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D-galactose (D-gal) is a reducing sugar widely distributed in food. In a pregnant animal model exposed to D-gal, D-gal was found to have toxic effects on both the mother and foetus through oxidative stress. However, little is known about the effect of D-gal exposure on the placenta and its underlying mechanism. In this study, we evaluated the effects of D-gal on HTR8/SVneo cells and the mechanisms in vitro. In the present study, the activity of HTR8/SVneo human trophoblasts decreased in a time- and concentration-dependent manner after exposure to D-gal. D-gal resulted in premature senescence of HTR8/SVneo cells, as confirmed by assessing β-galactosidase (SA-β-gal) activity and the expression of senescence-related factor p21. We also verified the damage of oxidative stress induced by D-gal by measuring the expression of reactive oxygen species (ROS), sirtuin 1 (SIRT1) and forkhead box O (FOXO) 3a. SRT1720, as a SIRT1 activator, mitigated D-gal-induced oxidative stress and senescence by upregulating SIRT1 and FOXO3a expression and reducing ROS production. Our data suggest that D-gal may induce HTR8/SVneo premature ageing through the SIRT1/FOXO3a/ROS signalling pathway mediated by oxidative stress and that SIRT1 protects cells from this damage.

Background Stress, herd transfer, and food changes experienced by nursery and fattening pigs can lead to reduced performance, reduced digestion and absorption, and impaired intestinal health. Given the role of essential oils in relieving stress and improving animal welfare, we hypothesized that essential oils may improve pig performance via promoting gut health and gut homeostasis laid by EOs supplementation during nursery continuously impacts performance in fattening pigs. Results A total of 100 piglets (Landrace × Large White; weighted 8.08 ± 0.34 kg, weaned at d 28) were randomly selected and divided into 2 treatments: (1) basal diet (Con); (2) basal diet supplement with 0.1% complex essential oils (CEO). The experiment period was 42 days. Then weaned piglets’ growth performance and indications of intestinal health were assessed. Compared to the Con group, dietary supplemented CEO enhanced BW at 14 d (P P P P P Conclusions Therefore, the strategy of adding CEO to pig diets as a growth promoter and enhancing intestinal health is feasible.

Genomic MET amplification and exon 14 skipping are currently clinically recognized biomarkers for stratifying subsets of non-small cell lung cancer (NSCLC) patients according to the predicted response to c-Met inhibitors (c-Metis), yet the overall clinical benefit of this strategy is quite limited. Notably, c-Met protein overexpression, which occurs in approximately 20–25% of NSCLC patients, has not yet been clearly defined as a clinically useful biomarker. An optimized strategy for accurately classifying patients with c-Met overexpression for decision-making regarding c-Meti treatment is lacking. Herein, we found that SYK regulates the plasticity of cells in an epithelial state and is associated with their sensitivity to c-Metis both in vitro and in vivo in PDX models with c-Met overexpression regardless of MET gene status. Furthermore, TGF-β1 treatment resulted in SYK transcriptional downregulation, increased Sp1-mediated transcription of FRA1, and restored the mesenchymal state, which conferred resistance to c-Metis. Clinically, a subpopulation of NSCLC patients with c-Met overexpression coupled with SYK overexpression exhibited a high response rate of 73.3% and longer progression-free survival with c-Meti treatment than other patients. SYK negativity coupled with TGF-β1 positivity conferred de novo and acquired resistance. In summary, SYK regulates cell plasticity toward a therapy-sensitive epithelial cell state. Furthermore, our findings showed that SYK overexpression can aid in precisely stratifying NSCLC patients with c-Met overexpression regardless of MET alterations and expand the population predicted to benefit from c-Met-targeted therapy.

The farnesoid X receptor (FXR) regulates inflammation and immune responses in a subset of immune-mediated diseases. We previously reported that FXR expression promotes tumor cell proliferation in non–small cell lung cancer (NSCLC). Here we study the relevance of FXR to the immune microenvironment of NSCLC. We found an inverse correlation between FXR and PD-L1 expression in a cohort of 408 NSCLC specimens; from this, we identified a subgroup of FXRhighPD-L1low patients. We showed that FXR downregulates PD-L1 via transrepression and other mechanisms in NSCLC. Cocultured with FXRhighPD-L1low NSCLC cell lines, effector function and proliferation of CD8+ T cell in vitro are repressed. We also detected downregulation of PD-L1 in FXR-overexpressing Lewis lung carcinoma (LLC) mouse syngeneic models, indicating an FXRhighPD-L1low subtype in which FXR suppresses tumor-infiltrating immune cells. Anti–PD-1 therapy was effective against FXRhighPD-L1low mouse LLC tumors. Altogether, our findings demonstrate an immunosuppressive role for FXR in the FXRhighPD-L1low NSCLC subtype and provide translational insights into therapeutic response in PD-L1low NSCLC patients treated with anti–PD-1. We recommend FXRhighPD-L1low as a biomarker to predict responsiveness to anti–PD-1 immunotherapy.

Supplementary Table 1, Supplementary Figures 1-7

BackgroundThe suppressor of cytokine signaling 3 (SOCS3) is the negative feedback regulator of the JAK-STAT signaling pathway. The purpose of our study was to investigate the SOCS3 status in colon primary tumor and lung metastasis and its relationship with macrophages.MethodsThe SOCS3 expression pattern and its relationship with the immune response in pan-cancer was investigated using multiple methods. Samples and corresponding clinical information of 32 colon cancer patients with lung metastasis were collected, and the CD68, CD163, and SOCS3 status were conducted using immunohistochemistry (IHC). The relationship between SOCS3 status and macrophage markers was analyzed. Besides, we explored the molecular mechanisms of SOCS3 in lung metastasis via the TCGA database.ResultsHigh SOCS3 expression was more inclined to poor prognosis and was positively correlated with main immune cell infiltration in almost each cancer type, especially in colon cancer. Compared with the colon primary tumor, lung metastasis harbored higher CD163 and SOCS3 expression, and high SOCS3 expression was more likely to be associated with high CD163 expression in lung metastasis. Besides, the exceptional differentially expressed genes in lung metastasis significantly enriched in immune responses and regulations.ConclusionsSOCS3 possessed value as a prognostic marker and target for immunotherapeutic intervention in different tumors and might be a potential target of tumor progression and tumor immunotherapy in colon cancer.

Ferroptosis is a non-apoptotic regulated cell death caused by iron accumulation and subsequent lipid peroxidation. Currently, the therapeutic role of ferroptosis on cancer is gaining increasing interest. Baicalin an active component in Scutellaria baicalensis Georgi with anticancer potential various cancer types; however, the effects of baicalein on bladder cancer and the underlying molecular mechanisms remain largely unknown. In the study, we investigated the effect of baicalin on bladder cancer cells 5637 and KU-19-19. As a result, we show baicalin exerted its anticancer activity by inducing apoptosis and cell death in bladder cancer cells. Subsequently, we for the first time demonstrate baicalin-induced ferroptotic cell death in vitro and in vivo, accompanied by reactive oxygen species (ROS) accumulation and intracellular chelate iron enrichment. The ferroptosis inhibitor deferoxamine but not necrostatin-1, chloroquine (CQ), N-acetyl-l-cysteine, l-glutathione reduced, or carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (Z-VAD-FMK) rescued baicalin-induced cell death, indicating ferroptosis contributed to baicalin-induced cell death. Mechanistically, we show that ferritin heavy chain 1 (FTH1) was a key determinant for baicalin-induced ferroptosis. Overexpression of FTH1 abrogated the anticancer effects of baicalin in both 5637 and KU19-19 cells. Taken together, our data for the first time suggest that the natural product baicalin exerts its anticancer activity by inducing FTH1-dependent ferroptosis, which will hopefully provide a prospective compound for bladder cancer treatment., Graphical abstract Baicalin exerts its anticancer activity in bladder cancer by inducing ferritin heavy chain 1 (FTH1)-dependent ferroptosis, which will hopefully provide great therapeutic potential for bladder cancer treatment.Image 1

Background Alexithymia is a common psychological disorder. However, few studies have investigated its prevalence and predictors in patients with chronic obstructive pulmonary disease (COPD). Therefore, we aimed to determine the prevalence and predictors of alexithymia in Chinese patients. Methods This cross-sectional study included 842 COPD patients to assess the prevalence and predictors of alexithymia using the 20-item Toronto Alexithymia Scale (TAS-20). We used the Hospital Anxiety and Depression Scale (HADS) to assess anxiety and depression, the modified British Medical Research Council dyspnea Rating Scale (mMRC) to assess dyspnea, St. George's Respiratory Questionnaire (SGRQ) to assess quality of life, and the age-adjusted Charlson comorbidity index (ACCI) to assess comorbidities. Alexithymia-related predictors were identified using univariate and multivariate logistic regression analyses. Results The prevalence of alexithymia in COPD patients was 23.6% (199/842). Multivariate analysis showed that age [odds ratio (OR) 0.886; 95% confidence interval (CI) 0.794–0.998], body mass index (OR 0.879; 95% CI 0.781–0.989), HADS-anxiety (OR 1.238; 95% CI 1.097–1.396), HADS-depression (OR 1.178; 95% CI 1.034–1.340), mMRC (OR 1.297; 95% CI 1.274–1.320), SGRQ (OR 1.627; 95% CI 1.401–1.890), ACCI (OR 1.165; 95% CI 1.051–1.280), and GOLD grade (OR 1.296; 95% CI 1.256–1.337) were independent predictors for alexithymia in patients with COPD. Conclusions The prevalence of alexithymia was high in Chinese COPD patients. Anxiety, depression, dyspnea, quality of life, comorbidities, and disease severity are independent risk factors, and age and BMI are predictive factors for alexithymia in COPD patients.

Background:Whether whey protein supplementation can reduce the occurrence of hypoproteinemia in patients with acute critically ill neurological diseases on the basis of standard intact EN has not been confirmed by randomized controlled clinical trials. Objective:We evaluated the effect of whey protein powder on serum albumin in acute critically ill neurological patients. Methods:Critically ill neurological patients expected to stay longer than 7 days were randomized. For the intact protein formula (IPF) group, only an intact protein formula was given. For the whey protein supplementation formula (WPF) group, whey protein powder was added on the basis of an intact protein formula. Results: The serum albumin level in the WPF group was higher than that in the IPF group (31.92 ± 4.48 / 29.55 ± 4.31, P = 0.005, 95%CI 0.746 −3.981). There was no significant difference in the complications of enteral nutrition treatment between the two groups (p＞0.05). The serum albumin levels in the WPF group was higher than that in the IPF group for patients 60 years or older and for stroke patients respectively (P＜0.05). Interleukin-6 (OR = -0.023, P = 0.018, 95%CI -0.042 − -0.004) and procalcitonin (OR = -8.331, P = 0.004, 95%CI -13.931 − -2.730) were negatively independently correlated with the serum albumin levels respectively. There was no significant difference in the mRS between the two groups at 14 days and 90 days after onset (p＞0.05). Conclusion: Whey protein supplementation can improve the severity of hypoproteinemia in critically ill patients with neurological disease, especially in elderly patients and in patients with stroke. At the same time, we need to pay more attention to persistent inflammatory responses and secondary infections. Further clinical studiesat different levels are needed to discover more evidence to help better managethese patients. URL: https://clinicaltrials.gov/ct2/show/NCT04361357?term=04361357&draw=2&rank=1. Registration ID: NCT04361357

Supplementary Material 1

Ferrihydrite and magnetite enhanced anaerobic digestion through dissimilatory iron reduction and direct interspecies electron transfer (DIET), respectively.

Cellular senescence is a key factor in the development of intervertebral disc degeneration (IVDD). Age-associated decreases in NAD+ levels play a critical role in regulating cellular senescence. Previous studies have found that small extracellular vesicles (sEVs) secreted by adipocytes (Adipo-sEVs) or adipose tissue are abundant in nicotinamide phosphoribosyltransferase (NAMPT), which is the key NAD+ biosynthetic enzyme in mammals. Systemic injection of these sEVs significantly improves physical activity and extends the lifespan of aged mice by increasing NAD+ levels. However, to date, the therapeutic potential of Adipo-sEVs in other age-associated disease models, such as IVDD, has not been explored. In this study, we investigated the therapeutic effects of Adipo-sEVs on senescence of nucleus pulposus cells (NPCs) and cartilaginous endplate cells (EPCs). In vitro, Adipo-sEVs could rejuvenate the senescence of NPCs and EPCs. Age-related dysfunctions were also ameliorated by Adipo-sEVs by delivering NAMPT and activating NAD+ biosynthesis and the Sirt1 pathway. Further in vivo experiments revealed that Adipo-sEV-mediated delivery of NAMPT attenuated IVDD in rats by rejuvenating senescent NPCs and EPCs. Collectively, the results indicate a new cell-free tool and provide a promising sEV-mediated delivery method of NAMPT as a therapeutic approach for IVDD clinically.

Stress or stress-induced intestinal disturbances, especially diarrhea, are the main triggers for inflammatory bowel disease and irritable bowel syndrome. Diarrhea and intestinal inflammatory disease afflict patients around the world, and it has become a huge burden on the global health care system. Drinking sodium metasilicate-based alkaline mineral water (SM-based AMW) exerts a potential therapeutic effect in gastrointestinal disorders, including gut inflammation, and diarrhea, but the supportive evidence on animal studies and mechanism involved remain unreported. The maternally separated (MS) piglet (Newly weaned piglet) is an excellent model to investigate the treatment of diarrhea in infant. This study aims to determine whether drinking SM-based AMW confers diarrhea resistance in maternally separated (MS) piglets under weaning stress and what the underlying mechanisms are involved. 240 newly weaned piglets were randomly divided into the Control group and the sodium metasilicate pentahydrate (SMP) group. A decreased diarrhea incidence was observed in SMP treatment piglets. The intestine injury and activated stress hormones (COR and ACTH) induced by weaning was alleviated by SM-based AMW. This may be related to the improvement of intestinal microflora structure and function by SMP, especially the increase of s_copri abundance. Meanwhile, SMP maintained the integrity of the duodenal mucus barrier in MS piglets. Importantly, by targeting NF-κB inhibition via the microbiota-gut interaction, SM-based AMW alleviated intestinal inflammation, maintained fluid homeostasis by modulating aquaporins and fluid transporter expression, and enhanced barrier integrity by suppressing MLCK/p-MLC signaling. Therefore, drinking metasilicate-based alkaline mineral water confers diarrhea resistance in MS piglets via the microbiota-gut interaction.

Diarrhea has the fourth-highest mortality rate of all diseases and causes a large number of infant deaths each year. The maternally separated (MS) piglet (newly weaned piglet) is an excellent model to investigate the treatment of diarrhea in infants. Drinking alkaline mineral water has the potential to be therapeutic in gastrointestinal disorders, particularly diarrhea, but the supporting evidence from system studies and the mechanisms involved have yet to be reported.This study aims to determine whether drinking alkaline mineral water confers diarrhea resistance in MS piglets under weaning stress and what the fundamental mechanisms involved are.MS piglets were used to create a stress-induced intestinal disorder-diarrhea susceptibility model. A total of 240 MS piglets were randomly divided into two groups (6 pens/group and 20 piglets/pen). IPEC-J2 cell line was used for in vitro evaluation. An alkaline mineral complex (AMC) water was employed, and its effect on the hypothalamus-pituitary-adrenocortical (HPA) axis, gut microbes, gut morphology, and intestinal epithelial cell (IEC) proliferation and differentiation were investigated using a variety of experimental methodology.AMC water reduced diarrhea rate in MS piglets by inhibiting the HPA axis, ameliorating gut microbiota structure, and stimulating IEC proliferation and differentiation. Apparently, the brain-microbe-gut axis is linked with AMC water conferring diarrhea resistance in piglets. Mechanistically, AMC water decreased stress hormones (COR and Hpt) secretion by suppressing HPA axis, which then increased the abundance of beneficial gut microbes; accordingly, maintained the proliferation of IEC and promoted the differentiation of intestinal stem cells (ISC) into goblet cell and Paneth cell by activating the Wnt/β-catenin signaling pathway. In the absence of gut microbiota (in vitro), AMC activated the LPS-induced Wnt/β-catenin signaling inhibition in IPEC-J2 cells and significantly increased the number of Lgr5 + cells, whereas had no effect on IPEC-J2 differentiation.Drinking alkaline mineral water confers diarrhea resistance in MS piglets by maintaining intestinal epithelial regeneration via the brain-microbe-gut axis; thus, this study provides a potential prevention strategy for young mammals at risk of diarrhea.

Background: Suppressor of cytokine signaling (SOCS) is a family of proteins that respond to cytokine, growth factor and other signals, and can regulate various functions of tumor cells. The purpose of our study was to investigate the prognostic performance and biological function of SOCS3 in bladder cancer. Methods: The clinical information of 80 patients with bladder cancer at Zhejiang Provincial People’s Hospital was collected and the SOCS3 protein level was detected by immunohistochemistry. The relationship between SOCS3 status and clinical parameters and the prognosis was analyzed. Besides, we explored the biological function of SOCS3 in bladder cancer. Results: The expression of SOCS3 in bladder cancer tissues was lower than that in normal tissues at the protein level and transcription level (P < 0.001). The low expression group of SOCS3 was more inclined to high staging and high grading. The prognosis of the high expression group of SOCS3 was significantly better than that of the low expression group of SOCS3 in non-muscle-invasive bladder cancer patients (P = 0.037). Also, ectopic expression of SOCS3 reduced the cell proliferation and migration ability of the bladder cancer cell line. Conclusions: Our findings imply that SOCS3 is a potential prognostic factor for non-muscle-invasive bladder cancer, and plays a tumor suppressor role in bladder cancer.

Efficient utilization of organic materials based on the rich resources in the karst region can promote soil fertility. Microorganisms have a crucial influence on soil phosphorus availability.

Tumor metastasis occurs in lung cancer, resulting in tumor progression and therapy failure. Anoikis is a mechanism of apoptosis that combats tumor metastasis; it inhibits the escape of tumor cells from the native extracellular matrix to other organs. Deciphering the regulators and mechanisms of anoikis in cancer metastasis is urgently needed to treat lung cancer. Several natural and synthetic products exhibit the pro-anoikis potential in lung cancer cells and in vivo models. These products include artonin E, imperatorin, oroxylin A, lupalbigenin, sulforaphane, renieramycin M, avicequinone B, and carbenoxolone. This review summarizes the current understanding of the molecular mechanisms of anoikis regulation and relevant regulators involved in lung cancer metastasis and discusses the therapeutic potential of targeting anoikis in the treatment of lung cancer metastasis.

To investigate the effects of acupuncture on phosphorylated P38 mitogen-activated protein kinase (p-P38MAPK), intercellular adhesion molecule-1 (ICAM-1), interferon γ (IFN-γ), and eosinophilic granulocytes (EOS) in lung tissue of asthmatic rats, and to explore the mechanism of acupuncture in regulating the apoptosis of EOS.Clean-grade male Wistar rats were randomly divided into normal, model, dexamethasone and acupuncture groups, 8 rats in each group. The asthmatic model was established by intraperitoneal injection of mixture suspension (1 mL) of 10% ovalbumin and 10% Al(OH)_3+ normal saline, followed by inhalation of atomized 1% ovalbumin solution for 30 min, once daily for 2 weeks to trigger occurrence of asthmatic symptoms. The rats in dexamethasone group were intraperitoneally injected with 0.9 mg/kg dexamethasone since day 15 once a day for two consecutive weeks. In the acupuncture group, bilateral "Feishu" (BL13), "Pishu" (BL20), "Shenshu" (BL23), "Dingchuan" (EX-B1), and "Danzhong" (CV17) were selected for acupuncture treatment once every other day since day 15 for two consecutive weeks. Uniform reinforcing and reducing manipulation was carried out, and the needles were retained for 30 min. The pathological changes of the lung tissue were observed by hematoxylin-eosin (HE) staining. The apoptosis of EOS in the lung tissue of rats was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. The expression of p-P38MAPK in the lung tissue was detected by Western blot. The protein and mRNA levels of ICAM-1 and IFN-γ in the lung tissue were determined by immunohistochemistry and real-time PCR, respectively.The results of HE staining showed that the pulmonary alveoli and surrounding tissues were intact with no inflammatory cell infiltration in the normal group. The model group showed massive exudation of inflammatory materials and thickened pulmonary interstitium. The dexamethasone group and acupuncture group showed less damage of the alveolar structure and only a small number of inflammatory cells around the airway. Compared with the normal group, the apoptosis rate of EOS in lung tissue was decreased (Acupuncture may inhibit the P38MAPK signaling pathway, down-regulate ICAM-1 expression, and up-regulate IFN-γ expression to promote the apoptosis of EOS and reduce EOS aggregation, thus alleviating the inflammatory response of airway in asthma.

In this retrospective study, we have explored the anatomical factors that lead to the development of radiation necrosis (RN) in the setting of stereotactic radiosurgery (SRS) for melanoma brain metastases (MBM). Between 2014 and 2018, 137 patients underwent SRS for 311 MBM. Lesions were assessed according to anatomical zones: zone 1—peripheral grey-white matter junction and cortical mantle, zone 2—deep white matter, including tumours located at base of sulci, zone 3—tumours adjacent to ependymal lining or in deep locations such as brainstem, basal ganglia and thalamus. Other anatomical factors including lobes, medial-peripheral, supra or infratentorial locations were also recorded. In all, 12.4% (n = 17) of patients and 6.1% (n = 20) of lesions developed RN, actuarial incidence of RN at 12 and 24 months was 10% and 14.2% respectively. Zone 2 lesions recorded the highest rate of development of RN (n = 7/19; 36%), zone 3 (N = 4/24; 16%) and zone 1 (n = 9/268; 3%). Five of 17 patients developed symptomatic RN and 7/17 patients underwent surgery for RN. This study raises awareness of the increased likelihood of deep lesions particularly in white matter structures to develop RN after SRS. Further studies including larger cohorts would be useful in identifying statistical differences in the rate of development of RN in different anatomical zones.

Objective This study is a retrospective evaluation of patients with L4-5 highly down-migrated lumbar disc herniation (LDH) operated with interlaminar endoscopic lumbar discectomy (IELD) versus transforaminal endoscopic lumbar discectomy (TELD). Methods From January 2015 to December 2018, 77 patients with L4-5 highly down-migrated LDH were divided into 2 groups according to different surgical approaches. There were 40 patients who underwent IELD, and 37 patients who underwent TELD. The operation time, hospital stay, Oswestry Disability Index, clinical outcome according with modified MacNab criteria, Visual Analog Scale (VAS) scores, and complications were compared between the IELD and TELD groups. Results Seventy-seven patients were included, 40 and 37 patients underwent IELD and TELD, respectively. The IELD and TELD groups both achieved a significant improvement in Oswestry Disability Index, back and leg VAS scores, and clinical outcome postoperation. Mean operating and x-ray times during operation were significantly shorter in the IELD group than in the TELD group (41.8 vs. 50.3, 1.8 vs. 13.7). There were 3 patients who experienced recurrence in the IELD group and 2 in the TELD group. In the TELD group, there were 3 patients who required revision surgery due to incompletely removed disc fragment. All patients in the IELD group were treated successfully. There was no other complication in these cases. Conclusions Both IELD and TELD could be a good alternative option for highly down-migrated LDH in L4-L5. IELD may have advantages in operation time and x-ray times during operation compared with TELD.

Regeneration of chronic skin wounds in tissue is still a key challenge in regenerative medicine because of the accumulation of senescent cells and increasing secretion of "senescence-associated secretory phenotype"-(SASP) in the wound site. Recently, some studies have reported that small extracellular vesicles (sEVs) derived from stem cells can alleviate cellular senescence with very low risk of tumorigenesis and immune responses. As our previous studies have shown that urine-derived stem cells (USCs) can be obtained easily and noninvasively and sEVs derived from USCs (USC-sEVs) have capabilities of regenerating tissue injuries, using USC-sEVs to enhance chronic skin wound healing in aged tissue might be a feasible and efficient strategy. Therefore, in this study, the USC-sEVs were collected and firstly loaded in a human acellular amniotic membrane (HAAM) for controlled releasing and locating the USC-sEVs in the wound site before they were implanted into a chronic skin wound in aged mice. In vivo results showed that the USC-sEVs in HAAM could effectively accelerate the wound healing by ameliorating cellular senescence and reducing the secretion of SASP in the aged skin wounds. To elucidate the mechanism, USC-sEVs were used to in vitro culture human dermal fibroblasts (HDFs) and results showed that USC-sEVs could rejuvenate senescent fibroblasts by reversing the aging phenotypes of senescent HDFs and efficiently reducing the secretion of SASP after they activated the Sirt1 pathway. Therefore, USC-sEVs are efficient for enhancing wound healing in aged mice by ameliorating cellular senescence.

This article proposes a wearable assistive system based on artificial intelligence (AI) edge computing techniques to help visually impaired consumers safely use marked crosswalks, or zebra crossings. The proposed wearable assistive system consists of a pair of smart sunglasses, a waist-mounted intelligent device, and an intelligent walking cane (stick). A deep learning technique is adopted for zebra crossing image recognition in real time. Visually impaired consumers need to wear the proposed smart sunglasses and waist-mounted intelligent device and hold the proposed intelligent walking cane when they approach a zebra crossing. When a visually impaired pedestrian reaches a zebra crossing, they will immediately receive a message about the current situation at the crossing and the traffic light signal. Experimental results show that the accuracy of real-time zebra crossing recognition of the proposed system can reach up to 90%.