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- Ma, Yue, et al.
(författare)
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Acid suppressants use and risk of atherosclerotic cardiovascular disease in middle-aged and older adults
- 2022
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Ingår i: Atherosclerosis. - : Elsevier BV. - 0021-9150. ; 358, s. 47-54
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Tidskriftsartikel (refereegranskat)abstract
- Background and aims: Concerns regarding adverse events associated with the use of acid suppressants have increased. However, the impact of proton pump inhibitors (PPIs) and histamine‐2 receptor antagonists (H2RAs) on the risk of atherosclerotic cardiovascular disease (ASCVD) remains unknown. This study aimed to estimate the risk of ASCVD in association with the use of PPIs and H2RAs. Methods: This prospective cohort study included participants without cardiovascular diseases or anti-hypertensive treatment at baseline (2006–2010) in the UK Biobank. The outcomes were ASCVD and each subtype (coronary artery disease, myocardial infarction, peripheral artery disease, and ischemic stroke). The association was estimated by Cox proportional-hazards models. Results: Among 316,730 individuals (aged 50–88 years), during a median of 12.5 years of follow-up, we documented 13,503 (4.3%) incident ASCVD. Regular PPIs use was associated with a higher risk of ASCVD (HR: 1.16, 95% CI: 1.09–1.23) and every subtype of ASCVD. Among each type of PPIs, omeprazole (HR: 1.19, 95% CI: 1.11–1.28), lansoprazole (HR: 1.11, 95% CI: 1.02–1.22), and pantoprazole (HR: 1.40, 95% CI: 1.00–1.97) were associated with a higher risk of ASCVD. Stratification analysis showed that PPIs use was associated with a higher risk of ASCVD among individuals without indications of medications for PPIs. In addition, use of H2RAs was not related to the risk of ASCVD (HR: 0.97, 95% CI: 0.85–1.11). Conclusions: PPIs were associated with increased risk of ASCVD, particularly amongst participants without indications for medication. Our findings are of important practical significance and suggest that clinicians should be cautious in prophylactic use of PPIs.
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- Sun, Miao, et al.
(författare)
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Maternal androgen excess reduce placental and fetal weights, increase placental steroidogenesis and leads to long-term health effects in their female offspring.
- 2012
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Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 1522-1555 .- 0193-1849. ; 303:11
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Tidskriftsartikel (refereegranskat)abstract
- Here we tested the hypothesis that excess maternal androgen in late pregnancy reduces placental and fetal growth, increases placental steroidogenesis, and adversely affects glucose and lipid metabolism in adult female offspring. Pregnant Wistar rats were randomly assigned to treatment with testosterone (daily injections of 5 mg free testosterone from gestational day 16 to 19) or vehicle alone. In experiment 1, fetal and placental weights, circulating maternal testosterone, estradiol, and corticosterone levels, and placental protein expression and distribution of estrogen receptors α and ß, androgen receptor, and 17 beta-hydroxysteroid dehydrogenase 2 were determined. In experiment 2, birth weights, postnatal growth rates, circulating testosterone, estradiol, and corticosterone levels, insulin sensitivity, adipocyte size, lipid profiles, and the presence of non-alcoholic fatty liver were assessed in female adult offspring. Treatment with testosterone reduced placental and fetal weights and increased placental expression of all four proteins. The offspring of testosterone-treated dams were born with intrauterine growth restriction, however at 6 weeks of age there was no difference in body weight between the offspring of testosterone-, and control-treated rats. At 10-11 weeks of age, the offspring of the testosterone-treated dams had less fat mass and smaller adipocyte size than those born to control rats and had no difference in insulin sensitivity. Circulating triglyceride levels were higher in the offspring of testosterone-treated dams and they developed non-alcoholic fatty liver as adults. We demonstrate for the first time that prenatal testosterone exposure alters placental steroidogenesis and leads to dysregulation of lipid metabolism in their adult female offspring.
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- Wang, Yong, et al.
(författare)
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Research on Pharmaceutical Supply Chain Decision-Making Model Considering Output and Demand Fluctuations
- 2024
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Ingår i: IEEE Access. - : Institute of Electrical and Electronics Engineers (IEEE). - 2169-3536. ; 12, s. 61629-61641
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Tidskriftsartikel (refereegranskat)abstract
- In response to the evolving pharmaceutical supply chain market, which is shifting from a seller's to a buyer's market, this study introduces an innovative decision-making model that addresses the volatility in output and demand. Our primary innovation lies in the development of a "revenue-sharing plus margin" collaborative decision-making optimization model, designed to enhance supply chain coordination amidst uncertainty. By establishing a revenue function, we propose a coordinated approach that leverages both revenue-sharing coefficients and profit margins to achieve Pareto improvements for supply chain partners. Through numerical analysis, we identify an optimal value range for the model's parameters, demonstrating the model's efficacy in balancing the expected returns for both suppliers and retailers. The study's contributions are threefold: (1) the introduction of a novel decision-making model tailored to the pharmaceutical supply chain, (2) the provision of a clear framework for comparing collaborative versus decentralized decision-making outcomes, and (3) the empirical validation of the model through case studies, showcasing its superiority in overall supply chain efficiency. This research significantly extends the current literature by providing a nuanced understanding of how supply chain coordination can be optimized under conditions of uncertainty. The findings underscore the importance of collaborative decision-making in achieving supply chain stability and offer practical insights for supply chain management in the pharmaceutical industry.
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- Yang, Xinming, et al.
(författare)
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Cryptotanshinone reverses reproductive and metabolic disturbances in prenatally androgenized rats via regulation of signaling mechanisms and androgen synthesis.
- 2011
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Ingår i: American journal of physiology. Regulatory, integrative and comparative physiology. - : American Physiological Society. - 1522-1490 .- 0363-6119. ; 300:4
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Tidskriftsartikel (refereegranskat)abstract
- This trial explores (i) prenatally androgenized (PNA) rats as a model of polycystic ovary syndrome (PCOS) and (ii) reproductive and metabolic effects of cryptotanshinone in PNA ovaries. On days 16-18 of pregnancy, 10 rats were injected with testosterone propionate (PNA mothers) and 10 with sesame oil (control mothers). At age 3 mo, 12 female offspring from each group were randomly assigned to receive saline and 12 cryptotanshinone treatment during 2 weeks. Before treatment, compared with the 24 controls, the 24 PNA rats had (i) disrupted estrus cycles, (ii) higher 17-hydroxyprogesterone, (P = 0.030), androstenedione (P = 0.016), testosterone and insulin (Ps = 0.000), and glucose (P = 0.047) levels, and (iii) higher areas under the curve (AUC) for glucose (AUC-Glu, P = 0.025) and homeostatic model assessment for insulin resistance (HOMA-IR, P = 0.008). After treatment, compared with vehicle-treated PNA rats, cryptotanshinone-treated PNA rats had (i) improved estrus cycles (P = 0.045), (ii) reduced 17-hydroxyprogesterone (P = 0.041), androstenedione (P = 0.038), testosterone (P = 0.003), glucose (P = 0.036), and insulin (P = 0.041) levels, and (iii) lower AUC-Glu (P = 0.045) and HOMA-IR (P = 0.024). Western blot showed that cryptotanshinone reversed the altered protein expressions of insulin receptor substrate-1 and -2, phosphatidylinositol 3-kinase p85α, glucose transporter-4, ERK-1, and 17α-hydroxylase within PNA ovaries. We conclude that PNA model rats exhibit reproductive and metabolic phenotypes of human PCOS and that regulation of key molecules in insulin signaling and androgen synthesis within PNA ovaries may explain cryptotanshinone's therapeutic effects.
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- Zhou, Lihui, et al.
(författare)
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Association of impaired lung function with dementia, and brain magnetic resonance imaging indices : a large population-based longitudinal study
- 2022
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Ingår i: Age and Ageing. - : Oxford University Press (OUP). - 1468-2834 .- 0002-0729. ; 51:11
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: to examine the association between different patterns of impaired lung function with the incident risk of dementia and magnetic resonance imaging (MRI)-based brain structural features. METHODS: in UK Biobank, a total of 308,534 dementia-free participants with valid lung function measures (forced expiratory volume in 1 s [FEV1] and forced vital capacity [FVC]) were included. Association was assessed using Cox proportional hazards regression model. Furthermore, the association between impaired lung function and brain MRI biomarkers related to cognitive function was analysed among 30,159 participants. RESULTS: during a median follow-up of 12.6 years, 3,607 incident all-cause dementia cases were recorded. Restrictive impairment (hazard ratio [HR], 1.42; 95% confidence interval [CI], 1.27-1.60) and obstructive impairment (HR, 1.28; 95% CI, 1.15-1.42) were associated with higher risk of all-cause dementia. The restricted cubic splines indicated FEV1% predicted and FVC % predicted had reversed J-shaped associations with dementia. Participants with impaired lung function have higher risks of all-cause dementia across all apolipoprotein E (APOE) risk categories, whereas associations were stronger among those of low APOE risk (P for interaction = 0.034). In addition, restrictive and obstructive impairment were linked to lower total (β: -0.075, SE: 0.021, Pfdr = 0.002; β: -0.033, SE: 0.017, Pfdr = 0.069) and frontoparietal grey matter volumes, higher white matter hyperintensity, poorer white matter integrity, lower hippocampus (β: -0.066, SE: 0.024, Pfdr = 0.017; β: -0.051, SE: 0.019, Pfdr = 0.019) and other subcortical volumes. CONCLUSIONS: participants with restrictive and obstructive impairments had a higher risk of dementia. Brain MRI indices further supported adverse effects and provided insight into potential pathophysiology biomarkers.
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