bluuebunny/crossref_metadata_2025_split huggingface dataset:
Crosstalk between skeletal muscle ratio and cholesterol metabolism disorders: a cross-section study
Authors: Wang Yunle , Hu Jun , Shen Hui , Liu Chunxing , Yang Lijuan 
Published: July 2024

Abstract
Background
Dysfunction of cholesterol metabolism may be associated with low skeletal muscle mass. This study aimed to explore the relationship between skeletal muscle mass and cholesterol metabolic disorders in adults.

Methods
The data of a total of 5949 people with complete medical history data, biochemical data and body composition analysis were recruited. According to the serum cholesterol, low density lipoprotein (LDL), high density lipoprotein (HDL) and nonHDL, the population was divided into a disorder group and a normal group. Independent sample t tests, chi-square tests, Pearson's correlation analyses and binary logistic regression analyses were used to study the effect of body composition on abnormal cholesterol metabolism. According to BMI and sex, the population was divided into different subgroups, and binary logistic regression analysis was used to study the effect of the skeletal mass ratio on cholesteral metabolic disorders in different subgroups.

Results
There were significant differences in sex, alcohol consumption, body weight, BMI, skeletal muscle mass index (SMI) [total skeletal muscle mass (kg)/height 2 (m2)] and skeletal muscle mass ratio (SMR) [total skeletal muscle mass (kg)/weight (kg) *100] between the disorder group (hypercholesterolemia, hyper-LDL, lower-HDL and hyper-nonHDL) and the normal group. Pearson correlation analysis revealed that the SMR was negatively correlated, while the SMI was positively correlated with cholesterol metabolic disorders in both sexes. The overweight group was older and had a greater SMI, abnormal cholesteral metabolism ratio and lower SMR than the normal-weight group. In the normal-weight group, the SMR was an independent protective factor against different kinds of cholesteral metabolic disorders in both sexes, while the SMI was a risk factor. In the overweight subgroup, the protective effect on HDL and nonHDL metabolism remained in the male subgroup but disappeared in the female subgroup. However, the SMI was an independent risk factor for different kinds of cholesteral metabolic disorders in both sexes.

Conclusions
SMR was an independent protective factor against cholesterol metabolic disorders in both males and females, especially in the normal weight group. SMI was an independent risk factor, especially in the overweight group.
Sclerotherapy for the intraoral ranula with bleomycin: technical considerations and preliminary experience
Authors: Zhang Hong-Yu , Su Li-Wen , Sun Huan , Rui Chao-Chen , Wu Yang 
Published: July 2024

AbstractRanula is a mucous cyst that occurs in the sublingual gland (SLG) in the floor of the mouth. It can be classified into two types based on origins: One is the the lesser sublingual gland (LSLG) in the anterior segment and the Rivini duct, which is connected to it, and the other is the greater sublingual gland (GSLG) in the posterior segment. Because of the anatomical characteristics, surgical resection of the cysts carries the risk of damaging adjacent tissues and has a high recurrence rate. Intralesional injection of sclerotherapy may be a better alternative treatment. We summarized 65 cases of ranula treated with intralesional injections of bleomycin(BML). According to the origin of the ranula, 60 cases were from the LSLG and the Rivini duct, and 5 cases were from the GSLG. The results showed that 60 cases of ranula from LSLG and Rivini ducts were 100% cured during the follow-up period. The median number of injections for all patients was 1.16. All 5 cases of ranula from the GSLG did not wholly recover. This study confirmed that BLM intralesional injection is a safe and effective treatment modality for cysts from LSLG or the ducts of Rivini rather than GSLG. Therefore, before treatment, it is necessary to determine the type and origin of the cyst by characterizing its morphology to ensure the effectiveness of the treatment.
Oncologists’ palliative care referral behaviour: testing utility of social exchange theory as an explanatory framework
Authors: Salins Naveen , Hughes Sean , Preston Nancy 
Published: July 2024

Abstract
Background
Adults and children with cancer are referred to palliative care infrequently or late. Oncologists often gatekeep these referrals. Social exchange theory is used to explain physician referral behaviour in various clinical settings. Its utility in a cancer palliative care setting is not known.

Methods
We used Karl Popper’s hypothetico-deductive approach to test the hypothesis. The hypothesis was that social exchange theory is a helpful framework for explaining oncologists’ palliative care referral behaviour in a cancer setting. The utility of the theoretical framework was tested against the empiric findings of a systematic review and original research.

Results
Most components of social exchange theory known to explain physician referral behaviour like beliefs about the provider or service, emotions triggered during the professional engagement, its symbolism and stigma, the complexity of the referral task, efforts needed to achieve it, its cost, benefit, and value were similar in a cancer setting. Empirical findings suggest that oncologists provided strategies and solutions to better palliative care integration instead of comparing their existing engagement with potential alternatives and choosing them.

Conclusion
Social exchange theory was found to be helpful in explaining oncologists’ palliative care referral behaviour. To further develop the social exchange theory based on the data used to test it, it is recommended to include feedback and solutions as a component of the theoretical framework alongside a comparison level for alternatives.
A pseudonymized corpus of occupational health narratives for clinical entity recognition in Spanish
Authors: Dunstan Jocelyn , Vakili Thomas , Miranda Luis , Villena Fabián , Aracena Claudio , Quiroga Tamara , Vera Paulina , Viteri Valenzuela Sebastián , Rocco Victor 
Published: July 2024

AbstractDespite the high creation cost, annotated corpora are indispensable for robust natural language processing systems. In the clinical field, in addition to annotating medical entities, corpus creators must also remove personally identifiable information (PII). This has become increasingly important in the era of large language models where unwanted memorization can occur. This paper presents a corpus annotated to anonymize personally identifiable information in 1,787 anamneses of work-related accidents and diseases in Spanish. Additionally, we applied a previously released model for Named Entity Recognition (NER) trained on referrals from primary care physicians to identify diseases, body parts, and medications in this work-related text. We analyzed the differences between the models and the gold standard curated by a physician in detail. Moreover, we compared the performance of the NER model on the original narratives, in narratives where personal information has been masked, and in texts where the personal data is replaced by another similar surrogate value (pseudonymization). Within this publication, we share the annotation guidelines and the annotated corpus.
Novel transcriptional regulation of the GAP promoter in Pichia pastoris towards high expression of heterologous proteins
Authors: Lin Xiangna , Ding Weiqiu , Zheng Shaoyan , Wu Lianna , Chen Xue , Xie Chunfang , Liu Daling , Yao Dongsheng 
Published: July 2024

Abstract
Background
Pichia pastoris (Komagataella phaffii) is a promising production host, but the usage of methanol limits its application in the medicine and food industries.

Results
To improve the constitutive expression of heterologous proteins in P. pastoris, four new potential transcription regulators (Loc1p, Msn2p, Gsm1p, Hot1p) of the glyceraldehyde triphosphate dehydrogenase promoter (pGAP) were revealed in this study by using cellulase E4 as reporter gene. On this basis, a series of P. pastoris strains with knockout or overexpression of transcription factors were constructed and the deletion of transcription factor binding sites on pGAP was confirmed. The results showed that Loc1p and Msn2p can inhibit the activity of pGAP, while Gsm1p and Hot1p can enhance the activity of pGAP; Loc1p, Gsm1p and Hot1p can bind directly to pGAP, while Msn2p must be treated to expose the C-terminal domain to bind to pGAP. Moreover, manipulating a single transcription factor led to a 0.96-fold to 2.43-fold increase in xylanase expression. In another model protein, aflatoxin oxidase, knocking out Loc1 based on AFO-∆Msn2 strain resulted in a 0.63-fold to 1.4-fold increase in expression. It can be demonstrated that the combined use of transcription factors can further improve the expression of exogenous proteins in P. pastoris.

Conclusion
These findings will contribute to the construction of pGAP-based P. pastoris systems towards high expression of heterologous proteins, hence improving the application potential of yeast.
The lncRNA LINC01605 promotes the progression of pancreatic ductal adenocarcinoma by activating the mTOR signaling pathway
Authors: Zhu Yu-Heng , Jia Qin-Yuan , Yao Hong-Fei , Duan Zong-Hao , Ma Xue-Shi-Yu , Zheng Jia-Hao , Yin Yi-Fan , Liu Wei , Zhang Jun-Feng , Hua Rong , Ma Ding , Sun Yong-Wei , Yang Jian-Yu , Liu De-Jun , Huo Yan-Miao 
Published: July 2024

Abstract
Background
This study investigated the molecular mechanism of long intergenic non-protein coding RNA 1605 (LINC01605) in the process of tumor growth and liver metastasis of pancreatic ductal adenocarcinoma (PDAC).

Methods
LINC01605 was filtered out with specificity through TCGA datasets (related to DFS) and our RNA-sequencing data of PDAC tissue samples from Renji Hospital. The expression level and clinical relevance of LINC01605 were then verified in clinical cohorts and samples by immunohistochemical staining assay and survival analysis. Loss- and gain-of-function experiments were performed to estimate the regulatory effects of LINC01605 in vitro. RNA-seq of LINC01605-knockdown PDAC cells and subsequent inhibitor-based cellular function, western blotting, immunofluorescence and rescue experiments were conducted to explore the mechanisms by which LINC01605 regulates the behaviors of PDAC tumor cells. Subcutaneous xenograft models and intrasplenic liver metastasis models were employed to study its role in PDAC tumor growth and liver metastasis in vivo.

Results
LINC01605 expression is upregulated in both PDAC primary tumor and liver metastasis tissues and correlates with poor clinical prognosis. Loss and gain of function experiments in cells demonstrated that LINC01605 promotes the proliferation and migration of PDAC cells in vitro. In subsequent verification experiments, we found that LINC01605 contributes to PDAC progression through cholesterol metabolism regulation in a LIN28B-interacting manner by activating the mTOR signaling pathway. Furthermore, the animal models showed that LINC01605 facilitates the proliferation and metastatic invasion of PDAC cells in vivo.

Conclusions
Our results indicate that the upregulated lncRNA LINC01605 promotes PDAC tumor cell proliferation and migration by regulating cholesterol metabolism via activation of the mTOR signaling pathway in a LIN28B-interacting manner. These findings provide new insight into the role of LINC01605 in PDAC tumor growth and liver metastasis as well as its value for clinical approaches as a metabolic therapeutic target in PDAC.
EBP1 promotes the malignant biological behaviors of kidney renal clear cell carcinoma through activation of p38/HIF-1α signaling pathway
Authors: Meng Huan , Cao Shuxia , Tian Shengri , Huo Jiaqi , Li Xiangdan , Xu Dongyuan , Liu Lan 
Published: July 2024

Abstract
Background
Kidney Renal Clear Cell Carcinoma (KIRC) is a common malignant tumor of the urinary system, and its incidence is increasing. ERBB3 binding protein (EBP1) is upregulated in various cancers. However, the connection between EBP1 and KIRC has not been reported.

Methods
The expression of EBP1 in normal kidney tissue and KIRC tissue was analyzed through database and tissue microarray. EBP1 was knocked down in KIRC cell lines, and its impact on KIRC proliferation was assessed through CCK-8, soft agar assay, and flow cytometry. Scratch and transwell assays were used to evaluate the influence of EBP1 on KIRC invasion and migration. Nude mice tumor experiment were conducted to examine the effect of EBP1 on tumor tissue. Database analysis explored potential pathways involving EBP1, and validation was performed through Western blot experiments and p38 inhibitor.

Results
EBP1 is upregulated in KIRC and significantly correlates with clinical staging, pathological grading, and lymph node metastasis in patients. The mechanism research showed that knocking down EBP1 inhibited KIRC proliferation, invasion, and migration and inhibited p38 phosphorylation and the expression of hypoxia-inducible factor-1α (HIF-1α) in KIRC. p-38 inhibitor (SB203580) inhibits p38 phosphorylation and HIF-1α expression and suppresses cell viability in a concentration-dependent manner, but has no effect on EBP1 expression. HEK 293T cells overexpressing EBP1 showed increased expression of phosphorylated p38 and HIF-1α and enhanced cell viability, however, SB203580 inhibited this effect of EBP1.

Conclusion
EBP1 may promote the occurrence and development of KIRC by regulating the expression of p38/HIF-1α signaling pathway.

Graphical Abstract
Histogenetic insights and genetic landscape of fibromatosis-like undifferentiated gastric carcinoma: a focused study
Authors: Wang Yang-Kun , Wang Su-Nan , Liao Xing-Hai , Wang Zhi-Qiang , Li Ping , Yun Tian , Meng De-Qi 
Published: July 2024

Abstract
Background
The aim of this study was to elucidate the histogenesis and genetic underpinnings of fibromatosis-like undifferentiated gastric carcinoma (FLUGC), a rare pathological entity.

Method
Through a detailed analysis of seven cases, including histopathological evaluation, CTNNB1 gene mutation screening, human epidermal growth factor receptor 2 (HER2) protein level quantification, and HER2 gene amplification assessment to identify the pathological and molecular characteristics of FLUGC.

Results
Of the seven patients in this study, five were male and two were female (age: 39–73 years). Four patients presented with lesions in the gastric antrum and three had lesions in the lateral curvature of the stomach. Histopathologically, over 90% of the tumor consisted of aggressive fibromatosis-like tissue, including proliferating spindle fibroblasts and myofibroblasts and varying amounts of collagenous fibrous tissues. Undifferentiated cancer cells, accounting for less than 10%, were dispersed among the aggressive fibromatosis-like tissues. These cells were characterized by their small size and were relatively sparse without glandular ducts or nested mass-like structures. Immunophenotyping results showed positive expression of CKpan, CDX2, villin, and p53 in undifferentiated cancer cells; positive expression of vimentin in aggressive fibromatosis-like tissue; positive cytoplasmic expression of β-catenin; and focal cytoplasmic positive expression of smooth muscle actin (SMA). Genetic analysis did not reveal any mutations in the CTNNB1 gene test, nor was there amplification in the HER2 gene fluorescence in situ hybridization (FISH) test. Additionally, the Epstein-Barr encoding region (EBER) of in situ hybridization was negative; and the mismatch repair (MMR) protein was positive. Programmed cell death-1 (PD-1) was < 1–5%; programmed cell death ligand 1 (PD-L1): TPS = 1–4%, CPS = 3–8.

Conclusion
The study highlights the significance of CTNNB1, HER2, EBER, and MMR as pivotal genetic markers in FLUGC, underscoring their relevance for diagnosis and clinical management. The rarity and distinct pathological features of FLUGC emphasize the importance of accurate diagnosis to prevent underdiagnosis or misdiagnosis and to raise awareness within the medical community.
Heat stress induced piRNA alterations in pachytene spermatocytes and round spermatids
Authors: Mehta Poonam , Sethi Shruti , Yadav Santosh Kumar , Gupta Gopal , Singh Rajender 
Published: July 2024

Abstract
Background
Spermatogenesis is a temperature-sensitive process, and elevation in temperature hampers this process quickly and significantly. We studied the molecular effects of testicular heating on piRNAs and gene expression in rat testicular germ cells.

Methods
We generated a cryptorchid rat model by displacing the testis from the scrotal sac (34 °C) to the abdominal area (37 °C) and sacrificed animals after 1 day, 3 days, and 5 days. Pachytene spermatocytes and round spermatids were purified using elutriation centrifugation and percoll gradient methods. We performed transcriptome sequencing in pachytene spermatocytes and round spermatids to identify differentially expressed piRNAs and their probable targets, i.e., TE transcripts and mRNAs.

Results
As a result of heat stress, we observed significant upregulation of piRNAs and TE transcripts in testicular germ cells. In addition to this, piRNA biogenesis machinery and heat shock proteins (Hsp70 and Hsp90 family members) were upregulated. mRNAs have also been proposed as targets for piRNAs; therefore, we shortlisted certain piRNA-mRNA pairs with an inverse relationship of expression. We observed that in testicular heat stress, the heat shock proteins go hand-in-hand with the upregulation of piRNA biogenesis machinery. The dysregulation of piRNAs in heat-stressed germ cells, increased ping-pong activity, and disturbed expression of piRNA target transcripts suggest a connection between piRNAs, mRNAs, and TE transcripts.

Conclusions
In heat stress, piRNAs, piRNA machinery, and heat shock proteins are activated to deal with low levels of stress, which is followed by a rescue approach in prolonged stressaccompained by high TE activity to allow genetic mutations, perhaps for survival and adaptability.
Unveiling viewpoints on national food environment policies in the Dutch newspaper discourse: an interpretative media content analysis
Authors: Droog Nine M. S. , Dijkstra Coosje S. , van Selm Naomi , Poelman Maartje P. , Mackenbach Joreintje D. 
Published: July 2024

Abstract
Background
National food environment policies can contribute to the reduction of diet-related non-communicable diseases. Yet, their implementation in the Netherlands remains low. It has been hypothesized that the media can play a pivotal role in inducing spikes in policy attention, thereby shaping political action. The aim of this study was to examine the discourse on food policies in Dutch newspaper articles between 2000–2022, by analyzing arguments used by various actors.

Methods
A systematic search in Nexis Uni was used to identify newspaper articles that covered national-level Dutch food environment policies published in seven Dutch national newspapers between 2000–2022. Covered policies were classified into six domains including food composition, labeling, promotion, prices, provision and retail and into the four stages of the policy cycle; policy formulation, decision-making, implementation, and evaluation. A grey literature search was used to identify food policies implemented during 2000–2022. Descriptive statistics were used to summarize coverage of policies over time, policy type and policy stage. An interpretive content analysis was performed on a random subsample of the newspaper articles to determine the actors, viewpoints and arguments of the food policies.

Results
We identified 896 relevant newspaper articles. The coverage of food policies in newspapers was initially low but peaked in 2018/2021/2022. Through grey literature search we identified 6 food policies which were implemented or adjusted between 2000–2022. The majority of the newspaper articles reported on food pricing policies and were discussed in the policy formulation stage. Academics (mainly supportive) were the most and food industry (mostly opposing) the least cited actors. Supportive arguments highlighted health consequences, health inequalities and collective responsibility, whereas opposing arguments focused on unwanted governmental interference and ineffectiveness of policies.

Conclusions
Dutch newspaper articles covering food policies represented a variety of actors and arguments, with individual versus collective responsibility for food choices playing a central role in the arguments. These insights may serve as a basis for further research into why certain arguments are used and their effect on policy attention and implementation.
The vast majority of somatic mutations in plants are layer-specific
Authors: Goel Manish , Campoy José A. , Krause Kristin , Baus Lisa C. , Sahu Anshupa , Sun Hequan , Walkemeier Birgit , Marek Magdalena , Beaudry Randy , Ruiz David , Huettel Bruno , Schneeberger Korbinian 
Published: July 2024

Abstract
Background
Plant meristems are structured organs consisting of distinct layers of stem cells, which differentiate into new plant tissue. Mutations in meristematic layers can propagate into large sectors of the plant. However, the characteristics of meristematic mutations remain unclear, limiting our understanding of the genetic basis of somaclonal phenotypic variation.

Results
Here, we analyse the frequency and distribution of somatic mutations in an apricot tree. We separately sequence the epidermis (developing from meristem layer 1) and the flesh (developing from meristem layer 2) of several fruits sampled across the entire tree. We find that most somatic mutations (> 90%) are specific to individual layers. Interestingly, layer 1 shows a higher mutation load than layer 2, implying different mutational dynamics between the layers. The distribution of somatic mutations follows the branching of the tree. This suggests that somatic mutations are propagated to developing branches through axillary meristems. In turn, this leads us to the unexpected observation that the genomes of layer 1 of distant branches are more similar to each other than to the genomes of layer 2 of the same branches. Finally, using single-cell RNA sequencing, we demonstrate that layer-specific mutations were only transcribed in the cells of the respective layers and can form the genetic basis of somaclonal phenotypic variation.

Conclusions
Here, we analyse the frequency and distribution of somatic mutations with meristematic origin. Our observations on the layer specificity of somatic mutations outline how they are distributed, how they propagate, and how they can impact clonally propagated crops.