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See Working with Events for other ways of subscribing to events. How do I see device events?ĭevice event logs can be found in the console in the device’s general information page. Next, recreate your device as documented in the Using the API section. In this case, the device will not appear in The Things Stack Console, so you need to check if it is present in the Join Server/Network Server/Application Server components using the following command:Ĭurl -X DELETE '' -H 'Accept: application/json' -H 'Authorization: Bearer ' You can also register the device using another JoinEUI, but keep in mind that you will need to configure that JoinEUI in the device as well.ĭuplicate identifiers: This error occurs when an end device is deleted from the Identity Server, but the device entry persists in the Join Server, Network Server and Application Server databases. If someone already registered an end device with this combination of DevEUI and JoinEUI, you can contact the manufacturer to check if your EUIs are correct and/or provide you new EUIs. You can also register the device using another JoinEUI, but keep in mind that you will need to configure that JoinEUI in the device as well.Īn end device with JoinEUI and DevEUI is already registered in another tenant: Within The Things Stack deployment, only a single end device can be registered with a certain combination of DevEUI and JoinEUI/AppEUI, across all tenants. If you previously registered an end device with this combination of DevEUI and JoinEUI, you can delete the existing device and repeat the registration. See ID and EUI constraints for more information.Īn end device with JoinEUI and DevEUI is already registered as in application : Within The Things Stack deployment, only a single end device can be registered with a certain combination of DevEUI and JoinEUI/AppEUI. ID already taken: Another end device in the application is using this ID. Here are some common errors and solutions: I receive an error when registering an end device. This section provides help for common issues and frequently asked questions you may have when adding devices. Sex steroids are mainly synthesized by the gonads (testis and ovary), but the adrenals constitute an additional source ( Vanderschueren et al. Overall, current evidence suggests that skeletal sexual dimorphism is not just the end result of differences in sex steroid secretion between the sexes, but depends on gender differences in GH–IGF1 and mechanical sensitivity to loading as well. AR and ERβ signaling may limit the osteogenic response to loading in males and females respectively, while ERα may stimulate the response of bone to mechanical stimulation in the female skeleton. In addition, sex hormones and their receptors have an impact on the mechanical sensitivity of the growing skeleton. Estrogen/ERα-mediated effects in males may – at least partly – depend on interaction with IGF1. Both the AR and ERα pathways are needed to optimize radial cortical bone expansion, whereas AR signaling alone is the dominant pathway for normal male trabecular bone development. Androgens not only act directly on bone through the androgen receptor (AR) but also activate estrogen receptor-α or -β (ERα or ERβ) following aromatization into estrogens. Estrogens limit periosteal bone expansion but stimulate endosteal bone apposition in females, whereas androgens stimulate radial bone expansion in males. GH–IGF1 action is likely to be the most important determinant of sex differences in bone mass. Recent findings have redefined the traditional concept of sex hormones as the main regulators of skeletal sexual dimorphism. Structural gender differences in bone mass – characterized by wider but not thicker bones – are generally attributed to opposing sex steroid actions in men and women. |
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