Programmable and Modularized Gas Sensor Integrated by 3D Printing.

The rapid advancement of intelligent manufacturing technology has enabled electronic equipment to achieve synergistic design and programmable optimization through computer-aided engineering. Three-dimensional (3D) printing, with the unique characteristics of near-net-shape forming and mold-free fabrication, serves as an effective medium for the materialization of digital designs into usable devices. This methodology is particularly applicable to gas sensors, where performance can be collaboratively optimized by the tailored design of each internal module including composition, microstructure, and architecture. Meanwhile, diverse 3D printing technologies can realize modularized fabrication according to the application requirements. The integration of artificial intelligence software systems further facilitates the output of precise and dependable signals. Simultaneously, the self-learning capabilities of the system also promote programmable optimization for the hardware, fostering continuous improvement of gas sensors for dynamic environments. This review investigates the latest studies on 3D-printed gas sensor devices and relevant components, elucidating the technical features and advantages of different 3D printing processes. A general testing framework for the performance evaluation of customized gas sensors is proposed. Additionally, it highlights the superiority and challenges of programmable and modularized gas sensors, providing a comprehensive reference for material adjustments, structure design, and process modifications for advanced gas sensor devices.

Analysis of the prognostic factors of simultaneous integrated boost-intensity modulated radiation therapy (SIB-IMRT) in 220 cases of locally advanced squamous esophageal cancer: a retrospective cohort study.

Background: Esophageal cancer is one of the most common malignant tumors in China. Patients with advanced esophageal cancer often cannot be treated by surgery; in these cases, radiation therapy is usually applied. However, there are currently few studies on the clinical efficacy of this treatment method. The present study aimed to investigate and observe the clinical efficacy and related prognostic factors of simultaneous integrated boost-intensity modulated radiation therapy (SIB-IMRT) in esophageal squamous carcinoma, and to provide a reference for clinicians in radiotherapy (RT) departments. Methods: The clinical and follow-up data of 220 patients with esophageal squamous carcinoma admitted to the First Affiliated Hospital of Bengbu Medical College from January 2017 to December 2018 were retrospectively analyzed to assess the relevant prognostic factors and analyze their effects on 3-year overall survival (OS) and progression-free survival (PFS). The prognostic influencing factors were analyzed using the log-rank test and Cox multi-factor regression analysis. Results: The median follow-up time was 56.0 months (3.0 to 66.0 months). The 1-, 2-, and 3-year survival rates were 68.6%, 49.1%, and 36.3%, respectively, for the entire cohort, and the 1-, 2-, and 3-year PFS rates were 52.3%, 37.7%, and 25.5%, respectively. The median OS time was 24 months [95% confidence interval (CI): 19.16-28.84 months] and the median PFS time was 15 months (95% CI: 11.04-18.96 months). The multifactorial analysis results showed that gender, RT dose, treatment modality, absolute lymphocyte count (ALC), and gross tumor volume (GTV) were independent prognostic factors affecting 3-year OS (P<0.05); while gender, N-stage, RT dose, and GTV were independent prognostic factors affecting 3-year PFS (P<0.05). Conclusions: In the SIB-IMRT era, the survival of esophageal squamous cell carcinoma (ESCC) patients treated with radical (chemo)radiotherapy is relatively satisfactory. As a single-institution study on radiation therapy for esophageal cancer, this study yielded accurate results that help to provide references for subsequent related studies and clinicians' selection of treatment options.

Analysis of Immunotherapy Combined with Radiotherapy in Patients with Brain Metastasis of Driver Gene-Negative Non-Small-Cell Lung Cancer.

Purpose: To observe the remission rate and side effects of immunotherapy combined with radiotherapy in patients with brain metastasis of driver gene-negative non-small-cell lung cancer (NSCLC). Methods: 152 patients with NSCLC brain metastasis admitted to our hospital from January 2019 to December 2021 were selected as the research objects. Patients were divided into a single group (85 cases) and a combined group (67 cases) according to treatment methods. The therapeutic effects and side effects of the single group and combined group were compared. In addition, the patients who received immunotherapy combined with radiotherapy were divided into three subgroups: A, B, and C, and the therapeutic effects and side effects of different radiotherapy modes were compared among group A [whole brain radiotherapy (WBRT)], group B (WBRT combined with local radiotherapy) and group C (local radiotherapy). Results: The objective response rate (ORR) and disease control rate (DCR) in the combined group were higher than those in the single group (P < 0.05). The incidence of reactive capillary hyperplasia and immune-related pneumonia in the combined group were higher than that in the single group (P < 0.05). There was no significant difference in the incidence of other side effects between the two groups (P > 0.05). ORR and DCR in group B were higher than those in group A (P < 0.05). There was no significant difference in the incidence of side effects among the three groups (P > 0.05). Conclusion: Immunotherapy combined with radiotherapy is effective in patients with brain metastasis of driver gene-negative NSCLC, which can improve the disease control rate without increasing the side effects. In addition, WBRT combined with local push radiotherapy is effective and safe. Clinical Study Registration Number. The Clinical study registration number is K2019086.

Haptoglobin is an early indicator of survival after radiation-induced severe injury and bone marrow transplantation in mice.

BACKGROUND: Hematopoietic stem cell transplantation (HSCT) is the main treatment for acute radiation sickness, especially after fatal radiation. The determination of HSCT for radiation patients is mainly based on radiation dose, hemogram and bone marrow injury severity. This study aims to explore a better biomarker of acute radiation injury from the perspective of systemic immune response. METHODS: C57BL/6J female mice were exposed to total body irradiation (TBI) and partial body irradiation (PBI). Changes in haptoglobin (Hp) level in plasma were shown at different doses and time points after the exposure and treatment with amifostine or bone marrow transplantation. Student's t-test/two tailed test were used in two groups. To decide the Hp levels as a predictor of the radiation dose in TBI and PBI, multiple linear regression analysis were performed. The ability of biomarkers to identify two groups of different samples was determined by the receiver operating characteristic (ROC) curve. The results were expressed as mean ± standard deviation (SD). Significance was set at P value < 0.05, and P value < 0.01 was set as highly significant. Survival distribution was determined by log-rank test. RESULTS: In this study, we found that Hp was elevated dose-dependently in plasma in the early post-irradiation period and decreased on the second day, which can be used as a molecular indicator for early dose assessment. Moreover, we detected the second increase of Hp on the 3rd and 5th days after the lethal irradiation at 10 Gy, which was eliminated by amifostine, a radiation protection drug, while protected mice from death. Most importantly, bone marrow transplantation (BMT) on the 3rd and 5th day after 10 Gy radiation improved the 30-days survival rate, and effectively accelerated the regression of secondary increased Hp level. CONCLUSIONS: Our study suggests that Hp can be used not only as an early molecule marker of radiation injury, but also as an important indicator of bone marrow transplantation therapy for radiation injury, bringing new scientific discoveries in the diagnosis and treatment of acute radiation injury from the perspective of systemic immunity.

N6-Methyladenosine-Related lncRNAs Are Anticipated Biomarkers for Sarcoma Patients.

Background: Soft tissue sarcomas (STSs) are rare tumors and occur at any site in the body. Our goal was to identify a putative molecular mechanism for N6-methyladenosine (m6A) lncRNA alteration and to develop predictive biomarkers for sarcoma. Methods: The lncRNA levels were obtained from TCGA datasets. Pearson correlation analysis was used to select all the lncRNAs that are connected to m6A. An m6A-related lncRNA model was built using LASSO Cox regression. To assess the prognostic efficiency of the model and potential lncRNAs, we performed univariate survival analysis and receiver operating characteristic (ROC) analysis. We also performed enrichment analysis to evaluate the roles of the potential genes. Finally, quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to confirm m6A-related lncRNA expression in tissues. Results: Following Pearson correlation analysis on TCGA datasets, we identified 78 m6A-related lncRNAs. Next, we used LASSO Cox regression analysis and identified 13 m6A-related lncRNAs as prognostic lncRNAs. After calculating risk scores, sarcoma patients were divided into high- and low-risk groups depending on the median of risk scores. We also found that these lncRNAs were immune associated via enrichment analysis. Conclusions: Here, we found that SNHG1, FIRRE, and YEATS2-AS1 could serve as biomarkers to predict overall survival of sarcoma patients, which provides a new insight into treatment of STS.

BPIFA2 as a Novel Early Biomarker to Identify Fatal Radiation Injury After Radiation Exposure.

Background: Current dosimeters cannot cope with the two tasks of medical rescue in the early stage of nuclear accident, the accurate determination of radiation exposure and the identification of patients with fatal radiation injury. As radiation can cause alterations in serum components, it is feasible to develop biomarkers for radiation injury from serum. This study aims to investigate whether serum BPIFA2 could be used as a potential biomarker of predicting fatal radiation injury in the early stage after nuclear accident. Methods: A rabbit anti-mouse BPIFA2 polyclonal antibody was prepared to detect the expression of BPIFA2. C57BL/6J female mice were exposed to total body radiation (TBI) at different dose and Partial body radiation (PBI) at lethal dose to detect the dynamic changes of BPIFA2 in serum at different time points after irradiation by Western blot assay. Results: BPIFA2 in mice serum were significantly increased at 1-12 h post-irradiation at .5-10 Gy, and increased again significantly at 3 d after 10 Gy irradiation with associated with mortality closely. It also increased rapidly after PBI and was closely related to injury degree, regardless whether the salivary glands were irradiated. Conclusions: The increase of serum BPIFA2 is a novel early biomarker not only for identifying radiation exposure, but also for fatal radiation injury playing a vital role in rational use of medical resources, and greater efficiency of medical treatment to minimize casualties.

Early Biomarkers Associated with P53 Signaling for Acute Radiation Injury.

Accurate dose assessment within 1 day or even 12 h after exposure through current methods of dose estimation remains a challenge, in response to a large number of casualties caused by nuclear or radiation accidents. P53 signaling pathway plays an important role in DNA damage repair and cell apoptosis induced by ionizing radiation. The changes of radiation-induced P53 related genes in the early stage of ionizing radiation should compensate for the deficiency of lymphocyte decline and γ-H2AX analysis as novel biomarkers of radiation damage. Bioinformatic analysis was performed on previous data to find candidate genes from human peripheral blood irradiated in vitro. The expression levels of candidate genes were detected by RT-PCR. The expressions of screened DDB2, AEN, TRIAP1, and TRAF4 were stable in healthy population, but significantly up-regulated by radiation, with time specificity and dose dependence in 2-24 h after irradiation. They are early indicators for medical treatment in acute radiation injury. Their effective combination could achieve a more accurate dose assessment for large-scale wounded patients within 24 h post exposure. The effective combination of p53-related genes DDB2, AEN, TRIAP1, and TRAF4 is a novel biodosimetry for a large number of people exposed to acute nuclear accidents.

Lipidomic Profiling for Serum Biomarkers in Mice Exposed to Ionizing Radiation.

Radiation biodosimeters are required urgently for fast and accurate evaluation of absorbed dose for irradiated individuals. Lipidomics has appeared as a credible technique for identification and quantification of lipid for researching biomarker of diseases. We performed a lipidomic profile on mice serum at time points of 6, 24, and 72 hours after 0, 2, 5.5, 7, and 8 Gy irradiation to select radiation-responsive lipids and conducted Kyoto Encyclopedia of Genes and Genome pathway enrichment analysis to recognize the pathways and network changes. Then, Pearson correlation analysis was performed to evaluate the feasibility of radiation-responsive lipids to estimate radiation dose. Seven radiation-responsive lipids including PC (18:2/18:2), PC (18:0/18:2), Lyso PC 18:1, PC (18:0/20:4), SM (D18:0/24:1), PC (16:0/18:1), and Lyso PC 18:2 were identified in which glycerophospholipid metabolism presented as the most significant pathway, and they all presented good linear correlation with the irradiated dose. This study identified 7 radiation-responsive lipids in mice serum and certificate their feasibility of dose estimation as biodosimeters.

Type 2 diabetes mitigation in the diabetic Goto-Kakizaki rat by elevated bile acids following a common-bile-duct surgery.

OBJECTIVE: Elevated plasma bile acids after bariatric surgery are thought to explain type 2 diabetes mellitus (T2DM) remission. Bile acids can bind to and activate the nuclear receptor farnesoid-X receptor (FXR) by regulating lipid and glucose metabolism. We performed a surgical procedure (ligation of the common bile duct and external biliary drainage [LBD]) in the diabetic Goto-Kakizaki (GK) rat in order to investigate its effect on bile acids metabolism and T2DM mitigation. MATERIAL/METHODS: LBD surgery and sham control surgery were performed on diabetic GK rats. The concentrations of total bile acids and blood glucose were analyzed by an automatic analyzer. Intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (ITT) were used to monitor blood glucose level. Expression of genes involved in bile acid metabolism (FXR, CYP7A, et al.) and glycolipid metabolism (G6Pase, PEPCK, et al) was analyzed using qRT-PCR. The protein levels of pAKT, AKT and pGSK3ß were tested by western blot. The morphological alterations of the liver and epididymal fat were monitored by H&E staining. RESULTS: LBD increased plasma total bile acids, improved hepatic insulin sensitivity, and eventually mitigated T2DM, whereas food intake and body weight were unaltered. Post-LBD, the levels of total bile acids were elevated from 24.80±7.12 to 61.44±6.40 and the concentration of fast blood glucose was decreased from 204.7±11.06mg/dL to 109.3±5.4mg/dL. IPGTT and ITT showed that LBD operation improved insulin sensitivity in GK rats. Clusters of FXR signaling target genes were altered in the liver, such as FXR, CYP7A, G6Pase and PEPCK. These contributed to sustained bile acid homeostasis, and they ameliorated hepatic endoplasmic reticulum (ER) stress, increased energy expenditure, and reduced gluconeogenesis, resulting in a substantial improvement in hepatic insulin sensitivity. LBD also significantly reduced epididymal fat tissue and decreased the size of adipocytes. CONCLUSION: These results demonstrate that the elevated bile acids observed in LBD-operated GK rats link insulin sensitivity improvement to T2DM mitigation, recapitulating the metabolic effects of bariatric surgery. Our investigation establishes a model for a focused study of bile acids in the context of bariatric surgery that may contribute to the identification of therapeutics for T2DM.

Toll-like receptor 5 agonism protects mice from radiation pneumonitis and pulmonary fibrosis.

Radiation pneumonitis and pulmonary fibrosis are the main complications with radiotherapy for thoracic neoplasms, directly limiting the efficient dose in clinical application and currently there are few medicines that effectively function as radioprotectants. However, a TLR5 agonist, CBLB502, was confirmed to have protective efficacy against hematopoietic and gastrointestinal radiation syndromes in mice and primates. This study points to a new direction for protection against thoracic radiation-induced pulmonary syndromes and skin injury by CBLB502. We utilized the TUNEL assay, pathological analysis and immunohistochemistry to obtain evidence that CBLB502 could alleviate the occurrence of radiation pneumonitis and pulmonary fibrosis as well as radiation- induced skin injury. It may thus play a promising role in facilitating clinical radiotherapy of thoracic neoplasms.

Toll-like receptor 5 agonist inhibition of growth of A549 lung cancer cells in vivo in a Myd88 dependent manner.

The purpose of this study was to examine the effect of a Toll-like receptor 5 (TLR5) agonist, CBLB502, on the growth and radiosensitivity of A549 lung cancer cells in vivo. Expression of myeloid differentiation factor 88 (MyD88) or TLR5 was stably knocked down in human lung cancer cells (A549) using lentivirus expressing short hairpin RNA targeting human MyD88 or TLR5. Lack of MyD88 or TLR5 expression enhanced tumor growth in mouse xenografts of A549 lung cancer cells. CBLB502 inhibited the growth of A549 lung cancer cells, not A549-MyD88-KD cells in vivo in the murine xenograft model. Our results showed that the inhibition of A549 by CBLB502 in vivo was realized through regulating the expression of neutrophil recruiting cytokines and neutrophil infiltration. Finally, we found that activation of TLR5 signaling did not affect the radiosensitivity of tumors in vivo.

Repair of articular cartilage defects with tissue-engineered osteochondral composites in pigs.

To compare the results of repair of knee cartilage defects with tissue-engineered osteochondral composites and tissue-engineered cartilage in pigs. Autologous chondrocytes and osteoblasts were seeded on scaffolds of polylactic-co-glycolic acid (PLGA) and tricalcium phosphate (TCP) to generate tissue-engineered cartilage and tissue-engineered bone, respectively. The tissue-engineered osteochondral composite was formed by a chondrocyte-PLGA construct sutured to an osteoblast-TCP construct with an absorbable suture. Cartilage defects were surgically created at the weightbearing surface of the bilateral femoral medial condyles of 12 mini-pigs. Thus, 24 defects in 12 pigs were randomly assigned to three treatment groups: tissue-engineered osteochondral composite group, tissue-engineered cartilage group, and blank control group. Six months after surgery, the regenerated cartilage was scored macroscopically and histologically. The compressive properties and glycosaminoglycan (GAG) content of the cartilage were also assessed. The gross grading scale indicated that the mean scores of the tissue-engineered osteochondral composite group were significantly higher than those of the tissue-engineered cartilage group. According to the International Cartilage Repair Society (ICRS) Visual Histological Assessment Scale, the scores of the osteochondral composite group were significantly better than those of the tissue-engineered cartilage group and blank control group. Assessment of compressive properties and GAG content showed better repair results in the osteochondral composite group than those of the tissue-engineered cartilage group. Using tissue-engineered osteochondral composites to repair cartilage defects was better than that of tissue-engineered cartilage.