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Article ; Online: Hyperkalemia, Bradycardia, and Cardiac Arrest during Percutaneous Declotting of an Arteriovenous Graft.

Wiltrout, Charles

2010 Volume 27, Issue 2, Page(s) 241–244

Language	English
Publishing date	2010-07-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	848341-3
ISSN	1098-8963 ; 0739-9529
ISSN (online)	1098-8963
ISSN	0739-9529
DOI	10.1055/s-0030-1253520
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Article: Hyperkalemia, Bradycardia, and Cardiac Arrest during Percutaneous Declotting of an Arteriovenous Graft

Wiltrout, Charles

Seminars in Interventional Radiology

(Musculoskeletal Interventions)

2010 Volume 27, Issue 02, Page(s) 241–244

Series title	Musculoskeletal Interventions
Language	English
Publishing date	2010-05-18
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	848341-3
ISSN	1098-8963 ; 0739-9529
ISSN (online)	1098-8963
ISSN	0739-9529
DOI	10.1055/s-0030-1253520
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Article ; Online: Calcaneal bone mineral density in young adults prescribed selective serotonin reuptake inhibitors.

Seifert, Charles F / Wiltrout, Tara R

Clinical therapeutics

2013 Volume 35, Issue 9, Page(s) 1412–1417

Abstract: Background: Several previous studies have reported both an association between selective serotonin reuptake inhibitors (SSRI) and decreased bone mineral density and increased fractures, but no previous studies have specifically evaluated bone health in ... ...

Abstract	Background: Several previous studies have reported both an association between selective serotonin reuptake inhibitors (SSRI) and decreased bone mineral density and increased fractures, but no previous studies have specifically evaluated bone health in young adults who have a history of SSRI use. Objective: The purpose was to characterize the effect SSRI use in early adulthood on bone mineral density. Methods: A cross-sectional study was conducted on subjects who voluntarily responded to recruitment methods for the study. Young adults aged 18 to 25 years who were currently or had previously taken an SSRI for a minimum of 3 consecutive months were included in the study. A subject interview was conducted on each patient to collect background information. Each subject's calcaneal bone mineral density was then measured with an ultrasonometer. Results: Complete data were collected on 51 subjects. The median duration of SSRI use was 24 ± 54 months. A significant negative correlation was observed between SSRI duration and calcaneal ultrasound T-score (r = -0.53, P < 0.001) which was unchanged in depressed subjects. Subjects on continuous SSRIs for >24 months had a significantly lower median T-score (0.30 ± 0.93) than subjects taking SSRIs for ≤ 24 months (0.90 ± 0.81; P = 0.0010). Conclusions: In this young relatively healthy population who were following most of the recommendations to improve bone health, a significant negative correlation was observed between the duration of SSRI use and bone mineral density. Subjects who were on SSRIs for longer than 24 months had a significantly lower T-score. Further large scale longitudinal studies are needed in this younger population to determine the effects of chronic SSRI use on bone health.
MeSH term(s)	Bone Density/drug effects ; Calcaneus/physiology ; Cross-Sectional Studies ; Depression/drug therapy ; Female ; Fractures, Bone/etiology ; Healthy Volunteers ; Humans ; Male ; Osteoporosis/chemically induced ; Reproducibility of Results ; Risk Factors ; Serotonin Uptake Inhibitors/adverse effects ; Serotonin Uptake Inhibitors/therapeutic use ; Young Adult
Chemical Substances	Serotonin Uptake Inhibitors
Language	English
Publishing date	2013-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	603113-4
ISSN	1879-114X ; 0149-2918
ISSN (online)	1879-114X
ISSN	0149-2918
DOI	10.1016/j.clinthera.2013.07.423
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Article ; Online: Correction of coagulopathy for percutaneous interventions.

Wiltrout, Charles / Kondo, Kimi L

Seminars in interventional radiology

2012 Volume 27, Issue 4, Page(s) 338–347

Abstract: Due to medical illness or pharmacotherapy, patients undergoing percutaneous interventions often have abnormal hemostasis. Its etiology may include alterations in the protein-based coagulation system, thrombocytopenia, deficient platelet function, or ... ...

Abstract	Due to medical illness or pharmacotherapy, patients undergoing percutaneous interventions often have abnormal hemostasis. Its etiology may include alterations in the protein-based coagulation system, thrombocytopenia, deficient platelet function, or mixed deficits such as disseminated intravascular coagulation. In this article, the authors review the basic science of each of these etiologies, as well as their available methods of correction. They also review the evidence and guidelines regarding the assessment and treatment of coagulopathy in image-guided procedures. The periprocedural bleeding risk and the urgency of a given procedure guide the management of abnormal hemostasis in this patient population.
Language	English
Publishing date	2012-05-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	848341-3
ISSN	1098-8963 ; 0739-9529
ISSN (online)	1098-8963
ISSN	0739-9529
DOI	10.1055/s-0030-1267857
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Article: Correction of Coagulopathy for Percutaneous Interventions

Wiltrout, Charles / Kondo, Kimi L

Seminars in Interventional Radiology

2010 Volume 27, Issue 04, Page(s) 338–347

Abstract	Due to medical illness or pharmacotherapy, patients undergoing percutaneous interventions often have abnormal hemostasis. Its etiology may include alterations in the protein-based coagulation system, thrombocytopenia, deficient platelet function, or mixed deficits such as disseminated intravascular coagulation. In this article, the authors review the basic science of each of these etiologies, as well as their available methods of correction. They also review the evidence and guidelines regarding the assessment and treatment of coagulopathy in image-guided procedures. The periprocedural bleeding risk and the urgency of a given procedure guide the management of abnormal hemostasis in this patient population.
Keywords	Anticoagulation ; platelets ; coagulopathy ; disseminated intravascular coagulation ; reversal
Language	English
Publishing date	2010-11-19
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	848341-3
ISSN	1098-8963 ; 0739-9529
ISSN (online)	1098-8963
ISSN	0739-9529
DOI	10.1055/s-0030-1267857
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Article: Configurational and nonconfigurational interactions between odorants in binary mixtures.

Wiltrout, Charles / Dogra, Samriti / Linster, Christiane

Behavioral neuroscience

2003 Volume 117, Issue 2, Page(s) 236–245

Abstract: Studies on odor mixture perception suggest that although odor components can often be identified in mixtures, mixtures can also give rise to novel perceptual qualities that are not present in the components. Using an olfactory habituation task, the ... ...

Abstract	Studies on odor mixture perception suggest that although odor components can often be identified in mixtures, mixtures can also give rise to novel perceptual qualities that are not present in the components. Using an olfactory habituation task, the authors evaluated how the perceptual similarity between components in a mixture affects the perceptual quality of the mixture itself. Rats perceived binary mixtures composed of similar components as different from their 2 components, whereas binary mixtures composed of dissimilar components were perceived as very similar to their components. Results show that for both types of mixtures, pretraining to Component A reduces subsequent learning about Component B in rats trained in the presence of A.
MeSH term(s)	Animals ; Conditioning (Psychology)/drug effects ; Conditioning (Psychology)/physiology ; Discrimination (Psychology)/drug effects ; Discrimination (Psychology)/physiology ; Discrimination Learning/physiology ; Drug Interactions ; Generalization (Psychology) ; Male ; Odorants ; Perception/physiology ; Rats ; Rats, Sprague-Dawley ; Reaction Time/drug effects ; Smell/drug effects ; Smell/physiology
Language	English
Publishing date	2003-04
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	230159-3
ISSN	1939-0084 ; 0735-7044
ISSN (online)	1939-0084
ISSN	0735-7044
DOI	10.1037/0735-7044.117.2.236
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Article: Repairing brain after stroke: a review on post-ischemic neurogenesis.

Wiltrout, Charles / Lang, Bradley / Yan, Yiping / Dempsey, Robert J / Vemuganti, Raghu

Neurochemistry international

2007 Volume 50, Issue 7-8, Page(s) 1028–1041

Abstract: Stroke is devastating as currently no therapies are available that can prevent stroke-induced neurological dysfunction in humans. With the recent observations that acute insults to adult brain stimulate new neuronal formation in various species of ... ...

Abstract	Stroke is devastating as currently no therapies are available that can prevent stroke-induced neurological dysfunction in humans. With the recent observations that acute insults to adult brain stimulate new neuronal formation in various species of animals, optimism is building for a possible regeneration of stroke-damaged brain. This article reviewed the advances in the understanding of the molecular mechanisms of the various steps of neurogenesis with an emphasis on the endogenous mediators and exogenous promoters of neural progenitor proliferation, migration and survival in the post-ischemic adult brain.
MeSH term(s)	Adult ; Animals ; Brain/physiology ; Brain/physiopathology ; Brain Ischemia/physiopathology ; Brain Ischemia/rehabilitation ; Cerebral Ventricles/physiopathology ; Dentate Gyrus/physiopathology ; Hippocampus/physiopathology ; Humans ; Inflammation ; Insulin-Like Growth Factor I/physiology ; Nerve Regeneration/physiology ; Neurotransmitter Agents/physiology ; Nitric Oxide/physiology ; Stroke/physiopathology ; Stroke Rehabilitation
Chemical Substances	Neurotransmitter Agents ; Nitric Oxide (31C4KY9ESH) ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2007-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2007.04.011
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Article ; Online: Adiposity induces lethal cytokine storm after systemic administration of stimulatory immunotherapy regimens in aged mice.

Mirsoian, Annie / Bouchlaka, Myriam N / Sckisel, Gail D / Chen, Mingyi / Pai, Chien-Chun Steven / Maverakis, Emanuel / Spencer, Richard G / Fishbein, Kenneth W / Siddiqui, Sana / Monjazeb, Arta M / Martin, Bronwen / Maudsley, Stuart / Hesdorffer, Charles / Ferrucci, Luigi / Longo, Dan L / Blazar, Bruce R / Wiltrout, Robert H / Taub, Dennis D / Murphy, William J

The Journal of experimental medicine

2014 Volume 211, Issue 12, Page(s) 2373–2383

Abstract: Aging is a contributing factor in cancer occurrence. We recently demonstrated that systemic immunotherapy (IT) administration in aged, but not young, mice resulted in induction of rapid and lethal cytokine storm. We found that aging was accompanied by ... ...

Abstract	Aging is a contributing factor in cancer occurrence. We recently demonstrated that systemic immunotherapy (IT) administration in aged, but not young, mice resulted in induction of rapid and lethal cytokine storm. We found that aging was accompanied by increases in visceral fat similar to that seen in young obese (ob/ob or diet-induced obese [DIO]) mice. Yet, the effects of aging and obesity on inflammatory responses to immunotherapeutics are not well defined. We determine the effects of adiposity on systemic IT tolerance in aged compared with young obese mice. Both young ob/ob- and DIO-generated proinflammatory cytokine levels and organ pathologies are comparable to those in aged ad libitum mice after IT, culminating in lethality. Young obese mice exhibited greater ratios of M1/M2 macrophages within the peritoneal and visceral adipose tissues and higher percentages of TNF(+) macrophages in response to αCD40/IL-2 as compared with young lean mice. Macrophage depletion or TNF blockade in conjunction with αCD40/IL-2 prevented cytokine storms in young obese mice and protected from lethality. Calorie-restricted aged mice contain less visceral fat and displayed reduced cytokine levels, protection from organ pathology, and protection from lethality upon αCD40/IL-2 administration. Our data demonstrate that adiposity is a critical factor in the age-associated pathological responses to systemic anti-cancer IT.
MeSH term(s)	Adiposity/immunology ; Aging/immunology ; Animals ; Caloric Restriction ; Cytokines/blood ; Cytokines/immunology ; Female ; Flow Cytometry ; Humans ; Immunotherapy/methods ; Inflammation Mediators/blood ; Inflammation Mediators/immunology ; Intra-Abdominal Fat/immunology ; Intra-Abdominal Fat/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Mice, Inbred C57BL ; Mice, Obese ; Neoplasms/immunology ; Neoplasms/therapy ; Obesity/genetics ; Obesity/immunology ; Obesity/metabolism ; Tumor Necrosis Factor-alpha/immunology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Cytokines ; Inflammation Mediators ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2014-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20140116
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Article ; Online: Aging predisposes to acute inflammatory induced pathology after tumor immunotherapy.

Bouchlaka, Myriam N / Sckisel, Gail D / Chen, Mingyi / Mirsoian, Annie / Zamora, Anthony E / Maverakis, Emanual / Wilkins, Danice E C / Alderson, Kory L / Hsiao, Hui-Hua / Weiss, Jonathan M / Monjazeb, Arta M / Hesdorffer, Charles / Ferrucci, Luigi / Longo, Dan L / Blazar, Bruce R / Wiltrout, Robert H / Redelman, Doug / Taub, Dennis D / Murphy, William J

The Journal of experimental medicine

2013 Volume 210, Issue 11, Page(s) 2223–2237

Abstract: Cancer commonly occurs in the elderly and immunotherapy (IT) is being increasingly applied to this population. However, the majority of preclinical mouse tumor models assessing potential efficacy and toxicities of therapeutics use young mice. We assessed ...

Abstract	Cancer commonly occurs in the elderly and immunotherapy (IT) is being increasingly applied to this population. However, the majority of preclinical mouse tumor models assessing potential efficacy and toxicities of therapeutics use young mice. We assessed the impact of age on responses to systemic immune stimulation. In contrast to young mice, systemic cancer IT regimens or LPS given to aged mice resulted in rapid and lethal toxicities affecting multiple organs correlating with heightened proinflammatory cytokines systemically and within the parenchymal tissues. This inflammatory response and increased morbidity with age was independent of T cells or NK cells. However, prior in vivo depletion of macrophages in aged mice resulted in lesser cytokine levels, increased survival, and decreased liver histopathology. Furthermore, macrophages from aged mice and normal human elderly volunteers displayed heightened TNF and IL-6 production upon in vitro stimulation. Treatment of both TNF knockout mice and in vivo TNF blockade in aged mice resulted in significant increases in survival and lessened pathology. Importantly, TNF blockade in tumor-bearing, aged mice receiving IT displayed significant anti-tumor effects. These data demonstrate the critical role of macrophages in the age-associated hyper-inflammatory cytokine responses to systemic immunostimulation and underscore the importance of performing preclinical assessments in aged mice.
MeSH term(s)	Aging/immunology ; Aging/pathology ; Animals ; CD40 Antigens/immunology ; Cytokines/toxicity ; Dose-Response Relationship, Drug ; Female ; Humans ; Immunotherapy ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Lipopolysaccharides/pharmacology ; Liver/drug effects ; Liver/enzymology ; Liver/pathology ; Macrophages/drug effects ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Survival Analysis ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	CD40 Antigens ; Cytokines ; Inflammation Mediators ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2013-09-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20131219
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Article: Activation of cutaneous protein kinase C alpha induces keratinocyte apoptosis and intraepidermal inflammation by independent signaling pathways.

Cataisson, Christophe / Joseloff, Elizabeth / Murillas, Rodolfo / Wang, Alice / Atwell, Coralyn / Torgerson, Sara / Gerdes, Michael / Subleski, Jeffrey / Gao, Ji-Liang / Murphy, Philip M / Wiltrout, Robert H / Vinson, Charles / Yuspa, Stuart H

Journal of immunology (Baltimore, Md. : 1950)

2003 Volume 171, Issue 5, Page(s) 2703–2713

Abstract: Skin keratinocytes are major mediators of host immune responses. The skin is also a target for immunologically based inflammation in many pathological states. Activation of protein kinase C (PKC) can induce cutaneous inflammation, but the precise role of ...

Abstract	Skin keratinocytes are major mediators of host immune responses. The skin is also a target for immunologically based inflammation in many pathological states. Activation of protein kinase C (PKC) can induce cutaneous inflammation, but the precise role of each of six cutaneous PKC isoforms (alpha, delta, epsilon, eta, zeta, mu) that regulate normal skin homeostasis or contribute to skin pathology has not been clarified. We generated transgenic mice that overexpress PKCalpha in the basal layer of the epidermis and the outer root sheath of hair follicles under the regulation of the bovine keratin 5 promoter. K5-PKCalpha transgenic mice exhibit severe intraepidermal neutrophilic inflammation and disruption of the epidermis and upper hair follicles when treated topically with 12-O-tetradecanoylphorbol-13-acetate (TPA). Both TPA and UVB cause apoptosis in transgenic skin, but only TPA evokes intraepidermal inflammation. TPA also induces apoptosis in cultured transgenic keratinocytes, and this is prevented by an AP-1 dominant-negative construct. However, inhibiting AP-1 in vivo does not abrogate intraepidermal inflammation. Transcripts for specific cytokines and chemokines are elevated in TPA-treated cultured transgenic keratinocytes, and conditioned culture medium from these cells promotes neutrophil migration in vitro. Chemokine expression and neutrophil migration are not diminished by inhibiting AP-1. Thus, PKCalpha activation induces keratinocyte apoptosis via an AP-1-dependent pathway and mediates chemokine induction and intraepidermal inflammation independently. This model system will be useful to define specific chemokines regulated by PKCalpha that promote intraepidermal neutrophilic inflammation, a condition that characterizes several human cutaneous diseases such as pustular psoriasis and acute generalized exanthematous pustulosis.
MeSH term(s)	Animals ; Apoptosis/physiology ; Cell Movement/genetics ; Cell Survival/genetics ; Cells, Cultured ; Chemokines/biosynthesis ; Cytokines/biosynthesis ; Enzyme Activation/genetics ; Enzyme Activation/immunology ; Epidermis/enzymology ; Epidermis/metabolism ; Epidermis/pathology ; Inflammation/enzymology ; Inflammation/genetics ; Inflammation/pathology ; Keratinocytes/enzymology ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; Protein Kinase C/biosynthesis ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Protein Kinase C/physiology ; Protein Kinase C-alpha ; Signal Transduction/genetics ; Signal Transduction/physiology ; Transcription Factor AP-1/physiology ; Transgenes
Chemical Substances	Chemokines ; Cytokines ; Transcription Factor AP-1 ; Prkca protein, mouse (EC 2.7.11.13) ; Protein Kinase C (EC 2.7.11.13) ; Protein Kinase C-alpha (EC 2.7.11.13)
Language	English
Publishing date	2003-07-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.171.5.2703
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