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  1. Article ; Online: Providing Outpatient Telehealth Services in the United States: Before and During Coronavirus Disease 2019.

    Brotman, Joshua J / Kotloff, Robert M

    Chest

    2020  Volume 159, Issue 4, Page(s) 1548–1558

    Abstract: Before coronavirus disease 2019 (COVID-19), telehealth evaluation and management (E/M) services were not widely used in the United States and often were restricted to rural areas or locations with poor access to care. Most Medicare beneficiaries could ... ...

    Abstract Before coronavirus disease 2019 (COVID-19), telehealth evaluation and management (E/M) services were not widely used in the United States and often were restricted to rural areas or locations with poor access to care. Most Medicare beneficiaries could not receive telehealth services in their homes. In response to the COVID-19 pandemic, Medicare, Medicaid, and commercial insurers relaxed restrictions on both coverage and reimbursement of telehealth services. These changes, together with the need for social distancing, transformed the delivery of outpatient E/M services through an increase in telehealth use. In some cases, the transition from in-person outpatient care to telehealth occurred overnight. Billing and claim submission for telehealth services is complicated; has changed over the course of the pandemic; and varies with each insurance carrier, making telehealth adoption burdensome. Despite these challenges, telehealth is beneficial for health-care providers and patients. Without additional legislation at the federal and state levels, it is likely that telehealth use will continue to decline after the COVID-19 public health emergency.
    MeSH term(s) Ambulatory Care ; COVID-19 ; Humans ; Medicaid ; Medicare ; Telemedicine ; United States
    Language English
    Publishing date 2020-11-25
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Review
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1016/j.chest.2020.11.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Gene signatures common to allograft rejection are associated with lymphocytic bronchitis.

    Greenland, John R / Wang, Ping / Brotman, Joshua J / Ahuja, Rahul / Chong, Tiffany A / Kleinhenz, Mary Ellen / Leard, Lorriana E / Golden, Jeffrey A / Hays, Steven R / Kukreja, Jasleen / Singer, Jonathan P / Rajalingam, Raja / Jones, Kirk / Laszik, Zoltan G / Trivedi, Neil N / Greenland, Nancy Y / Blanc, Paul D

    Clinical transplantation

    2019  Volume 33, Issue 5, Page(s) e13515

    Abstract: Lymphocytic bronchitis (LB) precedes chronic lung allograft dysfunction. The relationships of LB (classified here as Endobronchial or E-grade rejection) to small airway (A- and B-grade) pathologies are unclear. We hypothesized that gene signatures common ...

    Abstract Lymphocytic bronchitis (LB) precedes chronic lung allograft dysfunction. The relationships of LB (classified here as Endobronchial or E-grade rejection) to small airway (A- and B-grade) pathologies are unclear. We hypothesized that gene signatures common to allograft rejection would be present in LB. We studied LB in two partially overlapping lung transplant recipient cohorts: Cohort 1 included large airway brushes (6 LB cases and 18 post-transplant referents). Differential expression using DESeq2 was used for pathway analysis and to define an LB-associated metagene. In Cohort 2, eight biopsies for each pathology subtype were matched with pathology-free biopsies from the same subject (totaling 48 samples from 24 subjects). These biopsies were analyzed by multiplexed digital counting of immune transcripts. Metagene score differences were compared by paired t tests. Compared to referents in Cohort 1, LB demonstrated upregulation of allograft rejection pathways, and upregulated genes in these cases characterized an LB-associated metagene. We observed statistically increased expression in Cohort 2 for this LB-associated metagene and four other established allograft rejection metagenes in rejection vs paired non-rejection biopsies for both E-grade and A-grade subtypes, but not B-grade pathology. Gene expression-based categorization of allograft rejection may prove useful in monitoring lung allograft health.
    MeSH term(s) Adult ; Allografts ; Biomarkers/analysis ; Bronchitis/diagnosis ; Bronchitis/etiology ; Bronchitis/pathology ; Female ; Follow-Up Studies ; Gene Expression Profiling ; Graft Rejection/diagnosis ; Graft Rejection/etiology ; Graft Rejection/pathology ; Graft Survival ; Humans ; Lung Transplantation/adverse effects ; Lymphocytes/metabolism ; Lymphocytes/pathology ; Male ; Middle Aged ; Prognosis ; Prospective Studies
    Chemical Substances Biomarkers
    Language English
    Publishing date 2019-03-27
    Publishing country Denmark
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 639001-8
    ISSN 1399-0012 ; 0902-0063
    ISSN (online) 1399-0012
    ISSN 0902-0063
    DOI 10.1111/ctr.13515
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: CXCR3 enhances a T-cell-dependent epidermal proliferative response and promotes skin tumorigenesis.

    Winkler, Ashley E / Brotman, Joshua J / Pittman, Meredith E / Judd, Nancy P / Lewis, James S / Schreiber, Robert D / Uppaluri, Ravindra

    Cancer research

    2011  Volume 71, Issue 17, Page(s) 5707–5716

    Abstract: The chemokine receptor CXCR3 has been proposed to play a critical role in host antitumor responses. In this study, we defined CXCR3-expressing immune cell infiltration in human skin squamous cell carcinomas and then used CXCR3-deficient mice to assess ... ...

    Abstract The chemokine receptor CXCR3 has been proposed to play a critical role in host antitumor responses. In this study, we defined CXCR3-expressing immune cell infiltration in human skin squamous cell carcinomas and then used CXCR3-deficient mice to assess the contribution of CXCR3 to skin tumorigenesis. Our studies employed two established protocols for chemical skin carcinogenesis [methylcholanthrene (MCA) or 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) models]. CXCR3 deletion did not affect tumor development in the MCA model; however, CXCR3 was important in the DMBA/TPA model where gene deletion reduced the incidence of skin tumors. This decreased incidence of skin tumors did not reflect differences in epidermal development but rather was associated with reduced epidermal thickness and proliferation in CXCR3(-/-) mice, implicating the CXCR3 pathway in DMBA/TPA-induced epidermal inflammation and proliferation. Notably, CXCR3 expressed in CD4(+) and CD8(+) T cells was found to be important for enhanced epidermal proliferation. Specifically, CXCR3-deficient mice reconstituted with T cells isolated from wild-type mice treated with DMBA/TPA restored wild-type levels of epidermal proliferation in the mutant mice. Taken together, our findings establish that CXCR3 promotes epidermal tumorigenesis likely through a T-cell-dependent induction of keratinocyte proliferation.
    MeSH term(s) 9,10-Dimethyl-1,2-benzanthracene/pharmacology ; Animals ; Carcinoma, Squamous Cell/chemically induced ; Carcinoma, Squamous Cell/immunology ; Carcinoma, Squamous Cell/pathology ; Cell Proliferation ; Cell Transformation, Neoplastic/chemically induced ; Cell Transformation, Neoplastic/immunology ; Cell Transformation, Neoplastic/pathology ; Epidermis/drug effects ; Epidermis/immunology ; Epidermis/pathology ; Humans ; Lymphocytes, Tumor-Infiltrating/immunology ; Methylcholanthrene/pharmacology ; Mice ; Mice, Mutant Strains ; Receptors, CXCR3/genetics ; Receptors, CXCR3/immunology ; Skin Neoplasms/chemically induced ; Skin Neoplasms/immunology ; Skin Neoplasms/pathology ; T-Lymphocytes/immunology ; Tetradecanoylphorbol Acetate/pharmacology
    Chemical Substances Cxcr3 protein, mouse ; Receptors, CXCR3 ; Methylcholanthrene (56-49-5) ; 9,10-Dimethyl-1,2-benzanthracene (57-97-6) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
    Language English
    Publishing date 2011-07-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-11-0907
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Adipose tissue 12/15 lipoxygenase pathway in human obesity and diabetes.

    Lieb, David C / Brotman, Joshua J / Hatcher, Margaret A / Aye, Myo S / Cole, Banumathi K / Haynes, Bronson A / Wohlgemuth, Stephen D / Fontana, Mark A / Beydoun, Hind / Nadler, Jerry L / Dobrian, Anca D

    The Journal of clinical endocrinology and metabolism

    2014  Volume 99, Issue 9, Page(s) E1713–20

    Abstract: Context: Visceral adipose tissue (VAT) is a key contributor to chronic inflammation in obesity. The 12/15-lipoxygenase pathway (ALOX) is present in adipose tissue (AT) and leads to inflammatory cascades that are causal for the onset of insulin ... ...

    Abstract Context: Visceral adipose tissue (VAT) is a key contributor to chronic inflammation in obesity. The 12/15-lipoxygenase pathway (ALOX) is present in adipose tissue (AT) and leads to inflammatory cascades that are causal for the onset of insulin resistance in rodent models of obesity.
    Objective: The pathophysiology of the ALOX 12/15 pathway in human AT is unknown. We characterized the ALOX pathway in different AT depots in obese humans with or without type 2 diabetes (T2D).
    Design: This study includes a cross-sectional cohort of 46 morbidly obese (body mass index >39 kg/m(2)) nondiabetic (n = 25) and T2D (n = 21) subjects.
    Setting: This study was conducted at Eastern Virginia Medical School (Norfolk, Virginia) in collaboration with Sentara Metabolic and Weight Loss Surgery Center (Sentara Medical Group, Norfolk, Virginia).
    Patients: Twenty-five obese (body mass index 44.8 ± 4.4 kg/m(2)) nondiabetic (hemoglobin A1c 5.83% ± 0.27%) and 21 obese (43.4 ± 4.1 kg/m(2)) and T2D (hemoglobin A1c 7.66% ± 1.22%) subjects were included in the study. The subjects were age matched and both groups had a bias toward female gender.
    Main outcomes and measures: Expression of ALOX isoforms along with fatty acid substrates and downstream lipid metabolites were measured. Correlations with depot-specific inflammatory markers were also established.
    Results: ALOX 12 expression and its metabolite 12(S)-hydroxyeicosatetraenoic acid were significantly increased in the VAT of T2D subjects. ALOX 15A was exclusively expressed in VAT in both groups. ALOX 12 expression positively correlated with expression of inflammatory genes IL-6, IL-12a, CXCL10, and lipocalin-2.
    Conclusions: ALOX 12 may have a critical role in regulation of inflammation in VAT in obesity and T2D. Selective ALOX 12 inhibitors may constitute a new approach to limit AT inflammation in human obesity.
    MeSH term(s) Adolescent ; Adult ; Aged ; Arachidonate 12-Lipoxygenase/genetics ; Arachidonate 12-Lipoxygenase/metabolism ; Arachidonate 15-Lipoxygenase/genetics ; Arachidonate 15-Lipoxygenase/metabolism ; Biomarkers/metabolism ; Cross-Sectional Studies ; Diabetes Mellitus, Type 2/enzymology ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/immunology ; Fatty Acids/metabolism ; Female ; Gene Expression Regulation, Enzymologic/immunology ; Glycated Hemoglobin A/metabolism ; Humans ; Inflammation/enzymology ; Inflammation/genetics ; Inflammation/immunology ; Intra-Abdominal Fat/enzymology ; Intra-Abdominal Fat/immunology ; Lipid Metabolism/genetics ; Lipid Metabolism/immunology ; Male ; Middle Aged ; Obesity, Morbid/enzymology ; Obesity, Morbid/genetics ; Obesity, Morbid/immunology ; Young Adult
    Chemical Substances Biomarkers ; Fatty Acids ; Glycated Hemoglobin A ; hemoglobin A1c protein, human ; Arachidonate 12-Lipoxygenase (EC 1.13.11.31) ; ALOX12 protein, human (EC 1.13.11.31.) ; ALOX15 protein, human (EC 1.13.11.33) ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33)
    Language English
    Publishing date 2014-06-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/jc.2013-4461
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: ERK1/2 regulation of CD44 modulates oral cancer aggressiveness.

    Judd, Nancy P / Winkler, Ashley E / Murillo-Sauca, Oihana / Brotman, Joshua J / Law, Jonathan H / Lewis, James S / Dunn, Gavin P / Bui, Jack D / Sunwoo, John B / Uppaluri, Ravindra

    Cancer research

    2011  Volume 72, Issue 1, Page(s) 365–374

    Abstract: Carcinogen-induced oral cavity squamous cell carcinoma (OSCC) incurs significant morbidity and mortality and constitutes a global health challenge. To gain further insight into this disease, we generated cell line models from 7,12-dimethylbenz(a) ... ...

    Abstract Carcinogen-induced oral cavity squamous cell carcinoma (OSCC) incurs significant morbidity and mortality and constitutes a global health challenge. To gain further insight into this disease, we generated cell line models from 7,12-dimethylbenz(a)anthracene-induced murine primary OSCC capable of tumor formation upon transplantation into immunocompetent wild-type mice. Whereas several cell lines grew rapidly and were capable of metastasis, some grew slowly and did not metastasize. Aggressively growing cell lines displayed ERK1/2 activation, which stimulated expression of CD44, a marker associated with epithelial to mesenchymal transition and putative cancer stem cells. MEK (MAP/ERK kinase) inhibition upstream of ERK1/2 decreased CD44 expression and promoter activity and reduced cell migration and invasion. Conversely, MEK1 activation enhanced CD44 expression and promoter activity, whereas CD44 attenuation reduced in vitro migration and in vivo tumor formation. Extending these findings to freshly resected human OSCC, we confirmed a strict relationship between ERK1/2 phosphorylation and CD44 expression. In summary, our findings identify CD44 as a critical target of ERK1/2 in promoting tumor aggressiveness and offer a preclinical proof-of-concept to target this pathway as a strategy to treat head and neck cancer.
    MeSH term(s) Animals ; Carcinoma, Squamous Cell/enzymology ; Carcinoma, Squamous Cell/immunology ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Hyaluronan Receptors/immunology ; Lymphatic Metastasis ; Mice ; Mice, Inbred C57BL ; Mouth Neoplasms/enzymology ; Mouth Neoplasms/immunology ; Mouth Neoplasms/pathology
    Chemical Substances Hyaluronan Receptors ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2011-11-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-11-1831
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Prolongation of cardiac and islet allograft survival by a blocking hamster anti-mouse CXCR3 monoclonal antibody.

    Uppaluri, Ravindra / Sheehan, Kathleen C F / Wang, Liqing / Bui, Jack D / Brotman, Joshua J / Lu, Bao / Gerard, Craig / Hancock, Wayne W / Schreiber, Robert D

    Transplantation

    2008  Volume 86, Issue 1, Page(s) 137–147

    Abstract: Background: Acute allograft rejection requires a multifaceted immune response involving trafficking of immune cells into the transplant and expression of effector cell functions leading to graft destruction. The chemokine receptor CXCR3 and its ligands, ...

    Abstract Background: Acute allograft rejection requires a multifaceted immune response involving trafficking of immune cells into the transplant and expression of effector cell functions leading to graft destruction. The chemokine receptor CXCR3 and its ligands, CXCL9, CXCL10 and CXCL11, constitute an important pathway for effector cell recruitment posttransplant. However, analysis of CXCR3 expression and function has been hampered by a general lack of availability of a neutralizing anti-CXCR3 monoclonal antibody (mAb) for use in experimental models.
    Methods: We report the generation, characterization, and use of CXCR3-173, a new hamster mAb specific for mouse CXCR3 that recognizes CXCR3 on cells from wild-type but not CXCR3-/- mice.
    Results: Using CXCR3-173 mAb, we demonstrate CXCR3 expression on primary memory phenotype CD4+ and CD8+ T cells, naturally occurring CD4+CD25+ Foxp3+ regulatory T cells, natural killer T cells, and approximately 25% of NK cells. CXCR3-173 blocked chemotaxis in vitro in response to CXCL10 or CXCL11 but not CXCL9. When injected into mice, this mAb significantly prolonged both cardiac and islet allograft survival. When combined with a subtherapeutic regimen of rapamycin, CXCR3-173 mAb induced long-term (>100 day) survival of cardiac and islet allografts. The in vivo effects of CXCR3-173 mAb were not associated with effector lymphocyte depletion.
    Conclusion: These data highlight the utility of CXCR3-173 mAb in developing immunotherapeutic approaches to inhibit transplant rejection and potentially other immune-mediated diseases in murine models.
    MeSH term(s) Animals ; Antibodies, Monoclonal/pharmacology ; CD4-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/drug effects ; Cell Line ; Chemotaxis, Leukocyte/drug effects ; Cricetinae ; Cytokines/genetics ; Cytokines/metabolism ; Drug Therapy, Combination ; Graft Rejection/immunology ; Graft Rejection/pathology ; Graft Rejection/prevention & control ; Graft Survival/drug effects ; Heart Transplantation ; Immunosuppressive Agents/pharmacology ; Islets of Langerhans Transplantation ; Killer Cells, Natural/drug effects ; Lymphocyte Subsets/drug effects ; Lymphocyte Subsets/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Animal ; RNA, Messenger/metabolism ; Receptors, CXCR3/genetics ; Receptors, CXCR3/immunology ; Sirolimus/pharmacology ; T-Lymphocytes, Regulatory/drug effects ; Time Factors ; Transplantation, Homologous
    Chemical Substances Antibodies, Monoclonal ; Cxcr3 protein, mouse ; Cytokines ; Immunosuppressive Agents ; RNA, Messenger ; Receptors, CXCR3 ; Sirolimus (W36ZG6FT64)
    Language English
    Publishing date 2008-07-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 208424-7
    ISSN 1534-6080 ; 0041-1337
    ISSN (online) 1534-6080
    ISSN 0041-1337
    DOI 10.1097/TP.0b013e31817b8e4b
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