen-activated protein kinase (MAPK)signaling-mediated smoking-associated pulmonary vascular remodeling (PVR) plays an important role in the pathogenesis of group 3 pulmonary hypertension (PH). And G protein pathway suppressor 2 (GPS2) could suppress G-protein signaling such as Ras and MAPK, but its role in cigarette smoking -induced PVR (CS-PVR) is unclear.

Methods
An in vivo model of smoke-exposed rats was constructed to assess the role of GPS2 in smoking-induced PH and PVR. In vitro, the effects of GPS2 overexpression and silencing on the function of human pulmonary arterial smooth cells (HPASMCs) and the underlying mechanisms were explored.

Results
GPS2 expression was downregulated in rat pulmonary arteries (PAs) and HPASMCs after CS exposure. More importantly, CS-exposed rats with GPS2 overexpression had lower right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), and wall thickness (WT%) than those without. And enhanced proliferation and migration of HPASMCs induced by cigarette smoking extract (CSE) can be evidently inhibited by overexpressed GPS2. Besides, GPS2siRNA significantly enhanced the proliferation, and migration of HPASMCs as well as activated Ras and Raf/ERK signaling, while these effects were inhibited by zoledronic acid (ZOL). In addition, GPS2 promoter methylation level in rat PAs and HPASMCs was increased after CS exposure, and 5-aza-2-deoxycytidine (5-aza) inhibited CSE-induced GPS2 hypermethylation and downregulation in vitro.

Conclusions
GPS2 overexpression could improve the CS-PVR, suggesting that GPS2 might serve as a novel therapeutic target for PH-COPD in the future.

Graphical Abstract
Evidence of Plasmodium vivax circulation in western and eastern regions of Senegal: implications for malaria control
Authors: Badiane Aida S. , Ngom Bassirou , Ndiaye Tolla , Cunningham Deirdre , Campbell James , Gaye Amy , Sène Aita , Sy Mouhamad , Ndiaye Daouda , Nwakanma Davis , Langhorne Jean 
Published: May 2024

Abstract
Background
Malaria elimination in Senegal requires accurate diagnosis of all Plasmodium species. Plasmodium falciparum is the most prevalent species in Senegal, although Plasmodium malariae, Plasmodium ovale, and recently Plasmodium vivax have also been reported. Nonetheless, most malaria control tools, such as Histidine Rich Protein 2 rapid diagnosis test (PfHRP2-RDT,) can only diagnose P. falciparum. Thus, PfHRP2-RDT misses non-falciparum species and P. falciparum infections that fall below the limit of detection. These limitations can be addressed using highly sensitive Next Generation Sequencing (NGS). This study assesses the burden of the four different Plasmodium species in western and eastern regions of Senegal using targeted PCR amplicon sequencing.

Methods
Three thousand samples from symptomatic and asymptomatic individuals in 2021 from three sites in Senegal (Sessene, Diourbel region; Parcelles Assainies, Kaolack region; Gabou, Tambacounda region) were collected. All samples were tested using PfHRP2-RDT and photoinduced electron transfer polymerase chain reaction (PET-PCR), which detects all Plasmodium species. Targeted sequencing of the nuclear 18S rRNA and the mitochondrial cytochrome B genes was performed on PET-PCR positive samples.

Results
Malaria prevalence by PfHRP2-RDT showed 9.4% (94/1000) and 0.2% (2/1000) in Diourbel (DBL) and Kaolack (KL), respectively. In Tambacounda (TAM) patients who had malaria symptoms and had a negative PfHRP2-RDT were enrolled. The PET-PCR had a positivity rate of 23.5% (295/1255) overall. The PET-PCR positivity rate was 37.6%, 12.3%, and 22.8% in Diourbel, Kaolack, and Tambacounda, respectively. Successful sequencing of 121/295 positive samples detected P. falciparum (93%), P. vivax (2.6%), P. malariae (4.4%), and P. ovale wallikeri (0.9%). Plasmodium vivax was co-identified with P. falciparum in thirteen samples. Sequencing also detected two PfHRP2-RDT-negative mono-infections of P. vivax in Tambacounda and Kaolack.

Conclusion
The findings demonstrate the circulation of P. vivax in western and eastern Senegal, highlighting the need for improved malaria control strategies and accurate diagnostic tools to better understand the prevalence of non-falciparum species countrywide.
DNMT1-targeting remodeling global DNA hypomethylation for enhanced tumor suppression and circumvented toxicity in oral squamous cell carcinoma
Authors: Liu Yangfan , Sun Yu , Yang Jin , Wu Deyang , Yu Shuang , Liu Junjiang , Hu Tao , Luo Jingjing , Zhou Hongmei 
Published: May 2024

Abstract
Background
The faithful maintenance of DNA methylation homeostasis indispensably requires DNA methyltransferase 1 (DNMT1) in cancer progression. We previously identified DNMT1 as a potential candidate target for oral squamous cell carcinoma (OSCC). However, how the DNMT1- associated global DNA methylation is exploited to regulate OSCC remains unclear.

Methods
The shRNA-specific DNMT1 knockdown was employed to target DNMT1 on oral cancer cells in vitro, as was the use of DNMT1 inhibitors. A xenografted OSCC mouse model was established to determine the effect on tumor suppression. High-throughput microarrays of DNA methylation, bulk and single-cell RNA sequencing analysis, multiplex immunohistochemistry, functional sphere formation and protein immunoblotting were utilized to explore the molecular mechanism involved. Analysis of human samples revealed associations between DNMT1 expression, global DNA methylation and collaborative molecular signaling with oral malignant transformation.

Results
We investigated DNMT1 expression boosted steadily during oral malignant transformation in human samples, and its inhibition considerably minimized the tumorigenicity in vitro and in a xenografted OSCC model. DNMT1 overexpression was accompanied by the accumulation of cancer-specific DNA hypomethylation during oral carcinogenesis; conversely, DNMT1 knockdown caused atypically extensive genome-wide DNA hypomethylation in cancer cells and xenografted tumors. This novel DNMT1-remodeled DNA hypomethylation pattern hampered the dual activation of PI3K-AKT and CDK2-Rb and inactivated GSK3β collaboratively. When treating OSCC mice, targeting DNMT1 achieved greater anticancer efficacy than the PI3K inhibitor, and reduced the toxicity of blood glucose changes caused by the PI3K inhibitor or combination of PI3K and CDK inhibitors as well as adverse insulin feedback.

Conclusions
Targeting DNMT1 remodels a novel global DNA hypomethylation pattern to facilitate anticancer efficacy and minimize potential toxic effects via balanced signaling synergia. Our study suggests DNMT1 is a crucial gatekeeper regarding OSCC destiny and treatment outcome.
RICTOR/mTORC2 downregulation in BRAFV600E melanoma cells promotes resistance to BRAF/MEK inhibition
Authors: Ponzone Luca , Audrito Valentina , Landi Claudia , Moiso Enrico , Levra Levron Chiara , Ferrua Sara , Savino Aurora , Vitale Nicoletta , Gasparrini Massimiliano , Avalle Lidia , Vantaggiato Lorenza , Shaba Enxhi , Tassone Beatrice , Saoncella Stefania , Orso Francesca , Viavattene Daniele , Marina Eleonora , Fiorilla Irene , Burrone Giulia , Abili Youssef , Altruda Fiorella , Bini Luca , Deaglio Silvia , Defilippi Paola , Menga Alessio , Poli Valeria , Porporato Paolo Ettore , Provero Paolo , Raffaelli Nadia , Riganti Chiara , Taverna Daniela , Cavallo Federica , Calautti Enzo 
Published: May 2024

AbstractBackgroundThe main drawback of BRAF/MEK inhibitors (BRAF/MEKi)-based targeted therapy in the management of BRAF-mutated cutaneous metastatic melanoma (MM) is the development of therapeutic resistance. We aimed to assess in this context the role of mTORC2, a signaling complex defined by the presence of the essential RICTOR subunit, regarded as an oncogenic driver in several tumor types, including MM.MethodsAfter analyzing The Cancer Genome Atlas MM patients’ database to explore both overall survival and molecular signatures as a function of intra-tumor RICTOR levels, we investigated the effects of RICTOR downregulation in BRAFV600EMM cell lines on their response to BRAF/MEKi. We performed proteomic screening to identify proteins modulated by changes in RICTOR expression, and Seahorse analysis to evaluate the effects of RICTOR depletion on mitochondrial respiration. The combination of BRAFi with drugs targeting proteins and processes emerged in the proteomic screening was carried out on RICTOR-deficient cells in vitro and in a xenograft setting in vivo.ResultsLow RICTOR levels in BRAF-mutated MM correlate with a worse clinical outcome. Gene Set Enrichment Analysis of low-RICTOR tumors display gene signatures suggestive of activation of the mitochondrial Electron Transport Chain (ETC) energy production. RICTOR-deficient BRAFV600Ecells are intrinsically tolerant to BRAF/MEKi and anticipate the onset of resistance to BRAFi upon prolonged drug exposure. Moreover, in drug-naïve cells we observed a decline in RICTOR expression shortly after BRAFi exposure. In RICTOR-depleted cells, both mitochondrial respiration and expression of nicotinamide phosphoribosyltransferase (NAMPT) are enhanced, and their pharmacological inhibition restores sensitivity to BRAFi.ConclusionsOur work unveils an unforeseen tumor-suppressing role for mTORC2 in the early adaptation phase of BRAFV600Emelanoma cells to targeted therapy and identifies the NAMPT-ETC axis as a potential therapeutic vulnerability of low RICTOR tumors. Importantly, our findings indicate that the evaluation of intra-tumor RICTOR levels has a prognostic value in metastatic melanoma and may help to guide therapeutic strategies in a personalized manner.
Extracellular vesicles from senescent mesenchymal stromal cells are defective and cannot prevent osteoarthritis
Authors: Boulestreau Jérémy , Maumus Marie , Bertolino Giuliana M. , Toupet Karine , Jorgensen Christian , Noël Daniéle 
Published: May 2024

AbstractAge is the most important risk factor in degenerative diseases such as osteoarthritis (OA), which is associated with the accumulation of senescent cells in the joints. Here, we aimed to assess the impact of senescence on the therapeutic properties of extracellular vesicles (EVs) from human fat mesenchymal stromal cells (ASCs) in OA. We generated a model of DNA damage-induced senescence in ASCs using etoposide and characterized EVs isolated from their conditioned medium (CM). Senescent ASCs (S-ASCs) produced 3-fold more EVs (S-EVs) with a slightly bigger size and that contain 2-fold less total RNA. Coculture experiments showed that S-ASCs were as efficient as healthy ASCs (H-ASCs) in improving the phenotype of OA chondrocytes cultured in resting conditions but were defective when chondrocytes were proliferating. S-EVs were also impaired in their capacity to polarize synovial macrophages towards an anti-inflammatory phenotype. A differential protein cargo mainly related to inflammation and senescence was detected in S-EVs and H-EVs. Using the collagenase-induced OA model, we found that contrary to H-EVs, S-EVs could not protect mice from cartilage damage and joint calcifications, and were less efficient in protecting subchondral bone degradation. In addition, S-EVs induced a pro-catabolic and pro-inflammatory gene signature in the joints of mice shortly after injection, while H-EVs decreased hypertrophic, catabolic and inflammatory pathways. In conclusion, S-EVs are functionally impaired and cannot protect mice from developing OA.
A novel conductive microtubule hydrogel for electrical stimulation of chronic wounds based on biological electrical wires
Authors: Fan Weijing , Yang Xiao , Hu Xiaoming , Huang Renyan , Shi Hongshuo , Liu Guobin 
Published: May 2024

AbstractElectrical stimulation (ES) is considered a promising therapy for chronic wounds via conductive dressing. However, the lack of a clinically suitable conductive dressing is a serious challenge. In this study, a suitable conductive biomaterial with favorable biocompatibility and conductivity was screened by means of an inherent structure derived from the body based on electrical conduction in vivo. Ions condensed around the surface of the microtubules (MTs) derived from the cell’s cytoskeleton are allowed to flow in the presence of potential differences, effectively forming a network of biological electrical wires, which is essential to the bioelectrical communication of cells. We hypothesized that MT dressing could improve chronic wound healing via the conductivity of MTs applied by ES. We first developed an MT-MAA hydrogel by a double cross-linking method using UV and calcium chloride to improve chronic wound healing by ES. In vitro studies showed good conductivity, mechanical properties, biocompatibility, and biodegradability of the MT-MAA hydrogel, as well as an elevated secretion of growth factors with enhanced cell proliferation and migration ability in response to ES. The in vivo experimental results from a full-thickness diabetic wound model revealed rapid wound closure within 7d in C57BL/6J mice, and the wound bed dressed by the MT-MAA hydrogel was shown to have promoted re-epithelization, enhanced angiogenesis, accelerated nerve growth, limited inflammation phases, and improved antibacterial effect under the ES treatment. These preclinical findings suggest that the MT-MAA hydrogel may be an ideal conductive dressing for chronic wound healing. Furthermore, biomaterials based on MTs may be also promising for treating other diseases.