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Article: How many ELNs are optimal for breast cancer patients with more than three PLNs who underwent MRM? A large population-based study.

Wang, Xiaohui / Ji, Changbin / Chi, Huiying / Wang, Haiyong

2018 Volume 11, Page(s) 1005–1011

Abstract: Background: Few studies have focused on the optimal threshold of examed lymph nodes (ELNs) for breast cancer patients with more than three positive lymph nodes after modified radical mastectomy.: Materials and methods: The X-tile and the minimum : ... ...

Abstract	Background: Few studies have focused on the optimal threshold of examed lymph nodes (ELNs) for breast cancer patients with more than three positive lymph nodes after modified radical mastectomy. Materials and methods: The X-tile and the minimum Results: The results showed that 12 ELNs was the optimal threshold for these patients, and the patients with >12 ELNs had a better cancer-specific survival benefit compared with the patients with <12 ELNs ( Conclusion: The number 12 can be selected as the optimal threshold of ELNs for breast cancer patients with >3 positive lymph nodes after modified radical mastectomy.
Language	English
Publishing date	2018-02-26
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2495130-4
ISSN	1178-6930
ISSN	1178-6930
DOI	10.2147/OTT.S152936
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Article ; Online: Synergistic anticancer effects of bufalin and sorafenib by regulating apoptosis associated proteins.

Wang, Haiyong / Zhang, Chenyue / Chi, Huiying / Meng, Zhiqiang

Molecular medicine reports

2018 Volume 17, Issue 6, Page(s) 8101–8110

Abstract: As one of the most recognized and well‑known drugs for hepatocellular carcinoma (HCC), the antitumor effect of sorafenib against HCC remains to be improved. Bufalin has displayed an antitumor effect in HCC; however, whether the enhanced antitumor effect ... ...

Abstract	As one of the most recognized and well‑known drugs for hepatocellular carcinoma (HCC), the antitumor effect of sorafenib against HCC remains to be improved. Bufalin has displayed an antitumor effect in HCC; however, whether the enhanced antitumor effect may be generated with their combined treatment remains unclear. Therefore, in the present study, their combined effects on HCC proliferation and apoptosis were investigated. It was revealed that either bufalin or sorafenib suppressed PLC/PRF/5 and SMMC‑7721 cell proliferation in a concentration‑dependent manner following incubation for 24 h, and the inhibitory effect was augmented with their combined treatment. The synergistic effect peaked in HCC cells treated with 20 nM bufalin and 10 µM sorafenib. In addition, cell cycle and terminal deoxynucleotidyl transferase dUTP nick‑end labelling assays revealed that bufalin also enhanced sorafenib‑induced apoptosis. Colony formation assay demonstrated that combined treatment significantly suppressed HCC proliferation compared with treatment with either of them alone. Furthermore, B‑cell lymphoma 2‑associated X protein, caspase 7 and poly‑(adenosine diphosphate‑ribose) polymerase were upregulated in HCC cells with combined treatment. Taken together, the results of the present study revealed that the treatment of sorafenib combined with bufalin synergistically suppressed HCC proliferation and induced apoptosis. Therefore, bufalin combined with sorafenib may be a favorable treatment strategy for patients with HCC.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Bufanolides/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Drug Synergism ; Humans ; Male ; Mice ; Neoplasms/genetics ; Neoplasms/metabolism ; Niacinamide/analogs & derivatives ; Niacinamide/pharmacology ; Phenylurea Compounds/pharmacology ; Xenograft Model Antitumor Assays
Chemical Substances	Apoptosis Regulatory Proteins ; Bufanolides ; Phenylurea Compounds ; Niacinamide (25X51I8RD4) ; sorafenib (9ZOQ3TZI87) ; bufalin (U549S98QLW)
Language	English
Publishing date	2018-04-24
Publishing country	Greece
Document type	Journal Article
ISSN	1791-3004
ISSN (online)	1791-3004
DOI	10.3892/mmr.2018.8927
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Article ; Online: Synergistic anti-hepatoma effect of bufalin combined with sorafenib via mediating the tumor vascular microenvironment by targeting mTOR/VEGF signaling.

Wang, Haiyong / Zhang, Chenyue / Chi, Huiying / Meng, Zhiqiang

International journal of oncology

2018 Volume 52, Issue 6, Page(s) 2051–2060

Abstract: Sorafenib inhibits tumor growth primarily by inhibiting vessel formation, however, its efficacy requires improvement, therefore, the development of strategies which augment its antiangiogenic effect are of primary concern. Bufalin inhibits tumor cell ... ...

Abstract	Sorafenib inhibits tumor growth primarily by inhibiting vessel formation, however, its efficacy requires improvement, therefore, the development of strategies which augment its antiangiogenic effect are of primary concern. Bufalin inhibits tumor cell proliferation and metastasis, and induces apoptosis. In our previous study, it was demonstrated that the antiangiogenic effect of sorafenib was improved by bufalin in human umbilical vein endothelial cells (HUVECs). However, whether bufalin synergizes with sorafenib by affecting the tumor vascular microenvironment remains to be elucidated. In the present study, it was found that hepatocellular carcinoma (HCC) cell proliferation was inhibited by either bufalin or sorafenib following incubation for 24 h, and the inhibition was enhanced upon treatment with a combination of the two. Conditioned medium (CM), comprising supernatant from HCC cells was collected from each of the treatment groups. The migration and tubule formation were suppressed the most in the combination-CM treated HUVECs. The secretion of vascular endothelial growth factor (VEGF) was decreased in HCC cells treated with the combination-CM, as determined by an angiogenesis array, enzyme-linked immunosorbent assay (ELISA) and western blot analysis. The inhibition of tube formation in HUVECs treated with the combination-CM was reversed by incubation with VEGF. The in vivo experiments demonstrated that subcutaneous HCC cell tumors from mice treated with the combination treatment expressed the lowest levels of VEGF, as evidenced by immunohistochemistry and ELISA. Additionally, the level of phosphorylated mechanistic target of rapamycin (mTOR) was reduced in HUVECs pretreated with the phosphoinositide 3-kinase inhibitor PI103. Furthermore, the migration of HCC cells and HUVEC tube formation were attenuated by PI103 pretreatment. In conclusion, the results revealed a synergistic anti-hepatoma effect of bufalin combined with sorafenib via affecting the tumor vascular microenvironment by targeting mTOR/VEGF signaling.
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Bufanolides/administration & dosage ; Bufanolides/pharmacology ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival ; Culture Media, Conditioned/pharmacology ; Drug Synergism ; Gene Expression Regulation, Neoplastic/drug effects ; Human Umbilical Vein Endothelial Cells/cytology ; Human Umbilical Vein Endothelial Cells/drug effects ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Mice ; Niacinamide/administration & dosage ; Niacinamide/analogs & derivatives ; Niacinamide/pharmacology ; Phenylurea Compounds/administration & dosage ; Phenylurea Compounds/pharmacology ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/metabolism ; Tumor Microenvironment/drug effects ; Vascular Endothelial Growth Factor A/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Bufanolides ; Culture Media, Conditioned ; Phenylurea Compounds ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; Niacinamide (25X51I8RD4) ; sorafenib (9ZOQ3TZI87) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; bufalin (U549S98QLW)
Language	English
Publishing date	2018-04-02
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1154403-x
ISSN	1791-2423 ; 1019-6439
ISSN (online)	1791-2423
ISSN	1019-6439
DOI	10.3892/ijo.2018.4351
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Article ; Online: The appropriate number of ELNs for lymph node negative breast cancer patients underwent MRM: a population-based study.

Chi, Huiying / Zhang, Chenyue / Wang, Haiyong / Wang, Zhehai

Oncotarget

2017 Volume 8, Issue 39, Page(s) 65668–65676

Abstract: Whether number of examed lymph nodes (ELNs) would bring survival benefit for patients with negative lymph nodes after modified radical mastectomy (MRM) is uncertain. In our study, using the Surveillance Epidemiology and End Results (SEER) database ... ...

Abstract	Whether number of examed lymph nodes (ELNs) would bring survival benefit for patients with negative lymph nodes after modified radical mastectomy (MRM) is uncertain. In our study, using the Surveillance Epidemiology and End Results (SEER) database between 2004 and 2009, we screened the appropriate patients with negative lymph nodes underwent MRM. The Cox proportional hazard analysis was used to determine the effect of number of ELNs on cancer specific survival (CSS). The results showed that the number of ELNs was not an independent prognostic factor on CSS (
Language	English
Publishing date	2017-09-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.20052
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Article ; Online: Shen-Zhi-Ling oral solution improves learning and memory ability in Alzheimer's disease mouse model.

Chi, Huiying / Liu, Te / Pan, Weidong / Chen, Jiulin / Wu, Beiling / Yu, Zhihua / Chen, Chuan

Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan

2020 Volume 39, Issue 5, Page(s) 667–677

Abstract: Objective: To investigate the effector mechanisms and effector targets of Shen-Zhi-Ling (SZL) oral solution in the treatment of Alzheimer's disease (AD).: Methods: In this study, we carried out gavage with SZL oral solution in an APP/PS-1 ... ...

Abstract	Objective: To investigate the effector mechanisms and effector targets of Shen-Zhi-Ling (SZL) oral solution in the treatment of Alzheimer's disease (AD). Methods: In this study, we carried out gavage with SZL oral solution in an APP/PS-1 heterozygous double transgenic AD mouse model for 12 continuous weeks. Haematoxylin and eosin staining, Nissl staining and Annexin V/Propidium Iodide staining were used to detect the brain histopathology in AD mouse model. Immunofluorescence staining was used to detect the expression levels of autophagy's proteins. Morris water maze test was used to detect the learning and memory ability in AD mouse model. Results: Pathological results showed that neuronal loss in the hippocampus of mice in the SZL intervention group was significantly alleviated and the number of apoptotic neurons was significantly decreased compared with the control group (physiological saline and non-intervention groups). Immunofluorescence staining results showed that the expression of autophagy activators, Beclin-1 and LC3B, was significantly increased in the hippocampal neurons of mice of the SZL intervention group, while the expression of the apoptotic factor, caspase-3, was significantly decreased. At the same time, hippocampal accumulation of Aβ42 protein was significantly decreased. In addition, results of the water maze experiment showed that the latency period in mice from the SZL intervention group was significantly reduced. Conclusion: In summary, we believe that the SZL oral solution significantly activates autophagy in hippocampal neurons, effectively reducing the accumulation of Aβ42 peptides, alleviating neuronal injury and apoptosis, and ultimately improving the cognitive function in a mouse model of AD.
MeSH term(s)	Administration, Oral ; Alzheimer Disease/drug therapy ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Animals ; Autophagy/drug effects ; Disease Models, Animal ; Drugs, Chinese Herbal/administration & dosage ; Drugs, Chinese Herbal/therapeutic use ; Hippocampus/drug effects ; Hippocampus/pathology ; Hippocampus/physiopathology ; Memory/drug effects ; Mice ; Neurons/drug effects ; Neurons/pathology ; Solutions
Chemical Substances	Drugs, Chinese Herbal ; Solutions ; shen-zhi-ling
Language	English
Publishing date	2020-03-10
Publishing country	China
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603186-9
ISSN	2589-451X ; 0254-6272 ; 0255-2922
ISSN (online)	2589-451X ; 0254-6272
ISSN	0255-2922
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Zs.B 2564: Show issues

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Article: Effect of the herbal formulation Shen-Zhi-Ling on an APP/PS1 mouse model of Alzheimer's disease by modulating the biliverdin reductase/heme oxygenase 1 system.

Xing, Sanli / Shen, Dingzhu / Chen, Chuan / Wu, Beiling / Chi, Huiying

Experimental and therapeutic medicine

2017 Volume 14, Issue 3, Page(s) 1961–1966

Abstract: Shen-Zhi-Ling (SZL) oral liquid is a traditional Chinese medicine formula that is mainly used for the clinical treatment of mild to moderate Alzheimer's disease (AD). The aim of the present study was to investigate the effects and underlying mechanisms ... ...

Abstract	Shen-Zhi-Ling (SZL) oral liquid is a traditional Chinese medicine formula that is mainly used for the clinical treatment of mild to moderate Alzheimer's disease (AD). The aim of the present study was to investigate the effects and underlying mechanisms of SZL treatment on AD. APP/PS1 transgenic mice were utilized to evaluate the effect of SZL treatment (0.5 g/20 g/day). Morris water maze and Thioflavin S staining analyses were used to evaluate the cognitive impairment and β-amyloid plaques, respectively, while quantitative polymerase chain reaction and western blot analysis were performed to examine the mRNA and protein expression levels of heme oxygenase 1 (HO-1) and biliverdin reductase (BVR). Furthermore, immunofluorescence staining was used to measure the BVR and HO-1 protein levels in the hippocampus. The findings of the current study demonstrated that SZL treatment was able to ameliorate the impairment of memory and reduce the accumulation of amyloid plaques, and its ameliorating effects may be attributed to the modulation of the HO-1/BVR system in the hippocampus. These results indicate that SZL may be a possible complementary and alternative therapy to delay the development of AD.
Language	English
Publishing date	2017-07-09
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2017.4732
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Article ; Online: Cyclophosphamide promotes the proliferation inhibition of mouse ovarian granulosa cells and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.

Xiong, Ying / Liu, Te / Wang, Suwei / Chi, Huiying / Chen, Chuan / Zheng, Jin

Gene

2017 Volume 596, Page(s) 1–8

Abstract: The dysfunction of ovarian granulosa cells (OGCs) directly affects the premature ovarian failure (POF). In vivo experiments showed that cyclophosphamide significantly induced mouse ovarian atrophy and proliferation inhibition of OGCs. The expressions of ... ...

Abstract	The dysfunction of ovarian granulosa cells (OGCs) directly affects the premature ovarian failure (POF). In vivo experiments showed that cyclophosphamide significantly induced mouse ovarian atrophy and proliferation inhibition of OGCs. The expressions of p53, p66Shc and p16 were significantly higher in OGCs of the cyclophosphamide treatment group. MTT assay showed that cyclophosphamide effectively inhibited the proliferation of OGCs in vitro. SA-β-Gal staining showed that the OGCs in the cyclophosphamide treatment group had many senescent cells. And, the expression of p53, p66Shc, p16 and cleaved caspase-3 in the OGCs of the cyclophosphamide treatment group significant increases. The Northern blot showed that the intensity of the lncRNA-Meg3 hybridization signal of the OGCs in the cyclophosphamide treatment group was significantly higher than that in the control group. ChIP results confirmed the significant increase in the obtained p66Shc promoter DNA fragment, which was enriched on p53 protein, in the OGCs treated with cyclophosphamide. When cyclophosphamide treatment was conducted after siRNA-Meg3 was used, the expression of endogenous lncRNA-Meg3, p53, p66Shc, p16 and cleaved caspase-3 was significantly lower than that in the siRNA-Mock control group. In summary, cyclophosphamide promotes the proliferation inhibition of mouse OGCs and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.
MeSH term(s)	Animals ; Cell Proliferation/drug effects ; Cyclophosphamide/adverse effects ; Cyclophosphamide/pharmacology ; Disease Models, Animal ; Female ; Granulosa Cells/drug effects ; Granulosa Cells/metabolism ; Granulosa Cells/pathology ; Mice, Inbred C57BL ; Primary Ovarian Insufficiency/chemically induced ; Primary Ovarian Insufficiency/genetics ; Primary Ovarian Insufficiency/metabolism ; Primary Ovarian Insufficiency/pathology ; Promoter Regions, Genetic ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; RNA, Small Interfering ; Signal Transduction/drug effects ; Src Homology 2 Domain-Containing, Transforming Protein 1/genetics ; Src Homology 2 Domain-Containing, Transforming Protein 1/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	MEG3 non-coding RNA, mouse ; RNA, Long Noncoding ; RNA, Small Interfering ; Shc1 protein, mouse ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Tumor Suppressor Protein p53 ; Cyclophosphamide (8N3DW7272P)
Language	English
Publishing date	2017-01-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2016.10.011
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Article: [To investigate the strategy of Chinese medicine for prevention and treatment of atherosclerosis based on vascular aging].

Shen, Ding-Zhu / Chen, Chuan / Chi, Hui-Ying

Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine

2012 Volume 32, Issue 2, Page(s) 266–268

Abstract: Atherosclerosis, a chronic degenerative disease mainly attacks the middle-aged and the aged population as they grow old. Anti-angiocellular aging has gradually become a new strategy for atherosclerosis. In the process of atherosclerosis developing, ... ...

Abstract	Atherosclerosis, a chronic degenerative disease mainly attacks the middle-aged and the aged population as they grow old. Anti-angiocellular aging has gradually become a new strategy for atherosclerosis. In the process of atherosclerosis developing, endothelial cell renewing is speeding. Various biological function disorders that induce blood vessel aging emerge, which leads to changes of the telomere and telomerase, resulting in aged endothelial cells and dysfunction. Telomere and telomerase may play key roles in the etiological factors such as inflammation and AS plaque. In our previous work we have found that Chinese compounds with Shen invigorating effects could not only obviously ameliorate the symptoms and functions of the senility, but also show significant effects on restraining atherosclerosis. We should actively study the mechanisms of Chinese medicine for treating atherosclerosis from Shen, and the mechanisms of Shen invigorating compounds for regulating angiocellular aging through the telomere pathway, thus providing evidence for establishing vascular cell aging based atherosclerosis prevention and treatment strategies by Chinese medicine.
MeSH term(s)	Aging ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Endothelium, Vascular/pathology ; Humans ; Medicine, Chinese Traditional
Language	Chinese
Publishing date	2012-02
Publishing country	China
Document type	English Abstract ; Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1195456-5
ISSN	1003-5370
ISSN	1003-5370
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Article ; Online: Salidroside slows the progression of EA.hy926 cell senescence by regulating the cell cycle in an atherosclerosis model.

Sun, Lin / Dou, Fangfang / Chen, Jiulin / Chi, Huiying / Xing, Sanli / Liu, Te / Sun, Shenwei / Chen, Chuan

Molecular medicine reports

2018 Volume 17, Issue 1, Page(s) 257–263

Abstract: Aging is the major risk factor for diseases of the cardiovascular system, such as coronary atherosclerotic heart disease, but little is known about the relationship between atherosclerosis (AS) and age‑related declines in vascular structure and function. ...

Abstract	Aging is the major risk factor for diseases of the cardiovascular system, such as coronary atherosclerotic heart disease, but little is known about the relationship between atherosclerosis (AS) and age‑related declines in vascular structure and function. Here, we used histological analyses in combination with molecular biology techniques to show that lipid deposition in endothelial cell was accompanied by aging and growth arrest. Endothelial cell senescence is sufficient to cause AS; however, we found that salidroside reduced intracellular lipid deposition, slowed the progression of endothelial cell senescence and inhibited the expression of the senescence‑related molecules and phosphorylated the retinoblastoma (Rb) protein. Further study confirmed that salidroside increased the percent of S phase cells in oxidized low‑density lipoprotein (ox‑LDL)‑treated endothelial cells. Collectively, vascular endothelial cell function declined with age and AS, and our data suggested that salidroside prevented ox‑LDL‑treated endothelial cell senescence by promoting cell cycle progression from G0/G1 phase to S phase via Rb phosphorylation. We demonstrated for the first time the complex interactions between AS and endothelial cell senescence, and we believe that salidroside represents a promising therapy for senescence‑related AS.
MeSH term(s)	Animals ; Atherosclerosis/drug therapy ; Atherosclerosis/etiology ; Atherosclerosis/pathology ; Biomarkers ; Cell Cycle/drug effects ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line ; Cellular Senescence/drug effects ; Disease Models, Animal ; Endothelial Cells ; Gene Expression Regulation/genetics ; Genes, p53 ; Glucosides/pharmacology ; Humans ; Phenols/pharmacology
Chemical Substances	Biomarkers ; Cell Cycle Proteins ; Glucosides ; Phenols ; rhodioloside (M983H6N1S9)
Language	English
Publishing date	2018-01
Publishing country	Greece
Document type	Journal Article
ISSN	1791-3004
ISSN (online)	1791-3004
DOI	10.3892/mmr.2017.7872
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Article ; Online: Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR.

Liu, Te / Chi, Huiying / Chen, Jiulin / Chen, Chuan / Huang, Yongyi / Xi, Hao / Xue, Jun / Si, Yibing

Gene

2017 Volume 631, Page(s) 29–38

Abstract: Many studies have demonstrated that curcumin can effectively inhibit the proliferation, invasion, and tumorigenesis of prostate cancer cells in vitro and in vivo. In this study, ... ...

Abstract	Many studies have demonstrated that curcumin can effectively inhibit the proliferation, invasion, and tumorigenesis of prostate cancer cells in vitro and in vivo. In this study, CD44
MeSH term(s)	AC133 Antigen ; Animals ; Antineoplastic Agents, Phytogenic/pharmacology ; Binding, Competitive ; Biomarkers/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Curcumin/pharmacology ; Humans ; Hyaluronan Receptors ; Male ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs/metabolism ; Neoplasm Invasiveness ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/immunology ; RNA, Long Noncoding/metabolism ; RNA, Neoplasm/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	AC133 Antigen ; Antineoplastic Agents, Phytogenic ; Biomarkers ; Cell Cycle Proteins ; Hyaluronan Receptors ; Linc-RNA-RoR, human ; MIRN145 microRNA, human ; MicroRNAs ; PROM1 protein, human ; RNA, Long Noncoding ; RNA, Neoplasm ; Curcumin (IT942ZTH98)
Language	English
Publishing date	2017-10-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2017.08.008
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