External Funding Announcements
This page includes a compilation of relevant funding announcements from external funders, including the National Institutes of Health. Although this list is not exhaustive, we hope that it is helpful to investigators seeking new funding opportunities. This page will be continuously updated as we receive word of new announcements, so please check back regularly!
If you know of an announcement we should add, please forward it to Jackie Loeb at firstname.lastname@example.org.
This notice applies to due dates on or after September 8, 2022 and subsequent receipt dates through September 8, 2025.
NOT-HD-22-026: Notice of Special Interest (NOSI): Advancing Research on Early Pregnancy Loss
Release Date: July 5, 2022
Submit applications for this initiative using one of the following funding opportunity announcements (FOAs) or any reissues of these announcement through the expiration date of this notice.
PA-20-196- NIH Exploratory/Developmental Research Grant Program (Parent R21 Basic Experimental Studies with Humans Required)
Early Pregnancy loss (EPL), defined as a pregnancy loss occurring up to 20 weeks gestation, is a very common pregnancy complication, occurring in 12-15% of clinically recognized pregnancies, with increased prevalence associated with increasing maternal age. The use of highly sensitive hCG assays allows the detection of pregnancy earlier in gestation than the time of clinical recognition, and gives an even higher estimated loss of 50-70% of conceptions prior to the second trimester. To achieve a successful pregnancy, a series of strict embryonic and maternal conditions must be met, that include high quality embryos, favorable conditions for embryo implantation, receptive maternal endometrium and optimal uterine environment to sustain the conceptus to term. In addition, maternal immune tolerance and hormonal factors play a critical role. While approximately half of all cases of EPL appear to be due to embryonic aneuploidy, very little is known about the physiologic and pathophysiologic processes that underlie non-aneuploid EPL. As a result, there is also a lack of understanding for the underlying causes of recurrent pregnancy loss (RPL). This NOSI seeks to address these critical knowledge gaps by encouraging basic, translational and clinical studies on biological processes that may uncover potential etiologies of EPL and RPL. This includes research to understand implantation mechanistically and identify a range of key factors, involved in implantation and placentation that are important for early pregnancy establishment, including abnormalities that contribute to sporadic EPL and recurrent pregnancy loss.
The major gaps that this NOSI targets include, but are not limited to the following
Discovering novel contributing factors that disturb embryo implantation, placenta development, endometrial receptivity and decidualization that lead to EPL, as well as the mechanisms that govern these processes
Investigation into maternal- and paternal-derived factors in gametes that may be responsible for EPL
Errors in epigenetic reprogramming in gametes and preimplantation embryo and early pregnancy loss
Studies of immunological disorders (e.g., inflammatory cytokines, NK cell dysfunction) that contribute to EPL
Uncovering male factor contribution and underlying mechanisms that lead to EPL
Development of new model systems that allow mechanistic investigation
Studies of nutrition factor contribution to EPL (e.g., over- or under- nutrition and vitamin/protein factors)
Studies of dynamic communication between endometrium and embryo
Of Special Interest:
Studies that explore immune system interactions between endometrium and placenta or embryo
Model systems that allow mechanistic investigation of multi-component interactions – e.g., organoids and organs on a chip
Studies focused on the following topics will be given low priority unless there is a clear demonstration that they provide special advantages (diagnostics, risk prediction) over current approaches.
Genomic abnormalities, such as aneuploidy, and genetic determinants
Uterine structure anomalies, such as adenomyosis, intrauterine adhesions and fibroid