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: Synthetic decapeptides (N 206) covering the entire sequence of mouse liver fumarylacetoacetate hydrolase (FAH) were used to analyze the specificities of the autoantibodies (autoAb) elicited towards this enzyme in mice infected with mouse hepatitis virus (MHV). These autoAb bound mainly to N-and C-terminal FAH peptides, the most reactive sequences being 1e50 and 390e420, respectively. Surprisingly, although FAH sequence 1e50 shares a high degree of homology with various MHV proteins, the C-terminal portion does not. Moreover, whereas the autoAb reacted with homologous peptides surrounding residues 70, 160 and 360, non-similar sequences around residues 130, 210, 240, 250, and 300 were also recognized, indicating that autoAb were not restricted to epitopes with sequence homologies. There was also a lack of correlation between the amount of anti-MHV or anti-FAH antibodies produced and the reactivity towards the peptides. Moreover, the spectrum of peptides recognized by the autoAb of a given mouse did not change significantly with time, which suggests that the MHV-elicited autoimmune response does not induce an epitope recognition spreading. Finally, anti-FAH Ab produced after immunization with rat liver FAH recognized essentially the same mouse FAH regions than autoAb from MHV-infected mice. Results indicated that the induction of the autoAb is not only related to molecular or structural mimicry, but rather supports the Danger model, in which any aggression, in this case the MHV infection, is susceptible to trigger the production of autoAb.

Output: The peptide specificities of the autoantibodies elicited by mouse hepatitis virus A59

Input: Consider Input: Globally, there are a number of emerging pathogens. For most, there are no licensed vaccines available for human use, although there is ongoing research and development. However, given the extensive and increasing list of emerging pathogens and the investment required to bring vaccines into clinical use, the task is huge. Overlaid on this task is the risk of anti-microbial resistance (AMR) acquisition by micro-organisms which can endow a relatively harmless organism with pathogenic potential. Furthermore, climate change also introduces a challenge by causing some of the insect vectors and environmental conditions prevalent in tropical regions to begin to spread out from these traditional areas, thus increasing the risk of migration of zoonotic disease. Vaccination provides a defence against these emerging pathogens. However, vaccines for pathogens which cause severe, but occasional, disease outbreaks in endemic pockets have suffered from a lack of commercial incentive for development to a clinical standard, encompassing Phase III clinical trials for efficacy. An alternative is to develop such vaccines to request US Emergency Use Authorization (EUA), or equivalent status in the United States, Canada and the European Union, making use of a considerable number of regulatory mechanisms that are available prior to licensing. This review covers the status of vaccine development for some of the emerging pathogens, the hurdles that need to be overcome to achieve EUA or an equivalent regional or national status and how these considerations may impact vaccine development for the future, such that a more comprehensive stockpile of promising vaccines can be achieved.

Output: Vaccines for emerging pathogens: prospects for licensure

Input: Consider Input: RNA interference (RNAi) is a powerful method for specific gene silencing which may also lead to promising novel therapeutic strategies. It is mediated through small interfering RNAs (siRNAs) which sequence-specifically trigger the cleavage and subsequent degradation of their target mRNA. One critical factor is the ability to deliver intact siRNAs into target cells/organs in vivo. This review highlights the mechanism of RNAi and the guidelines for the design of optimal siRNAs. It gives an overview of studies based on the systemic or local application of naked siRNAs or the use of various nonviral siRNA delivery systems. One promising avenue is the the complexation of siRNAs with the polyethylenimine (PEI), which efficiently stabilizes siRNAs and, upon systemic administration, leads to the delivery of the intact siRNAs into different organs. The antitumorigenic effects of PEI/siRNA-mediated in vivo gene-targeting of tumor-relevant proteins like in mouse tumor xenograft models are described. RNAi is an evolutionarily conserved, sequence-specific, posttranscriptional gene silencing phenomenon. It is triggered by 2 Journal of Biomedicine and Biotechnology DNA DNA dsRNA dsRNA processing Dicer ATP siRNA ADP + P i Interferon response Nonspecific gene silencing RISC assembly RISC activation Binding of RISC to target mRNA mRNA degradation Cleavage Target mRNA Expression RISC ATP ADP + P i RISC Figure 1 : Mechanism of RNA interference (RNAi) in mammalian systems. Long double-stranded RNA molecules (dsRNA), which are expressed from DNA vectors (left red arrow) or directly enter the cell (center red arrow), are processed by the Dicer complex resulting in the formation of small inhibitory RNAs (siRNAs). Alternatively, to induce RNAi these small 21-23 bp duplexes are directly delivered into the cell (right red arrow). The siRNAs are incorporated into a nuclease-containing multiprotein complex called RISC, which becomes activated upon the ATP-dependent unwinding of the siRNA duplex by an RNA helicase. The now single-stranded siRNA guides the RISC complex to its complementary target mRNA which is then cleaved by the endonucleolytical activity of RISC. While the RISC complex is recovered for further cycles, the cleaved mRNA molecule is rapidly degraded due to its unprotected RNA ends.
Output: Review Article Delivery Systems for the Direct Application of siRNAs to Induce RNA Interference (RNAi) In Vivo