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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Question: Background: Influenza is a zoonotic disease that infects millions of people each year resulting in hundreds of thousands of deaths, and in turn devastating pandemics. Influenza is caused by influenza viruses, including influenza A virus (IAV). There are many subtypes of IAV but only a few seem to be able to adapt to humans and to cause disease. In 2013, an H7N9 IAV subtype emerged in China that does not cause clinical symptoms in its chicken host but leads to severe infections when transmitted into humans. Since 2013, there have been six epidemic waves of H7N9 with 1567 laboratory-confirmed human infections and 615 deaths. Pathogenicity of IAV is complex, but a crucial feature contributing to virulence is the activation of the hemagglutinin (HA) fusion protein by host proteases that triggers membrane fusion and leads to subsequent virus propagation. : 293T, VERO, and MDCK cells were used to conduct Western blot analysis, immunofluorescence assays, and pseudoparticle and live virus infections, and to evaluate H7N9 HA cleavage-activation. Results/Conclusions: We show that human matriptase/ST 14 is able to cleave H7N9 HA. Cleavage of H7N9 HA expressed in cell culture results in fusogenic HA and syncytia formation. In infection studies with viral pseudoparticles carrying matriptase/ ST 14-activated H7N9 HA, we observed a high infectivity of cells. Finally, human matriptase/ST 14 also activated H7N9 live virus which resulted in high infectivity. Our data demonstrate that human matriptase/ST 14 is a likely candidate protease to promote H7N9 infections in humans.

Answer: Human matriptase/ST 14 proteolytically cleaves H7N9 hemagglutinin and facilitates the activation of influenza A/Shanghai/2/2013 virus in cell culture


Question: We previously showed that erythropoietin (EPO) attenuates the morphological signs of spinal cord ischemia/reperfusion (I/R) injury in swine [1] without, however, improving neurological function. The clinical use of EPO has been cautioned most recently due to serious safety concerns arising from an increased mortality in acute stroke patients treated with EPO and simultaneously receiving systemic thrombolysis [2]. Carbamylated EPO (cEPO) is an EPO derivative without erythropoietic activity and devoid of the EPO side eff ects, but with apparently well maintained cytoprotective qualities [3]. We therefore tested the hypothesis whether cEPO may be equally effi cient as EPO in reducing morphological as well as functional aortic occlusion-induced spinal cord I/R injury. Methods In a randomized and blinded trial pigs received either vehicle (control, n = 9), EPO or cEPO, respectively (n = 9 each; 5,000 IU/kg over 30 minutes before and during the fi rst 4 hours of reperfusion). Animals underwent 30 minutes of thoracic aortic balloon occlusion with catheters placed immediately downstream of the A. subclavia and upstream of the aortic trifurcation. Spinal cord function was assessed by motor evoked potentials (MEP as percentage of the amplitude before aortic occlusion) and lower limb refl exes (assessed as the subjective strength of response) for a period of 10 hours after reperfusion. Tissue damage was evaluated using Nissl staining. Results Both EPO-treated and cEPO-treated animals presented with attenuated spinal cord injury in the Nissl staining (median (quartile) percentage of damaged neurons in the thoracic segments: control 27 (25,44), cEPO 8 (4,10), and EPO 5 (5,7), P <0.001 vs control group; in the lumbar segments: control 26 (19,32), cEPO 7 (5,13), EPO 8 (5,10), P <0.001 vs control group). However, while only cEPO treatment was associated with recovery of the MEP amplitude to pre-occlusion values when compared with the control group (P <0.05), lower limb refl ex response was comparably restored stronger in both treatment groups (P <0.05 vs control). Conclusions In a clinically relevant porcine model mimicking aortic crossclamping during vascular surgery repair of thoracic aortic aneurysm, cEPO protected spinal cord function and integrity as eff ective as EPO when applied at equipotent doses. Acknowledgements Supported by the Deutsche Forschungs gemeinschaft (SCHE 899/2-2). Figure 1 (abstract P2). Phenylbutyrate reduced the unfolded protein response. Introduction In awake, spontaneously breathing mice, inhaling hydrogen sulfi de (H 2 S) induced a hibernation-like metabolic state characterised by reduced energy expenditure and hypothermia [1], which protected against otherwise lethal hypoxia [2] and hemorrhage [3] as a result of impaired cellular energy metabolism [4]. Therefore, we investigated the metabolic eff ects of inhaled H 2 S in our model of resuscitated murine septic shock. Methods Sixteen hours after induction of sepsis by cecal ligation and puncture (CLP) or sham operation, anesthetized and mechanically ventilated mice received 100 ppm H 2 S or vehicle over 5 hours at body temperatures of 38 and 27°C, respectively. During the observation period, hyperdynamic hemodynamics were maintained by colloid resuscitation and noradrenaline infusion [5]. Endogenous glucose production was calculated from blood 13 C6-glucose isotope enrichment derived from the rate of appearance of stable, non-radioactive labeled 1,2,3,4,5,6-13 C6 glucose during continuous isotope infusion [6]. Whole-body glucose oxidation rate was derived from the total CO 2 -production rate, the mixed expiratory 13 CO 2 / 12 CO 2 isotope ratio and the 13 C6-glucose infusion rate after the steady state was achieved. Results While endogenous glucose production was not aff ected by hypothermia, it was signifi cantly higher in the septic animals when compared with the corresponding sham operated groups, most likely due to the ongoing noradrenaline infusion. In contrast, despite the catecholamine infusion and higher glucose release, whole body glucose oxidation was signifi cantly reduced in normothermic septic animals. During hypothermia, H 2 S shifted substrate towards preferential glucose utilisation, but this eff ect disappeared in the septic mice. Conclusions H 2 S inhalation alone does not infl uence glucose metabolism once temperature is maintained at normothermic levels in anesthetised and mechanically ventilated mice. The H 2 S-related shift of energy metabo lism towards preferential carbohydrate oxidation present during hypothermia is blunted during sepsis, possibly as a result of the ongoing catecholamine treatment.

Answer: P1 Comparison of carbamylated versus recombinant erythropoietin during spinal cord ischemia/reperfusion injury P2 Sodium 4-phenylbutylate protects against myocardial ischemia-reperfusion injury by reducing unfolded protein response-mediated apoptosis in mice P3 Time-dependent eff ects of intravenous H 2 S during long-term, resuscitated porcine hemorrhagic shock


Question: There is a continuing threat that the highly pathogenic avian influenza virus will cause future influenza pandemics. In this study, we screened a library of compounds that are biologically active and structurally diverse for inhibitory activity against influenza neuraminidase (NA). We found that aurintricarboxylic acid (ATA) is a potent inhibitor of NA activity of both group-1 and group-2 influenza viruses with IC 50 s (effective concentration to inhibit NA activity by 50%) values at low micromolar concentrations. ATA was equally potent in inhibiting the NA activity derived from wild-type NA and its H274Y mutant which renders NA resistance to inhibition by oseltamivir. Although ATA is structurally distinct from sialic acid, molecular modeling experiments suggested that ATA binds to NA at the enzyme's substrate binding site. These results indicate that ATA may be a good starting material for the design of a novel class of NA inhibitors for the treatment influenza viruses.

Answer:
Aurintricarboxylic acid inhibits influenza virus neuraminidase