instruction:
In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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Being madly in love with all the advances in minimally invasive medicine and technology I often tell my friends the stories of how interventional radiology (IR) changes lives. One of these unintended stories led to a much bigger audience of TED community and spread the word about IR far beyond the circle of my friends. As the TED slogan promised, participating in the event 1 made me realize that our ideas of better medicine are worth sharing. It also made me think that better communication with the public is possible, and it does not take genius. It takes a willingness to try. We know that IR with its broad procedural spectrum, safety of minimally invasive approach, lower requirement for anesthesia and hospitalization, and cost-effectiveness has a strong stand in the evolving universal healthcare practice model. But, as Goethe said, knowing is not enough; we must apply. 2 Then, how can we as medical community increase the exercise of IR procedures? The starting point is to accept that many people, including medical professionals, do not know what diseases we can treat and what diagnostic or therapeutic services we can provide. Either it is a palliative treatment of metastases, or elective embolization of uterine fibroids, or emergent lysis of pulmonary embolism-it is our responsibility to find the appropriate patients and let both patients and primary physicians know what options we have to offer.
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Journal Pre-proof Guest Editorial: Radiology Nurses Can Raise the Impact on Promoting IR

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Early innate and cell-intrinsic responses are essential to protect host cells against pathogens. In turn, viruses have developed sophisticated mechanisms to establish productive infections, counteracting the host innate immune responses. Increasing evidence indicates that these antiviral factors may have a dual role by directly inhibiting viral replication, as well as by sensing and transmitting signals to induce antiviral cytokines. Recent studies have pointed at new, unappreciated mechanisms of viral evasion of host innate protective responses including manipulating the host ubiquitin system. Viral inhibition of antiviral factors by ubiquitin-dependent degradation is emerging as critical evasion mechanism of the antiviral response. In addition, recent studies have uncovered new mechanisms by which viral encoded proteins inhibit ubiquitin and ubiquitin-like modification of host proteins involved innate immune signaling pathways. Here we discuss recent findings and novel strategies that viruses have developed to counteract these early innate antiviral defenses. Early events in viral infection include attachment to the host cell membrane and entry, release of the viral RNA, DNA, and protein complexes into the cytoplasm of the cell and early recognition by the host innate immune system. At each of these steps, host cells have developed mechanisms to limit virus infection. In turn, viruses have rapidly evolved to counteract host defenses by different mechanisms. Many recent studies have pointed at the importance of cell type and host specific expression of antiviral factors as critical for
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Viral evasion mechanisms of early antiviral responses involving regulation of ubiquitin pathways NIH Public Access

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Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is the cause of an atypical pneumonia that affected Asia, North America and Europe in 2002-2003. The viral spike (S) glycoprotein is responsible for mediating receptor binding and membrane fusion. Recent studies have proposed that the carboxyl terminal portion (S2 subunit) of the S protein is a class I viral fusion protein. The Wimley and White interfacial hydrophobicity scale was used to identify regions within the CoV S2 subunit that may preferentially associate with lipid membranes with the premise that peptides analogous to these regions may function as inhibitors of viral infectivity. Five regions of high interfacial hydrophobicity spanning the length of the S2 subunit of SARS-CoV and murine hepatitis virus (MHV) were identified. Peptides analogous to regions of the N-terminus or the pretransmembrane domain of the S2 subunit inhibited SARS-CoV plaque formation by 40-70% at concentrations of 15-30 M. Interestingly, peptides analogous to the SARS-CoV or MHV loop region inhibited viral plaque formation by >80% at similar concentrations. The observed effects were dose-dependent (IC50 values of 2-4 M) and not a result of peptide-mediated cell cytotoxicity. The antiviral activity of the CoV peptides tested provides an attractive basis for the development of new fusion peptide inhibitors corresponding to regions outside the fusion protein heptad repeat regions.
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Inhibition of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infectivity by peptides analogous to the viral spike protein NIH Public Access