Qing‐Yu He

Jinan University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Bin Li

State Key Laboratory of Respiratory Disease

Xuesong Sun

Jinan University

Jen‐Fu Chiu

National Health Research Institutes

Can‐Can Zheng

Guangzhou Medical University

Xingfeng Yin

Jinan University

Shujun Li

First Affiliated Hospital of Xinxiang Medical University

Zi-Jia Huang

Jinan University

Yan Li

Southern Medical University Shenzhen Hospital

Gong Zhang

Jinan University

Long Liao

Mianyang Central Hospital

Cooperative Institutions

Jinan University

343

Sun Yat-sen University

264

Chinese Academy of Sciences

253

European Foundation for the Study of Chronic Liver Failure

198

Chinese Academy of Medical Sciences & Peking Union Medical College

182

Sichuan University

171

University of Hong Kong

168

Fudan University

160

Peking University

150

Shanghai Jiao Tong University

139

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Omics Evidence: Single Nucleotide Variants Transmissions on Chromosome 20 in Liver Cancer Cell Lines

Journal of Proteome Research (2013)

Quanhui Wang Bo Wen Tong Wang Zhongwei Xu Xuefei Yin

Cancer genomics unveils many cancer-related mutations, including some chromosome 20 (Chr.20) genes. The mutated messages have been found in the corresponding mRNAs; however, whether they could be translated to proteins still requires more evidence. Herein, we proposed a transomics strategy to profile the expression status of human Chr.20 genes (555 in Ensembl v72). The data of transcriptome and translatome (the mRNAs bound with ribosome, translating mRNAs) revealed that ∼80% of the coding genes on Chr.20 were detected with mRNA signals in three liver cancer cell lines, whereas of the proteome identified, only ∼45% of the Chr.20 coding genes were detected. The high amount of overlapping of identified genes in mRNA and RNC-mRNA (ribosome nascent-chain complex-bound mRNAs, translating mRNAs) and the consistent distribution of the abundance averages of mRNA and RNC-mRNA along the Chr.20 subregions in three liver cancer cell lines indicate that the mRNA information is efficiently transmitted from transcriptional to translational stage, qualitatively and quantitatively. Of the 457 genes identified in mRNAs and RNC-mRNA, 136 were found to contain SNVs with 213 sites, and >40% of these SNVs existed only in metastatic cell lines, suggesting them as the metastasis-related SNVs. Proteomics analysis showed that 16 genes with 20 SNV sites were detected with reliable MS/MS signals, and some SNVs were further validated by the MRM approach. With the integration of the omics data at the three expression phases, therefore, we are able to achieve the overall view of the gene expression of Chr.20, which is constructive in understanding the potential trend of encoding genes in a cell line and exploration of a new type of markers related to cancers.

Ribosome profiling

Proteome

10.1021/pr400899b

Cite

Citations (16)

Correlation of imaging markers of cerebral small vessel disease with left ventricular disease: A review

MEDS Clinical Medicine (2023)

Qing‐Yu He Meiru Yi Hui Zhang

Cerebral small vessel disease (CSVD) is a combination of disorders that affects the small arteries, veins, and microvessels of the brain. It can be observed on cranial magnetic resonance imaging as cerebral white matter hyperintensity, enlarged perivascular spaces, cerebral microbleeds, cerebral atrophy, and lacunes. The underlying mechanisms of cerebral small vessel disease remain unclear. Recent studies have suggested that left ventricle-associated diseases can contribute to a better understanding of the pathogenesis of cerebral small-vessel disease. Epidemiologic and clinicopathologic data have uncovered evidence of a relationship between cerebral small vessel disease and left ventricular disease. The purpose of this paper is to explore the complex relationship between cerebral small vessel disease and left ventricular disease. Defining the relationship between cerebral small vessel disease and left ventricular-related diseases is crucial for early prevention of cerebral small vessel disease.

Cerebral atrophy

Leukoaraiosis

Cerebral ventricle

Perivascular space

10.23977/medsc.2023.040911

Cite

Citations (0)

Serum biomarkers of hepatitis B virus infected liver inflammation: A proteomic study

PROTEOMICS (2003)

Qing‐Yu He George Lau Yuan Zhou Siu–Tsan Yuen Marie C.M. Lin

Abstract Hepatitis B virus (HBV), a serious infectious and widespread human pathogen, represents a major health problem worldwide. Chronic HBV infection has a very high risk of evolving into hepatocellular carcinoma. Although considerable progress was made during the recent past, the pathogenesis of HBV infection is still elusive and a definite diagnosis of HBV infected liver information still relies on biopsy histological test. In this report, we used proteomics technology to globally examine HBV infected serum samples aiming at searching for disease‐associated proteins that can be used as serological biomarkers for diagnosis and/or target proteins for pathogenetic study. By comparing with normal and HBV negative serum samples, we found that at least seven proteins were significantly changed in HBV infected sera. These greatly altered proteins were identified to be haptoglobin β and α2 chain, apolipoprotein A‐I and A‐IV, α1‐antitrypsin, transthyretin and DNA topoisomerase IIβ. The alteration of these proteins is displayed not only in quantity but also in patterns (or specificity), which can be correlated with necroinflammatory scores. In particular, apolipoprotein A‐I presents heterogeneous change in expression level with different isoforms and α1‐antitrypsin produces evidently different fragments implying diverse cleavage pathways. These unique phenomena appear specific to HBV infection. A combination simultaneously considering the quantities and isoforms of these proteins could be a useful serum biomarker (or index) for HBV diagnosis and therapy.

Haptoglobin

Liver disease

Pathogenesis

Hepatitis B

Proteome

10.1002/pmic.200300394

Cite

Citations (159)

KCTD12 promotes tumorigenesis by facilitating CDC25B/CDK1/Aurora A-dependent G2/M transition

Oncogene (2017)

Y Zhong Jie Yang Wen Xu Yang Wang C-C Zheng

Cell cycle dysregulation leads to uncontrolled cell proliferation and tumorigenesis. Understanding the molecular mechanisms underlying cell cycle progression can provide clues leading to the identification of key proteins involved in cancer development. In this study, we performed proteomics analysis to identify novel regulators of the cell cycle. We found that potassium channel tetramerization domain containing 12 (KCTD12) was significantly upregulated in M phase compared with S phase. We also found that KCTD12 overexpression not only facilitated the G2/M transition and induced cancer cell proliferation, but also promoted the growth of subcutaneous tumors and Ki-67 proliferation index in mice. Regarding the mechanism underlying these phenomena, cyclin-dependent kinase 1 (CDK1) was identified as an interacting partner of KCTD12 by immunoprecipitation and mass spectrometry analysis, which showed that KCTD12 activated CDK1 and Aurora kinase A (Aurora A) and that the effects of KCTD12 on CDK1 phosphorylation and cell proliferation were abrogated by cell division cycle 25B (CDC25B) silencing. In addition, Aurora A phosphorylated KCTD12 at serine 243, thereby initiating a positive feedback loop necessary for KCTD12 to exert its cancer-promoting effects. Furthermore, we analyzed the expression levels of various genes and the correlations between the expression of these genes and survival using tumor tissue microarray and Gene Expression Omnibus (GEO) data sets. The data showed that KCTD12 expression was significantly upregulated in cervical and lung cancers. More importantly, high KCTD12 expression was associated with larger tumor sizes, higher pathological stages and poor patient survival. Collectively, our study demonstrate that KCTD12 binds to CDC25B and activates CDK1 and Aurora A to facilitate the G2/M transition and promote tumorigenesis and that Aurora A phosphorylates KCTD12 at serine 243 to trigger a positive feedback loop, thereby potentiating the effects of KCTD12. Thus, the KCTD12-CDC25B-CDK1-Aurora A axis has important implications for cancer diagnoses and prognoses.

Cyclin B1

10.1038/onc.2017.287

Cite

Citations (61)

Dietary Supplementation with Two Host-Associated Bacillus Velezensis Strains Enhances Growth, Antioxidant, and Gut Health in Micropterus Salmoides and Channa Argus

Haohang Zhao Zhiwen Wang Yiming Wen Deyu Ning Wei Li

10.2139/ssrn.5148440

Cite

Citations (0)

Mutations at the Histidine 249 Ligand Profoundly Alter the Spectral and Iron-Binding Properties of Human Serum Transferrin N-Lobe

Biochemistry (2000)

Qing‐Yu He Anne B. Mason Rowchanak Pakdaman N. Dennis Chasteen Bonnie K. Dixon

Human serum transferrin is an iron-binding and -transport protein which carries iron from the blood stream into various cells. Iron is held in two deep clefts located in the N- and C-lobes by coordinating to four amino acid ligands, Asp 63, Tyr 95, Tyr 188, and His 249 (N-lobe numbering), and to two oxygens from carbonate. We have previously reported the effect on the iron-binding properties of the N-lobe following mutation of the ligands Asp 63, Tyr 95, and Tyr 188. Here we report the profound functional changes which result from mutating His 249 to Ala, Glu, or Gln. The results are consistent with studies done in lactoferrin which showed that the histidine ligand is critical for the stability of the iron-binding site [H. Nicholson, B. F. Anderson, T. Bland, S. C. Shewry, J. W. Tweedie, and E. N. Baker (1997) Biochemistry 36, 341−346]. In the mutant H249A, the histidine ligand is disabled, resulting in a dramatic reduction in the kinetic stability of the protein toward loss of iron. The H249E mutant releases iron three times faster than wild-type protein but shows significant changes in both EPR spectra and the binding of anion. This appears to be the net effect of the metal ligand substitution from a neutral histidine residue to a negative glutamate residue and the disruption of the "dilysine trigger" [MacGillivray, R. T. A., Bewley, M. C., Smith, C. A., He, Q.-Y., Mason, A. B., Woodworth, R. C., and Baker, E. N. (2000) Biochemistry 39, 1211−1216]. In the H249Q mutant, Gln 249 appears not to directly contact the iron, given the similarity in the spectroscopic properties and the lability of iron release of this mutant to the H249A mutant. Further evidence for this idea is provided by the preference of both the H249A and H249Q mutants for nitrilotriacetate rather than carbonate in binding iron, probably because NTA is able to provide a third ligation partner. An intermediate species has been identified during the kinetic interconversion between the NTA and carbonate complexes of the H249A mutant. Thus, mutation of the His 249 residue does not abolish iron binding to the transferrin N-lobe but leads to the appearance of novel iron-binding sites of varying structure and stability.

10.1021/bi9915216

Cite

Citations (28)

Enucleation of the prostate for benign prostatic hyperplasia thulium laser versus holmium laser: a systematic review and meta-analysis

Lasers in Medical Science (2019)

Kaiwen Xiao Liang Zhou Qing‐Yu He Xiaoshuai Gao Guo Chen

10.1007/s10103-018-02697-x

Cite

Citations (27)

A hidden human proteome encoded by ‘non-coding’ genes

Nucleic Acids Research (2019)

Shaohua Lu Jing Zhang Xinlei Lian Li Sun Kun Meng

It has been a long debate whether the 98% 'non-coding' fraction of human genome can encode functional proteins besides short peptides. With full-length translating mRNA sequencing and ribosome profiling, we found that up to 3330 long non-coding RNAs (lncRNAs) were bound to ribosomes with active translation elongation. With shotgun proteomics, 308 lncRNA-encoded new proteins were detected. A total of 207 unique peptides of these new proteins were verified by multiple reaction monitoring (MRM) and/or parallel reaction monitoring (PRM); and 10 new proteins were verified by immunoblotting. We found that these new proteins deviated from the canonical proteins with various physical and chemical properties, and emerged mostly in primates during evolution. We further deduced the protein functions by the assays of translation efficiency, RNA folding and intracellular localizations. As the new protein UBAP1-AST6 is localized in the nucleoli and is preferentially expressed by lung cancer cell lines, we biologically verified that it has a function associated with cell proliferation. In sum, we experimentally evidenced a hidden human functional proteome encoded by purported lncRNAs, suggesting a resource for annotating new human proteins.

Proteome

Ribosome profiling

Human proteome project

ENCODE

Proteogenomics

10.1093/nar/gkz646

Cite

Citations (143)

Trends and risk factors analysis of NEC in preterm infants over 9 years

Egyptian Pediatric Association Gazette (2024)

Yi Yang Qing‐Yu He Min Yang Pinglin Zhang Lijun Su

Abstract Background Investigating the trend of changes in the occurrence of necrotizing enterocolitis (NEC) in preterm infants during 9 years and analyzing the risk factors of NEC with the purpose of providing reference for clinical diagnosis and treatment of NEC. Methods Clinical data of NEC in preterm infants with Bell’s stage ≥ II from January 2013 to December 2021 in the Neonatology Department of the Third Affiliated Hospital of Zunyi Medical University was retrospectively analyzed. Trends in the occurrence of NEC in preterm infants were analyzed by the trend chi-square test. Subsequently, the general data (sex, gestational age, singleton or multiple births, birth weight, serum albumin, alkaline phosphatase, sepsis, blood transfusion, mechanical ventilation, RDS, arterial catheterization) and perinatal data (intrauterine distress, turbid amniotic fluid, premature rupture of membranes, mode of delivery, fetal heart abnormalities, diabetes mellitus) were collected; then, the risk factors for NEC were analyzed by univariate and multivariate logistic-regression analysis. Results In the past 9 years, 77 cases of NEC occurred, with the incidence rate of 1.95%, and the incidence of NEC in preterm infants has been increasing year by year ( P < 0.05). The results of univariate analysis showed that the morbidity of NEC in preterm infants was associated with premature rupture of membranes, blood transfusion, sepsis, and the of serum albumin ( P < 0.05). Multivariate logistic regression analysis revealed that blood transfusion (OR = 2.232, 95% CI: 1.012–4.923) and sepsis (OR = 0.899, 95% CI: 0.809–3.915) were independent risk factors of NEC in preterm infants, while high serum albumin (OR = 0.899, 95% CI: 0.809–3.915) was an independent protective factor of NEC in preterm infants. Conclusion The morbidity of NEC is gradually increasing. Inhibition of infection and limitation of blood transfusion are effective measures to reduce the occurrence of NEC. Meanwhile, high serum albumin is a protective factor for NEC.

10.1186/s43054-024-00261-7

Cite

Citations (0)

Efficacy and Safety of All-oral, 12-week Ravidasvir Plus Ritonavir-boosted Danoprevir and Ribavirin in Treatment-naïve Noncirrhotic HCV Genotype 1 Patients: Results from a Phase 2/3 Clinical Trial in China

Journal of Clinical and Translational Hepatology (2019)

Xiaoyuan Xu Bo Feng Yujuan Guan Sujun Zheng Jifang Sheng

Background and Aims: Ravidasvir (RDV) is a new generation pangenotypic hepatitis C virus (HCV) NS5A inhibitor, with high barrier to baseline resistance-associated species. This is the first phase 2/3 study conducted in Mainland China confirming the efficacy and safety of RDV + ritonavir-boosted danoprevir + ribavirin for 12 weeks in treatment-naïve noncirrhotic patients with genotype 1 infection in a large population. Methods: In this multicenter, randomized, double-blinded, placebo-controlled phase 2/3 trial (NCT03362814), we enrolled 424 treatment-naïve, noncirrhotic adult HCV genotype 1 patients. All patients were randomized at 3:1 ratio to receive a combination of RDV 200mg once daily plus ritonavir-boosted danoprevir 100mg/100mg twice daily and oral ribavirin 1000/1200mg/day (body weight <75/≥75 kg) (n = 318) or placebo (n = 106) for 12 weeks. The primary end-point was the rate of sustained virologic response 12 weeks after the end of treatment, and the safety was evaluated and compared between treatment and placebo groups. Results: The overall rate of sustained virological response at 12 weeks after treatment is 99% (306/309, 95%, CI: 97%-100%) under per protocol set analysis. All patients harboring baseline NS5A resistance-associated species in the treatment group (76/76, per protocol set) achieved sustained virological response at 12 weeks after treatment. No treatment-related serious adverse events were reported. Laboratory abnormalities showed mild or moderate severity (grade 1 and grade 2) in liver function tests. Conclusions: In treatment-naïve, noncirrhotic HCV Chinese patients infected with HCV genotype 1, all-oral regimen of RDV + ritonavir-boosted danoprevir + ribavirin for 12 weeks was highly efficacious, safe, and well tolerated.

Ritonavir

Hepatitis C

Clinical endpoint

10.14218/jcth.2019.00033

Cite

Citations (15)