Sensors enable the detection of physiological indicators and pathological markers to assist in the diagnosis, treatment, and long-term monitoring of diseases, in addition to playing an essential role in the observation and evaluation of physiological activities. The development of modern medical activities cannot be separated from the precise detection, reliable acquisition, and intelligent analysis of human body information. Therefore, sensors have become the core of new-generation health technologies along with the Internet of Things (IoTs) and artificial intelligence (AI). Previous research on the sensing of human information has conferred many superior properties on sensors, of which biocompatibility is one of the most important. Recently, biocompatible biosensors have developed rapidly to provide the possibility for the long-term and in-situ monitoring of physiological information. In this review, we summarize the ideal features and engineering realization strategies of three different types of biocompatible biosensors, including wearable, ingestible, and implantable sensors from the level of sensor designing and application. Additionally, the detection targets of the biosensors are further divided into vital life parameters (e.g., body temperature, heart rate, blood pressure, and respiratory rate), biochemical indicators, as well as physical and physiological parameters based on the clinical needs. In this review, starting from the emerging concept of next-generation diagnostics and healthcare technologies, we discuss how biocompatible sensors revolutionize the state-of-art healthcare system unprecedentedly, as well as the challenges and opportunities faced in the future development of biocompatible health sensors.

Background: With the rapid development of surgical technics and instruments, more and more locally advanced non-small cell lung cancer (NSCLC) patients are being treated by minimally invasive surgery (MIS), including video-assisted thoracoscopic surgery (VATS) and robotic-assisted thoracic surgery (RATS). The aim of this retrospective study was to compare the perioperative and long-term outcomes of patients who underwent lobectomy by these two surgical approaches. Methods: We performed a retrospective review of the prospectively collected database of our hospital to identify patients with clinical stage IIB–IIIA NSCLC who underwent video-assisted thoracoscopic or robotic lobectomy. Perioperative outcomes, recurrence, and overall survival (OS) were compared. Results: From January 2014 to January 2017, there were at total of 121 patients, including 36 robotic lobectomy patients and 85 VATS lobectomy patients. One patient (2.8%) in the RATS group and 5 patients (5.9%) in the VATS group were converted to thoracotomy (P=0.79). No perioperative death was observed in both groups. The postoperative morbidity was similar between the two groups (13.9% for RATS vs. 15.3% for VATS; P=0.84). Robotic lobectomy was associated with a shorter length of postoperative hospital stay (4 vs. 5 d, P<0.01) and more counts of lymph nodes harvested (13 vs. 10, P<0.01). The median disease-free survival (DFS) for the RATS and VATS groups were 31.1 and 33.8 months, respectively. The corresponding 3-year DFS was 40.3% in the RATS group and 47.6% in the VATS group (P=0.74). The 3-year OS was 75.7% in RATS and 77.0% in the VATS group (P=0.75). Conclusions: For selected NSCLC patients with lymph node involvement, robotic lobectomy is safe and effective with a low complication rate and similar long-term outcome compared with VATS lobectomy. Moreover, the robotic approach resulted in shorter postoperative length of stay and greater lymph node assessment.

Background: Epithelial-to-mesenchymal transition (EMT) contributes to the invasion and metastasis of epithelial tumors. Sirtuin 6 (SIRT6), an NAD-dependent deacetylase, is known to promote metastasis of non-small cell lung cancer (NSCLC). Methods: In this work, we determined the role of SIRT6 in the EMT of NSCLC cells and identified the key EMT-related genes involved in the oncogenic activity of SIRT6. Results: We report that depletion of SIRT6 inhibits transforming growth factor-β1 (TGF-β1)-induced EMT in A549 and H1299 NSCLC cells, which is rescued by ectopic expression of SIRT6. Knockdown of SIRT6 leads to a reduction in Snail protein without affecting the mRNA level. Immunoprecipitation experiments demonstrate a physical association between SIRT6 and Snail. SIRT6 deacetylates Snail and prevents its proteasomal degradation. Silencing of Snail blunts SIRT6-induced NSCLC cell migration and invasion, while overexpression of Snail restores the invasion and EMT in SIRT6-depleted NSCLC cells. SIRT6 depletion leads to an upregulation of kruppel-like factor 4 (KLF4) and reduced Snail binding to the promoter of Klf4 in NSCLC cells. Knockdown of KLF4 rescues the invasive capacity in SIRT6-depleted NSCLC cells. Conversely, co-expression of KLF4 impairs SIRT6-induced aggressive behavior. In vivo data further demonstrate that SIRT6-induced NSCLC metastasis is antagonized by overexpression of KLF4. Conclusions: These findings provide mechanistic insights into the pro-metastatic activity of SIRT6 and highlight the role of the SIRT6/Snail/KLF4 axis in regulating EMT and invasion of NSCLC cells.