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Article ; Online: Retinal Ganglion Cell Survival and Axon Regeneration after Optic Nerve Injury: Role of Inflammation and Other Factors.

Wong, Kimberly A / Benowitz, Larry I

International journal of molecular sciences

2022 Volume 23, Issue 17

Abstract: The optic nerve, like most pathways in the mature central nervous system, cannot regenerate if injured, and within days, retinal ganglion cells (RGCs), the neurons that extend axons through the optic nerve, begin to die. Thus, there are few clinical ... ...

Abstract	The optic nerve, like most pathways in the mature central nervous system, cannot regenerate if injured, and within days, retinal ganglion cells (RGCs), the neurons that extend axons through the optic nerve, begin to die. Thus, there are few clinical options to improve vision after traumatic or ischemic optic nerve injury or in neurodegenerative diseases such as glaucoma, dominant optic neuropathy, or optic pathway gliomas. Research over the past two decades has identified several strategies to enable RGCs to regenerate axons the entire length of the optic nerve, in some cases leading to modest reinnervation of di- and mesencephalic visual relay centers. This review primarily focuses on the role of the innate immune system in improving RGC survival and axon regeneration, and its synergy with manipulations of signal transduction pathways, transcription factors, and cell-extrinsic suppressors of axon growth. Research in this field provides hope that clinically effective strategies to improve vision in patients with currently untreatable losses could become a reality in 5-10 years.
MeSH term(s)	Axons/metabolism ; Cell Survival ; Humans ; Inflammation/metabolism ; Nerve Regeneration/physiology ; Optic Nerve Injuries/metabolism ; Retinal Ganglion Cells/metabolism
Language	English
Publishing date	2022-09-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231710179
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Article ; Online: Full-length optic nerve regeneration in the absence of genetic manipulations.

Feng, Qian / Wong, Kimberly A / Benowitz, Larry I

JCI insight

2023 Volume 8, Issue 7

Abstract: The inability of mature retinal ganglion cells (RGCs) to regenerate axons after optic nerve injury can be partially reversed by manipulating cell-autonomous and/or -nonautonomous factors. Although manipulations of cell-nonautonomous factors could have ... ...

Abstract	The inability of mature retinal ganglion cells (RGCs) to regenerate axons after optic nerve injury can be partially reversed by manipulating cell-autonomous and/or -nonautonomous factors. Although manipulations of cell-nonautonomous factors could have higher translational potential than genetic manipulations of RGCs, they have generally produced lower levels of optic nerve regeneration. Here, we report that preconditioning resulting from mild lens injury (conditioning LI, cLI) before optic nerve damage induced far greater regeneration than LI after nerve injury or the pro-inflammatory agent zymosan given either before or after nerve damage. Unlike zymosan-induced regeneration, cLI was unaltered by depleting mature neutrophils or T cells or blocking receptors for known inflammation-derived growth factors (oncomodulin, stromal cell-derived factor 1, CCL5) and was only partly diminished by suppressing CCR2+ monocyte recruitment. Repeated episodes of LI led to full-length optic nerve regeneration, and pharmacological removal of local resident macrophages with the colony stimulating factor 1 receptor inhibitor PLX5622 enabled some axons to reinnervate the brain in just 6 weeks, comparable to the results obtained with the most effective genetic manipulations of RGCs. Thus, cell-nonautonomous interventions can induce high levels of optic nerve regeneration, paving the way to uncovering potent, translatable therapeutic targets for CNS repair.
MeSH term(s)	Humans ; Zymosan/pharmacology ; Nerve Regeneration/genetics ; Optic Nerve Injuries/drug therapy ; Optic Nerve Injuries/metabolism ; Retinal Ganglion Cells/physiology ; Axons/metabolism
Chemical Substances	Zymosan (9010-72-4)
Language	English
Publishing date	2023-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.164579
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Article: An Unusual Cause of Abdominal Ascites.

Wong, Kimberly A / Olson, Kristin A / Chak, Eric W

Case reports in gastroenterology

2018 Volume 12, Issue 2, Page(s) 420–424

Abstract: Abdominal ascites is most commonly caused by portal hypertension from liver cirrhosis. When present, portal hypertension is associated with an elevated serum-ascites albumin gradient (SAAG) ≥1.1 g/dL. In contrast, a SAAG < 1.1 g/dL suggests malignancy, ... ...

Abstract	Abdominal ascites is most commonly caused by portal hypertension from liver cirrhosis. When present, portal hypertension is associated with an elevated serum-ascites albumin gradient (SAAG) ≥1.1 g/dL. In contrast, a SAAG < 1.1 g/dL suggests malignancy, tuberculosis, pancreatitis, or nephrotic syndrome. Here, we present a case of low SAAG ascites caused by epithelioid peritoneal mesothelioma in a woman with no known liver disease. The diagnosis proved elusive until diagnostic laparoscopy with biopsy was performed.
Language	English
Publishing date	2018-08-21
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2440540-1
ISSN	1662-0631
ISSN	1662-0631
DOI	10.1159/000490660
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Article: Update on New Drugs and Those in Development for the Treatment of Primary Biliary Cholangitis.

Bahar, Runalia / Wong, Kimberly A / Liu, Chung H / Bowlus, Christopher L

Gastroenterology & hepatology

2018 Volume 14, Issue 3, Page(s) 154–163

Abstract: Primary biliary cholangitis (PBC) is an autoimmune inflammatory liver disease of the interlobular bile ducts that can lead to cirrhosis and liver failure. Until recently, the only effective treatment was ursodeoxycholic acid (UDCA). However, up to 40% of ...

Abstract	Primary biliary cholangitis (PBC) is an autoimmune inflammatory liver disease of the interlobular bile ducts that can lead to cirrhosis and liver failure. Until recently, the only effective treatment was ursodeoxycholic acid (UDCA). However, up to 40% of PBC patients have an inadequate response to UDCA and may continue to have disease progression. Several models have been developed, including the UK-PBC and GLOBE scores, to assist in identifying patients who may benefit from second-line therapies, such as the farnesoid X receptor (FXR) agonist obeticholic acid (OCA). The addition of OCA can significantly improve serum alkaline phosphatase and total bilirubin, which are strong surrogate markers of clinical outcomes in PBC. Other alternatives, including the peroxisome proliferator-activated receptor (PPAR)-α agonists fenofibrate and bezafibrate, may also improve liver biochemistries in PBC patients with an inadequate response to UDCA, but further study is needed to demonstrate their safety and long-term efficacy. Other novel agents, including those targeting the FXR pathway and PPAR-δ agonists, have shown promising results and may alter the therapeutic landscape of PBC in the near future. For now, OCA remains the only approved second-line agent for PBC patients with an inadequate response to UDCA while results of long-term studies of its safety and clinical benefit are awaited.
Language	English
Publishing date	2018-06-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2386402-3
ISSN	1554-7914
ISSN	1554-7914
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Article ; Online: Current Treatment Options for Primary Biliary Cholangitis.

Wong, Kimberly A / Bahar, Runalia / Liu, Chung H / Bowlus, Christopher L

Clinics in liver disease

2018 Volume 22, Issue 3, Page(s) 481–500

Abstract: Primary biliary cholangitis is a progressive, autoimmune disease of the interlobular bile ducts, leading to secondary damage of hepatocytes that may progress to cirrhosis and liver failure. Until recently, the only approved treatment was ursodeoxycholic ... ...

Abstract	Primary biliary cholangitis is a progressive, autoimmune disease of the interlobular bile ducts, leading to secondary damage of hepatocytes that may progress to cirrhosis and liver failure. Until recently, the only approved treatment was ursodeoxycholic acid. However, 40% of patients do not have an adequate response. Obeticholic acid was approved for treatment as add-on therapy in this group of patients. Off-label use of fibrates has also been reported to be effective. Several new therapies are in development and may further add to the treatment options available to patients with primary biliary cholangitis.
MeSH term(s)	Alkaline Phosphatase/metabolism ; Bezafibrate/therapeutic use ; Chenodeoxycholic Acid/analogs & derivatives ; Chenodeoxycholic Acid/therapeutic use ; Cholagogues and Choleretics/therapeutic use ; Comorbidity ; Drug Therapy, Combination ; Fenofibrate/therapeutic use ; Fibroblast Growth Factors/analogs & derivatives ; Humans ; Hypolipidemic Agents/therapeutic use ; Immunosuppressive Agents/therapeutic use ; Liver Cirrhosis, Biliary/drug therapy ; Liver Cirrhosis, Biliary/epidemiology ; Liver Cirrhosis, Biliary/metabolism ; Malnutrition/drug therapy ; Malnutrition/epidemiology ; Osteoporosis/drug therapy ; Osteoporosis/epidemiology ; Peroxisome Proliferator-Activated Receptors/agonists ; Receptors, Cytoplasmic and Nuclear/agonists ; Ursodeoxycholic Acid/therapeutic use
Chemical Substances	Cholagogues and Choleretics ; FGF19 protein, human ; Hypolipidemic Agents ; Immunosuppressive Agents ; Peroxisome Proliferator-Activated Receptors ; Receptors, Cytoplasmic and Nuclear ; obeticholic acid (0462Z4S4OZ) ; farnesoid X-activated receptor (0C5V0MRU6P) ; Chenodeoxycholic Acid (0GEI24LG0J) ; Fibroblast Growth Factors (62031-54-3) ; Ursodeoxycholic Acid (724L30Y2QR) ; Alkaline Phosphatase (EC 3.1.3.1) ; Fenofibrate (U202363UOS) ; Bezafibrate (Y9449Q51XH)
Language	English
Publishing date	2018-05-19
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1472315-3
ISSN	1557-8224 ; 1089-3261
ISSN (online)	1557-8224
ISSN	1089-3261
DOI	10.1016/j.cld.2018.03.003
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Article: An Unusual Cause of Abdominal Ascites

Wong, Kimberly A. / Olson, Kristin A. / Chak, Eric W.

Case Reports in Gastroenterology

2018 Volume 12, Issue 2, Page(s) 420–424

Institution	Department of Internal Medicine, University of California Davis School of Medicine, Sacramento, California, USA Department of Pathology, University of California Davis School of Medicine, Sacramento, California, USA Division of Gastroenterology and Hepatology, University of California Davis School of Medicine, Sacramento, California, USA
Abstract	Abdominal ascites is most commonly caused by portal hypertension from liver cirrhosis. When present, portal hypertension is associated with an elevated serum-ascites albumin gradient (SAAG) ≥1.1 g/dL. In contrast, a SAAG < 1.1 g/dL suggests malignancy, tuberculosis, pancreatitis, or nephrotic syndrome. Here, we present a case of low SAAG ascites caused by epithelioid peritoneal mesothelioma in a woman with no known liver disease. The diagnosis proved elusive until diagnostic laparoscopy with biopsy was performed.
Keywords	Ascites ; Liver ; Mesothelioma
Language	English
Publishing date	2018-08-21
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Single Case ; This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC).
ZDB-ID	2440540-1
ISSN	1662-0631 ; 1662-0631
ISSN (online)	1662-0631
ISSN	1662-0631
DOI	10.1159/000490660
Database	Karger publisher's database

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Article: Efficient retina formation requires suppression of both Activin and BMP signaling pathways in pluripotent cells.

Wong, Kimberly A / Trembley, Michael / Abd Wahab, Syafiq / Viczian, Andrea S

Biology open

2015 Volume 4, Issue 4, Page(s) 573–583

Abstract: Retina formation requires the correct spatiotemporal patterning of key regulatory factors. While it is known that repression of several signaling pathways lead to specification of retinal fates, addition of only Noggin, a known BMP antagonist, can ... ...

Abstract	Retina formation requires the correct spatiotemporal patterning of key regulatory factors. While it is known that repression of several signaling pathways lead to specification of retinal fates, addition of only Noggin, a known BMP antagonist, can convert pluripotent Xenopus laevis animal cap cells to functional retinal cells. The aim of this study is to determine the intracellular molecular events that occur during this conversion. Surprisingly, blocking BMP signaling alone failed to mimic Noggin treatment. Overexpressing Noggin in pluripotent cells resulted in a concentration-dependent suppression of both Smad1 and Smad2 phosphorylation, which act downstream of BMP and Activin signaling, respectively. This caused a decrease in downstream targets: endothelial marker, xk81, and mesodermal marker, xbra. We treated pluripotent cells with dominant-negative receptors or the chemical inhibitors, dorsomorphin and SB431542, which each target either the BMP or Activin signaling pathway. We determined the effect of these treatments on retina formation using the Animal Cap Transplant (ACT) assay; in which treated pluripotent cells were transplanted into the eye field of host embryos. We found that inhibition of Activin signaling, in the presence of BMP signaling inhibition, promotes efficient retinal specification in Xenopus tissue, mimicking the affect of adding Noggin alone. In whole embryos, we found that the eye field marker, rax, expanded when adding both dominant-negative Smad1 and Smad2, as did treating the cells with both dorsomorphin and SB431542. Future studies could translate these findings to a mammalian culture assay, in order to more efficiently produce retinal cells in culture.
Language	English
Publishing date	2015-03-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2632264-X
ISSN	2046-6390
ISSN	2046-6390
DOI	10.1242/bio.20149977
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Article ; Online: Retinal Ganglion Cell Axon Regeneration Requires Complement and Myeloid Cell Activity within the Optic Nerve.

Peterson, Sheri L / Li, Yiqing / Sun, Christina J / Wong, Kimberly A / Leung, Kylie S / de Lima, Silmara / Hanovice, Nicholas J / Yuki, Kenya / Stevens, Beth / Benowitz, Larry I

The Journal of neuroscience : the official journal of the Society for Neuroscience

2021 Volume 41, Issue 41, Page(s) 8508–8531

Abstract: Axon regenerative failure in the mature CNS contributes to functional deficits following many traumatic injuries, ischemic injuries, and neurodegenerative diseases. The complement cascade of the innate immune system responds to pathogen threat through ... ...

Abstract	Axon regenerative failure in the mature CNS contributes to functional deficits following many traumatic injuries, ischemic injuries, and neurodegenerative diseases. The complement cascade of the innate immune system responds to pathogen threat through inflammatory cell activation, pathogen opsonization, and pathogen lysis, and complement is also involved in CNS development, neuroplasticity, injury, and disease. Here, we investigated the involvement of the classical complement cascade and microglia/monocytes in CNS repair using the mouse optic nerve injury (ONI) model, in which axons arising from retinal ganglion cells (RGCs) are disrupted. We report that central complement C3 protein and mRNA, classical complement C1q protein and mRNA, and microglia/monocyte phagocytic complement receptor CR3 all increase in response to ONI, especially within the optic nerve itself. Importantly, genetic deletion of
MeSH term(s)	Animals ; Axons/immunology ; Axons/metabolism ; Complement C1q/immunology ; Complement C1q/metabolism ; Complement C3/immunology ; Complement C3/metabolism ; Female ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Nerve Regeneration/physiology ; Optic Nerve Injuries/immunology ; Optic Nerve Injuries/metabolism ; Optic Nerve Injuries/pathology ; Retinal Ganglion Cells/immunology ; Retinal Ganglion Cells/metabolism
Chemical Substances	Complement C3 ; Complement C1q (80295-33-6)
Language	English
Publishing date	2021-08-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.0555-21.2021
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Zs.A 1668: Show issues

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Article ; Online: AGER1 downregulation associates with fibrosis in nonalcoholic steatohepatitis and type 2 diabetes.

Dehnad, Ali / Fan, Weiguo / Jiang, Joy X / Fish, Sarah R / Li, Yuan / Das, Suvarthi / Mozes, Gergely / Wong, Kimberly A / Olson, Kristin A / Charville, Gregory W / Ali, Mohammed / Török, Natalie J

The Journal of clinical investigation

2020 Volume 130, Issue 8, Page(s) 4320–4330

Abstract: Type 2 diabetes is clinically associated with progressive necroinflammation and fibrosis in nonalcoholic steatohepatitis (NASH). Advanced glycation end-products (AGEs) accumulate during prolonged hyperglycemia, but the mechanistic pathways that lead to ... ...

Abstract	Type 2 diabetes is clinically associated with progressive necroinflammation and fibrosis in nonalcoholic steatohepatitis (NASH). Advanced glycation end-products (AGEs) accumulate during prolonged hyperglycemia, but the mechanistic pathways that lead to accelerated liver fibrosis have not been well defined. In this study, we show that the AGEs clearance receptor AGER1 was downregulated in patients with NASH and diabetes and in our NASH models, whereas the proinflammatory receptor RAGE was induced. These findings were associated with necroinflammatory, fibrogenic, and pro-oxidant activity via the NADPH oxidase 4. Inhibition of AGEs or RAGE deletion in hepatocytes in vivo reversed these effects. We demonstrate that dysregulation of NRF2 by neddylation of cullin 3 was linked to AGER1 downregulation and that induction of NRF2 using an adeno-associated virus-mediated approach in hepatocytes in vivo reversed AGER1 downregulation, lowered the level of AGEs, and improved proinflammatory and fibrogenic responses in mice on a high AGEs diet. In patients with NASH and diabetes or insulin resistance, low AGER1 levels were associated with hepatocyte ballooning degeneration and ductular reaction. Collectively, prolonged exposure to AGEs in the liver promotes an AGER1/RAGE imbalance and consequent redox, inflammatory, and fibrogenic activity in NASH.
MeSH term(s)	Animals ; Ascorbic Acid ; Cholecalciferol ; Dehydroepiandrosterone/analogs & derivatives ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Disease Models, Animal ; Down-Regulation ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Mice ; Mice, Knockout ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Nicotinic Acids ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology ; Plant Extracts ; Receptor for Advanced Glycation End Products/biosynthesis ; Receptor for Advanced Glycation End Products/genetics
Chemical Substances	AGER protein, human ; Ager protein, mouse ; HUM 5007 ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Nfe2l2 protein, mouse ; Nicotinic Acids ; Plant Extracts ; Receptor for Advanced Glycation End Products ; Cholecalciferol (1C6V77QF41) ; Dehydroepiandrosterone (459AG36T1B) ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2020-07-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI133051
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Article ; Online: Optic nerve regeneration: A long view.

Yin, Yuqin / De Lima, Silmara / Gilbert, Hui-Ya / Hanovice, Nicholas J / Peterson, Sheri L / Sand, Rheanna M / Sergeeva, Elena G / Wong, Kimberly A / Xie, Lili / Benowitz, Larry I

Restorative neurology and neuroscience

2019 Volume 37, Issue 6, Page(s) 525–544

Abstract: The optic nerve conveys information about the outside world from the retina to multiple subcortical relay centers. Until recently, the optic nerve was widely believed to be incapable of re-growing if injured, with dire consequences for victims of ... ...

Abstract	The optic nerve conveys information about the outside world from the retina to multiple subcortical relay centers. Until recently, the optic nerve was widely believed to be incapable of re-growing if injured, with dire consequences for victims of traumatic, ischemic, or neurodegenerative diseases of this pathway. Over the past 10-20 years, research from our lab and others has made considerable progress in defining factors that normally suppress axon regeneration and the ability of retinal ganglion cells, the projection neurons of the retina, to survive after nerve injury. Here we describe research from our lab on the role of inflammation-derived growth factors, suppression of inter-cellular signals among diverse retinal cell types, and combinatorial therapies, along with related studies from other labs, that enable animals with optic nerve injury to regenerate damaged retinal axons back to the brain. These studies raise the possibility that vision might one day be restored to people with optic nerve damage.
MeSH term(s)	Animals ; Axons/metabolism ; Axons/ultrastructure ; Humans ; Inflammation Mediators/metabolism ; Nerve Regeneration/physiology ; Optic Nerve/physiology ; Optic Nerve/ultrastructure ; Optic Nerve Injuries/metabolism ; Optic Nerve Injuries/pathology ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/ultrastructure
Chemical Substances	Inflammation Mediators
Language	English
Publishing date	2019-10-09
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1017098-4
ISSN	1878-3627 ; 0922-6028
ISSN (online)	1878-3627
ISSN	0922-6028
DOI	10.3233/RNN-190960
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