The American Journal of Chinese Medicine Impact Factor & Information

Publisher: Institute for Advanced Research in Asian Science and Medicine, World Scientific Publishing

Journal description

Current impact factor: 2.63

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.625
2012 Impact Factor 2.281
2011 Impact Factor 1.979
2010 Impact Factor 1.383
2009 Impact Factor 1.422
2008 Impact Factor 1.058
2007 Impact Factor 1.122
2006 Impact Factor 0.71
2005 Impact Factor 0.743
2004 Impact Factor 0.593
2003 Impact Factor 0.627
2002 Impact Factor 0.738
2001 Impact Factor 0.511
2000 Impact Factor 0.583
1999 Impact Factor 0.532
1998 Impact Factor 0.293
1997 Impact Factor 0.329
1996 Impact Factor 0.453
1995 Impact Factor 0.07
1994 Impact Factor 0.06
1993 Impact Factor 0.147
1992 Impact Factor 0.052

Impact factor over time

Impact factor

Additional details

5-year impact 1.97
Cited half-life 6.30
Immediacy index 0.23
Eigenfactor 0.00
Article influence 0.28
Website American Journal of Chinese Medicine website
Other titles The American journal of Chinese medicine, Mei-chou Chung-kuo i hsüeh tsa chih
ISSN 0192-415X
OCLC 4655940
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

World Scientific Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Author's pre-print on any website or open access repository
    • Author's post-print on author's personal website, institutional repository, subject repository or funding agency designated repository
    • Publisher's version/PDF cannot be used
    • Set statement to accompany pre-print and authors post-print - see policy
    • Must link to publisher version with DOI
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Akebia Saponin D (ASD) or asperosaponin VI is the most abundant constituent of the rhizome of Dipsacus asper, which has been used for the treatment of lower back pain, traumatic hematoma and bone fractures. In recent years, it was reported that ASD was a potential treatment strategy for Alzheimer's disease (AD). However, the low bioavailability of ASD limited its clinical utility. Microcrystalline preparation is one of the effective methods to improve drug absorption. The drugs prepared by different methods can present different solid forms (polymorphs), and different polymorphs have significantly different bioavailabilities. The objective of this study was to prepare ASD polymorphs using the different preparation processes and to evaluate their physicochemical properties and oral absorption. ASD-2 obtained by the antisolvent process was simpler and had higher recovery (78.5%) than that of ASD-1 by a two-step macroporous resin column separation (56.5%). The ASD polymorphs were characterized using differential scanning calorimetry (DSC), thermogravimetry analysis (TGA), powder X-ray diffraction (PXRD) and scanning electron microscopy (SEM). The results revealed that ASD-2 existed in microcrystalline form, while ASD-1 was amorphous. Furthermore, the equilibrium solubility, dissolution in aqueous solution and pharmacokinetic parameters of the samples were determined. ASD-2 showed lower aqueous solubility than that of ASD-1 (p < 0.01). In addition, ASD-2 showed lower dissolution with only 65% of the drug released while ASD-1 had a higher dissolution with 99% of drug released at the end of the 180 min testing period. Although ASD-1 significantly increased solubility and dissolution, the AUC 0-20h of ASD-2 was 4.3 times that of the amorphous ASD-1 in vivo. Data suggest that the microcrystalline preparation of ASD-2 is not only reasonable in economy and suitable for large-scale preparation, but also a promising method to enhance bioavailability of ASD.
    The American Journal of Chinese Medicine 05/2015; DOI:10.1142/S0192415X15500329
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    ABSTRACT: Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and injury is one of the major atherogenic factors. This study is aimed to investigate the protective effect of celery seed extract (CSE) on ox-LDL-induced injury of macrophages and the underlying signaling pathway. RAW264.7 macrophages were pre-incubated with CSE for 24 h, followed by stimulation with ox-LDL. Oil red O staining and enzymatic colorimetry indicated CSE significantly lessened lipid droplets and total cholesterol (TC) content in ox-LDL-injured macrophages. ELISA revealed that CSE decreased the secretion of inflammatory cytokine TNF-α and IL-6 by 12-27% and 5-15% respectively. MTT assay showed CSE promoted cell viability by 16-40%. Cell apoptosis was also analyzed by flow cytometry and laser scanning confocal microscope and the data indicated CSE inhibited ox-LDL-induced apoptosis of macrophages. Meanwhile, western blot analysis showed CSE suppressed NF-κBp65 and notch1 protein expressions stimulated by ox-LDL in macrophages. These results suggest that CSE inhibits ox-LDL-induced macrophages injury via notch1/NF-κB pathway.
    The American Journal of Chinese Medicine 04/2015; DOI:10.1142/S0192415X15500287
  • The American Journal of Chinese Medicine 03/2015; 43(2):1-13.
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    ABSTRACT: Ginsenoside Rg1 has been reported to possess anti-inflammatory activities, but the effects of Rg1 on the shear induced MCP-1 upregulation mechanism on endothelial cells (ECs) remain to be determined. In this study, we show that Rg1 down modulates shear induced pro-inflammatory cytokine MCP-1 gene expression and monocytes adhesion without potential cell toxicity. The negative effects on monocytes adhesion is due to a decrease in MCP-1 protein release. Furthermore, the inhibitory effect of Rg1 on the phosphorylation level of ERK, p38, and JNK mitogen-activated protein kinase (MAPK) induced by shear stress (SS) is similar with that of specific chemical inhibitors for MAPK pathways activation. These results demonstrate that ginsenoside Rg1 inhibits the shear induced inflammation by suppressing the MAPK pathway. This suggests that Rg1 may serve as a novel anti-inflammatory agent for inflammation-induced cardiovascular diseases treatment.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500202
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    ABSTRACT: Cholinergic dysfunction and oxidation stress are the dominant mechanisms of memory deficit in Alzheimer's disease (AD). This study describes how ferulic acid (FA) ameliorates cognitive deficits induced by mecamylamine (MECA), scopolamine (SCOP), central acetylcholinergic neurotoxin ethylcholine mustard aziridinium ion (AF64A) and amyloid β peptide (Aβ1-40). This study also elucidates the role of anti-oxidant enzymes and cholinergic marker acetylcholinesterase (AChE) in the reversal of FA from Aβ1-40-induced cognitive deficits in rats. At 100 mg/kg, FA attenuated impairment induced by MECA and SCOP plus MECA; however, this improvement was not blocked by the peripheral muscarinic receptor antagonist scopolamine methylbromide (M-SCOP). At 100 and 300 mg/kg, FA also attenuated the impairment of inhibitory passive avoidance induced by AF64A. Further, FA attenuated the performance impairment and memory deficit induced by Aβ1-40 in rats, as did vitamin E/C. FA reversed the deterioration of superoxide dismutase (SOD) and AChE activities, and the glutathione disulfide (GSSG) and glutathione (GSH) levels in the cortex and hippocampus. Vitamin E/C only selectively reversed deterioration in the hippocampus. We suggest that FA reduced the progression of cognitive deficits by activating central muscarinic and nicotinic receptors and anti-oxidant enzymes.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500214
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    ABSTRACT: To systematically evaluate the efficacy and safety of Danhong injection (DH) in treating acute coronary syndrome (ACS), randomized controlled trials (RCTs) regarding ACS treated by DH were searched in Chinese and English electronic databases from inception until June 2013. Two reviewers independently retrieved RCTs and extracted information. The Cochrane risk of bias method was used to assess the quality of the included studies, and a meta-analysis was conducted with Review Manager 5.2 software. About 26 RCTs with 2660 participants were included. The methodological quality was usually not high, and only one study used a randomized, double-blinded method. The meta-analysis indicated that on the basis of conventional therapy with Western medicine (WM), DH was more effective in increasing the total effective rate [ RR = 1.24, 95%CI (1.17, 1.32), p < 0.00001]. Additionally, DH can decrease inflammatory cytokines, including high sensitive C-reactive protein (Hs-CRP) and interleukin-6 (IL-6), lower plasma viscosity, plasma endothelin-1 (ET-1) and brain natriuretic peptide (BNP), reduce the generation of myeloperoxidase (MPO), and decrease the number of T-wave inversion. There were no adverse drug reactions (ADR) reported in the experimental group, while one case occurred in the control group. Based on the systematic review, DH combined with WM was effective in the treatment of ACS. However, the safety of DH in the treatment of ACS should be further carefully interpreted by more large-scale and double-blind RCTs.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500135
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    ABSTRACT: We assessed the therapeutic effects of lumbrokinase, a group of enzymes extracted from the earthworm, on peripheral-nerve regeneration using well-defined sciatic nerve lesion paradigms in diabetic rats induced by the injection of streptozotocin (STZ). We found that lumbrokinase therapy could improve the rats' circulatory blood flow and promote the regeneration of axons in a silicone rubber conduit after nerve transection. Lumbrokinase treatment could also improve the neuromuscular functions with better nerve conductive performances. Immunohistochemical staining showed that lumbrokinase could dramatically promote calcitonin gene-related peptide (CGRP) expression in the lamina I-II regions in the dorsal horn ipsilateral to the injury and cause a marked increase in the number of macrophages recruited within the distal nerve stumps. In addition, the lumbrokinase could stimulate the secretion of interleukin-1 (IL-1), nerve growth factor (NGF), platelet-derived growth factor (PDGF), and transforming growth factor-β (TGF-β) in dissected diabetic sciatic nerve segments. In conclusion, the administration of lumbrokinase after nerve repair surgery in diabetic rats was found to have remarkable effects on promoting peripheral nerve regeneration and functional recovery.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500147
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    ABSTRACT: Lobelia chinensis Lour (LcL) is a popular herb that has been widely used as folk medicine in China for the treatment of fever, lung cancer, and inflammation for hundreds of years. Recently, several studies have shown that the anti-inflammatory properties were correlated with the inhibition of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) from the NF-kB pathway. The aim of this study was to evaluate the anti-oxidative and anti-inflammatory activities of L. chinensis. Both suppressive activities on LPS-induced nitric oxide production in RAW264.7 macrophages in vitro and the acute rat lung injury model in vivo were studied. The results showed that the menthanol extract of LcL and its fractions within the range of 62.5-250 μg/mL did not induce cytotoxicity (p < 0.001). The ethyl acetate fraction of LcL showed better NO inhibition activity than other fractions. On the other hand, the Lc-EA (62.5, 125, 250 mg/kg) pretreated rats showed a decrease in the pro-inflammatory cytokines (TNF-α, IL-β, IL-6) and inhibited iNOS, COX-2 expression through the NF-kB pathway. These results suggested that L. chinensis exhibited an anti-inflammatory effect through the NF-kB pathways.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500184
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    ABSTRACT: Dioscorea nipponica Makino, a popular folk medicine, exerts anti-inflammation properties. The present study investigated the therapeutic effect of the total saponins from Dioscorea nipponica Makino (TSDN) on aplastic anemia (AA) and possible immune regulation mechanisms. Using a mouse model of AA, three different doses of TSDN were orally administrated for 14 consecutive days. We first demonstrated that TSDN was found to be effective in alleviating pancytopenia with a hypocellular bone marrow as compared with AA model group. Moreover, gastrogavage administration of a medium dose of TSDN was found to dramatically increase the percentage of CD4(+) cells in bone marrow nucleated cells (BMNC) and restore the CD4(+)/CD8(+) ratio. The pro-inflammatory cytokine concentrations of IL-2 and IFN-γ were significantly decreased, and anti-inflammatory cytokine IL-4 was significantly increased in culture supernatant of BMNC. Further investigations showed that TSDN obviously inhibited Fas-FasL-induced BMNC apoptosis as well as effectively suppressed intracellular apoptosis protein of caspase-3 and -8 expressions. Taken together, these findings suggested that TSDN could alleviate AA by elevating the CD4(+)/CD8(+) T-cell ratio, inhibiting inflammatory Th1-cytokines, and exerting anti-apoptosis effects.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500196
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    ABSTRACT: Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500226
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    ABSTRACT: Kaempferol is a biologically active component present in various plants. The hepatoprotective effect of kaempferol in drug-induced liver injury has been proven, while its effect against alcoholic liver injury (ALI) remains unclear. Hence, the present study aimed to evaluate the effect of kaempferol against ALI in mice. The experimental ALI mice model was developed and the mice were treated with different doses of kaempferol for 4 weeks. The liver functions were observed by monitoring the following parameters: Aspartate aminotransferase (AST/GOT) and alanine aminotransferase (ALT/GPT) levels in serum; histopathological studies of liver tissue; oxidative stress by hydrogen peroxide ( H 2 O 2), superoxide dismutase (SOD) and glutathione (GSH); the lipid peroxidation status by malondialdehyde (MDA) and lipid accumulation by triglyceride (TG) level in serum; and the expression levels and activities of a key microsomal enzyme cytochrome 2E1 (CYP2E1), by both in vitro and in vivo methods. The ALI mice (untreated) showed clear symptoms of liver injury, such as significantly increased levels of oxidative stress, lipid peroxidation and excessive CYP2E1 expression and activity. The mice treated with different kaempferol dosages exhibited a significant decrease in the oxidative stress as well as lipid peroxidation, and increased anti-oxidative defense activity. The kaempferol treatment has significantly reduced the expression level and activity of hepatic CYP2E1, thus indicating that kaempferol could down regulate CYP2E1. These findings show the hepatoprotective properties of kaempferol against alcohol-induced liver injury by attenuating the activity and expression of CYP2E1 and by enhancing the protective role of anti-oxidative defense system.
    The American Journal of Chinese Medicine 03/2015; DOI:10.1142/S0192415X15500160
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    ABSTRACT: Celastrol is a natural terpenoid isolated from Tripterygium wilfordii, a well-known Chinese medicinal herb that presents anti-proliferative activities in several cancer cell lines. Here, we investigated whether celastrol induces apoptosis on hepatocellular carcinoma Bel-7402 cells and further explored the underlying molecular mechanisms. Celastrol caused a dose- and time-dependent growth inhibition and apoptosis of Bel-7402 cells. It increased apoptosis through the up-regulation of Bax and the down-regulation of Bcl-2 in Bel-7402 cells. Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. These results indicated that celastrol could induce apoptosis in Bel-7402 cells, which may be associated with the activation of the mitochondria-mediated pathway.
    The American Journal of Chinese Medicine 02/2015; 43(01):1-12. DOI:10.1142/S0192415X15500093
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    ABSTRACT: α-Phellandrene (α-PA) is a cyclic monoterpene. To investigate the induction of autophagy by α-PA and its mechanism, human liver tumor cells (J5) were incubated with α-PA and analyzed for cell viability and the molecular regulation of pre-autophagosome origination and autophagosome formation. According to the results, PI3K-I, mTOR, and Akt protein levels were decreased after α-PA treatment compared to those of the control group (p < 0.05). The phosphorylation of Bcl-2, and PI3K-III, LC3-II and Beclin-1 protein levels in J5 cells were increased after α-PA treatment (p < 0.05). In addition, α-PA up-regulated nuclear p53 and down-regulated cytoplasmic p53 expression in J5 cells. The NF-κB pathway was activated, as indicated by increase in cytosolic phosphorylated IκB, nuclear NF-κB levels, and the DNA-binding activity of NF-κB after α-PA treatment in J5 cells (p < 0.05). These results suggest that α-PA can induce J5 cell autophagy by regulating mTOR and LC-3II expression, p53 signaling, and NF-κB activation in J5 cells.
    The American Journal of Chinese Medicine 02/2015; 43(01):1-16. DOI:10.1142/S0192415X15500081
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    ABSTRACT: Cochinchina Momordica Seed, which is the dried ripe seed of Momordica cochinchinensis (Lour.) Spreng, has been used as a mainly anticancer ingredient for many years in China. This study aims at investigating the roles of an ethanol-soluble extract of Cochinchina Momordica Seed (ECMS) in suppressing the proliferation and metastasis of human lung cancer cells, and further elucidating underlying molecular mechanisms. Our researches suggest that ECMS dose-dependently decreased the survival rates of A549 and H1299 cells, and inhibited the migration and invasion in A549 cells. ECMS-induced apoptosis was accompanied by up-regulation of p53, Bax and the down-regulation of Bcl-2, PI-3K/Akt signal pathway, and resulted in the dissipation of mitochondrial membrane potential (ΔΨm) and sequentially activated caspase-3 cascade. Pre-treated with specific inhibitors, LY294002 (PI-3K inhibitor) and BAY11-7082 (NF-κB inhibitor) could enhance the anti-proliferation effects of ECMS on A549 cells. Furthermore, ECMS could increase the level of E-cadherin and decrease of the level of STAT-3 and MMP-2, and scarcely affected the expression of VEGF, and resulted in the inhibition of migration and invasion. Pre-treated with specific inhibitors, WP1066 (STAT-3 inhibitor) and TIMP-2 (MMP-2 inhibitor) could enhance the inhibitory effects of ECMS on migration. In conclusion, the current data demonstrated ECMS inhibited the proliferation of A549 cells by inducing apoptosis, at least partly through the activation of p53 and inactivation of PI-3K/Akt signaling. STAT-3 and MMP-2 pathways may be partly involved in anti-metastasis activities of ECMS. Hence, ECMS might be a promising candidate for the therapy of the non-small cell lung cancer by regulating multiple molecular targets.
    The American Journal of Chinese Medicine 02/2015; 43(01):1-18. DOI:10.1142/S0192415X1550010X
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    ABSTRACT: This study was designed to determine the antinociceptive effect and related neuronal mechanism of electroacupuncture (EA) on paclitaxel (PTX)-induced neuropathic pain in mice. PTX (4 mg/kg, i.p.) was administered once a day for 5 consecutive days to induce neuropathic pain. EA stimulation (2 mA, 2 Hz, 30 min) was applied at the ST36 acupoint bilaterally once in every 2 days. Repeated EA stimulation significantly attenuated PTX-induced mechanical allodynia and thermal hyperalgesia. In a separate set of experiment, the antinociceptive effect of a single EA stimulation 8 days after PTX treatment was reduced by intrathecal pretreatment with naloxone (opioid receptor antagonist), idazoxan (alpha2-adrenoceptor antagonist) or propranolol (beta-adrenoceptor antagonist), but not prazosin (alpha1-adrenoceptor antagonist). Moreover, EA remarkably suppressed the PTX-enhanced phosphorylation of the NMDA receptor NR2B subunit in the spinal dorsal horn, and intrathecal pretreatment of naloxone, idazoxan (IDA) or propranolol blocked the effect of EA. In conclusion, EA stimulation at the ST36 acupoint significantly diminished PTX-induced neuropathic pain in mice via the mediation of spinal opioid receptor, alpha2- and beta-adrenoceptors.
    The American Journal of Chinese Medicine 02/2015; 43(01):1-14. DOI:10.1142/S0192415X15500044
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    ABSTRACT: Sho-saiko-to is an herbal medicine that is known to have diverse pharmacological activities and has been used for the treatment of various infectious diseases. Here, we examined the effects of baicalin, a compound isolated from Sho-saiko-to, and the effects of the iron chelator quinolinic acid on the Fenton reaction. The control reaction mixture contained 0.1 M 5,5-dimethyl-1-pyrroline N-oxide (DMPO), 0.2 mM H 2 O 2, 0.2 mM FeSO 4( NH 4)2 SO 4, and 40 mM sodium phosphate buffer (pH 7.4). Upon the addition of 0.6 mM baicalin or quinolinic acid to the control reaction mixture, the ESR peak heights of DMPO/ OH radical adducts were measured as 32% ± 1% (baicalin) and 166% ± 27% (quinolinic acid) of that of the control mixture. In order to clarify why baicalin and quinolinic acid exerted opposite effects on the formation of hydroxyl radicals, we measured oxygen consumption in the presence of either compound. Upon the addition of 0.6 mM baicalin (or quinolinic acid) to the control reaction mixture without DMPO and H 2 O 2, the relative oxygen consumption rates were found to be 449% ± 40% (baicalin) and 18% ± 9% (quinolinic acid) of that of the control mixture without DMPO and H 2 O 2, indicating that baicalin facilitated the transfer of electrons from Fe (2+) to dissolved oxygen. Thus, the great majority of Fe (2+) turned into Fe (3+), and the formation of hydroxyl radicals was subsequently inhibited in this reaction.
    The American Journal of Chinese Medicine 02/2015; 43(01):1-15. DOI:10.1142/S0192415X15500068
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    ABSTRACT: Scutellariae radix is one of the most widely used anticancer herbal medicines in several Asian countries, including Korea, Japan, and China. Squamous cell carcinoma (SCC) is one of the most common head and neck carcinomas, which is highly invasive and metastatic, and can potentially develop chemoresistance. Therefore, new effective treatment methods are urgently needed. We determined the effects of Scutellariae radix on SCC-25 cells using the WST-1 assay, F-actin staining, flow cytometry analysis, immunofluorescence staining, and western blot analysis. Scutellariae radix treatment inhibited SCC-25 cell growth in a dose- and time-dependent manner, but it did not inhibit HaCaT (human keratinocyte) cell growth. Changes in cell morphology and disruption of filamentous (F)-actin organization were observed. Scutellariae radix-induced apoptosis as indicated by the translocation of cytochrome c and apoptosis-inducing factor (AIF) into the nucleus and cytosol. Scutellariae radix-induced an increase in cells with sub-G1 DNA content, and increased Bax, cleaved caspase-3, caspase-7, caspase-9, DNA fragmentation factor 45 (DFF 45), and poly(ADP-ribose) polymerase-1 (PARP-1) expression levels. Furthermore, increased expression of phosphorylated mitogen-activated protein kinase (MAPK)-related proteins was detected. The antitumor effect of Scutellariae radix was due to decreased cell proliferation, changes in cell morphology, and the activation of caspase and MAPK pathways. Taken together, the findings of this study highlight the anticancer activity of Scutellariae radix in chemoresistant SCC-25 oral squamous carcinoma cells.
    The American Journal of Chinese Medicine 02/2015; 43(01):1-15. DOI:10.1142/S0192415X15500111