TASK DEFINITION: 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".
PROBLEM: Paragraph: We have previously reported that the 3C-like proteinase of the coronavirus infectious bronchitis virus (IBV) is responsible for processing of the 1a and 1a/1b polyproteins to three mature products of 24, 10, and 100 kDa (Liu et al., 1994 (Liu et al., , 1997 Ng and Liu, 1998) . The C-terminal cleavage site of the 100-kDa protein was defined to be the Q 891(1b) -S 892(1b) dipeptide bond encoded by nucleotides 15, 129 to 15, 134 (Liu and Brown, 1995). In this report, other cleavage sites of the 3C-like proteinase in the polyprotein encoded by the ORF 1b region were mapped by coexpression, deletion, and site-directed mutagenesis studies. Using two ORF 1b-specific antisera, V58 and V17, three more Q-S(G) dipeptide bonds, encoded by nucleotides 16,929 to 16,934, 18,492 to 18,497, and 19,506 to 19,511, respectively, were demonstrated to be the cleavage sites of the 3C-like proteinase. Cleavage at these four positions would result in the release of four mature products with molecular masses of approximately 68, 58, 39, and 35 kDa. Among them, the 39-and 35-kDa proteins were specifically identified in IBV-infected cells. Taken together with the 100-kDa protein previously identified, these results suggest that the ORF 1b region of IBV mRNA1 may be able to encode five mature products. 
 Title: Proteolytic Mapping of the Coronavirus Infectious Bronchitis Virus 1b Polyprotein: Evidence for the Presence of Four Cleavage Sites of the 3C-like Proteinase and Identification of Two Novel Cleavage Products

SOLUTION: False

PROBLEM: Paragraph: Cytokine expression patterns of T cells can be regulated by pre-commitment to stable effector phenotypes, further modification of moderately stable phenotypes, and quantitative changes in cytokine production in response to acute signals. We showed previously that the epidermal growth factor family member Amphiregulin is expressed by T cell receptor-activated mouse CD4 T cells, particularly Th2 cells, and helps eliminate helminth infection. Here we report a detailed analysis of the regulation of Amphiregulin expression by human T cell subsets. Signaling through the T cell receptor induced Amphiregulin expression by most or all T cell subsets in human peripheral blood, including naive and memory CD4 and CD8 T cells, Th1 and Th2 in vitro T cell lines, and subsets of memory CD4 T cells expressing several different chemokine receptors and cytokines. In these different T cell types, Amphiregulin synthesis was inhibited by an antagonist of protein kinase A, a downstream component of the cAMP signaling pathway, and enhanced by ligands that increased cAMP or directly activated protein kinase A. Prostaglandin E2 and adenosine, natural ligands that stimulate adenylyl cyclase activity, also enhanced Amphiregulin synthesis while reducing synthesis of most other cytokines. Thus, in contrast to mouse T cells, Amphiregulin synthesis by human T cells is regulated more by acute signals than precommitment of T cells to a particular cytokine pattern. This may be appropriate for a cytokine more involved in repair than attack functions during most inflammatory responses. 
 Title: The Acute Environment, Rather than T Cell Subset Pre- Commitment, Regulates Expression of the Human T Cell Cytokine Amphiregulin

SOLUTION: False

PROBLEM: Paragraph: Influenza viruses exhibit a fascinating level of antigenic heterogeneity that facilitates re-infection in the human population. The human antibody repertoire also manifests endless capability for variation in the genes that specify the portion of antibody molecules interacting with epitopes. A recent explosion of techniques for isolating human monoclonal antibodies to viruses has led to isolation of new antibodies that allow glimpses into the molecular basis for recognition and escape that underlies the constant antigenic drift in influenza surface proteins. These studies also reveal evidence for lifelong persistence of immunity to some influenza viruses. 
 Title: Recent Advances in the Study of Human Antibody Responses to Influenza Virus Using Optimized Human Hybridoma Approaches

SOLUTION:
True