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.

Input: Consider Input: 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.

Output: Surveillance of travel-associated diseases at two referral centres in Marseille, France: a 12-year survey

Input: Consider Input: For over 30 years, HIV/AIDS has wreaked havoc in the world. In the absence of an effective vaccine for HIV, development of new anti-HIV agents is urgently needed. We previously identified the antiviral activities of the scorpion-venom-peptidederived mucroporin-M1 for three RNA viruses (measles viruses, SARS-CoV, and H5N1). In this investigation, a panel of scorpion venom peptides and their derivatives were designed and chosen for assessment of their anti-HIV activities. A new scorpion venom peptide derivative Kn2-7 was identified as the most potent anti-HIV-1 peptide by screening assays with an EC 50 value of 2.76 mg/ml (1.65 mM) and showed low cytotoxicity to host cells with a selective index (SI) of 13.93. Kn2-7 could inhibit all members of a standard reference panel of HIV-1 subtype B pseudotyped virus (PV) with CCR5-tropic and CXCR4tropic NL4-3 PV strain. Furthermore, it also inhibited a CXCR4-tropic replication-competent strain of HIV-1 subtype B virus. Binding assay of Kn2-7 to HIV-1 PV by Octet Red system suggested the anti-HIV-1 activity was correlated with a direct interaction between Kn2-7 and HIV-1 envelope. These results demonstrated that peptide Kn2-7 could inhibit HIV-1 by direct interaction with viral particle and may become a promising candidate compound for further development of microbicide against HIV-1.

Output: Anti-HIV-1 Activity of a New Scorpion Venom Peptide Derivative Kn2-7

Input: Consider Input: cally active but which do not bind antibody 259 have been prepared recently; cells transformed by such mutants were not altered morphologically, nor did they show greatly inhibited thymidine incorporation, after injection of antibody 259 26 It is assumed that while viral oncogenes function without normal control, their mechanism of action is similar to that of related cellular genes. Here we have presented evidence to support this idea in the case of growth factor receptor-like molecules and related oncogenes. It is therefore possible that these data might aid in understanding the way in which cellular genes interact in the control of normal proliferation. Our results indicate that some receptor-like oncogenes depend on ras proteins while some cytoplasmic oncogenes do not. There are, of course, numerous oncogenes which we have not yet tested which might behave differently from those described here. With this limitation in mind and on the basis of our present data, we propose that an important class of proliferative signals are received at the cell surface by receptor molecules such as growth factor receptors, and the c-ras proteins are essential in the transfer of these signals to cytoplasmic effectors having serine kinase activity; the effectors then modify target molecules which are directly involved in initiating a proliferative cycle. Accordingly, if the cytoplasmic effector were mutated such that it functioned without activation, proliferation would continue independently of c-ras proteins. Receptor molecules, on the other hand, would always require c-ras to stimulate proliferation. While our data are consistent with the above scheme, they do not exclude many other possibilities involving multiple metabolic pathways and more complex interactions. For example, we have not reported results with nuclear oncogenes owing to their difficulty in transforming NIH 3T3 cells. The proposed scheme is primarily attractive because of its similarity to the carefully studied mechanism of signal transduction involving cyclic AMP. While it is unlikely that cyclic AMP itself regulates proliferation 27 , G-regulatory proteins with enzymatic similarities to c-ras proteins are involved. These regulatory proteins control signal transduction from cell-surface receptors to cytoplasmic serine kinase effector molecules by regulating adenyl cyclase activity28. While the present study has examined only one aspect of what is likely to be a highly complex system for regulating proliferation, it does provide a means of functionally comparing separate viral oncogenes. Injection of antibody has been used in other studies to characterize the types of molecules responsible for tumour cell proliferation. Like NIH 3T3 cells transformed by mos or raj genes, many tumour cells show no inhibition of proliferation when injected with anti-ras antibody. In this way their proliferation is distinct from that of the normal cell types studied, each of which was efficiently inhibited by the injected antibodyl6.
Output: Viral particles induce Ia antigen expression on astrocytes