In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

Example Input: Paragraph: Background: Pseudomonas aeruginosa (PA) is an opportunistic Gram-negative bacterium that causes serious life threatening and nosocomial infections including pneumonia. PA has the ability to alter host genome to facilitate its invasion, thus increasing the virulence of the organism. Sphingosine-1-phosphate (S1P), a bioactive lipid, is known to play a key role in facilitating infection. Sphingosine kinases (SPHK) 1&2 phosphorylate sphingosine to generate S1P in mammalian cells. We reported earlier that Sphk2 −/− mice offered significant protection against lung inflammation, compared to wild type (WT) animals. Therefore, we profiled the differential expression of genes between the protected group of Sphk2 −/− and the wild type controls to better understand the underlying protective mechanisms related to the Sphk2 deletion in lung inflammatory injury. Whole transcriptome shotgun sequencing (RNA-Seq) was performed on mouse lung tissue using NextSeq 500 sequencing system. Results: Two-way analysis of variance (ANOVA) analysis was performed and differentially expressed genes following PA infection were identified using whole transcriptome of Sphk2 −/− mice and their WT counterparts. Pathway (PW) enrichment analyses of the RNA seq data identified several signaling pathways that are likely to play a crucial role in pneumonia caused by PA such as those involved in: 1. Immune response to PA infection and NF-κB signal transduction; 2. PKC signal transduction; 3. Impact on epigenetic regulation; 4. Epithelial sodium channel pathway; 5. Mucin expression; and 6. Bacterial infection related pathways. Our genomic data suggests a potential role for SPHK2 in PA-induced pneumonia through elevated expression of inflammatory genes in lung tissue. Further, validation by RT-PCR on 10 differentially expressed genes showed 100% concordance in terms of vectoral changes as well as significant fold change. (Continued on next page) 
 Title: Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung
Example Output: False

Example Input: Paragraph: As simple organisms with a parasite nature, viruses have become masters in manipulating and subvert cellular components, including host proteins and organelles, to improve viral replication. Therefore, the understanding of viral strategies to manipulate cell function disrupting plant defenses and enhancing viral infection cycles is fundamental to the production of virus-resistant plant lines. After invading susceptible plants, viruses create conditions that favor local and systemic infections by suppressing multiple layers of innate host defenses while use cellular machinery to own benefit. Viral interference in interlinked essential cellular functions results in phenotypic changes and disease symptoms, which debilitates plants favoring infection establishment. Herein in this review, the novelty it will be the discussion about the strategies used by (+) single strand RNA viruses to affect cellular processes and components to improve viral replication, in parallel to overcome plant defenses, favoring disease establishment by applying in one action using the same viral protein to coordinate viral replication and breaking down plant defense. This focus on plant-virus interaction was never done before, and this knowledge has the potential to help in the development of new strategies to produce resistant plants. 
 Title: Killing two birds with one stone: How do Plant Viruses Break Down Plant Defenses and Manipulate Cellular Processes to Replicate Themselves?
Example Output: True

Example Input: Paragraph: To extend the frontier of genome editing and enable the radical redesign of mammalian genomes, we developed a set of dead-Cas9 base editor (dBE) variants that allow editing at tens of thousands of loci per cell by overcoming the cell death associated with DNA double-strand breaks (DSBs) and single-strand breaks (SSBs). We used a set of gRNAs targeting repetitive elementsranging in target copy number from about 31 to 124,000 per cell. dBEs enabled survival after 5 large-scale base editing, allowing targeted mutations at up to ~13,200 and ~2610 loci in 293T and human induced pluripotent stem cells (hiPSCs), respectively, three orders of magnitude greater than previously recorded. These dBEs can overcome current on-target mutation and toxicity barriers that prevent cell survival after large-scale genome engineering. One Sentence Summary: Base editing with reduced DNA nicking allows for the simultaneous 10 
 Title: Enabling large-scale genome editing by reducing DNA nicking
Example Output:
True