LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 105

Search options

  1. Article: Dynamic and scalable assessment of the senescence-associated secretory phenotype (SASP).

    Malaquin, Nicolas / Rodier, Francis

    Methods in cell biology

    2022  Volume 181, Page(s) 181–195

    Abstract: Dual-faced cellular senescence is responsible for beneficial biological processes and for age-related pathologies. Senescent cells under stable proliferation arrest develop numerous senescence-associated phenotypes such as the potent pro-inflammatory ... ...

    Abstract Dual-faced cellular senescence is responsible for beneficial biological processes and for age-related pathologies. Senescent cells under stable proliferation arrest develop numerous senescence-associated phenotypes such as the potent pro-inflammatory secretome called the senescence-associated secretory phenotype (SASP). The SASP shapes the senescent microenvironment and influences the biology of adjacent cells, including the modulation of proliferation and migration/invasion, reinforcement/induction of peripheral senescence, and immune cell activity or recruitment. The SASP is a dynamic process with multiple waves of secreted factors described to interlace over a period of many days. Whether the senescence phenotype reaches a mature stable state remains controversial. Overall, the complexity of the context-dependent and timely SASP compositions and its varied microenvironmental impact demonstrate the importance of properly assessing SASP over time. In this chapter, we focus on scalable and dynamic experimental procedures to prepare SASP conditioned medium over time from cells receiving senescence-inducing stimuli. This SASP-containing conditioned medium can be used to assess the composition of the SASP, study SASP-related signaling pathways or evaluate the paracrine microenvironmental impact of senescent cells.
    MeSH term(s) Senescence-Associated Secretory Phenotype ; Culture Media, Conditioned/pharmacology ; Cellular Senescence/genetics ; Cells, Cultured ; Phenotype
    Chemical Substances Culture Media, Conditioned
    Language English
    Publishing date 2022-12-05
    Publishing country United States
    Document type Journal Article
    ISSN 0091-679X
    ISSN 0091-679X
    DOI 10.1016/bs.mcb.2022.10.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Targeted Anti-Cancer Provascular Therapy Using Ultrasound, Microbubbles, and Nitrite to Increase Radiotherapy Efficacy.

    Michon, Simon / Rodier, Francis / Yu, François T H

    Bioconjugate chemistry

    2022  Volume 33, Issue 6, Page(s) 1093–1105

    Abstract: Hypoxia is an important mechanism of resistance to radiation therapy in many human malignancies including prostate cancer. It has been recently shown that ultrasound targeted microbubble cavitation (UTMC) can increase blood perfusion in skeletal muscle ... ...

    Abstract Hypoxia is an important mechanism of resistance to radiation therapy in many human malignancies including prostate cancer. It has been recently shown that ultrasound targeted microbubble cavitation (UTMC) can increase blood perfusion in skeletal muscle by triggering nitric oxide signaling. Interestingly, this effect was amplified with a sodium nitrite coinjection. Since sodium nitrite has been shown to synergize with radiotherapy (RT), we hypothesized that UTMC with a sodium nitrite coinjection could further radiosensitize solid tumors by increasing blood perfusion and thus reduce tumor hypoxia. We evaluated (1) the ability of UTMC with and without nitrite to increase perfusion in muscle (mouse hindlimbs) and human prostate tumors using different pulse lengths and pressure; (2) the efficacy of this approach as a provascular therapy given directly before RT in the human prostate subcutaneous xenografts PC3 tumor model. Using long pulses with various pressures, in muscle, the provascular response following UTMC was strong (6.61 ± 4.41-fold increase in perfusion post-treatment). In tumors, long pulses caused an increase in perfusion (2.42 ± 1.38-fold) at lower mechanical index (MI = 0.25) but not at higher MI (0.375, 0.5, and 0.750) when compared to control (no UTMC). However, when combined with RT, UTMC with long pulses (MI = 0.25) did not improve tumor growth inhibition. With short pulses, in muscle, the provascular response following UTMC (SONOS) + nitrite was strong (13.74 ± 8.60-fold increase in perfusion post-treatment). In tumors, UTMC (SONOS) + nitrite also caused a provascular response (1.94 ± 1.20-fold increase in perfusion post-treatment) that lasted for at least 10 min, but not with nitrite alone. Interestingly, the blunted provascular response observed for long pulses at higher MI without nitrite was reversed with the addition of nitrite. UTMC (SONOS) with and without nitrite caused an increase in perfusion in tumors. The provascular response observed for UTMC (SONOS) + nitrite was confirmed by histology. Finally, there was an improved growth inhibition for the 8 Gy RT dose + nitrite + UTMC group vs 8 Gy RT + nitrite alone. This effect was not significant with mice treated by UTMC + nitrite and receiving doses of 0 or 2 Gy RT. In conclusion, UTMC + nitrite increased blood flow leading to an increased efficacy of higher doses of RT in our tumor model, warranting further study of this strategy.
    MeSH term(s) Animals ; Humans ; Male ; Mice ; Microbubbles ; Muscle, Skeletal/blood supply ; Neoplasms ; Sodium Nitrite/pharmacology ; Sodium Nitrite/therapeutic use ; Ultrasonography
    Chemical Substances Sodium Nitrite (M0KG633D4F)
    Language English
    Publishing date 2022-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1024041-x
    ISSN 1520-4812 ; 1043-1802
    ISSN (online) 1520-4812
    ISSN 1043-1802
    DOI 10.1021/acs.bioconjchem.1c00510
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Detection of the senescence-associated secretory phenotype (SASP).

    Rodier, Francis

    Methods in molecular biology (Clifton, N.J.)

    2013  Volume 965, Page(s) 165–173

    Abstract: Cellular senescence suppresses cancer by eliminating potentially oncogenic cells, participates in tissue repair, contributes to cancer therapy, and promotes organismal aging. Numerous activities of senescent cells depend on the aptitude of these cells to ...

    Abstract Cellular senescence suppresses cancer by eliminating potentially oncogenic cells, participates in tissue repair, contributes to cancer therapy, and promotes organismal aging. Numerous activities of senescent cells depend on the aptitude of these cells to secrete myriads of bioactive molecules, a behavior termed the senescence-associated secretory phenotype (SASP). The SASP supports cell-autonomous functions like the senescence-associated growth arrest, and mediates paracrine interactions between senescent cells and their surrounding microenvironment. The biological functions and the regulation of the SASP are beginning to emerge, and current SASP assessment techniques include the analysis of SASP factors at the mRNA level, the direct measurement of factors inside or outside the cell (i.e., secreted), and the detection of SASP-provoked cellular responses. Here, we focus on a simple approach to collect SASP-conditioned media in order to directly measure secreted SASP factors using sandwich enzyme-linked immunosorbent assay. As an example, we discuss the assessment of the major SASP factor interleukin-6 in senescent human fibroblasts. Supplemental notes are provided to easily adapt this procedure to other SASP factors, change cell types, or scale the techniques for different volumes or high-throughput measurements. These techniques should facilitate the discovery of novel functions and regulators of the SASP.
    MeSH term(s) Cell Culture Techniques ; Cellular Senescence ; Culture Media, Conditioned/chemistry ; Enzyme-Linked Immunosorbent Assay/methods ; Fibroblasts/cytology ; Fibroblasts/secretion ; Humans ; Phenotype
    Chemical Substances Culture Media, Conditioned
    Language English
    Publishing date 2013
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-62703-239-1_10
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: DCBLD1 is associated with the integrin signaling pathway and has prognostic value in non-small cell lung and invasive breast carcinoma.

    Cardin, Guillaume B / Bernard, Monique / Rodier, Francis / Christopoulos, Apostolos

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 12753

    Abstract: Germline single nucleotide polymorphisms in the promoter region of the DCBLD1 gene are associated with non-smoking cases of both non-small cell lung carcinoma (NSCLC) and human papillomavirus-negative head and neck cancer. However the clinical relevance ... ...

    Abstract Germline single nucleotide polymorphisms in the promoter region of the DCBLD1 gene are associated with non-smoking cases of both non-small cell lung carcinoma (NSCLC) and human papillomavirus-negative head and neck cancer. However the clinical relevance and function of DCBLD1 remain unclear. This multicenter retrospective study was designed to evaluate the prognostic value and function of DCBLD1 in the four main solid cancers: NSCLC, invasive breast carcinoma, colorectal adenocarcinoma and prostate adenocarcinoma. We included the following cohorts: GSE81089 NSCLC, METABRIC invasive breast carcinoma, GSE14333 colorectal adenocarcinoma, GSE70770 prostate adenocarcinoma and The Cancer Genome Atlas (TCGA) Firehose Legacy cohorts of all four cancers. DCBLD1 gene expression was associated with a worse overall survival in multivariate analyses for both NSCLC cohorts (TCGA: P = 0.03 and GSE81089: P = 0.04) and both invasive breast carcinoma cohorts (TCGA: P = 0.02 and METABRIC: P < 0.001). Patients with high DCBLD1 expression showed an upregulation of the integrin signaling pathway in comparison to those with low DCBLD1 expression in the TCGA NSCLC cohort (FDR = 5.16 × 10
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; DNA Copy Number Variations ; Down-Regulation ; Female ; Humans ; Integrins/metabolism ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Male ; Membrane Proteins/genetics ; Middle Aged ; Neoplasm Invasiveness ; Prognosis ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Retrospective Studies ; Signal Transduction ; Up-Regulation
    Chemical Substances DCBLD1 protein, human ; Integrins ; Membrane Proteins
    Language English
    Publishing date 2021-06-17
    Publishing country England
    Document type Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-92090-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: Quantifying Senescence-Associated Phenotypes in Primary Multipotent Mesenchymal Stromal Cell Cultures.

    Nadeau, Stéphanie / Cheng, Anastasia / Colmegna, Inés / Rodier, Francis

    Methods in molecular biology (Clifton, N.J.)

    2019  Volume 2045, Page(s) 93–105

    Abstract: Cellular senescence is a tumor suppressor mechanism that removes potentially neoplastic cells from the proliferative pool. Senescent cells naturally accumulate with advancing age; however, excessive/aberrant accumulation of senescent cells can disrupt ... ...

    Abstract Cellular senescence is a tumor suppressor mechanism that removes potentially neoplastic cells from the proliferative pool. Senescent cells naturally accumulate with advancing age; however, excessive/aberrant accumulation of senescent cells can disrupt normal tissue function. Multipotent mesenchymal stromal cells (MSCs), which are actively evaluated as cell-based therapy, can undergo replicative senescence or stress-induced premature senescence. The molecular characterization of MSCs senescence can be useful not only for understanding the clinical correlations between MSCs biology and human age or age-related diseases but also for identifying competent MSCs for therapeutic applications. Because MSCs are involved in regulating the hematopoietic stem cell niche, and MSCs dysfunction has been implicated in age-related diseases, the identification and selective removal of senescent MSC may represent a potential therapeutic target. Cellular senescence is generally defined by senescence-associated (SA) permanent proliferation arrest (SAPA) accompanied by persistent DNA damage response (DDR) signaling emanating from persistent DNA lesions including damaged telomeres. Alongside SA cell cycle arrest and DDR signaling, a plethora of phenotypic hallmarks help define the overall senescent phenotype including a potent SA secretory phenotype (SASP) with many microenvironmental functions. Due to the complexity of the senescence phenotype, no single hallmark is alone capable of identifying senescent MSCs. This protocol highlights strategies to validate MSCs senescence through the measurements of several key SA hallmarks including lysosomal SA Beta-galactosidase activity (SA-βgal), cell cycle arrest, persistent DDR signaling, and the inflammatory SASP.
    MeSH term(s) Cell Cycle Checkpoints/genetics ; Cell Cycle Checkpoints/physiology ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Cell Proliferation/genetics ; Cell Proliferation/physiology ; Cells, Cultured ; Cellular Senescence/genetics ; Cellular Senescence/physiology ; Cytokines/metabolism ; DNA Damage ; Deoxyuridine/analogs & derivatives ; Deoxyuridine/metabolism ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Humans ; Inflammation/metabolism ; Mesenchymal Stem Cells/enzymology ; Mesenchymal Stem Cells/metabolism ; Mesenchymal Stem Cells/physiology ; Mesenchymal Stem Cells/radiation effects ; Multipotent Stem Cells/enzymology ; Multipotent Stem Cells/metabolism ; Multipotent Stem Cells/physiology ; Multipotent Stem Cells/radiation effects ; Phenotype ; Signal Transduction/genetics ; Telomere/genetics ; Telomere/metabolism ; Workflow ; beta-Galactosidase/metabolism
    Chemical Substances Cytokines ; beta-Galactosidase (EC 3.2.1.23) ; 5-ethynyl-2'-deoxyuridine (G373S00W2J) ; Deoxyuridine (W78I7AY22C)
    Language English
    Publishing date 2019-04-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/7651_2019_217
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: DCBLD1 is associated with the integrin signaling pathway and has prognostic value in non-small cell lung and invasive breast carcinoma

    Guillaume B. Cardin / Monique Bernard / Francis Rodier / Apostolos Christopoulos

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Volume 11

    Abstract: Abstract Germline single nucleotide polymorphisms in the promoter region of the DCBLD1 gene are associated with non-smoking cases of both non-small cell lung carcinoma (NSCLC) and human papillomavirus-negative head and neck cancer. However the clinical ... ...

    Abstract Abstract Germline single nucleotide polymorphisms in the promoter region of the DCBLD1 gene are associated with non-smoking cases of both non-small cell lung carcinoma (NSCLC) and human papillomavirus-negative head and neck cancer. However the clinical relevance and function of DCBLD1 remain unclear. This multicenter retrospective study was designed to evaluate the prognostic value and function of DCBLD1 in the four main solid cancers: NSCLC, invasive breast carcinoma, colorectal adenocarcinoma and prostate adenocarcinoma. We included the following cohorts: GSE81089 NSCLC, METABRIC invasive breast carcinoma, GSE14333 colorectal adenocarcinoma, GSE70770 prostate adenocarcinoma and The Cancer Genome Atlas (TCGA) Firehose Legacy cohorts of all four cancers. DCBLD1 gene expression was associated with a worse overall survival in multivariate analyses for both NSCLC cohorts (TCGA: P = 0.03 and GSE81089: P = 0.04) and both invasive breast carcinoma cohorts (TCGA: P = 0.02 and METABRIC: P < 0.001). Patients with high DCBLD1 expression showed an upregulation of the integrin signaling pathway in comparison to those with low DCBLD1 expression in the TCGA NSCLC cohort (FDR = 5.16 × 10–14) and TCGA invasive breast carcinoma cohort (FDR = 1.94 × 10–05).
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2021-06-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    More links

    Kategorien

  7. Article ; Online: mTOR as a senescence manipulation target: A forked road.

    Saoudaoui, Sarah / Bernard, Monique / Cardin, Guillaume B / Malaquin, Nicolas / Christopoulos, Apostolos / Rodier, Francis

    Advances in cancer research

    2021  Volume 150, Page(s) 335–363

    Abstract: Cellular senescence, cancer and aging are highly interconnected. Among many important molecular machines that lie at the intersection of this triad, the mechanistic (formerly mammalian) target of rapamycin (mTOR) is a central regulator of cell metabolism, ...

    Abstract Cellular senescence, cancer and aging are highly interconnected. Among many important molecular machines that lie at the intersection of this triad, the mechanistic (formerly mammalian) target of rapamycin (mTOR) is a central regulator of cell metabolism, proliferation, and survival. The mTOR signaling cascade is essential to maintain cellular homeostasis in normal biological processes or in response to stress, and its dysregulation is implicated in the progression of many disorders, including age-associated diseases. Accordingly, the pharmacological implications of mTOR inhibition using rapamycin or others rapalogs span the treatment of various human diseases from immune disorders to cancer. Importantly, rapamycin is one of the only known pan-species drugs that can extend lifespan. The molecular and cellular mechanisms explaining the phenotypic consequences of mTOR are vast and heavily studied. In this review, we will focus on the potential role of mTOR in the context of cellular senescence, a tumor suppressor mechanism and a pillar of aging. We will explore the link between senescence, autophagy and mTOR and discuss the opportunities to exploit senescence-associated mTOR functions to manipulate senescence phenotypes in age-associated diseases and cancer treatment.
    MeSH term(s) Aging/physiology ; Animals ; Antineoplastic Agents/therapeutic use ; Autophagy/physiology ; Cellular Senescence/genetics ; Humans ; Molecular Targeted Therapy/methods ; Molecular Targeted Therapy/trends ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Protein Kinase Inhibitors/therapeutic use ; TOR Serine-Threonine Kinases/physiology
    Chemical Substances Antineoplastic Agents ; Protein Kinase Inhibitors ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
    Language English
    Publishing date 2021-03-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 127-2
    ISSN 2162-5557 ; 0065-230X
    ISSN (online) 2162-5557
    ISSN 0065-230X
    DOI 10.1016/bs.acr.2021.02.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Senolytic Targeting of Bcl-2 Anti-Apoptotic Family Increases Cell Death in Irradiated Sarcoma Cells.

    Lafontaine, Julie / Cardin, Guillaume B / Malaquin, Nicolas / Boisvert, Jean-Sébastien / Rodier, Francis / Wong, Philip

    Cancers

    2021  Volume 13, Issue 3

    Abstract: Radiotherapy (RT) is a key component of cancer treatment. Most of the time, radiation is given after surgery but for soft-tissue sarcomas (STS), pre-surgical radiation is commonly utilized. However, despite improvements in RT accuracy, the rate of local ... ...

    Abstract Radiotherapy (RT) is a key component of cancer treatment. Most of the time, radiation is given after surgery but for soft-tissue sarcomas (STS), pre-surgical radiation is commonly utilized. However, despite improvements in RT accuracy, the rate of local recurrence remains high and is the major cause of death for patients with STS. A better understanding of cell fates in response to RT could provide new therapeutic options to enhance tumour cell killing by RT and facilitate surgical resection. Here, we showed that irradiated STS cell cultures do not die but instead undergo therapy-induced senescence (TIS), which is characterized by proliferation arrest, senescence-associated β-galactosidase activity, secretion of inflammatory cytokines and persistent DNA damage. STS-TIS was also associated with increased levels of the anti-apoptotic Bcl-2 family of proteins which rendered cells targetable using senolytic Bcl-2 inhibitors. As oppose to radiation alone, the addition of senolytic agents Venetoclax (ABT-199) or Navitoclax (ABT-263) after irradiation induced a rapid apoptotic cell death in STS monolayer cultures and in a more complex three-dimensional culture model. Together, these data suggest a new promising therapeutic approach for sarcoma patients who receive neoadjuvant RT. The addition of senolytic agents to radiation treatments may significantly reduce tumour volume prior to surgery and thereby improve the clinical outcome of patients.
    Language English
    Publishing date 2021-01-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13030386
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article ; Online: Radiotherapy on-chip: microfluidics for translational radiation oncology.

    Chermat, Rodin / Ziaee, Maryam / Mak, David Y / Refet-Mollof, Elena / Rodier, Francis / Wong, Philip / Carrier, Jean-François / Kamio, Yuji / Gervais, Thomas

    Lab on a chip

    2022  Volume 22, Issue 11, Page(s) 2065–2079

    Abstract: The clinical importance of radiotherapy in the treatment of cancer patients justifies the development and use of research tools at the fundamental, pre-clinical, and ultimately clinical levels, to investigate their toxicities and synergies with systemic ... ...

    Abstract The clinical importance of radiotherapy in the treatment of cancer patients justifies the development and use of research tools at the fundamental, pre-clinical, and ultimately clinical levels, to investigate their toxicities and synergies with systemic agents on relevant biological samples. Although microfluidics has prompted a paradigm shift in drug discovery in the past two decades, it appears to have yet to translate to radiotherapy research. However, the materials, dimensions, design versatility and multiplexing capabilities of microfluidic devices make them well-suited to a variety of studies involving radiation physics, radiobiology and radiotherapy. This review will present the state-of-the-art applications of microfluidics in these fields and specifically highlight the perspectives offered by radiotherapy on-a-chip in the field of translational radiobiology and precision medicine. This body of knowledge can serve both the microfluidics and radiotherapy communities by identifying potential collaboration avenues to improve patient care.
    MeSH term(s) Drug Discovery/methods ; Humans ; Lab-On-A-Chip Devices ; Microfluidics ; Precision Medicine ; Radiation Oncology
    Language English
    Publishing date 2022-05-31
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2056646-3
    ISSN 1473-0189 ; 1473-0197
    ISSN (online) 1473-0189
    ISSN 1473-0197
    DOI 10.1039/d2lc00177b
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article ; Online: Manipulating senescence in health and disease: emerging tools.

    Cheng, Shuofei / Rodier, Francis

    Cell cycle (Georgetown, Tex.)

    2015  Volume 14, Issue 11, Page(s) 1613–1614

    MeSH term(s) Apoptosis/drug effects ; Apoptosis/physiology ; Cell Transformation, Neoplastic/pathology ; Cellular Senescence/physiology ; Models, Biological ; Optical Imaging ; Stress, Physiological/physiology ; Tacrolimus/analogs & derivatives ; Tacrolimus/pharmacology
    Chemical Substances AP20187 ; Tacrolimus (WM0HAQ4WNM)
    Language English
    Publishing date 2015-04-30
    Publishing country United States
    Document type Editorial
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2015.1039359
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top