Anja Schmidt

Pharmaceutical companies fund much biomedical research, yet many journals restrict open access publishing options for peer-reviewed articles reporting commercially funded research. Expanded publishing options, such as funder-neutral publishing policies, will help address this inequity.

Open Science aims to fight misinformation and improve trust in scientific research; it encourages the reliability and accessibility of evidence, reduces inequalities through the democratisation of scientific knowledge and focuses scientific endeavours on issues of societal significance. As a multisponsor collaboration committed to driving positive change, Open Pharma has a multifaceted vision for scientific research publications funded by pharmaceutical companies (‘company research publications’) that aligns strongly with Open Science tenets. This new vision statement outlines our forward-looking principles for company research publications, both for short-term attainment (‘immediate’) and long-term commitment (‘ultimate’). Together, the principles provide a framework for positive collective action by all stakeholders involved in the development and dissemination of peer-reviewed company research publications. Underpinned by our central commitment to transparency for company research publications, we outline goals for: universal access to these publications; provision of peer-reviewed plain language summaries of the publications to aid comprehension among non-specialist readers; leveraging author and institutional metadata to advance transparency, discoverability and research impact; working towards FAIR (Findability, Accessibility, Interoperability, and Reuse) data principles through cross-sector consensus and action, and disclosure of patient involvement in research and its reporting to support transparency and encourage a research ecosystem attuned to patient centricity. We call on all stakeholders to realise the Open Pharma Vision and achieve an open and trusted future for company research publications that will ultimately advance patient care and improve global health.

Background and objective: Acne is a common dermatologic condition that extends into middle age, particularly among women, and is associated with substantial healthcare resource utilization. Drospirenone (DRSP), a synthetic progestin, has anti-androgenic activity, and women using DRSP 3.0 mg/ethinyl estradiol (EE) 0.02 mg as a 24/4 regimen (DRSP/EE-24/4) for contraception also may use it for treatment of moderate acne. The study used a US national healthcare database to assess acne-related healthcare resource utilization among women aged 18–45 years before (pre-index) and after (post-index) initiation of DRSP/EE-24/4. Methods: Resource utilization and costs were evaluated by age group (18–25, 26–35, or 36–45 years) and by type of acne medication (systemic antibiotic, topical, or anti-androgen). Results: Data for 1340 women were evaluated. Overall, drug costs, medical costs, and total costs were decreased by 38%, 37%, and 37%, respectively (p < 0.0001 for all) between the pre-index and post-index periods; significant differences were evident across age groups and acne medication categories. Total costs were significantly decreased for patients (41%) and healthcare plans (36%; p < 0.0001 for both) overall and across age groups and drug classes. Acne-related claims and number of days using acne medication were reduced (by 37% each; p < 0.0001 for both). Study limitations: The study was retrospective in design and had a limited follow-up period. Database limitations restricted assessment of medication compliance and adherence. Conclusion: DRSP/EE-24/4 use was associated with substantial reductions in acne-related healthcare resource utilization, and reductions occurred regardless of age or type of acne medication. DRSP/EE-24/4 therefore represents a cost-effective option for the treatment of acne among women using DRSP/EE-24/4 for oral contraception.

The role of the immune system in the pathogenesis of endometriosis remains elusive. It has been shown that patients have an altered peritoneal environment with increased levels of inflammatory cytokines, activated macrophages and reduced clearance of retrogradely transported endometrial fragments. However, it is not known if this unique inflammatory situation is cause or consequence of endometriosis. This study investigates the impact of a pre-existing peritoneal inflammation on endometriosis establishment in a mouse model. Endometriosis was induced by intraperitoneal injection of enhanced green fluorescent protein (EGFP)-expressing endometrium in mice. In parallel, a peritonitis model was established via intraperitoneal injection of thioglycolate medium (TM). Finally, endometriosis was induced in the inflamed peritoneal cavity and lesion establishment as well as morphological and histological characteristics were analysed. Induction of endometriosis in an inflamed peritoneal cavity resulted in fewer lesions and significantly lower sum of lesion surface area per mouse in the TM-treated group. Additionally, a higher amount of non-attached debris could be detected in the peritoneal cavity of TM-treated mice. An intraperitoneal inflammation decreases endometriosis establishment in this mouse model. Thus, a pre-existing peritoneal inflammation might not be a factor favouring the development of endometriosis.

The retinoic acid (RA) synthesizing enzymes, retinaldehyde dehydrogenases (RALDH), are expressed in specific spatial and temporal patterns in uterine tissues during estrous cycle and early pregnancy in mice. Expression of RALDH1 and 2 has been shown to be induced by estrogen treatment within the uterus. In this study, we determined the influence of progesterone and 17‐ß‐estradiol on the uterine expression of the RA‐metabolizing enzyme CYP26A1 after specific time intervals (1, 4, 24, and 48 hr after treatment of ovariectomized mice). In a following experiment, we investigated the influence of gestagen (promegestone 0.3 mg/kg body weight), estrogen (estradiol 3 µg/kg), their combination, as well as the antagonizing anti‐progesterone hormone (RU 486 10 mg/kg) on the uterine expression of CYP26A1. Expression of CYP26A1 was localized using in situ hybridization and quantified using RT‐PCR. CYP26A1 mRNA expression was strongly—although transiently—induced in uterine endometrial epithelial and glandular cells after administration of gestagen or the combination of gestagen + estrogen, but not by estrogen alone. These observations were confirmed by semi‐quantitative RT‐PCR experiments on whole uteri. Thus, we show that the expression of CYP26A1 in endometrial epithelial cells is regulated by progesterone and not significantly influenced by co‐administration of estrogen. These data indicate an additional level of hormonal control of endogenous RA levels in the mouse uterus, where its synthesis would rely on estrogen‐dependent expression of RALDH enzymes, whereas its active metabolism would be triggered by progesterone‐induced CYP26A1 expression. Mol. Reprod. Dev.

The active metabolite of vitamin A, retinoic acid (RA), plays an important role in the female reproductive system. The synthesis of RA is tightly regulated by the activity of retinaldehyde dehydrogenases (Raldh). Among these, Raldh1 and Raldh2 exhibit specific temporal and spatial expression patterns in the mouse uterus, both during the oestrous cycle and early pregnancy. In the present study, we have assessed whether oestradiol and progesterone directly influence the uterine expression of Raldh1 and Raldh2 in ovariectomised mice. We investigated the effect of gestagen (promegestone 0.3 mg kg-1 bodyweight), oestrogen (oestradiol 3 µg kg-1 bodyweight) and their combination on the uterine expression of Raldh2. Expression was analysed using in situ hybridisation and quantified using real-time detection reverse transcription–polymerase chain reaction. The results show that the expression of Raldh2 is rapidly (within 1–4 h) induced in stromal cells by oestrogen, but not by gestagen, treatment, whereas combined oestrogen + gestagen treatment leads to a more prolonged (48 h) response. In contrast, oestrogen, but not progesterone, treatment downregulates (within 4–24 h) Raldh1 expression in the uterine glandular epithelium. We conclude that the uterine RA concentrations are regulated by oestrogens via an effect on the expression of the Raldh synthesising enzymes. Such a regulation is consistent with the natural fluctuations of Raldh expression during the oestrous cycle, early pregnancy and blastocyst implantation.

Objective Nonuniformity in suppression of spermatogenesis induced by various hormones or hormone combinations has impeded the development of an effective hormonal male contraceptive. The basis for th...