TASK DEFINITION: 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.
PROBLEM: Keywords: interferon, interferon-stimulated genes, tumor necrosis factor-related apoptosis-inducing ligand, acute lung injury, innate immunity, influenza, respiratory syncytial virus, coronavirus FiGURe 1 | PRRs and their downstream signaling pathways in virus-induced iFN induction. In viral infection, type I IFNs are induced by TLR, RLR, CLR, and cytosolic nucleic acid sensors. Cell membrane-located TLRs ligate to viral envelope proteins (e.g., TLR2/herpes simplex virus), upon which they recruit MyD88. MyD88 interacts with IRAK kinase (IRAK-1, -2, or -4) that either directly activate IRF1 or interact with TRAF6, which induces IRF7 or assembles with TAK1. TAK1 forms a complex with TAB-1/-2 and -3 and subsequently either activates the MAPK kinases p38 and JNK, leading to AP-1 phosphorylation and nuclear translocation, or induces ubiquitination of NEMO followed by IκB degradation and NFκB activation. Endosomal TLRs recognizing viral nucleic acid and signal via the adaptor protein MyD88 (for TLR7/8/9) or interact with TRIF (for TLR3) followed by TRAF3, TANK, and TBK1 activation. TBK1 and IKKε then phosphorylate and activate IRF3 and IRF7. Additionally, TRIF can interact with TRAF6 to initiate TAK1 signaling. Both RLRs, RIG-I and MDA-5, recognize nucleic acid contents in the cytoplasm and stimulate the mitochondrial anchored IPS-1 for dimerization followed by TRADD recruitment that acts via TRAF3 on IRF3 and IRF7. Additionally, IPS-1 can interact with FADD and RIP1 to activate NFκB via IKK activated by caspase-8 and -10. Also PKR signaling results in NFκB activation and nuclear translocation. The dsDNA sensor cGAS produces cGAMP that activates ER-located STING that via TBK1 induces IRF3 translocation and type I IFN production. CLRs play a minor role in viral recognition; however, DC-SIGN activates the small GTPase Ras and Raf protein kinase, followed by NFκB activation. Type III IFN are induced by TLR3, TLR9, and via RIG-I and peroxisomal-resident IPS-1. Especially IRF1, but also NFκB, IRF3, and IRF7 are implicated in IFN-λ production, with the latter being stabilized by Med23.

SOLUTION: The impact of the interferon/TNF- Related Apoptosis-inducing Ligand Signaling Axis on Disease Progression in Respiratory viral infection and Beyond

PROBLEM: Most acute respiratory infections (ARIs) in children are due to viral etiology, and represent an important cause of mortality and morbidity in children <5 years old in developing countries. The pathogens that cause ARIs vary geographically and by season, and viruses serve a major role. In the present study, the distribution of the seven respiratory viruses that are more prevalent in Southern European countries were retrospectively analyzed in a Southern Italy Hospital, that centralizes pediatric diseases from the Naples province. Viruses were categorized by a FilmArray Respiratory Panel, and demonstrated no substantial differences in sex, age and seasonal viruses distribution. However, all the investigated viruses had a higher detection rate in the surrounding municipalities than in the metropolitan area of Naples. In recent years, the association between air pollution and respiratory infections has become an increasing public health concern. The data in this study support this association in the surrounding areas of Naples extensively contaminated by environmental toxic agents. In these areas, characterization of the epidemiology of ARIs is required to implement a prevention and control program.

SOLUTION: Characterization of respiratory infection viruses in hospitalized children from Naples province in Southern Italy

PROBLEM: Inhibition of extracellular matrix (ECM) degradation may represent a mechanism for cardiac protection against ischemia. Extracellular matrix metalloproteinase inducer (EMMPRIN) is highly expressed in response to acute myocardial infarction (AMI), and induces activation of several matrix metalloproteinases (MMPs), including gelatinases MMP-2 and MMP-9. We targeted EMMPRIN with paramagnetic/fluorescent micellar nanoparticles conjugated with the EMMPRIN binding peptide AP-9 (NAP9), or an AP-9 scrambled peptide as a negative control (NAPSC). We found that NAP9 binds to endogenous EMMPRIN in cultured HL1 myocytes and in mouse hearts subjected to ischemia/reperfusion (IR). Injection of NAP9 at the time of or one day after IR, was enough to reduce progression of myocardial cell death when compared to Control and NAPSC injected mice (infarct size in NAP9 injected mice: 32%±6.59 vs Control: 46%±9.04 or NAPSC injected mice: 48%±7.64). In the same way, cardiac parameters were recovered to almost healthy levels (LVEF NAP9 63% ± 7.24 vs Control 42% ± 4.74 or NAPSC 39% ± 6.44), whereas ECM degradation was also reduced as shown by inhibition of MMP-2 and MMP-9 activation. Cardiac magnetic resonance (CMR) scans have shown a signal enhancement in the left ventricle of NAP9 injected mice with respect to non-injected, and to mice injected with NAPSC. A positive correlation between CMR enhancement and Evans-Blue/TTC staining of infarct size was calculated (R:0.65). Taken together, these results point to EMMPRIN targeted nanoparticles as a new approach to the mitigation of ischemic/reperfusion injury.

SOLUTION:
EMMPRIN-Targeted Magnetic Nanoparticles for In Vivo Visualization and Regression of Acute Myocardial Infarction