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As industrial safety increases, various industrial accident prevention technologies using smart factory technology are being studied. However, small and medium enterprises (SMEs), which account for the majority of industrial accidents, are having difficulties in preventing industrial accidents by applying these smart factory technologies due to practical problems. In this study, customized monitoring and warning systems for each type of industrial accident were developed and applied to the actual field. Through this, we demonstrated industrial accident prevention technology through appropriate smart factory technology used by SMEs. A customized monitoring system using vision, current, temperature, and gas sensors was established for the four major disaster types: worker body access, short circuit and overcurrent, fire and burns due to high temperature, and emission of hazardous gas. In addition, a notification method suitable for each work environment was applied so that the monitored risk factors could be recognized quickly, and real-time data transmission and display enabled workers and managers to understand the disaster risk effectively. Through the application and demonstration of these appropriate smart factory technologies, the spread of these industrial safety technologies is to be discussed.

본 연구에서는 리그닌 기반 다공성 탄소(lignin-based porous carbon; LBPC)를 수산화칼륨(KOH)으로 활성화할 때 온도가 비표면적과 전기화학적 특성에 미치는 영향을 알아보았다. 리그닌과 acrylonitrile을 그라프트 중합으로 합성한 리그닌-polyacrylonitrile (PAN) 공중합체를 전구체로 하여 LBPC를 제조한 후 LBPC를 KOH로 600, 700, 800, 900℃에서 활성화하여 활성화 처리한 LBPC (KA-LBPC-6, 7, 8, 9)를 제조하였다. KA-LBPC의 표면 특성을 알아보기 위해 주사전자현미경으로 관찰하였으며, 비표면적 분석을 통해 기공 특성을 파악하였다. 전기화학적 특성은 3전극 시스템으로 분석하였다. 실험 결과 SEM 사진상에서 활성화 처리에 의한 미세기공 형성을 관찰하였다. KA-LBPC-7의 비표면적은 2480.1 ㎡/g, 미세기공 부피는 0.64 ㎤/g, 중기공 부피는 0.76 ㎤/g으로 KA-LBPC 중에서 가장 좋은 기공 특성을 보였다. 전기화학적 특성 역시 2 mV/s의 주사속도에서 비정전용량이 151.3 F/g이었던 KA-LBPC-7이 가장 좋은 것으로 나타났다.

Characteristics of a discharged liquid jet in near-nozzle are determined by the in-flow turbulences generated by the evolution of inflow vortices and cavitation. High-fidelity simulations have indicated that such physical processes can generate ultrafast turbulent fluctuations (in the range of MHz) originating from the nature of turbulence by the interaction between the large and small-scale turbulence in the flow. Detecting ultrafast turbulent oscillations while resolving small-scale turbulences in the optically dense near-nozzle liquid jet has not been observed through experimental methods so far. In this study, therefore, ultrafast x-ray phase-contrast imaging, which can provide a clear image in the near-field using a high-energy x-ray source, was applied to observe the fluctuation of flow velocity in the near-field to obtain the ultrafast turbulent oscillations at the discharged jet. To capture the ultrafast variance of flow velocity originating from the nature of turbulence, the high imaging frequency was applied up to 1.2 MHz. With the implemented methodology, turbulence intensity distributions of discharged liquid jets were measured for various injection pressures and nozzle geometries. Such turbulence intensity results were also correlated with the initial dispersion angle of the spray. In addition, the turbulence length scales, which can be detected through the current methodology, were estimated and discussed considering standard-length scales. The results showed that the current experimental method introduced in this study can provide important insights into the turbulence characteristics of spray by resolving Taylor scale turbulences and can provide valuable validation data and boundary conditions for reliable spray simulations.

Background and purpose Kaempferol is a natural flavonoid widely investigated in various fields due to its antioxidant, anti-cancer, and anti-inflammatory activities, but few studies have shown its inhibitory effect on T cell activation. This study examined the therapeutic potential of kaempferol in atopic dermatitis by modulating T cell activation. Experimental approach Effects of kaempferol on T cell activation and the underlying mechanisms were investigated in Jurkat cells and mouse CD4+ T cells. A model of atopic dermatitis in mice was used to determine its therapeutic potential on T cell-mediated conditions in vivo. Western blots, RT-PCR, pulldown assays and ELISA were used, along with histological analysis of skin. Key results Pretreatment with kaempferol reduced CD69 expression and production of inflammatory cytokines including IL-2 from activated Jurkat cells and murine CD4+ T cells without cytotoxicity. Pulldown assays revealed that kaempferol physically binds to MRP-1 in T cells, inhibiting the action of MRP-1. In activated T cells, kaempferol suppressed JNK phosphorylation and the TAK1-IKKα mediated NF-κB pathway. Oral administration of kaempferol to mice showed improved manifestation of atopic dermatitis, a T cell-mediated condition. Western blot results showed that, as in the in vitro studies, decreased phosphorylation of JNK was associated with down-regulated MRP-1 activity in vivo, in the kaempferol-treated mice in the atopic dermatitis model. Conclusion and implications Kaempferol regulates T cell activation by inhibiting MRP-1 activity in activated T cells, thus showing protective effects against T cell mediated disease in vivo.

Persimmon leaf extracts (PLE) have been widely used as a traditional medicine in East Asian countries. The effects of persimmon leaves, including antioxidant, antiinflammatory, hypotensive, and anti-allergy effects, have been investigated; however, there is little evidence on the inhibition of T cell activation in vitro and effects on T cell-related diseases, such as atopic dermatitis (AD), in vivo by persimmon leaves. PLE (50 μg/mL) effectively attenuated the mRNA levels of IL-2 in Jurkat T cells stimulated with PMA/A23187 and Staphylococcus enterotoxin E-loaded Raji B cells without causing cytotoxicity. In Jurkat T cells stimulated with PMA/A23187, treatment with 50 μg/mL PLE blocked the translocation of p65 and IκBα degradation. Moreover, the JNK signaling pathway in Jurkat T cells stimulated with PMA/A23187 was affected by treatment with PLE. The oral administration of PLE markedly attenuated AD manifestations in mice, including ear thickness, IgE levels, and lymph node sizes. These results indicate PLE significantly blocked T cell activation via NF-κB signaling and the JNK pathway. This suggests underlying mechanisms of PLE involving the control of effector cytokines produced by activated T cells in ear tissue and lymph nodes, as well as the infiltration of mast cells and the therapeutic potential of AD.

Smart factory is the main keyword in the field of manufacturing processes about the fourth industrial revolution. To realize the smart factory, making all pieces of device into smart devices that are connected to the centralized system to enable a real-time exchange of information is essential. Sound can be efficient means to make devices as smart devices because sound can contain the status information of various devices simultaneously, and it can be recorded easily outside of a device using only a microphone. In this study, multi-device operation monitoring system by analyzing sound is developed. Mic arrays for acquiring the sound were installed at the outside the devices and recorded the sounds from several devices simultaneously. By analyzing the recorded sound with log-mel spectrogram and Convolutional Neuron Network (CNN), the system could detect the operational status of three devices with an accuracy of 71–92 %. To improve the performance, virtual data set was created by composition of individual device operating sounds of different intensities. With this virtual data set, accuracy can be enhanced to 87 % ∼ 99 % accuracy and, required sound data amount could be reduced. Developed system was applied successfully in monitoring experiments in two different environments: a workshop in which hand-operated device was used and a factory with a computer numerical control machine and verifying the performance.

Methamphetamine (METH) is an extremely addictive drug that has raised serious public health concerns recently. METH addiction not only results in neuronal cytotoxicity, but it also affects immune cell activity, including T lymphocytes. 6,4,7[Formula: see text]-trihydroxyflavanone (THF), isolated from Dalbergia odorifera, has been studied for its antibacterial activity, but evidence for whether THF has an anti-cytotoxic and protective effect on T cell activation exposed to METH is lacking. In this study, results showed that treatment with THF was not cytotoxic to Jurkat T cells but dose-dependently mitigated the cytotoxicity induced by exposure to METH. The Western blot results demonstrating pre-treatment with THF maintained the expression of anti-apoptotic proteins and phosphorylation of PI3K/Akt/mTOR downregulated by treatment with METH. Furthermore, we found that decreased expression of IL-2 and CD69 by METH exposure was partially restored, and viability was significantly prevented by pre-treatment with THF in activated T cells. These findings were involved in re-elevated expression of anti-apoptotic proteins as well as recovered pathways including MAPK/PI3K/Akt/mTOR in activated T cells pre-exposed to METH. Our results suggest beneficial effects of THF against the cytotoxic and immune-modulating effect of METH on T cells and therapeutic potential of THF for patients with immunodeficiency caused by METH addiction.

The material extrusion (ME) process is one of the most widely used 3D printing processes, especially considering its use of inexpensive materials. However, the error known as the “spaghetti-shape error,” related to filament tangling, is a common problem associated with the ME process. Once occurring, this issue, which consumes both time and materials, requires a restart of the entire process. In order to prevent this, the user must constantly monitor the process. In this research, a failure detection method which uses a webcam and deep learning is developed for the ME process. The webcam captures images and then analyzes them by machine learning based on a convolutional neural network (CNN), showing outstanding performance in both image classification and the recognition of objects. Sample images were trained based on a modified Visual Geometry Group Network (VGGNet) model and the trained model was evaluated, resulting in 97% accuracy. The pre-trained model was tested on a 3D printer monitoring system for its ability to recognize the “spaghetti-shape-error” and was able to detect 96% of abnormal deposition processes. The proposed method can analyze the ME process in real time and informs the user or halts the process when abnormal printing is detected.

The precise location of the Master Knot of Henry (MKH) has important clinical significance, but its anatomical definition has not been agreed upon. The purpose of this study is to present a linear regression equation for predicting length variables based on foot length, by evaluating the correlation of length variables related to flexor hallucis longus (FHL) and flexor digitorum longus (FDL), with respect to the location of the MKH. A total of 95 limbs were dissected from 48 adult cadavers, and were fixed in formalin. Measurements were made for the length parameter, with reference to the landmark. The relevance between length variables was analyzed through simple correlation analysis and linear regression analysis. The foot length was 213.69 ± 17.53 mm, MKH-great toe distal phalanx was 140.16 ± 14.69 mm, MKH-FHL insertion was 124.55 ± 13.46 mm, MKH-little toe distal phalanx was 121.79 ± 13.41 mm, MKH-FDL little toe insertion was 109.07 ± 14.16 mm, and the FHL-FDL angle was 33.15 ± 5.39. The correlation coefficient between all the length variables for foot length showed a high positive correlation. We derived a regression equation that can predict the length of each variable. This regression formula is considered to be highly useful because it can estimate the positional relationship of the MKH relatively simply.

Background and objectives: EZH2 is overexpressed in hepatocellular carcinoma (HCC) and is correlated with poor prognosis. However, its clinical significance and molecular mechanism have not been studied in HCC. In this study, clinical and prognostic values of EZH2 was studied using Total Cancer Genome Atlas (TCGA) data and then, these data were confirmed in Huh1 and HepG2 cell lines. Materials and Methods: We used the TCGA database from cBioPortal. In addition, we analyzed EZH2 mRNA levels in HCC cell lines and its correlation with STAT3 and EZH2. Results: According to TCGA, EZH2 had a prognostic value in various cancers, especially in HCC. Furthermore, EZH2 in HCC was correlated with N stage (p = 0.045) and alpha-fetoprotein (AFP) > 20 ng/mL (p < 0.01). However, a negative association between EZH2 and age (p = 0.027) was found. The overall survival result of HCC was significantly poorer in patients with high EZH2 expression. In addition, the recurrence rate was also significantly higher in patients with high expression of EZH2 than those with low expression (χ2 = 16.10, p < 0.001). EZH2 expression was negatively correlated with STAT3 expression among EZH2-associated genes (R = −0.163, p = 0.002). EZH2 expression level was down-regulated to 50% or less compared to the control group treated negative siRNA. MTT assays showed that EZH2-siRNA affected on the viability of HCC cell line significantly. Conclusions: In conclusion, the overexpression of EZH2 was an independent biomarker for poor outcomes of HCC. However, more in vivo studies are required to identify the downstream target genes in HCC to improve our understanding of the biological role of EZH2 in HCC.

Triacsins are a family of natural products containing an N-hydroxytriazene moiety not found in any other known secondary metabolites. Though many studies have examined the biological activity of triacsins in lipid metabolism, the biosynthesis of triacsins has remained unknown. Here, we report the identification of the triacsin biosynthetic gene cluster in Streptomyces aureofaciens ATCC 31442. Bioinformatic analysis of the gene cluster led to the discovery of the tacrolimus producer Streptomyces tsukubaensis NRRL 18488 as a new triacsin producer. In addition to targeted gene disruption to identify necessary genes for triacsin production, stable isotope feeding was performed in vivo to advance the understanding of N-hydroxytriazene biosynthesis.

Periodontitis is a set of chronic inflammatory diseases caused by the accumulation of Gram-negative bacteria on teeth, resulting in gingivitis, pocket formation, alveolar bone loss, tissue destruction, and tooth loss. In this study, the contents of ginsenosides isolated from Panax ginseng fruit extract were quantitatively analyzed, and the anti-inflammatory effects were evaluated in human periodontal ligament cells. The major ginsenosides, Re, Ra8, and Rf, present in ginseng fruit were simultaneously analyzed by a validated method using high-performance liquid chromatography with a diode-array detector, Re, Ra8, and Rf content per 1 g of P. ginseng fruit extract was 1.01 ± 0.03, 0.33 ± 0.01, and 0.55 ± 0.04 mg, respectively. Ginsenosides-Re, -Ra8, and -Rf inhibited the production of pro-inflammatory factors and the expression of important cytokines in periodontitis by inducing the expression of heme oxygenase 1 (HO-1), promoting osteoblast differentiation of periodontal ligament cells, suppressing alveolar bone loss, and promoting the expression of osteoblast-specific genes, such as alp, opn, and runx2. An inhibitory effect of these ginsenosides on periodontitis and alveolar bone loss was observed via the regulation of HO-1 and subsequent epidermal growth factor receptor (EGFR) signaling. Silencing EGFR with EGFR siRNA confirmed that the effect of ginsenosides on HO-1 is mediated by EGFR. In conclusion, this study evaluated the contents of ginsenosides-Re, -Ra8, and -Rf isolated from P. ginseng fruit extract. Therefore, these results provide important basic data for future P. ginseng fruit component studies and suggest that ginsenosides Re, Ra8, and Rf have potential as future treatment options for periodontitis.

Methamphetamine (METH) is a synthetic psychostimulant drug that has detrimental effects on the health of its users. Although it has been investigated as a cause of neurodegenerative disease due to its neurotoxicity, whether small molecules derived from natural products attenuate these side effects remains elusive. 6,7,4′-trihydroxyflavanone (THF) is a flavanone family that possesses various pharmacological activities, including anti-rheumatic, anti-ischemic, anti-inflammatory, anti-osteoclastogenic, and protective effects against METH-induced deactivation of T cells. However, little is known about whether THF protects neuronal cells from METH-induced neurotoxicity. Here, we investigated the protective effects of THF on neurotoxicity induced by METH exposure by enhancing the Nrf2/HO-1 and PI3K/Akt/mTOR signaling pathways in SH-SY5y cells. Treatment with THF did not lead to cytotoxicity, but attenuated METH-induced neurotoxicity by modulating the expression of apoptosis-related proteins, METH-induced oxidative stress, and PI3K/Akt/mTOR phosphorylation in METH-exposed SH-SY5y cells. Moreover, we found THF induced Nrf2 nuclear translocation and HO-1 expression. An inhibitor assay confirmed that the induction of HO-1 by THF attenuates METH-induced neurotoxicity. Therefore, we suggest that THF preserves neuronal cells from METH-induced neurotoxicity by upregulating HO-1 expression through the Nrf2 and PI3K/Akt/mTOR signaling pathways. Thus, THF has therapeutic potential for use in the treatment of METH-addicts suffering from neurodegenerative diseases.

A flexible and bioactive scaffold for adipose tissue engineering was fabricated and evaluated by dual nozzle three-dimensional printing. A highly elastic poly (L-lactide-co-ε-caprolactone) (PLCL) copolymer, which acted as the main scaffolding, and human adipose tissue derived decellularized extracellular matrix (dECM) hydrogels were used as the printing inks to form the scaffolds. To prepare the three-dimensional (3D) scaffolds, the PLCL co-polymer was printed with a hot melting extruder system while retaining its physical character, similar to adipose tissue, which is beneficial for regeneration. Moreover, to promote adipogenic differentiation and angiogenesis, adipose tissue-derived dECM was used. To optimize the printability of the hydrogel inks, a mixture of collagen type I and dECM hydrogels was used. Furthermore, we examined the adipose tissue formation and angiogenesis of the PLCL/dECM complex scaffold. From in vivo experiments, it was observed that the matured adipose-like tissue structures were abundant, and the number of matured capillaries was remarkably higher in the hydrogel–PLCL group than in the PLCL-only group. Moreover, a higher expression of M2 macrophages, which are known to be involved in the remodeling and regeneration of tissues, was detected in the hydrogel–PLCL group by immunofluorescence analysis. Based on these results, we suggest that our PLCL/dECM fabricated by a dual 3D printing system will be useful for the treatment of large volume fat tissue regeneration.

Inflammatory bowel disease (IBD) is an immune disorder that develops due to chronic inflammation in several cells. It is known that colorectal and T cells are mainly involved in the pathogenesis of IBD. Chrysophanol is an anthraquinone family member that possesses several bioactivities, including anti-diabetic, anti-tumor, and inhibitory effects on T cell activation. However, it is unknown whether chrysophanol suppresses the activity of colorectal cells. In this study, we found that chrysophanol did not induce cytotoxicity in HT-29 colorectal cells. Pre-treatment with chrysophanol inhibited the mRNA levels of pro-inflammatory cytokines in tumor necrosis factor-α (TNF-α)-stimulated HT-29 cells. Western blot analysis revealed that pre-treatment with chrysophanol mitigates p65 translocation and the mitogen-activated protein kinase (MAPK) pathway in activated HT-29 cells. Results from the in vivo experiment confirmed that oral administration of chrysophanol protects mice from dextran sulfate sodium (DSS)-induced IBD. Chrysophanol administration attenuates the expression of pro-inflammatory cytokines in colon tissues of the DSS-induced IBD model. In addition, we found that oral administration of chrysophanol systemically decreased the expression of effector cytokines from mesenteric lymph nodes. Therefore, these data suggest that chrysophanol has a potent modulatory effect on colorectal cells as well as exhibiting a beneficial potential for curing IBD in vivo.

Since hypoxia-induced neurotoxicity is one of the major causes of neurodegenerative disorders, including the Alzheimer’s disease, continuous efforts to find a novel antioxidant from natural products are required for public health. 6,7,4′-trihydroxyflavanone (THF), isolated from Dalbergia odorifera, has been shown to inhibit osteoclast formation and have an antibacterial activity. However, no evidence has reported whether THF has a protective role against hypoxia-induced neurotoxicity. In this study, we found that THF is not cytotoxic, but pre-treatment with THF has a cytoprotective effect on CoCl2-induced hypoxia by restoring the expression of anti-apoptotic proteins in SH-SY5y cells. In addition, pre-treatment with THF suppressed CoCl2-induced hypoxia-related genes including HIF1α, p53, VEGF, and GLUT1 at the mRNA and protein levels. Pre-treatment with THF also attenuated the oxidative stress occurred by CoCl2-induced hypoxia by preserving antioxidant proteins, including SOD and CAT. We revealed that treatment with THF promotes HO-1 expression through Nrf2 nuclear translocation. An inhibitor assay using tin protoporphyrin IX (SnPP) confirmed that the enhancement of HO-1 by pre-treatment with THF protects SH-SY5y cells from CoCl2-induced neurotoxicity under hypoxic conditions. Our results demonstrate the advantageous effects of THF against hypoxia-induced neurotoxicity through the HO-1/Nrf2 signaling pathway and provide a therapeutic insight for neurodegenerative disorders.

Colitis is a multifactorial disorder that mostly occurs in the gastrointestinal tract. Despite improvements in mucosal inflammation research, little is known regarding the small bioactive molecules that are beneficial for regulating T cells and colon cell activity. 6,7,4′-trihydroxyflavanone (THF) is a flavanone that possesses anti-osteoclastogenesis activity and exerts protective effects against methamphetamine-induced immunotoxicity. Whether THF mitigates intestinal inflammation by regulating T cells and colon cell activity remains unknown. In the present study, Jurkat and HT-29 cells were used for in vitro experiments, and dextran sulfate sodium (DSS)-induced colitis model in mice was used for in vivo experiment. We observed that THF did not have a negative effect on the viability of Jurkat and HT-29 cells. Quantitative PCR and Western blot analysis revealed that THF regulates the activity of Jurkat cells and HT-29 cells via the NFκB and MAPK pathways under stimulated conditions. In the DSS-induced colitis model, oral administration of THF attenuated the manifestations of DSS-induced colitis, including a reduction in body weight, shrinkage of the colon, and enhanced expression of pro-inflammatory cytokines in the colon and mesenteric lymph nodes. These data suggest that THF alleviates DSS-induced colitis by modulating the activity of T cells and colon cells in vivo.

The endoscopic features between herpes simplex virus (HSV) and cytomegalovirus (CMV) esophagitis overlap significantly, and hence the differential diagnosis between HSV and CMV esophagitis is sometimes difficult. Therefore, we developed a machine-learning-based classifier to discriminate between CMV and HSV esophagitis. We analyzed 87 patients with HSV esophagitis and 63 patients with CMV esophagitis and developed a machine-learning-based artificial intelligence (AI) system using a total of 666 endoscopic images with HSV esophagitis and 416 endoscopic images with CMV esophagitis. In the five repeated five-fold cross-validations based on the hue–saturation–brightness color model, logistic regression with a least absolute shrinkage and selection operation showed the best performance (sensitivity, specificity, positive predictive value, negative predictive value, accuracy, and area under the receiver operating characteristic curve: 100%, 100%, 100%, 100%, 100%, and 1.0, respectively). Previous history of transplantation was included in classifiers as a clinical factor; the lower the performance of these classifiers, the greater the effect of including this clinical factor. Our machine-learning-based AI system for differential diagnosis between HSV and CMV esophagitis showed high accuracy, which could help clinicians with diagnoses.

Methamphetamine (METH) is a highly addictive drug that induces irreversible damage to neuronal cells and pathological malfunction in the brain. Aromadendrin, isolated from the flowers of Chionanthus retusus, has been shown to have anti-inflammatory or anti-tumor activity. Nevertheless, it has been reported that METH exacerbates neurotoxicity by inducing endoplasmic reticulum (ER) stress via the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in neuronal cells. There is little evidence that aromadendrin protects cells from neurotoxicity induced by METH. In this study, we found that aromadendrin partially suppressed the METH-induced cell death in SH-SY5y cells without causing cytotoxicity. Aromadendrin regulated METH-induced ER stress by preserving the phosphorylation of the PI3K/Akt/mTOR signaling pathway in METH-exposed SH-SY5y cells. In addition, aromadendrin mitigated METH-induced autophagic and the apoptotic pathways in METH-exposed SH-SY5y cells. Mechanistic studies revealed that pre-treatment with aromadendrin restored the expression of anti-apoptotic proteins in METH-exposed conditions. The inhibitor assay confirmed that aromadendrin-mediated restoration of mTOR phosphorylation protected cells from autophagy and apoptosis in METH-exposed cells. Therefore, these findings suggest that aromadendrin relatively has a protective effect on SH-SY5y cells against autophagy and apoptosis induced by METH via regulation of ER stress and the PI3K/Akt/mTOR signaling pathway.

Immune checkpoint blockade therapy has provided clinical benefit to some patients with advanced cancer including melanoma and non-small cell lung cancer. However, many patients still fail to respond to single immune checkpoint blockade therapy. The need for combination therapies to increase anti-tumor responses is becoming important. Interleukin-4 receptor (IL4R) is frequently overexpressed in various cancer types and promotes tumor cell survival. PD-L1, a well-known immune checkpoint, is up-regulated in malignant tumors and inhibits T-cell activity. In this study, we aimed at a combination therapy using an IL4R-targeted cytotoxic peptide and PD-L1-blocking peptide. To target IL4R-high tumor cells, we exploited IL4RPep-1-KLA composed of IL4RPep-1, an IL4R-binding peptide, and (KLAKLAK)2, a cytotoxic peptide. IL4RPep-1-KLA induced necrosis as well as apoptosis of IL4R-expressing tumor cells and increased the secretion of CRT, HMGB1, and ATP, well-known markers of immunogenic cell death (ICD). Flow cytometry analysis showed that the conditioned medium of tumor cells treated with IL4RPep-1-KLA enhanced the expression of CD86 and CD80 on dendritic cells, suggesting the activation and maturation of dendritic cells through ICD. Sequential treatment with IL4RPep-1-KLA followed by PD-L1Pep-2, a PD-L1-blocking peptide, during the co-culture of tumor cells and CD8+ T-cells activated T-cell activity including T-cell proliferation and cytokine secretion more efficiently than single treatment with IL4RPep-1-KLA or PD-L1Pep-2, or simultaneous treatment. These results suggest that sequential, combined treatment with the IL4R-targeted cytotoxic peptide and PD-L1-blocking peptide can induce ICD of tumor cells and maturation of dendritic cells and subsequently activate T-cells. This treatment is a promising strategy for cancer immunotherapy. Citation Format: Nawon Park, Byungheon Lee, Hyunsu Lee. Combined treatment with interleukin-4 receptor-targeted cytotoxic peptide and PD-L1-blocking peptide efficiently induces immunogenic cell death of tumor cells and activates T-cell activity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3422.