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Background: Underlying diseases have a statistically significant positive correlation to sudden death. However, sudden unexplained death (SUD) is different from sudden death, as there is no clinical evidence to support the sudden death due to the original underlying disease, nor a lethal pathological basis to be found during autopsy. In addition, SUD are more common in young, previously healthy individuals, usually without any signs of disease, with no positive lesions found after autopsy. Therefore, a causal relationship between SUD and the underlying disease needs to be further explored. This study aimed to explore the role that common underlying diseases play in patients with SUD and to reveal the correlation between them.
Methods: The medical records, history and case information of 208 patients with SUD were collected for the survey. All these SUD occurred in the emergency room of Peking University Third Hospital from January 2006 to December 2009. The patients were stratified by with and without common underlying diseases. To examine possible associations between the underlying diseases and the cause of unexplained sudden death, the chi-squared and Fisher's exact tests were used.
Results: Among the 208 patients, 65 were diagnosed with common underlying diseases while 143 were not. Within these two groups, there were 45 patients for whom the clear cause of death was determined. However, there were no statistically significant differences or strong associations (χ(2) = 1.238, P > 0.05) between the 11 patients with (16.90%) and 34 without (23.78%) common underlying disease among these 45 patients. We also found that occurrence of the common underlying diseases, such as neurological system, cardiovascular and pulmonary system diseases, are not statistically significant (P > 0.05) in the diagnosis of the SUD.
Conclusion: Common underlying diseases make no obvious contributions to SUD and are not useful in diagnosing the underlying reasons for death.
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Sci China Life Sci
September 2025
State Key Laboratory of Plant Environmental Resilience, College of Life Sciences, Zhejiang University, Hangzhou, 310058, China.
Diurnal floret opening and closure (DFOC) is essential for rice reproductive development and hybrid breeding, yet transcriptional dynamics and underlying regulatory networks remain poorly characterized. Here, we conducted high-temporal-resolution transcriptomic analyses of lodicules to dissect DFOC regulatory networks in two japonica rice cultivars. Analysis of differentially expressed genes (DEGs) uncovered core genes shared by both cultivars, primarily associated with jasmonic acid (JA) signaling and cell wall remodeling.
View Article and Find Full Text PDFBr J Cancer
September 2025
Institute of Life Sciences, Bhubaneswar, Odisha, India.
Background: Docetaxel is the most common chemotherapy regimen for several neoplasms, including advanced OSCC (Oral Squamous Cell Carcinoma). Unfortunately, chemoresistance leads to relapse and adverse disease outcomes.
Methods: We performed CRISPR-based kinome screening to identify potential players of Docetaxel resistance.
Nat Metab
September 2025
Department of Clinical and Biomedical Sciences, Faculty of Health and Life Sciences, University of Exeter, Exeter, UK.
Young-onset monogenic disorders often show variable penetrance, yet the underlying causes remain poorly understood. Uncovering these influences could reveal new biological mechanisms and enhance risk prediction for monogenic diseases. Here we show that polygenic background substantially shapes the clinical presentation of maturity-onset diabetes of the young (MODY), a common monogenic form of diabetes that typically presents in adolescence or early adulthood.
View Article and Find Full Text PDFNat Commun
September 2025
Department of Preventive Medicine, Keck School of Medicine, University of Southern California Norris Comprehensive Cancer Center, Los Angeles, 90033, California, USA.
NPJ Antimicrob Resist
September 2025
Department of Systems Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Studying how antibacterials operate at subinhibitory concentrations reveals how they impede normal growth. While previous works demonstrated drugs can impact multiple aspects of growth, such as prolonging the doubling time or reducing the maximal bacterial load, a systematic understanding of this phenomenon is lacking. It remains unknown if common principles dictate how drugs interfere with growth.
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