CC-BY 4.0 International license perpetuity. It is made available under a preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in Highlights Women with preeclampsia have increased risk of cardiovascular disease later in life but the mechanism is poorly understood. "In silico" analyses of publically available datasets provided overlapping biomarkers and pathogenic pathways between preeclampsia, hypertension and heart failure with preserved ejection fraction (HFpEF). These data could be utilised in the future studies that may lead to the development of better risk stratification strategies or preventative treatments for women post preeclampsia.
Non-unions continue to present a challenge to trauma surgeons, as current treatment options are limited, duration of treatment is long, and the outcome often unsatisfactory. Additionally, standard treatment with autologous bone grafts is associated with comorbidity at the donor site. Therefore, alternatives to autologous bone grafts and further therapeutic strategies to improve on the outcome and reduce cost for care providers are desirable. In this study in Sprague–Dawley rats we employed a recently established sequential defect model, which provides a platform to test new potential therapeutic strategies on non-unions while gaining mechanistic insight into their actions. The effects of a combinatorial treatment of a bone graft substitute (HACaS+G) implantation and systemic PTH administration was assessed by µ-CT, histological analysis, and bio-mechanical testing and compared to monotreatment and controls. Although neither PTH alone nor the combination of a bone graft substitute and PTH led to the formation of a stable union, our data demonstrate a clear osteoinductive and osteoconductive effect of the bone graft substitute. Additionally, PTH administration was shown to induce vascularization, both as a single adjuvant treatment and in combination with the bone graft substitute. Thus, systemic PTH administration is a potential synergistic co-treatment to bone graft substitutes.
Corresponding authorsHighlights Women with preeclampsia have increased risk of cardiovascular disease later in life but the mechanism is poorly understood. "In silico" analyses of publically available datasets provided overlapping biomarkers and pathogenic pathways between preeclampsia, hypertension and heart failure with preserved ejection fraction (HFpEF). These data could be utilised in the future studies that may lead to the development of better risk stratification strategies or preventative treatments for women post preeclampsia. AbstractObjectives: Preeclampsia is a cardiovascular pregnancy complication which occurs in 5-10% of pregnancies that can lead to a number of pregnancy complications including maternal and foetal death. Long-term, preeclampsia is associated with up to 8-fold increased risk of cardiovascular disease (CVD) for both mothers and their offspring. The lack of mechanistic data in relation to the causes or consequences of preeclampsia has prevented the development of effective therapeutic or monitoring strategies. Study design:This study investigates common underlying mechanisms of preeclampsia and CVD, specifically hypertension and heart failure with preserved ejection fraction (HFpEF)using "in silico" approach of publicly available datasets. Integrated techniques were designed to mine data repositories and identify relevant biomarkers associated with these three conditions. Main outcomes measures:The knowledge base tools were employed that enabled the analysis of these biomarkers to discover potential molecular and biological links between these three conditions.Results: Our bioinformatics "in silico" analyses of the publically available datasets identified 76 common biomarkers between preeclampsia, hypertension and HFpEF. These biomarkers were representative of 29 pathways commonly enriched across the three conditions which were largely related to inflammation, metabolism, angiogenesis, remodelling, haemostasis, apoptosis, endoplasmic reticulum (ER) stress signalling and the renin-angiotensin-aldosterone (RAAS) system. Conclusions:This bioinformatics approach which uses the wealth of scientific data available in public repositories can be helpful to gain a deeper understanding of the overlapping pathogenic mechanisms of associated diseases, which could be explored as biomarkers or targets to prevent long-term cardiovascular complications such as hypertension and HFpEF following preeclampsia. Abstract word count: 244 wordsMain text word count: 2580 words Total word count: 4653 words
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