Prioritisation also led to poor resource utilisation and short-lived effects of extra capacity. Departments where prioritisation is causing long waits can improve their situation by temporarily bringing capacity above demand and introducing "first come, first served" instead of prioritisation. CONCLUSION A poor appointment allocation policy can build long waiting times, even when capacity is sufficient to meet demand. By bringing waiting times down and going away from prioritisation, the waiting list size and average waiting times at the studied department could be maintained almost 90% below the current level - without requiring permanent change in the capacity/demand ratio.Despite progressive universal drug coverage and pharmaceutical policies found in other countries, Canada remains the only developed nation with a publicly funded healthcare system that does not include universal coverage for prescription drugs. In the absence of a national pharmacare plan, a province may choose to cover a specific sub-population for certain drugs. Although different provinces have individually attempted to extend coverage to certain subpopulations within their jurisdictions, out-of-pocket expenses on drugs and pharmaceutical products (OPEDP) accounts for a large proportion of out-of-pocket health expenses (OPHE) that are catastrophic in nature. Pharmaceutical drug coverage is a major source of public scrutiny among politicians and policy-makers in Canada. In this editorial, we focus on social inequalities in the burden of OPEDP in Canada. Prescription drugs are inconsistently covered under patchworks of public insurance coverage, and this inconsistency represents a major source of inequity of healthcare financing. Residents of certain provinces, rural households and Canadians from poorer households are more likely to be affected by this inequity and suffer disproportionately higher proportions of catastrophic out-of-pocket expenses on drugs and pharmaceutical products (COPEDP). Universal pharmacare would reduce COPEDP and promote a more equitable healthcare system in Canada.The genus-level recognition of monophyletic short-legged toads ( Brachytarsophrys) has been recently implicated in the taxonomic debate of Megophrys sensu lato. In the present study, Brachytarsophrys is reasonably regarded as a distinct genus based on significant morphological differentiations and recent molecular analyses. Furthermore, a comprehensive review of this genus is performed, with two species groups proposed based on morphological differences and phylogenetic relationships. Particularly, Brachytarsophrys platyparietus is removed as a synonym of Brachytarsophrys carinense and considered a valid species due to significant genetic divergence and distinct morphological differences. In addition, a new species, Brachytarsophrys orientalis sp. nov., is described based on a series of specimens collected from southeastern China. This work takes the member species of the genus Brachytarsophrys to seven, suggesting that the diversity of Brachytarsophrys is underestimated. In addition, the genus levels of other monophyletic groups within the subfamily Megophryinae are discussed.5α-dihydrotestosterone (5α-DHT) is the most potent natural androgen. 5α-DHT elicits a multitude of physiological actions, in a host of tissues, including prostate, seminal vesicles, hair follicles, skin, kidney, and lacrimal and meibomian glands. However, the physiological role of 5α-DHT in human physiology, remains questionable and, at best, poorly appreciated. Recent emerging literature supports a role for 5α-DHT in the physiological function of liver, pancreatic b-cell function and survival, ocular function and prevention of dry eye disease and kidney physiological function. Thus, inhibition of 5α-reductases with finasteride or dutasteride to reduce 5α-DHT biosynthesis in the course of treatment of benign prostatic hyperplasia (BPH) or male pattern hair loss, known as androgenetic alopecia (AGA) my induces a novel form of tissue specific androgen deficiency and contributes to a host of pathophysiological conditions, that are yet to be fully recognized.  https://www.selleckchem.com/products/bi-3802.html  Here, we advance the concept that blockade of 5α-reductases by finasteride or dutasteride in a mechanism-based, irreversible, inhabitation of 5α-DHT biosynthesis results in a novel state of androgen deficiency, independent of circulating testosterone levels. Finasteride and dutasteride are frequently prescribed for long-term treatment of lower urinary tract symptoms in men with BPH and in men with AGA. This treatment may result in development of non-alcoholic fatty liver diseases (NAFLD), insulin resistance (IR), type 2 diabetes (T2DM), dry eye disease, potential kidney dysfunction, among other metabolic dysfunctions. We suggest that long-term use of finasteride and dutasteride may be associated with health risks including NAFLD, IR, T2DM, dry eye disease and potential kidney disease. Copyright © 2020 Korean Society for Sexual Medicine and Andrology.PURPOSE In this study, we tested whether the resveratrol-enriched peanut sprout extracts cultivated with fermented sawdust medium (PSEFS) could suppress benign prostatic hyperplasia (BPH) in vitro and in vivo. MATERIALS AND METHODS The mode of action of PSEFS was estimated by employing high-performance liquid chromatography analysis, MTT assay, cell counting, cell cycle analysis, immunoblots, and immunoprecipitation and electrophoretic mobility shift assay. In vivo efficacy of PSEFS was analyzed in BPH animal model via immunostaining and enzyme-linked immunosorbent assay. RESULTS We selected the Yesan peanut sprout variety, which contains the highest level of resveratrol. The resveratrol levels in PSEFS were higher than those obtained with hydroponic technology. PSEFS treatment induced cell cycle arrest at the G1-phase by downregulating CDK4 and cyclin D1 via p21WAF1 induction in the RWPE-1 and WPMY prostate cells, thereby decreasing their proliferation. Treatment with PSEFS decreased ERK1/2 phosphorylation and increased JNK phosphorylation. The levels of DNA-bound transcription factors associated with proliferation (nuclear factor-κB, Sp-1, and AP-1) decreased upon PSEFS treatment in both prostate cells. Additionally, the levels of the molecular markers of BPH development (5α-reductase, androgen receptor, fibroblast growth factor, Bcl-2, and Bax) also changed by the addition of PSEFS. Finally, in a testosterone propionate-induced BPH model in rats, PSEFS administration attenuated the size, weight, and thickness of prostate tissues with no signs of death. CONCLUSIONS These results showed that PSEFS inhibited BPH both in vitro and in vivo and might be useful in the development of a potential BPH therapy. Copyright © 2020 Korean Society for Sexual Medicine and Andrology.