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.

[EX Q]: We have previously reported that the apathogenic Tula hantavirus induces apoptosis in Vero E6 epithelial cells. To assess the molecular mechanisms behind the induced apoptosis we studied the effects of hantavirus infection on cellular signaling pathways which promote cell survival. We previously also observed that the Tula virus-induced cell death process is augmented by external TNF-α. Since TNF-α is involved in the pathogenesis of hantavirus-caused hemorrhagic fever with renal syndrome (HFRS) we investigated its effects on HFRS-causing hantavirus-infected cells. We studied both apathogenic (Tula and Topografov) and pathogenic (Puumala and Seoul) hantaviruses for their ability to regulate cellular signaling pathways and observed a direct virusmediated down-regulation of external signal-regulated kinases 1 and 2 (ERK1/2) survival pathway activity, which was dramatically enhanced by TNF-α. The fold of ERK1/2 inhibition correlated with viral replication efficiencies, which varied drastically between the hantaviruses studied. We demonstrate that in the presence of a cytokine TNF-α, which is increased in HFRS patients, hantaviruses are capable of inactivating proteins that promote cell survival (ERK1/ 2). These results imply that hantavirus-infected epithelial cell barrier functions might be compromised in diseased individuals and could at least partially explain the mechanisms of renal dysfunction and the resulting proteinuria seen in HFRS patients.
[EX A]: Virology Journal Hantaviruses and TNF-alpha act synergistically to induce ERK1/2 inactivation in Vero E6 cells

[EX Q]: 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.
[EX A]: Journal Pre-proof Guest Editorial: Radiology Nurses Can Raise the Impact on Promoting IR

[EX Q]: During the replication cycle of Sindbis virus minus-strand synthesis stops normally at the time that plus-strand synthesis reaches a maximum rate. We have isolated and characterized revertants of ts24, a member of the A complementation group of Sindbis HR mutants, that we had demonstrated previously to have a temperature-sensitive defect in the regulation of minus-strand synthesis. These revertants of t&4 replicated efficiently at 40' but nevertheless retained the temperature sensitive defect in the regulation of minus-strand synthesis: they continued to synthesize minus strands late in the replication cycle at 40" but not at 30" and in the presence or absence of protein synthesis. Although failure to regulate the synthesis of minus strands resulted in continuous minus-strand synthesis and in the accumulation of minus strands, the rate of plus-strand synthesis was not increased concertedly. Minus strands synthesized after the rate of plus-strand synthesis had become constant were demonstrated to be utilized as templates for 26 S mRNA synthesis. Thus, the change from an increasing to a constant rate of plus-strand synthesis during the alphavirus replication cycle cannot be governed solely by the number of minus strands that accumulate in infected cells. We present a model for the preferential utilization of minus strands as a mechanism for the cessation of minus-strand synthesis that occurs normally during alphavirus replication.
[EX A]:
The Effect of Loss of Regulation of Minus-Strand RNA Synthesis on Sindbis Virus Replication