Background Testicular hypoplasia can affect the sexual and reproductive ability in adulthood, and even increase the risk of cancer. Abnormal development of the gubernaculum is one of the important factors of testicular hypoplasia. Therefore, a study of the structure and function of the gubernaculum is an important but neglected new breakthrough point for investigating the normal/abnormal development of the testis. Previous findings showed that Insulin like factor 3 (INSL3) is a key factor regulating the growth of gubernaculum, however, the mechanism by which INSL3 acts on the gubernaculum remains unknown. Therefore, we probed the mechanism associated with INSL3-induced the proliferation, migration, and apoptosis of gubernacular cells in mice. Methods A culture cell model of neonatal mice gubernaculum is established by INSL3 intervention. We blocked PLC/PKC signaling pathway with U73122 pretreat to investigate the role of the PLC/PKC signaling pathway. The changes of cell proliferation, migration, and apoptosis were detected by molecular biological methods. In addition, the levels of PCNA and F-action were detected by immunofluorescence and western blotting. Results We found that INSL3 can promote the proliferation and migration of gubernacular cells and inhibit their apoptosis, meanwhile, INSL3 significantly up-regulated PLC/PKC protein phosphorylation. However, treatment with the PLC/PKC signaling pathway inhibitor U73122 significantly inhibited these effects of INSL3. Besides, we found that INSL3 could up-regulate the protein expression level of PCNA and F-actin, while the PCNA and F-actin expression was significantly weakened after U73122 pretreatment. Conclusions This research revealed that INSL3 binding to RXFP2 may up-regulate the expression levels of PCNA and F-actin by activating the PLC/PKC signaling pathway to promote the proliferation and migration of gubernacular cells. It suggests that the RXFP2-PLC/PKC axis may serve as a novel molecular mechanism by which INSL3 regulates growth of the gubernaculum.
Ephedrine is thought to exert behavioural effects primarily through actions on the central nervous system. However, the neuromechanism underlying the effects of ephedrine addiction still remains unclear. Our study aimed to establish chronic ephedrine addiction models in rhesus monkeys and to investigate the neuromechanism of chronic ephedrine addiction using the behavioural methods combined with resting-state blood oxygenation level dependent-functional magnetic resonance imaging (BOLD-fMRI). Monkeys in the ephedrine addiction group (n = 6) received intramuscular injections of ephedrine using a dose escalation method, with a chronic model established in 8 weeks, while in the control group (n = 4), monkeys received a pure 0.9% saline injection. The weight and behaviors of the monkeys were observed throughout the treatment. All monkeys underwent the brain MR scans for two times (before treatment and after treatment had been discontinued). After molding, the weight of the ephedrine group was significantly reduced, while the weight of the control group increased significantly. Compared with the control group, the ephedrine addicted monkeys showed more abnormal behaviors related to addiction. In fMRI study, the ephedrine addicted monkeys showed more increased brain activation than that of the control group, mainly including the prefrontal cortex(PFC) and anterior cingulate cortex (ACC), the left ventral tegmental area(VTA), right insula, right amygdala, hippocampus, left thalamus, and left cerebellum.We hypothesize that the principal neuromechanism underlying chronic ephedrine addiction involves multiple abnormal brain neuron circuits, mainly in the PFC and the limbic system, and is closely related to addictive behaviors.
Background: Abdominal wound dehiscence (AWD) is a major complication of abdominal surgery, neonates are a group with a high risk of AWD, which has serious consequences or can even result in death. The purpose of this study is to explore the risk factors for neonatal AWD.Methods: The clinical data for 453 cases of neonatal laparotomy from June 2009 to June 2020 were retrospectively analyzed, among which 27 cases of AWD were found. Nine factors, including gender, age at admission, weight at admission, preterm delivery, level of preoperative anemia, hypoalbuminemia, operation time, incision length, and incision type, were analyzed to explore their correlation with neonatal AWD.Results: The incidence of neonatal AWD was 6.0% (27/453), of which partial wound dehiscence 4.9% (22/453) and complete wound dehiscence 1.1% (5/453). Anemia, hypoproteinemia, and wound contamination were the main risk factors for neonatal AWD. The AWD-free survival rates for infants with severe anemia and mild to moderate anemia were 83.3% and 91.2%, respectively. The AWD-free survival rates for those with hypoproteinemia, type II and type III incision were 88.0%, 95.1% and 87.1%, respectively.Conclusion: Neonatal AWD is closely related to anemia, hypoproteinemia, and incision contamination. It is of great significance for the prevention of neonatal AWD to strengthen nutritional support, correct preoperative anemia, and control infection.Trial registration: Research Registry, researchregistry5350. Registered 01 February 2020 - Retrospectively registered, https://www.researchregistry.com/browse-the-registry#home/registrationdetails/5e359028eef79c001577fa18/
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