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1. Mapping the distribution of Nipah virus infections: a geospatial modelling analysis

Author: Sun, Yan-Qun, Zhang, Yuan-Yuan, Liu, Mei-Chen, Chen, Jin-Jin, Li, Ting-Ting, Liu, Yan-Ning, Zhang, Ling-Yu, Wang, Tao, Yu, Lin-Jie, Che, Tian-Le, Tang, Tian, Xu, Qiang, Lv, Chen-Long, Jiang, Bao-Gui, Golding, Nick, Mehlman, Max L, Hay, Simon I, Fang, Li-Qun, and Liu, Wei
Abstract: Nipah virus is a zoonotic paramyxovirus responsible for disease outbreaks with high fatality rates in south and southeast Asia. However, knowledge of the potential geographical extent and risk patterns of the virus is poor. We aimed to establish an integrated spatiotemporal and phylogenetic database of Nipah virus infections in humans and animals across south and southeast Asia.
Published: 2024
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2. MolLoG: A Molecular Level Interpretability Model Bridging Local to Global for Predicting Drug Target Interactions

Author: Feng, Bao-Ming, Zhang, Yuan-Yuan, Zhou, Xiao-Chen, Wang, Jin-Long, and Feng, Yin-Fei
Abstract: Developing new pharmaceuticals is a costly and time-consuming endeavor fraught with significant safety risks. A critical aspect of drug research and disease therapy is discerning the existence of interactions between drugs and proteins. The evolution of deep learning (DL) in computer science has been remarkably aided in this regard in recent years. Yet, two challenges remain: (i) balancing the extraction of profound, local cohesive characteristics while warding off gradient disappearance and (ii) globally representing and understanding the interactions between the drug and target local attributes, which is vital for delivering molecular level insights indispensable to drug development. In response to these challenges, we propose a DL network structure, MolLoG, primarily comprising two modules: local feature encoders (LFE) and global interactive learning (GIL). Within the LFE module, graph convolution networks and leap blocks capture the local features of drug and protein molecules, respectively. The GIL module enables the efficient amalgamation of feature information, facilitating the global learning of feature structural semantics and procuring multihead attention weights for abstract features stemming from two modalities, providing biologically pertinent explanations for black-box results. Finally, predictive outcomes are achieved by decoding the unified representation via a multilayer perceptron. Our experimental analysis reveals that MolLoG outperforms several cutting-edge baselines across four data sets, delivering superior overall performance and providing satisfactory results when elucidating various facets of drug–target interaction predictions.
Published: 2024
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3. Enzyme-assisted extraction of essential oil from Cinnamomum longepaniculatum(Gamble) N. Chao ex H. W. Li and anxiolytic activity

Author: Wang, Chen-Wei, Zhang, Yuan-Yuan, Zhang, Xue, Zheng, Kai-Li, Cong, Ying, Yang, Lei, and Zhang, Lin
Abstract: This work was designed to evaluate the effect of four enzyme-assisted extraction (EAE) combined hydrodistillation (HD) methods on the yield, microstructure and chemical composition of essential oil (EO) from leaves of Cinnamomum longepaniculatum(Gamble) N. Chao ex H. W. Li. The chemical composition of EO was analyzed using gas chromatography-mass spectrometry. Changes in the microstructure of leaf residues were observed by scanning electron microscopy. Response surface methodology was used to predict the best conditions for the EO extraction with the most effective enzyme pretreatment. Further, the anxiolytic effect and mechanism of the optimized EO were investigated by the open-field test (OFT), elevated plus-maze test (EPMT), hole-board test (HBT) and the assay of neurotransmitter concentrations (5-hydroxytryptamine, 5-HT; γ-aminobutyric acid, GABA; norepinephrine, NE). The results showed that different enzyme pretreatments increased the yield and quality of EO and disrupted the cell wall. The circumscribed-β-glucan/hemicellulose enzyme (1:1) pretreatment (4.33%) was the most effective compared to the enzyme-free group (2.82%). The optimum extraction process conditions were: pH:5, enzymolysis time: 67 min and digestion temperature: 48.5 °C. Under these conditions, the maximum yield of EO was 4.37%. After inhalation of EO, mice showed significant anxiolytic effects in EPMT, HBT, and OFT. In addition, EO significantly down-regulated 5-hydroxytryptamine and NE levels and up-regulated GABA levels. Cinnamomum longepaniculatumEO may be related to 5-HTergic, GABAergic and NEergic neurotransmitter systems for better anxiolytic effect.
Published: 2024
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4. Prognostic Factors and Outcomes in Patients With Septic Shock After Allogeneic Hematopoietic Stem Cell Transplantation

Author: Huang, Qiu-Sha, Han, Tian-Xiao, Fu, Hai-Xia, Meng, Han, Zhao, Peng, Wu, Ye-Jun, He, Yun, Zhu, Xiao-Lu, Wang, Feng-Rong, Zhang, Yuan-Yuan, Mo, Xiao-Dong, Han, Wei, Yan, Chen-Hua, Wang, Jing-Zhi, Chen, Huan, Chen, Yu-Hong, Han, Ting-Ting, Lv, Meng, Chen, Yao, Wang, Yu, Xu, Lan-Ping, Liu, Kai-Yan, Huang, Xiao-Jun, and Zhang, Xiao-Hui
Abstract: •Outcomes in patients who developed septic shock after allo-HSCT were poor.•Gram-negative bacilli accounted for 61.5% of the positive isolates.•Escherichia coliwas the dominant isolated pathogen.•Patients with late-onset septic shock had a significantly worse outcome.•Of patients with sepsis-induced coagulopathy, the 28-day mortality rate was 88.1%.
Published: 2024
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5. Heterozygosity analysis of spontaneous 2nfemale gametes and centromere mapping of the diploid Hevea brasiliensisbased on full-sib triploid populations

Author: Zhang, Yuan-yuan, Li, Hong-kun, Huang, Xiao, Yuan, Yu-jiao, Zhang, Xiao-fei, Gao, Xin-sheng, Wang, Xiang-jun, Wei, Ming-ming, Huang, Hua-sun, and Li, Weiguo
Abstract: Key message: Unreduced megagametophytes via second-division restitution were confirmed through heterozygosity analysis, and four candidate physical centromeres of rubber were located for the first time. Abstract: The evaluation of maternal heterozygosity restitution (MHR) is vital in identifying the mechanism of 2ngametogenesis and assessing the utilization value of 2ngametes. In this study, three full-sib triploid populations were employed to evaluate the MHR of 2nfemale gametes of rubber tree clone GT1 and to confirm their genetic derivation. The 2nfemale gametes of GT1 were derived from second-division restitution (SDR) and transmitted more than half of the parental heterozygosity. In addition, low recombination frequency markers were developed, and four candidate physical centromeres of rubber tree were located for the first time. The confirmation that 2nfemale gametes of rubber tree clone GT1 are derived from SDR provides insights into the molecular mechanisms of 2ngametogenesis. In addition, the identified centromere location will aid in the development of centromeric markers for the rapid identification of the 2ngametogenesis mechanism.
Published: 2024
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6. GPS-Based Ionospheric Tomography From the Combination of PolSAR and E-CHAIM

Author: Wang, Cheng, Zhao, Hai-Sheng, Wang, Li-Ming, Cao, Le, Xing, Zan-Yang, and Zhang, Yuan-Yuan
Abstract: The utilization of global positioning system (GPS) for 3-D ionospheric electron density reconstruction, i.e., computerized ionospheric tomography (CIT), provides significant importance in investigating the internal structure, variations, and disturbances within the ionosphere. However, the ill-posed problem caused by insufficient observational data or uneven distribution will rely heavily on the selection of initial values, which are typically derived from empirical models with low precision. Aiming at this issue, this article uses the total electron content (TEC) obtained by the spaceborne full-polarization synthetic aperture radar (PolSAR) to correct the Empirical Canadian High Arctic Ionospheric Model (E-CHAIM), thus improving the authenticity of the initial value. This study makes full use of the advantages of low-frequency full-PolSAR in ionospheric sounding, including high precision and resolution, as well as all-day and all-weather operation without a ground receiver. Therefore, the precision of GPS-based tomography can be enhanced, particularly for small-scale anomalies, and it is also simple and easy to achieve. Numerical and measured experiments using GPS, incoherent scatter radar (ISR), PolSAR, and E-CHAIM data in Alaska demonstrate that the reconstruction accuracy of the proposed CIT is significantly improved than that of the tomography results using only empirical model. In addition, the effects of PolSAR system errors and voxel size on CIT are analyzed to demonstrate the robustness of the method proposed in this article.
Published: 2024
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7. Salvage haploidentical transplantation for graft failure after first haploidentical allogeneic stem cell transplantation: an updated experience

Author: Ma, Rui, Zhu, Dan-Ping, Zhang, Xiao-Hui, Xu, Lan-Ping, Wang, Yu, Mo, Xiao-Dong, Lv, Meng, Zhang, Yuan-Yuan, Cheng, Yi-Fei, Yan, Chen-Hua, Chen, Yu-Hong, Chen, Yao, Wang, Jing-Zhi, Wang, Feng-Rong, Han, Ting-Ting, Kong, Jun, Wang, Zhi-Dong, Han, Wei, Chen, Huan, Chang, Ying-Jun, He, Yun, Xu, Zheng-Li, Zheng, Feng-Mei, Fu, Hai-Xia, Liu, Kai-Yan, Huang, Xiao-Jun, and Sun, Yu-Qian
Abstract: Graft failure is a fatal complication following allogeneic stem cell transplantation where a second transplantation is usually required for salvage. However, there are no recommended regimens for second transplantations for graft failure, especially in the haploidentical transplant setting. We recently reported encouraging outcomes using a novel method (haploidentical transplantation from a different donor after conditioning with fludarabine and cyclophosphamide). Herein, we report updated outcomes in 30 patients using this method. The median time of the second transplantation was 96.5 (33–215) days after the first transplantation. Except for one patient who died at +19d and before engraftment, neutrophil engraftments were achieved in all patients at 11 (8–24) days, while platelet engraftments were achieved in 22 (75.8%) patients at 17.5 (9–140) days. The 1-year OS and DFS were 60% and 53.3%, and CIR and TRM was 6.7% and 33.3%, respectively. Compared with the historical group, neutrophil engraftment (100% versus 58.5%, p< 0.001) and platelet engraftment (75.8% versus 32.3%, p< 0.001) were better in the novel regimen group, and OS was also improved (60.0% versus 26.4%, p= 0.011). In conclusion, salvage haploidentical transplantation from a different donor using the novel regimen represents a promising option to rescue patients with graft failure after the first haploidentical transplantation.
Published: 2024
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8. Human amniotic epithelial stem cell is a cell therapy candidate for preventing acute graft-versus-host disease

Author: Yang, Peng-jie, Zhao, Xiang-yu, Kou, Yao-hui, Liu, Jia, Ren, Xiang-yi, Zhang, Yuan-yuan, Wang, Zhi-dong, Ge, Zhen, Yuan, Wei-xin, Qiu, Chen, Tan, Bing, Liu, Qin, Shi, Yan-na, Jiang, Yuan-qing, Qiu, Cong, Guo, Li-he, Li, Jin-ying, Huang, Xiao-jun, and Yu, Lu-yang
Abstract: Graft-versus-host disease (GVHD), an immunological disorder that arises from donor T cell activation through recognition of host alloantigens, is the major limitation in the application of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Traditional immunosuppressive agents can relieve GVHD, but they induce serious side effects. It is highly required to explore alternative therapeutic strategy. Human amniotic epithelial stem cells (hAESCs) were recently considered as an ideal source for cell therapy with special immune regulatory property. In this study, we evaluated the therapeutic role of hAESCs in the treatment of GVHD, based on our previous developed cGMP-grade hAESCs product. Humanized mouse model of acute GVHD (aGVHD) was established by injection of huPBMCs via the tail vein. For prevention or treatment of aGVHD, hAESCs were injected to the mice on day -1 or on day 7 post-PBMC infusion, respectively. We showed that hAESCs infusion significantly alleviated the disease phenotype, increased the survival rate of aGVHD mice, and ameliorated pathological injuries in aGVHD target organs. We demonstrated that hAESCs directly induced CD4+T cell polarization, in which Th1 and Th17 subsets were downregulated, and Treg subset was elevated. Correspondingly, the levels of a series of pro-inflammatory cytokines were reduced while the levels of the anti-inflammatory cytokines were upregulated in the presence of hAESCs. We found that hAESCs regulated CD4+subset polarization in a paracrine mode, in which TGFβ and PGE2 were selectively secreted to mediate Treg elevation and Th1/Th17 inhibition, respectively. In addition, transplanted hAESCs preserved the graft-versus-leukemia (GVL) effect by inhibiting leukemia cell growth. More intriguingly, hAESCs infusion in HSCT patients displayed potential anti-GVHD effect with no safety concerns and confirmed the immunoregulatory mechanisms in the preclinical study. We conclude that hAESCs infusion is a promising therapeutic strategy for post-HSCT GVHD without compromising the GVL effect. The clinical trial was registered at www.clinicaltrials.govas #NCT03764228.
Published: 2024
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9. Repair of dysfunctional bone marrow endothelial cells alleviates aplastic anemia

Author: Tang, Shu-Qian, Xing, Tong, Lyu, Zhong-Shi, Guo, Li-Ping, Liang, Mi, Li, Chen-Yuan, Zhang, Yuan-Yuan, Wang, Yu, Xu, Lan-Ping, Zhang, Xiao-Hui, Huang, Xiao-Jun, and Kong, Yuan
Abstract: Aplastic anemia (AA) is a life-threatening disease characterized by bone marrow (BM) failure and pancytopenia. As an important component of the BM microenvironment, endothelial cells (ECs) play a crucial role in supporting hematopoiesis and regulating immunity. However, whether impaired BM ECs are involved in the occurrence of AA and whether repairing BM ECs could improve hematopoiesis and immune status in AA remain unknown. In this study, a classical AA mouse model and VE-cadherin blocking antibody that could antagonize the function of ECs were used to validate the role of BM ECs in the occurrence of AA. N-acetyl-L-cysteine (NAC, a reactive oxygen species scavenger) or exogenous EC infusion was administered to AA mice. Furthermore, the frequency and functions of BM ECs from AA patients and healthy donors were evaluated. BM ECs from AA patients were treated with NAC in vitro, and then the functions of BM ECs were evaluated. We found that BM ECs were significantly decreased and damaged in AA mice. Hematopoietic failure and immune imbalance became more severe when the function of BM ECs was antagonized, whereas NAC or EC infusion improved hematopoietic and immunological status by repairing BM ECs in AA mice. Consistently, BM ECs in AA patients were decreased and dysfunctional. Furthermore, dysfunctional BM ECs in AA patients led to their impaired ability to support hematopoiesis and dysregulate T cell differentiation toward proinflammatory phenotypes, which could be repaired by NAC in vitro. The reactive oxygen species pathway was activated, and hematopoiesis- and immune-related signaling pathways were enriched in BM ECs of AA patients. In conclusion, our data indicate that dysfunctional BM ECs with impaired hematopoiesis-supporting and immunomodulatory abilities are involved in the occurrence of AA, suggesting that repairing dysfunctional BM ECs may be a potential therapeutic approach for AA patients.
Published: 2023
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10. Avapritinib is effective for treatment of minimal residual disease in acute myeloid leukemia with t (8;21) and kit mutation failing to immunotherapy after allogeneic hematopoietic stem cell transplantation

Author: Kong, Jun, Zheng, Feng-Mei, Wang, Zhi-Dong, Zhang, Yuan-Yuan, Cheng, Yi-Fei, Fu, Hai-Xia, Lv, Meng, Chen, Huan, Xu, Lan-Ping, Zhang, Xiao-Hui, Huang, Xiao-Jun, and Wang, Yu
Abstract: In patients with t(8;21) acute myeloid leukemia (AML) with recurrent measurable residual disease (MRD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT), pre-emptive interferon-α therapy and donor lymphocyte infusion are noneffective in 30%–50% of patients. Avapritinib is a novel tyrosine kinase inhibitor targeting KIT mutations. We retrospectively report about 20 patients with t(8;21) AML and KIT mutations treated with avapritinib after allo-HSCT with MRD and most failing to respond to immunotherapy. Reduction of RUNX1-RUNX1T1after 1 month of treatment was ≥1 log in 12 patients (60%), which became negative in 4 patients (20%). In 13 patients who received avapritinib for ≥3 months, the reduction was ≥1 log in all patients, which became negative in 7 patients (53.8%). The median follow-up time was 5.5 (2.0–10.0) months from avapritinib initiation to the last follow-up. Three patients underwent hematologic relapse and survived. Among all 20 patients, RUNX1-RUNX1T1transcripts turned negative in 9 patients (45%). The efficacy did not differ significantly between D816 and non-D816 KIT mutation groups. The main adverse effect was hematological toxicity, which could generally be tolerated. In summary, avapritinib was effective for MRD treatment in patients with t(8;21) AML with KIT mutations failing to respond to immunotherapy after allo-HSCT.
Published: 2023
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11. A Prognostic Model Based on Clinical Biomarkers for Heart Failure in Adult Patients Following Allogeneic Hematopoietic Stem Cell Transplantation

Author: Zhang, Ao-Bei, Wang, Chen-Cong, Zhao, Peng, Tong, Ke-Ting, He, Yun, Zhu, Xiao-Lu, Fu, Hai-Xia, Wang, Feng-Rong, Mo, Xiao-Dong, Wang, Yu, Zhao, Xiang-Yu, Zhang, Yuan-Yuan, Han, Wei, Chen, Huan, Chen, Yao, Yan, Chen-Hua, Wang, Jing-Zhi, Han, Ting-Ting, Sun, Yu-Qian, Chen, Yu-Hong, Chang, Ying-Jun, Xu, Lan-Ping, Liu, Kai-Yan, Huang, Xiao-Jun, and Zhang, Xiao-Hui
Abstract: •Our model is the first to predict heart failure mortality following allogeneic hematopoietic stem cell transplantation.•The BLIPS score demonstrated high discrimination and calibration power.•The model can provide early identification of patients with heart failure, with a higher 2-month mortality rate.
Published: 2023
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12. A rapid and sensitive LC-ESI-MS/MS method for determining vincristine in micro-volumes of plasma for pediatric cancer patients

Author: Zhang, Yuan-Yuan, Wang, Jie, Li, Li, Wu, Chun-Ying, Chu, Chen-Chao, Guo, Hong-Li, Li, Tao, Chen, Feng, Zhou, Li, and Hu, Ya-Hui
Abstract: Vincristine is a natural vinca alkaloid drug, which is widely used in pediatric cancer treatment with dose-dependent neurotoxicity. Thus far, little is known about the association between neurotoxicity and plasma vincristine concentration, which markedly varies among individuals. Routine therapeutic drug monitoring (TDM) can be seen as a reliable strategy to improve efficacy and reduce side effects. Therefore, a rapid, sensitive, and reproducible method is critical for the clinical implementation of TDM. In this study, micro-volume (50 μL) human plasma samples were prepared by a simple one-step protein precipitation method with acetonitrile. Chromatographic separation of vincristine and its internal standard vincristine-d3from background noise was achieved on a Kinetex C18 column (2.1 mm × 50 mm, 1.7 μm) with a gradient elution program at a flow rate of 0.3 mL min−1in 4 min. The mass spectrometric detection was performed in electrospray ionization multiple reaction monitoring mode using the ion transitions of 825.4 → 765.1 for vincristine, and 828.2 → 768.2 for vincristine-d3, respectively. As a result, no matrix effect was observed. The lower limit of quantification was 0.5 ng mL−1with a precision of 14.6% and an accuracy of 97.4%. The calibration curve was linear from 0.5 to 100 ng mL−1(r2> 0.99, n= 8). The intra- and inter-batch precision and accuracy, recovery, and stability of the new method were all within the acceptable criteria. The method was successfully applied to monitor the vincristine concentration for six pediatric cancer patients. Arguably, such proactive TDM of vincristine may be helpful to manage the treatment for these cancer patients.
Published: 2023
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13. Clinical risk factors and prognostic model for patients with bronchiolitis obliterans syndrome after hematopoietic stem cell transplantation

Author: Huang, Qiu-Sha, Han, Tian-Xiao, Chen, Qi, Wu, Jin, Zhao, Peng, Wu, Ye-Jun, He, Yun, Zhu, Xiao-Lu, Fu, Hai-Xia, Wang, Feng-Rong, Zhang, Yuan-Yuan, Mo, Xiao-Dong, Han, Wei, Yan, Chen-Hua, Wang, Jing-Zhi, Chen, Huan, Chen, Yu-Hong, Han, Ting-Ting, Lv, Meng, Chen, Yao, Wang, Yu, Xu, Lan-Ping, Liu, Kai-Yan, Huang, Xiao-Jun, and Zhang, Xiao-Hui
Abstract: Bronchiolitis obliterans syndrome (BOS) is a common and potentially devastating noninfectious pulmonary complication after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Currently, predictive tools for BOS are not available. We aimed to identify the clinical risk factors and establish a prognostic model for BOS in patients who undergo allo-HSCT. We retrospectively identified a cohort comprising 195 BOS patients from 6100 consecutive patients who were allografted between 2008 and 2022. The entire cohort was divided into a derivation cohort and a validation cohort based on the time of transplantation. Via multivariable Cox regression methods, declining forced expiratory volume at 1 s (FEV1) to <40%, pneumonia, cGVHD except lung, and respiratory failure were found to be independent risk factors for the 3-year mortality of BOS. A risk score called FACT was constructed based on the regression coefficients. The FACT model had an AUC of 0.863 (95% CI: 0.797–0.928) in internal validation and 0.749 (95% CI: 0.621–0.876) in external validation. The calibration curves showed good agreement between the FACT-predicted probabilities and actual observations. The FACT risk score will help to identify patients at high risk and facilitate future research on developing novel, effective interventions to personalize treatment.
Published: 2023
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14. Machine learning algorithm as a prognostic tool for venous thromboembolism in allogeneic transplant patients

Author: Deng, Rui-Xin, Zhu, Xiao-Lu, Zhang, Ao-Bei, He, Yun, Fu, Hai-Xia, Wang, Feng-Rong, Mo, Xiao-Dong, Wang, Yu, Zhao, Xiang-Yu, Zhang, Yuan-Yuan, Han, Wei, Chen, Huan, Chen, Yao, Yan, Chen-Hua, Wang, Jing-Zhi, Han, Ting-Ting, Chen, Yu-Hong, Chang, Ying-Jun, Xu, Lan-Ping, Huang, Xiao-Jun, and Zhang, Xiao-Hui
Abstract: [Display omitted]
Published: 2023
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15. Rapid determination of plasma vigabatrin by LC-ESI-MS/MS supporting therapeutic drug monitoring in children with infantile spasms

Author: Wang, Jie, Zhang, Yuan-Yuan, Guo, Hong-Li, Hu, Ya-Hui, Lu, Xiao-Peng, Wang, Shan-Shan, Wu, Chun-Feng, and Chen, Feng
Abstract: Vigabatrin is one of the second-generation anti-seizure medications (ASMs) designated orphan drugs by the FDA for monotherapy for pediatric patients with infantile spasms from 1 month to 2 years of age. Vigabatrin is also indicated as the adjunctive therapy for adults and pediatric patients 10 years of age and older with refractory complex partial seizures. Ideally, the vigabatrin treatment entails achieving complete seizure freedom without significant adverse effects, and the therapeutic drug monitoring (TDM) will make a significant contribution to this aim, which provides a pragmatic approach to such epilepsy care in that the dose tailoring can be undertaken for uncontrollable seizures and in cases of clinical toxicity guided by the drug concentrations. Thus, reliable assays are mandatory for TDM to be valuable, and blood, plasma, or serum are the matrixes of choice. In this study, a simple, rapid, and sensitive LC-ESI-MS/MS method for the measurement of plasma vigabatrin was developed and validated. The sample clean-up was performed by an easy-to-use method, i.e., protein precipitation using acetonitrile (ACN). Chromatographic separation of vigabatrin and vigabatrin-13C,d2(internal standard) was achieved on the Waters symmetry C18 column (4.6 mm × 50 mm, 3.5 μm) with isocratic elution at a flow rate of 0.35 mL min−1. The target analyte was completely separated by elution with a highly aqueous mobile phase for 5 min, without any endogenous interference. The method showed good linearity over the 0.010–50.0 μg mL−1concentration range with a correlation coefficient r2= 0.9982. The intra-batch and inter-batch precision and accuracy, recovery, and stability of the method were all within the acceptable parameters. Moreover, the method was successfully used in pediatric patients treated with vigabatrin and also provided valuable information for clinicians by monitoring plasma vigabatrin levels in our hospital.
Published: 2023
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16. Mapping the global distribution of spotted fever group rickettsiae: a systematic review with modelling analysis

Author: Zhang, Yuan-Yuan, Sun, Yan-Qun, Chen, Jin-Jin, Teng, Ai-Ying, Wang, Tao, Li, Hao, Hay, Simon I, Fang, Li-Qun, Yang, Yang, and Liu, Wei
Abstract: Emerging and re-emerging spotted fever group (SFG) rickettsioses are increasingly recognised worldwide as threats to public health, yet their global distribution and associated risk burden remain poorly understood.
Published: 2023
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17. Mixed chimaerism is associated with poorer long-term failure-free survival among aplastic anaemia patients receiving HLA-matched donor transplantation

Author: Xu, Zheng-Li, Xu, Lan-Ping, Zhang, Yuan-Yuan, Cheng, Yi-Fei, Mo, Xiao-Dong, Han, Ting-Ting, Wang, Feng-Rong, Yan, Chen-Hua, Sun, Yu-Qian, Chen, Yu-Hong, Tang, Fei-Fei, Han, Wei, Wang, Yu, Zhang, Xiao-Hui, Liu, Kai-Yan, and Huang, Xiao-Jun
Published: 2023
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18. Wetting and corrosion behavior between magnesia–carbon refractory and converter slags with different MgO contents

Author: Bai, Rui-qiang, Liu, Si-yang, Mao, Fei-xiong, Zhang, Yuan-yuan, Yang, Xin, and He, Zhi-jun
Abstract: The influence of MgO content in slag on wetting and corrosion behavior between slag and MgO–C refractory was investigated. It can be known from the high-temperature wetting experiment that as the MgO content in the slag increases, the final contact angle between the slag and the MgO–C refractory gradually increases and the penetration depth of the slag into the refractory gradually decreases from 60.54 μm (when the MgO content is 8%) to 28.11 μm (when the MgO content is 12%). The CaO and SiO2in the slag penetrate into the MgO–C refractory along the pores or surface cracks formed by carbon oxidation and react with MgO to generate a large amount of low-melting compound CaO–MgO–SiO2, which accelerates the corrosion of the refractory. As the MgO content in slag increases, the viscosity of the slag increases and the fluidity becomes worse, so that the mass transfer and diffusion of molecules or ions in the slag are weakened. In addition, the increase in MgO reduces the activity of FeO in the slag, which inhibits the interfacial chemical reaction, thereby weakening the wetting effect caused by the reaction.
Published: 2022
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19. The ENPP1 Q121 variant predicts major cardiovascular events in high-risk individuals: evidence for interaction with obesity in diabetic patients

Author: Bacci, Simonetta, Rizza, Stefano, Prudente, Sabrina, Spoto, Belinda, Powers, Christine, Facciorusso, Antonio, Pacilli, Antonio, Lauro, Davide, Testa, Alessandra, Zhang, Yuan-Yuan, Di Stolfo, Giuseppe, Mallamaci, Francesca, Tripepi, Giovanni, Xu, Rui, Mangiacotti, Davide, Aucella, Filippo, Lauro, Renato, Gervino, Ernest V., Hauser, Thomas H., Copetti, Massimiliano, De Cosmo, Salvatore, Pellegrini, Fabio, Zoccali, Carmine, Federici, Massimo, Doria, Alessandro, and Trischitta, Vincenzo
Subjects: Single nucleotide polymorphisms -- Research -- Genetic aspects -- Health aspects, Cardiovascular diseases -- Genetic aspects -- Risk factors -- Diagnosis -- Research, Diabetics -- Health aspects -- Research, Health
Abstract: OBJECTIVE--Insulin resistance (IR) and cardiovascular disease may share a common genetic background. We investigated the role of IR-associated ENPP1 K121Q polymorphism (rs1044498) on cardiovascular disease in high-risk individuals. RESEARCH DESIGN AND METHODS--A prospective study (average follow-up, 37 months) was conducted for major cardiovascular events (myocardial infarction [MI], stroke, cardiovascular death) from the Gargano Heart Study (GHS; n = 330 with type 2 diabetes and coronary artery disease), the Tor Vergata Atherosclerosis Study (TVAS; n = 141 who had MI), and the Cardiovascular Risk Extended Evaluation in Dialysis (CREED) database (n = 266 with end-stage renal disease). Age at MI was investigated in cross-sectional studies of 339 type 2 diabetic patients (n = 169 from Italy, n = 170 from the U.S.). RESULTS--Incidence of cardiovascular events per 100 person--years was 4.2 in GHS, 10.8 in TVAS, and 11.7 in CREED. Hazard ratios (HRs) for KQ+QQ versus individuals carrying the K121/K121 genotype (KK) individuals were 1.47 (95% CI 0.80-2.70) in GHS, 2.31 (95% CI 1.22-4.34) in TVAS, and 1.36 (95% CI 0.88-2.10) in CREED, and 1.56 (95% CI 1.15-2.12) in the three cohorts combined. In the 395 diabetic patients, the Q121 variant predicted cardiovascular events among obese but not among nonobese individuals (HR 5.94 vs. 0.62, P = 0.003 for interaction). A similar synergism was observed in cross-sectional studies, with age at MI being 3 years younger in Q121 carriers than in KK homozygotes among obese but not among nonobese patients (P = 0.035 for interaction). CONCLUSIONS--The ENPP1 K121Q polymorphism is an independent predictor of major cardiovascular events in high-risk individuals. In type 2 diabetes, this effect is exacerbated by obesity. Future larger studies are needed to confirm our finding. Diabetes 60:1000-1007, 2011, Morbidity and mortality due to cardiovascular disease (CVD) are highly prevalent (1), mostly because of the epidemics of obesity and type 2 diabetes (2-4). Environmental and genetic factors both contribute [...]
Published: 2011
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20. Serum macrophage migration-inhibitory factor as a diagnostic and prognostic biomarker for gastric cancer

Author: Xia, Harry Hua-Xiang, Yang, Yi, Chu, Kent-Man, Gu, Qing, Zhang, Yuan-Yuan, He, Hua, Wong, Wai Man, Leung, Suet-Yi, Yuen, Siu-Tsan, Yuen, Man-Fung, Chan, Annie O.O., and Wong, Benjamin C.Y.
Subjects: Stomach cancer -- Diagnosis, Stomach cancer -- Patient outcomes, Stomach cancer -- Research, Macrophages -- Analysis, Dyspepsia -- Research, Health
Published: 2009

21. Selective bromodomain and extra-terminal bromodomain inhibitor inactivates macrophages and hepatic stellate cells to inhibit liver inflammation and fibrosis

Author: Fu, Rong, Zu, Shi-Jia, Liu, Yan-Jun, Li, Jia-Cheng, Dang, Wen-Zhen, Liao, Li-Ping, Liu, Li-Ping, Chen, Pan-Yu, Huang, He-Ming, Wu, Kang-Hui, Zhou, Bing, Pan, Qin, Luo, Cheng, Zhang, Yuan-Yuan, and Li, Guang-Ming
Abstract: ABSTRACTLiver fibrosis occurs following inflammation triggered by the integrated actions of activated liver-resident macrophages (Kupffer cells) and hepatic stellate cells (HSCs), and the multiplicity of these mechanisms complicates drug therapy. Here, we demonstrate that the selective bromodomain and extra-terminal (BET) bromodomain inhibitor compound38 can block both the Janus kinase-signal transducer and activator of transcription and mitogen-activated protein kinase signaling pathways in macrophages, which decreased their secretion of proinflammatory cytokines in a dose-dependent manner. The inactivation of macrophages attenuated lipopolysaccharide-induced injurious inflammation concurrent with a reduction in F4/80+ cells, proinflammatory cytokine levels, and neutrophil infiltration. Moreover, compound 38 inhibited the Wnt/β-catenin and transforming growth factor-beta/SMAD signaling pathways to abolish the activation of HSCs. In vivo, compound 38 significantly decreased the collagen deposition and fibrotic area of a CCl4-induced liver fibrosis model, and restored the deficiency of activated HSCs and the upregulation of liver inflammation. These results highlight the potential role of compound 38 in treating liver fibrosis considering its simultaneous inhibitory effects on liver inflammation and related fibrosis.
Published: 2022
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22. Insights and implications of sexual dimorphism in osteoporosis

Author: Zhang, Yuan-Yuan, Xie, Na, Sun, Xiao-Dong, Nice, Edouard C., Liou, Yih-Cherng, Huang, Canhua, Zhu, Huili, and Shen, Zhisen
Abstract: Osteoporosis, a metabolic bone disease characterized by low bone mineral density and deterioration of bone microarchitecture, has led to a high risk of fatal osteoporotic fractures worldwide. Accumulating evidence has revealed that sexual dimorphism is a notable feature of osteoporosis, with sex-specific differences in epidemiology and pathogenesis. Specifically, females are more susceptible than males to osteoporosis, while males are more prone to disability or death from the disease. To date, sex chromosome abnormalities and steroid hormones have been proven to contribute greatly to sexual dimorphism in osteoporosis by regulating the functions of bone cells. Understanding the sex-specific differences in osteoporosis and its related complications is essential for improving treatment strategies tailored to women and men. This literature review focuses on the mechanisms underlying sexual dimorphism in osteoporosis, mainly in a population of aging patients, chronic glucocorticoid administration, and diabetes. Moreover, we highlight the implications of sexual dimorphism for developing therapeutics and preventive strategies and screening approaches tailored to women and men. Additionally, the challenges in translating bench research to bedside treatments and future directions to overcome these obstacles will be discussed.
Published: 2024
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23. Author Correction: Insights and implications of sexual dimorphism in osteoporosis

Author: Zhang, Yuan-Yuan, Xie, Na, Sun, Xiao-Dong, Nice, Edouard C., Liou, Yih-Cherng, Huang, Canhua, Zhu, Huili, and Shen, Zhisen
Published: 2024
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24. Tag polymorphisms at the A20 (TNFAIP3) locus are associated with lower gene expression and increased risk of coronary artery disease in type 2 diabetes

Author: Boonyasrisawat, Watip, Eberle, Delphine, Bacci, Simonetta, Zhang, Yuan-Yuan, Nolan, David, Gervino, Ernest V., Johnstone, Michael T., Trischitta, Vincenzo, Shoelson, Steven E., and Doria, Alessandro
Subjects: Diabetes -- Research, Genetic polymorphisms -- Research -- Genetic aspects, Tumor necrosis factor -- Research -- Genetic aspects, Type 2 diabetes -- Genetic aspects -- Care and treatment -- Research, Health, Care and treatment, Research, Genetic aspects
Abstract: A20 or tumor necrosis factor (TNF)-induced protein 3 (TNFAIP3) is a negative regulator of nuclear factor-κB (NF-κB). We have investigated whether polymorphisms in this gene are associated with increased atherosclerosis in diabetic patients. Five tag single nucleotide polymorphisms (SNPs) were typed in 479 type 2 diabetic patients from Boston, including 239 coronary artery disease (CAD)-positive case subjects and 240 CAD-negative control subjects. Two tag SNPs (rs5029930 and rs610604) were independently associated with CAD; adjusted odds ratios (ORs) for minor allele carriers were 2.3 (95% CI 1.4-3.8, P = 0.001) and 2.0 (1.3-2.9, P = 0.0008), respectively. The association with rs610604 was dependent on glycemic control, with ORs of 3.9 among subjects with A1C ≤ 7.0% and 1.2 for those with A1C >7.0% (P for interaction = 0.015). A similar interaction pattern was found among 231 CAD-positive and 332 CAD-negative type 2 diabetic patients from Italy (OR 2.2, P = 0.05 vs. OR 0.9, P = 0.63 in the low vs. high A1C strata, P for interaction = 0.05). Quantitative RT-PCR in blood mononuclear cells from 83 nondiabetic subjects showed that rs610604 and rs5029930 minor allele homozygotes have 30-45% lower levels of A20 mRNA than major allele homozygotes, and heterozygotes have intermediate levels (P = 0.04 and 0.028, respectively). These findings point to variability in the A20/TNFAIP3 gene as a modulator of CAD risk in type 2 diabetes. This effect is mediated by allelic differences in A20 expression., Patients with type 2 diabetes experience a two- to fourfold increase in the risk of cardiovascular death compared with nondiabetic subjects (1). The increase in cardiovascular mortality is mainly secondary [...]
Published: 2007

25. Common haplotypes at the adiponectin receptor 1 (ADIPOR1) locus are associated with increased risk of coronary artery disease in type 2 diabetes

Author: Soccio, Teresa, Zhang, Yuan-Yuan, Bacci, Simonetta, Mlynarski, Wojciech, Placha, Grzegorz, Raggio, Greer, Di Paola, Rosa, Marucci, Antonella, Johnstone, Michael T., Gervino, Ernest V., Abumrad, Nada A., Klein, Samuel, Trischitta, Vincenzo, and Doria, Alessandro
Subjects: Haplotypes -- Research -- Genetic aspects, Diabetes -- Research, Genetic variation -- Research -- Genetic aspects, Type 2 diabetes -- Genetic aspects -- Causes of -- Research, Health, Research, Genetic aspects, Causes of
Abstract: Adiponectin, an adipokine facilitating insulin action, has antiatherogenic effects. This study investigated whether common polymorphisms in the adiponectin receptor 1 (ADIPOR1) gene mediating these effects influence the risk of coronary artery disease (CAD) in type 2 diabetes. Linkage disequilibrium analysis of 28 single nucleotide polymorphisms (SNPs) spanning the entire ADIPOR1 locus revealed two haplotype blocks that could be tagged by six SNPs. These six markers were typed in two populations of CAD-positive and -negative subjects with type 2 diabetes, one from Boston (n = 411) and the other from Italy (n = 533). In the Boston population, the three tags of the more 3' block were all significantly associated with CAD (P = 0.001-0.01). A similar trend, although not significant, was found in Italian subjects. Haplotype analysis of the combined populations revealed different haplotype distributions in case and control subjects (P = 0.0002), with one common haplotype being associated in homozygotes with a greater than threefold increase in cardiovascular risk (odds ratio 3.6 [95% CI 1.8-7.2]). Some of the genotypes associated with increased cardiovascular risk were associated with 30-40% lower ADIPOR1 mRNA levels in blood mononuclear cells (n = 60) and adipose tissue biopsies (n = 28) (P = 0.001-0.014). Our findings point to genetic variability at the ADIPOR1 locus as a strong determinant of CAD susceptibility in type 2 diabetes., Increased susceptibility to atherosclorosis originates from unbalanced activity of pro- and antiatherogenic factors, which are both environmental and genetic in origin (1). The nature of the genetic component is poorly [...]
Published: 2006

26. The K121Q polymorphism of the ENPP1/PC-1 Gene is associated with insulin resistance/atherogenic phenotypes, including earlier onset of type 2 diabetes and myocardial infarction

Author: Bacci, Simonetta, Ludovico, Ornella, Prudente, Sabrina, Zhang, Yuan-Yuan, Di Paola, Rosa, Mangiacotti, Davide, Rauseo, Anna, Nolan, David, Duffy, Jill, Fini, Grazia, Salvemini, Lucia, Amico, Cesare, Vigna, Carlo, Pellegrini, Fabio, Menzaghi, Claudia, Doria, Alessandro, and Trischitta, Vincenzo
Subjects: Heart attack -- Risk factors -- Drug therapy -- Genetic aspects -- Health aspects, Insulin resistance -- Health aspects -- Drug therapy -- Genetic aspects -- Risk factors, Type 2 diabetes -- Risk factors -- Genetic aspects -- Drug therapy -- Health aspects, Health, Drug therapy, Genetic aspects, Risk factors, Health aspects
Abstract: Insulin resistance (IR) is pathogenic for type 2 diabetes and coronary artery disease (CAD). The K121Q polymorphism of the ENPP1/PC-1 gene is associated with IR. Our aim was to investigate the role of the 121Q variant on the risk of type 2 diabetes and CAD. Nondiabetic control subjects (n = 638), type 2 diabetic patients without CAD (n = 535), and type 2 diabetic patients with CAD (n = 434) from Italy and the U.S. were studied. The proportion of 121Q carriers progressively increased in the three groups (27.4, 28.8, and 33.2%, respectively; adjusted P value -0.027). Among diabetic patients (n = 969), 121Q carriers had an increased risk of developing type 2 diabetes before the age of 65 years (adjusted odds ratio [OR] 2.26, 95% CI 1.26-4.03; P = 0.006) and having a myocardial infarction (MI) (n = 156) by 50 years of age (3.17, 1.46-6.88, P = 0.007). The 121Q variant was also associated with an increased risk for CAD (1.47, 1.01-2.18; P = 0.049) in diabetic patients who did not smoke (n = 546). In conclusion, the ENPP1/PC-1 121Q variant is associated with a progressive deterioration of the IR-atherogenic phenotype; among diabetic individuals, it is also associated with earlier onset of type 2 diabetes and MI., Although it is well accepted that insulin resistance (IR) is partly under genetic control, the genes that are involved are mostly unknown (1-5). IR is pathogenic for type 2 diabetes [...]
Published: 2005

27. Natural product 1,2,3,4,6-penta-O-galloyl-β-D-glucopyranose is a reversible inhibitor of glyceraldehyde 3-phosphate dehydrogenase

Author: Li, Wen, Liao, Li-ping, Song, Ning, Liu, Yan-jun, Ding, Yi-luan, Zhang, Yuan-yuan, Zhou, Xiao-ru, Sun, Zhong-ya, Xiao, Sen-hao, Wang, Hong-bo, Lu, Jing, Zhang, Nai-xia, Jiang, Hua-liang, Chen, Kai-xian, Liu, Chuan-peng, Zheng, Jie, Zhao, Ke-hao, and Luo, Cheng
Abstract: Aerobic glycolysis, also known as the Warburg effect, is a hallmark of cancer cell glucose metabolism and plays a crucial role in the activation of various types of immune cells. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) catalyzes the conversion of D-glyceraldehyde 3-phosphate to D-glycerate 1,3-bisphosphate in the 6th critical step in glycolysis. GAPDH exerts metabolic flux control during aerobic glycolysis and therefore is an attractive therapeutic target for cancer and autoimmune diseases. Recently, GAPDH inhibitors were reported to function through common suicide inactivation by covalent binding to the cysteine catalytic residue of GAPDH. Herein, by developing a high-throughput enzymatic screening assay, we discovered that the natural product 1,2,3,4,6-penta-O-galloyl-β-D-glucopyranose (PGG) is an inhibitor of GAPDH with Ki= 0.5 μM. PGG blocks GAPDH activity by a reversible and NAD+and Pi competitive mechanism, suggesting that it represents a novel class of GAPDH inhibitors. In-depth hydrogen deuterium exchange mass spectrometry (HDX-MS) analysis revealed that PGG binds to a region that disrupts NAD+and inorganic phosphate binding, resulting in a distal conformational change at the GAPDH tetramer interface. In addition, structural modeling analysis indicated that PGG probably reversibly binds to the center pocket of GAPDH. Moreover, PGG inhibits LPS-stimulated macrophage activation by specific downregulation of GAPDH-dependent glucose consumption and lactate production. In summary, PGG represents a novel class of GAPDH inhibitors that probably reversibly binds to the center pocket of GAPDH. Our study sheds new light on factors for designing a more potent and specific inhibitor of GAPDH for future therapeutic applications.
Published: 2022
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28. P300/CBP inhibition sensitizes mantle cell lymphoma to PI3Kδ inhibitor idelalisib

Author: Zhou, Xiao-ru, Li, Xiao, Liao, Li-ping, Han, Jie, Huang, Jing, Li, Jia-cheng, Tao, Hong-ru, Fan, Shi-jie, Chen, Zhi-feng, Li, Qi, Chen, Shi-jie, Ding, Hong, Yang, Ya-xi, Zhou, Bing, Jiang, Hua-liang, Chen, Kai-xian, Zhang, Yuan-yuan, Huang, Chuan-xin, and Luo, Cheng
Abstract: Mantle cell lymphoma (MCL) is a lymphoproliferative disorder lacking reliable therapies. PI3K pathway contributes to the pathogenesis of MCL, serving as a potential target. However, idelalisib, an FDA-approved drug targeting PI3Kδ, has shown intrinsic resistance in MCL treatment. Here we report that a p300/CBP inhibitor, A-485, could overcome resistance to idelalisib in MCL cells in vitro and in vivo. A-485 was discovered in a combinational drug screening from an epigenetic compound library containing 45 small molecule modulators. We found that A-485, the highly selective catalytic inhibitor of p300 and CBP, was the most potent compound that enhanced the sensitivity of MCL cell line Z-138 to idelalisib. Combination of A-485 and idelalisib remarkably decreased the viability of three MCL cell lines tested. Co-treatment with A-485 and idelalisib in Maver-1 and Z-138 MCL cell xenograft mice for 3 weeks dramatically suppressed the tumor growth by reversing the unsustained inhibition in PI3K downstream signaling. We further demonstrated that p300/CBP inhibition decreased histone acetylation at RTKs gene promoters and reduced transcriptional upregulation of RTKs, thereby inhibiting the downstream persistent activation of MAPK/ERK signaling, which also contributed to the pathogenesis of MCL. Therefore, additional inhibition of p300/CBP blocked MAPK/ERK signaling, which rendered maintaining activation to PI3K-mTOR downstream signals p-S6 and p-4E-BP1, thus leading to suppression of cell growth and tumor progression and eliminating the intrinsic resistance to idelalisib ultimately. Our results provide a promising combination therapy for MCL and highlight the potential use of epigenetic inhibitors targeting p300/CBP to reverse drug resistance in tumor.
Published: 2022
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29. α-Glucosidase Inhibitory Activities and the Interaction Mechanism of Novel Spiro-Flavoalkaloids from YingDe Green Tea

Author: Hou, Zhi-Wei, Chen, Chen-Hui, Ke, Jia-Ping, Zhang, Yuan-Yuan, Qi, Yan, Liu, Shi-Yu, Yang, Zi, Ning, Jing-Ming, and Bao, Guan-Hu
Abstract: Flavoalkaloids are a unique class of compounds in tea, most of which have an N-ethyl-2-pyrrolidinone moiety substituted at the A ring of a catechin skeleton. 1-Ethyl-5-hydroxy-pyrrolidone, a decomposed product of theanine, was supposed to be the key intermediate to form tea flavoalkaloids. However, we have also detected another possible theanine intermediate, 1-ethyl-5-oxopyrrolidine-2-carboxylic acid, and speculated if there are related conjugated catechins. Herein, four novel spiro-flavoalkaloids with a spiro-γ-lactone structural moiety were isolated from Yingde green tea (Camellia sinensisvar. assamica) in our continuing exploration of new chemical constituents from tea. The structures of the new compounds, spiro-flavoalkaloids A-D (1–4), were further elucidated by extensive nuclear magnetic resonance (NMR) spectroscopy together with the calculated 13C NMR, IR, UV–vis, high-resolution mass, optical rotation, experimental, and calculated circular dichroism spectra. We also provided an alternative pathway to produce these novel spiro-flavoalkaloids. Additionally, their α-glucosidase inhibitory activities were determined with IC50values of 3.34 (1), 5.47 (2), 22.50 (3), and 15.38 (4) μM. Docking results revealed that compounds 1and 2mainly interacted with residues ASP-215, ARG-442, ASP-352, GLU-411, HIS-280, ARG-315, and ASN-415 of α-glucosidase through hydrogen bonds. The fluorescence intensity of α-glucosidase could be quenched by compounds 1and 2in a static style.
Published: 2022
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30. The lower relapse rate and better survival advantages of haploidentical allograft compared with HLA-matched sibling donor allografts for intermediate- and adverse-risk AML patients with pretransplantation minimal residual disease

Author: Wang, Ming, Wang, Bixia, Xu, Lan-Ping, Wang, Yu, Zhang, Xiao-Hui, Cheng, Yi-fei, Sun, Yu-Qian, Zhang, Yuan-Yuan, Liu, Yan-Rong, Chang, Ying-Jun, Liu, Kai-Yan, and Huang, Xiao-Jun
Published: 2022
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31. GDF11 promotes wound healing in diabetic mice via stimulating HIF-1ɑ-VEGF/SDF-1ɑ-mediated endothelial progenitor cell mobilization and neovascularization

Author: Zhang, Ying, Zhang, Yi-yuan, Pan, Zhen-wei, Li, Qing-qi, Sun, Li-hua, Li, Xin, Gong, Man-yu, Yang, Xue-wen, Wang, Yan-ying, Li, Hao-dong, Xuan, Li-na, Shao, Ying-chun, Li, Meng-meng, Zhang, Ming-yu, Yu, Qi, Li, Zhange, Zhang, Xiao-fang, Liu, Dong-hua, Zhu, Yan-meng, Tan, Zhong-yue, Zhang, Yuan-yuan, Liu, Yun-qi, Zhang, Yong, Jiao, Lei, and Yang, Bao-feng
Abstract: Non-healing diabetic wounds (DW) are a serious clinical problem that remained poorly understood. We recently found that topical application of growth differentiation factor 11 (GDF11) accelerated skin wound healing in both Type 1 DM (T1DM) and genetically engineered Type 2 diabetic db/db(T2DM) mice. In the present study, we elucidated the cellular and molecular mechanisms underlying the action of GDF11 on healing of small skin wound. Single round-shape full-thickness wound of 5-mm diameter with muscle and bone exposed was made on mouse dorsum using a sterile punch biopsy 7 days following the onset of DM. Recombinant human GDF11 (rGDF11, 50 ng/mL, 10 μL) was topically applied onto the wound area twice a day until epidermal closure (maximum 14 days). Digital images of wound were obtained once a day from D0 to D14 post-wounding. We showed that topical application of GDF11 accelerated the healing of full-thickness skin wounds in both type 1 and type 2 diabetic mice, even after GDF8 (a muscle growth factor) had been silenced. At the cellular level, GDF11 significantly facilitated neovascularization to enhance regeneration of skin tissues by stimulating mobilization, migration and homing of endothelial progenitor cells (EPCs) to the wounded area. At the molecular level, GDF11 greatly increased HIF-1ɑ expression to enhance the activities of VEGF and SDF-1ɑ, thereby neovascularization. We found that endogenous GDF11 level was robustly decreased in skin tissue of diabetic wounds. The specific antibody against GDF11 or silence of GDF11 by siRNA in healthy mice mimicked the non-healing property of diabetic wound. Thus, we demonstrate that GDF11 promotes diabetic wound healing via stimulating endothelial progenitor cells mobilization and neovascularization mediated by HIF-1ɑ-VEGF/SDF-1ɑ pathway. Our results support the potential of GDF11 as a therapeutic agent for non-healing DW.
Published: 2022
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32. Effect of visual distraction on pain in adults undergoing colonoscopy: a meta-analysis

Author: Zhang, Yuan-Yuan, Vimala, Ramoo, Chui, Ping Lei, and Hilmi, Ida Normiha
Abstract: Background: Pain is a contributing factor to the low compliance rate for performing a colonoscopy on screening for colorectal cancer. Purpose: This meta-analysis aimed to evaluate the effect of visual distraction on adults undergoing colonoscopy. Methods: We searched PubMed, EMBASE, Web of Science, and Cochrane Library Database from their inception to February 2022. Randomized controlled trials comparing visual distraction with non-visual distraction were considered for inclusion. The fixed-effects and random-effects models were used to pool the data from individual studies and the Cochrane risk of bias assessment tool was used to determine the methodology quality. Results: This meta-analysis included four studies (N= 301) for pain level and total procedure time, three studies (N= 181) for satisfaction score, three studies (N= 196) for anxiety level, and four studie (N= 402) for willingness to repeat the procedure. The pooled analysis shown that significantly lower pain levels (SMD, − 0.25; 95% CI − 0.47 to − 0.02; P= 0.03), higher satisfaction score with the procedure (SMD, 0.63; 95% CI, 0.33 to 0.93; P< 0.0001), and higher willingness to repeat the procedure (OR, 2.66; 95% CI 1.70 to 4.17; P< 0.0001) in the visual distraction group than those in the non-visual distraction group, with no significant differences in total procedure time (SMD,− 0.07; 95% CI − 0.30 to 0.15; P= 0.53) or anxiety level (SMD,− 0.27; 95% CI − 0.55 to 0.01; P= 0.06). Conclusions: Visual distraction improved the patient’s pain, satisfaction, and willingness to repeat the procedure. Thus, visual stimulation is an effective way to reduce pain during colonoscopy and should be recommended.
Published: 2022
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33. Distinct Immune Homeostasis Remodeling Patterns after HLA-Matched and Haploidentical Transplantation

Author: Guo, Huidong, Guo, Liping, Wang, Bixia, Wang, Ming, Hong, Yan, Mo, Xiao-Dong, Sun, Yuqian, Zhang, Yuan-Yuan, Wang, Zhidong, Kong, Jun, Yan, Chen-Hua, Wang, Yu, Xu, Lan-Ping, Zhang, Xiaohui, Chang, Ying-Jun, and Huang, Xiao-Jun
Published: 2022
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34. A prognostic model (BATAP) with external validation for patients with transplant-associated thrombotic microangiopathy

Author: Zhao, Peng, Wu, Ye-jun, He, Yun, Chong, Shan, Qu, Qing-yuan, Deng, Rui-xin, Sun, Xiao-wan, Huang, Qiu-sha, Liu, Xiao, Zhu, Xiao-lu, Wang, Feng-rong, Zhang, Yuan-yuan, Mo, Xiao-dong, Han, Wei, Wang, Jing-zhi, Wang, Yu, Chen, Huan, Chen, Yu-hong, Zhao, Xiang-yu, Chang, Ying-jun, Xu, Lan-ping, Liu, Kai-yan, Huang, Xiao-jun, and Zhang, Xiao-hui
Abstract: Transplant-associated thrombotic microangiopathy (TA-TMA) is a potentially life-threatening complication following allogeneic hematopoietic stem cell transplantation (allo-HSCT). Information on markers for early prognostication remains limited, and no predictive tools for TA-TMA are available. We attempted to develop and validate a prognostic model for TA-TMA. A total of 507 patients who developed TA-TMA following allo-HSCT were retrospectively identified and separated into a derivation cohort and a validation cohort, according to the time of transplantation, to perform external temporal validation. Patient age (odds ratio [OR], 2.371; 95% confidence interval [CI], 1.264-4.445), anemia (OR, 2.836; 95% CI, 1.566-5.138), severe thrombocytopenia (OR, 3.871; 95% CI, 2.156-6.950), elevated total bilirubin (OR, 2.716; 95% CI, 1.489-4.955), and proteinuria (OR, 2.289; 95% CI, 1.257-4.168) were identified as independent prognostic factors for the 6-month outcome of TA-TMA. A risk score model termed BATAP (Bilirubin, Age, Thrombocytopenia, Anemia, Proteinuria) was constructed according to the regression coefficients. The validated c-statistic was 0.816 (95%, CI, 0.766-0.867) and 0.756 (95% CI, 0.696-0.817) for the internal and external validation, respectively. Calibration plots indicated that the model-predicted probabilities correlated well with the actual observed frequencies. This predictive model may facilitate the prognostication of TA-TMA and contribute to the early identification of high-risk patients.
Published: 2021
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35. Gossypol, a novel modulator of VCP, induces autophagic degradation of mutant huntingtin by promoting the formation of VCP/p97-LC3-mHTT complex

Author: Li, Xiao-jing, Zhang, Yuan-yuan, Fu, Yu-hua, Zhang, Hao, Li, He-xuan, Li, Quan-fu, Li, Hai-ling, Tan, Ren-ke, Jiang, Chen-xiao, Jiang, Wei, Li, Zeng-xia, Luo, Cheng, Lu, Bo-xun, and Dang, Yong-jun
Abstract: Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder caused by toxic aggregates of mutant huntingtin protein (mHTT) in the brain. Decreasing mHTT is a potential strategy for therapeutic purpose of HD. Valosin-containing protein (VCP/p97) is a crucial regulator of proteostasis, which regulates the degradation of damaged protein through proteasome and autophagy pathway. Since VCP has been implicated in pathogenesis of HD as well as other neurodegenerative diseases, small molecules that specifically regulate the activity of VCP may be of therapeutic benefits for HD patients. In this study we established a high-throughput screening biochemical assay for VCP ATPase activity measurement and identified gossypol, a clinical approved drug in China, as a novel modulator of VCP. Gossypol acetate dose-dependently inhibited the enzymatic activity of VCP in vitro with IC50of 6.53±0.6 μM. We further demonstrated that gossypol directly bound to the interface between the N and D1 domains of VCP. Gossypol acetate treatment not only lowered mHTT levels and rescued HD-relevant phenotypes in HD patient iPS-derived Q47 striatal neurons and HD knock-in mouse striatal cells, but also improved motor function deficits in both Drosophilaand mouse HD models. Taken together, gossypol acetate acted through a gain-of-function way to induce the formation of VCP-LC3-mHTT ternary complex, triggering autophagic degradation of mHTT. This study reveals a new strategy for treatment of HD and raises the possibility that an existing drug can be repurposed as a new treatment of neurodegenerative diseases.
Published: 2021
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36. Bulsufan decreases the incidence of mixed chimaerism in HLA-matched donor transplantation for severe aplastic anaemia

Author: Xu, Lan-Ping, Xu, Zheng-Li, Zhang, Yuan-Yuan, Cheng, Yi-Fei, Mo, Xiao-Dong, Han, Ting-Ting, Wang, Feng-Rong, Yan, Chen-Hua, Sun, Yu-Qian, Chen, Yu-Hong, Tang, Fei-Fei, Han, Wei, Wang, Yu, Zhang, Xiao-Hui, Liu, Kai-Yan, and Huang, Xiao-Jun
Published: 2022
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37. Atomically Dispersed Co to an End-Adsorbing Molecule for Excellent Biomimetically and Prime Sensitively Detecting O2•–Released from Living Cells

Author: Zou, Zhuo, Shi, Zhuan Zhuan, Wu, Jing Gao, Wu, Chao, Zeng, Qing Xin, Zhang, Yuan Yuan, Zhou, Guang Dong, Wu, Xiao Shuai, Li, Juan, Chen, Hong, Yang, Hong Bin, and Li, Chang Ming
Abstract: Single-atom catalysis efficiently exposes the catalytic sites to reactant molecules while rendering opportunity to investigate the catalysis mechanisms at atomic levels for scientific insights. Here, for the first time, atomically dispersed Co atoms are synthesized as biomimetic “enzymes” to monitor superoxide anions (O2•–), delivering ultraordinary high sensitivity (710.03 μA·μM–1·cm–2), low detection limit (1.5 nM), and rapid response time (1.2 s), ranking the best among all the reported either bioenzymatic or biomimetic O2•–biosensors. The sensor is further successfully employed to real-time monitor O2•–released from living cells. Moreover, theoretical calculation and analysis associated with experimental results discover that a mode of end adsorption of the negatively charged O2•–on the Co3+atom rather than a bridge or/and side adsorption of the two atoms of O2•–on two Co3+atoms, respectively, plays an important role in the single-atomic catalysis toward O2•–oxidation, which not only facilitates faster electron transfer but also offers better selectivity. This work holds great promise for an inexpensive and sensitive atomic biomimetic O2•–sensor for bioresearch and clinic diagnosis, while revealing that the adsorption mode plays a critical role in single-atom catalysis for a fundamental insight.
Published: 2021
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38. Fragmenlt Recombination Design, Synthesis, and Safener Activity of Novel Ester-Substituted Pyrazole Derivatives

Author: Jia, Ling, Gao, Shuang, Zhang, Yuan-Yuan, Zhao, Li-Xia, Fu, Ying, and Ye, Fei
Abstract: Fenoxaprop-p-ethyl (FE), a type of acetyl-CoA carboxylase (ACCase) inhibitor, has been extensively applied to a variety of crop plants. It can cause damage to wheat (Triticum aestivum) even resulting in the death of the crop. On the prerequisite of not reducing herbicidal efficiency on target weed species, herbicide safeners selectively protect crops from herbicide injury. Based on fragment splicing, a series of novel substituted pyrazole derivatives was designed to ultimately address the phytotoxicity to wheat caused by FE. The title compounds were synthesized in a one-pot way and characterized viainfrared spectroscopy, 1H nuclear magnetic resonance, 13C nuclear magnetic resonance, and high-resolution mass spectrometry. The bioactivity assay proved that the FE phytotoxicity to wheat could be reduced by most of the title compounds. The molecular docking model indicated that compound IV-21prevented fenoxaprop acid (FA) from reaching or acting with ACCase. The absorption, distribution, metabolism, excretion, and toxicity predictions demonstrated that compound IV-21exhibited superior pharmacokinetic properties to the commercialized safener mefenpyr-diethyl. The current work revealed that a series of newly substituted pyrazole derivatives presented strong herbicide safener activity in wheat. This may serve as a potential candidate structure to contribute to the further protection of wheat from herbicide injury.
Published: 2021
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39. PTPL1 suppresses lung cancer cell migration via inhibiting TGF-β1-induced activation of p38 MAPK and Smad 2/3 pathways and EMT

Author: Zhu, Ning, Zhang, Xiu-juan, Zou, Hai, Zhang, Yuan-yuan, Xia, Jing-wen, Zhang, Peng, Zhang, You-zhi, Li, Jing, Dong, Liang, Wumaier, Gulinuer, and Li, Sheng-qing
Abstract: Epithelial-mesenchymal transition (EMT) enables dissemination of neoplastic cells and onset of distal metastasis of primary tumors. However, the regulatory mechanisms of EMT by microenvironmental factors such as transforming growth factor-β (TGF-β) remain largely unresolved. Protein tyrosine phosphatase L1 (PTPL1) is a non-receptor protein tyrosine phosphatase that plays a suppressive role in tumorigenesis of diverse tissues. In this study we investigated the role of PTPL1/PTPN13 in metastasis of lung cancer and the signaling pathways regulated by PTPL1 in terms of EMT of non-small cell lung cancer (NSCLC) cells. We showed that the expression of PTPL1 was significantly downregulated in cancerous tissues of 23 patients with NSCLC compared with adjacent normal tissues. PTPL1 expression was positively correlated with overall survival of NSCLC patients. Then we treated A549 cells in vitro with TGF-β1 (10 ng/mL) and assessed EMT. We found that knockdown of PTPL1 enhanced the migration and invasion capabilities of A549 cells, through enhancing TGF-β1-induced EMT. In nude mice bearing A549 cell xenografts, knockdown of PTPL1 significantly promoted homing of cells and formation of tumor loci in the lungs. We further revealed that PTPL1 suppressed TGF-β-induced EMT by counteracting the activation of canonical Smad2/3 and non-canonical p38 MAPK signaling pathways. Using immunoprecipitation assay we demonstrated that PTPL1 could bind to p38 MAPK, suggesting that p38 MAPK might be a direct substrate of PTPL1. In conclusion, these results unravel novel mechanisms underlying the regulation of TGF-β signaling pathway, and have implications for prognostic assessment and targeted therapy of metastatic lung cancer.
Published: 2021
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40. Ruscogenin attenuates particulate matter-induced acute lung injury in mice via protecting pulmonary endothelial barrier and inhibiting TLR4 signaling pathway

Author: Wang, Yu-wei, Wu, Yun-hao, Zhang, Jia-zhi, Tang, Jia-hui, Fan, Rui-ping, Li, Fang, Yu, Bo-yang, Kou, Jun-ping, and Zhang, Yuan-yuan
Abstract: The inhalation of particulate matter (PM) is closely related to respiratory damage, including acute lung injury (ALI), characterized by inflammatory fluid edema and disturbed alveolar-capillary permeability. Ruscogenin (RUS), the main active ingredient in the traditional Chinese medicine Ophiopogonis japonicus, has been found to exhibit anti-inflammatory activity and rescue LPS-induced ALI. In this study, we investigated whether and how RUS exerted therapeutic effects on PM-induced ALI. RUS (0.1, 0.3, 1 mg·kg−1·d−1) was orally administered to mice prior to or after intratracheal instillation of PM suspension (50 mg/kg). We showed that RUS administration either prior to or after PM challenge significantly attenuated PM-induced pathological injury, lung edema, vascular leakage and VE-cadherin expression in lung tissue. RUS administration significantly decreased the levels of cytokines IL-6 and IL-1β, as well as the levels of NO and MPO in both bronchoalveolar lavage fluid (BALF) and serum. RUS administration dose-dependently suppressed the phosphorylation of NF-κB p65 and the expression of TLR4 and MyD88 in lung tissue. Furthermore, TLR4 knockout partly diminished PM-induced lung injury, and abolished the protective effects of RUS in PM-instilled mice. In conclusion, RUS effectively alleviates PM-induced ALI probably by inhibition of vascular leakage and TLR4/MyD88 signaling. TLR4 might be crucial for PM to initiate pulmonary lesion and for RUS to exert efficacy against PM-induced lung injury.
Published: 2021
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41. Screening of coexpression genes of immune cells in breast cancer tissues

Author: Zhang, Yuan-Yuan and Gan, Yi-Min
Abstract: This study aimed to investigate immune cell infiltration (ICI) in breast cancer tissues and its impact on the prognosis of patients. The whole transcriptome sequencing data sets of breast tissue (GSE126125, GSE190275 and GSE45498) were downloaded from Gene Expression Omnibus database. Data sets, including 281 breast cancer tissue samples and 59 normal breast tissue samples. In this study, the CIBERSORT algorithm was used to calculate the infiltration content of 22 immune cells subtypes in breast cancer tissues and normal breast tissues. The ICI between normal and breast cancer tissue samples was examined through the Rank-sum test. Furthermore, Kaplan–Meier and the log-rank test were used for survival analysis. Univariate and multivariate COX analysis was used to screen the prognostic risk factors of breast cancer based on ICI. The correlation between 22 kinds of immune cells was analyzed by the Pearson test. The results of univariate COX analysis indicated that resting dendritic cells, eosinophils, resting mast cells, monocytes, and memory CD4 T cells resting were protective factors for the prognosis of breast cancer patients (hazard ratio [HR] < 1, P< .05). The activation of macrophage M0 and mast cells were also prognostic risk factors for breast cancer patients (HR > 1, P< .05). Besides, multivariate COX analysis showed that resting mast cells were independent protective factors for the prognosis of breast cancer patients (HR < 1, P< .05). Macrophage M0 and mast cell activation were independent risk factors for the prognosis of breast cancer patients (HR > 1, P< .05). High infiltration of macrophage M0 and activated mast cells is associated with poor prognosis. Meanwhile, macrophage M0 and activated mast cells promote breast cancer progression. Low infiltration of resting mast cells is associated with poor prognosis, which inhibits breast cancer progression.
Published: 2024
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42. Limited Aggregation Behavior of β-Conglycinin and Its Terminating Effect on Glycinin Aggregation during Heating at pH 7.0

Author: Guo, Jian, Yang, Xiao-Quan, He, Xiu-Ting, Wu, Na-Na, Wang, Jin-Mei, Gu, Wei, and Zhang, Yuan-Yuan
Abstract: In this work, different thermal aggregation behaviors of soy β-conglycinin and glycinin at pH 7.0 were characterized with size exclusion chromatography and low-angle light scattering. Limited aggregation that grew via the consumption of “monomers” was detected in β-conglycinin, forming soluble aggregates. For glycinin, the association between the aggregates that led to the appearance of insoluble materials was observed. Heated with β-conglycinin, the assembly between the glycinin aggregates was terminated and its solubility was recovered. The structure of the soluble and insoluble aggregates was analyzed by small-angle X-ray scattering and dynamic light scattering. Unlike the β-conglycinin soluble aggregates that possessed limited size and less compact conformation, particles with a denser core and a less dense outer shell were found in the glycinin insoluble aggregates. Evidence is presented to reveal the transition between the soluble and insoluble aggregates and the role of β-conglycinin in the solubilization of the soy protein aggregates during heating.
Published: 2024
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43. Construction of C(sp2)–X (X = Br, Cl) Bonds through a Copper-Catalyzed Atom-Transfer Radical Process: Application for the 1,4-Difunctionalization of Isoquinolinium Salts

Author: Sun, Qiu, Zhang, Yuan-Yuan, Sun, Jing, Han, Ying, Jia, Xiaodong, and Yan, Chao-Guo
Abstract: A highly efficient Cu-catalyzed 1,4-difunctionalization of isoquinolinium salts was developed with ether and X–(X = Br, Cl) as the halogen source under mild conditions. This transformation involves the combination of oxidative coupling and copper-catalyzed halogen atom-transfer radical processes. This method not only provides an efficient way to prepare various substituted azaarenes but also achieves the selective construction of C(sp2)–X (X = Br, Cl) bonds from a halogen anion and nucleophilic carbon atom via a free-radical process.
Published: 2024
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44. Acute Cholecystitis Following Allogeneic Hematopoietic Stem Cell Transplantation: Clinical Features, Outcomes, Risk Factors, and Prediction Model

Author: Zhang, Zhuangyi, He, Yun, Zhu, Xiao-Lu, Liu, Xiao, Fu, Hai-Xia, Wang, Feng-Rong, Mo, Xiao-Dong, Wang, Yu, Zhang, Yuan-Yuan, Han, Wei, Chen, Yao, Yan, Chen-Hua, Wang, Jing-Zhi, Chen, Yu-Hong, Chang, Ying-Jun, Xu, Lan-Ping, Liu, Kai-Yan, Huang, Xiao-Jun, and Zhang, Xiao-Hui
Abstract: Acute cholecystitis (AC) is a potentially fatal complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT); however, only limited information is available on its clinical features, outcomes, and risk management strategies. This retrospective, nested, case–control study included 6701 patients undergoing allo-HSCT at our center from January 2004 to June 2019. In total, 72 patients (1.1%) were diagnosed with AC; among these, acute acalculous cholecystitis had a slightly higher prevalence (42 patients, 58.3%). Patients with moderate and severe AC exhibited remarkably worse overall survival (P = .001) and non-relapse mortality (P = .011) than others. Survival of haploidentical HSCT recipients with AC was comparable to that for patients with human leukocyte antigen (HLA)-identical donors. Age ≥ 18 years, antecedent stage II to IV acute graft-versus-host disease, and total parenteral nutrition were identified as potential risk factors for AC following allo-HSCT, while haploidentical transplantations were not more susceptible to AC than HLA-identical HSCT. Based on these criteria, a risk score model was developed and validated to estimate the probability of AC following allo-HSCT. The model separates all patients into low-, intermediate-, and high-risk groups and thereby provides a basis for early detection of this complication in the management of allo-HSCT.
Published: 2021
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45. The Antitumor Effects of Icaritin Against Breast Cancer is Related to Estrogen Receptors

Author: Tao, Cheng-Cheng, Wu, Yue, Gao, Xiang, Qiao, Ling, Yang, Ying, Li, Fang, Zou, Jie, Wang, Yu-Hao, Zhang, Shu-Yu, Li, Chang-Long, Zhang, Yuan-Yuan, and Sun, Xiao-Dong
Abstract: Objective: We aim to investigate the anticancer effects and mechanisms of icaritin against breast cancer. Materials and Methods: Both estrogen receptor (ER) positive breast cancer cells MCF- 7 and ER-negative MDA-MB-231 cells were employed. We examined the effects of icaritin on the proliferation and migration by wound healing assay and transwell assay. Cell apoptosis and cell cycle of MCF-7 and MDA-MB-231 cells were analyzed using Flow cytometry. Cell autophagy of MCF-7 and MDA-MB-231 cells was assessed by western blotting, acridine orange staining and confocal microscopy. We also detected the expression of apoptosis-related genes by western blotting. In addition, an autophagy inhibitor was used to investigate whether cytoprotective autophagy was induced. Meanwhile, an ER inhibitor was utilized to explore whether ER was involved in autophagy. Results: Icaritin inhibited the proliferation and migration, and induced cell cycle arrest of both MDA-MB-231 and MCF-7 cells. Icaritin significantly induced apoptosis of MDA-MB- 231 cells by activating caspase-3. And icaritin stimulated autophagy in MCF-7 cells, as evidenced by increased LC3II/LC3I, enhanced p62 degradation, the accumulation of endogenous LC3 puncta formation, and the increased autophagy flux. Icaritin induced autophagy through upregulating the phosphorylation of AMPK and ULK1. Chloroquine, an autophagy inhibitor, increased icaritin-induced apoptosis and proliferation inhibition of MCF-7 cells. Meanwhile, tamoxifen, an ER inhibitor, reversed icaritin-induced autophagy and proliferation inhibition of MCF-7 cells. Conclusion: Our study demonstrated that the antitumor effects of icaritin against breast cancer are related to ER, which suggested that the status of ER should be considered in the clinical application of icaritin.
Published: 2021
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46. Histone deacetylase inhibitor givinostat attenuates nonalcoholic steatohepatitis and liver fibrosis

Author: Huang, He-ming, Fan, Shi-jie, Zhou, Xiao-ru, Liu, Yan-jun, Li, Xiao, Liao, Li-ping, Huang, Jing, Shi, Cui-cui, Yu, Liang, Fu, Rong, Fan, Jian-gao, Zhang, Yuan-yuan, Luo, Cheng, and Li, Guang-ming
Abstract: Nonalcoholic steatohepatitis (NASH) is a common chronic liver disease that is increasingly prevalent worldwide. Liver inflammation is an important contributor to disease progression from nonalcoholic fatty liver (NAFL) to NASH, but there is a lack of efficient therapies. In the current study we evaluated the therapeutic potential of givinostat, a histone deacetylase (HDAC) inhibitor, in the treatment of NASH in vivo and in vitro. Liver inflammation was induced in mice by feeding a methionine- and choline-deficient diet (MCD) or a fructose, palmitate, cholesterol diet (FPC). The mice were treated with givoinostat (10 mg·kg−1·d−1, ip) for 8 or 10 weeks. At the end of the experiment, the livers were harvested for analysis. We showed that givoinostat administration significantly alleviated inflammation and attenuated hepatic fibrosis in MCD-induced NASH mice. RNA-seq analysis of liver tissues form MCD-fed mice revealed that givinostat potently blocked expression of inflammation-related genes and regulated a broad set of lipid metabolism-related genes. In human hepatocellular carcinoma cell line HepG2 and human derived fetal hepatocyte cell line L02, givinostat significantly decreased palmitic acid-induced intracellular lipid accumulation. The benefit of givinostat was further confirmed in FPC-induced NASH mice. Givinostat administration significantly attenuated hepatic steatosis, inflammation as well as liver injury in this mouse model. In conclusion, givinostat is efficacious in reversing diet-induced NASH, and may serve as a therapeutic agent for the treatment of human NASH.
Published: 2021
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47. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1

Author: Klionsky, Daniel J., Abdel-Aziz, Amal Kamal, Abdelfatah, Sara, Abdellatif, Mahmoud, Abdoli, Asghar, Abel, Steffen, Abeliovich, Hagai, Abildgaard, Marie H., Abudu, Yakubu Princely, Acevedo-Arozena, Abraham, Adamopoulos, Iannis E., Adeli, Khosrow, Adolph, Timon E., Adornetto, Annagrazia, Aflaki, Elma, Agam, Galila, Agarwal, Anupam, Aggarwal, Bharat B., Agnello, Maria, Agostinis, Patrizia, Agrewala, Javed N., Agrotis, Alexander, Aguilar, Patricia V., Ahmad, S. Tariq, Ahmed, Zubair M., Ahumada-Castro, Ulises, Aits, Sonja, Aizawa, Shu, Akkoc, Yunus, Akoumianaki, Tonia, Akpinar, Hafize Aysin, Al-Abd, Ahmed M., Al-Akra, Lina, Al-Gharaibeh, Abeer, Alaoui-Jamali, Moulay A., Alberti, Simon, Alcocer-Gómez, Elísabet, Alessandri, Cristiano, Ali, Muhammad, Alim Al-Bari, M. Abdul, Aliwaini, Saeb, Alizadeh, Javad, Almacellas, Eugènia, Almasan, Alexandru, Alonso, Alicia, Alonso, Guillermo D., Altan-Bonnet, Nihal, Altieri, Dario C., Álvarez, Élida M. C., Alves, Sara, Alves da Costa, Cristine, Alzaharna, Mazen M., Amadio, Marialaura, Amantini, Consuelo, Amaral, Cristina, Ambrosio, Susanna, Amer, Amal O., Ammanathan, Veena, An, Zhenyi, Andersen, Stig U., Andrabi, Shaida A., Andrade-Silva, Magaiver, Andres, Allen M., Angelini, Sabrina, Ann, David, Anozie, Uche C., Ansari, Mohammad Y., Antas, Pedro, Antebi, Adam, Antón, Zuriñe, Anwar, Tahira, Apetoh, Lionel, Apostolova, Nadezda, Araki, Toshiyuki, Araki, Yasuhiro, Arasaki, Kohei, Araújo, Wagner L., Araya, Jun, Arden, Catherine, Arévalo, Maria-Angeles, Arguelles, Sandro, Arias, Esperanza, Arikkath, Jyothi, Arimoto, Hirokazu, Ariosa, Aileen R., Armstrong-James, Darius, Arnauné-Pelloquin, Laetitia, Aroca, Angeles, Arroyo, Daniela S., Arsov, Ivica, Artero, Rubén, Asaro, Dalia Maria Lucia, Aschner, Michael, Ashrafizadeh, Milad, Ashur-Fabian, Osnat, Atanasov, Atanas G., Au, Alicia K., Auberger, Patrick, Auner, Holger W., Aurelian, Laure, Autelli, Riccardo, Avagliano, Laura, Ávalos, Yenniffer, Aveic, Sanja, Aveleira, Célia Alexandra, Avin-Wittenberg, Tamar, Aydin, Yucel, Ayton, Scott, Ayyadevara, Srinivas, Azzopardi, Maria, Baba, Misuzu, Backer, Jonathan M., Backues, Steven K., Bae, Dong-Hun, Bae, Ok-Nam, Bae, Soo Han, Baehrecke, Eric H., Baek, Ahruem, Baek, Seung-Hoon, Baek, Sung Hee, Bagetta, Giacinto, Bagniewska-Zadworna, Agnieszka, Bai, Hua, Bai, Jie, Bai, Xiyuan, Bai, Yidong, Bairagi, Nandadulal, Baksi, Shounak, Balbi, Teresa, Baldari, Cosima T., Balduini, Walter, Ballabio, Andrea, Ballester, Maria, Balazadeh, Salma, Balzan, Rena, Bandopadhyay, Rina, Banerjee, Sreeparna, Banerjee, Sulagna, Bánréti, Ágnes, Bao, Yan, Baptista, Mauricio S., Baracca, Alessandra, Barbati, Cristiana, Bargiela, Ariadna, Barilà, Daniela, Barlow, Peter G., Barmada, Sami J., Barreiro, Esther, Barreto, George E., Bartek, Jiri, Bartel, Bonnie, Bartolome, Alberto, Barve, Gaurav R., Basagoudanavar, Suresh H., Bassham, Diane C., Bast, Robert C., Basu, Alakananda, Batoko, Henri, Batten, Isabella, Baulieu, Etienne E., Baumgarner, Bradley L., Bayry, Jagadeesh, Beale, Rupert, Beau, Isabelle, Beaumatin, Florian, Bechara, Luiz R.G., Beck, George R., Beers, Michael F., Begun, Jakob, Behrends, Christian, Behrens, Georg M.N., Bei, Roberto, Bejarano, Eloy, Bel, Shai, Behl, Christian, Belaid, Amine, Belgareh-Touzé, Naïma, Bellarosa, Cristina, Belleudi, Francesca, Belló Pérez, Melissa, Bello-Morales, Raquel, Beltran, Jackeline Soares de Oliveira, Beltran, Sebastián, Benbrook, Doris Mangiaracina, Bendorius, Mykolas, Benitez, Bruno A., Benito-Cuesta, Irene, Bensalem, Julien, Berchtold, Martin W., Berezowska, Sabina, Bergamaschi, Daniele, Bergami, Matteo, Bergmann, Andreas, Berliocchi, Laura, Berlioz-Torrent, Clarisse, Bernard, Amélie, Berthoux, Lionel, Besirli, Cagri G., Besteiro, Sebastien, Betin, Virginie M., Beyaert, Rudi, Bezbradica, Jelena S., Bhaskar, Kiran, Bhatia-Kissova, Ingrid, Bhattacharya, Resham, Bhattacharya, Sujoy, Bhattacharyya, Shalmoli, Bhuiyan, Md. Shenuarin, Bhutia, Sujit Kumar, Bi, Lanrong, Bi, Xiaolin, Biden, Trevor J., Bijian, Krikor, Billes, Viktor A., Binart, Nadine, Bincoletto, Claudia, Birgisdottir, Asa B., Bjorkoy, Geir, Blanco, Gonzalo, Blas-Garcia, Ana, Blasiak, Janusz, Blomgran, Robert, Blomgren, Klas, Blum, Janice S., Boada-Romero, Emilio, Boban, Mirta, Boesze-Battaglia, Kathleen, Boeuf, Philippe, Boland, Barry, Bomont, Pascale, Bonaldo, Paolo, Bonam, Srinivasa Reddy, Bonfili, Laura, Bonifacino, Juan S., Boone, Brian A., Bootman, Martin D., Bordi, Matteo, Borner, Christoph, Bornhauser, Beat C., Borthakur, Gautam, Bosch, Jürgen, Bose, Santanu, Botana, Luis M., Botas, Juan, Boulanger, Chantal M., Boulton, Michael E., Bourdenx, Mathieu, Bourgeois, Benjamin, Bourke, Nollaig M., Bousquet, Guilhem, Boya, Patricia, Bozhkov, Peter V., Bozi, Luiz H. M., Bozkurt, Tolga O., Brackney, Doug E., Brandts, Christian H., Braun, Ralf J., Braus, Gerhard H., Bravo-Sagua, Roberto, Bravo-San Pedro, José M., Brest, Patrick, Bringer, Marie-Agnès, Briones-Herrera, Alfredo, Broaddus, V. Courtney, Brodersen, Peter, Brodsky, Jeffrey L., Brody, Steven L., Bronson, Paola G., Bronstein, Jeff M., Brown, Carolyn N., Brown, Rhoderick E., Brum, Patricia C., Brumell, John H., Brunetti-Pierri, Nicola, Bruno, Daniele, Bryson-Richardson, Robert J., Bucci, Cecilia, Buchrieser, Carmen, Bueno, Marta, Buitrago-Molina, Laura Elisa, Buraschi, Simone, Buch, Shilpa, Buchan, J. Ross, Buckingham, Erin M., Budak, Hikmet, Budini, Mauricio, Bultynck, Geert, Burada, Florin, Burgoyne, Joseph R., Burón, M. Isabel, Bustos, Victor, Büttner, Sabrina, Butturini, Elena, Byrd, Aaron, Cabas, Isabel, Cabrera-Benitez, Sandra, Cadwell, Ken, Cai, Jingjing, Cai, Lu, Cai, Qian, Cairó, Montserrat, Calbet, Jose A., Caldwell, Guy A., Caldwell, Kim A., Call, Jarrod A., Calvani, Riccardo, Calvo, Ana C., Calvo-Rubio Barrera, Miguel, Camara, Niels OS, Camonis, Jacques H., Camougrand, Nadine, Campanella, Michelangelo, Campbell, Edward M., Campbell-Valois, François-Xavier, Campello, Silvia, Campesi, Ilaria, Campos, Juliane C., Camuzard, Olivier, Cancino, Jorge, Candido de Almeida, Danilo, Canesi, Laura, Caniggia, Isabella, Canonico, Barbara, Cantí, Carles, Cao, Bin, Caraglia, Michele, Caramés, Beatriz, Carchman, Evie H., Cardenal-Muñoz, Elena, Cardenas, Cesar, Cardenas, Luis, Cardoso, Sandra M., Carew, Jennifer S., Carle, Georges F., Carleton, Gillian, Carloni, Silvia, Carmona-Gutierrez, Didac, Carneiro, Leticia A., Carnevali, Oliana, Carosi, Julian M., Carra, Serena, Carrier, Alice, Carrier, Lucie, Carroll, Bernadette, Carter, A. Brent, Carvalho, Andreia Neves, Casanova, Magali, Casas, Caty, Casas, Josefina, Cassioli, Chiara, Castillo, Eliseo F., Castillo, Karen, Castillo-Lluva, Sonia, Castoldi, Francesca, Castori, Marco, Castro, Ariel F., Castro-Caldas, Margarida, Castro-Hernandez, Javier, Castro-Obregon, Susana, Catz, Sergio D., Cavadas, Claudia, Cavaliere, Federica, Cavallini, Gabriella, Cavinato, Maria, Cayuela, Maria L., Cebollada Rica, Paula, Cecarini, Valentina, Cecconi, Francesco, Cechowska-Pasko, Marzanna, Cenci, Simone, Ceperuelo-Mallafré, Victòria, Cerqueira, João J., Cerutti, Janete M., Cervia, Davide, Cetintas, Vildan Bozok, Cetrullo, Silvia, Chae, Han-Jung, Chagin, Andrei S., Chai, Chee-Yin, Chakrabarti, Gopal, Chakrabarti, Oishee, Chakraborty, Tapas, Chakraborty, Trinad, Chami, Mounia, Chamilos, Georgios, Chan, David W., Chan, Edmond Y. W., Chan, Edward D., Chan, H.Y. Edwin, Chan, Helen H., Chan, Hung, Chan, Matthew T.V., Chan, Yau Sang, Chandra, Partha K., Chang, Chih-Peng, Chang, Chunmei, Chang, Hao-Chun, Chang, Kai, Chao, Jie, Chapman, Tracey, Charlet-Berguerand, Nicolas, Chatterjee, Samrat, Chaube, Shail K., Chaudhary, Anu, Chauhan, Santosh, Chaum, Edward, Checler, Frédéric, Cheetham, Michael E., Chen, Chang-Shi, Chen, Guang-Chao, Chen, Jian-Fu, Chen, Liam L., Chen, Leilei, Chen, Lin, Chen, Mingliang, Chen, Mu-Kuan, Chen, Ning, Chen, Quan, Chen, Ruey-Hwa, Chen, Shi, Chen, Wei, Chen, Weiqiang, Chen, Xin-Ming, Chen, Xiong-Wen, Chen, Xu, Chen, Yan, Chen, Ye-Guang, Chen, Yingyu, Chen, Yongqiang, Chen, Yu-Jen, Chen, Yue-Qin, Chen, Zhefan Stephen, Chen, Zhi, Chen, Zhi-Hua, Chen, Zhijian J., Chen, Zhixiang, Cheng, Hanhua, Cheng, Jun, Cheng, Shi-Yuan, Cheng, Wei, Cheng, Xiaodong, Cheng, Xiu-Tang, Cheng, Yiyun, Cheng, Zhiyong, Chen, Zhong, Cheong, Heesun, Cheong, Jit Kong, Chernyak, Boris V., Cherry, Sara, Cheung, Chi Fai Randy, Cheung, Chun Hei Antonio, Cheung, King-Ho, Chevet, Eric, Chi, Richard J., Chiang, Alan Kwok Shing, Chiaradonna, Ferdinando, Chiarelli, Roberto, Chiariello, Mario, Chica, Nathalia, Chiocca, Susanna, Chiong, Mario, Chiou, Shih-Hwa, Chiramel, Abhilash I., Chiurchiù, Valerio, Cho, Dong-Hyung, Choe, Seong-Kyu, Choi, Augustine M.K., Choi, Mary E., Choudhury, Kamalika Roy, Chow, Norman S., Chu, Charleen T., Chua, Jason P., Chua, John Jia En, Chung, Hyewon, Chung, Kin Pan, Chung, Seockhoon, Chung, So-Hyang, Chung, Yuen-Li, Cianfanelli, Valentina, Ciechomska, Iwona A., Cifuentes, Mariana, Cinque, Laura, Cirak, Sebahattin, Cirone, Mara, Clague, Michael J., Clarke, Robert, Clementi, Emilio, Coccia, Eliana M., Codogno, Patrice, Cohen, Ehud, Cohen, Mickael M., Colasanti, Tania, Colasuonno, Fiorella, Colbert, Robert A., Colell, Anna, Čolić, Miodrag, Coll, Nuria S., Collins, Mark O., Colombo, María I., Colón-Ramos, Daniel A., Combaret, Lydie, Comincini, Sergio, Cominetti, Márcia R., Consiglio, Antonella, Conte, Andrea, Conti, Fabrizio, Contu, Viorica Raluca, Cookson, Mark R., Coombs, Kevin M., Coppens, Isabelle, Corasaniti, Maria Tiziana, Corkery, Dale P., Cordes, Nils, Cortese, Katia, Costa, Maria do Carmo, Costantino, Sarah, Costelli, Paola, Coto-Montes, Ana, Crack, Peter J., Crespo, Jose L., Criollo, Alfredo, Crippa, Valeria, Cristofani, Riccardo, Csizmadia, Tamas, Cuadrado, Antonio, Cui, Bing, Cui, Jun, Cui, Yixian, Cui, Yong, Culetto, Emmanuel, Cumino, Andrea C., Cybulsky, Andrey V., Czaja, Mark J., Czuczwar, Stanislaw J., D’Adamo, Stefania, D’Amelio, Marcello, D’Arcangelo, Daniela, D’Lugos, Andrew C., D’Orazi, Gabriella, da Silva, James A., Dafsari, Hormos Salimi, Dagda, Ruben K., Dagdas, Yasin, Daglia, Maria, Dai, Xiaoxia, Dai, Yun, Dai, Yuyuan, Dal Col, Jessica, Dalhaimer, Paul, Dalla Valle, Luisa, Dallenga, Tobias, Dalmasso, Guillaume, Damme, Markus, Dando, Ilaria, Dantuma, Nico P., Darling, April L., Das, Hiranmoy, Dasarathy, Srinivasan, Dasari, Santosh K., Dash, Srikanta, Daumke, Oliver, Dauphinee, Adrian N., Davies, Jeffrey S., Dávila, Valeria A., Davis, Roger J., Davis, Tanja, Dayalan Naidu, Sharadha, De Amicis, Francesca, De Bosscher, Karolien, De Felice, Francesca, De Franceschi, Lucia, De Leonibus, Chiara, de Mattos Barbosa, Mayara G., De Meyer, Guido R.Y., De Milito, Angelo, De Nunzio, Cosimo, De Palma, Clara, De Santi, Mauro, De Virgilio, Claudio, De Zio, Daniela, Debnath, Jayanta, DeBosch, Brian J., Decuypere, Jean-Paul, Deehan, Mark A., Deflorian, Gianluca, DeGregori, James, Dehay, Benjamin, Del Rio, Gabriel, Delaney, Joe R., Delbridge, Lea M. D., Delorme-Axford, Elizabeth, Delpino, M. Victoria, Demarchi, Francesca, Dembitz, Vilma, Demers, Nicholas D., Deng, Hongbin, Deng, Zhiqiang, Dengjel, Joern, Dent, Paul, Denton, Donna, DePamphilis, Melvin L., Der, Channing J., Deretic, Vojo, Descoteaux, Albert, Devis, Laura, Devkota, Sushil, Devuyst, Olivier, Dewson, Grant, Dharmasivam, Mahendiran, Dhiman, Rohan, di Bernardo, Diego, Di Cristina, Manlio, Di Domenico, Fabio, Di Fazio, Pietro, Di Fonzo, Alessio, Di Guardo, Giovanni, Di Guglielmo, Gianni M., Di Leo, Luca, Di Malta, Chiara, Di Nardo, Alessia, Di Rienzo, Martina, Di Sano, Federica, Diallinas, George, Diao, Jiajie, Diaz-Araya, Guillermo, Díaz-Laviada, Inés, Dickinson, Jared M., Diederich, Marc, Dieudé, Mélanie, Dikic, Ivan, Ding, Shiping, Ding, Wen-Xing, Dini, Luciana, Dinić, Jelena, Dinic, Miroslav, Dinkova-Kostova, Albena T., Dionne, Marc S., Distler, Jörg H.W., Diwan, Abhinav, Dixon, Ian M.C., Djavaheri-Mergny, Mojgan, Dobrinski, Ina, Dobrovinskaya, Oxana, Dobrowolski, Radek, Dobson, Renwick C.J., Đokić, Jelena, Dokmeci Emre, Serap, Donadelli, Massimo, Dong, Bo, Dong, Xiaonan, Dong, Zhiwu, 2nd Dorn, Gerald W., Dotsch, Volker, Dou, Huan, Dou, Juan, Dowaidar, Moataz, Dridi, Sami, Drucker, Liat, Du, Ailian, Du, Caigan, Du, Guangwei, Du, Hai-Ning, Du, Li-Lin, du Toit, André, Duan, Shao-Bin, Duan, Xiaoqiong, Duarte, Sónia P., Dubrovska, Anna, Dunlop, Elaine A., Dupont, Nicolas, Durán, Raúl V., Dwarakanath, Bilikere S., Dyshlovoy, Sergey A., Ebrahimi-Fakhari, Darius, Eckhart, Leopold, Edelstein, Charles L., Efferth, Thomas, Eftekharpour, Eftekhar, Eichinger, Ludwig, Eid, Nabil, Eisenberg, Tobias, Eissa, N. Tony, Eissa, Sanaa, Ejarque, Miriam, El Andaloussi, Abdeljabar, El-Hage, Nazira, El-Naggar, Shahenda, Eleuteri, Anna Maria, El-Shafey, Eman S., Elgendy, Mohamed, Eliopoulos, Aristides G., Elizalde, María M., Elks, Philip M., Elsasser, Hans-Peter, Elsherbiny, Eslam S., Emerling, Brooke M., Emre, N. C. Tolga, Eng, Christina H., Engedal, Nikolai, Engelbrecht, Anna-Mart, Engelsen, Agnete S.T., Enserink, Jorrit M., Escalante, Ricardo, Esclatine, Audrey, Escobar-Henriques, Mafalda, Eskelinen, Eeva-Liisa, Espert, Lucile, Eusebio, Makandjou-Ola, Fabrias, Gemma, Fabrizi, Cinzia, Facchiano, Antonio, Facchiano, Francesco, Fadeel, Bengt, Fader, Claudio, Faesen, Alex C., Fairlie, W. 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Razaul, Karmakar, Parimal, Katare, Rajesh G., Kato, Masaru, Kaufmann, Stefan H.E., Kauppinen, Anu, Kaushal, Gur P., Kaushik, Susmita, Kawasaki, Kiyoshi, Kazan, Kemal, Ke, Po-Yuan, Keating, Damien J., Keber, Ursula, Kehrl, John H., Keller, Kate E., Keller, Christian W., Kemper, Jongsook Kim, Kenific, Candia M., Kepp, Oliver, Kermorgant, Stephanie, Kern, Andreas, Ketteler, Robin, Keulers, Tom G., Khalfin, Boris, Khalil, Hany, Khambu, Bilon, Khan, Shahid Y., Khandelwal, Vinoth Kumar Megraj, Khandia, Rekha, Kho, Widuri, Khobrekar, Noopur V., Khuansuwan, Sataree, Khundadze, Mukhran, Killackey, Samuel A., Kim, Dasol, Kim, Deok Ryong, Kim, Do-Hyung, Kim, Dong-Eun, Kim, Eun Young, Kim, Eun-Kyoung, Kim, Hak-Rim, Kim, Hee-Sik, Kim, Hyung-Ryong, Kim, Jeong Hun, Kim, Jin Kyung, Kim, Jin-Hoi, Kim, Joungmok, Kim, Ju Hwan, Kim, Keun Il, Kim, Peter K., Kim, Seong-Jun, Kimball, Scot R., Kimchi, Adi, Kimmelman, Alec C., Kimura, Tomonori, King, Matthew A., Kinghorn, Kerri J., Kinsey, Conan G., Kirkin, Vladimir, Kirshenbaum, Lorrie A., Kiselev, Sergey L., Kishi, Shuji, Kitamoto, Katsuhiko, Kitaoka, Yasushi, Kitazato, Kaio, Kitsis, Richard N., Kittler, Josef T., Kjaerulff, Ole, Klein, Peter S., Klopstock, Thomas, Klucken, Jochen, Knævelsrud, Helene, Knorr, Roland L., Ko, Ben C.B., Ko, Fred, Ko, Jiunn-Liang, Kobayashi, Hotaka, Kobayashi, Satoru, Koch, Ina, Koch, Jan C., Koenig, Ulrich, Kögel, Donat, Koh, Young Ho, Koike, Masato, Kohlwein, Sepp D., Kocaturk, Nur M., Komatsu, Masaaki, König, Jeannette, Kono, Toru, Kopp, Benjamin T., Korcsmaros, Tamas, Korkmaz, Gözde, Korolchuk, Viktor I., Korsnes, Mónica Suárez, Koskela, Ali, Kota, Janaiah, Kotake, Yaichiro, Kotler, Monica L., Kou, Yanjun, Koukourakis, Michael I., Koustas, Evangelos, Kovacs, Attila L., Kovács, Tibor, Koya, Daisuke, Kozako, Tomohiro, Kraft, Claudine, Krainc, Dimitri, Krämer, Helmut, Krasnodembskaya, Anna D., Kretz-Remy, Carole, Kroemer, Guido, Ktistakis, Nicholas T., Kuchitsu, Kazuyuki, Kuenen, Sabine, Kuerschner, Lars, Kukar, Thomas, Kumar, Ajay, Kumar, Ashok, Kumar, Deepak, Kumar, Dhiraj, Kumar, Sharad, Kume, Shinji, Kumsta, Caroline, Kundu, Chanakya N., Kundu, Mondira, Kunnumakkara, Ajaikumar B., Kurgan, Lukasz, Kutateladze, Tatiana G., Kutlu, Ozlem, Kwak, SeongAe, Kwon, Ho Jeong, Kwon, Taeg Kyu, Kwon, Yong Tae, Kyrmizi, Irene, La Spada, Albert, Labonté, Patrick, Ladoire, Sylvain, Laface, Ilaria, Lafont, Frank, Lagace, Diane C., Lahiri, Vikramjit, Lai, Zhibing, Laird, Angela S., Lakkaraju, Aparna, Lamark, Trond, Lan, Sheng-Hui, Landajuela, Ane, Lane, Darius J. R., Lane, Jon D., Lang, Charles H., Lange, Carsten, Langel, Ülo, Langer, Rupert, Lapaquette, Pierre, Laporte, Jocelyn, LaRusso, Nicholas F., Lastres-Becker, Isabel, Lau, Wilson Chun Yu, Laurie, Gordon W., Lavandero, Sergio, Law, Betty Yuen Kwan, Law, Helen Ka-wai, Layfield, Rob, Le, Weidong, Le Stunff, Herve, Leary, Alexandre Y., Lebrun, Jean-Jacques, Leck, Lionel Y.W., Leduc-Gaudet, Jean-Philippe, Lee, Changwook, Lee, Chung-Pei, Lee, Da-Hye, Lee, Edward B., Lee, Erinna F., Lee, Gyun Min, Lee, He-Jin, Lee, Heung Kyu, Lee, Jae Man, Lee, Jason S., Lee, Jin-A, Lee, Joo-Yong, Lee, Jun Hee, Lee, Michael, Lee, Min Goo, Lee, Min Jae, Lee, Myung-Shik, Lee, Sang Yoon, Lee, Seung-Jae, Lee, Stella Y., Lee, Sung Bae, Lee, Won Hee, Lee, Ying-Ray, Lee, Yong-ho, Lee, Youngil, Lefebvre, Christophe, Legouis, Renaud, Lei, Yu L., Lei, Yuchen, Leikin, Sergey, Leitinger, Gerd, Lemus, Leticia, Leng, Shuilong, Lenoir, Olivia, Lenz, Guido, Lenz, Heinz Josef, Lenzi, Paola, León, Yolanda, Leopoldino, Andréia M., Leschczyk, Christoph, Leskelä, Stina, Letellier, Elisabeth, Leung, Chi-Ting, Leung, Po Sing, Leventhal, Jeremy S., Levine, Beth, Lewis, Patrick A., Ley, Klaus, Li, Bin, Li, Da-Qiang, Li, Jianming, Li, Jing, Li, Jiong, Li, Ke, Li, Liwu, Li, Mei, Li, Min, Li, Min, Li, Ming, Li, Mingchuan, Li, Pin-Lan, Li, Ming-Qing, Li, Qing, Li, Sheng, Li, Tiangang, Li, Wei, Li, Wenming, Li, Xue, Li, Yi-Ping, Li, Yuan, Li, Zhiqiang, Li, Zhiyong, Li, Zhiyuan, Lian, Jiqin, Liang, Chengyu, Liang, Qiangrong, Liang, Weicheng, Liang, Yongheng, Liang, YongTian, Liao, Guanghong, Liao, Lujian, Liao, Mingzhi, Liao, Yung-Feng, Librizzi, Mariangela, Lie, Pearl P. Y., Lilly, Mary A., Lim, Hyunjung J., Lima, Thania R.R., Limana, Federica, Lin, Chao, Lin, Chih-Wen, Lin, Dar-Shong, Lin, Fu-Cheng, Lin, Jiandie D., Lin, Kurt M., Lin, Kwang-Huei, Lin, Liang-Tzung, Lin, Pei-Hui, Lin, Qiong, Lin, Shaofeng, Lin, Su-Ju, Lin, Wenyu, Lin, Xueying, Lin, Yao-Xin, Lin, Yee-Shin, Linden, Rafael, Lindner, Paula, Ling, Shuo-Chien, Lingor, Paul, Linnemann, Amelia K., Liou, Yih-Cherng, Lipinski, Marta M., Lipovšek, Saška, Lira, Vitor A., Lisiak, Natalia, Liton, Paloma B., Liu, Chao, Liu, Ching-Hsuan, Liu, Chun-Feng, Liu, Cui Hua, Liu, Fang, Liu, Hao, Liu, Hsiao-Sheng, Liu, Hua-feng, Liu, Huifang, Liu, Jia, Liu, Jing, Liu, Julia, Liu, Leyuan, Liu, Longhua, Liu, Meilian, Liu, Qin, Liu, Wei, Liu, Wende, Liu, Xiao-Hong, Liu, Xiaodong, Liu, Xingguo, Liu, Xu, Liu, Xuedong, Liu, Yanfen, Liu, Yang, Liu, Yang, Liu, Yueyang, Liu, Yule, Livingston, J. Andrew, Lizard, Gerard, Lizcano, Jose M., Ljubojevic-Holzer, Senka, LLeonart, Matilde E., Llobet-Navàs, David, Llorente, Alicia, Lo, Chih Hung, Lobato-Márquez, Damián, Long, Qi, Long, Yun Chau, Loos, Ben, Loos, Julia A., López, Manuela G., López-Doménech, Guillermo, López-Guerrero, José Antonio, López-Jiménez, Ana T., López-Pérez, Óscar, López-Valero, Israel, Lorenowicz, Magdalena J., Lorente, Mar, Lorincz, Peter, Lossi, Laura, Lotersztajn, Sophie, Lovat, Penny E., Lovell, Jonathan F., Lovy, Alenka, Lőw, Péter, Lu, Guang, Lu, Haocheng, Lu, Jia-Hong, Lu, Jin-Jian, Lu, Mengji, Lu, Shuyan, Luciani, Alessandro, Lucocq, John M., Ludovico, Paula, Luftig, Micah A., Luhr, Morten, Luis-Ravelo, Diego, Lum, Julian J., Luna-Dulcey, Liany, Lund, Anders H., Lund, Viktor K., Lünemann, Jan D., Lüningschrör, Patrick, Luo, Honglin, Luo, Rongcan, Luo, Shouqing, Luo, Zhi, Luparello, Claudio, Lüscher, Bernhard, Luu, Luan, Lyakhovich, Alex, Lyamzaev, Konstantin G., Lystad, Alf Håkon, Lytvynchuk, Lyubomyr, Ma, Alvin C., Ma, Changle, Ma, Mengxiao, Ma, Ning-Fang, Ma, Quan-Hong, Ma, Xinliang, Ma, Yueyun, Ma, Zhenyi, MacDougald, Ormond A., Macian, Fernando, MacIntosh, Gustavo C., MacKeigan, Jeffrey P., Macleod, Kay F., Maday, Sandra, Madeo, Frank, Madesh, Muniswamy, Madl, Tobias, Madrigal-Matute, Julio, Maeda, Akiko, Maejima, Yasuhiro, Magarinos, Marta, Mahavadi, Poornima, Maiani, Emiliano, Maiese, Kenneth, Maiti, Panchanan, Maiuri, Maria Chiara, Majello, Barbara, Major, Michael B., Makareeva, Elena, Malik, Fayaz, Mallilankaraman, Karthik, Malorni, Walter, Maloyan, Alina, Mammadova, Najiba, Man, Gene Chi Wai, Manai, Federico, Mancias, Joseph D., Mandelkow, Eva-Maria, Mandell, Michael A., Manfredi, Angelo A., Manjili, Masoud H., Manjithaya, Ravi, Manque, Patricio, Manshian, Bella B., Manzano, Raquel, Manzoni, Claudia, Mao, Kai, Marchese, Cinzia, Marchetti, Sandrine, Marconi, Anna Maria, Marcucci, Fabrizio, Mardente, Stefania, Mareninova, Olga A., Margeta, Marta, Mari, Muriel, Marinelli, Sara, Marinelli, Oliviero, Mariño, Guillermo, Mariotto, Sofia, Marshall, Richard S., Marten, Mark R., Martens, Sascha, Martin, Alexandre P.J., Martin, Katie R., Martin, Sara, Martin, Shaun, Martín-Segura, Adrián, Martín-Acebes, Miguel A., Martin-Burriel, Inmaculada, Martin-Rincon, Marcos, Martin-Sanz, Paloma, Martina, José A., Martinet, Wim, Martinez, Aitor, Martinez, Ana, Martinez, Jennifer, Martinez Velazquez, Moises, Martinez-Lopez, Nuria, Martinez-Vicente, Marta, Martins, Daniel O., Martins, Joilson O., Martins, Waleska K., Martins-Marques, Tania, Marzetti, Emanuele, Masaldan, Shashank, Masclaux-Daubresse, Celine, Mashek, Douglas G., Massa, Valentina, Massieu, Lourdes, Masson, Glenn R., Masuelli, Laura, Masyuk, Anatoliy I., Masyuk, Tetyana V., Matarrese, Paola, Matheu, Ander, Matoba, Satoaki, Matsuzaki, Sachiko, Mattar, Pamela, Matte, Alessandro, Mattoscio, Domenico, Mauriz, José L., Mauthe, Mario, Mauvezin, Caroline, Maverakis, Emanual, Maycotte, Paola, Mayer, Johanna, Mazzoccoli, Gianluigi, Mazzoni, Cristina, Mazzulli, Joseph R., McCarty, Nami, McDonald, Christine, McGill, Mitchell R., McKenna, Sharon L., McLaughlin, BethAnn, McLoughlin, Fionn, McNiven, Mark A., McWilliams, Thomas G., Mechta-Grigoriou, Fatima, Medeiros, Tania Catarina, Medina, Diego L., Megeney, Lynn A., Megyeri, Klara, Mehrpour, Maryam, Mehta, Jawahar L., Meijer, Alfred J., Meijer, Annemarie H., Mejlvang, Jakob, Meléndez, Alicia, Melk, Annette, Memisoglu, Gonen, Mendes, Alexandrina F., Meng, Delong, Meng, Fei, Meng, Tian, Menna-Barreto, Rubem, Menon, Manoj B., Mercer, Carol, Mercier, Anne E., Mergny, Jean-Louis, Merighi, Adalberto, Merkley, Seth D., Merla, Giuseppe, Meske, Volker, Mestre, Ana Cecilia, Metur, Shree Padma, Meyer, Christian, Meyer, Hemmo, Mi, Wenyi, Mialet-Perez, Jeanne, Miao, Junying, Micale, Lucia, Miki, Yasuo, Milan, Enrico, Milczarek, Małgorzata, Miller, Dana L., Miller, Samuel I., Miller, Silke, Millward, Steven W., Milosevic, Ira, Minina, Elena A., Mirzaei, Hamed, Mirzaei, Hamid Reza, Mirzaei, Mehdi, Mishra, Amit, Mishra, Nandita, Mishra, Paras Kumar, Misirkic Marjanovic, Maja, Misasi, Roberta, Misra, Amit, Misso, Gabriella, Mitchell, Claire, Mitou, Geraldine, Miura, Tetsuji, Miyamoto, Shigeki, Miyazaki, Makoto, Miyazaki, Mitsunori, Miyazaki, Taiga, Miyazawa, Keisuke, Mizushima, Noboru, Mogensen, Trine H., Mograbi, Baharia, Mohammadinejad, Reza, Mohamud, Yasir, Mohanty, Abhishek, Mohapatra, Sipra, Möhlmann, Torsten, Mohmmed, Asif, Moles, Anna, Moley, Kelle H., Molinari, Maurizio, Mollace, Vincenzo, Møller, Andreas Buch, Mollereau, Bertrand, Mollinedo, Faustino, Montagna, Costanza, Monteiro, Mervyn J., Montella, Andrea, Montes, L. Ruth, Montico, Barbara, Mony, Vinod K., Monzio Compagnoni, Giacomo, Moore, Michael N., Moosavi, Mohammad A., Mora, Ana L., Mora, Marina, Morales-Alamo, David, Moratalla, Rosario, Moreira, Paula I., Morelli, Elena, Moreno, Sandra, Moreno-Blas, Daniel, Moresi, Viviana, Morga, Benjamin, Morgan, Alwena H., Morin, Fabrice, Morishita, Hideaki, Moritz, Orson L., Moriyama, Mariko, Moriyasu, Yuji, Morleo, Manuela, Morselli, Eugenia, Moruno-Manchon, Jose F., Moscat, Jorge, Mostowy, Serge, Motori, Elisa, Moura, Andrea Felinto, Moustaid-Moussa, Naima, Mrakovcic, Maria, Muciño-Hernández, Gabriel, Mukherjee, Anupam, Mukhopadhyay, Subhadip, Mulcahy Levy, Jean M., Mulero, Victoriano, Muller, Sylviane, Münch, Christian, Munjal, Ashok, Munoz-Canoves, Pura, Muñoz-Galdeano, Teresa, Münz, Christian, Murakawa, Tomokazu, Muratori, Claudia, Murphy, Brona M., Murphy, J. Patrick, Murthy, Aditya, Myöhänen, Timo T., Mysorekar, Indira U., Mytych, Jennifer, Nabavi, Seyed Mohammad, Nabissi, Massimo, Nagy, Péter, Nah, Jihoon, Nahimana, Aimable, Nakagawa, Ichiro, Nakamura, Ken, Nakatogawa, Hitoshi, Nandi, Shyam S., Nanjundan, Meera, Nanni, Monica, Napolitano, Gennaro, Nardacci, Roberta, Narita, Masashi, Nassif, Melissa, Nathan, Ilana, Natsumeda, Manabu, Naude, Ryno J., Naumann, Christin, Naveiras, Olaia, Navid, Fatemeh, Nawrocki, Steffan T., Nazarko, Taras Y., Nazio, Francesca, Negoita, Florentina, Neill, Thomas, Neisch, Amanda L., Neri, Luca M., Netea, Mihai G., Neubert, Patrick, Neufeld, Thomas P., Neumann, Dietbert, Neutzner, Albert, Newton, Phillip T., Ney, Paul A., Nezis, Ioannis P., Ng, Charlene C.W., Ng, Tzi Bun, Nguyen, Hang T. T., Nguyen, Long T., Ni, Hong-Min, Ní Cheallaigh, Clíona, Ni, Zhenhong, Nicolao, M. Celeste, Nicoli, Francesco, Nieto-Diaz, Manuel, Nilsson, Per, Ning, Shunbin, Niranjan, Rituraj, Nishimune, Hiroshi, Niso-Santano, Mireia, Nixon, Ralph A., Nobili, Annalisa, Nobrega, Clevio, Noda, Takeshi, Nogueira-Recalde, Uxía, Nolan, Trevor M., Nombela, Ivan, Novak, Ivana, Novoa, Beatriz, Nozawa, Takashi, Nukina, Nobuyuki, Nussbaum-Krammer, Carmen, Nylandsted, Jesper, O’Donovan, Tracey R., O’Leary, Seónadh M., O’Rourke, Eyleen J., O’Sullivan, Mary P., O’Sullivan, Timothy E., Oddo, Salvatore, Oehme, Ina, Ogawa, Michinaga, Ogier-Denis, Eric, Ogmundsdottir, Margret H., Ogretmen, Besim, Oh, Goo Taeg, Oh, Seon-Hee, Oh, Young J., Ohama, Takashi, Ohashi, Yohei, Ohmuraya, Masaki, Oikonomou, Vasileios, Ojha, Rani, Okamoto, Koji, Okazawa, Hitoshi, Oku, Masahide, Oliván, Sara, Oliveira, Jorge M. A., Ollmann, Michael, Olzmann, James A., Omari, Shakib, Omary, M. Bishr, Önal, Gizem, Ondrej, Martin, Ong, Sang-Bing, Ong, Sang-Ging, Onnis, Anna, Orellana, Juan A., Orellana-Muñoz, Sara, Ortega-Villaizan, Maria Del Mar, Ortiz-Gonzalez, Xilma R., Ortona, Elena, Osiewacz, Heinz D., Osman, Abdel-Hamid K., Osta, Rosario, Otegui, Marisa S., Otsu, Kinya, Ott, Christiane, Ottobrini, Luisa, Ou, Jing-hsiung James, Outeiro, Tiago F., Oynebraten, Inger, Ozturk, Melek, Pagès, Gilles, Pahari, Susanta, Pajares, Marta, Pajvani, Utpal B., Pal, Rituraj, Paladino, Simona, Pallet, Nicolas, Palmieri, Michela, Palmisano, Giuseppe, Palumbo, Camilla, Pampaloni, Francesco, Pan, Lifeng, Pan, Qingjun, Pan, Wenliang, Pan, Xin, Panasyuk, Ganna, Pandey, Rahul, Pandey, Udai B., Pandya, Vrajesh, Paneni, Francesco, Pang, Shirley Y., Panzarini, Elisa, Papademetrio, Daniela L., Papaleo, Elena, Papinski, Daniel, Papp, Diana, Park, Eun Chan, Park, Hwan Tae, Park, Ji-Man, Park, Jong-In, Park, Joon Tae, Park, Junsoo, Park, Sang Chul, Park, Sang-Youel, Parola, Abraham H., Parys, Jan B., Pasquier, Adrien, Pasquier, Benoit, Passos, João F., Pastore, Nunzia, Patel, Hemal H., Patschan, Daniel, Pattingre, Sophie, Pedraza-Alva, Gustavo, Pedraza-Chaverri, Jose, Pedrozo, Zully, Pei, Gang, Pei, Jianming, Peled-Zehavi, Hadas, Pellegrini, Joaquín M., Pelletier, Joffrey, Peñalva, Miguel A., Peng, Di, Peng, Ying, Penna, Fabio, Pennuto, Maria, Pentimalli, Francesca, Pereira, Cláudia MF, Pereira, Gustavo J.S., Pereira, Lilian C., Pereira de Almeida, Luis, Perera, Nirma D., Pérez-Lara, Ángel, Perez-Oliva, Ana B., Pérez-Pérez, María Esther, Periyasamy, Palsamy, Perl, Andras, Perrotta, Cristiana, Perrotta, Ida, Pestell, Richard G., Petersen, Morten, Petrache, Irina, Petrovski, Goran, Pfirrmann, Thorsten, Pfister, Astrid S., Philips, Jennifer A., Pi, Huifeng, Picca, Anna, Pickrell, Alicia M., Picot, Sandy, Pierantoni, Giovanna M., Pierdominici, Marina, Pierre, Philippe, Pierrefite-Carle, Valérie, Pierzynowska, Karolina, Pietrocola, Federico, Pietruczuk, Miroslawa, Pignata, Claudio, Pimentel-Muiños, Felipe X., Pinar, Mario, Pinheiro, Roberta O., Pinkas-Kramarski, Ronit, Pinton, Paolo, Pircs, Karolina, Piya, Sujan, Pizzo, Paola, Plantinga, Theo S., Platta, Harald W., Plaza-Zabala, Ainhoa, Plomann, Markus, Plotnikov, Egor Y., Plun-Favreau, Helene, Pluta, Ryszard, Pocock, Roger, Pöggeler, Stefanie, Pohl, Christian, Poirot, Marc, Poletti, Angelo, Ponpuak, Marisa, Popelka, Hana, Popova, Blagovesta, Porta, Helena, Porte Alcon, Soledad, Portilla-Fernandez, Eliana, Post, Martin, Potts, Malia B., Poulton, Joanna, Powers, Ted, Prahlad, Veena, Prajsnar, Tomasz K., Praticò, Domenico, Prencipe, Rosaria, Priault, Muriel, Proikas-Cezanne, Tassula, Promponas, Vasilis J., Proud, Christopher G., Puertollano, Rosa, Puglielli, Luigi, Pulinilkunnil, Thomas, Puri, Deepika, Puri, Rajat, Puyal, Julien, Qi, Xiaopeng, Qi, Yongmei, Qian, Wenbin, Qiang, Lei, Qiu, Yu, Quadrilatero, Joe, Quarleri, Jorge, Raben, Nina, Rabinowich, Hannah, Ragona, Debora, Ragusa, Michael J., Rahimi, Nader, Rahmati, Marveh, Raia, Valeria, Raimundo, Nuno, Rajasekaran, Namakkal-Soorappan, Ramachandra Rao, Sriganesh, Rami, Abdelhaq, Ramírez-Pardo, Ignacio, Ramsden, David B., Randow, Felix, Rangarajan, Pundi N., Ranieri, Danilo, Rao, Hai, Rao, Lang, Rao, Rekha, Rathore, Sumit, Ratnayaka, J. Arjuna, Ratovitski, Edward A., Ravanan, Palaniyandi, Ravegnini, Gloria, Ray, Swapan K., Razani, Babak, Rebecca, Vito, Reggiori, Fulvio, Régnier-Vigouroux, Anne, Reichert, Andreas S., Reigada, David, Reiling, Jan H., Rein, Theo, Reipert, Siegfried, Rekha, Rokeya Sultana, Ren, Hongmei, Ren, Jun, Ren, Weichao, Renault, Tristan, Renga, Giorgia, Reue, Karen, Rewitz, Kim, Ribeiro de Andrade Ramos, Bruna, Riazuddin, S. Amer, Ribeiro-Rodrigues, Teresa M., Ricci, Jean-Ehrland, Ricci, Romeo, Riccio, Victoria, Richardson, Des R., Rikihisa, Yasuko, Risbud, Makarand V., Risueño, Ruth M., Ritis, Konstantinos, Rizza, Salvatore, Rizzuto, Rosario, Roberts, Helen C., Roberts, Luke D., Robinson, Katherine J., Roccheri, Maria Carmela, Rocchi, Stephane, Rodney, George G., Rodrigues, Tiago, Rodrigues Silva, Vagner Ramon, Rodriguez, Amaia, Rodriguez-Barrueco, Ruth, Rodriguez-Henche, Nieves, Rodriguez-Rocha, Humberto, Roelofs, Jeroen, Rogers, Robert S., Rogov, Vladimir V., Rojo, Ana I., Rolka, Krzysztof, Romanello, Vanina, Romani, Luigina, Romano, Alessandra, Romano, Patricia S., Romeo-Guitart, David, Romero, Luis C., Romero, Montserrat, Roney, Joseph C., Rongo, Christopher, Roperto, Sante, Rosenfeldt, Mathias T., Rosenstiel, Philip, Rosenwald, Anne G., Roth, Kevin A., Roth, Lynn, Roth, Steven, Rouschop, Kasper M.A., Roussel, Benoit D., Roux, Sophie, Rovere-Querini, Patrizia, Roy, Ajit, Rozieres, Aurore, Ruano, Diego, Rubinsztein, David C., Rubtsova, Maria P., Ruckdeschel, Klaus, Ruckenstuhl, Christoph, Rudolf, Emil, Rudolf, Rüdiger, Ruggieri, Alessandra, Ruparelia, Avnika Ashok, Rusmini, Paola, Russell, Ryan R., Russo, Gian Luigi, Russo, Maria, Russo, Rossella, Ryabaya, Oxana O., Ryan, Kevin M., Ryu, Kwon-Yul, Sabater-Arcis, Maria, Sachdev, Ulka, Sacher, Michael, Sachse, Carsten, Sadhu, Abhishek, Sadoshima, Junichi, Safren, Nathaniel, Saftig, Paul, Sagona, Antonia P., Sahay, Gaurav, Sahebkar, Amirhossein, Sahin, Mustafa, Sahin, Ozgur, Sahni, Sumit, Saito, Nayuta, Saito, Shigeru, Saito, Tsunenori, Sakai, Ryohei, Sakai, Yasuyoshi, Sakamaki, Jun-Ichi, Saksela, Kalle, Salazar, Gloria, Salazar-Degracia, Anna, Salekdeh, Ghasem H., Saluja, Ashok K., Sampaio-Marques, Belém, Sanchez, Maria Cecilia, Sanchez-Alcazar, Jose A., Sanchez-Vera, Victoria, Sancho-Shimizu, Vanessa, Sanderson, J. Thomas, Sandri, Marco, Santaguida, Stefano, Santambrogio, Laura, Santana, Magda M., Santoni, Giorgio, Sanz, Alberto, Sanz, Pascual, Saran, Shweta, Sardiello, Marco, Sargeant, Timothy J., Sarin, Apurva, Sarkar, Chinmoy, Sarkar, Sovan, Sarrias, Maria-Rosa, Sarkar, Surajit, Sarmah, Dipanka Tanu, Sarparanta, Jaakko, Sathyanarayan, Aishwarya, Sathyanarayanan, Ranganayaki, Scaglione, K. Matthew, Scatozza, Francesca, Schaefer, Liliana, Schafer, Zachary T., Schaible, Ulrich E., Schapira, Anthony H.V., Scharl, Michael, Schatzl, Hermann M., Schein, Catherine H., Scheper, Wiep, Scheuring, David, Schiaffino, Maria Vittoria, Schiappacassi, Monica, Schindl, Rainer, Schlattner, Uwe, Schmidt, Oliver, Schmitt, Roland, Schmidt, Stephen D., Schmitz, Ingo, Schmukler, Eran, Schneider, Anja, Schneider, Bianca E., Schober, Romana, Schoijet, Alejandra C., Schott, Micah B., Schramm, Michael, Schröder, Bernd, Schuh, Kai, Schüller, Christoph, Schulze, Ryan J., Schürmanns, Lea, Schwamborn, Jens C., Schwarten, Melanie, Scialo, Filippo, Sciarretta, Sebastiano, Scott, Melanie J., Scotto, Kathleen W., Scovassi, A. Ivana, Scrima, Andrea, Scrivo, Aurora, Sebastian, David, Sebti, Salwa, Sedej, Simon, Segatori, Laura, Segev, Nava, Seglen, Per O., Seiliez, Iban, Seki, Ekihiro, Selleck, Scott B., Sellke, Frank W., Selsby, Joshua T., Sendtner, Michael, Senturk, Serif, Seranova, Elena, Sergi, Consolato, Serra-Moreno, Ruth, Sesaki, Hiromi, Settembre, Carmine, Setty, Subba Rao Gangi, Sgarbi, Gianluca, Sha, Ou, Shacka, John J., Shah, Javeed A., Shang, Dantong, Shao, Changshun, Shao, Feng, Sharbati, Soroush, Sharkey, Lisa M., Sharma, Dipali, Sharma, Gaurav, Sharma, Kulbhushan, Sharma, Pawan, Sharma, Surendra, Shen, Han-Ming, Shen, Hongtao, Shen, Jiangang, Shen, Ming, Shen, Weili, Shen, Zheni, Sheng, Rui, Sheng, Zhi, Sheng, Zu-Hang, Shi, Jianjian, Shi, Xiaobing, Shi, Ying-Hong, Shiba-Fukushima, Kahori, Shieh, Jeng-Jer, Shimada, Yohta, Shimizu, Shigeomi, Shimozawa, Makoto, Shintani, Takahiro, Shoemaker, Christopher J., Shojaei, Shahla, Shoji, Ikuo, Shravage, Bhupendra V., Shridhar, Viji, Shu, Chih-Wen, Shu, Hong-Bing, Shui, Ke, Shukla, Arvind K., Shutt, Timothy E., Sica, Valentina, Siddiqui, Aleem, Sierra, Amanda, Sierra-Torre, Virginia, Signorelli, Santiago, Sil, Payel, Silva, Bruno J. de Andrade, Silva, Johnatas D., Silva-Pavez, Eduardo, Silvente-Poirot, Sandrine, Simmonds, Rachel E., Simon, Anna Katharina, Simon, Hans-Uwe, Simons, Matias, Singh, Anurag, Singh, Lalit P., Singh, Rajat, Singh, Shivendra V., Singh, Shrawan K., Singh, Sudha B., Singh, Sunaina, Singh, Surinder Pal, Sinha, Debasish, Sinha, Rohit Anthony, Sinha, Sangita, Sirko, Agnieszka, Sirohi, Kapil, Sivridis, Efthimios L., Skendros, Panagiotis, Skirycz, Aleksandra, Slaninová, Iva, Smaili, Soraya S., Smertenko, Andrei, Smith, Matthew D., Soenen, Stefaan J., Sohn, Eun Jung, Sok, Sophia P. M., Solaini, Giancarlo, Soldati, Thierry, Soleimanpour, Scott A., Soler, Rosa M., Solovchenko, Alexei, Somarelli, Jason A., Sonawane, Avinash, Song, Fuyong, Song, Hyun Kyu, Song, Ju-Xian, Song, Kunhua, Song, Zhiyin, Soria, Leandro R., Sorice, Maurizio, Soukas, Alexander A., Soukup, Sandra-Fausia, Sousa, Diana, Sousa, Nadia, Spagnuolo, Paul A., Spector, Stephen A., Srinivas Bharath, M. M., St. Clair, Daret, Stagni, Venturina, Staiano, Leopoldo, Stalnecker, Clint A., Stankov, Metodi V., Stathopulos, Peter B., Stefan, Katja, Stefan, Sven Marcel, Stefanis, Leonidas, Steffan, Joan S., Steinkasserer, Alexander, Stenmark, Harald, Sterneckert, Jared, Stevens, Craig, Stoka, Veronika, Storch, Stephan, Stork, Björn, Strappazzon, Flavie, Strohecker, Anne Marie, Stupack, Dwayne G., Su, Huanxing, Su, Ling-Yan, Su, Longxiang, Suarez-Fontes, Ana M., Subauste, Carlos S., Subbian, Selvakumar, Subirada, Paula V., Sudhandiran, Ganapasam, Sue, Carolyn M., Sui, Xinbing, Summers, Corey, Sun, Guangchao, Sun, Jun, Sun, Kang, Sun, Meng-xiang, Sun, Qiming, Sun, Yi, Sun, Zhongjie, Sunahara, Karen K.S., Sundberg, Eva, Susztak, Katalin, Sutovsky, Peter, Suzuki, Hidekazu, Sweeney, Gary, Symons, J. David, Sze, Stephen Cho Wing, Szewczyk, Nathaniel J., Tabęcka-Łonczynska, Anna, Tabolacci, Claudio, Tacke, Frank, Taegtmeyer, Heinrich, Tafani, Marco, Tagaya, Mitsuo, Tai, Haoran, Tait, Stephen W. G., Takahashi, Yoshinori, Takats, Szabolcs, Talwar, Priti, Tam, Chit, Tam, Shing Yau, Tampellini, Davide, Tamura, Atsushi, Tan, Chong Teik, Tan, Eng-King, Tan, Ya-Qin, Tanaka, Masaki, Tanaka, Motomasa, Tang, Daolin, Tang, Jingfeng, Tang, Tie-Shan, Tanida, Isei, Tao, Zhipeng, Taouis, Mohammed, Tatenhorst, Lars, Tavernarakis, Nektarios, Taylor, Allen, Taylor, Gregory A., Taylor, Joan M., Tchetina, Elena, Tee, Andrew R., Tegeder, Irmgard, Teis, David, Teixeira, Natercia, Teixeira-Clerc, Fatima, Tekirdag, Kumsal A., Tencomnao, Tewin, Tenreiro, Sandra, Tepikin, Alexei V., Testillano, Pilar S., Tettamanti, Gianluca, Tharaux, Pierre-Louis, Thedieck, Kathrin, Thekkinghat, Arvind A., Thellung, Stefano, Thinwa, Josephine W., Thirumalaikumar, V.P., Thomas, Sufi Mary, Thomes, Paul G., Thorburn, Andrew, Thukral, Lipi, Thum, Thomas, Thumm, Michael, Tian, Ling, Tichy, Ales, Till, Andreas, Timmerman, Vincent, Titorenko, Vladimir I., Todi, Sokol V., Todorova, Krassimira, Toivonen, Janne M., Tomaipitinca, Luana, Tomar, Dhanendra, Tomas-Zapico, Cristina, Tomić, Sergej, Tong, Benjamin Chun-Kit, Tong, Chao, Tong, Xin, Tooze, Sharon A., Torgersen, Maria L., Torii, Satoru, Torres-López, Liliana, Torriglia, Alicia, Towers, Christina G., Towns, Roberto, Toyokuni, Shinya, Trajkovic, Vladimir, Tramontano, Donatella, Tran, Quynh-Giao, Travassos, Leonardo H., Trelford, Charles B., Tremel, Shirley, Trougakos, Ioannis P., Tsao, Betty P., Tschan, Mario P., Tse, Hung-Fat, Tse, Tak Fu, Tsugawa, Hitoshi, Tsvetkov, Andrey S., Tumbarello, David A., Tumtas, Yasin, Tuñón, María J., Turcotte, Sandra, Turk, Boris, Turk, Vito, Turner, Bradley J., Tuxworth, Richard I., Tyler, Jessica K., Tyutereva, Elena V., Uchiyama, Yasuo, Ugun-Klusek, Aslihan, Uhlig, Holm H., Ułamek-Kozioł, Marzena, Ulasov, Ilya V., Umekawa, Midori, Ungermann, Christian, Unno, Rei, Urbe, Sylvie, Uribe-Carretero, Elisabet, Üstün, Suayib, Uversky, Vladimir N, Vaccari, Thomas, Vaccaro, Maria I., Vahsen, Björn F., Vakifahmetoglu-Norberg, Helin, Valdor, Rut, Valente, Maria J., Valko, Ayelén, Vallee, Richard B., Valverde, Angela M., Van den Berghe, Greet, van der Veen, Stijn, Van Kaer, Luc, van Loosdregt, Jorg, van Wijk, Sjoerd J.L., Vandenberghe, Wim, Vanhorebeek, Ilse, Vannier-Santos, Marcos A., Vannini, Nicola, Vanrell, M. Cristina, Vantaggiato, Chiara, Varano, Gabriele, Varela-Nieto, Isabel, Varga, Máté, Vasconcelos, M. Helena, Vats, Somya, Vavvas, Demetrios G., Vega-Naredo, Ignacio, Vega-Rubin-de-Celis, Silvia, Velasco, Guillermo, Velázquez, Ariadna P., Vellai, Tibor, Vellenga, Edo, Velotti, Francesca, Verdier, Mireille, Verginis, Panayotis, Vergne, Isabelle, Verkade, Paul, Verma, Manish, Verstreken, Patrik, Vervliet, Tim, Vervoorts, Jörg, Vessoni, Alexandre T., Victor, Victor M., Vidal, Michel, Vidoni, Chiara, Vieira, Otilia V., Vierstra, Richard D., Viganó, Sonia, Vihinen, Helena, Vijayan, Vinoy, Vila, Miquel, Vilar, Marçal, Villalba, José M., Villalobo, Antonio, Villarejo-Zori, Beatriz, Villarroya, Francesc, Villarroya, Joan, Vincent, Olivier, Vindis, Cecile, Viret, Christophe, Viscomi, Maria Teresa, Visnjic, Dora, Vitale, Ilio, Vocadlo, David J., Voitsekhovskaja, Olga V., Volonté, Cinzia, Volta, Mattia, Vomero, Marta, Von Haefen, Clarissa, Vooijs, Marc A., Voos, Wolfgang, Vucicevic, Ljubica, Wade-Martins, Richard, Waguri, Satoshi, Waite, Kenrick A., Wakatsuki, Shuji, Walker, David W., Walker, Mark J., Walker, Simon A., Walter, Jochen, Wandosell, Francisco G., Wang, Bo, Wang, Chao-Yung, Wang, Chen, Wang, Chenran, Wang, Chenwei, Wang, Cun-Yu, Wang, Dong, Wang, Fangyang, Wang, Feng, Wang, Fengming, Wang, Guansong, Wang, Han, Wang, Hao, Wang, Hexiang, Wang, Hong-Gang, Wang, Jianrong, Wang, Jigang, Wang, Jiou, Wang, Jundong, Wang, Kui, Wang, Lianrong, Wang, Liming, Wang, Maggie Haitian, Wang, Meiqing, Wang, Nanbu, Wang, Pengwei, Wang, Peipei, Wang, Ping, Wang, Ping, Wang, Qing Jun, Wang, Qing, Wang, Qing Kenneth, Wang, Qiong A., Wang, Wen-Tao, Wang, Wuyang, Wang, Xinnan, Wang, Xuejun, Wang, Yan, Wang, Yanchang, Wang, Yanzhuang, Wang, Yen-Yun, Wang, Yihua, Wang, Yipeng, Wang, Yu, Wang, Yuqi, Wang, Zhe, Wang, Zhenyu, Wang, Zhouguang, Warnes, Gary, Warnsmann, Verena, Watada, Hirotaka, Watanabe, Eizo, Watchon, Maxinne, Wawrzyńska, Anna, Weaver, Timothy E., Wegrzyn, Grzegorz, Wehman, Ann M., Wei, Huafeng, Wei, Lei, Wei, Taotao, Wei, Yongjie, Weiergräber, Oliver H., Weihl, Conrad C., Weindl, Günther, Weiskirchen, Ralf, Wells, Alan, Wen, Runxia H., Wen, Xin, Werner, Antonia, Weykopf, Beatrice, Wheatley, Sally P., Whitton, J. 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Wei-Lynn, Wu, An-Guo, Wu, Chengbiao, Wu, Jian, Wu, Junfang, Wu, Kenneth K., Wu, Min, Wu, Shan-Ying, Wu, Shengzhou, Wu, Shu-Yan, Wu, Shufang, Wu, William K.K., Wu, Xiaohong, Wu, Xiaoqing, Wu, Yao-Wen, Wu, Yihua, Xavier, Ramnik J., Xia, Hongguang, Xia, Lixin, Xia, Zhengyuan, Xiang, Ge, Xiang, Jin, Xiang, Mingliang, Xiang, Wei, Xiao, Bin, Xiao, Guozhi, Xiao, Hengyi, Xiao, Hong-tao, Xiao, Jian, Xiao, Lan, Xiao, Shi, Xiao, Yin, Xie, Baoming, Xie, Chuan-Ming, Xie, Min, Xie, Yuxiang, Xie, Zhiping, Xie, Zhonglin, Xilouri, Maria, Xu, Congfeng, Xu, En, Xu, Haoxing, Xu, Jing, Xu, JinRong, Xu, Liang, Xu, Wen Wen, Xu, Xiulong, Xue, Yu, Yakhine-Diop, Sokhna M.S., Yamaguchi, Masamitsu, Yamaguchi, Osamu, Yamamoto, Ai, Yamashina, Shunhei, Yan, Shengmin, Yan, Shian-Jang, Yan, Zhen, Yanagi, Yasuo, Yang, Chuanbin, Yang, Dun-Sheng, Yang, Huan, Yang, Huang-Tian, Yang, Hui, Yang, Jin-Ming, Yang, Jing, Yang, Jingyu, Yang, Ling, Yang, Liu, Yang, Ming, Yang, Pei-Ming, Yang, Qian, Yang, Seungwon, Yang, Shu, Yang, Shun-Fa, Yang, Wannian, Yang, Wei Yuan, Yang, Xiaoyong, Yang, Xuesong, Yang, Yi, Yang, Ying, Yao, Honghong, Yao, Shenggen, Yao, Xiaoqiang, Yao, Yong-Gang, Yao, Yong-Ming, Yasui, Takahiro, Yazdankhah, Meysam, Yen, Paul M., Yi, Cong, Yin, Xiao-Ming, Yin, Yanhai, Yin, Zhangyuan, Yin, Ziyi, Ying, Meidan, Ying, Zheng, Yip, Calvin K., Yiu, Stephanie Pei Tung, Yoo, Young H., Yoshida, Kiyotsugu, Yoshii, Saori R., Yoshimori, Tamotsu, Yousefi, Bahman, Yu, Boxuan, Yu, Haiyang, Yu, Jun, Yu, Jun, Yu, Li, Yu, Ming-Lung, Yu, Seong-Woon, Yu, Victor C., Yu, W. Haung, Yu, Zhengping, Yu, Zhou, Yuan, Junying, Yuan, Ling-Qing, Yuan, Shilin, Yuan, Shyng-Shiou F., Yuan, Yanggang, Yuan, Zengqiang, Yue, Jianbo, Yue, Zhenyu, Yun, Jeanho, Yung, Raymond L., Zacks, David N., Zaffagnini, Gabriele, Zambelli, Vanessa O., Zanella, Isabella, Zang, Qun S., Zanivan, Sara, Zappavigna, Silvia, Zaragoza, Pilar, Zarbalis, Konstantinos S., Zarebkohan, Amir, Zarrouk, Amira, Zeitlin, Scott O., Zeng, Jialiu, Zeng, Ju-deng, Žerovnik, Eva, Zhan, Lixuan, Zhang, Bin, Zhang, Donna D., Zhang, Hanlin, Zhang, Hong, Zhang, Hong, Zhang, Honghe, Zhang, Huafeng, Zhang, Huaye, Zhang, Hui, Zhang, Hui-Ling, Zhang, Jianbin, Zhang, Jianhua, Zhang, Jing-Pu, Zhang, Kalin Y.B., Zhang, Leshuai W., Zhang, Lin, Zhang, Lisheng, Zhang, Lu, Zhang, Luoying, Zhang, Menghuan, Zhang, Peng, Zhang, Sheng, Zhang, Wei, Zhang, Xiangnan, Zhang, Xiao-Wei, Zhang, Xiaolei, Zhang, Xiaoyan, Zhang, Xin, Zhang, Xinxin, Zhang, Xu Dong, Zhang, Yang, Zhang, Yanjin, Zhang, Yi, Zhang, Ying-Dong, Zhang, Yingmei, Zhang, Yuan-Yuan, Zhang, Yuchen, Zhang, Zhe, Zhang, Zhengguang, Zhang, Zhibing, Zhang, Zhihai, Zhang, Zhiyong, Zhang, Zili, Zhao, Haobin, Zhao, Lei, Zhao, Shuang, Zhao, Tongbiao, Zhao, Xiao-Fan, Zhao, Ying, Zhao, Yongchao, Zhao, Yongliang, Zhao, Yuting, Zheng, Guoping, Zheng, Kai, Zheng, Ling, Zheng, Shizhong, Zheng, Xi-Long, Zheng, Yi, Zheng, Zu-Guo, Zhivotovsky, Boris, Zhong, Qing, Zhou, Ao, Zhou, Ben, Zhou, Cefan, Zhou, Gang, Zhou, Hao, Zhou, Hong, Zhou, Hongbo, Zhou, Jie, Zhou, Jing, Zhou, Jing, Zhou, Jiyong, Zhou, Kailiang, Zhou, Rongjia, Zhou, Xu-Jie, Zhou, Yanshuang, Zhou, Yinghong, Zhou, Yubin, Zhou, Zheng-Yu, Zhou, Zhou, Zhu, Binglin, Zhu, Changlian, Zhu, Guo-Qing, Zhu, Haining, Zhu, Hongxin, Zhu, Hua, Zhu, Wei-Guo, Zhu, Yanping, Zhu, Yushan, Zhuang, Haixia, Zhuang, Xiaohong, Zientara-Rytter, Katarzyna, Zimmermann, Christine M., Ziviani, Elena, Zoladek, Teresa, Zong, Wei-Xing, Zorov, Dmitry B., Zorzano, Antonio, Zou, Weiping, Zou, Zhen, Zou, Zhengzhi, Zuryn, Steven, Zwerschke, Werner, Brand-Saberi, Beate, Dong, X. Charlie, Kenchappa, Chandra Shekar, Li, Zuguo, Lin, Yong, Oshima, Shigeru, Rong, Yueguang, Sluimer, Judith C., Stallings, Christina L., and Tong, Chun-Kit
Abstract: ABSTRACTIn 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fideautophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021
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48. Comparison of hemorrhagic and ischemic stroke after allogeneic hematopoietic stem cell transplantation

Author: Cai, Xuan, Fu, Hai-Xia, Mo, Xiao-Dong, Wang, Yu, Zhang, Yuan-Yuan, Wu, Jin, Han, Wei, Tang, Fei-Fei, Gui, Ruo-Yun, Chen, Huan, Chen, Yao, Zhao, Peng, Yan, Chen-Hua, Wang, Jing-Zhi, Chen, Yu-Hong, Chang, Ying-Jun, Xu, Lan-Ping, Liu, Kai-Yan, Huang, Xiao-Jun, and Zhang, Xiao-Hui
Abstract: Stroke is an important complication following allogeneic hematopoietic stem cell transplantation (allo-HSCT). Nevertheless, few studies have been published to analyzed the occurrence and prognosis of stroke after allo-HSCT. From January 2007 to December 2018 in Peking University People’s Hospital, 6449 patients received HSCT and there were 2.3% of patients diagnosed with stroke after allo-HSCT (hemorrhagic: 1.0%, ischemic: 1.3%). The median time to hemorrhagic and ischemic stroke after HSCT was 161 days and 137 days, respectively. In total, 8.4% of patients experienced neurological sequelae. The outcome was much worse in patients with stroke than in control subjects. The comparison of prognosis showed no statistical differences between patients with hemorrhagic stroke and those with ischemic stroke. Significant risk factors for hemorrhagic stroke were pretransplant central nervous system leukemia (CNSL), and delayed platelet engraftment. Risk factors associated with the occurrence of ischemic stroke included high-risk disease, prior venous thromboembolism (VTE), grade III–IV acute graft-versus-host disease (aGVHD), and thrombotic microangiopathy (TMA). Haplo-identical transplantation was not a risk factor for stroke and had no impact on the prognosis compared with HLA-matched HSCT. Altogether, these results show that stroke is a severe complication after allo-HSCT. The prognosis of posttransplant stroke did not differ between hemorrhagic and ischemic stroke.
Published: 2020
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49. Posterior reversible encephalopathy syndrome (PRES) after haploidentical haematopoietic stem cell transplantation: incidence, risk factors and outcomes

Author: Chen, Qi, Zhao, Xin, Fu, Hai-Xia, Chen, Yu-Hong, Zhang, Yuan-Yuan, Wang, Jing-Zhi, Wang, Yu, Wang, Feng-Rong, Mo, Xiao-Dong, Han, Wei, Chen, Huan, Chang, Ying-Jun, Xu, Lan-Ping, Liu, Kai-Yan, Huang, Xiao-Jun, and Zhang, Xiao-Hui
Abstract: Posterior reversible encephalopathy syndrome (PRES) is a gradually recognised neurological complication of allogenic haematopoietic stem cell transplantation (allo-HSCT). However, there is a paucity of information on PRES after haploidentical HSCT (haplo-HSCT). We performed a retrospective nested case-control study in patients following haplo-HSCT for malignant and nonmalignant haematologic diseases between January 2009 and December 2018 in our centre. A total of 45 patients were diagnosed with PRES after transplant, accounting for an incidence of 1.17%. Grades II to IV acute graft-versus-host disease (aGVHD) (HR 2.370, 95% CI 1.277–4.397, p= 0.006) and hypertension (HR 14.466, 95% CI 7.107–29.443, p< 0.001) were identified as risk factors for developing PRES after haplo-HSCT. There was no difference in overall survival (OS), disease-free survival (DFS), the cumulative incidence of relapse or nonrelapse mortality (NRM) between patients with PRES and controls without PRES following haplo-HSCT in either adults or children. All but one patient with PRES showed nearly complete clinical and neurologic recovery. In conclusion, PRES is a rare condition with benign outcomes following haplo-HSCT. Further multicentre prospective studies are needed to confirm the results and help to establish the standard therapy for posttransplant PRES.
Published: 2020
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50. Successful hematopoietic stem cell transplantation with haploidentical donors and non-irradiation conditioning in patients with Fanconi anemia

Author: Wang, Jing-Zhi, Huang, Xiao-Jun, Zhang, Yuan-Yuan, Tang, Fei-Fei, Han, Ting-Ting, Mo, Xiao-Dong, Sun, Yu-Qian, Chen, Yu-Hong, Wang, Yu, Zhang, Xiao-Hui, Xu, Lan-Ping, and Lyu, Peng
Published: 2021
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