bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chronic rapid eye movement sleep deprivation aggravates the pathogenesis of Alzheimer’s disease by decreasing brain O-GlcNAc cycling in mice
Authors: Kim Dong Yeol , Kim Sang-Min , Han Inn-Oc 
Published: July 2024

AbstractThis study investigated the role of O-GlcNAc cycling in Alzheimer’s disease-related changes in brain pathophysiology induced by chronic REM sleep deprivation (CSD) in mice. CSD increased amyloid beta (Aβ) and p-Tau accumulation and impaired learning and memory (L/M) function. CSD decreased dendritic length and spine density. CSD also increased the intensity of postsynaptic density protein-95 (PSD-95) staining. All of these Alzheimer’s disease (AD) pathogenic changes were effectively reversed through glucosamine (GlcN) treatment by enhancing O-GlcNAcylation. Interestingly, the lelvel of O-GlcNAcylated-Tau (O-Tau) exhibited an opposite trend compared to p-Tau, as it was elevated by CSD and suppressed by GlcN treatment. CSD increased neuroinflammation, as indicated by elevated levels of glial fibrillary acidic protein and IBA-1-positive glial cells in the brain, which were suppressed by GlcN treatment. CSD promoted the phosphorylation of GSK3β and led to an upregulation in the expression of endoplasmic reticulum (ER) stress regulatory proteins and genes. These alterations were effectively suppressed by GlcN treatment. Minocycline not only suppressed neuroinflammation induced by CSD, but it also rescued the decrease in O-GlcNAc levels caused by CSD. Minocycline also reduced AD neuropathy without affecting CSD-induced ER stress. Notably, overexpressing O-GlcNAc transferase in the dentate gyrus region of the mouse brain rescued CSD-induced cognitive dysfunction, neuropathy, neuroinflammation, and ER stress responses. Collectively, our findings reveal that dysregulation of O-GlcNAc cycling underlies CSD-induced AD pathology and demonstrate that restoration of OGlcNAcylation protects against CSD-induced neurodegeneration.
An exploration of the influence of ZnO NPs treatment on germination of radish seeds under salt stress based on the YOLOv8-R lightweight model
Authors: Ouyang Zhiqian , Fu Xiuqing , Zhong Zhibo , Bai Ruxiao , Cheng Qianzhe , Gao Ge , Li Meng , Zhang Haolun , Zhang Yaben 
Published: July 2024

Abstract
Background
Since traditional germination test methods have drawbacks such as slow efficiency, proneness to error, and damage to seeds, a non-destructive testing method is proposed for full-process germination of radish seeds, which improves the monitoring efficiency of seed quality.

Results
Based on YOLOv8n, a lightweight test model YOLOv8-R is proposed, where the number of parameters, the amount of calculation, and size of weights are significantly reduced by replacing the backbone network with PP-LCNet, the neck part with CCFM, the C2f of the neck part with OREPA, the SPPF with FocalModulation, and the Detect of the head part with LADH. The ablation test and comparative test prove the performance of the model. With adoption of germination rate, germination index, and germination potential as the three vitality indicators, the seed germination phenotype collection system and YOLOv8-R model are used to analyze the full time-series sequence effects of different ZnO NPs concentrations on germination of radish seeds under varying degrees of salt stress.

Conclusions
The results show that salt stress inhibits the germination of radish seeds and that the inhibition effect is more obvious with the increased concentration of NaCl solution; in cultivation with deionized water, the germination rate of radish seeds does not change significantly with increased concentration of ZnO NPs, but the germination index and germination potential increase initially and then decline; in cultivation with NaCl solution, the germination rate, germination potential and germination index of radish seeds first increase and then decline with increased concentration of ZnO NPs.
Challenges and innovations in the surgical treatment of advanced Dupuytren disease by percutaneous needle fasciotomy: indications, limitations, and medico-legal implications
Authors: Basile Giuseppe , Amadei Federico , Prevot Luca Bianco , Tronconi Livio Pietro , Ciccarelli Antonello , Bolcato Vittorio , Zaami Simona 
Published: July 2024

Abstract
Background
Dupuytren disease, a chronic thickening and retraction of the palmar aponeurosis of the hands, may result in permanent and progressive flexion of one or more fingers. Percutaneous needle fasciotomy is a simple method that uses a hypodermic needle usually performed under local anaesthesia. The study aim was to report the postoperative results and complications using a percutaneous approach to treat Dupuytren contracture in a consecutive series of patients with advanced Dupuytren disease, also considering the relevant medico-legal implications.

Methods
Retrospective multicentre study of all patients with Tubiana stage 3–4 Dupuytren contracture treated with percutaneous needle aponeurotomy, with no ultrasound assistance, from 2012 to 2022. Patient demographics, disease severity, treatment-related complications, and the incidence of recurrence were identified. An overview of therapeutic treatment options has accounted for 52 relevant sources spanning the 2007–2023 time period.

Results
Overall, 41.7% (N = 200) of patients were females, the mean age was 72 years (60–89), the right hand was treated in 54.2% (N = 260) of patients. The little finger was involved in 50% of the patients. The 12 months mean PED was 9°, the mean quickDASH was 8, the mean URAM 6. Minor complications were reported in 18.7% (N = 90) of patients, typically skin lacerations (83.3%) with no clinical sequelae, and no major complications were reported. Recurrence occurred in 30% (N = 144) of patients.

Conclusions
Percutaneous needle fasciotomy is safe and reliable even in patients with advanced Dupuytren disease, resulting in predictably acceptable outcome with low risk of complications.
Astrocytic autophagy plasticity modulates Aβ clearance and cognitive function in Alzheimer’s disease
Authors: Kim Suhyun , Chun Heejung , Kim Yunha , Kim Yeyun , Park Uiyeol , Chu Jiyeon , Bhalla Mridula , Choi Seung-Hye , Yousefian-Jazi Ali , Kim Sojung , Hyeon Seung Jae , Kim Seungchan , Kim Yeonseo , Ju Yeon Ha , Lee Seung Eun , Lee Hyunbeom , Lee Kyungeun , Oh Soo-Jin , Hwang Eun Mi , Lee Junghee , Lee C. Justin , Ryu Hoon 
Published: July 2024

Abstract
Background
Astrocytes, one of the most resilient cells in the brain, transform into reactive astrocytes in response to toxic proteins such as amyloid beta (Aβ) in Alzheimer’s disease (AD). However, reactive astrocyte-mediated non-cell autonomous neuropathological mechanism is not fully understood yet. We aimed our study to find out whether Aβ-induced proteotoxic stress affects the expression of autophagy genes and the modulation of autophagic flux in astrocytes, and if yes, how Aβ-induced autophagy-associated genes are involved Aβ clearance in astrocytes of animal model of AD.

Methods
Whole RNA sequencing (RNA-seq) was performed to detect gene expression patterns in Aβ-treated human astrocytes in a time-dependent manner. To verify the role of astrocytic autophagy in an AD mouse model, we developed AAVs expressing shRNAs for MAP1LC3B/LC3B (LC3B) and Sequestosome1 (SQSTM1) based on AAV-R-CREon vector, which is a Cre recombinase-dependent gene-silencing system. Also, the effect of astrocyte-specific overexpression of LC3B on the neuropathology in AD (APP/PS1) mice was determined. Neuropathological alterations of AD mice with astrocytic autophagy dysfunction were observed by confocal microscopy and transmission electron microscope (TEM). Behavioral changes of mice were examined through novel object recognition test (NOR) and novel object place recognition test (NOPR).

Results
Here, we show that astrocytes, unlike neurons, undergo plastic changes in autophagic processes to remove Aβ. Aβ transiently induces expression of LC3B gene and turns on a prolonged transcription of SQSTM1 gene. The Aβ-induced astrocytic autophagy accelerates urea cycle and putrescine degradation pathway. Pharmacological inhibition of autophagy exacerbates mitochondrial dysfunction and oxidative stress in astrocytes. Astrocyte-specific knockdown of LC3B and SQSTM1 significantly increases Aβ plaque formation and GFAP-positive astrocytes in APP/PS1 mice, along with a significant reduction of neuronal marker and cognitive function. In contrast, astrocyte-specific overexpression of LC3B reduced Aβ aggregates in the brain of APP/PS1 mice. An increase of LC3B and SQSTM1 protein is found in astrocytes of the hippocampus in AD patients.

Conclusions
Taken together, our data indicates that Aβ-induced astrocytic autophagic plasticity is an important cellular event to modulate Aβ clearance and maintain cognitive function in AD mice.
Advances in the application of gas vesicles in medical imaging and disease treatment
Authors: Feng Renjie , Lan Jie , Goh Meei Chyn , Du Meng , Chen Zhiyi 
Published: July 2024

AbstractThe gas vesicle (GV) is like a hollow nanoparticle consisting of an internal gas and a protein shell, which mainly consists of hydrophobic gas vesicle protein A (GvpA) and GvpC attached to the surface. GVs, first discovered in cyanobacteria, are mainly produced by photosynthetic bacteria (PSB) and halophilic archaea. After being modified and engineered, GVs can be utilized as contrast agents, delivery carriers, and immunological boosters for disease prevention, diagnosis, and treatment with good results due to their tiny size, strong stability and non-toxicity advantages. Many diagnostic and therapeutic approaches based on GV are currently under development. In this review, we discuss the source, function, physical and chemical properties of GV, focus on the current application progress of GV, and put forward the possible application prospect and development direction of GV in the future.
Exploring the impact of GSTM1 as a novel molecular determinant of survival in head and neck cancer patients of African descent
Authors: Yang Fan , Chen Fanghui , Shay Chloe , Chen Georgia Z. , Saba Nabil F. , Teng Yong 
Published: July 2024

Abstract
Background
Blacks/African American (BAA) patients diagnosed with head and neck squamous cell carcinoma (HNSCC) have worse survival outcomes than White patients. However, the mechanisms underlying racial disparities in HNSCC have not been thoroughly characterized.

Methods
Data on gene expression, copy number variants (CNVs), gene mutations, and methylation were obtained from 6 head and neck cancer datasets. Comparative bioinformatics analysis of the above genomic features was performed between BAAs and Whites. The expression pattern of GSTM1 was validated by immunohistochemistry using tumor tissue microarray (TMA). Effect of GSTM1 knockdown were assessed by cell proliferation, colony formation, and tumor development in an orthotopic mouse model. The changes in protein kinases were determined using the Proteome Profiler Human Phospho-Kinase Array Kit in HNSCC cells with or without GSTM1 knockdown.

Results
We identified ancestry-related differential genomic profiles in HNSCC. Specifically, in BAA HNSCC, FAT1 mutations were associated with its gene expression, SALL3 gene expression correlated with its gene CNVs, and RTP4 gene expression showed an inverse correlation with its methylation. Notably, GSTM1 emerged as a prognostic risk factor for BAA HNSCC, with high gene CNVs and expression levels correlating with poor overall survival in BAA patients. Immunohistochemistry results from newly developed in-house TMA validated the expression pattern of GSTM1 between BAA HNSCC and White HNSCC. In an orthotopic mouse model, GSTM1 knockdown significantly inhibited malignant progression in tumors derived from BAAs. In contrast, loss of GSTM1 did not affect the development of HNSCC originating in Whites. Mechanistically, GSTM1 knockdown suppressed HSP27 phosphorylation and β-catenin in BAA HNSCC cells, but not in White HNSCC cells. This differential effect at least partially contributes to tumor development in BAA patients.

Conclusion
This study identifies GSTM1 as a novel molecular determinant of survival in HNSCC patients of African descent. It also provides a molecular basis for future research focused on identifying molecular determinants and developing therapeutic interventions to improve outcomes for BAA patients with HNSCC.
Epigenetic mechanism of RBM15 in affecting cisplatin resistance in laryngeal carcinoma cells by regulating ferroptosis
Authors: Liang Yue , Zhong Haoyue , Zhao Yi , Tang XiaoMin , Pan Chunchen , Sun Jingwu , Sun Jiaqiang 
Published: July 2024

AbstractLaryngeal carcinoma (LC) is a common cancer of the respiratory tract. This study aims to investigate the role of RNA-binding motif protein 15 (RBM15) in the cisplatin (DDP) resistance of LC cells. LC-DDP-resistant cells were constructed. RBM15, lysine-specific demethylase 5B (KDM5B), lncRNA Fer-1 like family member 4 (FER1L4), lncRNA KCNQ1 overlapping transcript 1 (KCNQ1OT1), glutathione peroxidase 4 (GPX4), and Acyl-CoA synthetase long-chain family (ACSL4) was examined. Cell viability, IC50, and proliferation were assessed after RBM15 downregulation. The enrichment of insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) and N6-methyladenosine (m6A) on KDM5B was analyzed. KDM5B mRNA stability was measured after actinomycin D treatment. A tumor xenograft assay was conducted to verify the role of RBM15 in LC. Results showed that RBM15 was upregulated in LC and its knockdown decreased IC50, cell viability, proliferation, glutathione, and upregulated iron ion content, ROS, malondialdehyde, ACSL4, and ferroptosis. Mechanistically, RBM15 improved KDM5B stability in an IGF2BP3-dependent manner, resulting in FER1L4 downregulation and GPX4 upregulation. KDM5B increased KCNQ1OT1 and inhibited ACSL4. KDM5B/KCNQ1OT1 overexpression or FER1L4 knockdown promoted DDP resistance in LC by inhibiting ferroptosis. In conclusion, RBM15 promoted KDM5B expression, and KDM5B upregulation inhibited ferroptosis and promoted DDP resistance in LC by downregulating FER1L4 and upregulating GPX4, as well as by upregulating KCNQ1OT1 and inhibiting ACSL4. Silencing RBM15 inhibited tumor growth in vivo.
Prostate cancers with distinct transcriptional programs in Black and White men
Authors: Kim Minhyung , Tamukong Patrick , Galvan Gloria Cecilia , Yang Qian , De Hoedt Amanda , Freeman Michael R. , You Sungyong , Freedland Stephen 
Published: July 2024

Abstract
Background
Black men are at a higher risk of prostate cancer (PC) diagnosis and present with more high-grade PC than White men in an equal access setting. This study aimed to identify differential transcriptional regulation between Black and White men with PC.

Methods
We performed microarray of radical prostatectomy tissue blocks from 305 Black and 238 White men treated at the Durham Veterans Affairs Medical Center. Differential expression, gene set enrichment analysis, master regulator analysis, and network modeling were conducted to compare gene expression by race. Findings were validated using external datasets that are available in the Gene Expression Omnibus (GEO) database. The first was a multi-institutional cohort of 1152 prostate cancer patients (596 Black, 556 White) with microarray data (GEO ID: GSE169038). The second was an Emory cohort of 106 patients (22 Black, 48 White, 36 men of unknown race) with RNA-seq data (GEO ID: GSE54460). Additionally, we analyzed androgen receptor (AR) chromatin binding profiles using paired AR ChIP-Seq datasets from Black and White men (GEO IDs: GSE18440 and GSE18441).

Results
We identified 871 differentially expressed genes between Black and White men. White men had higher activity of MYC-related pathways, while Black men showed increased activity of inflammation, steroid hormone responses, and cancer progression-related pathways. We further identified the top 10 transcription factors (TFs) in Black patients, which formed a transcriptional regulatory network centered on the AR. The activities of this network and the pathways were significantly different in Black vs. White men across multiple cohorts and PC molecular subtypes.

Conclusions
These findings suggest PC in Black and White men have distinct tumor transcriptional profiles. Furthermore, a highly interactive TF network centered on AR drives differential gene expression in Black men. Additional study is needed to understand the degree to which these differences in transcriptional regulatory elements contribute to PC health disparities.
Sex-related differences regarding headache triggered by low barometric pressure in Japan
Authors: Fujimoto Takuma , Iwata Hiroki , Kobayashi Noriko , Kondo Shingo , Yamaura Katsunori 
Published: July 2024

Abstract
Purpose
The prevalence of migraine headache is higher in women. Low barometric pressure is a factor in headache triggering, but sex-related differences have not been identified. The purpose of this study was to examine sex-related differences in headache triggered by low barometric pressure.

Methods
Study subjects aged 20–49 years were randomly selected from a research company’s (Macromill, Inc.) web panel. Those with chronic migraine or tension-type headache invited to complete a web-based self-administered questionnaire. Logistic regression analysis was performed with the objective variable as the Headache Impact Test-6 (HIT-6) high scores (56 or more) or headache triggered by low barometric pressure.

Results
Participants were 332 women and 337 men in the headache population. HIT-6 high scores were associated with age at headache occurrence 20 years or younger (OR: odds ratio 1.85, 95% CI: confidence interval 1.15–2.99, p = 0.012) and headache triggered by low barometric pressure (OR 2.11, 95%CI 1.51–2.94, p < 0.001). Headache triggered by low barometric pressure was significantly associated with women (OR 2.92, 95%CI 2.12–4.02, p < 0.001).

Conclusions
Headache triggered by low barometric pressure were related to sex-related differences. It was suggested that a sex-specific treatment approach for headache triggering is needed.
A differential expression of an identical mutation in CYP17A1 gene in two infertility patients: a case report
Authors: Rabinovich Elay , Hershko-Klement Anat , Bentov Yaakov 
Published: July 2024

Abstract
Background
17-Hydroxylase deficiency is the rarest form of congenital adrenal hyperplasia, a disorder that affects steroidogenesis, causing abnormal hormone levels. Studies have shown a clear association between 17-hydroxylase deficiency and primary infertility, but a definite protocol to treat the disorder has not been determined yet.

Case presentation
Case I presents a 24-year-old Caucasian Israeli-Arab female who experienced 6 years of infertility. Before her initial visit to our clinic, she underwent three laparoscopic ovarian cystectomies, had an unsuccessful in vitro fertilization cycle, and was treated with combined oral contraceptives. Her hormonal profile was tested, and the results led to genetic counseling and the diagnosis of non-classical congenital adrenal hyperplasia. She was treated with estradiol, glucocorticoids, and transdermal testosterone. After hormonal levels were lowered, in vitro fertilization cycles were initiated, and the patient had a spontaneous ovulation. In case II, a 20-year-old Caucasian Israeli-Arab female presented for infertility evaluation owing to her oligomenorrhea. Her vitals and physical examination had normal results. The investigation of her abnormal hormonal profile led her to be referred to genetic testing, where the results showed the same genetic mutation as seen in case I.

Conclusion
Both cases highlight the distinctiveness of the condition, where an identical mutation in the gene responsible for the same enzyme can bring about diverse phenotypes. Case I offers a potential treatment protocol for this rare disorder.
Insights into ionizing radiation-induced bone marrow hematopoietic stem cell injury
Authors: Zhang Yimin , Chen Xinliang , Wang Xinmiao , Chen Jun , Du Changhong , Wang Junping , Liao Weinian 
Published: July 2024

AbstractWith the widespread application of nuclear technology across various fields, ionizing radiation-induced injuries are becoming increasingly common. The bone marrow (BM) hematopoietic tissue is a primary target organ of radiation injury. Recent researches have confirmed that ionizing radiation-induced hematopoietic dysfunction mainly results from BM hematopoietic stem cells (HSCs) injury. Additionally, disrupting and reshaping BM microenvironment is a critical factor impacting both the injury and regeneration of HSCs post radiation. However, the regulatory mechanisms of ionizing radiation injury to BM HSCs and their microenvironment remain poorly understood, and prevention and treatment of radiation injury remain the focus and difficulty in radiation medicine research. In this review, we aim to summarize the effects and mechanisms of ionizing radiation-induced injury to BM HSCs and microenvironment, thereby enhancing our understanding of ionizing radiation-induced hematopoietic injury and providing insights for its prevention and treatment in the future.
The plasma viral communities associate with clinical profiles in a large-scale haematological patients cohort
Authors: Ma Shuai , Yin Yuyao , Guo Yifan , Yao Chaoqun , Xu Siqi , Luo Qingqing , Yin Guankun , Wang Shuyi , Wang Qi , Chen Hongbin , Wang Ruobing , Jin Longyang , Liang Guanxiang , Wang Hui 
Published: July 2024

Abstract
Background
Haematological patients exhibit immune system abnormalities that make them susceptible to viral infections. Understanding the relationship between the virome in the blood plasma of haematological patients and their clinical characteristic is crucial for disease management. We aimed to explore the presence of viral pathogens and identify close associations between viral infections and various clinical features.

Results
A total of 21 DNA viruses and 6 RNA viruses from 12 virus families were identified from 1383 patients. Patients with haematological diseases exhibited significantly higher diversity, prevalence, and co-detection rates of viral pathogens. During fever episodes, pathogen detection was notably higher, with Epstein-Barr virus (EBV) and Mucorales infections being the most probable culprits for fever symptoms in non-haematological patients. The detection rate of torque teno virus (TTV) significantly increases in haematological patients after transplantation and during primary lung infections. Additionally, TTV-positive patients demonstrate significantly higher absolute neutrophil counts, while C-reactive protein and procalcitonin levels are notably lower. Furthermore, TTV, cytomegalovirus, and parvovirus B19 (B19V) were found to be more prevalent in non-neutropenic patients, while non-viral pathogenic infections, such as Gram-negative bacteria and Mucorales, were more common in neutropenic patients. Pegivirus C (HPgV-C) infection often occurred post-transplantation, regardless of neutropenia. Additionally, some viruses such as TTV, B19V, EBV, and HPgV-C showed preferences for age and seasonal infections.

Conclusions
Analysis of the plasma virome revealed the susceptibility of haematological patients to plasma viral infections at specific disease stages, along with the occurrence of mixed infections with non-viral pathogens. Close associations were observed between the plasma virome and various clinical characteristics, as well as clinical detection parameters. Understanding plasma virome aids in auxiliary clinical diagnosis and treatment, enabling early prevention to reduce infection rates in patients and improve their quality of life.