Yu Hu

University of Chinese Academy of Sciences

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Chunyan Sun

Union Hospital

Wei Lü

Ningbo Institute of Industrial Technology

Ya-Dan Wang

Chinese Academy of Sciences

Jun Qin

Hubei University of Medicine

Lu Zhang

Southern Medical University

Zhang‐Bo Chu

Union Hospital

Yicong Deng

Anhui Polytechnic University

Xuelei Wang

Shanghai East Hospital

Yi Zang

University of Chinese Academy of Sciences

Yan Zhang

Shanghai Jiao Tong University

Cooperative Institutions

Chinese Academy of Sciences

Huazhong University of Science and Technology

University of Chinese Academy of Sciences

Union Hospital

Shanghai Jiao Tong University

Chinese Academy of Medical Sciences & Peking Union Medical College

Xi'an Jiaotong University

Tongji Hospital

Shanghai Institute of Nutrition and Health

Research Center for Eco-Environmental Sciences

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Hepatitis B virus reactivation in a chronic myeloid leukemia patient treated with imatinib mesylate.

PubMed (2012)

Ya-Dan Wang Guohui Cui Mian Li Bhuveshwarnath Gowrea Jia Xia

Imatinib mesylate is a molecular targeted agent for treating chronic myeloid leukemia (CML) and gastrointestinal stromal tumor. Although imatinib mesylate is not regarded as an immunosuppressive agent, few studies have also shown that it may impair immune response. In this report, we present a case of transient hepatitis B virus (HBV) reactivation during imatinib mesylate treatment for CML.

Imatinib Mesylate

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Citations (23)

[Study of brain-derived neurotrophic factor activating TrkB signaling cascades in the pathogenesis of multiple myeloma].

PubMed (2008)

Chunyan Sun Yu Hu Tao Guo Jing Huang Lu Zhang

To explore the significance of abnormal expression of brain-derived neurotrophic factor (BDNF)/TrkB in the development and evolution of multiple myeloma (MM) and the involved signaling pathways.The effect of BDNF on the cell viability of human myeloma cell line (HMCL) (RPMI8226, U266, KM3) was determined by trypan blue dye-exclusion. MTT assay was used to evaluate the cytotoxicity of tested chemotherapeutic agents. The effect of BDNF on the phosphorylation of TrkB was determined by Western blot. A human myeloma xenograft animal model was used to evaluate the effects of BDNF on tumor growth and survival time.BDNF at 50 microg/L triggered significant increase in cell viability of HMCL. BDNF protected KM3 cells from melphalan and vincristine. The viability of KM3 cells exposed to varying concentrations of melphalan with and without 50 microg/L BDNF showed that BDNF induced almost a 2-fold and a 3-fold increase in melphalan and vincristine toxicity respectively. BDNF treatment increased MM cell growth in xenografted MM model (3240.9 mm3 vs 1032.7 mm3 ) (P <0.05). Intratumoral injection of BDNF also significantly reduced survival time (13 d vs 21 d) (P <0.05). The phosphorylated TrkB level was increased significantly after treated by exogenous BDNF. BDNF-triggered migration in RPMI8226 cells was completely abrogated by a Trk tyrosine kinase inhibitor K252a.BDNF can activate TrkB signaling cascades resulting in MM cells growth, migration, and chemoprotection and appears to have a major contribution to the pathogenesis of MM.

Viability assay

MTT assay

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Research progress of hyperleukocytic acute leukemia

Guoji shuxue ji xueyexue zazhi (2019)

Yu Hu Bo Zheng

Acute hyperleukocytic leukemia (AHL) refers to acute leukemia patients whose peripheral white blood cell count(WBC) is more than 100×109/L. It is called hyperleukocytosis (HL), when peripheral WBC is more than 100×109/L. It is common in acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). AHL has a rapid onset, rapid progress, high early mortality and poor prognosis, which is a critical disease in hematology department. Because of its complications such as leukostasis, tumor lysis syndrome (TLS), disseminated intravascular coagulation (DIC), patients′ lives are threatened and need urgent intervention. Therefore, how to reduce the early mortality of patients with AHL is an important research topic. This article reviews the epidemiology, pathophysiology and clinical manifestations of AHL, especially the current treatment options. Key words: Leukocytosis; Leukemia; Tumor lysis syndrome; Acute hyperleukocytic leukemia; Lyperleukocytosis; Early mortality; Epidemiologic studies; Leukostasis

Leukostasis

Leukocytosis

Hematology

10.3760/cma.j.issn.1673-419x.2019.06.013

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ZMYND8 mediated liquid condensates spatiotemporally decommission the latent super-enhancers during macrophage polarization

Nature Communications (2021)

Pan Jia Xiang Li Xuelei Wang Liangjiao Yao Yingying Xu

Abstract Super-enhancers (SEs) govern macrophage polarization and function. However, the mechanism underlying the signal-dependent latent SEs remodeling in macrophages remains largely undefined. Here we show that the epigenetic reader ZMYND8 forms liquid compartments with NF-κB/p65 to silence latent SEs and restrict macrophage-mediated inflammation. Mechanistically, the fusion of ZMYND8 and p65 liquid condensates is reinforced by signal-induced acetylation of p65. Then acetylated p65 guides the ZMYND8 redistribution onto latent SEs de novo generated in polarized macrophages, and consequently, recruit LSD1 to decommission latent SEs. The liquidity characteristic of ZMYND8 is critical for its regulatory effect since mutations coagulating ZMYND8 into solid compartments disable the translocation of ZMYND8 and its suppressive function. Thereby, ZMYND8 serves as a molecular rheostat to switch off latent SEs and control the magnitude of the immune response. Meanwhile, we propose a phase separation model by which the latent SEs are fine-tuned in a spatiotemporal manner.

Macrophage polarization

10.1038/s41467-021-26864-x

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Prenatal Exposure to Ketamine Leads to Anxiety-Like Behaviors and Dysfunction in Bed Nucleus of Stria Terminalis

The International Journal of Neuropsychopharmacology (2020)

Jing Sun Jianbang Lin Xiaolong Feng Zhonghua Lu Taian Liu

Both the clinical and preclinical studies have suggested embryonic or infant exposure to ketamine, a general anesthetic, pose a great threat to the developing brain. However, it remains unclear how ketamine may contribute to the brain dysfunctions.A mouse model of prenatal exposure to ketamine was generated by i.m. injection and continuous i.p. infusion of pregnant mice. Open field test and elevated plus maze test were used to analyze the behavioral alterations induced by ketamine. Immunostaining by c-Fos was used to map the neuron activity. Chemogenetic modulation of the neurons was used to rescue the abnormal neuron activity and behaviors.Here we show that mice prenatally exposed to ketamine displayed anxiety-like behaviors during adulthood, but not during puberty. C-Fos immunostaining identified abnormal neuronal activity in Bed Nucleus of the Stria Terminalis, the silencing of which by chemogenetics restores the anxiety-like behaviors.Taken together, these results demonstrate a circuitry mechanism of ketamine-induced anxiety-like behaviors.

Elevated plus maze

c-Fos

10.1093/ijnp/pyaa002

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Fer-1 Protects against Isoflurane-Induced Ferroptosis in Astrocytes and Cognitive Impairment in Neonatal Mice

Neurotoxicity Research (2024)

Peng Zhang Xiaotong Shi Danyi He Yu Hu Yongchao Zhang

10.1007/s12640-024-00706-2

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MicroRNA-135a Regulates VEGFC Expression and Promotes Luteinized Granulosa Cell Apoptosis in Polycystic Ovary Syndrome

Reproductive Sciences (2020)

Yifang Wei Shenglian Lu Yu Hu Guo Li Xiaoyu Wu

Hyperandrogenism

10.1007/s43032-020-00155-0

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Nanoscale Zinc-Based Metal–Organic Frameworks Induce Neurotoxicity by Disturbing the Metabolism of Catecholamine Neurotransmitters

Environmental Science & Technology (2023)

Shuang Liu Jingcun Dong Xiaolong Fang Xueting Yan He Zhang

As a group of new nanomaterials, nanoscale metal–organic frameworks (MOFs) are widely applied in the biomedical field, exerting unknown risks to the human body, especially the central nervous system. Herein, the impacts of MOF-74-Zn nanoparticles on neurological behaviors and neurotransmitter metabolism are explored in both in vivo and in vitro assays modeled by C57BL/6 mice and PC12 cells, respectively. The mice exhibit increased negative-like behaviors, as demonstrated by the observed decrease in exploring behaviors and increase in despair-like behaviors in the open field test and forced swimming test after exposure to low doses of MOF-74-Zn nanoparticles. Disorders in the catecholamine neurotransmitter metabolism may be responsible for the MOF-74-Zn-induced abnormal behaviors. Part of the reason for this is the inhibition of neurotransmitter synthesis caused by restrained neurite extension. In addition, MOF-74-Zn promotes the translocation of more calcium into the cytoplasm, accelerating the release and uptake and finally resulting in an imbalance between synthesis and catabolism. Taken together, the results from this study indicate the human toxicity risks of nanoscale low-toxicity metal-based MOFs and provide valuable insight into the rational and safe use of MOF nanomaterials.

Neurotoxicity

10.1021/acs.est.2c09740

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Citations (14)

Chronic myeloid leukemia and BCR/ABL signal pathways are not associated with AKT1 pleckstrin homology domain (E17K) mutations

European Journal Of Haematology (2009)

Yanli He Jine Zheng Yanjie Hu Hong Xiao Jun Liu

Hematology

Pleckstrin homology domain

10.1111/j.1600-0609.2009.01350.x

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Citations (3)

Poster: the Sign Rule and Beyond: Boundary Effects, Flexibility, and Noise Correlations in Population Codes

Yu Hu Joel Zylberberg Eric Shea‐Brown

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