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: Multilateral agencies define and operationalized health and development in a variety of ways. The World Health Organization (WHO) and the World Bank are two dominant actors in health and development. Each espouses a different ideal of health as it relates to the process of development. The WHO defines health as a human right, and focuses on health outcomes as inputs to and the result of development. The World Bank's approach to development focuses largely on macro-economic growth as input to human capabilities. The World Bank became a leading actor in international health policy in the 1990s when it operationalized health as an outcome of financial and health care systems. This chapter looks at programming efforts by the WHO and the World Bank to foster development via investment in health or through macro-economic adjustment. Results are mixed. Efforts to improve primary care were successful in improving health outcomes of children under five, but made little impact on maternal mortality. Structural adjustment programs achieved moderate success with medium-to long-term economic growth but increased health inequities. These mixed achievements resulted in an effort by the United Nations to foster a multi-sectoral approach to development espoused in the Millennium Development Goals and Sustainable Development Goals. 
 Title: International Organizations and Their Approaches to Fostering Development
Example Output: True

Example Input: Paragraph: The spread of the COVID-19 caused by the SARS-CoV-2 outbreak has been growing since its first identification in December 2019. The publishing of the first SARS-CoV-2 genome made a valuable source of data to study the details about its phylogeny, evolution, and interaction with the host. Protein-protein binding assays have confirmed that Angiotensin-converting enzyme 2 (ACE2) is more likely to be the cell receptor via which the virus invades the host cell. In the present work, we provide an insight into the interaction of the viral spike Receptor Binding Domain (RBD) from different coronavirus isolates with host ACE2 protein. By calculating : bioRxiv preprint 2 the binding energy between RBD and ACE2, we highlighted the putative jump in the affinity from a progenitor form of SARS-CoV-2 to the current virus responsible for COVID-19 outbreak. Our result was consistent with the phylogeny analysis and corroborates the opinion that the interface segment of the spike protein RBD might be acquired by SARS-CoV-2 via a complex evolutionary process rather than mutation accumulation. We also highlighted the relevance of Q493 and P499 amino acid residues of SARS-CoV-2 RBD for binding to hACE2 and maintaining the stability of the interface. Moreover, we show from the structural analysis that it is unlikely for the interface residues to be the result of human engineering. Finally, we studied the impact of eight different variants located at the interaction surface of ACE2, on the complex formation with SARS-CoV-2 RBD. We found that none of them is likely to disrupt the interaction with the viral RBD of SARS-CoV-2. 
 Title: Interaction of the spike protein RBD from SARS-CoV-2 with ACE2: similarity with SARS-CoV, hot-spot analysis and effect of the receptor polymorphism
Example Output: False

Example Input: Paragraph: Theiler's murine encephalomyelitis virus (TMEV) is a member of the genus Cardiovirus in the Picornaviridae, a family of positive-sense single-stranded RNA viruses. Previously, we demonstrated that in the related cardiovirus, Encephalomyocarditis virus, a programmed ؊1 ribosomal frameshift (؊1 PRF) occurs at a conserved G_GUU_UUU sequence within the 2B-encoding region of the polyprotein open reading frame (ORF). Here we show that ؊1 PRF occurs at a similar site during translation of the TMEV genome. In addition, we demonstrate that a predicted 3= RNA stem-loop structure at a noncanonical spacing downstream of the shift site is required for efficient frameshifting in TMEV and that frameshifting also requires virus infection. Mutating the G_GUU_UUU shift site to inhibit frameshifting results in an attenuated virus with reduced growth kinetics and a small-plaque phenotype. Frameshifting in the virus context was found to be extremely efficient at 74 to 82%, which, to our knowledge, is the highest frameshifting efficiency recorded to date for any virus. We propose that highly efficient ؊1 PRF in TMEV provides a mechanism to escape the confines of equimolar expression normally inherent in the single-polyprotein expression strategy of picornaviruses. Many viruses utilize programmed ؊1 ribosomal frameshifting (؊1 PRF) to produce different protein products at a defined ratio, or to translate overlapping ORFs to increase coding capacity. With few exceptions, ؊1 PRF occurs on specific "slippery" heptanucleotide sequences and is stimulated by RNA structure beginning 5 to 9 nucleotides (nt) downstream of the slippery site. Here we describe an unusual case of ؊1 PRF in Theiler's murine encephalomyelitis virus (TMEV) that is extraordinarily efficient (74 to 82% of ribosomes shift into the alternative reading frame) and, in stark contrast to other examples of ؊1 PRF, is dependent upon a stem-loop structure beginning 14 nt downstream of the slippery site. Furthermore, in TMEV-based reporter constructs in transfected cells, efficient frameshifting is critically dependent upon virus infection. We suggest that TMEV evolved frameshifting as a novel mechanism for removing ribosomes from the message (a "ribosome sink") to downregulate synthesis of the 3=-encoded replication proteins. 
 Title: Characterization of Ribosomal Frameshifting in Theiler's Murine Encephalomyelitis Virus
Example Output:
True