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Article ; Online: Adipose-derived Mesenchymal Stromal Cells Modulate Lipid Metabolism and Lipid Droplet Biogenesis via AKT/mTOR -PPARγ Signalling in Macrophages.

Souza-Moreira, Luciana / Soares, Vinicius Cardoso / Dias, Suelen da Silva Gomes / Bozza, Patricia T

2019 Volume 9, Issue 1, Page(s) 20304

Abstract: Mesenchymal stromal cells (MSCs) are a potential therapy for many chronic inflammatory diseases due to their regenerative, immunologic and anti-inflammatory properties. The two-way dialogue between MSCs and macrophages is crucial to tissue regeneration ... ...

Abstract	Mesenchymal stromal cells (MSCs) are a potential therapy for many chronic inflammatory diseases due to their regenerative, immunologic and anti-inflammatory properties. The two-way dialogue between MSCs and macrophages is crucial to tissue regeneration and repair. Previous research demonstrated that murine adipose-derived MSC conditioned medium (ASCcm) reprograms macrophages to an M2-like phenotype which protects from experimental colitis and sepsis. Here, our focus was to determine the molecular mechanism of lipid droplet biogenesis in macrophages re-educated using ASCcm. Adipose-derived MSC conditioned medium promotes phosphorylation of AKT/mTOR pathway proteins in macrophages. Furthermore, increased expression of PPARγ, lipid droplet biogenesis and PGE
MeSH term(s)	Adipose Tissue/cytology ; Cell Communication ; Lipid Droplets/metabolism ; Lipid Metabolism ; Macrophages/metabolism ; Mesenchymal Stem Cells/metabolism ; Models, Biological ; PPAR gamma/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	PPAR gamma ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2019-12-30
Publishing country	England
Document type	Journal Article ; 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/s41598-019-56835-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Correction: SARS-CoV-2 engages inflammasome and pyroptosis in human primary monocytes.

Ferreira, André C / Soares, Vinicius Cardoso / de Azevedo-Quintanilha, Isaclaudia G / Dias, Suelen da Silva Gomes / Fintelman-Rodrigues, Natalia / Sacramento, Carolina Q / Mattos, Mayara / de Freitas, Caroline S / Temerozo, Jairo R / Teixeira, Lívia / Hottz, Eugenio Damaceno / Barreto, Ester A / Pão, Camila R R / Palhinha, Lohanna / Miranda, Milene / Bou-Habib, Dumith Chequer / Bozza, Fernando A / Bozza, Patrícia T / Souza, Thiago Moreno L

Cell death discovery

2021 Volume 7, Issue 1, Page(s) 116

Language	English
Publishing date	2021-05-19
Publishing country	United States
Document type	Published Erratum
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-021-00477-1
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Article: SARS-CoV-2 engages inflammasome and pyroptosis in human primary monocytes.

Ferreira, André C / Soares, Vinicius Cardoso / de Azevedo-Quintanilha, Isaclaudia G / Dias, Suelen da Silva Gomes / Fintelman-Rodrigues, Natalia / Sacramento, Carolina Q / Mattos, Mayara / de Freitas, Caroline S / Temerozo, Jairo R / Teixeira, Lívia / Damaceno Hottz, Eugenio / Barreto, Ester A / Pão, Camila R R / Palhinha, Lohanna / Miranda, Milene / Bou-Habib, Dumith Chequer / Bozza, Fernando A / Bozza, Patrícia T / Souza, Thiago Moreno L

Cell death discovery

2021 Volume 7, Issue 1, Page(s) 43

Abstract: Infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with leukopenia and uncontrolled inflammatory response in critically ill patients. A better comprehension of SARS-CoV-2-induced monocyte death is essential ... ...

Abstract	Infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with leukopenia and uncontrolled inflammatory response in critically ill patients. A better comprehension of SARS-CoV-2-induced monocyte death is essential for the identification of therapies capable to control the hyper-inflammation and reduce viral replication in patients with 2019 coronavirus disease (COVID-19). Here, we show that SARS-CoV-2 engages inflammasome and triggers pyroptosis in human monocytes, experimentally infected, and from patients under intensive care. Pyroptosis associated with caspase-1 activation, IL-1ß production, gasdermin D cleavage, and enhanced pro-inflammatory cytokine levels in human primary monocytes. At least in part, our results originally describe mechanisms by which monocytes, a central cellular component recruited from peripheral blood to respiratory tract, succumb to control severe COVID-19.
Language	English
Publishing date	2021-03-01
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-021-00428-w
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Article: Non-permissive SARS-CoV-2 infection in human neurospheres.

Pedrosa, Carolina da S G / Goto-Silva, Livia / Temerozo, Jairo R / Souza, Leticia R Q / Vitória, Gabriela / Ornelas, Isis M / Karmirian, Karina / Mendes, Mayara A / Gomes, Ismael C / Sacramento, Carolina Q / Fintelman-Rodrigues, Natalia / Soares, Vinicius Cardoso / Dias, Suelen da Silva Gomes / Salerno, José Alexandre / Puig-Pijuan, Teresa / Oliveira, Julia T / Aragão, Luiz G H S / Torquato, Thayana C Q / Veríssimo, Carla /

Biagi, Diogo / Cruvinel, Estela M / Dariolli, Rafael / Furtado, Daniel R / Borges, Helena L / Bozza, Patrícia T / Rehen, Stevens / Souza, Thiago Moreno L / Guimarães, Marília Zaluar P

bioRxiv : the preprint server for biology

2021

Abstract: Coronavirus disease 2019 (COVID-19) was initially described as a viral infection of the respiratory tract. It is now known, however, that several other organs are affected, including the brain. Neurological manifestations such as stroke, encephalitis, ... ...

Abstract	Coronavirus disease 2019 (COVID-19) was initially described as a viral infection of the respiratory tract. It is now known, however, that several other organs are affected, including the brain. Neurological manifestations such as stroke, encephalitis, and psychiatric conditions have been reported in COVID-19 patients, but the neurotropic potential of the virus is still debated. Herein, we sought to investigate SARS-CoV-2 infection in human neural cells. We demonstrated that SARS-CoV-2 infection of neural tissue is non-permissive, however, it can elicit inflammatory response and cell damage. These findings add to the hypothesis that most of the neural damage caused by SARS-CoV-2 infection is due to a systemic inflammation leading to indirect harmful effects on the central nervous system despite the absence of local viral replication.
Keywords	covid19
Language	English
Publishing date	2021-06-17
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.09.11.293951
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Article ; Online: The neuropeptides VIP and PACAP inhibit SARS-CoV-2 replication in monocytes and lung epithelial cells and decrease the production of proinflammatory cytokines in infected cells

Temerozo, Jairo R. / Sacramento, Carolina Q. / Fintelman-Rodrigues, Natalia / Pao, Camila R. R. / Freitas, Caroline S. de / Dias, Suelen da Silva Gomes / Ferreira, AndrÃ© C / Mattos, Mayara / Soares, Vinicius Cardoso / Teixeira, LÃvia / Azevedo-Quintanilha, Isaclaudia G. de / Bozza, Fernando A. / Bozza, PatrÃcia T. / Souza, Thiago Moreno L. / Bou-Habib, Dumith Chequer

bioRxiv

Abstract: Infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), may elicit uncontrolled and damaging inflammatory reactions, due to an excessive immune response and dysregulated ... ...

Abstract	Infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), may elicit uncontrolled and damaging inflammatory reactions, due to an excessive immune response and dysregulated production of cytokines and chemokines. Thus, it is critical to identify compounds able to inhibit virus replication and thwart the excessive inflammatory reaction and tissue lesions secondary to SARS-CoV-2 infection. Here, we show that the neuropeptides VIP and PACAP, molecules endowed with immunoregulatory properties, were able to inhibit SARS-CoV-2 RNA synthesis/replication in human monocytes and viral production in lung epithelial cells. VIP and PACAP protected these cells from virus-induced cytopathicity, reduced the production of proinflammmatory mediators, and prevented the SARS-CoV-2-induced NF-kB activation, which is critically involved in the production of inflammatory mediators. Both neuropeptides promoted CREB activation in infected monocytes, a transcription factor with antiapoptotic activity and also a negative regulator of NF-kB. As a possible host response to control patient inflammation, we identified that VIP levels were elevated in plasma from patients with severe forms of COVID-19, correlating with the inflammatory marker CRP and survival on those patients. Since a synthetic form of VIP is clinically approved in Europe and under two clinical trials for patients with COVID-19, our results provide the scientific evidence to further support clinical investigation of these neuropeptides against COVID-19.
Keywords	covid19
Publisher	BioRxiv; WHO
Document type	Article ; Online
Note	WHO #Covidence: #220806
DOI	10.1101/2020.07.25.220806
Database	COVID19

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Article ; Online: The neuropeptides VIP and PACAP inhibit SARS-CoV-2 replication in monocytes and lung epithelial cells and decrease the production of proinflammatory cytokines in infected cells.

Temerozo, Jairo R. / Sacramento, Carolina Q. / Fintelman-Rodrigues, Natalia / Pao, Camila R. R. / de Freitas, Caroline S. / Dias, Suelen da Silva Gomes / Ferreira, André C / Mattos, Mayara / Soares, Vinicius Cardoso / Teixeira, Lívia / de Azevedo-Quintanilha, Isaclaudia G. / Kurtz, Pedro / Bozza, Fernando A. / Bozza, Patrícia T. / Souza, Thiago Moreno L. / Bou-Habib, Dumith Chequer

bioRxiv

Abstract	Infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), may elicit uncontrolled and damaging inflammatory reactions, due to an excessive immune response and dysregulated production of cytokines and chemokines. Thus, it is critical to identify compounds able to inhibit virus replication and thwart the excessive inflammatory reaction and tissue lesions secondary to SARS-CoV-2 infection. Here, we show that the neuropeptides VIP and PACAP, molecules endowed with immunoregulatory properties, were able to inhibit SARS-CoV-2 RNA synthesis/replication in human monocytes and viral production in lung epithelial cells. VIP and PACAP protected these cells from virus-induced cytopathicity, and reduced the production of proinflammmatory mediators. VIP and PACAP prevented the SARS-CoV-2-induced NF-kB activation, which is critically involved in the production of inflammatory mediators, and promoted CREB activation, a transcription factor with antiapoptotic activity and also a negative regulator of NF-kB, in infected monocytes. By imparing this signaling loop, VIP and PACAP prevented NF-kB-dependent production of proinflammatory cytokines. As a possible host response to control patient inflammation, we identified that VIP levels were elevated in plasma from patients with severe forms of COVID-19, correlating with the inflammatory marker CRP and survival on those patients. Since a synthetic form of VIP is clinically approved in Europe and under two clinical trials for patients with COVID-19, our results provide the scientific evidence to further support clinical investigation of these neuropeptides against COVID-19.
Keywords	covid19
Language	English
Publishing date	2020-07-26
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2020.07.25.220806
Database	COVID19

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Article ; Online: SARS-CoV-2 induces inflammasome-dependent pyroptosis and downmodulation of HLA-DR in human monocytes, which can be prevented by atazanavir.

Ferreira, Andre Costa / Soares, Vinicius Cardoso / Quintanilha, Isaclaudia Gomes de Azevedo / Dias, Suelen da Silva Gomes / Rodrigues, Natalia Fintelman / Sacramento, Carolina Queiroz / Mattos, Mayara / Freitas, Caroline S / Temerozo, Jairo R / Teixeira, Livia / Hottz, Eugenio D / Barreto, Ester / Pao, Camila RR / Palhinha, Lohanna / Miranda, Milene / Bou-Habib, Dumith C / Bozza, Fernando A / Bozza, Patricia T / Lopes e Souza, Thiago M

medRxiv

Abstract	Infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with leukopenia and uncontrolled inflammatory response in critically ill patients. A better comprehension of SARS-CoV-2-induced monocytes death is essential for the identification of therapies capable to control the hyper-inflammation and reduce viral replication in patients with COVID-19. Here, we show that SARS-CoV-2 induces inflammasome activation and cell death by pyroptosis in human monocytes, experimentally infected and in patients under intensive care. Pyroptosis was dependent on caspase-1 engagement, prior to IL-1beta production and inflammatory cell death. Monocytes exposed to SARS-CoV-2 downregulate HLA-DR, suggesting a potential limitation to orchestrate the immune response. Our results originally describe the mechanism by which monocytes, a central cellular component recruited from peripheral blood to respiratory tract, succumb in patients with severe 2019 coronavirus disease (COVID-19), and emphasize the need for identifying anti-inflammatory and antiviral strategies to prevent SARS-CoV-2-induced pyroptosis.
Keywords	covid19
Language	English
Publishing date	2020-08-31
Publisher	Cold Spring Harbor Laboratory Press
Document type	Article ; Online
DOI	10.1101/2020.08.25.20182055
Database	COVID19

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Article ; Online: A cannabinoid receptor agonist shows anti-inflammatory and survival properties in human SARS-CoV-2-infected iPSC-derived cardiomyocytes

Aragao, Luiz Guilherme H.S. / Oliveira, Julia T / Temerozo, Jairo R / Mendes, Mayara A / Salerno, Jose Alexandre / Pedrosa, Carolina da S. G. / Puig-Pijuan, Teresa / Verissimo, Carla / Ornelas, Isis M / Torquato, Thayana / Vitoria, Gabriela / Sacramento, Carolina Q. / Fintelman-Rodrigues, Natalia / Dias, Suelen da Silva Gomes / Cardoso Soares, Vinicius / Souza, Leticia R. Q. / Karmirian, Karina / Goto-Silva, Livia / Biagi, Diogo /

Cruvinel, Estela M. / Dariolli, Rafael / Furtado, Daniel R. / Bozza, Patricia T. / Borges, Helena L. / Souza, Thiago Moreno L. / Guimaraes, Marilia Zaluar P. / Rehen, Stevens

bioRxiv

Abstract: Coronavirus disease 2019 (COVID-19) is caused by acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can infect several organs and lead to loss of vital organ function, especially impacting respiratory capacity. Among the extrapulmonary ... ...

Abstract	Coronavirus disease 2019 (COVID-19) is caused by acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can infect several organs and lead to loss of vital organ function, especially impacting respiratory capacity. Among the extrapulmonary manifestations of COVID-19 is myocardial injury, caused both directly and indirectly by SARS-CoV-2, and which is associated with a high risk of mortality. One of the hallmarks of severe COVID-19 is the cytokine storm, at which point the immune system malfunctions, leading to possible organ failure and death. Cannabinoids are known to have anti-inflammatory properties by negatively modulating the release of pro-inflammatory cytokines. Herein, we investigated the effects of the cannabinoid agonist WIN 55,212-2 (WIN) on SARS-CoV-2-infected human iPSC-derived cardiomyocytes (hiPSC-CMs). Although WIN did not modulate angiotensin-converting enzyme II, nor reduced SARS-CoV-2 infection and replication in hiPSC-CMs at the conditions tested, it had anti-inflammatory and protective effects by reducing the levels of interleukins 6, 8,18 and tumor necrosis factor-alpha (TNF-α) and lactate dehydrogenase (LDH) activity in these cells without causing hypertrophic cardiac damage. These findings suggest that cannabinoids should be further investigated as an alternative therapeutic tool for the treatment of COVID-19.
Keywords	covid19
Language	English
Publishing date	2021-02-21
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2021.02.20.431855
Database	COVID19

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Article ; Online: Inhibition of SARS-CoV-2 infection in human cardiomyocytes by targeting the Sigma-1 receptor disrupts cytoskeleton architecture and contractility

Salerno, José Alexandre / Torquato, Thayana / Temerozo, Jairo R / Goto-Silva, Livia / Mendes, Mayara A. / Sacramento, Carolina Q. / Fintelman-Rodrigues, Natalia / Vitoria, Gabriela / Souza, Leticia R. Q. / Ornelas, Isis M. / Veríssimo, Carla / Karmirian, Karina / Pedrosa, Carolina da S. G. / Dias, Suelen da Silva Gomes / Soares, Vinicius Cardoso / Aragão, Luiz Guilherme H.S. / Puig-Pijuan, Teresa / Salazar, Vinicius W / Dariolli, Rafael /

Biagi, Diogo / Furtado, Daniel Rodrigues / Borges, Helena L. / Bozza, Patrícia T / Guimarães, Marília Zaluar P. / Souza, Thiago Moreno L. / Rehen, Stevens

bioRxiv

Abstract: Heart dysfunction, represented by conditions such as myocarditis and arrhythmia, has been reported in COVID-19 patients. Therapeutic strategies focused on the cardiovascular system, however, remain scarce. The Sigma-1 receptor (S1R) has been recently ... ...

Abstract	Heart dysfunction, represented by conditions such as myocarditis and arrhythmia, has been reported in COVID-19 patients. Therapeutic strategies focused on the cardiovascular system, however, remain scarce. The Sigma-1 receptor (S1R) has been recently proposed as a therapeutic target because its inhibition reduces SARS-CoV-2 replication. To investigate the role of S1R in SARS-CoV-2 infection in the heart, we used human cardiomyocytes derived from induced pluripotent stem cells (hiPSC-CM) as an experimental model. Here we show that the S1R antagonist NE-100 decreases SARS-CoV-2 infection and viral replication in hiPSC-CMs. Also, NE-100 reduces cytokine release and cell death associated with infection. Because S1R is involved in cardiac physiology, we investigated the effects of NE-100 in cardiomyocyte morphology and function. We show that NE-100 compromises cytoskeleton integrity and reduces beating frequency, causing contractile impairment. These results show that targeting S1R to challenge SARS-CoV-2 infection may be a useful therapeutic strategy but its detrimental effects in vivo on cardiac function should not be ignored.
Keywords	covid19
Language	English
Publishing date	2021-02-21
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2021.02.20.432092
Database	COVID19

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Article ; Online: In vitro antiviral activity of the anti-HCV drugs daclatasvir and sofosbuvir against SARS-CoV-2, the aetiological agent of COVID-19.

Sacramento, Carolina Q / Fintelman-Rodrigues, Natalia / Temerozo, Jairo R / Da Silva, Aline de Paula Dias / Dias, Suelen da Silva Gomes / da Silva, Carine Dos Santos / Ferreira, André C / Mattos, Mayara / Pão, Camila R R / de Freitas, Caroline S / Soares, Vinicius Cardoso / Hoelz, Lucas Villas Bôas / Fernandes, Tácio Vinício Amorim / Branco, Frederico Silva Castelo / Bastos, Mônica Macedo / Boechat, Núbia / Saraiva, Felipe B / Ferreira, Marcelo Alves / Jockusch, Steffen /

The Journal of antimicrobial chemotherapy

2021 Volume 76, Issue 7, Page(s) 1874–1885

Abstract: Background: Current approaches of drug repurposing against COVID-19 have not proven overwhelmingly successful and the SARS-CoV-2 pandemic continues to cause major global mortality. SARS-CoV-2 nsp12, its RNA polymerase, shares homology in the nucleotide ... ...

Abstract	Background: Current approaches of drug repurposing against COVID-19 have not proven overwhelmingly successful and the SARS-CoV-2 pandemic continues to cause major global mortality. SARS-CoV-2 nsp12, its RNA polymerase, shares homology in the nucleotide uptake channel with the HCV orthologue enzyme NS5B. Besides, HCV enzyme NS5A has pleiotropic activities, such as RNA binding, that are shared with various SARS-CoV-2 proteins. Thus, anti-HCV NS5B and NS5A inhibitors, like sofosbuvir and daclatasvir, respectively, could be endowed with anti-SARS-CoV-2 activity. Methods: SARS-CoV-2-infected Vero cells, HuH-7 cells, Calu-3 cells, neural stem cells and monocytes were used to investigate the effects of daclatasvir and sofosbuvir. In silico and cell-free based assays were performed with SARS-CoV-2 RNA and nsp12 to better comprehend the mechanism of inhibition of the investigated compounds. A physiologically based pharmacokinetic model was generated to estimate daclatasvir's dose and schedule to maximize the probability of success for COVID-19. Results: Daclatasvir inhibited SARS-CoV-2 replication in Vero, HuH-7 and Calu-3 cells, with potencies of 0.8, 0.6 and 1.1 μM, respectively. Although less potent than daclatasvir, sofosbuvir alone and combined with daclatasvir inhibited replication in Calu-3 cells. Sofosbuvir and daclatasvir prevented virus-induced neuronal apoptosis and release of cytokine storm-related inflammatory mediators, respectively. Sofosbuvir inhibited RNA synthesis by chain termination and daclatasvir targeted the folding of secondary RNA structures in the SARS-CoV-2 genome. Concentrations required for partial daclatasvir in vitro activity are achieved in plasma at Cmax after administration of the approved dose to humans. Conclusions: Daclatasvir, alone or in combination with sofosbuvir, at higher doses than used against HCV, may be further fostered as an anti-COVID-19 therapy.
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; COVID-19 ; Carbamates ; Chlorocebus aethiops ; Humans ; Imidazoles ; Pharmaceutical Preparations ; Pyrrolidines ; RNA, Viral ; SARS-CoV-2 ; Sofosbuvir/pharmacology ; Valine/analogs & derivatives ; Vero Cells
Chemical Substances	Antiviral Agents ; Carbamates ; Imidazoles ; Pharmaceutical Preparations ; Pyrrolidines ; RNA, Viral ; Valine (HG18B9YRS7) ; daclatasvir (LI2427F9CI) ; Sofosbuvir (WJ6CA3ZU8B)
Language	English
Publishing date	2021-04-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	191709-2
ISSN	1460-2091 ; 0305-7453
ISSN (online)	1460-2091
ISSN	0305-7453
DOI	10.1093/jac/dkab072
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