Women suffering from absolute uterine factor infertility (AUFI), due to either lack of a uterus or one unable to sustain neonatal viability, presented as one of the last frontiers in conquering infertility. Following systematic animal research for over a decade, uterus transplantation was tested as a treatment for AUFI in 2012, which culminated in the first human live birth in 2014. The development of uterus transplantation from mouse to human has followed both the Moore Criteria for introduction of a surgical innovation and the IDEAL concept for evaluation of a novel major surgical procedure. In this article we review the important pre-clinical animal and human studies that paved the way for the successful introduction of human uterus transplantation a decade ago. We discuss this in the context of the Moore Criteria and describe the different procedures of preparation, surgeries, post-operative monitoring, and use of assisted reproduction in human uterus transplantation. We review the world-wide activities and associated results in the context of the IDEAL concept for evaluation of surgical innovation and appraise the ethical considerations relevant to uterus transplantation. We conclude that rigorous application of the Moore Criteria and strict alignment with the IDEAL concept has resulted in the establishment of uterus transplantation as a novel, safe and effective infertility therapy that is now being used worldwide for the treatment of women suffering from AUFI.

Electrophysiological studies have long established themselves as reliable methods for assessing the functional state of the brain and spinal cord, the degree of neurodegeneration, and evaluating the effectiveness of therapy. In addition, they can be used to diagnose, predict functional outcomes, and test the effectiveness of therapeutic and rehabilitation programs not only in clinical settings, but also at the preclinical level. Considering the urgent need to develop potential stimulators of neuroregeneration, it seems relevant to obtain objective data when modeling neurological diseases in animals. Thus, in the context of the application of electrophysiological methods, not only the comparison of the basic characteristics of bioelectrical activity of the brain and spinal cord in humans and animals, but also their changes against the background of neurodegenerative and post-traumatic processes are of particular importance. In light of the above, this review will contribute to a better understanding of the results of electrophysiological assessment in neurodegenerative and post-traumatic processes as well as the possibility of translating these methods from model animals to humans.

The aim of this paper is to explore and assess various strategies for monitoring antimicrobial consumption (AMC) in animals, within the context of the One Health approach. Recent studies have shed light on the limited surveillance and data collection for AMC in animals. Using the United States Center for Disease Control and Prevention Policy Analytical Framework, we assess global, national, and farm-level surveillance strategies on public health impact and feasibility using evidence from primary, secondary, and grey literature. From this, we identify key policy mechanisms that support the adoption of surveillance while providing specific recommendations. We find that a global strategy, though valuable for benchmarking and policy guidance, faces participation and data visibility challenges. National-level surveillance offers direct inputs into national action plans but struggles with data uniformity and comparability. Farm-level surveillance, while resource-intensive, provides the most granular data for informing specific interventions. We advocate for a multi-faceted approach to AMC surveillance, emphasizing that legal mandates and financial incentives are crucial for encouraging surveillance participation, along with international cooperation for enhancing participation and data quality. Drawing parallels with public reporting challenges in other sectors can provide valuable lessons on how to address data collection, analysis, and reporting barriers.

The mutation rate is a pivotal biological characteristic, intricately governed by natural selection and historically garnering considerable attention. Recent advances in high-throughput sequencing and analytical methodologies have profoundly transformed our understanding in this domain, ushering in an unprecedented era of mutation rate research. This paper aims to provide a comprehensive overview of the key concepts and methodologies frequently employed in the study of mutation rates. It examines various types of mutations, explores the evolutionary dynamics and associated theories, and synthesizes both classical and contemporary hypotheses. Furthermore, this review comprehensively explores recent advances in understanding germline and somatic mutations in animals and offers an overview of experimental methodologies, mutational patterns, molecular mechanisms, and driving forces influencing variations in mutation rates across species and tissues. Finally, it proposes several potential research directions and pressing questions for future investigations.
突变率是生命演化过程中的一个重要参数。它受到自然选的择精细调控，因此在演化生物学的研究历史上备受关注。近年来，随着高通量测序的发展和突变分析方法的进步，我们对突变率的理解有了显著地加深，突变的研究进入了一个前所未有的新时代。该文总结和讨论了突变研究中常见的演化生物学概念和经典的理论方法：我们首先详细介绍了突变的类型；之后，在此基础上探索前人提出的与演化动力学相关的理论模型；最后对经典假说与当代理论进行深入探讨和比较。此外，该文全面总结了动物生殖细胞和体细胞突变的最新进展：我们概述了这些研究过程中使用的实验方法、突变模式、突变的分子机制以及影响突变率变化的因素，并探讨了物种间和相同个体不同组织间突变率的差异。最终，我们概述了突变研究中未来潜在的研究方向和亟待解决的科学问题。.

OBJECTIVE: Peri-implant diseases, being the most common implant-related complications, significantly impact the normal functioning and longevity of implants. Experimental models play a crucial role in discovering potential therapeutic approaches and elucidating the mechanisms of disease progression in peri-implant diseases. This narrative review comprehensively examines animal models and common modeling methods employed in peri-implant disease research and innovatively summarizes the in vitro models of peri-implant diseases.
METHODS: Articles published between 2015 and 2023 were retrieved from PubMed/Medline, Web of Science, and Embase. All studies focusing on experimental models of peri-implant diseases were included and carefully evaluated.
RESULTS: Various experimental models of peri-implantitis have different applications and advantages. The dog model is currently the most widely utilized animal model in peri-implant disease research, while rodent models have unique advantages in gene knockout and systemic disease induction. In vitro models of peri-implant diseases are also continuously evolving to meet different experimental purposes.
CONCLUSIONS: The utilization of experimental models helps simplify experiments, save time and resources, and promote advances in peri-implant disease research. Animal models have been proven valuable in the early stages of drug development, while technological advancements have brought about more predictive and relevant in vitro models.
CONCLUSIONS: This review provides clear and comprehensive model selection strategies for researchers in the field of peri-implant diseases, thereby enhancing understanding of disease pathogenesis and providing possibilities for developing new treatment strategies.

UNASSIGNED: Ankle arthrodesis is one of the treatments of choice, particularly in late-stage and unstable diabetic Charcot arthropathy. Unfortunately, poor healing capacity might play a role in the high nonunion rate (10-40%). The advancement in regenerative medicine opens a new horizon for enhancing fusion after ankle arthrodesis in patients with poor healing capacity. However, a suitable small animal model is warranted to study the effectivity of these regenerative medicine approaches. Streptozotocin (STZ)-induced diabetes models and adjuvant-induced arthritis models with complete Freund\'s adjuvant are two established models. However, no study has combined those two models to make a diabetic arthritic model that more closely resembles the condition in Charcot arthropathy.
UNASSIGNED: Twenty male Sprague-Dawley rats were assigned into five groups, consisting of one control group, and four diabetic groups which were induced by STZ injection and a high-fat diet. Among these diabetic rats, two groups received complete Freund\'s adjuvant (CFA) injections to the left ankle of the hind limb. The control group, one of the diabetic-only groups, and one of the arthritic-diabetic-induced groups were euthanized at 4 weeks after STZ induction, and the remainder were euthanized 6 weeks after STZ induction. Clinical, radiological, and histological examinations were then compared in all five groups.
UNASSIGNED: Diabetic status was successfully achieved in the model, which was maintained until the completion of the study. The CFA-induced ankles were significantly larger than the contralateral ankles in all groups (p<0.05). Histopathological evaluation confirmed arthritic changes in the CFA-induced group with less variability after 4 weeks of arthritis induction.
UNASSIGNED: This rat model of arthritic diabetic mimics the progressive and chronic nature of Charcot arthropathy in humans. This model can be further use to study treatments that might enhance the fusion rate in ankle arthrodesis in healing-defective patients such as those with diabetes.
UNASSIGNED: 5.

BACKGROUND: Recent advancements in molecular diagnostics have unveiled a multitude of allergen molecules (AMs) associated with animal sensitizations, revealing significant cross- and co-sensitization patterns among these seemingly distinct allergens.
METHODS: We investigated the sensitization profiles of 120 children, sensitized to at least one of the 14 AMs from cat, dog, or horse using the Alex test, employing correlations and hierarchical clusters to explore relationship between sensitizations.
RESULTS: Sensitizations to Fel d 1, Can f 4/5, and Equ c 4 differ from other cat, dog, and horse AM sensitizations, suggesting they may represent genuine sensitizations for their respective animals. High correlations were observed among various AMs, including lipocalins (Can f 1/2/6, Fel d 4/7, and Equ c 1), serum albumins (Fel d 2, Can f 3, and Equ c 3), and uteroglobins (Fel d 1 and Can f_Fd1). Hierarchical clustering of sensitizations identified two similarity clusters and one dissimilarity cluster, providing an estimation of the likelihood of cross-reactivity. Additionally, our method facilitated speculation regarding cross-, co-, or genuine sensitization. Moreover, we noted a potential increase in the number and level of sensitized animal AMs concurrent with increased sensitization to other aeroallergens with advancing age. No significant difference was detected for the presence or absence of various types of allergic comorbidities.
CONCLUSIONS: Correlations and hierarchical clustering can unveil the extent and magnitude of cross-, co-, and genuine sensitization relationships among animal AMs. These insights can be leveraged to enhance artificial intelligence algorithms, improving diagnostic accuracy through the integration of other measures of sensitization.

The causes of forgetting in working memory (WM) remain a source of debate in cognitive psychology, partly because it has always been challenging to probe the complex neural mechanisms that govern rapid cognitive processes in humans. In this review, we argue that neural, and more precisely animal models, provide valuable tools for exploring the precise mechanisms of WM forgetting. First, we discuss theoretical perspectives concerning WM forgetting in humans. Then, we present neuronal correlates of WM in animals, starting from the initial evidence of delay activity observed in the prefrontal cortex to the later synaptic theory of WM. In the third part, specific theories of WM are discussed, including the notion that silent versus non-silent activity is more consistent with the processes of refreshing and decay proposed in human cognitive models. The review concludes with an exploration of the relationship between long-term memory and WM, revealing connections between these two forms of memory through the long-term synaptic hypothesis, which suggests that long-term storage of interference can potentially disrupt WM.

Alzheimer\'s disease is characterized, in part, by the accumulation of β-amyloid (Aβ) in the brain. Aβ is produced via the proteolysis of APP by BACE1 and γ-secretase. Since BACE1 is the rate-limiting enzyme in the production of Aβ, and a target for therapeutics, it is of interest to know when its proteolytic function evolved and for what purpose. Here, we take a functional evolutionary approach to show that BACE1 likely evolved from a gene duplication event near the base of the animal clade and that BACE1 APP/Aβ proteolytic function evolved during early animal diversification, hundreds of millions of years before the evolution of the APP/Aβ substrate. Our examination of BACE1 APP/Aβ proteolytic function includes cnidarians, ctenophores, and choanoflagellates. The most basal BACE1 ortholog is found in cnidarians, while ctenophores, placozoa, and choanoflagellates have genes equally orthologous to BACE1 and BACE2. BACE1 from a cnidarian (Hydra) can cleave APP to release Aβ, pushing back the date of the origin of its function to near the origin of animals. We tested more divergent BACE1/2 genes from a ctenophore (Mnemiopsis) and a choanoflagellate (Monosiga), and neither has this activity. These findings indicate that the specific proteolytic function of BACE1 evolved during the very earliest diversification of animals, most likely after a gene-duplication event.

Osteoarthritis (OA) is a degenerative disease with a high prevalence in the elderly population, but our understanding of its mechanisms remains incomplete. Analysis of serum exosomal small RNA sequencing data from clinical patients and gene expression data from OA patient serum and cartilage obtained from the GEO database revealed a common dysregulated miRNA, miR-199b-5p. In vitro cell experiments demonstrated that miR-199b-5p inhibits chondrocyte vitality and promotes extracellular matrix degradation. Conversely, inhibition of miR-199b-5p under inflammatory conditions exhibited protective effects against damage. Local viral injection of miR-199b-5p into mice induced a decrease in pain threshold and OA-like changes. In an OA model, inhibition of miR-199b-5p alleviated the pathological progression of OA. Furthermore, bioinformatics analysis and experimental validation identified Gcnt2 and Fzd6 as potential target genes of MiR-199b-5p. Thus, these results indicated that MiR-199b-5p/Gcnt2 and Fzd6 axis might be a novel therapeutic target for the treatment of OA.