bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distinct uric acid trajectories are associated with incident cardiac conduction block
Authors: Li Na , Cui Liufu , Shu Rong , Song Haicheng , Wang Jierui , Chen Shuohua , Tse Gary , Zhang Nan , Yang Xuemei , Xu Wenqi , Wu Shouling , Liu Tong 
Published: February 2024

Abstract
Background
The association of longitudinal uric acid (UA) changes with cardiac conduction block risk is unclear. We aimed to identify the trajectories of UA and explore its association with cardiac conduction block.

Methods
A total of 67,095 participants with a mean age of 53.12 years were included from the Kailuan cohort in Tangshan, China, who were free of cardiac conduction block and with repeated measurements of UA from 2006 to 2012. UA trajectories during 2006 to 2012 were identified by group-based trajectory modeling. Cox proportional hazard regression models were used to assess the association of UA trajectories with cardiac conduction block.

Results
We categorized three observed discrete trajectories of UA during 2006–2012 period: low-stable, moderate-stable, and high-stable. Over a median follow-up of 6.19 years, we identified 1405 (2.09%) incident cardiac conduction block. Compared to those in the low-stable trajectory, the adjusted hazard ratios (HRs) (95% confidence interval [CI]) of cardiac conduction block in the moderate-stable and high-stable trajectory were 1.30 (1.16–1.47) and 1.86 (1.56–2.22), and HRs of atrioventricular block were 1.39 (1.12–1.72) and 2.90 (2.19–3.83), and HRs of bundle branch blocks were 1.27 (1.10–1.47) and 1.43 (1.13–1.79). Notably, although the average UA level in the moderate-stable UA trajectory group is within the normal range, the risk of cardiac conduction block has increased.

Conclusions
The moderate-stable and high-stable trajectories are associated with increased risk for new-onset cardiac conduction block. Monitoring UA trajectories may assist in identifying subpopulations at higher risk for cardiac conduction block.
Machine learning prediction of future amyloid beta positivity in amyloid-negative individuals
Authors: Moradi Elaheh , Prakash Mithilesh , Hall Anette , Solomon Alina , Strange Bryan , Tohka Jussi ,   for the Alzheimer’s Disease Neuroimaging Initiative
Published: February 2024

Abstract
Background
The pathophysiology of Alzheimer’s disease (AD) involves $$\beta$$
β
-amyloid (A$$\beta$$
β
) accumulation. Early identification of individuals with abnormal $$\beta$$
β
-amyloid levels is crucial, but A$$\beta$$
β
quantification with positron emission tomography (PET) and cerebrospinal fluid (CSF) is invasive and expensive.

Methods
We propose a machine learning framework using standard non-invasive (MRI, demographics, APOE, neuropsychology) measures to predict future A$$\beta$$
β
-positivity in A$$\beta$$
β
-negative individuals. We separately study A$$\beta$$
β
-positivity defined by PET and CSF.

Results
Cross-validated AUC for 4-year A$$\beta$$
β
conversion prediction was 0.78 for the CSF-based and 0.68 for the PET-based A$$\beta$$
β
definitions. Although not trained for the clinical status-change prediction, the CSF-based model excelled in predicting future mild cognitive impairment (MCI)/dementia conversion in cognitively normal/MCI individuals (AUCs, respectively, 0.76 and 0.89 with a separate dataset).

Conclusion
Standard measures have potential in detecting future A$$\beta$$
β
-positivity and assessing conversion risk, even in cognitively normal individuals. The CSF-based definition led to better predictions than the PET-based definition.
Computed tomography-based body composition parameters can predict short-term prognosis in ulcerative colitis patients
Authors: Lu Jun , Xu Hui , Shi Haiyun , Zheng Jing , Cheng Tianxin , Zhou Minsi , Han Xinjun , Wang Yuxin , Meng Xuxu , Li Xiaoyang , Jiang Jiahui , Li Peng , Yang Zhenghan , Xu Lixue 
Published: February 2024

Abstract
Objectives
Emerging evidence suggests a potential relationship between body composition and short-term prognosis of ulcerative colitis (UC). Early and accurate assessment of rapid remission based on conventional therapy via abdominal computed tomography (CT) images has rarely been investigated. This study aimed to build a prediction model using CT-based body composition parameters for UC risk stratification.

Methods
In total, 138 patients with abdominal CT images were enrolled. Eleven quantitative parameters related to body composition involving skeletal muscle mass, visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) were measured and calculated using a semi-automated segmentation method. A prediction model was established with significant parameters using a multivariable logistic regression. The receiver operating characteristic (ROC) curve was plotted to evaluate prediction performance. Subgroup analyses were implemented to evaluate the diagnostic efficiency of the prediction model between different disease locations, centers, and CT scanners. The Delong test was used for statistical comparison of ROC curves.

Results
VAT density, SAT density, gender, and visceral obesity were significantly statistically different between remission and invalidation groups (all p < 0.05). The accuracy, sensitivity, specificity, and area under the ROC curve (AUC) of the prediction model were 82.61%, 95.45%, 69.89%, and 0.855 (0.792–0.917), respectively. The positive predictive value and negative predictive value were 70.79% and 93.88%, respectively. No significant differences in the AUC of the prediction model were found in different subgroups (all p > 0.05).

Conclusions
The predicting model constructed with CT-based body composition parameters is a potential non-invasive approach for short-term prognosis identification and risk stratification. Additionally, VAT density was an independent predictor for escalating therapeutic regimens in UC cohorts.

Critical relevance statement
The CT images were used for evaluating body composition and risk stratification of ulcerative colitis patients, and a potential non-invasive prediction model was constructed to identify non-responders with conventional therapy for making therapeutic regimens timely and accurately.

Key points
• CT-based prediction models help divide patients into invalidation and remission groups in UC.
• Results of the subgroup analysis confirmed the stability of the prediction model with a high AUC (all > 0.820).
• The visceral adipose tissue density was an independent predictor of bad short-term prognosis in UC.

Graphical Abstract
Liver imaging and pregnancy: what to expect when your patient is expecting
Authors: Porrello Giorgia , Cannella Roberto , Bernuau Jacques , Agman Antoine , Brancatelli Giuseppe , Dioguardi Burgio Marco , Vilgrain Valérie 
Published: February 2024

AbstractLiver diseases in pregnancy can be specific to gestation or only coincidental. In the latter case, the diagnosis can be difficult. Rapid diagnosis of maternal-fetal emergencies and situations requiring specialized interventions are crucial to preserve the maternal liver and guarantee materno-fetal survival. While detailed questioning of the patient and a clinical examination are highly important, imaging is often essential to reach a diagnosis of these liver diseases and lesions. Three groups of liver diseases may be observed during pregnancy: (1) diseases related to pregnancy: intrahepatic cholestasis of pregnancy, pre-eclampsia, eclampsia, hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome, and acute fatty liver of pregnancy; (2) liver diseases that are more frequent during or exacerbated by pregnancy: acute herpes simplex hepatitis, Budd-Chiari syndrome, hemorrhagic hereditary telangiectasia, hepatocellular adenoma, portal vein thrombosis, and cholelithiasis; (3) coincidental conditions, including acute hepatitis, incidental focal liver lesions, metabolic dysfunction–associated steatotic liver disease, cirrhosis, hepatocellular carcinoma, liver abscesses and parasitosis, and liver transplantation. Specific knowledge of the main imaging findings is required to reach an early diagnosis, for adequate follow-up, and to avoid adverse consequences in both the mother and the fetus.Critical relevance statement Pregnancy-related liver diseases are the most important cause of liver dysfunction in pregnant patients and, in pregnancy, even common liver conditions can have an unexpected turn. Fear of radiations should never delay necessary imaging studies in pregnancy.Key points• Pregnancy-related liver diseases are the most frequent cause of liver dysfunction during gestation.• Fear of radiation should never delay necessary imaging studies.• Liver imaging is important to assess liver emergencies and for the diagnosis and follow-up of any other liver diseases.• Common liver conditions and lesions may take an unexpected turn during pregnancy.• Pregnancy-specific diseases such as pre-eclampsia and HELLP syndrome must be rapidly identified. However, imaging should never delay delivery when it is considered to be urgent for maternal-fetal survival.
Graphical Abstract
Review of strategies to reduce the contamination of the water environment by gadolinium-based contrast agents
Authors: Dekker Helena M. , Stroomberg Gerard J. , Van der Molen Aart J. , Prokop Mathias 
Published: February 2024

AbstractGadolinium-based contrast agents (GBCA) are essential for diagnostic MRI examinations. GBCA are only used in small quantities on a per-patient basis; however, the acquisition of contrast-enhanced MRI examinations worldwide results in the use of many thousands of litres of GBCA per year. Data shows that these GBCA are present in sewage water, surface water, and drinking water in many regions of the world. Therefore, there is growing concern regarding the environmental impact of GBCA because of their ubiquitous presence in the aquatic environment. To address the problem of GBCA in the water system as a whole, collaboration is necessary between all stakeholders, including the producers of GBCA, medical professionals and importantly, the consumers of drinking water, i.e. the patients. This paper aims to make healthcare professionals aware of the opportunity to take the lead in making informed decisions about the use of GBCA and provides an overview of the different options for action.In this paper, we first provide a summary on the metabolism and clinical use of GBCA, then the environmental fate and observations of GBCA, followed by measures to reduce the use of GBCA. The environmental impact of GBCA can be reduced by (1) measures focusing on the application of GBCA by means of weight-based contrast volume reduction, GBCA with higher relaxivity per mmol of Gd, contrast-enhancing sequences, and post-processing; and (2) measures that reduce the waste of GBCA, including the use of bulk packaging and collecting residues of GBCA at the point of application.Critical relevance statement This review aims to make healthcare professionals aware of the environmental impact of GBCA and the opportunity for them to take the lead in making informed decisions about GBCA use and the different options to reduce its environmental burden.Key points• Gadolinium-based contrast agents are found in sources of drinking water and constitute an environmental risk.• Radiologists have a wide spectrum of options to reduce GBCA use without compromising diagnostic quality.• Radiology can become more sustainable by adopting such measures in clinical practice.
Graphical Abstract
The value of periportal hyperintensity sign from gadobenate dimeglumine-enhanced hepatobiliary phase MRI for predicting clinical outcomes in patients with decompensated cirrhosis
Authors: Cong Lanqing , Deng Yan , Cai Shuo , Wang Gongzheng , Zhao Xinya , He Jingzhen , Zhao Songbo , Wang Li 
Published: February 2024

Abstract
Objectives
To determine the value of periportal hyperintensity sign from gadobenate dimeglumine (Gd-BOPTA)-enhanced hepatobiliary phase (HBP) magnetic resonance imaging (MRI) for predicting clinical outcomes in patients with decompensated cirrhosis.

Methods
A total of 199 cirrhotic patients who underwent Gd-BOPTA-enhanced MRI were divided into control group (n  =  56) and decompensated cirrhosis group (n  =  143). The presence of periportal hyperintensity sign on HBP MRI was recorded. The Cox regression model was used to investigate the association between periportal hyperintensity sign and clinical outcomes.

Results
There was a significant difference in the frequency of periportal hyperintensity sign on HBP between compensated and decompensated cirrhotic patients (p  <  0.05). After a median follow-up of 29.0 months (range, 1.0–90.0 months), nine out of 143 patients (6.2%) with decompensated cirrhosis died. Periportal hyperintensity sign on HBP MRI was a significant risk factor for death (hazard ratio (HR)  =  23.677; 95% confidence interval (CI)  =  4.759–117.788; p  =  0.0001), with an area under the curve (AUC) of 0.844 (95% CI  =  0.774–0.899). Thirty patients (20.9%) developed further decompensation. Periportal hyperintensity sign on HBP MRI was also a significant risk factor for further decompensation (HR  =  2.594; 95% CI  =  1.140–5.903; p  =  0.023).

Conclusions
Periportal hyperintensity sign from Gd-BOPTA-enhanced HBP MRI is valuable for predicting clinical outcomes in patients with decompensated cirrhosis.

Critical relevance statement
Periportal hyperintensity sign from gadobenate dimeglumine-enhanced hepatobiliary phase magnetic resonance imaging is a new noninvasive method to predict clinical outcomes in patients with decompensated cirrhosis.

Key points
• There was a significant difference in the frequency of periportal hyperintensity sign on HBP between compensated and decompensated cirrhotic patients.
• Periportal hyperintensity sign on the hepatobiliary phase was a significant risk factor for death in patients with decompensated cirrhosis.
• Periportal hyperintensity sign on the hepatobiliary phase was a significant risk factor for further decompensation in patients with decompensated cirrhosis.

Graphical Abstract
Azathioprine and hydroxychloroquine overdose in Sjögren’s syndrome patient with hypocalcemia: a case report
Authors: Kooshki Alireza , Mehrpour Omid , Nakhaee Samaneh 
Published: February 2024

AbstractIntroductionHydroxychloroquine and azathioprine have been routinely used to control and treat primary and secondary Sjögren’s syndrome, which potentially triggered some overdoses by these drugs. Toxicity from hydroxychloroquine and azathioprine manifests in the form of cardiac conduction abnormalities, nausea, vomiting, and muscle weakness. Recognizing these unique drug overdoses and management of these toxicities is important. This case report aims to expand our current understanding of these drug overdoses and their management and also underscores the importance of anticipating and identifying fewer common complications, such as hypocalcemia.Case reportA 34-year-old Persian woman with a history of Sjögren’s syndrome presented to the emergency department 3.5–4 hours after an intentional overdose of hydroxychloroquine and azathioprine and severe hypotension and loss of consciousness. Although the patient was regularly taking other medications, such as fluoxetine, naproxen, and prednisolone, she explicitly clarified that these were not the substances involved in her overdose. Early investigations showed hypokalemia (2.4 mEq/L), hypocalcemia (7.5 mg/dL), and hypoglycemia (65 mg/dL). She was also diagnosed with metabolic acidosis and respiratory alkalosis. The electrocardiogram showed changes in favor of hypokalemia; other lab tests were run on the patient. Supportive treatments were applied, including rapid intravenous fluid dextrose 5%, normal saline, potassium chloride 30 mEq, and calcium gluconate 100 mg. The patient was managed and monitored overnight in the emergency room and recovered without residual side effects.ConclusionHydroxychloroquine and azathioprine toxicity are considered rare, but it is likely to increase in frequency given the prevalence and increase in autoimmune diseases and the increasing usage of these drugs in treating such diseases. We found hypocalcemia as the presentation to this patient, which needs further investigation into the probable mechanism. Clinicians need to consider the unique effects of hydroxychloroquine and azathioprine poisoning and initiate appropriate emergency interventions to improve the outcomes in similar patients.
Oxidized SOD1 accelerates cellular senescence in neural stem cells
Authors: Guan Teng , Guo Ying , Zhou Ting , Yu Qiang , Sun Jingyi , Sun Baoliang , Zhang Guohui , Kong Jiming 
Published: February 2024

Abstract
Background
Neural stem cells (NSCs), especially human NSCs, undergo cellular senescence characterized by an irreversible proliferation arrest and loss of stemness after prolonged culture. While compelling correlative data have been generated to support the oxidative stress theory as one of the primary determinants of cellular senescence of NSCs, a direct cause-and-effect relationship between the accumulation of oxidation-mediated damage and cellular senescence of NSCs has yet to be firmly established. Human SOD1 (hSOD1) is susceptible to oxidation. Once oxidized, it undergoes aberrant misfolding and gains toxic properties associated with age-related neurodegenerative disorders. The present study aims to examine the role of oxidized hSOD1 in the senescence of NSCs.

Methods
NSCs prepared from transgenic mice expressing the wild-type hSOD1 gene were maintained in culture through repeated passages. Extracellular vesicles (EVs) were isolated from culture media at each passage. To selectively knock down oxidized SOD1 in NSCs and EVs, we used a peptide-directed chaperone-mediated protein degradation system named CT4 that we developed recently.

Results
In NSCs expressing the hSOD1 from passage 5, we detected a significant increase of oxidized hSOD1 and an increased expression of biomarkers of cellular senescence, including upregulation of P53 and SA-β-Gal and cytoplasmic translocation of HMGB1. The removal of oxidized SOD1 remarkably increased the proliferation and stemness of the NSCs. Meanwhile, EVs derived from senescent NSCs carrying the wild-type hSOD1 contained high levels of oxidized hSOD1, which could accelerate the senescence of young NSCs and induce the death of cultured neurons. The removal of oxidized hSOD1 from the EVs abolished their senescence-inducing activity. Blocking oxidized SOD1 on EVs with the SOD1 binding domain of the CT4 peptide mitigated its toxicity to neurons.

Conclusion
Oxidized hSOD1 is a causal factor in the cellular senescence of NSCs. The removal of oxidized hSOD1 is a strategy to rejuvenate NSCs and to improve the quality of EVs derived from senescent cells.
“When everyone is responsible, no one takes responsibility”: exploring pediatric physiotherapy services in Israel
Authors: Waiserberg Nilly , Horev Tuvia , Feder-Bubis Paula 
Published: February 2024

Abstract
Background
According to Israel's National Health Insurance Law (1994), the Ministry of Health is responsible for the provision of health services in the country including physiotherapy services; moreover, the Special Education Law (1988), stipulates that physiotherapy services for children with motor disabilities, as well as other allied health services, are provided by the Ministry of Education in educational settings. Thus, children with motor disabilities are entitled PT services under two different laws by two different ministries.

Method
To describe the physiotherapy services for children with motor disabilities and examine how policymakers view these services, we conducted a qualitative study including in-depth semi-structured interviews with 10 policymakers from the Ministry of Health and the Ministry of Education, and the national directors of physiotherapy services from three of the four health maintenance organizations in Israel.

Results
Study results indicate that there is an array of physiotherapy services and providers. Despite the regulation of these services for children with motor disabilities, uncertainty and lack of knowledge were found about various issues. Therefore, the thematic analysis was structured around four descriptive questions: Where do the children receive physiotherapy? Who is eligible for physiotherapy treatment and who receives treatment? What interventions do children with motor disabilities receive? Who provides therapy for children with motor disabilities?

Conclusions
Policymakers are dubious regarding the provision of these services, questioning whether children with motor disabilities receive physiotherapy services according to their needs. In addition, the abundance of suppliers does not necessarily improve the quality of services provided to children with motor disabilities, which may ultimately harm their developmental potential.
Some existence results for a differential equation and an inclusion of fractional order via (convex) F-contraction mapping
Authors: Roomi Vahid , Afshari Hojjat , Kalantari Sabileh 
Published: February 2024

AbstractThe existence of solutions for a class of μ-Caputo fractional differential equations and an inclusion problem equipped with nonlocal μ-integral boundary conditions are investigated. We use F-contraction, convex F-contraction, and some consequences to achieve the desired goals. Finally, some examples are provided to illustrate the results.
Therapeutics for neurodegenerative diseases by targeting the gut microbiome: from bench to bedside
Authors: Ma Yuan-Yuan , Li Xin , Yu Jin-Tai , Wang Yan-Jiang 
Published: February 2024

AbstractThe aetiologies and origins of neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD), are complex and multifaceted. A growing body of evidence suggests that the gut microbiome plays crucial roles in the development and progression of neurodegenerative diseases. Clinicians have come to realize that therapeutics targeting the gut microbiome have the potential to halt the progression of neurodegenerative diseases. This narrative review examines the alterations in the gut microbiome in AD, PD, ALS and HD, highlighting the close relationship between the gut microbiome and the brain in neurodegenerative diseases. Processes that mediate the gut microbiome–brain communication in neurodegenerative diseases, including the immunological, vagus nerve and circulatory pathways, are evaluated. Furthermore, we summarize potential therapeutics for neurodegenerative diseases that modify the gut microbiome and its metabolites, including diets, probiotics and prebiotics, microbial metabolites, antibacterials and faecal microbiome transplantation. Finally, current challenges and future directions are discussed.