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  1. Article: Chryseobacterium Indologenes

    Das, Parijat / Karade, Santosh / Kaur, Kanwaljit / Ramamurthy, Ravi / Ranjan, Praveer

    Journal of clinical and diagnostic research : JCDR

    2017  Volume 11, Issue 6, Page(s) DD07–DD08

    Abstract: Chryseobacterium ... ...

    Abstract Chryseobacterium indologenes
    Language English
    Publishing date 2017-06-01
    Publishing country India
    Document type Case Reports
    ZDB-ID 2775283-5
    ISSN 0973-709X ; 2249-782X
    ISSN (online) 0973-709X
    ISSN 2249-782X
    DOI 10.7860/JCDR/2017/27237.10047
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: AMP-Activated Protein Kinase (AMPK) and Energy-Sensing in the Brain.

    Ramamurthy, Santosh / Ronnett, Gabriele

    Experimental neurobiology

    2012  Volume 21, Issue 2, Page(s) 52–60

    Abstract: 5'-adenosine monophosphate-activated protein kinase (AMPK) is an evolutionarily conserved cellular and organismal energy integrator that responds to numerous stimuli with the overall intention to facilitate energy conservation and enhance energy balance ... ...

    Abstract 5'-adenosine monophosphate-activated protein kinase (AMPK) is an evolutionarily conserved cellular and organismal energy integrator that responds to numerous stimuli with the overall intention to facilitate energy conservation and enhance energy balance while also affecting cellular survival and behaviors. AMPK has been appreciated for many years to function in peripheral organs that contribute to the generation or disposition of cellular energy, while its role in the brain has been only recently elucidated. While acknowledged to respond to organismal energy balance, we now recognize that energy balance within neurons also affects the brain's response to these peripheral signals. In this review, we discuss AMPK's regulation and its ever-expanding role as a neuronal energy integrator at both the cellular and systems levels.
    Language English
    Publishing date 2012-06-12
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2639017-6
    ISSN 2093-8144 ; 2093-8144
    ISSN (online) 2093-8144
    ISSN 2093-8144
    DOI 10.5607/en.2012.21.2.52
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Chryseobacterium Indologenes Pneumonitis in an Infant

    Parijat Das / Santosh Karade / Kanwaljit Kaur / Ravi Ramamurthy / Praveer Ranjan

    Journal of Clinical and Diagnostic Research, Vol 11, Iss 6, Pp DD07-DD

    A Case Report

    2017  Volume 08

    Abstract: Chryseobacterium indologenes, a non-fermentative Gram-negative bacilli distributed widely in nature, is an emerging nosocomial pathogen, inherently resistant to a wide range of antibiotics. There is limited number of C. indologenes infections reported ... ...

    Abstract Chryseobacterium indologenes, a non-fermentative Gram-negative bacilli distributed widely in nature, is an emerging nosocomial pathogen, inherently resistant to a wide range of antibiotics. There is limited number of C. indologenes infections reported from India. We report a case of C. indologenes associated pneumonia in a three-month-old infant with congenital heart disease. This case highlights the importance of prompt diagnostic workup and targeted antibiotic therapy for its effective management.
    Keywords drug resistance ; nosocomial infection ; pneumonia ; tachypnoea ; Medicine ; R
    Language English
    Publishing date 2017-06-01T00:00:00Z
    Publisher JCDR Research and Publications Private Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: AKAP-mediated feedback control of cAMP gradients in developing hippocampal neurons.

    Gorshkov, Kirill / Mehta, Sohum / Ramamurthy, Santosh / Ronnett, Gabriele V / Zhou, Feng-Quan / Zhang, Jin

    Nature chemical biology

    2017  Volume 13, Issue 4, Page(s) 425–431

    Abstract: Cyclic AMP (cAMP) and protein kinase A (PKA), classical examples of spatially compartmentalized signaling molecules, are critical axon determinants that regulate neuronal polarity and axon formation, yet little is known about micro-compartmentalization ... ...

    Abstract Cyclic AMP (cAMP) and protein kinase A (PKA), classical examples of spatially compartmentalized signaling molecules, are critical axon determinants that regulate neuronal polarity and axon formation, yet little is known about micro-compartmentalization of cAMP and PKA signaling and its role in developing neurons. Here, we revealed that cAMP forms a gradient in developing hippocampal neurons, with higher cAMP levels in more distal regions of the axon compared to other regions of the cell. Interestingly, this cAMP gradient changed according to the developmental stage and depended on proper anchoring of PKA by A-kinase anchoring proteins (AKAPs). Disrupting PKA anchoring to AKAPs increased the cAMP gradient in early-stage neurons and led to enhanced axon elongation. Our results provide new evidence for a local negative-feedback loop, assembled by AKAPs, for the precise control of a growth-stage-dependent cAMP gradient to ensure proper axon growth.
    MeSH term(s) A Kinase Anchor Proteins/metabolism ; Animals ; Cells, Cultured ; Cyclic AMP/metabolism ; Feedback, Physiological ; Hippocampus/cytology ; Neurons/metabolism ; Rats ; Rats, Sprague-Dawley
    Chemical Substances A Kinase Anchor Proteins ; Cyclic AMP (E0399OZS9N)
    Language English
    Publishing date 2017-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2202962-X
    ISSN 1552-4469 ; 1552-4450
    ISSN (online) 1552-4469
    ISSN 1552-4450
    DOI 10.1038/nchembio.2298
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  5. Article ; Online: Polarized activities of AMPK and BRSK in primary hippocampal neurons.

    Sample, Vedangi / Ramamurthy, Santosh / Gorshkov, Kirill / Ronnett, Gabriele V / Zhang, Jin

    Molecular biology of the cell

    2015  Volume 26, Issue 10, Page(s) 1935–1946

    Abstract: 5'-Adenosine monophosphate-activated protein kinase (AMPK) is a master metabolic regulator that has been shown to inhibit the establishment of neuronal polarity/axogenesis under energy stress conditions, whereas brain-specific kinase (BRSK) promotes the ... ...

    Abstract 5'-Adenosine monophosphate-activated protein kinase (AMPK) is a master metabolic regulator that has been shown to inhibit the establishment of neuronal polarity/axogenesis under energy stress conditions, whereas brain-specific kinase (BRSK) promotes the establishment of axon-dendrite polarity and synaptic development. However, little information exists regarding the localized activity and regulation of these kinases in developing neurons. In this study, using a fluorescence resonance energy transfer (FRET)-based activity reporter that responds to both AMPK and BRSK, we found that BRSK activity is elevated in the distal region of axons in polarized hippocampal neurons before any stimulation and does not respond to either Ca(2+) or 2-deoxyglucose (2-DG) stimulation. In contrast, AMPK activity is stimulated by either Ca(2+) or 2-DG in the soma, dendrites, and axons of hippocampal neurons, with maximal stimulated activity observed in the distal region of the axon. Our study shows that the activities of both AMPK and BRSK are polarized in developing hippocampal neurons, with high levels in the distal region of extended axons.
    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Animals ; Cell Polarity ; Cells, Cultured ; Cercopithecus aethiops ; Fluorescence Resonance Energy Transfer ; Hippocampus/enzymology ; Hippocampus/growth & development ; Neurogenesis/physiology ; Neurons/enzymology ; Neurons/physiology ; Rats ; Rats, Sprague-Dawley ; Receptor, EphA5/metabolism
    Chemical Substances Receptor, EphA5 (EC 2.7.10.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2015-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1098979-1
    ISSN 1939-4586 ; 1059-1524
    ISSN (online) 1939-4586
    ISSN 1059-1524
    DOI 10.1091/mbc.E14-02-0764
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Developing a head for energy sensing: AMP-activated protein kinase as a multifunctional metabolic sensor in the brain.

    Ramamurthy, Santosh / Ronnett, Gabriele V

    The Journal of physiology

    2006  Volume 574, Issue Pt 1, Page(s) 85–93

    Abstract: The 5'-adenosine monophosphate-activated protein kinase (AMPK) is a metabolic and stress sensor that has been functionally conserved throughout eukaryotic evolution. Activation of the AMPK system by various physiological or pathological stimuli that ... ...

    Abstract The 5'-adenosine monophosphate-activated protein kinase (AMPK) is a metabolic and stress sensor that has been functionally conserved throughout eukaryotic evolution. Activation of the AMPK system by various physiological or pathological stimuli that deplete cellular energy levels promotes activation of energy restorative processes and inhibits energy consumptive processes. AMPK has a prominent role not only as a peripheral sensor of energy balance, but also in the CNS as a multifunctional metabolic sensor. Recent work suggests that AMPK plays an important role in maintaining whole body energy balance by coordinating feeding behaviour through the hypothalamus in conjunction with peripheral energy expenditure. In addition, brain AMPK is activated by energy-poor conditions induced by hypoxia, starvation, and ischaemic stroke. Under these conditions, AMPK is activated as a protective response in an attempt to restore cellular homeostasis. However in vivo, it appears that the overall consequence of activation of AMPK is more complex than previously imagined, in that over-activation may be deleterious rather than neuroprotective. This review discusses recent findings that support the role of AMPK in brain as a multidimensional energy sensor and the consequences of its activation or inhibition under physiological and pathological states.
    MeSH term(s) AMP-Activated Protein Kinase Kinases ; Animals ; Brain/physiology ; Energy Metabolism/physiology ; Fatty Acids/metabolism ; Feeding Behavior/physiology ; Glucose/metabolism ; Homeostasis/physiology ; Humans ; Protein Kinases/metabolism
    Chemical Substances Fatty Acids ; Protein Kinases (EC 2.7.-) ; AMP-Activated Protein Kinase Kinases (EC 2.7.11.3) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2006-05-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/jphysiol.2006.110122
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Recombinant Adenosine Deaminase Ameliorates Inflammation, Vascular Disease, and Fibrosis in Preclinical Models of Systemic Sclerosis.

    Zhang, Yun / Zhu, Honglin / Layritz, Florian / Luo, Hui / Wohlfahrt, Thomas / Chen, Chih-Wei / Soare, Alina / Bergmann, Christina / Ramming, Andreas / Groeber, Florian / Reuter, Christian / Fornasini, GianFranco / Soukhareva, Nadejda / Schreiber, Brian / Ramamurthy, Santosh / Amann, Kerstin / Schett, Georg / Distler, Jörg H W

    Arthritis & rheumatology (Hoboken, N.J.)

    2020  Volume 72, Issue 8, Page(s) 1385–1395

    Abstract: Objective: Systemic sclerosis (SSc) is characterized by fibrosis, vascular disease, and inflammation. Adenosine signaling plays a central role in fibroblast activation. We undertook this study to evaluate the therapeutic effects of adenosine depletion ... ...

    Abstract Objective: Systemic sclerosis (SSc) is characterized by fibrosis, vascular disease, and inflammation. Adenosine signaling plays a central role in fibroblast activation. We undertook this study to evaluate the therapeutic effects of adenosine depletion with PEGylated adenosine deaminase (PEG-ADA) in preclinical models of SSc.
    Methods: The effects of PEG-ADA on inflammation, vascular remodeling, and tissue fibrosis were analyzed in Fra-2 mice and in a B10.D2→BALB/c (H-2
    Results: PEG-ADA effectively inhibited myofibroblast differentiation and reduced pulmonary fibrosis by 34.3% (with decreased collagen expression) (P = 0.0079; n = 6), dermal fibrosis by 51.8% (P = 0.0006; n = 6), and intestinal fibrosis by 17.7% (P = 0.0228; n = 6) in Fra-2 mice. Antifibrotic effects of PEG-ADA were also demonstrated in sclerodermatous chronic GVHD (reduced by 38.4%) (P = 0.0063; n = 8), and in a human full-thickness skin model. PEG-ADA treatment decreased inflammation and corrected the M2/Th2/group 2 innate lymphoid cell 2 bias. Moreover, PEG-ADA inhibited proliferation of pulmonary vascular smooth muscle cells (reduced by 40.5%) (P < 0.0001; n = 6), and prevented thickening of the vessel walls (reduced by 39.6%) (P = 0.0028; n = 6) and occlusions of pulmonary arteries (reduced by 63.9%) (P = 0.0147; n = 6). Treatment with PEG-ADA inhibited apoptosis of microvascular endothelial cells (reduced by 65.4%) (P = 0.0001; n = 6) and blunted the capillary rarefication (reduced by 32.5%) (P = 0.0199; n = 6). RNA sequencing demonstrated that treatment with PEG-ADA normalized multiple pathways related to fibrosis, vasculopathy, and inflammation in Fra-2 mice.
    Conclusion: Treatment with PEG-ADA ameliorates the 3 cardinal features of SSc in pharmacologically relevant and well-tolerated doses. These findings may have direct translational implications, as PEG-ADA has already been approved by the Food and Drug Administration for the treatment of patients with ADA-deficient severe combined immunodeficiency disease.
    MeSH term(s) Adenosine Deaminase/pharmacology ; Animals ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Disease Models, Animal ; Fibroblasts/drug effects ; Fibrosis/drug therapy ; Fibrosis/immunology ; Fibrosis/pathology ; Fos-Related Antigen-2/metabolism ; Graft vs Host Disease/drug therapy ; Graft vs Host Disease/immunology ; Graft vs Host Disease/pathology ; Humans ; Immunity, Innate/drug effects ; Inflammation ; Mice ; Mice, Inbred BALB C ; Models, Anatomic ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/immunology ; Pulmonary Fibrosis/pathology ; Scleroderma, Systemic/drug therapy ; Scleroderma, Systemic/immunology ; Scleroderma, Systemic/pathology ; Skin/drug effects ; Skin/immunology ; Skin/pathology ; Vascular Diseases/drug therapy ; Vascular Diseases/immunology ; Vascular Diseases/pathology
    Chemical Substances Fos-Related Antigen-2 ; Adenosine Deaminase (EC 3.5.4.4)
    Language English
    Publishing date 2020-06-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.41259
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Thromboxane A receptor-mediated cell proliferation, survival and gene expression in oligodendrocytes.

    Lin, Xin / Ramamurthy, Santosh K / Le Breton, Guy C

    Journal of neurochemistry

    2005  Volume 93, Issue 2, Page(s) 257–268

    Abstract: Thromboxane A(2) receptors (TP) were previously localized to discrete regions in the rat brain on myelinated fiber tracts and oligodendrocytes (OLGs). The present studies extended these findings and investigated the effects of TP signaling on cell ... ...

    Abstract Thromboxane A(2) receptors (TP) were previously localized to discrete regions in the rat brain on myelinated fiber tracts and oligodendrocytes (OLGs). The present studies extended these findings and investigated the effects of TP signaling on cell proliferation, survival, and gene expression in OLG progenitor cells (OPCs) and OLGs. It was found that the TP agonist, U46619 stimulated the proliferation of OPCs and promoted the survival of mature OLGs. Examination of the early gene expression events involved in OPC proliferation, revealed that c-fos expression was substantially increased by U46619 stimulation. Treatment of OPCs or OLGs with U46619 caused activation of the mitogen-activated protein kinases (MAPK) ERK 1/2. In OPCs this activation was blocked by inhibition of src. However, in OLGs this phosphorylation was not only blocked by inhibition of src but also by inhibition of protein kinase C (PKC). Furthermore, U46619 was found to increase CREB phosphorylation in both OPCs and OLGs. Similar to ERK 1/2 activation, there was a divergence in the mechanism of the TP-mediated CREB response for each cell type. Specifically, U46619 activation was attenuated by src and protein kinase A (PKA) inhibition in OPCs, whereas in OLGs this effect was blocked by inhibition of src, PKA as well as by inhibition of PKC. Collectively, these results provide the first demonstration that TP-activated nuclear signaling events are involved in the proliferation of OPCs, the survival of mature OLGs, and the stimulation of gene expression.
    MeSH term(s) 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid/pharmacology ; Animals ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cell Survival/physiology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Oligodendroglia/cytology ; Oligodendroglia/drug effects ; Oligodendroglia/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Thromboxane A2, Prostaglandin H2/agonists ; Receptors, Thromboxane A2, Prostaglandin H2/biosynthesis ; Receptors, Thromboxane A2, Prostaglandin H2/genetics ; Receptors, Thromboxane A2, Prostaglandin H2/physiology
    Chemical Substances Receptors, Thromboxane A2, Prostaglandin H2 ; 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid (76898-47-0)
    Language English
    Publishing date 2005-04
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/j.1471-4159.2004.02969.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Recombinant Adenosine Deaminase Ameliorates Inflammation, Vascular Disease, and Fibrosis in Preclinical Models of Systemic Sclerosis

    Zhang, Yun / Zhu, Honglin / Layritz, Florian / Luo, Hui / Wohlfahrt, Thomas / Chen, Chih-Wei / Soare, Alina / Bergmann, Christina / Ramming, Andreas / Groeber-Becker, Florian / Reuter, Christian / Fornasini, GianFranco / Soukhareva, Nadejda / Schreiber, Brian / Ramamurthy, Santosh / Amann, Kerstin / Schett, Georg / Distler, Jörg H.W

    2020  

    Abstract: S.1385-1395 ... Objective Systemic sclerosis (SSc) is characterized by fibrosis, vascular disease, and inflammation. Adenosine signaling plays a central role in fibroblast activation. We undertook this study to evaluate the therapeutic effects of adenosine ...

    Abstract S.1385-1395

    Objective Systemic sclerosis (SSc) is characterized by fibrosis, vascular disease, and inflammation. Adenosine signaling plays a central role in fibroblast activation. We undertook this study to evaluate the therapeutic effects of adenosine depletion with PEGylated adenosine deaminase (PEG‐ADA) in preclinical models of SSc. Methods The effects of PEG‐ADA on inflammation, vascular remodeling, and tissue fibrosis were analyzed in Fra‐2 mice and in a B10.D2RTBALB/c (H‐2d) model of sclerodermatous chronic graft‐versus‐host disease (GVHD). The effects of PEG‐ADA were confirmed in vitro in a human full‐thickness skin model. Results PEG‐ADA effectively inhibited myofibroblast differentiation and reduced pulmonary fibrosis by 34.3% (with decreased collagen expression) (P = 0.0079; n = 6), dermal fibrosis by 51.8% (P = 0.0006; n = 6), and intestinal fibrosis by 17.7% (P = 0.0228; n = 6) in Fra‐2 mice. Antifibrotic effects of PEG‐ADA were also demonstrated in sclerodermatous chronic GVHD (reduced by 38.4%) (P = 0.0063; n = 8), and in a human full‐thickness skin model. PEG‐ADA treatment decreased inflammation and corrected the M2/Th2/group 2 innate lymphoid cell 2 bias. Moreover, PEG‐ADA inhibited proliferation of pulmonary vascular smooth muscle cells (reduced by 40.5%) (P < 0.0001; n = 6), and prevented thickening of the vessel walls (reduced by 39.6%) (P = 0.0028; n = 6) and occlusions of pulmonary arteries (reduced by 63.9%) (P = 0.0147; n = 6). Treatment with PEG‐ADA inhibited apoptosis of microvascular endothelial cells (reduced by 65.4%) (P = 0.0001; n = 6) and blunted the capillary rarefication (reduced by 32.5%) (P = 0.0199; n = 6). RNA sequencing demonstrated that treatment with PEG‐ADA normalized multiple pathways related to fibrosis, vasculopathy, and inflammation in Fra‐2 mice. Conclusion Treatment with PEG‐ADA ameliorates the 3 cardinal features of SSc in pharmacologically relevant and well‐tolerated doses. These findings may have direct translational implications, as PEG‐ADA has already been ...
    Keywords adenosine deaminase ; collagen ; transcription factor Fra 2 ; systemic sclerosis ; skin fibrosis ; 666 ; 660 ; 616 ; 610 ; 620
    Subject code 610
    Language English
    Publishing country de
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: AMPK in the brain: its roles in energy balance and neuroprotection.

    Ronnett, Gabriele V / Ramamurthy, Santosh / Kleman, Amy M / Landree, Leslie E / Aja, Susan

    Journal of neurochemistry

    2009  Volume 109 Suppl 1, Page(s) 17–23

    Abstract: Adenosine monophosphate-activated protein kinase (AMPK) senses metabolic stress and integrates diverse physiological signals to restore energy balance. Multiple functions are indicated for AMPK in the CNS. While all neurons sense their own energy status, ...

    Abstract Adenosine monophosphate-activated protein kinase (AMPK) senses metabolic stress and integrates diverse physiological signals to restore energy balance. Multiple functions are indicated for AMPK in the CNS. While all neurons sense their own energy status, some integrate neuro-humoral signals to assess organismal energy balance. A variety of disease states may involve AMPK, so determining the underlying mechanisms is important. We review the impact of altered AMPK activity under physiological (hunger, satiety) and pathophysiological (stroke) conditions, as well as therapeutic manipulations of AMPK that may improve energy balance.
    MeSH term(s) Animals ; Brain Chemistry/drug effects ; Brain Chemistry/physiology ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Energy Metabolism/drug effects ; Energy Metabolism/physiology ; Enzyme Activation/physiology ; Humans ; Oxidative Stress/physiology
    Chemical Substances Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Language English
    Publishing date 2009-04-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/j.1471-4159.2009.05916.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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