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Qi Cao, BM, PhD

Academic Title:

Assistant Professor

Primary Appointment:

Diagnostic Radiology and Nuclear Medicine

Location:

Gudelsky Building, C250a

Phone (Primary):

410-328-9586

Phone (Secondary):

410-706-5414

Fax:

410-328-1600

Education and Training

  • Anhui Medical University, Hefei, China, MD, 1985
  • University of Newcastle, NSW, Australia, Ph.D, 1999
  • Residency, Mount Sinai School of Medicine Internal Medicine (Bronx), 2009
  • Residency, University of Maryland at Baltimore, 2013

Biosketch

Dr. Cao is a physician scientist at the UMB after I complished my residency in 2013. Before this appointment, I have studied molecular biology in alcoholic liver disease and non-alcoholic liver disease in the Mount Sinai School of Medicine in New York. I have published more than 40 articles in peer review journals.

Dr. Cao has research interest in molecular imaging in the diagnosis of liver fibrosis and alcoholic liver disease-caused neurological dysfunction. In addition, Dr. Cao has research interest in treatment and prevention of alcoholic liver disease. His research projects are supported by NIH grants and other grants.

Research/Clinical Keywords

Molecular Imaging, PET/CT, MRS, Alcoholic Liver Disease, Molecular Biology, Histopathology, Immunohistochemistry, Neurological Dysfunction, Alcoholic Liver Disease-Caused Neurological Dysfunction, Oxidative Stress, Alcoholic Liver Disease Therapy, Breast Cancer, Brown Fat, HCC, Radiation Therapy.

Highlighted Publications

Cao Q, Batey R, Pang G, Russell A, Clancy R. IL-6, IFN-gamma and TNF-alpha production by liver-associated T cells and acute liver injury in rats administered concanavalin A. Immunol Cell Biol. 1998; 76:542-549. PMID: 9893032

Cao Q, Mak KM, Lieber CS. Leptin represses matrix metalloproteinase-1 gene expression in LX2 human hepatic stellate cells. J Hepatol. 2007; 46:124-133. PMID: 17030072

Cao Q, Hersl J, La H, Smith M, Jenkins J, Goloubeva O, Dilsizian V, Tkaczuk K, Chen W, Jones L. A pilot study of FDG PET/CT detects a link between brown adipose tissue and breast cancer. BMC Cancer. 2014; 14:126. doi: 10.1186/1471-2407-14-126. PMID: 24564204

Additional Publication Citations

Cao Q, Mak KM, Lieber CS. Dilinoleoylphosphatidylcholine decreases TGF-beta1-induced collagen mRNA by inhibiting p38 MAPK in hepatic stellate cells. Am J Physiol Gastrointestinal & Liver Physiol2002; 283(5):G1051-G1061.

Lieber CS, Leo MA, Mak KM, Xu YQ, Cao Q, Ren CL, Ponomarenko A, DeCarli LM. Model of non-alcoholic fatty liver disease, including steatohepatitis. Am. J. ClinNutr.2004; 79(3):502-9.

Cao Q, Mak KM, Ren CL, and Lieber CS. Leptinstimulates tissue inhibitor of metalloproteinase-1 in human hepatic stellate cells: respective roles of the JAK-STAT and JAK-mediated H2O2-depedent MAPK pathways. J. Biol. Chem. 2004; 279(6):4292-4304.

Cao Q, Mak KM, and Lieber CS. Cytochrome P4502E1 primes macrophages to increase TNF-alpha production in response to lipopolysaccharide. Am J. PhysiolGastrointest Liver PhysiolJuly 2005; 289(1):G95-G107.

Liu H, Zheng F, Cao Q, Ren B, Zhu L, Striker G, Vlassara H. Amelioration of oxidant stress by the defensin lysozyme. Am. J. Physiol. EndocrinolMetab. May 2006; 290(5):E824-E832.

Cao Q, K Mak, Lieber CS. Leptin represses matrix metalloproteinase-1 gene expression in LX-2 human hepatic stellate cells. Journal of Hepatology 2007; 46(1):124-33.

You M, Cao Q, Liang X, Ajmo JM, Ness GC. Mammalian sirtuin 1 is involved in the protective action of dietary saturated fat against alcoholic fatty liver in mice. J Nutr. 2008; 138(3):497-501.

Chen W, Cao Q, Dilsizian V. Variation of heart-to-mediastinal ratio in (123) I-mIBG cardiac sympathetic imaging: it's affecting factors and potential corrections. CurrCardiol Rep. 2011; 13(2):132-7.

Cao Q, and Chen W. FDG PET imaging of large-vessel vasculitis. PET Clinic. 2012; 7:227-232.

Chen W, Cao Q and Dilsizian V. Reply to the letter by Ben F. Bulten et al. regarding "Interobserver Variability of Heart-to-Mediastinum Ratio in I-123 MIBG Sympathetic Imaging"Current Cardiology Reports. 2012;14(4):391.

Klein T, Dilsizian V, Cao Q, Chen W, Dickfeld T. The potential role of iodine-123 metaiodobeuanidine imaging for identifying sustained ventricular tachycardia in patients with cardiomyopathy. 2013;15:359.

Cao Q, Lu M, Heath J, Hausner PF, Alexander, RH, Dilsizian V, and Chen W. F-18 FDG PET/CT in a recurrent diffuse malignant peritoneal mesothelioma. Clinical Nuclear Medicine 2012; 37:492-494.

Singh SN, Cao Q, Gojo I, Rapoport AP, Akpek G. Durable complete remission after single agent decitabine in AML relapsing in extramedullary sites after allo-SCT.Bone Marrow Transplant.2012;47(7):1008-1009.

Cao Q, Lu M,Huebner T,Dilsizian V, and Chen W. F-18 FDG PET/CT in a Rare Malignant Extra-skeletal Osteosarcoma. Radiology. Clin. Nuc. Med. 2013;38(9):e367-369.

Complete List of Published Work in My Bibliography.

http://www.ncbi.nlm.nih.gov/sites/myncbi/qi.cao.1/bibliography/49422376/public/?sort=date&direction=ascending

Research Interests

1. During my post-graduate training (Ph.D.) in Australia and my working period as a research fellow in New York, my early publications addressed the fact that alcohol as a primary cellular sensitization factor can sensitize intrahepatic immune cells (intrahepatic Kupffer cells, intrahepatic CD4+ and CD8+ cells), as well as hepatic stellate cells (HSCs). When those alcohol-sensitized intrahepatic immune cells are stimulated with second pathological stimulators, specifically endotoxin, alcohol-metabolites such as acetaldehyde, oxidants (e.g., H2O2), and other mediators (e.g., IL-1, IL-6, TNF-a, and TGF-b), those cells can be over-activated. The over-activated cells can directly and synergistically cause liver injuries such as alcoholic steatosis, steatohepatitis, and alcoholic liver fibrosis/cirrhosis. Specifically intrahepatic Kupffer cells can over-produce inflammatory mediators (e.g., TNFa) via complicated intracellular signal pathways. Intrahepatic CD4+ and CD8+ cells can over-produce INFg, TNFa, IL-6 and IL-1. These cytokines may cause steatosis and hepatitis. HSCs stimulated by TGFb, LPS, H2O2 /menadione or leptin can overproduce collagen leading to liver fibrosis. These experiments were successfully completed in in vitro cell culture studies of intrahepatic Kupffer cells, intrahepatic CD4+ and CD8+ cells, as well as HSCs isolated from livers of alcohol-fed rats and commercial cell lines. To directly investigate oxidative stress formation-mediated TNF-a generation, I successfully established RAW macrophage cell lines with over-expression of the CYP450 2E1 gene. The published results confirmed that over-expression of the CYP450 2E1 can lead to increased production of oxidative stress that promoted TNF-a generation via the PI3K-MAPK pathways.

During my tenure at Mount Sinai in New York, my publications also addressed that antioxidants dilinoleoylphosphatidylcholine (DLPC), s-adenosylmethionine (SAMe), and a combination of SAMe and DLPC might playan important role in the prevention of ASH, ALF, and non-alcoholic steatohepatitis (NASH). Those experiments were completed in various rat and baboon models of ASH, ALF, and NASH.  In the study of antioxidant mechanisms of DLPC and SAMe, our published results showed that these antioxidants can diminish generation ofTNFaby Kupffer cells treated with LPS or / menadione. These antioxidants also diminished collagen formation by HSCs isolated from alcohol-fed rat livers and from LX2, a human HSC cell line. Overall, DLPC and SAMe treatment resulted in diminished liver damage in alcohol-fed rats and baboons compared to control. Further investigations demonstrated that oxidative stress mediated PI3K-MAPK pathways played an important role in the generation of TNF a by Kupffer cells and collagen formation by HSCs. DLPC and SAMe diminished TNF a by Kupffer cells and collagen synthesis by HSCs via lessening intracellular oxidative stress formation.

During my work at University of South Florida, in Tampa, FL, my publication addressed how high saturated fat (HSF) diet diminished the development of alcoholic fatty liver in mice. The HSF diet suppressed the increase in mature hepatic sterol regulatory element binding protein 1 (SREBP-1) and prevented increased mRNA of the SREBP-1-regulated lipogenic enzymes.  Sirtuin 1 (SIRT1), a NAD+-dependent class III histone deacetylase, was upregulated by ethanol administration in mice fed the HSF diet. The HSF diet blocked histone H3 at lysine 9 (lys9) hyperacetylation and attenuated association of acetylated histone H3-Lys9 with the promoters of mitochondrial glycerol-3-phosphate acyltransferase and stearoyl-CoA desaturase 1 in the livers of the ethanol-fed mice. These results suggested that the protective effects of HSF diet against the development of alcoholic liver steatosis might occur via regulation of the hepatic SIRT1-SREBP-1-histone H3 axis, suppressing the expression of genes encoding lipogenic enzymes and slowing the synthesis of hepatic fatty acids. 

2. In addition to the contributions described above, with a team of collaborators, I directly contributed my experiences into ALD studies by investigating (1) the role of Janus kinase-phosphatidylinositol 3-kinase-Akt (JAKs-PI3K-Akt) pathway in leptin-induced collagen type I in a human HSC cell line, LX-2, and (2) pharmaceutical Flavonoids against alcoholic fatty liver in rats associated with down-regulation of adipose differentiation-related protein expression. I also collaborated with other labs by contributions of my experiences in oxidative stress-mediated tissue injuries to studies of triterpene acids of Eriobotrya japonica (Thunb.) Lindl. Leaf against macrophage producing  oxidative stress-mediated  tissue injuries resulting in  two publications  (not listed) and oxidative stress-mediated tissue injuries in the cardiovascular lab at Mount Sinai, NYC resulting in one publication.

3. During my busy residency clinical training, I actively submitted applications for two grants: (1) The RSNA resident research grant, in which a combination of my previous ALD study experiences with my imaging training generated a method of noninvasive molecular imaging in the diagnosis of early stage ALF; and (2) the University of Maryland innovative research grant. I was awarded these two grants. This financial support initiated my academic career development. In addition, I collaborated with other investigators to conduct an NIH-supported retrospective clinical project on the prevalence of brown adipose tissue (BAT) activity on FDG PET/CT in patients with breast cancer. BAT has been proposed to play a key role in breast cancer progression. The study data demonstrated that prevalence of BAT was 3-fold greater than in age- and body weight-matched patients with other solid tumor malignancies; this difference is particularly striking among younger women aged < =55. The retrospective clinical data provided support to pursue prospective clinical and translational studies to further define the role of BAT in breast cancer development and progression.

4. After completing my residency. I am appointed as a physician and scientist in the same Department of Diagnostic Radiology and Nuclear Medicine. I work hard in my research project and collaborate with Dr. Su Xu, an expert in small animal imaging of MR and senior MR scholar at the same department and Dr. Jiabei Wang, an expert and senior scholar in substance abuse-related NDF research in the School of Pharmacy at the same campus. I discovered a lack of research on the progressive changes of NDF in animals from early stage ALD to late stage ALD. Since I have animal models of early to late stage ALD available, I would like to quantify progressive changes of NBCs in specific brain regions in the same models. Our preliminary studies in the late stage ALD demonstrate repeatable findings with significant differences between the two experimental groups. We want to move forward to quantify NBCs in specific brain regions and corresponding behavior changes in early stage ALD from steatosis, steatohepatitis and early stage liver fibrosis. This line of studies will help us to establish reliable and repeatable diagnosis parameters of NBCs in early stage ALD-related NDF in a preclinical setting, then in a clinical setting. These early findings of abnormal NBCs will finally help clinicians to manage those patients early and effectively before irreversible brain damage occurs.

My goal is:

  1. to study the molecular imaging PET/CT and MR in the diagnosis and monitoring treatment response of liver disease and liver cancers.
  2. to collaborate with other investigators in various projects by using molecular imaging techniques including PET/CT and MR.

My lab includes:

  1. a lab for molecular biology with cell isolation and culture from animal tissues in rats and mice with alcoholic fatty liver, alcoholic hepatitis and alcoholic fibrosis. ELISA, Western blotting, PCR, etc.
  2. full access to small animal imaging PET/CT and MR.

Clinical Specialty Details

  • My clinical specialty is nulcear medicine including PET/CT imaging, myocardial imaging, bone scan, thyroid and parathyroid scan, and more.
  • FDG PET/CT imaging for staging, treatment response and restaging of cancers.
  • SPECT imaging for diagnoosis of various diseases in the brain, lungs, heart, liver, kidneys, stomach, GI tract, skeleton, thyroid and parathyroid.
  • Radioation therepy for thyroid and cancers.
  • FDG PET vaibility study for myocardial scarring verusus hibernating but viable myocardium.
  • Rb-82 PET myocardial perfusion study for diagnosis of myocardial ischemia and infarction.

Awards and Affiliations

  • 04/1994–04/1999: Overseas Postgraduate Research Scholarship, Australia
  • 04/1994–04/1999: University of Newcastle Postgraduate Research Scholarship, University of Newcastle, Australia
  • 10/1997: Travel Awards for International Symposium on Alcohol Induced Immunopathology, Louisiana
  • 2012-2013: RSNA resident/fellow research grant winner
  • 05/2013: Roentgen Research Award, RSNA Research and Education Foundation.

Grants and Contracts

Current Ongoing Grants

Research and Innovation Seed Grant of University of Maryland, College Park (UMD) and Baltimore (UMB) campuses

18F-proline PET/CT in the functional diagnosis of early-stage non-alcoholic liver fibrosis in CGI-58 knockout mice.

Cao (PI)

Period: 10/20126/2015

The goal of this project is to study 18F-proline PET/CT in the diagnosis of early-stage liver fibrosis at the HSC level by small animal PET/CT imaging in liver-specific CGI-58 knockout (LivKO) mice. LivKO mice on a standard chow diet displayed relatively rapid formation of microvesicular and macrovesicular panlobular steatosis, and then progressed to advanced non-alcoholic fatty liver disease (NAFLD) stages over time, including lobular inflammation and centrilobular fibrosis via abnormally increased production of oxidative stress, inflammatory mediators TNFa, IL-1, and IL-6, and TGF-b. This model would be useful for study of molecular imaging in the diagnosis and monitoring of the progression of NAFLD.

Chair Foundation of the Department of Diagnostic Radiology and Nuclear Medicine.

Hyperpolarization MRS (HMRS) and 18F-proline PET/CT in the functional diagnosis of early-stage alcoholic/non-alcoholic liver fibrosis in IRAK-1 knockout mice.

Cao (PI)

Period: 08/2014 - 10/2015

The goal of this project is to study MRS in the evaluation of hepatocellular metabolism of alcohol and the quantification of alcohol metabolite acetate within livers in IRAK-1 knockout mice fed with/out alcohol. Those results will be correlated with HSC activation and hepatic collagen accumulation by 18F-proline PET/CT. IRAK-1 knockout mice on Lieber-DeCarli liquid ethanol diets plus treatment with endotoxin, or CCl4 demonstrated reduced formation of steatosis, inflammation, and fibrosis via decreased production of oxidative stress, inflammatory mediators, and TGF-b, indicating the important role of the TLR-IRAK-MAPK pathway in endotoxin-mediated collagen production by HSC.

Completed Research Support

GE Healthcare and Radiology Society of North America (RSNA) Resident Research Award.

18F-proline noninvasive PET/CT imaging in the functional diagnosis of early-stage alcoholic liver fibrosis in BALB/C mice fed with Lieber-DeCarli liquid ethanol diets. Cao (PI)

Period:7/1/2012 - 12/31/2014

The goal of this project was (1) to evaluate the role of proline in collagen synthesis using 3H-labeled proline in an in vitro culture system of HSCs isolated from livers of animals with AS, ASH, early stage alcoholic liver fibrosis (EAF), and late stage alcoholic liver fibrosis (LAF) by using a beta counter technique, (2) to establish 18F-proline in the distribution of critical organs in animals with AS, ASH, EAF, and LAF, and (3) to study the role of 18F-proline PET/CT in the diagnosis of early-stage liver fibrosis at the HSC level in animals with AS, ASH, EAF, and LAF by small animal PET/CT imaging. With the support of the RSNA resident research funding, the PI achieved preliminary results of radiotracer-labeled proline uptake in collagen synthesis using 3H-labeled proline in an in vitro culture system of HSCs isolated from livers of animals with LAF by using a beta counter technique. Our results also displayed significant correlation between incorporation of 3H proline into HSCs and collagen accumulation in in vitro culture medium of HSCs isolated from livers of chow-fed rats, alcohol-fed rats, and in culture medium of LX2, a human HSC cell line. Because 18F proline has been successfully applied for imaging lung fibrosis, these data indicated that 18F proline might be employed for the evaluation for noninvasive imaging of alcoholic liver fibrosis.

Australian Bushel Foundation Award

"Molecular mechanism study of alcoholic liver disease in rats"

(Co-Investigator 100%) PI: Robert Batey

04/1994-05/1999

My doctorate project of the role of intrahepatic T lymphocytes in molecular and pathological

mechanisms of alcoholic hepatitis was completed at the Department of Gastroenterology, John

Hunter Hospital, University of Newcastle, NSW, Australia.

The National Institute on Alcohol Abuse and Alcoholism Grant, AA-11115

"Alcohol abuse and hepatitis C fibrosis"

(Co-Investigator 100%) PI: Charles Lieber, Mount Sinai School of Medicine

05/1999–06/2007

Clinical trial of antioxidants dilinoleoylphosphatidylcholine and s-adenosylmethionine in the revention and therapy of hepatitis C and alcoholic hepatic fibrosis in patients with alcohol abuse and/or hepatitis C. Total Direct Costs: $5,000,000.

The National Institute on Alcohol Abuse and Alcoholism Grant, R01 AT001583-01A1

"Synergistic Nutraceutical Effects of dilinoleoylphosphatidylcholine and s-adenosylmethionine"

(Co-Investigator 100%) PI: Charles Lieber, Mount Sinai School of Medicine

05/1999–06/2007

Laboratory study of antioxidants dilinoleoylphosphatidylcholine and s-adenosylmethionine in the treatment of alcoholic and non-alcoholic (high fat) liver diseases in rats and baboons.

Total Direct Costs: $3,000,000

NIH/NIAAA Grants AA013623 and NIH AA015951

"Mammalian Sirtuin 1 in the protective action of dietary saturated fat against alcoholic fatty liver"

(Co-Investigator 100%) PI: Dr. Min You, University of South Florida

05/1999–06/2007

The Department of Veterans Affairs Grants

"Antioxidants in preventive role of alcoholic liver disease in rats"

(Co-Investigator 100%) PI: Dr. Charles Lieber, Mount Sinai School of Medicine

05/1999–06/2007

The Kingsbridge Research Foundation and the Christopher D. Smithers Foundation Award

"Antioxidants in preventive role of alcoholic liver disease in rats"

(Co-Investigator 100%) PI: Dr. Charles Lieber, Mount Sinai School of Medicine

05/1999–06/2007

These grants were used to study the treatment and prevention of alcoholic liver disease as well as the molecular mechanism of the alcoholic liver disease in Dr. Charles Lieber’s laboratory (New York, NY).

National Science Foundation of China

"The regulation of leptin in the collagen type 1 synthesis via PI3K-MAPK pathway"

Principle Investigator 100%. Anhui Medical University

07/2005-06/2007 - $400,000 RMB

National Institutes of Health/National Cancer Institute grant # CA167268.

"Brown fat activity by FDG PET/CT imaging may be associated with the pathogenesis of breast cancer in female patients with breast cancer"

(Co-Investigator), University of Maryland School of Medicine

09/2010 – 12/2013

Professional Activity

Academic Memberships:

  • 2010–2015:     Member, Radiological Society of North America
  • 2010–2015:     Member, Member, American College ofRadiology
  • 2010–Present: Member, Society of Nuclear Medicine and Molecular Imaging
  • 2010–Present: Member,Brain Imaging Council of SNMMI
  • 2010-Present:  Member, Mid-Eastern Chapter
  • 2013–2016:     Member, American Association for Study of Liver Disease
  • 2014–Present: Member, Research Society on Alcoholism

Editorial Board Member/Reviewer of the Journals

2014-current Board member, Austin Radiology

Austin Publishing Group
47 Hook ST
Altona Meadows
VIC, Melbourne 3028
Tel: +61-386447414
Email: radiology@austinpublishinggroup.net

2014-current Board member, Austin Journal of Nuclear Medicine and Radiotherapy

Austin Publishing Group
3126 Riverside Station Blvd
Secaucus,
New Jersey 07094, USA
Tel: 201-655-707
http://www.austinpublishinggroup.com/nuclear-medicine-radiotherapy
www.austinpublishinggroup.com

2015-current Reviewer, Alcohol and Alcoholism

www.alcalc.oupjournals.org
University of Catholue de Louvain
Biology of Comportment
Tel: +32(0) 10 47 43 84
Fax: +32(0) 10 47 40 94
Email: dewitte@uclouvain.be

2016-current Review Editor for Editorial Board of Signaling

Frontiers in Cell and Developmental Biology
Frontiers Editorial Office
EPFL - Innovation Square, Building I
CH – 1015 Lausanne
Switzerland
Tel +41(0)21 510 17 11
Fax +41 (0)21 510 17 01