Factors of research groups’ productivity: the case of the Ural Federal University

Relevance. One of the main goals of state university support programs in Russia is to increase the number of scientific publications. In 2021, Project 5-100 was replaced by the program PRIORITY 2030 (Strategic Academic Leadership Program). The new program increased the significance of the factors affecting the number of publications in universities and the issue of the optimal allocation of funding among research groups.Research objective. This study examines the factors that affect the productivity of research groups at the university. Unlike the majority of other studies on this topic, this study analyzes scientific productivity at the level of research groups.Data and methods. The study was possible due to the availability of data for 79 research groups at the Ural Federal University for the period from 2014 to 2020. The total number of articles and the number of articles in journals with an impact factor of more than two were used as indicators of research groups’ performance. To determine the factors influencing these indicators, we used econometric models for panel data. We used two separate samples: for social sciences and humanities and for other sciences.Results. We identified the following factors affecting the performance of research groups: the number of participants, the age of the research group, the supervisor’s scientific age, and the amount of funding (the possibility of obtaining more funds or being denied funds). The most interesting result is the following: the supervisor's scientific age and increased funding have a negative impact on the group’s performance. The article provides possible explanations for these results.Conclusion. Since the purpose of creating and funding research groups is primarily to increase their productivity, the results may be in favor of younger supervisors. University managers may also be interested in the ambiguous impact of increased funding: we suppose that research groups are more motivated not by the actual funding but by the prospective amount they may get.Merit, Expertise and Measuremen

Does Reverse Causality Underlie the Temporal Relationship between Depression and Crohn's Disease?

Background: Studies suggest that there is a temporal relationship between depression and Crohn's disease (CD) activity. However, these studies assumed a unidirectional relationship and did not examine the possibility of reverse causality and the risk of a spurious association due to the overlap of symptoms underlying the depression-CD relationship. We evaluated the existence of reverse causality reflected in a possible bidirectional relationship between patient-reported CD activity and an affective-cognitive dimension of depression. Methods: We studied 3307 adult volunteers with a self-reported diagnosis of CD who completed a baseline survey that included demographics, CD activity, and an affective-cognitive index of depression. Crohn's disease status and the affective-cognitive index of depression were also measured 6 and 12 months after the baseline evaluation. We used structural equation models to evaluate whether the effect of depression on future CD activity is stronger than the effect of CD activity on future depression. We calculated the likelihood that each of these hypotheses is supported by the data and calculated the likelihood ratio to provide a relative measure of which hypothesis best accounts for the data. Results: The results of the informative hypothesis testing showed the most support for the hypothesis stating that an affective-cognitive dimension of depression is a stronger predictor of patient-reported CD activity than the converse. Conclusions: The hypothesis that an affective-cognitive dimension of depression predicts patient-reported exacerbation of CD is 218 times more likely to account for the data than the converse

Genetic insights into biological mechanisms governing human ovarian ageing

Reproductive longevity is essential for fertility and influences healthy ageing in women, but insights into its underlying biological mechanisms and treatments to preserve it are limited. Here we identify 290 genetic determinants of ovarian ageing, assessed using normal variation in age at natural menopause in approximately 200,000 women of European ancestry. These common alleles were associated with clinical extremes of age at natural menopause; women in the top 1% of genetic susceptibility have an equivalent risk of premature ovarian insufficiency to those carrying monogenic FMR1 premutations. The identified loci implicate a broad range of DNA damage response (DDR) processes and include loss-of-function variants in key DDR-associated genes. Integration with experimental models demonstrates that these DDR processes act across the lifecourse to shape the ovarian reserve and its rate of depletion. Furthermore, we demonstrate that experimental manipulation of DDR pathways highlighted by human genetics increases fertility and extends reproductive life in mice. Causal inference analyses using the identified genetic variants indicate that extending reproductive life in women improves bone health and reduces risk of type 2 diabetes, but increases the risk of hormone-sensitive cancers. These findings provide insight into the mechanisms that govern ovarian ageing, when they act, and how they might be targeted by therapeutic approaches to extend fertility and prevent disease

Understanding the genetic complexity of puberty timing across the allele frequency spectrum

Pubertal timing varies considerably and is associated with later health outcomes. We performed multi-ancestry genetic analyses on ~800,000 women, identifying 1,080 signals for age at menarche. Collectively, these explained 11% of trait variance in an independent sample. Women at the top and bottom 1% of polygenic risk exhibited ~11 and ~14-fold higher risks of delayed and precocious puberty, respectively. We identified several genes harboring rare loss-of-function variants in ~200,000 women, including variants in ZNF483, which abolished the impact of polygenic risk. Variant-to-gene mapping approaches and mouse gonadotropin-releasing hormone neuron RNA sequencing implicated 665 genes, including an uncharacterized G-protein-coupled receptor, GPR83, which amplified the signaling of MC3R, a key nutritional sensor. Shared signals with menopause timing at genes involved in DNA damage response suggest that the ovarian reserve might signal centrally to trigger puberty. We also highlight body size-dependent and independent mechanisms that potentially link reproductive timing to later life disease