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.

Example Input: strains of infectious bronchitis virus (IBV) were isolated from the vaccinated chicken flocks in Sichuan province, China. The S1 genes of the isolates were amplified and sequenced. Phylogenetic analysis revealed that the 19 isolates and 37 reference IBV strains can be grouped into eight genotypes. Although IBVs of Taiwan-I type, massachusetts type, and proventriculitis type were isolated, but most isolates were LX4 genotype. Homology analysis of the sequences of S1 genes of the 19 isolates and 37 reference IBV strains revealed that the identity of the nucleotides and amino acid sequences of the S1 genes between the 15 LX4-type isolates and other IBV strains were 71.9-99.3% and 72.1-99.1%, respectively, while those of the analyzed IBV of LX4 type were 96.0-99.9% and 94.3-99.8%, respectively. The results from this study and other published results in the GenBank database showed that isolates circulating in Sichuan province in recent years were mainly LX4 genotype, which is the predominant genotype circulated in China in recent years.
Example Output: Genetic analysis revealed LX4 genotype strains of avian infectious bronchitis virus became predominant in recent years in Sichuan area, China

Example Input: Background: Chemokines and chemokine receptors cooperate to promote immune cell recruitment to the central nervous system (CNS). In this study, we investigated the roles of CXCR2 and CXCL1 in leukocyte recruitment to the CNS using a murine model of neuroinflammation. Methods: Wild-type (WT), CXCL1 −/− , and CXCR2 −/− mice each received an intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS). Esterase staining and intravital microscopy were performed to examine neutrophil recruitment to the brain. To assess endothelial activation in these mice, the expression of adhesion molecules was measured via quantitative real-time polymerase chain reaction (PCR) and Western blotting. To identify the cellular source of functional CXCR2, chimeric mice were generated by transferring bone marrow cells between the WT and CXCR2 −/− mice. Results: Expression levels of the chemokines CXCL1, CXCL2, and CXCL5 were significantly increased in the brain following the i.c.v. injection of LPS. CXCR2 or CXCL1 deficiency blocked neutrophil infiltration and leukocyte recruitment in the cerebral microvessels. In the CXCR2 −/− and CXCL1 −/− mice, the cerebral endothelial expression of adhesion molecules such as P-selectin and VCAM-1 was dramatically reduced. Furthermore, the bone marrow transfer experiments demonstrated that CXCR2 expression on CNS-residing cells is essential for cerebral endothelial activation and leukocyte recruitment. Compared with microglia, cultured astrocytes secreted a much higher level of CXCL1 in vitro. Astrocyte culture conditioned medium significantly increased the expression of VCAM-1 and ICAM-1 in cerebral endothelial cells in a CXCR2-dependent manner. Additionally, CXCR2 messenger RNA (mRNA) expression in cerebral endothelial cells but not in microglia or astrocytes was increased following tumor necrosis factor-α (TNF-α) stimulation. The intravenous injection of the CXCR2 antagonist SB225002 significantly inhibited endothelial activation and leukocyte recruitment to cerebral microvessels. Conclusions: CXCL1 secreted by astrocytes and endothelial CXCR2 play essential roles in cerebral endothelial activation and subsequent leukocyte recruitment during neuroinflammation.
Example Output: CXCR2 is essential for cerebral endothelial activation and leukocyte recruitment during neuroinflammation

Example Input: The rapid identification of highly specific and potent drug candidates continues to be a substantial challenge with traditional pharmaceutical approaches. Moreover, many targets have proven to be intractable to traditional small-molecule and protein approaches. Therapeutics based on RNA interference (RNAi) offer a powerful method for rapidly identifying specific and potent inhibitors of disease targets from all molecular classes. Numerous proof-of-concept studies in animal models of human disease demonstrate the broad potential application of RNAi therapeutics. The major challenge for successful drug development is identifying delivery strategies that can be translated to the clinic. With advances in this area and the commencement of multiple clinical trials with RNAi therapeutic candidates, a transformation in modern medicine may soon be realized. The RNase Dicer initiates RNAi by cleaving double-stranded RNA substrates into small fragments of about 21-25 nucleotides in length (Fig. 1) . These siRNA duplexes are incorporated into a protein complex called the RNA-induced silencing complex (RISC; Fig. 1 ). Biochemical analysis identified Argonaute 2 (Ago2) as the protein in RISC responsible for mRNA cleavage 3 , and the crystal structure of RNA-bound Ago2 has been reported, revealing key interactions 4 . Before RISC activation, the sense (nonguide) strand of the siRNA duplex is cleaved by Ago2, in the same manner as it cleaves mRNA substrates 5,6 . Preventing sense-strand cleavage by chemical modification can reduce siRNA potency in vitro; however, experimental context is important, as siRNAs with highly stabilized (uncleavable) sense strands can be highly active. Small-molecule pharmaceutical drugs, almost without exception, meet the 'Lipinski Rules' , criteria including high lipophilicity and molecular weight of not more than 500. In sharp contrast, siRNAs naturally lack these drug-like properties owing to their large size (two turns of a nucleic acid double helix), nearly 40 anionic charges due to the phosphodiester backbone, and high molecular weight (over 13 kDa). In aqueous solution, with their sugar-phosphate backbone exposed to water, siRNAs are extremely hydrophilic and heavily hydrated. Furthermore, siRNAs are unstable in serum as a result of degradation by serum nucleases, contributing to their short half-lives in vivo 7 . Although the molecular weight of siRNAs cannot be reduced, these molecules can be made more 'drug-like' through judicious use of chemical modification to the sugars, backbone or bases of the oligoribonucleotides. Chemically modified siRNA duplexes have been evaluated in cellbased assays and in animal models. The modifications discussed are
Example Output:
RNAi therapeutics: a potential new class of pharmaceutical drugs R E V I E W