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Article: Postoperative Seroma Deep to Mesh after Laparoscopic Ventral Hernia Repair: Computed Tomography Appearance and Implications for Treatment.

Scott, Paul D / Harold, Kristi L / Craft, Randall O / Roberts, Catherine Celeste

2015 Volume 3, Issue 1, Page(s) 128

Abstract: We report the development of a seroma deep to a mesh prosthesis used for laparoscopic ventral hernia repair (LVHR). Seroma formation anterior to mesh after LVHR is very common; however, the formation of a deep seroma has been rarely reported in the ... ...

Abstract	We report the development of a seroma deep to a mesh prosthesis used for laparoscopic ventral hernia repair (LVHR). Seroma formation anterior to mesh after LVHR is very common; however, the formation of a deep seroma has been rarely reported in the literature and the imaging appearance of a seroma posterior to mesh after LVHR has not been previously described. We present the imaging appearance and our clinical results of aspirating two seromas posterior to mesh after LVHR.
Language	English
Publishing date	2015-11-06
Publishing country	Netherlands
Document type	Case Reports
ZDB-ID	2406300-9
ISSN	1930-0433
ISSN	1930-0433
DOI	10.2484/rcr.v3i1.128
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Article ; Online: Prospective comparative study of quantitative X-ray (QXR) versus dual energy X-ray absorptiometry to determine the performance of QXR as a predictor of bone health for adult patients in secondary care.

Rangan, Amar / Tuck, Stephen P / Scott, Paul D / Kottam, Lucksy / Jafari, Maya / Watson, Terence / Lopez, Ben / Crone, Ben / Whitbread, Tim / Ratcliffe, Adam

BMJ open

2021 Volume 11, Issue 12, Page(s) e051021

Abstract: Objectives: To evaluate a method of quantitative X-ray (QXR) for obtaining bone health information from standard radiographs aimed at identifying early signs of osteoporosis to enable improved referral and treatment. This QXR measurement is performed by ...

Abstract	Objectives: To evaluate a method of quantitative X-ray (QXR) for obtaining bone health information from standard radiographs aimed at identifying early signs of osteoporosis to enable improved referral and treatment. This QXR measurement is performed by postexposure analysis of standard radiographs, meaning bone health data can be acquired opportunistically, alongside routine imaging. Design: The relationship between QXR and dual energy X-ray absorptiometry (DEXA) was demonstrated with a phantom study. A prospective clinical study was conducted to establish areal bone mineral density (aBMD) prediction model and a risk prediction model of a non-normal DEXA outcome. This was then extrapolated to a larger patient group with DEXA referral data. Setting: Secondary care National Health Service Hospital. Participants: 126 consenting adult patients from a DEXA clinic. Interventions: All participants underwent a DEXA scan to determine BMD at the lumbar spine (L2-L4) and both hips. An additional Antero-Posterior pelvis X-ray on a Siemens Ysio, fixed digital radiograph system was performed for the study. Outcome: Performance of QXR as a risk predictor for non-normal (osteoporotic) BMD. Results: Interim clinical study data from 78 patients confirmed a receiver operator curve (area under the ROC curve) of 0.893 (95% CI 0.843 to 0.942) for a risk prediction model of non-normal DEXA outcome. Extrapolation of these results to a larger patient group of 11 029 patients indicated a positive predictive value of 0.98 (sensitivity of 0.8) for a population of patients referred to DEXA under current clinical referral criteria. Conclusions: This study confirms that the novel QXR method provides accurate prediction of a DEXA outcome. Trial registration number: ISRCTN98160454; Pre-results.
MeSH term(s)	Absorptiometry, Photon/methods ; Adult ; Bone Density ; Humans ; Lumbar Vertebrae/diagnostic imaging ; Prospective Studies ; Secondary Care ; State Medicine ; X-Rays
Language	English
Publishing date	2021-12-24
Publishing country	England
Document type	Journal Article
ZDB-ID	2599832-8
ISSN	2044-6055 ; 2044-6055
ISSN (online)	2044-6055
ISSN	2044-6055
DOI	10.1136/bmjopen-2021-051021
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Article ; Online: Unexpected complexity in the interference activity of a cloned influenza defective interfering RNA.

Meng, Bo / Bentley, Kirsten / Marriott, Anthony C / Scott, Paul D / Dimmock, Nigel J / Easton, Andrew J

Virology journal

2017 Volume 14, Issue 1, Page(s) 138

Abstract: Background: Defective interfering (DI) viruses are natural antivirals made by nearly all viruses. They have a highly deleted genome (thus being non-infectious) and interfere with the replication of genetically related infectious viruses. We have ... ...

Abstract	Background: Defective interfering (DI) viruses are natural antivirals made by nearly all viruses. They have a highly deleted genome (thus being non-infectious) and interfere with the replication of genetically related infectious viruses. We have produced the first potential therapeutic DI virus for the clinic by cloning an influenza A DI RNA (1/244) which was derived naturally from genome segment 1. This is highly effective in vivo, and has unexpectedly broad-spectrum activity with two different modes of action: inhibiting influenza A viruses through RNA interference, and all other (interferon-sensitive) respiratory viruses through stimulating interferon type I. Results: We have investigated the RNA inhibitory mechanism(s) of DI 1/244 RNA. Ablation of initiation codons does not diminish interference showing that no protein product is required for protection. Further analysis indicated that 1/244 DI RNA interferes by replacing the cognate full-length segment 1 RNA in progeny virions, while interfering with the expression of genome segment 1, its cognate RNA, and genome RNAs 2 and 3, but not genome RNA 6, a representative of the non-polymerase genes. Conclusions: Our data contradict the dogma that a DI RNA only interferes with expression from its cognate full-length segment. There is reciprocity as cloned segment 2 and 3 DI RNAs inhibited expression of RNAs from a segment 1 target. These data demonstrate an unexpected complexity in the mechanism of interference by this cloned therapeutic DI RNA.
MeSH term(s)	Defective Viruses/genetics ; Defective Viruses/immunology ; Defective Viruses/isolation & purification ; HEK293 Cells ; Humans ; Influenza A virus/genetics ; Influenza A virus/growth & development ; Interferon Type I/metabolism ; RNA Interference ; RNA, Viral/genetics ; RNA, Viral/metabolism
Chemical Substances	Interferon Type I ; RNA, Viral
Language	English
Publishing date	2017-07-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2160640-7
ISSN	1743-422X ; 1743-422X
ISSN (online)	1743-422X
ISSN	1743-422X
DOI	10.1186/s12985-017-0805-6
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Article ; Online: A Defective Interfering Influenza RNA Inhibits Infectious Influenza Virus Replication in Human Respiratory Tract Cells: A Potential New Human Antiviral.

Smith, Claire M / Scott, Paul D / O'Callaghan, Christopher / Easton, Andrew J / Dimmock, Nigel J

Viruses

2016 Volume 8, Issue 8

Abstract: Defective interfering (DI) viruses arise during the replication of influenza A virus and contain a non-infective version of the genome that is able to interfere with the production of infectious virus. In this study we hypothesise that a cloned DI ... ...

Abstract	Defective interfering (DI) viruses arise during the replication of influenza A virus and contain a non-infective version of the genome that is able to interfere with the production of infectious virus. In this study we hypothesise that a cloned DI influenza A virus RNA may prevent infection of human respiratory epithelial cells with infection by influenza A. The DI RNA (244/PR8) was derived by a natural deletion process from segment 1 of influenza A/PR/8/34 (H1N1); it comprises 395 nucleotides and is packaged in the DI virion in place of a full-length genome segment 1. Given intranasally, 244/PR8 DI virus protects mice and ferrets from clinical influenza caused by a number of different influenza A subtypes and interferes with production of infectious influenza A virus in cells in culture. However, evidence that DI influenza viruses are active in cells of the human respiratory tract is lacking. Here we show that 244/PR8 DI RNA is replicated by an influenza A challenge virus in human lung diploid fibroblasts, bronchial epithelial cells, and primary nasal basal cells, and that the yield of challenge virus is significantly reduced in a dose-dependent manner indicating that DI influenza virus has potential as a human antiviral.
MeSH term(s)	Administration, Intranasal ; Animals ; Antiviral Agents/administration & dosage ; Antiviral Agents/metabolism ; Defective Viruses/genetics ; Disease Models, Animal ; Epithelial Cells/virology ; Ferrets ; Fibroblasts/virology ; Humans ; Influenza A Virus, H1N1 Subtype/drug effects ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H1N1 Subtype/physiology ; Mice ; Orthomyxoviridae Infections/prevention & control ; RNA, Viral/administration & dosage ; RNA, Viral/metabolism ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; RNA, Viral
Language	English
Publishing date	2016-08-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v8080237
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Article ; Online: Defective interfering virus protects elderly mice from influenza

Easton Andrew J / Marriott Anthony C / Meng Bo / Scott Paul D / Dimmock Nigel J

Virology Journal, Vol 8, Iss 1, p

2011 Volume 212

Abstract: Abstract Background We have identified and characterised a defective-interfering (DI) influenza A virus particles containing a highly deleted segment 1 RNA that has broad-spectrum antiviral activity. In young adult mice it exerts protection against ... ...

Abstract	Abstract Background We have identified and characterised a defective-interfering (DI) influenza A virus particles containing a highly deleted segment 1 RNA that has broad-spectrum antiviral activity. In young adult mice it exerts protection against several different subtypes of influenza A virus (defined here as homologous or genetically compatible protection) and against a paramyxovirus and an influenza B virus (heterologous or genetically unrelated protection). Homologous protection is mediated by replication competition between the deleted and full-length genomes, and heterologous protection occurs through stimulation of innate immunity, especially interferon type I. Methods A single dose of the protective DI virus was administered intranasally to elderly mice at -7, -1 and +1 days relative to intranasal challenge with influenza A virus. Results A single dose of the DI virus given 1 or 7 days protected elderly mice, reducing a severe, sometimes fatal disease to a subclinical or mild infection. In contrast, all members of control groups treated with inactivated DI virus before challenge became extremely ill and most died. Despite the subclinical/mild nature of their infection, protected mice developed solid immunity to a second infectious challenge. Conclusions The defective interfering virus is effective in preventing severe influenza A in elderly mice and may offer a new approach to protection of the human population.
Keywords	elderly ; defective-interfering virus ; geriatric ; influenza ; mice ; treatment ; Microbiology ; QR1-502 ; Science ; Q ; DOAJ:Microbiology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences ; Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	616
Language	English
Publishing date	2011-05-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Defective interfering influenza virus confers only short-lived protection against influenza virus disease: Evidence for a role for adaptive immunity in DI virus-mediated protection in vivo

Scott, Paul D / Meng, Bo / Marriott, Anthony C / Easton, Andrew J / Dimmock, Nigel J

Vaccine. 2011 Sept. 2, v. 29, no. 38

2011

Abstract: We have shown earlier that a single dose of cloned defective interfering (DI) influenza A virus strongly protects mice from disease following a lethal challenge with different subtypes of influenza A virus. These animals suffered no clinical disease but ... ...

Abstract	We have shown earlier that a single dose of cloned defective interfering (DI) influenza A virus strongly protects mice from disease following a lethal challenge with different subtypes of influenza A virus. These animals suffered no clinical disease but experienced a subclinical infection which rendered them immune to reinfection with the same challenge virus. However, little is known about how DI virus achieves such protection. Here we investigated the role of adaptive immunity in DI virus-mediated protection using severe-combined immunodeficient (SCID) mice, which lack competence in both B- and T-cell compartments but retain NK cell activity. SCID mice which were treated with DI virus and infected with influenza virus initially remained completely well, while infected litter mates that received UV-inactivated DI virus became seriously ill and died. However, after 10 days of good health, the DI virus-protected SCID mice developed a clinical disease that was similar, but not completely identical, to the acute influenza disease. Disease was delayed longer by a higher dose of DI virus. We excluded the possibilities that the DI virus load in the lungs had declined, that the DI RNA sequence had changed so that it no longer interfered with the infectious genome, or that infectious virus had become resistant to the DI virus. These data show that while DI virus provides full protection from the acute disease in the absence of adaptive immunity, that same immunity is essential for clearing the infection. This indicates that the conventional view that DI virus-induced protection is mediated solely by competition for replication with the challenge virus is incorrect for influenza virus.
Keywords	Orthomyxoviridae ; RNA ; T-lymphocytes ; acute course ; adaptive immunity ; genome ; influenza ; lungs ; mice ; nucleotide sequences ; severe combined immunodeficiency ; vaccines ; viral load ; viruses
Language	English
Dates of publication	2011-0902
Size	p. 6584-6591.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	605674-x
ISSN	1873-2518 ; 0264-410X
ISSN (online)	1873-2518
ISSN	0264-410X
DOI	10.1016/j.vaccine.2011.06.114
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Article ; Online: Results of laparoscopic Heller myotomy for extreme megaesophagus: an alternative to esophagectomy.

Scott, Paul D / Harold, Kristi L / Heniford, B Todd / Jaroszewski, Dawn E

Surgical laparoscopy, endoscopy & percutaneous techniques

2009 Volume 19, Issue 3, Page(s) 198–200

Abstract: Heller myotomy is recognized as the optimal treatment for achalasia. However, treatment of the markedly dilated esophagus has been debated in the literature. Although esophagectomy has been the standard treatment historically, several studies have ... ...

Abstract	Heller myotomy is recognized as the optimal treatment for achalasia. However, treatment of the markedly dilated esophagus has been debated in the literature. Although esophagectomy has been the standard treatment historically, several studies have examined successful treatment of achalasia with laparoscopic Heller myotomy in the setting of a markedly dilated esophagus (>6 cm). Patients with extreme megaesophagus (>10 cm) are often treated with esophagectomy. We report the successful treatment of 4 patients with extreme megaesophagus with laparoscopic Heller myotomy. Three of the 4 patients also had Toupet fundoplication. The average esophageal diameter was 11.2 cm (10 to 12 cm). In addition to severe dysphagia, all patients had preoperative signs, symptoms, and radiographic evidence of esophageal compression of their heart and lungs. All patients reported relief of their preoperative symptoms. Esophagectomy has not been required to maintain adequate clinical results in any of our patients. We conclude that laparoscopic Heller myotomy is an appropriate alternative to esophagectomy and can be offered to patients with extreme megaesophagus.
MeSH term(s)	Esophageal Achalasia/diagnosis ; Esophageal Achalasia/surgery ; Esophagoscopy ; Follow-Up Studies ; Humans ; Laparoscopy/methods ; Muscle, Smooth/surgery ; Retrospective Studies ; Tomography, X-Ray Computed ; Treatment Outcome
Language	English
Publishing date	2009-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	1475108-2
ISSN	1534-4908 ; 1530-4515 ; 1051-7200
ISSN (online)	1534-4908
ISSN	1530-4515 ; 1051-7200
DOI	10.1097/SLE.0b013e3181a6dd58
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Article ; Online: Defective interfering virus protects elderly mice from influenza.

Scott, Paul D / Meng, Bo / Marriott, Anthony C / Easton, Andrew J / Dimmock, Nigel J

Virology journal

2011 Volume 8, Page(s) 212

Abstract: Background: We have identified and characterised a defective-interfering (DI) influenza A virus particles containing a highly deleted segment 1 RNA that has broad-spectrum antiviral activity. In young adult mice it exerts protection against several ... ...

Abstract	Background: We have identified and characterised a defective-interfering (DI) influenza A virus particles containing a highly deleted segment 1 RNA that has broad-spectrum antiviral activity. In young adult mice it exerts protection against several different subtypes of influenza A virus (defined here as homologous or genetically compatible protection) and against a paramyxovirus and an influenza B virus (heterologous or genetically unrelated protection). Homologous protection is mediated by replication competition between the deleted and full-length genomes, and heterologous protection occurs through stimulation of innate immunity, especially interferon type I. Methods: A single dose of the protective DI virus was administered intranasally to elderly mice at -7, -1 and +1 days relative to intranasal challenge with influenza A virus. Results: A single dose of the DI virus given 1 or 7 days protected elderly mice, reducing a severe, sometimes fatal disease to a subclinical or mild infection. In contrast, all members of control groups treated with inactivated DI virus before challenge became extremely ill and most died. Despite the subclinical/mild nature of their infection, protected mice developed solid immunity to a second infectious challenge. Conclusions: The defective interfering virus is effective in preventing severe influenza A in elderly mice and may offer a new approach to protection of the human population.
MeSH term(s)	Animals ; Body Weight ; Defective Viruses ; Disease Models, Animal ; Female ; Immunity, Innate ; Influenza A virus/immunology ; Influenza A virus/pathogenicity ; Influenza B virus/immunology ; Influenza B virus/pathogenicity ; Interferons/immunology ; Male ; Mice ; Mice, Inbred C3H ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/pathology ; Orthomyxoviridae Infections/prevention & control ; Orthomyxoviridae Infections/virology ; Rodent Diseases/immunology ; Rodent Diseases/pathology ; Rodent Diseases/prevention & control ; Rodent Diseases/virology ; Severity of Illness Index ; Virus Replication
Chemical Substances	Interferons (9008-11-1)
Language	English
Publishing date	2011-05-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1743-422X
ISSN (online)	1743-422X
DOI	10.1186/1743-422X-8-212
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Article ; Online: Defective interfering influenza A virus protects in vivo against disease caused by a heterologous influenza B virus.

Scott, Paul D / Meng, Bo / Marriott, Anthony C / Easton, Andrew J / Dimmock, Nigel J

The Journal of general virology

2011 Volume 92, Issue Pt 9, Page(s) 2122–2132

Abstract: Influenza A and B viruses are major human respiratory pathogens that contribute to the burden of seasonal influenza. They are both members of the family Orthomyxoviridae but do not interact genetically and are classified in different genera. Defective ... ...

Abstract	Influenza A and B viruses are major human respiratory pathogens that contribute to the burden of seasonal influenza. They are both members of the family Orthomyxoviridae but do not interact genetically and are classified in different genera. Defective interfering (DI) influenza viruses have a major deletion of one or more of their eight genome segments, which renders them both non-infectious and able to interfere in cell culture with the production of infectious progeny by a genetically compatible, homologous virus. It has been shown previously that intranasal administration of a cloned DI influenza A virus, 244/PR8, protects mice from various homologous influenza A virus subtypes and that it also protects mice from respiratory disease caused by a heterologous virus belonging to the family Paramyxoviridae. The mechanisms of action in vivo differ, with homologous and heterologous protection being mediated by probable genome competition and type I interferon (IFN), respectively. In the current study, it was shown that 244/PR8 also protects against disease caused by a heterologous influenza B virus (B/Lee/40). Protection from B/Lee/40 challenge was partially eliminated in mice that did not express a functional type I IFN receptor, suggesting that innate immunity, and type I IFN in particular, are important in mediating protection against this virus. It was concluded that 244/PR8 has the ability to protect in vivo against heterologous IFN-sensitive respiratory viruses, in addition to homologous influenza A viruses, and that it acts by fundamentally different mechanisms.
MeSH term(s)	Animals ; Cross Protection ; Defective Viruses/immunology ; Disease Models, Animal ; Female ; Immunity, Innate ; Influenza A virus/immunology ; Influenza B virus/immunology ; Interferon Type I/immunology ; Male ; Mice ; Orthomyxoviridae Infections/prevention & control ; Rodent Diseases/prevention & control
Chemical Substances	Interferon Type I
Language	English
Publishing date	2011-06-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219316-4
ISSN	1465-2099 ; 0022-1317
ISSN (online)	1465-2099
ISSN	0022-1317
DOI	10.1099/vir.0.034132-0
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Article ; Online: Defective interfering influenza virus confers only short-lived protection against influenza virus disease: evidence for a role for adaptive immunity in DI virus-mediated protection in vivo.

Scott, Paul D / Meng, Bo / Marriott, Anthony C / Easton, Andrew J / Dimmock, Nigel J

Vaccine

2011 Volume 29, Issue 38, Page(s) 6584–6591

Abstract	We have shown earlier that a single dose of cloned defective interfering (DI) influenza A virus strongly protects mice from disease following a lethal challenge with different subtypes of influenza A virus. These animals suffered no clinical disease but experienced a subclinical infection which rendered them immune to reinfection with the same challenge virus. However, little is known about how DI virus achieves such protection. Here we investigated the role of adaptive immunity in DI virus-mediated protection using severe-combined immunodeficient (SCID) mice, which lack competence in both B- and T-cell compartments but retain NK cell activity. SCID mice which were treated with DI virus and infected with influenza virus initially remained completely well, while infected litter mates that received UV-inactivated DI virus became seriously ill and died. However, after 10 days of good health, the DI virus-protected SCID mice developed a clinical disease that was similar, but not completely identical, to the acute influenza disease. Disease was delayed longer by a higher dose of DI virus. We excluded the possibilities that the DI virus load in the lungs had declined, that the DI RNA sequence had changed so that it no longer interfered with the infectious genome, or that infectious virus had become resistant to the DI virus. These data show that while DI virus provides full protection from the acute disease in the absence of adaptive immunity, that same immunity is essential for clearing the infection. This indicates that the conventional view that DI virus-induced protection is mediated solely by competition for replication with the challenge virus is incorrect for influenza virus.
MeSH term(s)	Adaptive Immunity ; Animals ; B-Lymphocytes/immunology ; Defective Viruses/immunology ; Influenza A virus/immunology ; Influenza Vaccines/administration & dosage ; Influenza Vaccines/immunology ; Killer Cells, Natural/immunology ; Lung/virology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, SCID ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/pathology ; Orthomyxoviridae Infections/prevention & control ; Orthomyxoviridae Infections/virology ; T-Lymphocytes/immunology ; Viral Load
Chemical Substances	Influenza Vaccines
Language	English
Publishing date	2011-07-14
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605674-x
ISSN	1873-2518 ; 0264-410X
ISSN (online)	1873-2518
ISSN	0264-410X
DOI	10.1016/j.vaccine.2011.06.114
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