tbuckley/cabot-search huggingface dataset:
When I use a word . . . Academic publishing: the impact factor
Authors: Jeffrey K Aronson
Journal: BMJ (2025)

The citation index, first seeded as an embryo by the information scientist Eugene Garfield in the 1950s, was delivered in the 1960s as a fully formed child, the Science Citation Index. Its twin brother was the journal impact factor. Defined as the average number of citations that a journal's citable papers receive, the impact factor was originally intended by Garfield to be a tracking device and a retrieval tool, particularly so that fraudulent, incomplete, or obsolete data could be more easily detected. However, since then it has been repeatedly used to assess the quality of authors' research, particularly for purposes of funding and awarding tenure, against Garfield's advice that this was not a legitimate use. This has led to a regrettable "publish or perish" culture in academic research, with knock-on effects, such as paper mills and predatory journals, and neglect of other academic contributions, such as teaching and mentoring, reviewing and editing scholarly texts, contributions to policy, and, in medical practice, work at the bedside or in the clinic, all of which have suffered as a result.
Effect of sotagliflozin on major adverse cardiovascular events: a prespecified secondary analysis of the SCORED randomised trial
Authors: Rahul Aggarwal, Deepak L Bhatt, Michael Szarek, Christopher P Cannon, Lawrence A Leiter, Silvio E Inzucchi, Renato D Lopes, Darren K McGuire, Julia B Lewis, Matthew C Riddle, Michael J Davies, Phillip Banks, Amy K Carroll, Benjamin M Scirica, Kausik K Ray, Mikhail N Kosiborod, David Z I Cherney, Jacob A Udell, Subodh Verma, R Preston Mason, Bertram Pitt, Ph Gabriel Steg
Journal: The Lancet Diabetes & Endocrinology (2025)
Association of life-course events with predictors of HIV risk behaviour and HIV acquisition in Manicaland, Zimbabwe: a longitudinal analysis of a population cohort
Authors: Michael Pickles, Simon Gregson, Louisa Moorhouse, Rufurwokuda Maswera, Blessing Tsenesa, Freedom Dzamatira, Phyllis Mandizvidza, Sophie Bagnay, Tawanda Dadirai, Brian Kumbirai Moyo, Owen Mugurungi, Constance Nyamukapa, Timothy B Hallett
Journal: The Lancet HIV (2025)

An individual's HIV risk, and consequently their HIV prevention needs, change over time. In this study we aimed to quantify these changes, examine which life-course events were associated with them, and investigate the extent to which those life-course events were associated with HIV acquisition. We used longitudinal data from eight rounds of a general population cohort in Manicaland province, eastern Zimbabwe, on sociodemographic and HIV risk behaviours, as well as HIV serostatus from the first seven rounds. We first visualised how HIV risk behaviours, comprised of having multiple, concurrent, non-regular, or transactional partners, condom non-use, drug use, and visiting bars, changed for individuals over time using Sankey diagrams. We then examined whether logistic regression models incorporating life-course events-namely, changes in marital or employment status, in-migration, or birth of a child-were more strongly associated with changes in HIV risk behaviour than models using only sociodemographic variables. Finally, we compared how well sociodemographic, HIV risk behaviour, and life-course events were associated with the person's risk of HIV acquisition as follows: we used logistic regression to identify which states (divided into sociodemographic, HIV risk behaviour, and life-course events) were most strongly associated with risk of HIV acquisition; based on this we use three models (corresponding to the three divisions) to identify the top 20% of individuals predicted to be at risk of acquiring HIV by each model, and computed what proportion of the actual HIV infection events occurred in that group. Between 1998 and 2021, 21 213 individuals were interviewed at least twice, contributing a total of 34 212 participant observations. In this setting, individuals had periods of HIV risk lasting less than 3 years; only 12·3% (102 of 831) of those reporting transactional sex had also reported this in the previous round. We found that life-course events such as changes in marital status, employment status, and in-migrant status were associated with these changes in HIV risk behaviour. Using life-course events, particularly ones related to changes in marital status, 23% and 30% more HIV acquisitions were identified than using HIV risk behaviours or sociodemographic information, respectively. HIV risk changes dynamically in this population, and life-course events could be a powerful way to understand changes in HIV risk behaviour and risk of HIV acquisition. Bill and Melinda Gates Foundation, UK Medical Research Council, and Department for International Development.
Decoding Immunobiology Through Genetic Errors of Immunity
Authors: Mackenzie J. Bender, Carrie L. Lucas
Journal: Annual Review of Immunology (2025)

Throughout biology, the pursuit of genotype-phenotype relationships has provided foundational knowledge upon which new concepts and hypotheses are built. Genetic perturbation, whether occurring naturally or in experimental settings, is the mainstay of mechanistic dissection in biological systems. The unbiased discovery of causal genetic lesions via forward genetics in patients who have a rare disease elucidates a particularly impactful set of genotype-phenotype relationships. Here, we review the field of genetic errors of immunity, often termed inborn errors of immunity (IEIs), in a framework aimed at highlighting the powerful real-world immunology insights provided collectively and individually by these (approximately) 500 disorders. By conceptualizing essential immune functions in a model of the adaptive arsenal of rapid defenses, we organize IEIs based on immune circuits in which sensors, relays, and executioners cooperate to carry out pathogen clearance functions in an effective yet regulated manner. We review and discuss findings from IEIs that not only reinforce known immunology concepts but also offer surprising phenotypes, prompting an opportunity to refine our understanding of immune system function.
Developmental Origins and Oncogenesis in Medulloblastoma
Authors: Karrie M. Kiang, Yogesh K.H. Wong, Soma Sengupta, Martine F. Roussel, Q. Richard Lu
Journal: Annual Review of Neuroscience (2025)

Medulloblastoma is the most common pediatric brain cancer and is broadly categorized into four molecular subgroups. Understanding the cell origins of medulloblastoma is crucial for preventing tumor formation and relapse. Recent single-cell transcriptomics studies have identified the potential cell lineage vulnerabilities and mechanisms underpinning malignant transformation in medulloblastoma. Emerging evidence suggests that genetic-epigenetic alterations specific to each subgroup lead to a lineage-specific stall in the neural developmental program and subsequent tumorigenesis. We discuss the putative cells of origin, plasticity, and heterogeneity within medulloblastoma subgroups and delve into the genetic and epigenetic changes that predispose cells to transformation. Additionally, we review the current insights into how cerebellar stem/progenitor cells and lineage plasticity impact medulloblastoma pathogenesis and highlight recent therapeutic advances targeting specific oncogenic vulnerabilities in this malignancy.
Anxiety and Related Disorders During the Perinatal Period
Authors: Nichole Fairbrother, Fiona L. Challacombe, Sheryl M. Green, Heather A. O'Mahen
Journal: Annual Review of Clinical Psychology (2025)

Anxiety and anxiety-related disorders are, as a group, the most common mental health conditions and are more common among women compared with among men. It is now evident that these disorders affect one in five pregnant and postpartum people and are more common than depression. For some disorders (e.g., obsessive–compulsive disorder), there is also evidence of an elevated risk for their development and exacerbation during perinatal periods. In this article, we review the literature pertaining to anxiety and anxiety-related disorders during the perinatal period. We also provide information related to pregnancy-specific anxiety and fear of childbirth constructs that exist outside of diagnostic classification but are particularly important in the perinatal context. We review the scope, prevalence, and etiology of these disorders as well as comorbidity, screening, assessment, and treatment. We conclude with an overview of some of the key gaps in knowledge and recommendations for future research.
Identifying major depressive disorder in older adults through naturalistic driving behaviors and machine learning
Authors: Chen Chen, David C. Brown, Noor Al-Hammadi, Sayeh Bayat, Anne Dickerson, Brenda Vrkljan, Matthew Blake, Yiqi Zhu, Jean-Francois Trani, Eric J. Lenze, David B. Carr, Ganesh M. Babulal
Journal: npj Digital Medicine (2025)

Abstract Depression in older adults is often underdiagnosed and has been linked to adverse outcomes, including motor vehicle crashes. With a growing population of older drivers in the United States, innovations in screening methods are needed to identify older adults at greatest risk of decline. This study used machine learning techniques to analyze real-world naturalistic driving data to identify depression status in older adults and examined whether specific demographics and medications improved model performance. We analyzed two years of GPS data from 157 older adults, including 81 with major depressive disorder, using XGBoost and logistic regression models. The top-performing model achieved an area under the curve of 0.86 with driving features combined with total medication use. These findings suggest that naturalistic driving data holds high potential as a functional digital neurobehavioral marker for AI identifying depression in older adults on a national scale, thereby ensuring equitable access to treatment.
From challenges and pitfalls to recommendations and opportunities: Implementing federated learning in healthcare
Authors: Ming Li, Pengcheng Xu, Junjie Hu, Zeyu Tang, Guang Yang
Journal: Medical Image Analysis (2025)

Federated learning holds great potential for enabling large-scale healthcare research and collaboration across multiple centers while ensuring data privacy and security are not compromised. Although numerous recent studies suggest or utilize federated learning based methods in healthcare, it remains unclear which ones have potential clinical utility. This review paper considers and analyzes the most recent studies up to May 2024 that describe federated learning based methods in healthcare. After a thorough review, we find that the vast majority are not appropriate for clinical use due to their methodological flaws and/or underlying biases which include but are not limited to privacy concerns, generalization issues, and communication costs. As a result, the effectiveness of federated learning in healthcare is significantly compromised. To overcome these challenges, we provide recommendations and promising opportunities that might be implemented to resolve these problems and improve the quality of model development in federated learning with healthcare.
Past, present and future epidemiology of echinococcosis in China based on nationwide surveillance data 2004–2022
Authors: Xu Wang, Yan Kui, Chui-Zhao Xue, Qian Wang, Can-Jun Zheng, Jiang-Shan Zhao, Ya-Ming Yang, Xiao-Feng Jiang, Qu-Zhen Gong-Sang, Xiao Ma, Yu Feng, Xiang-Lin Wu, Sa Chen, Fan-Ka Li, Wen-Jie Yu, Ben-Fu Li, Bai-Xue Liu, Ying Wang, Li-Ying Wang, Shi-Jie Yang, Zheng-Huan Wang, Wei Hu, Yu-Juan Shen, Wen-Bao Zhang, Philip S Craig, Wei-Ping Wu, Ning Xiao, Shuai Han, Xiao-Nong Zhou, Shi-Zhu Li, Jian-Ping Cao
Journal: Journal of Infection (2025)

We evaluated the epidemiological characteristics of echinococcosis, a global public health threat, in China to inform global control efforts. Descriptive, statistical, cluster, spatial, and trend analyses were used to evaluate the epidemiology at national, provincial, and county levels based on 2004-2022 nationwide surveillance data from China. Between 2004 and 2022, China recorded 72,676 cystic echinococcosis (CE) cases, 11,465 alveolar echinococcosis (AE) cases, and 5703 others, with an average annual cases per million (ANpM) of 3.45. Females had a higher incidence (ANpM = 3.87) than males (3.05), with most cases (41.15%) in the 30-49 age group, mainly among herders (38.76%) and farmers (37.82%). Seven provinces (Xizang, Qinghai, Xinjiang, Ningxia, Gansu, Sichuan, and Inner Mongolia) accounted for 98.12% of cases, with the Tibetan Plateau showing the highest rates (ANpMs = 155.51 for CE, 46.95 for AE). Surgery and case fatality rates were 39.45% and 5.23% in key surveillance regions (KSRs). Prevalence among residents (0.20%), livestock (1.33%), rodents (1.30%), and dogs (1.26%) declined with increased control funding in KSRs. Between 2023 and 2030, there will be an estimated 20,096 new cases and 45,323 cases requiring treatment. The prevalence of echinococcosis has been alleviated in China, but significant control challenges remain, requiring sustained and targeted control measures.
A national registry study evaluated the landscape of kidney transplantation among presumed unauthorized immigrants in the United States.
Authors: Gayathri Menon, Garyn T Metoyer, Yiting Li, Yusi Chen, Sunjae Bae, Mario P DeMarco, Brian P Lee, Pablo C Loarte-Campos, Babak J Orandi, Dorry L Segev, Mara A McAdams-DeMarco
Journal: Kidney International (2025)
Glucose-Dependent Insulinotropic Polypeptide in Incretin Physiology: Role in Health and Disease
Authors: M Michael Wolfe, Michael O Boylan, Wiliam W Chin
Journal: Endocrine Reviews (2025)

Abstract Glucose-dependent insulinotropic polypeptide (GIP) is a 42-amino acid hormone that is synthesized and released from upper intestinal enteroendocrine K-cells in response to the ingestion of glucose or fat. The structure of GIP places it in the secretin/vasoactive intestinal polypeptide family of gastrointestinal regulatory peptides. Although originally named “gastric inhibitory polypeptide” on the basis of its ability to inhibit gastric acid secretion, GIP accounts for 60%-80% of the postprandial insulin response, consistent with the notion that this regulatory peptide constitutes the principal physiological incretin. Under normal conditions, GIP plays a major role in nutrient deposition and storage, both directly through its insulin mimetic properties and indirectly by enhancing insulin release. GIP is overexpressed in obese individuals, which may exacerbate insulin resistance manifested by many patients with type 2 diabetes mellitus. Enhanced postprandial secretion of GIP also initiates a vicious cycle characterized by increased nutrient uptake and storage in adipocytes, leading to insulin resistance and hyperinsulinemia, which then further increases adipocyte nutrient uptake and storage. Despite the deleterious consequences of GIP overexpression, when combined with glucagon-like peptide-1 analogues, GIP agonism has been demonstrated to provide benefit in treating obesity by mechanisms currently not fully elucidated. In contrast, consistent with the etiologic role of GIP overexpression in the pathogenesis of obesity, both genetic abrogation and immunoneutralization of GIP signaling have been shown to reduce the development of obesity in preclinical models. Whether these beneficial effects of GIP antagonism will be extended to humans needs to be determined.
Linking vaccine adjuvant mechanisms of action to function
Authors: Elana Ben-Akiva, Asheley Chapman, Tianyang Mao, Darrell J. Irvine
Journal: Science Immunology (2025)

Vaccines deliver an immunogen in a manner designed to safely provoke an immune response, leading to the generation of memory T and B cells and long-lived antibody-producing plasma cells. Adjuvants play a critical role in vaccines by controlling how the immune system is exposed to the immunogen and providing inflammatory cues that enable productive immune priming. However, mechanisms of action underlying adjuvant function at the molecular, cell, and tissue levels are diverse and often poorly understood. Here, we review the current understanding of mechanisms of action underlying adjuvants used in subunit protein/polysaccharide vaccines and mRNA vaccines, discuss where possible how these mechanisms of action link to downstream effects on the immune response, and identify knowledge gaps that will be important to fill in order to enable the continued development of more effective adjuvants for challenging pathogens such as HIV and emerging threats.
TRAF3 is critical for initial T follicular helper cell specification via coordination of the IL-6R/IL-2R–BCL6 signaling nexus
Authors: Peng Shao, Regina M. Antonetti, Tina Arkee, Emma L. Hornick, Hai Hui Xue, Gail A. Bishop, Noah S. Butler
Journal: Science Immunology (2025)

CD4 + T follicular helper (T FH ) cells are essential for orchestrating robust humoral immunity, yet the signals that initiate T FH cell differentiation are not fully understood. We identified that the adapter protein TRAF3 was required for T FH cell differentiation and function during systemic inflammatory infections. Loss of CD4 + T cell–intrinsic TRAF3 impaired chromatin remodeling and transcriptional programming essential for T FH cell initiation and instead augmented T H 1 development and function. TRAF3-deficient CD4 + T cells exhibited altered interleukin-6 (IL-6) and IL-2 responsiveness, which were coupled to failures in BCL6 expression. Enforced expression of either IL-6 receptor or BCL6 or blockade of IL-2 signaling was sufficient to rescue T FH cell differentiation. Human CD4 + T cells lacking TRAF3 exhibited impaired T FH polarization, supporting a conserved mechanism by which TRAF3 regulates CD4 + T cell fate determination. Thus, TRAF3 functions at the nexus of cytokine, transcriptional, and epigenetic nodes that promote the T FH cell specification during infection.
An international perspective on the future of systemic sclerosis research
Authors: David J. Abraham, Carol M. Black, Christopher P. Denton, Jörg H. W. Distler, Robyn Domsic, Carol Feghali-Bostwick, Pravitt Gourh, Monique Hinchcliff, Fred Kolling, Masataka Kuwana, Robert Lafyatis, Ulf Landegren, J. Matthew Mahoney, Javier Martin, Marco Matucci-Cerinic, Zsuzsanna H. McMahan, Ana L. Mora, Luc Mouthon, Marlene Rabinovitch, Mauricio Rojas, Kristofer Rubin, Maria Trojanowska, John Varga, Michael L. Whitfield, Armando Gabrielli, Thomas Krieg
Journal: Nature Reviews Rheumatology (2025)
Towards understanding cancer dormancy over strategic hitching up mechanisms to technologies
Authors: Sumin Yang, Jieun Seo, Jeonghyeon Choi, Sung-Hyun Kim, Yunmin Kuk, Kyung Chan Park, Mingon Kang, Sangwon Byun, Jae-Yeol Joo
Journal: Molecular Cancer (2025)

Delving into cancer dormancy has been an inherent task that may drive the lethal recurrence of cancer after primary tumor relief. Cells in quiescence can survive for a short or long term in silence, may undergo genetic or epigenetic changes, and can initiate relapse through certain contextual cues. The state of dormancy can be induced by multiple conditions including cancer drug treatment, in turn, undergoes a life cycle that generally occurs through dissemination, invasion, intravasation, circulation, immune evasion, extravasation, and colonization. Throughout this cascade, a cellular machinery governs the fate of individual cells, largely affected by gene regulation. Despite its significance, a precise view of cancer dormancy is yet hampered. Revolutionizing advanced single cell and long read sequencing through analysis methodologies and artificial intelligence, the most recent stage in the research tool progress, is expected to provide a holistic view of the diverse aspects of cancer dormancy.
Cost Sharing for Preferred Branded Drugs in Medicare Part D
Authors: Erin Trish, Barbara Blaylock, Karen Van Nuys
Journal: JAMA (2025)

This study uses data from the Centers for Medicare &amp;amp;amp; Medicaid Services Public Use Files to examine the use of co-payments and co-insurance for preferred brand-name drugs among Medicare Part D plans from 2020 to 2024 and characterize beneficiary exposure to these trends.
Prostate Cancer Mortality in Men Aged 70 Years Who Recently Underwent Prostate-Specific Antigen Screening
Authors: Dana H. Chung, Tanner J. Caverly, Matthew J. Schipper, Timothy P. Hofer, Roman Gulati, Brent S. Rose, Megan E. V. Caram, Phoebe A. Tsao, Kristian D. Stensland, David Elliott, Sameer D. Saini, Alex K. Bryant
Journal: JAMA Network Open (2025)

Importance Continuing prostate-specific antigen (PSA) screening after age 70 years might benefit men at high risk of prostate cancer–specific mortality (PCSM) or metastatic prostate cancer (mPCa), but the relative value of clinical factors (race and ethnicity, competing mortality, and PSA history) in identifying men at higher vs lower risk is unknown. Objective To examine the value of PSA levels, race and ethnicity, and competing mortality in risk stratification for PCSM and mPCa in men after age 70 years. Design, Setting, and Participants In this cohort study, clinical data of all men receiving health care through the Veterans Health Administration who turned age 70 years between 2008 and 2020 and had a normal screening PSA value between age 65 and 69 years (&amp;amp;lt;4 ng/mL [baseline PSA]) and no prior history of prostate cancer or biopsy were examined. The data cutoff date was December 26, 2023. Exposure The most recent screening PSA value from age 65 to 69 years, self-reported race and ethnicity, and competing mortality risk derived from a machine learning model. Main Outcome and Measures The 10-year absolute risk of PCSM and mPCa were determined using regression modeling. Results The cohort included 921 609 men who turned 70 years between 2008 and 2020; 11% of whom self-reported as Black and 82% as White race. Between age 65 and 70 years, 45% of patients had a baseline PSA of less than 1.00 ng/mL, and 32% had a baseline PSA of 1.00 to 1.99 ng/mL. Most patients (87%) continued to undergo screening past age 70 years, with little variation by competing mortality risk or race and ethnicity. The 10-year cumulative incidence of PCSM was 0.26% overall, and 95% of men had a 10-year risk less than 0.73%. Higher baseline PSA level between age 65 and 69 years was associated with 10-year PCSM risk (0.79% for 3.00-3.99 ng/mL vs 0.10% for 0.20-0.99 ng/mL), race and ethnicity (0.36% for Black vs 0.25% for White), and competing mortality (0.24% for the highest quintile vs 0.21% for the lowest quintile). Similar results were found for mPCa. Low PSA (0.20-0.99 ng/mL) was associated with very low PCSM and mPCa risk, even among Black men in the healthiest quintile of competing mortality risk (10-year PCSM risk, 0.08% [95% CI, 0.01%-0.44%]; 10-year mPCa risk 0.24% [95% CI, 0.10%-0.52%]). Conclusions and Relevance In this cohort study, the findings suggest that most men receiving care through the VHA continue PSA screening after age 70 years despite low absolute 10-year PCSM risks. The PSA values from age 65 to 69 years may be highly informative for adverse prostate cancer outcomes after age 70 years, with a PSA less than 1 ng/mL associated with a very low risk of long-term PCSM and mPCa.