Neuromorphic devices that can emulate the bionic sensory and perceptual functions of neural systems have great applications in personal healthcare monitoring, neuro-prosthetics, and human–machine interfaces. In order to realize bionic sensing and perception, it’s crucial to prepare neuromorphic devices with the function of perceiving environment in real-time. Up to now, lots of efforts have been made in the incorporation of the bio-inspired sensing and neuromorphic engineering in the booming artificial intelligence industry. In this review, we first introduce neuromorphic devices based on diverse materials and mechanisms. Then we summarize the progress made in the emulation of biological sensing and perception systems. Finally, the challenges and opportunities in these fields are also discussed.

Background This study aimed to explore the predictive value of integrin α7 (ITGA7) for acute myeloid leukemia (AML) risk and subsequently investigate its correlation with risk stratification and prognosis in AML patients. Methods Bone marrow samples were obtained from 196 de novo AML patients prior to initiation of treatment and from 50 subjects underwent bone marrow donation or bone marrow biopsy for non‐hematologic malignant disease (as controls). ITGA7 mRNA and protein expressions were detected by real‐time quantitative polymerase chain reaction and Western blot assays, respectively. In AML patients, the risk stratification was assessed, and complete remission (CR), event‐free survival (EFS), and overall survival (OS) were evaluated. Results Both ITGA7 mRNA and protein expressions were increased in AML patients compared with controls, and their expressions were correlated with poorer risk stratification. For prognosis, ITGA7 mRNA expression and protein expression were declined in CR patients compared to non‐CR patients. Meanwhile, both EFS and OS were shorter in ITGA7 mRNA high expression patients compared to ITGA7 mRNA low expression patients, as well as ITGA7 protein high expression patients compared to ITGA7 protein low expression patients. Conclusion Integrin α7 might serve as a potential biomarker for predicting increased AML risk and worse prognosis in AML patients.

The aim of this study was to evaluate the safety and clinical efficacy of a combined preoperative regimen consisting of volumetric modulated arc therapy–simultaneous integrated boost and capecitabine chemotherapy for distal rectal cancer. A total of 26 patients with locally advanced distal rectal cancer were enrolled from March 2015 to May 2016. The radiation dose fractionation was 58.75 Gy/25 fractions (2.35 Gy/fraction) for rectal tumor and pelvic lymph node metastasis and 50 Gy/25 fractions for pelvic lymph node stations, accompanied with simultaneous capecitabine chemotherapy. Completion of the simultaneous chemotherapy was ensued by 1 week of rest and then another cycle of induction chemotherapy with capecitabine. A radical rectal cancer surgery was performed 6 to 8 weeks after the simultaneous chemoradiotherapy. The primary end points were the complete pathological response rate and the postoperative sphincter preservation rate. All 26 patients completed the neoadjuvant chemoradiotherapy, among which 25 received surgical treatment. The postoperative complete pathological response rate was as high as 32% (8/25), while the sphincter preservation rate was 60% (15/25), the overall tumor/node (T/N) downstaging rate was 92% (23/25), and the R0 resection rate was 100%. During the chemoradiation, the most common adverse events were grade 1 and 2; grade 3 radiodermatitis occurred in 2 cases but no occurrence of acute adverse events occurred that were grade 4 and above. After the surgery, there was one case of ureteral injury and one case of intestinal obstruction, but no perioperative deaths occurred. In conclusion, the chemoradiation regimen of preoperative volumetric modulated arc therapy-simultaneous integrated boost (VMAT-SIB58.75Gy) and a single cycle of induction chemotherapy with capecitabine for patients with distal rectal cancer is safe and feasible with a satisfactory complete pathological response rate, sphincter preservation rate, and R0 resection rate.

IntroductionThe aim of the study was to investigate the changes in serum concentrations of nine vitamins in patients undergoing chemotherapy for lung cancer and explore their clinical values and influencing factors.Material and methodsPatients receiving chemotherapy for lung cancer in our centre from February 2018 to May 2020 were enrolled in this study. Serum concentrations of the nine vitamins including vitamins A, D, E, B9, B12, B1, C, B2, and B6 were measured in all subjects, and the changes in the concentrations of these vitamins were compared before and after 2 cycles of chemotherapy. In addition, the potential correlations of serum vitamin levels with age, gender, pathological type, and disease status were analysed.ResultsIn the 178 patients with lung cancer, there were different degrees of vitamin A, vitamin D, vitamin C, and in particular, vitamin B2 deficiencies. Before chemotherapy, the concentrations of vitamin A and vitamin C were significantly different between males and females and among patients in different clinical stages (both p < 0.05), the concentrations of vitamin C and vitamin B2 significantly differed among different pathological types of lung cancer (p < 0.05), and vitamin D level was significantly related to the disease status (p < 0.05). In addition, the proportion of vitamin B2 deficiency differed significantly among different pathological types (p < 0.05). There were significant differences in the concentrations of vitamins D, C, and B2 before and after chemotherapy (all p < 0.05). There was a correlation between the change of serum vitamin B1 concentration before and after chemotherapy and the change of body mass index (p < 0.05).ConclusionsDuring chemotherapy, lung cancer patients are more likely to develop vitamins A, D, C, and B2 deficiencies. Different vitamin deficiencies are related to gender, clinical stage, pathological type, and disease status. Vitamin determination and reasonable supplementation of nutrients in patients undergoing chemotherapy for lung cancer can help improve the nutritional status and increase chemotherapy tolerance.

Background. The development of lung adenocarcinoma (LUAD) involves the interactions between cell proliferation and death. Autophagy-dependent ferroptosis, a distinctive cell death process was implicated in a multitude of diseases, whereas no research revealing the relationship between autophagy-dependent ferroptosis and LUAD pathogenesis was reported. Thus, the primary objective was to explore the role and potential function of the autophagy-dependent ferroptosis-related genes in LUAD.Methods. Clinical information and transcriptome profiling of patients with LUAD were retrieved and downloaded from open-source databases. Autophagy-dependent ferroptosis-related genes were screened by published articles. The key gene was identified as the intersection between the differentially expressed genes and prognosis-related genes. Patients were divided into high- and low-risk groups using the expression level of the key gene. The validity of the key gene prognosis model was verified by survival analysis. The correlation between the clinical characteristics of LUAD and the expression level of the key gene was analyzed to explore the clinical significance and prognosis value. And the roles of the key gene in response to chemotherapy, immune microenvironment and tumor mutation burden were predicted. The validation of key gene expression levels were further performed by immunohistochemistry staining.Results. FANCD2, a key autophagy-dependent ferroptosis-related gene by searching database, was confirmed as an independent prognostic factor for LUAD occurrence. The high expression level of FANCD2 was associated with an advantaged TNM stage, a less chemotherapy sensitivity, a low ImmuneScore, which indicated a deactivation status in immune microenvironment, a high tumor mutation burden, and a poor survival for LUAD patients. Pathway enrichment analysis showed that FANCD2 were involved in response to oxidative stress and neutrophil mediated immunity. Immunohistochemistry staining showed that the expression level of FANCD2 is higher in LUAD patients than normal tissue samples, which was in accordance with the database report.Conclusion. FANCD2, a key gene related to autophagy-dependent ferroptosis, could work as a biomarker, which predicts the survival, chemotherapy sensitivity, tumor immunity and mutation burden of LUAD. Research of autophagy-dependent ferroptosis and targeting the FANCD2 may offer a new perspective for the treatment and improvement of prognosis in LUAD.