These findings indicate that in vivo and in vitro cytotoxic actions of chemotherapy drugs on the ovarian follicles and granulosa cells vary depending upon the their mechanism of action and the nature of the granulosa cells.

This review aims to introduce the novel concept of embryological target mining applied to interorgan crosstalk network genesis, and applies embryological target mining to multidrug-resistant essential hypertension (a prototype, complex, undertreated, multiorgan systemic syndrome) to uncover new treatment targets and critique why existing strategies fail. Briefly, interorgan crosstalk pathways represent the next frontier for target mining in molecular medicine. This is because stereotyped stepwise organogenesis presents a unique opportunity to infer interorgan crosstalk pathways that may be crucial to discovering novel treatment targets. Insights gained from this review will be applied to patient management in a clinician-directed fashion. . These terms will be used in the crosstalk-direct embryological target mining (CTD-ETM) analysis to come. | INTRODUCTION Multidrug | WHY DO EXISTING HYPERTENSIVE STRATEGIES FAIL IN COMPLIANT PATIENTS?The Guytonian theory implicates dysregulated renal sodium excretion as the key pathway in developing hypertension.

Low FEV was an important risk factor for future exacerbations. Downstaging of C1/D1 patients caused heterogeneity in A/B with including patients with low and high risk of future exacerbation. This resulted in a low discriminative power of GOLD 2017 regarding the risk of future exacerbation in groups A and B. This may cause underestimation of disease severity and inadequate treatment especially in A/B patients with low FEV .

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