Publications by authors named "Sagiv Aaron"

4 Publications

  • Page 1 of 1

Taming the "cobra": an approach to "cobra-like" formation seen in the Occlutech atrial septal defect and patent foramen ovale occluders.

Catheter Cardiovasc Interv 2012 Mar 12;79(4):678-80. Epub 2011 Dec 12.

Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.

Percutaneous closure of secundum atrial septal defect and patent foramen ovale has gained widespread use in recent years. We present a small series of four cases in which a "cobra-like" formation occurred in an Occlutech Figulla device during the deployment of the left disk, and propose a technique that may resolve this problem.
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http://dx.doi.org/10.1002/ccd.23303DOI Listing
March 2012

Intranasal transmission of hepatitis C virus: virological and clinical evidence.

Clin Infect Dis 2008 Oct;47(7):931-4

Molecular Virology Division, St. Luke's-Roosevelt Institute for Health Sciences/Columbia University.

Intranasal transmission of hepatitis C virus (HCV) via contaminated drug-sniffing implements is a potential but unconfirmed source of viral infection. We demonstrate the virological plausibility of intranasal transmission by confirming that blood and HCV RNA are present in the nasal secretions and drug-sniffing implements of HCV-infected intranasal drug users recruited from a community health clinic in New York City.
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http://dx.doi.org/10.1086/591699DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6545569PMC
October 2008

The critical role of human transcriptional repressor CTCF mRNA up-regulation in the induction of anti-HIV-1 responses in CD4(+) T cells.

Immunol Lett 2008 Apr 26;117(1):35-44. Epub 2007 Dec 26.

Molecular Virology Division, St. Luke's-Roosevelt Hospital Center, Columbia University Medical Center, New York, NY 10019, USA.

We have employed our CD4(+) T cell model named HIV-1 resistance factor (HRF(+)) to study the inducible anti-HIV-1 responses mediated through novel soluble molecules. We found that exposure to the soluble products of HRF(+) cells activated CCCTC-binding factor (CTCF) mRNA expression in HIV-1 susceptible primary and transformed CD4(+) T cells and overlapped with their acquisition of transient resistance to virus. Conversely, the interference with the expression of CTCF gene in HRF(+) cells reversed the resistant phenotype and eliminated the biological potential of their cell culture supernatant to induce "HRF-like" activity in target cells. Band-shift analysis upon the nuclear fractions from HIV-1 resistant cells showed that CTCF protein bound to HIV-1 promoter and this binding prevented the formation of NF-kappaB/LTR complex. This evidence suggests that CTCF is an intracellular effector of HRF activity and that the acquisition of resistance to HIV-1 in CD4(+) T cells is a consequence of the prior activation of CTCF gene by the soluble entity secreted by HRF(+) cells.
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http://dx.doi.org/10.1016/j.imlet.2007.11.017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2346778PMC
April 2008

Inhibition of HIV-1 or bacterial activation of macrophages by products of HIV-1-resistant human cells.

Immunol Cell Biol 2007 Nov-Dec;85(8):603-9. Epub 2007 Jul 17.

Molecular Virology Division, St Luke's-Roosevelt Hospital Center, Columbia University Medical Center, New York, NY, USA.

We have recently described the molecular basis of HIV-1 resistance factor (HRF)-mediated anti-viral activity in primary and transformed CD4 T cells. HRF+ cell culture supernatants or partially purified HRF were found to incapacitate the formation of the NF-kappaB/DNA complex, which is indispensable for long terminal promoter-driven transcription of virus genes. In this study, we tested whether HRF might have much broader activity against other organisms whose pathogenesis is linked to NF-kappaB activation. Specifically, we tested the effects of HRF on the NF-kappaB-mediated responses of primary macrophages to HIV-1 or several bacterial antigens. We found that exposure to HRF inhibited HIV-1 expression in macrophages and also induced the production of HRF-like activity by macrophages, which prevented replication of virus in HIV-1-infected peripheral blood lymphocytes cultured in the adjacent compartment. We investigated the mechanism of this inhibition and found that HRF impeded NF-kappaB/DNA binding in macrophages induced by either HIV-1 or lipopolysaccharide from several bacteria species, resulting in impaired tumor necrosis factor-alpha responses to these organisms.
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http://dx.doi.org/10.1038/sj.icb.7100092DOI Listing
February 2008
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