Infectious disease often occurs in small, independent outbreaks in populations with varying characteristics. Each outbreak by itself may provide too little information for accurate estimation of epidemic model parameters. Here we show that using standard stochastic epidemic models for each outbreak and allowing parameters to vary between outbreaks according to a linear predictor leads to a generalized linear model that accurately estimates parameters from many small and diverse outbreaks. By estimating initial growth rates in addition to transmission rates, we are able to characterize variation in numbers of initially susceptible individuals or contact patterns between outbreaks. With simulation, we find that the estimates are fairly robust to the data being collected at discrete intervals and imputation of about half of all infectious periods. We apply the method by fitting data from 75 norovirus outbreaks in health-care settings. Our baseline regression estimates are 0.0037 transmissions per infective-susceptible day, an initial growth rate of 0.27 transmissions per infective day, and a symptomatic period of 3.35 days. Outbreaks in long-term-care facilities had significantly higher transmission and initial growth rates than outbreaks in hospitals.
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http://dx.doi.org/10.1016/j.epidem.2013.12.002 | DOI Listing |
Cell Commun Signal
January 2025
Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.
Background: Ovarian cancer (OC), particularly high-grade serous ovarian carcinoma (HGSOC), is the leading cause of mortality from gynecological malignancies worldwide. Despite the initial effectiveness of treatment, acquired resistance to poly(ADP-ribose) polymerase inhibitors (PARPis) represents a major challenge for the clinical management of HGSOC, highlighting the necessity for the development of novel therapeutic strategies. This study investigated the role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a pivotal regulator of glycolysis, in PARPi resistance and explored its potential as a therapeutic target to overcome PARPi resistance.
View Article and Find Full Text PDFJ Med Case Rep
January 2025
Department of Surgery, Center for Endocrinology, Diabetes and Metabolism, Children's Hospital Los Angeles and Keck School of Medicine of USC, Los Angeles, CA, USA.
Background: Classic congenital adrenal hyperplasia, primarily due to 21-hydroxylase deficiency, leads to impaired cortisol and aldosterone production and excess adrenal androgens. Lifelong glucocorticoid therapy is required, often necessitating supraphysiological doses in youth to manage androgen excess and growth acceleration. These patients experience higher obesity rates, hypertension, and glucose metabolism issues, complicating long-term health management.
View Article and Find Full Text PDFNat Commun
January 2025
Sorbonne Université, CNRS, Laboratory of Computational and Quantitative Biology, LCQB, Paris, France.
Telomere shortening ultimately causes replicative senescence. However, identifying the mechanisms driving replicative senescence in cell populations is challenging due to the heterogeneity of telomere lengths and the asynchrony of senescence onset. Here, we present a mathematical model of telomere shortening and replicative senescence in Saccharomyces cerevisiae which is quantitatively calibrated and validated using data of telomerase-deficient single cells.
View Article and Find Full Text PDFZhonghua Fu Chan Ke Za Zhi
January 2025
Hospital Administration Office, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing100026, China.
To investigate the impact of preconception body mass index (BMI) on neonatal birth weight and the risk of macrosomia in pregnant women across various age groups. A cohort study was conducted, selecting pregnant women who underwent their initial prenatal assessment at Beijing Obstetrics and Gynecology Hospital from September 1st, 2018 to March 31st, 2020. Relevant data were collected from the hospital's electronic medical record system.
View Article and Find Full Text PDFDev Cell
January 2025
Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A8, Canada. Electronic address:
Distinguishing tumor maintenance genes from initiation, progression, and passenger genes is critical for developing effective therapies. We employed a functional genomic approach using the Lazy Piggy transposon to identify tumor maintenance genes in vivo and applied this to sonic hedgehog (SHH) medulloblastoma (MB). Combining Lazy Piggy screening in mice and transcriptomic profiling of human MB, we identified the voltage-gated potassium channel KCNB2 as a candidate maintenance driver.
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