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.

Q: Both antiseptic hand rubbing (AHR) using ethanol-based disinfectants (EBDs) and antiseptic hand washing (AHW) are important means of infection control to prevent seasonal influenza A virus (IAV) outbreaks. However, previous reports suggest a reduced efficacy of ethanol disinfection against pathogens in mucus. We aimed to elucidate the situations and mechanisms underlying the reduced efficacy of EBDs against IAV in infectious mucus. We evaluated IAV inactivation and ethanol concentration change using IAV-infected patients' mucus (sputum). Additionally, AHR and AHW effectiveness against infectious mucus adhering to the hands and fingers was evaluated in 10 volunteers. Our clinical study showed that EBD effectiveness against IAV in mucus was extremely reduced compared to IAV in saline. IAV in mucus remained active despite 120 s of AHR; however, IAV in saline was completely inactivated within 30 s. Due to the low rate of diffusion/convection because of the physical properties of mucus as a hydrogel, the time required for the ethanol concentration to reach an IAV inactivation level and thus for EBDs to completely inactivate IAV was approximately eight times longer in mucus than in saline. On the other hand, AHR inactivated IAV in mucus within 30 s when the mucus dried completely because the hydrogel characteristics were lost. Additionally, AHW rapidly inactivated IAV. Until infectious mucus has completely dried, infectious IAV can remain on the hands and fingers, even after appropriate AHR using EBD, thereby increasing the risk of IAV transmission. We clarified the ineffectiveness of EBD use against IAV in infectious mucus. IMPORTANCE Antiseptic hand rubbing (AHR) and antiseptic hand washing (AHW) are important to prevent the spread of influenza A virus (IAV). This study elucidated the situations/mechanisms underlying the reduced efficacy of AHR against infectious mucus derived from IAV-infected individuals and indicated the weaknesses of the current hand hygiene regimens. Due to the low rate of diffusion/convection because of the physical properties of mucus as a hydrogel, the efficacy of AHR using ethanolbased disinfectant against mucus is greatly reduced until infectious mucus adhering to the hands/fingers has completely dried. If there is insufficient time before treating the next patient (i.e., if the infectious mucus is not completely dry), medical staff should be aware that effectiveness of AHR is reduced. Since AHW is effective against both dry and nondry infectious mucus, AHW should be adopted to compensate for these weaknesses of AHR. FIG 1 Analysis of the physical properties of mucus from 19 influenza A virus-infected patients. (A) Rheological analysis: mean, maximum, and minimum viscosities of mucus (sputum) samples at different shear rates (left panel). Shown is a comparison of mucus and saline viscosities at different shear rates (right panel). (B) Average parameters measured for saline and mucus samples: contact angles, surface tension, and densities at different temperatures. (C) Time required for saline and mucus to completely dry (complete drying time). (D) Ethanol diffusion coefficients of saline and mucus exposed to an 80% ethanol concentration. Situations of Reduced Hand Hygiene Effectiveness September/October 2019 Volume 4 Issue 5 e00474-19 msphere.asm.org 3 FIG 6 Additional fluid simulation of changes in the ethanol concentrations in mucus. (A) Addition of 95 l of 80% ethanol to 5 l saline was modeled in OpenFOAM, demonstrating the disappearance over time of the region with Ͻ31% ethanol (shown in red). See also Movie S1. (B) Addition of 95 l of 80% ethanol to 5 l mucus was modeled. The simulation was performed under conditions of reduced viscosity (16.7% of the actual measurement value) because of the long time required for disappearance of the concentration region of Ͻ31%. See also Movie S2.

A: Situations Leading to Reduced Effectiveness of Current Hand Hygiene against Infectious Mucus from Influenza Virus- Infected Patients
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Q: Background: With increasing international travel and historically high numbers of residents visiting friends and relatives overseas, travel-associated illnesses are frequent in Marseille, France. We report the changing epidemiology of travel-related illnesses over a 12-year period. Methods: A single site GeoSentinel surveillance analysis was undertaken for 3460 ill returned travellers presenting to two public hospitals in Marseille, France from March 2003 to October 2015, with travel-related illnesses. Demographic characteristics, travel history, presenting symptoms and information on pre-travel consultations were collected. Results: There was a predominance of travel to sub-Saharan Africa, in particular to Comoros archipelago. Tourism was the main reason for travel (1591/3460, 46%), followed by visiting friends or relatives (VFR) (895/3460, 26%), with a mean duration of 29 days; 35% (1212/3460) of travellers reported a pre-travel health consultation. The most common syndromic diagnoses were febrile systemic illness (1343, 39%), dermatologic (716, 21%), gastrointestinal (340, 10%) and respiratory/ear-nose-throat (331, ENT) (10%). Hospitalization rates were highest amongst travellers from sub-Saharan Africa (858/ 1632, 53%), and VFR (573/ 895, 64%, P < 0.001). Frequent diagnoses included malaria (797, 23%), dengue (96, 2.77%) and chikungunya (75, 2.17%), reflecting global trends. Comparison of two periods (2003-10 to 2011-15) demonstrated an increase in chikungunya and decrease in malaria and influenza-like illness. We report an increase in ill travellers from the Caribbean, Middle East and South-East Asia. Conclusion: Surveillance of travellers provides relevant sentinel information on the changing epidemiology of infectious diseases across the globe, most notably for malaria, dengue and chikungunya. We demonstrate the use of travel surveillance in improving pre-travel consultation needs and to address autochthonous vector-borne viral risks.

A: Surveillance of travel-associated diseases at two referral centres in Marseille, France: a 12-year survey
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Q: Although pneumococcal pneumonia is one of the most common causes of death due to infectious diseases, little is known about pneumococci-lung cell interaction. Herein we tested the hypothesis that pneumococci activated pulmonary epithelial cell cytokine release by c-Jun-NH 2 -terminal kinase (JNK) Methods: Human bronchial epithelial cells (BEAS-2B) or epithelial HEK293 cells were infected with S. pneumoniae R6x and cytokine induction was measured by RT-PCR, ELISA and Bioplex assay. JNKphosphorylation was detected by Western blot and nuclear signaling was assessed by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP). JNK was modulated by the small molecule inhibitor SP600125 and AP1 by transfection of a dominant negative mutant. Results: S. pneumoniae induced the release of distinct CC and CXC, as well as Th1 and Th2 cytokines and growth factors by human lung epithelial cell line BEAS-2B. Furthermore, pneumococci infection resulted in JNK phosphorylation in BEAS-2B cells. Inhibition of JNK by small molecule inhibitor SP600125 reduced pneumococci-induced IL-8 mRNA expression and release of IL-8 and IL-6. One regulator of the il8 promoter is JNK-phosphorylated activator protein 1 (AP-1). We showed that S. pneumoniae timedependently induced DNA binding of AP-1 and its phosphorylated subunit c-Jun with a maximum at 3 to 5 h after infection. Recruitment of Ser 63/73 -phosphorylated c-Jun and RNA polymerase II to the endogenous il8 promoter was found 2 h after S. pneumoniae infection by chromatin immunoprecipitation. AP-1 repressor A-Fos reduced IL-8 release by TLR2-overexpressing HEK293 cells induced by pneumococci but not by TNFα. Antisense-constructs targeting the AP-1 subunits Fra1 and Fra2 had no inhibitory effect on pneumococci-induced IL-8 release. Conclusion: S. pneumoniae-induced IL-8 expression by human epithelial BEAS-2B cells depended on activation of JNK and recruitment of phosphorylated c-Jun to the il8 promoter.

A:
Respiratory Research Streptococcus pneumoniae induced c-Jun-N-terminal kinase-and AP-1 -dependent IL-8 release by lung epithelial BEAS-2B cells
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