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Dr. Dong  Chen  Md Phd Ms image

Dr. Dong Chen Md Phd Ms

200 1St St Sw
Rochester MN 55905
507 842-2511
Medical School: Other - 1992
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: Yes
Participates In EHR: No
License #:
NPI: 1033174370
Taxonomy Codes:
207ZP0105X

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Awards & Recognitions

About Us

Practice Philosophy

Conditions

Dr. Dong Chen is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:88187 Description:Flowcytometry/read 2-8 Average Price:$70.98 Average Price Allowed
By Medicare:
$61.72
HCPCS Code:85097 Description:Bone marrow interpretation Average Price:$49.31 Average Price Allowed
By Medicare:
$42.96
HCPCS Code:88342 Description:Immunohistochemistry Average Price:$43.82 Average Price Allowed
By Medicare:
$38.23
HCPCS Code:88305 Description:Tissue exam by pathologist Average Price:$39.17 Average Price Allowed
By Medicare:
$34.16
HCPCS Code:88319 Description:Enzyme histochemistry Average Price:$27.85 Average Price Allowed
By Medicare:
$24.28
HCPCS Code:85060 Description:Blood smear interpretation Average Price:$24.48 Average Price Allowed
By Medicare:
$21.37
HCPCS Code:88311 Description:Decalcify tissue Average Price:$12.74 Average Price Allowed
By Medicare:
$11.12
HCPCS Code:88313 Description:Special stains group 2 Average Price:$12.37 Average Price Allowed
By Medicare:
$10.80

HCPCS Code Definitions

85060
Blood smear, peripheral, interpretation by physician with written report
88187
Flow cytometry, interpretation; 2 to 8 markers
88305
Level IV - Surgical pathology, gross and microscopic examination Abortion - spontaneous/missed Artery, biopsy Bone marrow, biopsy Bone exostosis Brain/meninges, other than for tumor resection Breast, biopsy, not requiring microscopic evaluation of surgical margins Breast, reduction mammoplasty Bronchus, biopsy Cell block, any source Cervix, biopsy Colon, biopsy Duodenum, biopsy Endocervix, curettings/biopsy Endometrium, curettings/biopsy Esophagus, biopsy Extremity, amputation, traumatic Fallopian tube, biopsy Fallopian tube, ectopic pregnancy Femoral head, fracture Fingers/toes, amputation, non-traumatic Gingiva/oral mucosa, biopsy Heart valve Joint, resection Kidney, biopsy Larynx, biopsy Leiomyoma(s), uterine myomectomy - without uterus Lip, biopsy/wedge resection Lung, transbronchial biopsy Lymph node, biopsy Muscle, biopsy Nasal mucosa, biopsy Nasopharynx/oropharynx, biopsy Nerve, biopsy Odontogenic/dental cyst Omentum, biopsy Ovary with or without tube, non-neoplastic Ovary, biopsy/wedge resection Parathyroid gland Peritoneum, biopsy Pituitary tumor Placenta, other than third trimester Pleura/pericardium - biopsy/tissue Polyp, cervical/endometrial Polyp, colorectal Polyp, stomach/small intestine Prostate, needle biopsy Prostate, TUR Salivary gland, biopsy Sinus, paranasal biopsy Skin, other than cyst/tag/debridement/plastic repair Small intestine, biopsy Soft tissue, other than tumor/mass/lipoma/debridement Spleen Stomach, biopsy Synovium Testis, other than tumor/biopsy/castration Thyroglossal duct/brachial cleft cyst Tongue, biopsy Tonsil, biopsy Trachea, biopsy Ureter, biopsy Urethra, biopsy Urinary bladder, biopsy Uterus, with or without tubes and ovaries, for prolapse Vagina, biopsy Vulva/labia, biopsy
88311
Decalcification procedure (List separately in addition to code for surgical pathology examination)
88313
Special stain including interpretation and report; Group II, all other (eg, iron, trichrome), except stain for microorganisms, stains for enzyme constituents, or immunocytochemistry and immunohistochemistry
88319
Special stain including interpretation and report; Group III, for enzyme constituents
88342
Immunohistochemistry or immunocytochemistry, each separately identifiable antibody per block, cytologic preparation, or hematologic smear; first separately identifiable antibody per slide
85097
Bone marrow, smear interpretation

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

NPI
Doctor Name
Specialty
Count
1598732877
Hematology
254
1891832630
Hematology
167
1215901301
Cardiac Electrophysiology
142
1528044542
Medical Oncology
137
1104802347
Cardiovascular Disease (Cardiology)
125
1053399246
Hematology
117
1487671152
Hematology/Oncology
112
1871579672
Hematology/Oncology
102
1730151259
Cardiovascular Disease (Cardiology)
80
1962411231
Internal Medicine
79
*These referrals represent the top 10 that Dr. Chen has made to other doctors

Publications

Controlled self-assembly of a pyrene-based bolaamphiphile by acetate ions: from nanodisks to nanofibers by fluorescence enhancement. - Soft matter
In this paper, a pyrene moiety is incorporated into a bolaamphiphile to form a novel molecule denoted PRB. Above the critical micelle concentration, PRB forms nanodisks in the aqueous solution. The addition of acetate ions induces a morphological change in self-assembled aggregates, which convert into nanofibers with a diameter of several nanometers. More interestingly, along with the morphological change, the fluorescence of the assemblies was enhanced concomitantly, which can be attributed to the binding effect of acetate ions on pyridinium head groups of PRB.
Transplantation of Human Neural Progenitor Cells Expressing IGF-1 Enhances Retinal Ganglion Cell Survival. - PloS one
We have previously characterized human neuronal progenitor cells (hNP) that can adopt a retinal ganglion cell (RGC)-like morphology within the RGC and nerve fiber layers of the retina. In an effort to determine whether hNPs could be used a candidate cells for targeted delivery of neurotrophic factors (NTFs), we evaluated whether hNPs transfected with an vector that expresses IGF-1 in the form of a fusion protein with tdTomato (TD), would increase RGC survival in vitro and confer neuroprotective effects in a mouse model of glaucoma. RGCs co-cultured with hNPIGF-TD cells displayed enhanced survival, and increased neurite extension and branching as compared to hNPTD or untransfected hNP cells. Application of various IGF-1 signaling blockers or IGF-1 receptor antagonists abrogated these effects. In vivo, using a model of glaucoma we showed that IOP elevation led to reductions in retinal RGC count. In this model, evaluation of retinal flatmounts and optic nerve cross sections indicated that only hNPIGF-TD cells effectively reduced RGC death and showed a trend to improve optic nerve axonal loss. RT-PCR analysis of retina lysates over time showed that the neurotrophic effects of IGF-1 were also attributed to down-regulation of inflammatory and to some extent, angiogenic pathways. This study shows that neuronal progenitor cells that hone into the RGC and nerve fiber layers may be used as vehicles for local production and delivery of a desired NTF. Transplantation of hNPIGF-TD cells improves RGC survival in vitro and protects against RGC loss in a rodent model of glaucoma. Our findings have provided experimental evidence and form the basis for applying cell-based strategies for local delivery of NTFs into the retina. Application of cell-based delivery may be extended to other disease conditions beyond glaucoma.
Regulation of Adipose Tissue Inflammation and Insulin Resistance by MAP Kinase Phosphatase 5. - The Journal of biological chemistry
Obesity and metabolic disorders such as insulin resistance and type 2 diabetes have become a major threat to public health globally. The mechanisms that lead to insulin resistance in type 2 diabetes have not been well understood. In this study, we show that mice deficient in MAP kinase phosphatase 5 (MKP5) develop insulin resistance spontaneously at an early stage of life and glucose intolerance at a later age. Increased macrophage infiltration in the WAT of young MKP5-deficient mice correlates with the development of insulin resistance. Glucose intolerance in Mkp5-/- mice is accompanied by significantly increased visceral adipose weight, reduced AKT activation, enhanced p38 activity and increased inflammation in visceral adipose tissue when compared to wild-type (WT) mice. Deficiency of MKP5 resulted in increased inflammatory activation in macrophages. These findings thus demonstrate that MKP5 critically controls inflammation in the adipose tissues and the development of metabolic disorders.Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
Gradual-order enhanced stability: a frozen section of electrospun nanofibers for energy storage. - Nanoscale
A combination of electrospinning and a frozen section has been used to gradually lower the scale of the active materials, thus effectively avoiding nano-reunion, to a certain extent, during electrode fabrication. The as-fabricated electrode-based supercapacitor possesses high electrochemical capacitance and good stability. Our results demonstrate a universal top-down route for the controllable fabrication of homodisperse nanoparticle electrodes for use in high performance electrochemical devices.
[Association of human epicardial adipose tissue volume and inflammatory mediators with atherosclerosis and vulnerable coronary atherosclerotic plaque]. - Zhonghua xin xue guan bing za zhi
To investigate the relation of epicardial adipose tissue volume (EATV) determined by dual-source CT (DSCT) cardiac angiography and EAT-derived inflammatory factors to coronary heart disease (CHD) and vulnerable plaque.A total of 260 patients underwent cardiac computed tomography to evaluate stenosis of coronary artery, and blood samples were obtained from each patient. CHD was confirmed in 180 patients by DSA and CHD was excluded in the remaining 80 patients (NCHD). Vascular remodeling index and plaque vulnerability parameters (fatty volume, fibrous volume and calcification volume and fiber volume) were measured in CHD patients and correlation with EATV was analyzed. Epicardial adipose tissue (EAT) and intrathoracic adipose tissue (TAT) were collected from 40 CHD patients undergoing CABG surgery, and, mRNA and protein expressions of leptin and MMP9 were detected by RT-PCR and Western blot analysis.(1) The EATV was significantly higher in the CHD group than in NCHD group ((121.2 ± 40.6) mm(3) vs. (74.7 ± 18.1) mm(3), P = 0.01). (2) Subgroup analysis of the CHD patients demonstrated that EATV was significantly higher in patients with positive remodeling than in patients without positive remodeling ((97.6 ± 42.0) cm(3) vs. (75.5 ± 25.4) cm(3), P = 0.01). Lipid plaque volume was positively correlated with EATV (r = 0.34, P = 0.002); however, fiber plaque volume was negatively correlated with EATV (r = -0.30, P = 0.008). (3) Logistic regression analysis indicated that EATV was an independent risk factor for positive vascular remodeling (OR = 2.01, 95% CI: 1.30-2.32, P = 0.01). (4) mRNA and protein expression of leptin and MMP9 in EAT was significantly upregulated in 40 CHD patients who received CABG surgery compared to 40 NCHD patients (P < 0.01). However, there was no significant difference (P > 0.05) in mRNA and protein expression of leptin and MMP9 from the SAT between CHD and NCHD patients. (5) In the CHD group, leptin and MMP9 levels in EAT and EATV were positively correlated with lipid plaque volume and fibrous plaque volume (P < 0.05).EATV is an independent risk factors of coronary heart disease and plaque vulnerability; EAT secretion of inflammatory cytokines from CHD patients is significant increased compared to NCHD patients, EAT secretion of inflammatory cytokines are positively correlated with EATV, both of which are determinants affecting vascular remodeling. Reducing EATV might help to attenuate inflammation and plaque vulnerability and reduce the risk of coronary heart disease.
Ultrasensitive SERS detection of trinitrotoluene through capillarity-constructed reversible hot spots based on ZnO-Ag nanorod hybrids. - Nanoscale
A simple and efficient self-approach strategy was used to apply ultrasensitivity and self-revive ZnO-Ag hybrid surface-enhanced Raman scattering (SERS) sensors for the highly sensitive and selective detection of explosive TNT in both solution and vapour conditions. The good ultrasensitive sensing performance is a result of the abundant Raman hot spots, which were spontaneously formed in a reversible way by the self-approaching of flexible ZnO-Ag hybrid nanorods driven by the capillary force of solvent evaporation. Moreover, the enhancement effect was repeatedly renewed by the reconstruction of molecular bridges, which could selectively detect TNT with a lower limit of 4 × 10(-14) M. In addition, TNT vapor was also tested under this sensor, whereby once the ZnO-Ag NRs hybrid substrate was dipped in TNT, this substrate could detect the existence of TNT even in 5 detection cycles via a capillarity-constructed reversible hot spots approach. Compared with other pure Ag-based SERS sensors, this ZnO-Ag hybrid SERS sensor could rapidly self-revive SERS-activity by simple UV light irradiation and could retain stable SERS sensitivity for one month when used for TNT detection. This stable and ultrasensitive SERS substrate demonstrates a new route to eliminate the oxidized inactive problem of traditional Ag-based SERS substrates and suggests promising use in the applications of such hybrids as real-time online sensors for explosives detection.
The differential role of human macrophage in triggering secondary bystander effects after either gamma-ray or carbon beam irradiation. - Cancer letters
The abscopal effect could be an underlying factor in evaluating prognosis of radiotherapy. This study established an in vitro system to examine whether tumor-generated bystander signals could be transmitted by macrophages to further trigger secondary cellular responses after different irradiations, where human lung cancer NCI-H446 cells were irradiated with either γ-rays or carbon ions and co-cultured with human macrophage U937 cells, then these U937 cells were used as a bystander signal transmitter and co-cultured with human bronchial epithelial cells BEAS-2B. Results showed that U937 cells were only activated by γ-irradiated NCI-H446 cells so that the secondary injuries in BEAS-2B cells under carbon ion irradiation were weaker than γ-rays. Both TNF-α and IL-1α were involved in the γ-irradiation induced secondary bystander effect but only TNF-α contributed to the carbon ion induced response. Further assay disclosed that IL-1α but not TNF-α was largely responsible for the activation of macrophages and the formation of micronucleus in BEAS-2B cells. These data suggest that macrophages could transfer secondary bystander signals and play a key role in the secondary bystander effect of photon irradiation, while carbon ion irradiation has conspicuous advantage due to its reduced secondary injury.Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
Interleukin-17B Antagonizes Interleukin-25-Mediated Mucosal Inflammation. - Immunity
The interleukin-17 (IL-17) family of cytokines has emerged as a critical player in inflammatory diseases. Among them, IL-25 has been shown to be important in allergic inflammation and protection against parasitic infection. Here we have demonstrated that IL-17B, a poorly understood cytokine, functions to inhibit IL-25-driven inflammation. IL-17B and IL-25, both binding to the interleukin-17 receptor B (IL-17RB), were upregulated in their expression after acute colonic inflammation. Individual inhibition of these cytokines revealed opposing functions in colon inflammation: IL-25 was pathogenic but IL-17B was protective. Similarly opposing phenotypes were observed in Citrobacter rodentium infection and allergic asthma. Moreover, IL-25 was found to promote IL-6 production from colon epithelial cells, which was inhibited by IL-17B. Therefore, our data demonstrate that IL-17B is an anti-inflammatory cytokine in the IL-17 family.Copyright © 2015 Elsevier Inc. All rights reserved.
The T cell inhibitory molecule BTNL2 is upregulated in mild Plasmodium falciparum infection and is protective during experimental cerebral malaria. - The Journal of infectious diseases
Plasmodium falciparum infection can result in severe disease which is associated with elevated inflammation and vital organ dysfunction; however malaria endemic residents gain protection from lethal outcomes and manifest only mild symptoms during infection. To characterize host responses associated with this more effective antimalarial response, we characterized whole blood transcriptional profiles in Rwandan adults during a mild malaria episode and compared them to a convalescence sample. We observed transcriptional upregulation in many pathways, including Type-I IFN, IFN-γ, complement activation and nitric oxide during malaria infection, which provide benchmarks of mild disease physiology. Transcripts encoding negative regulators of T cell activation such as programmed death ligand 1 (PD-L1), programmed cell death 1 ligand 2 (PD-L2) and the butyrophilin family member BTNL2 were also increased. To support an important functional role for BTNL2 during malaria infection, we studied chimeric mice reconstituted with BTNL2(-/-) or wild type (WT) hematopoietic cells that were inoculated with P. berghei ANKA, a murine model of cerebral malaria. We found that BTNL2(-/-) chimeric mice had a significant loss of survival than WT counterparts. Collectively these data characterize the immune responses associated with mild malaria and uncovers a novel role for BTNL2 in the host response to malaria.© The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
pERK1/2 silencing sensitizes pancreatic cancer BXPC-3 cell to gemcitabine-induced apoptosis via regulating Bax and Bcl-2 expression. - World journal of surgical oncology
Our previous study has demonstrated that knockdown of activated ERK1/2(pERK1/2) sensitizes pancreatic cancer cells to chemotherapeutic drug gemcitabine (Gem) treatment. However, the details of this survival mechanism remain undefined. It has also shown that Bcl-2 confers resistance and Bax sensitizes to gemcitabine-induced apoptosis in pancreatic cancer cells. Furthermore, the extracellular signaling-regulated kinase (ERK) signaling pathway regulates Bcl-2/Bax expression ratio. We therefore tested the hypothesis that pancreatic cancer cells are resistant to gemcitabine and this resistance is due to activation of ERK1/2 and subsequent upregulation of Bcl-2 and downregulation of Bax.Pancreatic cancer cell BXPC-3 was used in the study. The effect of pharmacological inhibition of ERK1/2 on resistance of pancreatic cancer cells to apoptosis induced by treatment with gemcitabine was analyzed. The following methods were utilized: TUNEL and ELISA were used to detect apoptosis. Western blot was used to detect the protein expression.Gemcitabine treatment enhanced the activity of ERK1/2 in the BXPC-3 cells. Inhibition of the ERK1/2 by PD98059 could downregulate Bcl-2 and upregulate Bax and was associated with restoration of sensitivity to gemcitabine in BXPC-3 cells. Depletion of endogenous Bcl-2 expression by specific small interfering RNA transfection significantly increased gemcitabine-induced cell apoptosis. Combined treatment with PD98059 and Bax siRNA transfection could decrease gemcitabine-induced ERK1/2 and Bax activation, which subsequently resulted in decreased apoptosis.The upregulation of ERK1/2-dependent Bcl-2 and downregulation of ERK1/2-dependent Bax can protect human pancreatic cancer cells from gemcitabine-induced apoptosis. Targeting the ERK1/2-Bax/Bcl-2 pathway may in part lead to sensitization of pancreatic cancer to gemcitabine.

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