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Dr. Gregory  Woods  Md image

Dr. Gregory Woods Md

1126 Suffolk Dr
Richmond IN 47374
765 738-8742
Medical School: University Of Kansas School Of Medicine - 1983
Accepts Medicare: Yes
Participates In eRX: Yes
Participates In PQRS: Yes
Participates In EHR: No
License #: 01065273A
NPI: 1720073778
Taxonomy Codes:
207X00000X 207XX0005X

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Awards & Recognitions

About Us

Practice Philosophy

Conditions

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:20610 Description:Drain/inject joint/bursa Average Price:$209.01 Average Price Allowed
By Medicare:
$66.25
HCPCS Code:72110 Description:X-ray exam of lower spine Average Price:$174.42 Average Price Allowed
By Medicare:
$42.35
HCPCS Code:99215 Description:Office/outpatient visit est Average Price:$245.00 Average Price Allowed
By Medicare:
$133.18
HCPCS Code:73610 Description:X-ray exam of ankle Average Price:$121.40 Average Price Allowed
By Medicare:
$33.64
HCPCS Code:99203 Description:Office/outpatient visit new Average Price:$179.63 Average Price Allowed
By Medicare:
$99.32
HCPCS Code:73510 Description:X-ray exam of hip Average Price:$108.21 Average Price Allowed
By Medicare:
$30.17
HCPCS Code:73560 Description:X-ray exam of knee 1 or 2 Average Price:$105.55 Average Price Allowed
By Medicare:
$28.55
HCPCS Code:73030 Description:X-ray exam of shoulder Average Price:$98.70 Average Price Allowed
By Medicare:
$24.77
HCPCS Code:73562 Description:X-ray exam of knee 3 Average Price:$114.33 Average Price Allowed
By Medicare:
$41.63
HCPCS Code:72170 Description:X-ray exam of pelvis Average Price:$90.50 Average Price Allowed
By Medicare:
$24.13
HCPCS Code:73500 Description:X-ray exam of hip Average Price:$82.92 Average Price Allowed
By Medicare:
$22.93
HCPCS Code:99214 Description:Office/outpatient visit est Average Price:$156.64 Average Price Allowed
By Medicare:
$99.01
HCPCS Code:73565 Description:X-ray exam of knees Average Price:$76.90 Average Price Allowed
By Medicare:
$29.37
HCPCS Code:99213 Description:Office/outpatient visit est Average Price:$103.22 Average Price Allowed
By Medicare:
$66.84
HCPCS Code:99212 Description:Office/outpatient visit est Average Price:$75.13 Average Price Allowed
By Medicare:
$40.11
HCPCS Code:J1040 Description:Methylprednisolone 80 MG inj Average Price:$28.25 Average Price Allowed
By Medicare:
$6.75
HCPCS Code:J3301 Description:Triamcinolone acet inj NOS Average Price:$10.00 Average Price Allowed
By Medicare:
$1.69

HCPCS Code Definitions

99212
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A problem focused history; A problem focused examination; Straightforward medical decision making. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are self limited or minor. Typically, 10 minutes are spent face-to-face with the patient and/or family.
99214
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A detailed history; A detailed examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 25 minutes are spent face-to-face with the patient and/or family.
73560
Radiologic examination, knee; 1 or 2 views
99213
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: An expanded problem focused history; An expanded problem focused examination; Medical decision making of low complexity. Counseling and coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of low to moderate severity. Typically, 15 minutes are spent face-to-face with the patient and/or family.
72110
Radiologic examination, spine, lumbosacral; minimum of 4 views
73510
Radiologic examination, hip, unilateral; complete, minimum of 2 views
20610
Arthrocentesis, aspiration and/or injection; major joint or bursa (eg, shoulder, hip, knee joint, subacromial bursa)
73500
Radiologic examination, hip, unilateral; 1 view
72170
Radiologic examination, pelvis; 1 or 2 views
73030
Radiologic examination, shoulder; complete, minimum of 2 views
J3301
Injection, triamcinolone acetonide, not otherwise specified, 10 mg
J1040
Injection, methylprednisolone acetate, 80 mg
99215
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A comprehensive history; A comprehensive examination; Medical decision making of high complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 40 minutes are spent face-to-face with the patient and/or family.
99203
Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A detailed history; A detailed examination; Medical decision making of low complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate severity. Typically, 30 minutes are spent face-to-face with the patient and/or family.
73610
Radiologic examination, ankle; complete, minimum of 3 views
73565
Radiologic examination, knee; both knees, standing, anteroposterior
73562
Radiologic examination, knee; 3 views

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

NPI
Doctor Name
Specialty
Count
1982785309
Internal Medicine
735
1427015114
Diagnostic Radiology
429
1790768406
Family Practice
370
1013954304
Diagnostic Radiology
369
1124001458
Family Practice
352
1063405371
Orthopedic Surgery
352
1851357883
Diagnostic Radiology
329
1669406807
Anesthesiology
327
1568428217
Hematology/Oncology
272
1417010513
Diagnostic Radiology
244
*These referrals represent the top 10 that Dr. Woods has made to other doctors

Publications

A second transmissible cancer in Tasmanian devils. - Proceedings of the National Academy of Sciences of the United States of America
Clonally transmissible cancers are somatic cell lineages that are spread between individuals via the transfer of living cancer cells. There are only three known naturally occurring transmissible cancers, and these affect dogs, soft-shell clams, and Tasmanian devils, respectively. The Tasmanian devil transmissible facial cancer was first observed in 1996, and is threatening its host species with extinction. Until now, this disease has been consistently associated with a single aneuploid cancer cell lineage that we refer to as DFT1. Here we describe a second transmissible cancer, DFT2, in five devils located in southern Tasmania in 2014 and 2015. DFT2 causes facial tumors that are grossly indistinguishable but histologically distinct from those caused by DFT1. DFT2 bears no detectable cytogenetic similarity to DFT1 and carries a Y chromosome, which contrasts with the female origin of DFT1. DFT2 shows different alleles to both its hosts and DFT1 at microsatellite, structural variant, and major histocompatibility complex (MHC) loci, confirming that it is a second cancer that can be transmitted between devils as an allogeneic, MHC-discordant graft. These findings indicate that Tasmanian devils have spawned at least two distinct transmissible cancer lineages and suggest that transmissible cancers may arise more frequently in nature than previously considered. The discovery of DFT2 presents important challenges for the conservation of Tasmanian devils and raises the possibility that this species is particularly prone to the emergence of transmissible cancers. More generally, our findings highlight the potential for cancer cells to depart from their hosts and become dangerous transmissible pathogens.
Fucoidan Suppresses the Growth of Human Acute Promyelocytic Leukemia Cells In Vitro and In Vivo. - Journal of cellular physiology
Fucoidan, a natural component of seaweeds, is reported to have immunomodulatory and anti-tumor effects. The mechanisms underpinning these activities remain poorly understood. In this study, the cytotoxicity and anti-tumor activities of fucoidan were investigated in acute myeloid leukemia (AML) cells. The human AML cell lines NB4, KG1a, HL60, and K562 were treated with fucoidan and cell cycle, cell proliferation, and expression of apoptotic pathways molecules were analyzed. Fucoidan suppressed the proliferation and induced apoptosis through the intrinsic and extrinsic pathways in the acute promyelocytic leukemia (APL) cell lines NB4 and HL60, but not in KG1a and K562 cells. In NB4 cells, apoptosis was caspase-dependent as it was significantly attenuated by pre-treatment with a pan-caspase inhibitor. P21/WAF1/CIP1 was significantly up-regulated leading to cell cycle arrest. Fucoidan decreased the activation of ERK1/2 and down-regulated the activation of AKT through hypo-phosphorylation of Thr(308) residue but not Ser(473). In vivo, a xenograft model using the NB4 cells was employed. Mice were fed with fucoidan and tumor growth was measured following inoculation with NB4 cells. Subsequently, splenic natural killer (NK) cell cytotoxic activity was also examined. Oral doses of fucoidan significantly delayed tumor growth in the xenograft model and increased cytolytic activity of NK cells. Taken together, these data suggest that the selective inhibitory effect of fucoidan on APL cells and its protective effect against APL development in mice warrant further investigation of fucoidan as a useful agent in treatment of certain types of leukemia. J. Cell. Physiol. 231: 688-697, 2016. © 2015 Wiley Periodicals, Inc.© 2015 Wiley Periodicals, Inc.
Toll-like receptor signaling is functional in immune cells of the endangered Tasmanian devil. - Developmental and comparative immunology
Devil facial tumour disease (DFTD) is a fatally transmissible cancer that threatens the Tasmanian devil population. As Tasmanian devils do not produce an immune response against DFTD cells, an effective vaccine will require a strong adjuvant. Activation of innate immune system cells through toll-like receptors (TLRs) could provide this stimulation. It is unknown whether marsupials, including Tasmanian devils, express functional TLRs. We isolated RNA from peripheral blood mononuclear cells and, with PCR, detected transcripts for TLRs 2, 3, 4, 5, 6, 7, 8, 9, 10 and 13. Stimulation of the mononuclear cells with agonists to these TLRs increased the expression of downstream TLR signaling products (IL1α, IL6, IL12A and IFNβ). Our data provide the first evidence that TLR signaling is functional in the mononuclear cells of the Tasmanian devil. Future DFTD vaccination trials will incorporate TLR agonists to enhance the immune response against DFTD.Crown Copyright © 2015. Published by Elsevier Ltd. All rights reserved.
Immunology of a Transmissible Cancer Spreading among Tasmanian Devils. - Journal of immunology (Baltimore, Md. : 1950)
Devil facial tumor disease (DFTD) is a transmissible cancer that has killed most of the Tasmanian devil (Sarcophilus harrissii) population. Since the first case appeared in the mid-1990s, it has spread relentlessly across the Tasmanian devil's geographic range. As Tasmanian devils only exist in Tasmania, Australia, DFTD has the potential to cause extinction of this species. The origin of DFTD was a Schwann cell from a female devil. The disease is transmitted when devils bite each other around the facial areas, a behavior synonymous with this species. Every devil that is 'infected' with DFTD dies from the cancer. Once the DFTD cells have been transmitted, they appear to develop into a cancer without inducing an immune response. The DFTD cancer cells avoid allogeneic recognition because they do not express MHC class I molecules on the cell surface. A reduced genetic diversity and the production of immunosuppressive cytokines may also contribute.Copyright © 2015 by The American Association of Immunologists, Inc.
Fucoidan and cancer: a multifunctional molecule with anti-tumor potential. - Marine drugs
There is a wide variety of cancer types yet, all share some common cellular and molecular behaviors. Most of the chemotherapeutic agents used in cancer treatment are designed to target common deregulated mechanisms within cancer cells. Many healthy tissues are also affected by the cytotoxic effects of these chemical agents. Fucoidan, a natural component of brown seaweed, has anti-cancer activity against various cancer types by targeting key apoptotic molecules. It also has beneficial effects as it can protect against toxicity associated with chemotherapeutic agents and radiation. Thus the synergistic effect of fucoidan with current anti-cancer agents is of considerable interest. This review discusses the mechanisms by which fucoidan retards tumor development, eradicates tumor cells and synergizes with anti-cancer chemotherapeutic agents. Challenges to the development of fucoidan as an anti-cancer agent will also be discussed.
Mouse Model of Devil Facial Tumour Disease Establishes That an Effective Immune Response Can be Generated Against the Cancer Cells. - Frontiers in immunology
The largest carnivorous marsupial in Australia, the Tasmanian devil (Sarcophilus harrisii) is facing extinction in the wild due to a transmissible cancer known as Devil Facial Tumour Disease (DFTD). DFTD is a clonal cell line transmitted from host to host with 100% mortality and no known immunity. While it was first considered that low genetic diversity of the population of devils enabled the allograft transmission of DFTD recent evidence reveals that genetically diverse animals succumb to the disease. The lack of an immune response against the DFTD tumor cells may be due to a lack of immunogenicity of the tumor cells. This could facilitate transmission between devils. To test immunogenicity, mice were injected with viable DFTD cells and anti-DFTD immune responses analyzed. A range of antibody isotypes against DFTD cells was detected, indicating that as DFTD cells can induce an immune response they are immunogenic. This was supported by cytokine production, when splenocytes from mice injected with DFTD cells were cultured in vitro with DFTD cells and the supernatant analyzed. There was a significant production of IFN-γ and TNF-α following the first injection with DFTD cells and a significant production of IL-6 and IL-10 following the second injection. Splenocytes from naïve or immunized mice killed DFTD cells in in vitro cytotoxicity assays. Thus, they are also targets for immunological destruction. We conclude that as an immune response can be generated against DFTD cells they would be suitable targets for a vaccine.
Identification of dendritic cells, B cell and T cell subsets in Tasmanian devil lymphoid tissue; evidence for poor immune cell infiltration into devil facial tumors. - Anatomical record (Hoboken, N.J. : 2007)
The Tasmanian devil is under threat of extinction due to the transmissible devil facial tumor disease (DFTD). This fatal tumor is an allograft that does not induce an immune response, raising questions about the activity of Tasmanian devil immune cells. T and B cell analysis has been limited by a lack of antibodies, hence the need to produce such reagents. Amino acid sequence analysis revealed that CD4, CD8, IgM, and IgG were closely related to other marsupials. Monoclonal antibodies were produced against CD4, CD8, IgM, and IgG by generating bacterial fusion proteins. These, and commercial antibodies against CD1a and CD83, identified T cells, B cells and dendritic cells by immunohistochemistry. CD4(+) and CD8(+) T cells were identified in pouch young thymus, adult lymph nodes, spleen, bronchus- and gut-associated lymphoid tissue. Their anatomical distribution was characteristic of mammalian lymphoid tissues with more CD4(+) than CD8(+) cells in lymph nodes and splenic white pulp. IgM(+) and IgG(+) B cells were identified in adult lymph nodes, spleen, bronchus-associated lymphoid tissue and gut-associated lymphoid tissue, with more IgM(+) than IgG(+) cells. Dendritic cells were identified in lymph node, spleen and skin. This distribution is consistent with eutherian mammals and other marsupials, indicating they have the immune cell subsets for an anti-tumor immunity. Devil facial tumor disease tumors contained more CD8(+) than CD4(+) cells, but in low numbers. There were also low numbers of CD1a(+) and MHC class II(+) cells, but no CD83(+) IgM(+) or IgG(+) B cells, consistent with poor immune cell infiltration.© 2014 The Authors. The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology Published by Wiley Periodicals, Inc.
Flexion-distraction injuries of the thoracolumbar spine: open fusion versus percutaneous pedicle screw fixation. - Neurosurgical focus
Flexion-distraction injuries occur due to distractive forces causing disruption of the posterior and middle spinal columns. These fractures classically consist of a fracture line through the posterior bony elements; involvement of the posterior ligamentous complex is, however, common. Surgical treatment is often required for these unstable injuries to avoid neurological deterioration and posttraumatic kyphosis, and the surgery traditionally consists of an open posterior approach with instrumented fusion. Percutaneous pedicle screw fixation for these injuries, with the goal of minimal tissue disruption and preservation of normal anatomy while achieving adequate stabilization, has recently been reported in the literature, but to date, a direct comparative study comparing open and percutaneous fixation has not been reported. The authors report their experience treating these fractures with both techniques and review the available literature.Patients with flexion-distraction injury who were treated between May 2003 and March 2013 were prospectively followed. American Spinal Injury Association scores and degree of kyphotic angulation were recorded at admission, discharge, and follow-up. Data regarding intraoperative blood loss and operative time were obtained from a chart review. Patients treated with open versus minimally invasive procedures were compared.The authors identified 39 patients who suffered flexion-distraction injuries and were treated at their institution during the specified period; one of these patients declined surgery. All had injury to the posterior ligamentous complex. Open surgical procedures with pedicle screw fixation and posterolateral fusion were performed in 27 patients, while 11 patients underwent minimally invasive pedicle screw placement. Overall, there was improvement in kyphotic angulation at the time of discharge as well as most recent follow-up in both the open surgery and minimally invasive surgery (MIS) groups. The authors found no significant difference in American Spinal Injury Association score or the degree of kyphotic angulation between the MIS and open surgery groups. There was a trend toward shorter operative time for the MIS group, and patients who underwent minimally invasive procedures had significantly less blood loss.Minimally invasive percutaneous pedicle screw fixation appears to have similar efficacy in the treatment of flexion-distraction injuries and it allows for reduced blood loss and tissue damage compared with open surgical techniques. Therefore it should be considered as an option for the treatment of this type of injury.
Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer. - Proceedings of the National Academy of Sciences of the United States of America
Contagious cancers that pass between individuals as an infectious cell line are highly unusual pathogens. Devil facial tumor disease (DFTD) is one such contagious cancer that emerged 16 y ago and is driving the Tasmanian devil to extinction. As both a pathogen and an allograft, DFTD cells should be rejected by the host-immune response, yet DFTD causes 100% mortality among infected devils with no apparent rejection of tumor cells. Why DFTD cells are not rejected has been a question of considerable confusion. Here, we show that DFTD cells do not express cell surface MHC molecules in vitro or in vivo, due to down-regulation of genes essential to the antigen-processing pathway, such as β2-microglobulin and transporters associated with antigen processing. Loss of gene expression is not due to structural mutations, but to regulatory changes including epigenetic deacetylation of histones. Consequently, MHC class I molecules can be restored to the surface of DFTD cells in vitro by using recombinant devil IFN-γ, which is associated with up-regulation of the MHC class II transactivator, a key transcription factor with deacetylase activity. Further, expression of MHC class I molecules by DFTD cells can occur in vivo during lymphocyte infiltration. These results explain why T cells do not target DFTD cells. We propose that MHC-positive or epigenetically modified DFTD cells may provide a vaccine to DFTD. In addition, we suggest that down-regulation of MHC molecules using regulatory mechanisms allows evolvability of transmissible cancers and could affect the evolutionary trajectory of DFTD.
Ultraviolet radiation effects on the proteome of skin cells. - Advances in experimental medicine and biology
Proteomic studies to date have had limited use as an investigative tool in the skin's response to UV radiation. These studies used cell lines and reconstructed skin and have shown evidence of cell injury with oxidative damage and stress induced heat shock proteins. Others changes included altered cytokeratin and cytoskeletal proteins with enhanced expression of TRIM29 as the keratinocytes regenerate. The associated DNA repair requires polη, Rad18/Rad16 and Rev1. In the whole animal these events would be associated with inflammation, remodelling of the epidermis and modulation of the immune response. Longer term changes include ageing and skin cancers such as melanoma, squamous cell carcinoma and basal cell carcinoma. In the future proteomics will be used to explore these important aspects of photobiology. Better characterisation of the proteins involved should lead to a greater understanding of the skin's response to UV radiation.

Map & Directions

1126 Suffolk Dr Richmond, IN 47374
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