In mammals, reproductive synchrony and reproductive suppression usually are found in social, group-living species, which often display hierarchical relationships among related animals. Some individuals, particularly younger, philopatric females beyond the age of sexual maturity, may not raise offspring because they are suppressed by other individuals. Although brown bears (Ursus arctos) are a solitary species, the existence of socially induced delayed primiparity of philopatric females has been documented. Here we show further evidence for interactions of a population-regulatory nature that are typically associated with social species. We found that an adult female's probability of having cubs in a given year was influenced by whether or not her nearest neighboring adult female had cubs. At short distances (< or = 10 km) between the home range centroids of neighboring females, females with cubs had a negative effect on their neighboring female's probability of having cubs of the year. At distances >10 km and < or = 20 km, the effect reversed, and it disappeared beyond 20 km. We argue that reproductive suppression is probably caused by resource competition among females living close to each other. Previously, similar population regulation mechanisms have been found only in group-living mammals. Thus, social interactions and behavior in solitary carnivores may be more flexible than usually assumed.
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http://dx.doi.org/10.1890/07-1921.1 | DOI Listing |
HIV Med
January 2025
Centre for Immunology and Vaccinology, Imperial College London, London, UK.
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Background Endometriosis-related infertility and its treatment with assisted reproductive technologies (ART) have been broadly researched. Yet, underlying mechanisms of infertility, particularly in the absence of tubal dysfunction, remain unclear. While the impact of inflammatory milieu on the ovary and/or endometrium has been indicated as a contributing factor, recent evidence from euploid transfers and donor cycles questions the extent of these effects.
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January 2025
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
Background: Pathogenic or null mutations in WRN helicase is a cause of premature aging disease Werner syndrome (WS). WRN is known to protect somatic cells including adult stem cells from premature senescence. Loss of WRN in mesenchymal stem cells (MSCs) not only drives the cells to premature senescence but also significantly impairs the function of the stem cells in tissue repair or regeneration.
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December 2024
Scientific Research Institute for Biological Safety Problems, Ministry of Health of Kazakhstan, Almaty 080409, Kazakhstan.
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