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Menghan Yu,1 Xiaoshu Fu,1 Yanli Zhu,2 Miao Li,3 Min Wu,1 Entong Zhou,1 Hanwen Dong,1 Likun Wang,1 Ruoxi Wang,4 Fang Liu,2 Chunlai Jiang,1 Xiangwei Kong,5 Weiheng Su1,6 1National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, People’s Republic of China; 2People’s Hospital of Jiangyuan District, Baishan, Jilin Province, People’s Republic of China; 3Department of Neurosurgery, China-Japan Union Hospital, Jilin University, Changchun, People’s Republic of China; 4School of Public Health, Capital Medical University, Beijing, People’s Republic of China; 5Changchun University of Science and Technology, Changchun, People’s Republic of China; 6Key Laboratory for Molecular Enzymology and Engineering of the Ministry of Education, School of Life Sciences, Jilin University, Changchun, People’s Republic of ChinaCorrespondence: Weiheng Su, National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, People’s Republic of China, Email suweiheng@jlu.edu.cn Xiangwei Kong, Changchun University of Science and Technology, Changchun, People’s Republic of China, Email tenbpro@163.comPurpose: Tick-borne encephalitis virus (TBEV) infections result in severe central nervous system diseases in humans across Asia and Europe. In China, cases of tick-borne encephalitis are primarily caused by the Far East subtype of TBEV, which exhibits a distinct disease course compared to other extensively studied subtypes. However, there is limited knowledge regarding the nucleic acid and serological diagnostic characteristics of patients infected with the TBEV in China, which is the focus of investigation in the present study.Methods: This study established a TaqMan qPCR approach to detect TBEV RNA in the serum with optimal specificity, sensitivity, and precision. Using TaqMan qPCR and ELISA assay for TBEV IgM detection, serum samples from 63 hospitalized patients bitten by ticks in Northeast China were investigated for diagnostic characteristics.Results: Twenty-five patients were positive for viral RNA; nineteen patients were positive for IgM, and nine were positive for both viral RNA and IgM. Through comparative analysis, TBEV RNA copies were negatively correlated with the virus incubation period. IgM levels were positively correlated with the clinical symptom scores of patients. The severity of clinical symptoms and the length after the tick bite could be used to predict the IgM occurrence. Furthermore, IgM levels and viral RNA copies were not correlated in double-positive patients.Conclusion: Both nucleic acid and serological detection methods exhibited distinct windows for detecting TBEV infection, with some overlap, and were associated with specific correlated factors. This study provided novel insights into the diagnosis and course of TBEV-induced tick-borne encephalitis in China.Keywords: tick-borne encephalitis, TBE, tick-borne encephalitis virus, TBEV, TaqMan qPCR, IgM

The current study sought to understand the influence of cultural values on mental health attitudes and help-seeking behaviors in college students of diverse ethnic backgrounds. Asian and Latinx college students (N = 159) completed an online survey in which they reported on their adherence to cultural values as measured by ethnicity-specific cultural values and general attitudes towards mental health. Factor analysis revealed two common factors of cultural values irrespective of ethnicity: Interdependent Orientation (IO) and Cultural Obligation (CO). Regardless of ethnicity, the more students endorsed IO values, the less likely they were to perceive a need for mental health treatment. IO value adherence was also predictive of more negative attitudes towards mental health. CO values were not predictive of perceived need or help-seeking behaviors. Findings highlight the importance of understanding shared cultural values across ethnic-racial groups and considering how the multidimensionality of culture may help explain shared mental health behaviors crossing lines of ethnic group membership.

Ouyang H, Zhou E, Wang H. Onco Targets Ther. 2019:12;1147–1159 We, the Editors and Publisher of OncoTargets and Therapy, have retracted the following article. Following publication of the article, concerns were raised about the duplication of images from Figures 2, 3, 4 and 5 with images from other unrelated articles. Specifically, Images for Figure 2A have been duplicated with images for Figure 2C from Zheng, Z., Xiang, S., Wang, Y., Dong, Y., Li, Z., Xiang, Y…. Weng, X. (2020). NR4A1 promotes TNF‑α‑induced chondrocyte death and migration injury via activating the AMPK/Drp1/mitochondrial fission pathway Retraction in /10.3892/ijmm.2023.5288. International Journal of Molecular Medicine, 45, 151–161. https://doi.org/10.3892/ijmm.2019.4398 (RETRACTED) and Figure 4H from Qin, R., Zhang, L., Lin, D., Xiao, F., & Guo, L. (2019). Sirt1 inhibits HG-induced endothelial injury: Role of Mff-based mitochondrial fission and F‑actin homeostasis-mediated cellular migration. International Journal of Molecular Medicine, 44, 89–102. https://doi.org/10.3892/ijmm.2019.4185. Images for Figure 3A have been duplicated with images for Figure 5H from Ruibing Li, Ting Xin, Dandan Li, Chengbin Wang, Hang Zhu, Hao Zhou (2018) Therapeutic effect of Sirtuin 3 on ameliorating nonalcoholic fatty liver disease: The role of the ERK-CREB pathway and Bnip3-mediated mitophagy. Redox Biology, 18, 229–243. https://doi.org/10.1016/j.redox.2018.07.011 and Figure 5H from Lu C, Chen X, Wang Q, Xu X, Xu B. TNFα promotes glioblastoma A172 cell mitochondrial apoptosis via augmenting mitochondrial fission and repression of MAPK–ERK–YAP signaling pathways. Onco Targets Ther. 2018;11:7213–7227. https://doi.org/10.2147/OTT.S184337. Images for Figure 3C have been duplicated with images for Figure 4g and 5a from Song Lan, Jingfang Liu, Xiangying Luo, Changlong Bi (2019) RETRACTED ARTICLE: Effects of melatonin on acute brain reperfusion stress: role of Hippo signaling pathway and MFN2-related mitochondrial protection. Cell Stress and Chaperones, 24, 235–245. https://doi.org/10.1007/s12192-018-00960-2. Images for Figure 4E have been duplicated with images for Figure 3F from Zhao, Shu, Li, Peng, Wang, Peng, Yang, Jing, Song, Peng, Zhang, Dong and Zhou, Gang. “Nurr1 promotes lung cancer apoptosis via enhancing mitochondrial stress and p53-Drp1 pathway” Open Life Sciences, vol. 14, no. 1, 2019, pp. 262–274. https://doi.org/10.1515/biol-2019-0030. Images for Figure 5A have been duplicated with images for Figure 1a from Zhang, X., Li, F., Cui, Y. et al. RETRACTED ARTICLE: Mst1 overexpression combined with Yap knockdown augments thyroid carcinoma apoptosis via promoting MIEF1-related mitochondrial fission and activating the JNK pathway. Cancer Cell Int 19, 143 (2019). https://doi.org/10.1186/s12935-019-0860-8; Figure 2K from Peng Xu, Guofeng Zhang, Longgui Sha, Shuangxing Hou. RETRACTED: DUSP1 alleviates cerebral ischaemia reperfusion injury via inactivating JNKMff pathways and repressing mitochondrial fission. Life Sciences. 2018; 210:251–262. https://doi.org/10.1016/j.lfs.2018.08.049; Figures 4D and 5A from Yudong Xie, Yanping Lv, Yanli Zhang, Zhenzhen Liang, Lili Han, Yiyang Xie. LATS2 promotes apoptosis in non-small cell lung cancer A549 cells via triggering Mff-dependent mitochondrial fission and activating the JNK signaling pathway. Biomedicine & Pharmacotherapy. 2019;109:679–689. https://doi.org/10.1016/j.biopha.2018.10.097 and Figure 6A from Yao S, Yan W. Overexpression of Mst1 reduces gastric cancer cell viability by repressing the AMPK-Sirt3 pathway and activating mitochondrial fission. Onco Targets Ther. 2018;11:8465–8479. https://doi.org/10.2147/OTT.S180851. Images for Figure 5D have been duplicated with images for Figure 2a from Wan, J., Cui, J., Wang, L. et al. RETRACTED ARTICLE: Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC-1 cell apoptosis via activating the mROS-HtrA2/Omi pathways. Cancer Cell Int 18, 165 (2018). https://doi.org/10.1186/s12935-018-0665-1; Figure 6F from Jixuan Liu, Wei Yan, Xiaojing Zhao, Qian Jia, Jinda Wang, Huawei Zhang, Chunlei Liu, Kunlun He, Zhijun Sun. Sirt3 attenuates post-infarction cardiac injury via inhibiting mitochondrial fission and normalization of AMPK-Drp1 pathways. Cellular Signalling. 2019;53:1–13. https://doi.org/10.1016/j.cellsig.2018.09.009 and Figure 7D from Jun Qian, Dong Fang, Hong Lu, Yi Cao, Ji Zhang, Rong Ding, Lingchang Li, Jiege Huo. Tanshinone IIA promotes IL2-mediated SW480 colorectal cancer cell apoptosis by triggering INF2-related mitochondrial fission and activating the Mst1-Hippo pathway. Biomedicine & Pharmacotherapy. 2018; 108:1658–1669. https://doi.org/10.1016/j.biopha.2018.09.170. The authors did not respond to our queries and were unable to provide an explanation for the duplicated images or provide data for the study. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. We have been informed in our decision-making by our editorial policies and COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”.

YaLi Wu,1,* WenJuan Chen,1,* Mengfei Guo,1 Qi Tan,1 E Zhou,1 Jingjing Deng,1 Minglei Li,1 Jiangbin Chen,1 Zimo Yang,1 Yang Jin1– 3 1Department of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Diseases of National Health Commission, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 2Key Laboratory of Biological Targeted Therapy, the Ministry of Education, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 3Clinical Research Center for Major Respiratory Diseases in Hubei Province, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yang Jin, Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China, Email whuhjy@126.comAbstract: Extracellular vesicles (EVs) can contain DNA, RNA, proteins and metabolic molecules from primary origins; they are coated with a phospholipid bilayer membrane and released by cells into the extracellular matrix. EVs can be obtained from various body liquids, including the blood, saliva, cerebrospinal fluid, and urine. As has been proved, EVs-mediated transfer of biologically active molecules is crucial for various physiological and pathological processes. Extensive investigations have already begun to explore the diagnosis and prognosis potentials for EVs. Furthermore, research has continued to recognize the critical role of nucleic acids and proteins in EVs. However, our understanding of the comprehensive effects of metabolites in these nanoparticles is currently limited and in its infancy. Therefore, we have attempted to summarize the recent research into the metabolomics of EVs in relation to potential clinical applications and discuss the problems and challenges that have occurred, to provide more guidance for the future development in this field.Keywords: extracellular vesicles, metabolomics, metabolites, clinical application

Dongjiu Li,1,* Jiayin You,2,* Chengyu Mao,1,* En Zhou,1,* Zhihua Han,1 Junfeng Zhang,1 Tiantian Zhang,1 Changqian Wang1 1Department of Cardiology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, People’s Republic of China; 2Department of Emergency, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, People’s Republic of China*These authors contributed equally to this workCorrespondence: Tiantian Zhang; Changqian Wang, Email ZhangTT2022Dr@163.com; wangcqdr17@163.comObjective: Cardiomyocyte apoptosis critically contributes to ischemia reperfusion injury (IRI), which lacks effective therapeutic strategies. Circular RNAs (circRNAs) serve as novel diagnostic and therapeutic targets in various cardiovascular diseases. CircRNA Fbxl5 is one of the abundantly expressed circRNAs in the heart and its role in myocardial IRI remains elusive.Materials and Methods: Wild-type (WT) mice and neonatal mice ventricular myocytes (NMVMs) were used and subjected to myocardial IRI and anoxia reoxygenation (AR), respectively. Molecular and histological analyses and echocardiography were used to determine the extent of apoptosis, infarct size, and cardiac function.Results: We found that circRNA Fbxl5 was significantly upregulated in the myocardium, as well as in NMVMs subjected to AR. Knockdown of circRNA Fbxl5 ameliorated cardiomyocyte apoptosis, thereby decreasing infarct size and preserving cardiac function. Additionally, in vitro knockdown of circRNA Fbxl5 in NMVMs subjected to AR recapitulated the in vivo findings. Mechanistically, we identified that circRNA Fbxl5 directly sponged and suppressed the endogenous microRNA-146a (miR-146a), thereby weakening its inhibitory effect on MED1, which could further promote the apoptosis of cardiomyocytes.Conclusion: Our findings revealed a novel and critical role for circRNA Fbxl5 in regulating cardiomyocyte apoptosis, and added additional insight into circRNAs mediated during myocardial IRI. The underlying miR-146a-MED1 signaling serves as an important cascade in regulating the apoptosis of cardiomyocytes.Keywords: myocardial ischemia reperfusion injury, circular RNA, microRNA-146a, cardiomyocyte apoptosis

Yiye Zhu,1,2 Guoshun Huang,1,2 Yang Yang,1,2 Chen Yong,1,2 Xiang Yu,1,2 Gang Wang,3 Lan Yi,1,4 Kun Gao,1,4 Fang Tian,2 Shushu Qian,2 Enchao Zhou,1,4 Yanqin Zou1,3,4 1Department of Nephrology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People’s Republic of China; 2No. 1 Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People’s Republic of China; 3Zou’s Nephrology Medicine Intangible Cultural Heritage Inheritance Studio, Nanjing Boda Nephrology Hospital, Nanjing, Jiangsu, People’s Republic of China; 4Inheritance Studio of Traditional Chinese Medicine Master Yanqin Zou, Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu, People’s Republic of ChinaCorrespondence: Enchao Zhou; Yanqin Zou Tel +86-13851572603; +86-25-86538830Fax +86-25-86538830Email snk110@163.com; fsyy00650@njucm.edu.cnPurpose: Proteinuria is an independent risk factor of chronic kidney disease (CKD). Albumin-induced tubulointerstitial inflammation and epithelial-mesenchymal transition (EMT) via the activation of NLRP3 inflammasome is a potential therapeutic target for CKD. Suyin Detoxification Granule (SDG) improves proteinuria and postpones renal failure. However, the underlying mechanism is still unknown.Methods: Firstly, the rat model of renal failure was established using intragastric administration of adenine. Renal function, proteinuria, inflammatory indicators in serum, and renal pathology were assessed, and renal immunohistochemical staining of NLRP3 inflammasomes was performed after intervention with low and high concentrations of SDG. Secondly, the model of renal tubular epithelial HK-2 cells was established using albumin in vitro, and the cell viability, EMT phenotype, and the expression of proteins in the NLRP3 inflammasome signaling pathway were measured after the freeze-dried powder of Suyin Detoxification Prescription (SDP) and CY-09, which is a selective and direct NLRP3 inhibitor, were co-incubated with albumin. ATP, SOD, mitochondrial membrane potential, and ROS were further measured in vitro, and changes in the mitochondrial function after SDP intervention were observed. The mitochondrial antiviral signaling protein (MAVS) was knocked down using siRNA, and the interaction between MAVS and NLRP3 was verified using Western blotting, polymerase chain reaction (PCR), and immunofluorescence.Results: SDG improved renal function and proteinuria, alleviated renal fibrosis, and reduced serum inflammation and the expression of the components of the NLRP3 inflammasome in the kidney. In vitro, SDP and CY-09 enhanced cell viability after injury with albumin and inhibited pyroptosis induced by the NLRP3 inflammatory signaling pathway and expression of proteins involved in EMT. It was further found that SDP alleviated the mitochondrial dysfunction caused by albumin. The knockdown of MAVS reduced the expression of NLRP3 pathway proteins and their mRNA levels and also weakened the co-localization of NLRP3, thus, reducing cell pyroptosis.Conclusion: SDP protected renal tubular epithelial cells from cell pyroptosis and EMT by regulating the albumin-induced mitochondrial dysfunction/ MAVS/ NLRP3-ASC-caspase-1 inflammasome signaling pathway.Keywords: Suyin Detoxification Granule, renal tubular epithelial cells, mitochondrial dysfunction, MAVS, NLRP3 inflammasome, pyroptosis, EMT

The Reynolds number (Re) is an important parameter that can affect compressor performance. This study experimentally and numerically investigated the effect of Re variations on the efficiency and stall mechanisms for a three-stage axial flow compressor. In the experiment, the total pressure ratio, polytropic efficiency, and stalling mass flow rate were measured in a Re range varying from 1,100,000 to 55,000 to elucidate the Re effects. Unsteady three-dimensional numerical simulations were implemented to understand the stall mechanisms. The results indicate that the compressor efficiency and stall-pressure ratio begin to decrease remarkably as Re is reduced below a critical value, which is 220,000 in the case of the compressor studied. At a low Re, losses caused by the secondary flow near the hub and shroud increase remarkably, and the extended boundary layer separations at the blade suction surface further decrease the efficiency. The variation in Re changes the stallinitiated location. At higher Reynolds numbers, the interaction between the corner separation at the hub of stator 1 and the leakage flow through the blade tip gap induces a large vortex, which seriously blocks the blade passage. The blocking effect spreads to the aft stage and extends to higher spans, which results in the stall of the whole compressor. However, the blocking effect at the hub disappears at Re =55,000, and the interaction of the blade boundary layer separation near the shroud of rotor 1 and the tip leakage vortex causes a large blockage and then induces stall. The Re variation changes the radial flow transportation because of the varying effect on the aerodynamic performance of each blade element at different spans. This significantly influences the extent of the vortex near the end wall and ultimately changes the stall mechanisms. [ABSTRACT FROM AUTHOR]

Dongjiu Li,1,* Chengyu Mao,1,* En Zhou,1,* Jiayin You,2,* Erhe Gao,3 Zhihua Han,1 Yuqi Fan,1 Qing He,1 Changqian Wang1 1Department of Cardiology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, People’s Republic of China; 2Department of Emergency, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, People’s Republic of China; 3Center for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA*These authors contributed equally to this workCorrespondence: Changqian Wang Email wangcqdr17@163.comObjective: Post myocardial infarction (MI) fibrosis has been identified as an important factor in the progression of heart failure. Previous studies have revealed that microRNA-21 (miR-21) plays an important role in the pathogenesis of fibrosis. The purpose of this study was to explore the role of miR-21 in post-MI cardiac fibrosis.Material and Methods: MI was established in wild-type (WT) and miR-21 knockout (KO) mice. Primary mice cardiac fibroblasts (CFs) were isolated from WT and miR-21 KO mice and were treated with angiotensin II (Ang II) or Sprouty1 (Spry1) siRNA. Histological analysis and echocardiography were used to determine the extent of fibrosis and cardiac function.Results: Compared with WT mice, miR-21 KO mice displayed smaller fibrotic areas and decreased expression of fibrotic markers and inflammatory cytokines. In parallel, Ang II-induced myofibroblasts transformation was partially inhibited upon miR-21 KO in primary CFs. Mechanistically, we found that the expression of Spry1, a previously reported target of miR-21, was markedly increased in miR-21 KO mice post MI, further inhibiting ERK1/2 activation. In vitro studies showed that Ang II activated ERK1/2/TGF-β/Smad2/3 pathway. Phosphorylated Smad2/3 further enhanced the expression of α-SMA and FAP and may promote the maturation of miR-21, thereby downregulating Spry1. Additionally, these effects of miR-21 KO on fibrosis were reversed by siRNA-mediated knockdown of Spry1.Conclusion: Our findings suggest that miR-21 promotes post-MI fibrosis by targeting Spry1. Furthermore, it mediates a positive feedback on Ang II, thereby inducing the ERK/TGF-β/Smad pathway. Therefore, targeting the miR-21–Spry1 axis may be a promising therapeutic option for ameliorating post-MI cardiac fibrosis.Keywords: cardiac fibrosis, myocardial infarction, microRNA-21, Sprouty1, ERK/TGF-β/Smad signaling pathway

Hui Ouyang, Enxiang Zhou, Huan Wang Department of Breast and Thyroid Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Background and objective: Mst1-Hippo pathway and mitochondrial fragmentation participate in the progression of several types of cancers. However, their roles in breast cancer requires investigation. The aim of our study is to determine whether Mst1 overexpression regulates the viability of breast cancer cells via modulating mitochondrial fragmentation. Materials and methods: TUNEL staining, MTT assay and Western blotting were used to detect cancer cell death. Adenovirus-loaded Mst1 was transfected into cells to overexpress Mst1. Mitochondrial fragmentation was observed via immunofluorescence staining and Western blotting. Pathway blocker was used to detect whether Mst1 modulated cell death and mitochondrial fragmentation via JNK signaling pathway. Results: Our data showed that Mst1 overexpression promoted breast cancer cell death in a manner dependent on mitochondrial apoptosis. Mitochondrial oxidative stress, energy metabolism disorder, mitochondrial cyt-c liberation and mitochondrial apoptosis activation were observed after Mst1 overexpression. Furthermore, we demonstrated that Mst1 overexpression activated mitochondrial stress via triggering Drp1-related mitochondrial fragmentation, and that inhibition of Drp1-related mitochondrial fragmentation abrogated the proapoptotic effect of Mst1 overexpression on breast cancer cells. To this end, we found that Mst1 modulated Drp1 expression via the JNK signaling pathway, and that blockade of the JNK pathway attenuated mitochondrial stress and repressed apoptosis in Mst1-overexpressed cells. Conclusion: Altogether, our results identified a tumor suppressive role for Mst1 overexpression in breast cancer via activation of the JNK–Drp1 axis and subsequent initiation of fatal mitochondrial fragmentation. Given these findings, strategies to enhance Mst1 activity and elevate the JNK–Drp1–mitochondrial fragmentation cascade have clinical benefits for patients with breast cancer. Keywords: breast cancer, mitochondrial fragmentation, Mst1, JNK–Drp1 signaling pathway, mitochondrial dysfunction

Peiyang Ding,1,2 Teng Zhang,2,3 Yafei Li,1,2 Man Teng,2 Yaning Sun,2 Xiao Liu,2,4 Shujun Chai,2 Enmin Zhou,1 Qianyue Jin,2,5 Gaiping Zhang1,2,4,5 1College of Veterinary Medicine, Northwest A&F University, Yangling, 2Henan Provincial Key Laboratory of Animal Immunology, Henan Academy of Agricultural Sciences, 3College of Life Sciences, Henan Agricultural University, 4College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou, 5Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou, People’s Republic of China Abstract: Recent advancements in biotechnology have enabled the rapid identification and subsequent expression of pathogenic microbial major antigens that induce protective immune responses. However, subunit vaccines have not been successfully commercialized mainly due to the lack of sufficient levels of neutralizing antibodies (NAs). High levels of NA rely on the efficient recognition and cross-linking of multiple neutralizing epitopes with B-cell receptors (BCRs). Nanoparticles are able to display coupled antigenic arrays at high density and provide multiple binding molecular scenarios with BCRs. The high-resolution antigenic structure makes it possible to accurately display stable neutralizing epitopes. Therefore, the development of a nanovaccine that orientationally displays neutralizing epitopes is a feasible strategy. To address this hypothesis, the capsid (Cap) protein of porcine circovirus type 2 as model antigen was conjugated to gold nanoparticles (AuNPs) through direct reaction of the mercapto group of the unique cysteines with AuNPs, rendering Cap-AuNPs to have neutralizing epitopes on outer surface and an immunodominant epitope buried within the inner surface. In vitro studies showed that AuNPs promoted the phagocytosis of Cap protein and NA levels were significantly improved, meanwhile antibody levels against the immunodominant epitope was significantly reduced. In mouse studies, Cap-AuNP-immunized mice displayed a high production of interleukin (IL)-4, IL-10, and interferon-γ, suggesting that Cap-AuNPs can effectively activate CD4+ and CD8+ T cells and balance Th1 and Th2 cellular responses. This study presents a new vaccine design strategy based on antigen structure, where nanoparticles are coupled to antigens in well-ordered arrays and orientationally display neutralizing epitopes to enhance NA levels. Keywords: gold nanoparticles, porcine circovirus type 2, neutralizing antibody, epitopes, structure, orientationally display

Background: We conducted this study to assess the value of clinically relevant data for predicting the failure of removing urinary catheters among patients with intracerebral hemorrhage postoperatively. Materials and Methods: We retrospectively analyzed the medical records of all patients with intracerebral hemorrhage who underwent surgery for removal of intracerebral hematoma between January 2014 and December 2019, all of whom retained their urinary catheter. The patients were classified into 2 groups. Group A included patients who underwent successful removal of the catheter while group B included patients who underwent a failed removal. Univariate analysis was performed to determine the relationship between the failure of catheter removal and the patients' preoperative clinical characteristics. Independent prognostic predictors were identified using multivariate analyses. Results: The site of intracerebral hematoma (P =0.004), volume of hematoma (P <0.001), intraventricular hemorrhage (P <0.001), admitted Glasgow Coma Scale (GCS) (P <0.001), GCS before urinary catheter removal (P <0.001), smoking (P =0.011), herniation (P <0.001), urine protein (P =0.013), creatinine (P =0.037), and timing of urinary catheter removal (P <0.001) were significantly different among the 2 groups. Multiple logistical regression analysis indicated that GCS before urinary catheter removal (odds ratio=1.171; 95% confidence interval=1.050-1.306; P =0.005) and timing for urinary catheter removal (odds ratio=0.962; 95% confidence interval=0.944-0.981; P <0.001) were associated with failure of urinary catheter removal. Conclusions: This study demonstrated that GCS before urinary catheter removal and the timing of urinary catheter removal are independent factors associated with failure of urinary catheter removal among patients with intracerebral hemorrhage. [ABSTRACT FROM AUTHOR]