MIC19 Exerts Neuroprotective Role via Maintaining the Mitochondrial Structure in a Rat Model of Intracerebral Hemorrhage.

As an essential constituent of the mitochondrial contact site and cristae organization system (MICOS), MIC19 plays a crucial role in maintaining the stability of mitochondrial function and microstructure. However, the mechanisms and functions of MIC19 in intracerebral hemorrhage (ICH) remain unknown and need to be investigated. Sprague Dawley (SD) rats injected with autologous blood obtained from the caudal artery, and cultured neurons exposed to oxygen hemoglobin (OxyHb) were used to establish and emulate the ICH model in vivo and in vitro. Lentiviral vector encoding MIC19 or MIC19 short hairpin ribonucleic acid (shRNA) was constructed and administered to rats by intracerebroventricular injection to overexpress or knock down MIC19, respectively. First, MIC19 protein levels were increased after ICH modeling. After virus transfection and subsequent ICH modeling, we observed that overexpression of MIC19 could mitigate cell apoptosis and neuronal death, as well as abnormalities in mitochondrial structure and function, oxidative stress within mitochondria, and neurobehavioral deficits in rats following ICH. Conversely, knockdown of MIC19 had the opposite effect. Moreover, we found that the connection between MIC19 and SAM50 was disrupted after ICH, which may be a reason for the impairment of the mitochondrial structure after ICH. In conclusion, MIC19 exerts a protective role in the subsequent injury induced by ICH. The investigation of MIC19 may offer clinicians novel therapeutic insights for patients afflicted with ICH.

Application of Improved Robot-assisted Laparoscopic Telesurgery with 5G Technology in Urology.

The demand for telesurgery is rising rapidly, but robust evidence regarding the feasibility of its application in urology is still rare. From March to October 2021, a surgeon-controlled surgical robot in a tertiary hospital in Qingdao was used to remotely conduct robot-assisted laparoscopic radical nephrectomy (RN) in 29 patients located in eight primary hospitals. The median round-trip delay was 26 ms (interquartile range [IQR] 5) and the median distance between the primary hospital and the surgeon was 187 km (IQR 57). Both the master unit and the slave unit were guaranteed by network and mechanical engineers, and surgical assistants were well prepared on the patient side to prevent complications. The primary evaluation metric was the success rate, defined as the percentage of patients who underwent successful remote RN without conversion to other surgical procedures and no major intraoperative or postoperative complications. The results demonstrate that the combination of 5G technology and surgical robots is a novel potential telemedicine-based therapy choice for renal tumors. PATIENT SUMMARY: Our study shows that telesurgery using 5G technology is a safe and feasible treatment option for patients with kidney tumors. The total delay between the remote location and the operating rooms where surgery was being performed was just 200 ms. This approach could reduce health care costs and improve the quality of medical services accessed by patients.

Sam50 exerts neuroprotection by maintaining the mitochondrial structure during experimental cerebral ischemia/reperfusion injury in rats.

AIM: To investigate the role of Sam50, a barrel protein on the surface of the mitochondrial outer membrane, in cerebral ischemia-reperfusion (I/R) injury and its underlying mechanisms. METHODS: A middle cerebral artery occlusion/reperfusion (MCAO/R) model in adult male Sprague-Dawley rats was established in vivo, and cultured neurons were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) to simulate I/R injury in vitro. Lentiviral vector encoding Sam50 or Sam50 shRNA was constructed and administered to rats by intracerebroventricular injection to overexpress and knockdown Sam50, respectively. RESULTS: First, after MCAO/R induction, the mitochondrial structure was damaged, and Sam50 protein levels were increased responsively both in vivo and in vitro. Then, it was found that Sam50 overexpression could reduce infarction size, inhibit neuronal cell death, improve neurobehavioral disability, protect mitochondrial structure integrity, and ameliorate mitochondrial dysfunction, which was induced by I/R injury both in vivo and in vitro. However, Sam50 downregulation showed the opposite results and aggravated I/R injury by inducing neuronal cell death, neurobehavioral disability, and mitochondrial dysfunction. Moreover, we found that the interaction between Sam50 and Mic19 was broken off after OGD/R, showing that the Sam50-Mic19-Mic60 axis was breakage in neurons, which would be a reason for mitochondrial structure and function abnormalities induced by I/R injury. CONCLUSION: Sam50 played a vital role in the protection of neurons and mitochondria in cerebral I/R injury, which could be a novel target for mitochondrial protection and ameliorating I/R injury.