ABSTRACT
Long-term care refers to any support, both medical and non-medical, provided to the elderly with a chronic illness or disability due to physical or mental conditions. Since the cost of long-term care insurance is not inexpensive, low-cost devices and sensors can be used to create medical assistance systems to reduce human maintenance costs. The requirement of security and privacy under healthcare information protection is a critical issue for internet of medical things (IoMT) data transmission. In this paper, we designed an IoMT security robot for a long-term care system. The goal of this IoMT security robot is to provide secure transmission of the residents' private information. It is composed of three layers, namely, collection, encryption, and transmission. The function of the IoMT security robot is to first collect data from the patient or the elderly, then provide efficient data encryption, and deliver secured data transmission mechanisms to send the valuable data to the cloud. This IoMT security robot also has a server authentication mechanism, and a support IoT and IoMT devices inspection function. Our evaluation results showed that even when we utilized a low power consumption device like Raspberry Pi, AES algorithm achieved an encrypt and decrypt of 100-100 K bytes under 9 ms, which is a lot better than ECC, which takes about 104 ms. Further, we found that the AES only takes 0.00015 s to decrypt 100 Bytes data, which is way faster than the ECC algorithm, which takes 0.09 s.
ABSTRACT
BACKGROUND: Hypertension is a severe public health risk factor worldwide. Elevated angiotensin II (Ang II) produced by the renin-angiotensin-aldosterone system can lead to hypertension and its complications. METHOD: In this study, we addressed the cardiac-injury effects of Ang II and investigated the signaling mechanism induced by Ang II. Both H9c2 cardiomyoblast cells and neonatal rat cardiomyocytes were exposed to Ang II to observe hypertension-related cardiac apoptosis. RESULTS: The results of western blotting revealed that Ang II significantly attenuated the IGF1R-PI3K-AKT pathway via the Ang II-AT1 receptor axis and phosphatase and tensin homolog expression. Furthermore, real-time PCR showed that Ang II also activated miR-320-3p transcription to repress the PI3K-Akt pathway. In the heart tissue of spontaneously hypertensive rats, activation of the IGF1R survival pathway was also reduced compared with that in Wistar-Kyoto rats, especially in aged spontaneously hypertensive rats. CONCLUSION: Hence, we speculate that the Ang II-AT1 receptor axis induces both phosphatase and tensin homolog and miR-320-3p expression to downregulate the IGF1R-PI3K-AKT survival pathway and cause cell apoptosis in the heart.
