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| 2. |
- Abril, Jazmine, et al.
(författare)
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Associations between pregnancy-related factors and birth characteristics with risk of rare uterine cancer subtypes : a Nordic population-based case-control study
- 2024
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Ingår i: Cancer Causes and Control. - : Springer. - 0957-5243 .- 1573-7225. ; 35:5, s. 741-747
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Uterine sarcomas are a rare group of uterine malignancies. Due to the low incidence and changes in uterine sarcoma classification, risk factors are not well characterized. Our objective was to evaluate risk factors for uterine sarcoma and compare risk factors between uterine sarcoma, malignant mixed Mullerian tumors (MMMTs), and type I endometrial carcinomas.Methods: This nested case-control study utilized linked data from population-based medical birth and cancer registries in Denmark, Finland, Norway, and Sweden. Up to 10 controls were matched on country and birth year for each uterine cancer case. Using multivariable adjusted multinomial logistic regression, estimates of the associations between pregnancy-related factors and risk of uterine sarcoma, MMMTs, and type I endometrial carcinomas were determined.Results: Having a very-low-birth-weight infant (< 1500 vs. 2500-3999 g: OR [95% CI] 2.83 [1.61-4.96]) was associated with an increased risk of uterine sarcoma. Whereas, having a more recent pregnancy was associated with reduced risks of MMMT (< 10 vs. >= 30 years: 0.66 [0.20-2.23]) and type 1 endometrial carcinomas (0.35 [0.30-0.41]) but not uterine sarcomas (1.33 [0.90-1.98], p-heterogeneity < 0.01).Conclusion: Our study provides evidence that risk factors for uterine sarcoma and MMMT, previously grouped with uterine sarcomas, vary substantially. Additionally, MMMT and type I endometrial carcinomas are more similar than uterine sarcoma in that pregnancy complications like gestational hypertension and preeclampsia were associated with reduced risks of both but not uterine sarcoma, suggesting different etiologies.
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| 3. |
- Alm, Sven Erick, et al.
(författare)
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Stokastik
- 2008
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Bok (populärvet., debatt m.m.)
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| 4. |
- Arner, Erik, et al.
(författare)
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Adipocyte Turnover : Relevance to Human Adipose Tissue Morphology
- 2010
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Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 59:1, s. 105-109
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE-Adipose tissue may contain few large adipocytes (hypertrophy) or many small adipocytes (hyperplasia). We investigated factors of putative importance for adipose tissue morphology. RESEARCH DESIGN AND METHODS-Subcutaneous adipocyte size and total fat mass were compared in 764 subjects with BMI 18-60 kg/m(2). A morphology value was defined as tire difference between the measured adipocyte volume and the expected volume given by a curved-line fit for a given body fat mass and was related to insulin values. In 35 subjects, in vivo adipocyte turnover was measured by exploiting incorporation of atmospheric C-14 into DNA. RESULTS-Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but con-elated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (beta-coefficient = 0.3, P < 0.0001). Total adipocyte number and morphology were negatively related (r = -0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P < 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P < 0.001). The relative death rate (similar to 10% per year) or mean age of adipocytes (similar to 10 years) was not correlated with morphology. CONCLUSIONS-Adipose tissue morphology correlates with insulin measures and is linked to the total adipocyte number independently of sex and body fat level. Low generation rates of adipocytes associate with adipose tissue hypertrophy, whereas high generation rates associate with adipose hyperplasia. Diabetes 59:105-109, 2010
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| 5. |
- Ball, Frank, et al.
(författare)
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A network with tunable clustering, degree correlation and degree distribution, and an epidemic thereon
- 2013
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Ingår i: Journal of Mathematical Biology. - : Springer Science and Business Media LLC. - 0303-6812 .- 1432-1416. ; 66:4-5, s. 979-1019
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Tidskriftsartikel (refereegranskat)abstract
- A random network model which allows for tunable, quite general forms of clustering, degree correlation and degree distribution is defined. The model is an extension of the configuration model, in which stubs (half-edges) are paired to form a network. Clustering is obtained by forming small completely connected subgroups, and positive (negative) degree correlation is obtained by connecting a fraction of the stubs with stubs of similar (dissimilar) degree. An SIR (Susceptible Infective Recovered) epidemic model is defined on this network. Asymptotic properties of both the network and the epidemic, as the population size tends to infinity, are derived: the degree distribution, degree correlation and clustering coefficient, as well as a reproduction number , the probability of a major outbreak and the relative size of such an outbreak. The theory is illustrated by Monte Carlo simulations and numerical examples. The main findings are that (1) clustering tends to decrease the spread of disease, (2) the effect of degree correlation is appreciably greater when the disease is close to threshold than when it is well above threshold and (3) disease spread broadly increases with degree correlation when is just above its threshold value of one and decreases with when is well above one.
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| 6. |
- Ball, Frank, et al.
(författare)
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A stochastic SIR network epidemic model with preventive dropping of edges
- 2019
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Ingår i: Journal of Mathematical Biology. - : Springer Science and Business Media LLC. - 0303-6812 .- 1432-1416. ; 78:6, s. 1875-1951
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Tidskriftsartikel (refereegranskat)abstract
- A Markovian Susceptible Infectious Recovered (SIR) model is considered for the spread of an epidemic on a configuration model network, in which susceptible individuals may take preventive measures by dropping edges to infectious neighbours. An effective degree formulation of the model is used in conjunction with the theory of density dependent population processes to obtain a law of large numbers and a functional central limit theorem for the epidemic as the population size N, assuming that the degrees of individuals are bounded. A central limit theorem is conjectured for the final size of the epidemic. The results are obtained for both the Molloy-Reed (in which the degrees of individuals are deterministic) and Newman-Strogatz-Watts (in which the degrees of individuals are independent and identically distributed) versions of the configuration model. The two versions yield the same limiting deterministic model but the asymptotic variances in the central limit theorems are greater in the Newman-Strogatz-Watts version. The basic reproduction number R0 and the process of susceptible individuals in the limiting deterministic model, for the model with dropping of edges, are the same as for a corresponding SIR model without dropping of edges but an increased recovery rate, though, when R0>1, the probability of a major outbreak is greater in the model with dropping of edges. The results are specialised to the model without dropping of edges to yield conjectured central limit theorems for the final size of Markovian SIR epidemics on configuration-model networks, and for the size of the giant components of those networks. The theory is illustrated by numerical studies, which demonstrate that the asymptotic approximations are good, even for moderate N.
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| 7. |
- Ball, Frank, et al.
(författare)
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AN EPIDEMIC IN A DYNAMIC POPULATION WITH IMPORTATION OF INFECTIVES
- 2017
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Ingår i: The Annals of Applied Probability. - 1050-5164 .- 2168-8737. ; 27:1, s. 242-274
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Tidskriftsartikel (refereegranskat)abstract
- Consider a large uniformly mixing dynamic population, which has constant birth rate and exponentially distributed lifetimes, with mean population size n. A Markovian SIR (susceptible -> infective -> recovered) infectious disease, having importation of infectives, taking place in this population is analysed. The main situation treated is where n -> infinity, keeping the basic reproduction number R-0 as well as the importation rate of infectives fixed, but assuming that the quotient of the average infectious period and the average lifetime tends to 0 faster than 1/log n. It is shown that, as n -> infinity, the behaviour of the 3-dimensional process describing the evolution of the fraction of the population that are susceptible, infective and recovered, is encapsulated in a 1-dimensional regenerative process S = {S(t); t >= 0} describing the limiting fraction of the population that are susceptible. The process S grows deterministically, except at one random time point per regenerative cycle, where it jumps down by a size that is completely determined by the waiting time since the start of the regenerative cycle. Properties of the process S, including the jump size and stationary distributions, are determined.
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| 8. |
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| 9. |
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| 10. |
- Ball, Frank, et al.
(författare)
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Epidemics on networks with preventive rewiring
- 2022
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Ingår i: Random structures & algorithms (Print). - : Wiley. - 1042-9832 .- 1098-2418. ; 61:2, s. 250-297
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Tidskriftsartikel (refereegranskat)abstract
- A stochastic SIR (susceptible infective recovered) model is considered for the spread of an epidemic on a network, described initially by an Erdős–Rényi random graph, in which susceptible individuals connected to infectious neighbors may drop or rewire such connections. A novel construction of the model is used to derive a deterministic model for epidemics started with a positive fraction initially infected and prove convergence of the scaled stochastic model to that deterministic model as the population size . For epidemics initiated by a single infective that take off, we prove that for part of the parameter space, in the limit as , the final fraction infected is discontinuous in the infection rate at its threshold , thus not converging to 0 as . The discontinuity is particularly striking when rewiring is necessarily to susceptible individuals in that jumps from 0 to 1 as passes through .
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