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".

Input: Consider Input: Paragraph: M.N.); halromaihi@moph.gov.qa (H.A.-R.); malthani@moph.gov.qa (M.A.T.); dralmarri@moph.gov.qa (S.A.-M.); malhajri1@moph.gov.qa (M.A.) Abstract: MERS-CoV (Middle East respiratory syndrome corona virus) antibodies were detected in camels since 1983, but the first human case was only detected in 2012. This study sought to identify and quantify possible drivers for the MERS-CoV emergence and spillover to humans. A list of potential human, animal and environmental drivers for disease emergence were identified from literature. Trends in possible drivers were analyzed from national and international databases, and through structured interviews with experts in Qatar. The discovery and exploitation of oil and gas led to a 5-fold increase in Qatar GDP coupled with a 7-fold population growth in the past 30 years. The lifestyle gradually transformed from Bedouin life to urban sedentary life, along with a sharp increase in obesity and other comorbidities. Owing to substantial governmental support, camel husbandry and competitions flourished, exacerbating the already rapidly occurring desertification that forced banning of free grazing in 2005. Consequently, camels were housed in compact barns alongside their workers. The transition in husbandry leading to high density camel farming along with increased exposure to humans, combined with the increase of camel movement for the racing and breeding industry, have led to a convergence of factors driving spillover of MERS-CoV from camels to humans. 13 of 15 to provide "hard evidence" of causality. Nevertheless, this is the first comprehensive quantitative overview of possible drivers of MERS-CoV in Qatar. Several key changes were shown to involve camels, humans, the economy, and the environment in Qatar during the last 30 years. Our study indicates that the rapid increase in camel ownership, leading to the presence of camels from different origins in a high-density environment mixed together with human and other animal species may have offered the right circumstances for the virus to spread from camels to humans. The other key changes that were described collectively contributed to this situation. Further understanding of the drivers that led to the emergence of MERS-CoV can serve as input for MERS-CoV surveillance and control measures to prevent further spread of MERS-CoV and reduce transmission from camels to humans. 
 Title: viruses Drivers of MERS-CoV Emergence in Qatar

Output: True


Input: Consider Input: Paragraph: Clinical metagenomics (CMg) is the discipline that refers to the sequencing of all nucleic acid material present within a clinical specimen with the intent to recover clinically relevant microbial information. From a diagnostic perspective, next-generation sequencing (NGS) offers the ability to rapidly identify putative pathogens and predict their antimicrobial resistance profiles to optimize targeted treatment regimens. Since the introduction of metagenomics nearly a decade ago, numerous reports have described successful applications in an increasing variety of biological specimens, such as respiratory secretions, cerebrospinal fluid, stool, blood and tissue. Considerable advancements in sequencing and computational technologies in recent years have made CMg a promising tool in clinical microbiology laboratories. Moreover, costs per sample and turnaround time from specimen receipt to clinical management continue to decrease, making the prospect of CMg more feasible. Many difficulties, however, are associated with CMg and warrant further improvements such as the informatics infrastructure and analytical pipelines. Thus, the current review focuses on comprehensively assessing applications of CMg for diagnostic and subtyping purposes. Crown 
 Title: Highlighting Clinical Metagenomics for Enhanced Diagnostic Decision-making: A Step Towards Wider Implementation

Output: True


Input: Consider Input: Paragraph: Ubiquitin (UB) is a protein modifier that regulates many essential cellular processes. To initiate protein modification by UB, the E1 enzyme activates the C-terminal carboxylate of UB to launch its transfer through the E1-E2-E3 cascade onto target proteins. In this study, we used phage display to profile the specificity of the two human E1 enzymes, Ube1 and Uba6, towards the Cterminal sequence of UB ending with 71 LRLRGG 76 . Phage selection revealed that while Arg72 of UB is absolutely required for E1 recognition, UB residues at positions 71, 73 and 74 can be replaced with bulky aromatic side chains, and Gly75 of UB can be changed to Ser, Asp and Asn for efficient E1 activation. We have thus found that the E1 enzymes have substantial promiscuity regarding the UB C-terminal sequence. The UB variants from phage selection can also be transferred from E1 to E2 enzymes, however, they are blocked from further transfer to the E3 enzymes. This suggests that the C-terminal sequence of UB is important for its discharge from E2 and subsequent transfer to E3. In addition, we observed that the Leu73Phe and Leu73Tyr single mutants of UB are resistant to cleavage by deubiquitinating enzymes (DUBs), although they can be assembled by the E1-E2-E3 cascade into poly-UB chains, thus indicating differences in UB Cterminal specificities between the E1 and DUBs. Consequently these UB mutants may provide stability to UB polymers attached to cellular proteins and facilitate the elucidation of the biological signals encoded in the UB chains. Ubiquitin (UB) is a 76-residue protein that is attached to cellular proteins through an isopeptide bond between the C-terminal carboxylate of UB and the ε-amino group of a Lys residue on the modified protein. 1 Protein modifications by UB are associated with a myriad of cellular functions, including regulation of protein degradation, designation of protein 
 Title: Specificity of the E1-E2-E3 Enzymatic Cascade for Ubiquitin C- terminal Sequences Identified by Phage Display HHS Public Access Author manuscript Supplementary Material Refer to Web version on PubMed Central for supplementary material


Output: False