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".

Ex Input:
Paragraph: Brazzein protein comes from an edible fruit, which has a long history of being a staple in the local human diet in Africa. The attractive features of brazzein as a potential commercial sweetener include its small size (53 amino acid residues), its stability over wide ranges of temperature and pH, and the similarity of its sweetness to sucrose. Heterologous production of brazzein is complicated by the fact that the protein contains four disulfide bridges and requires a specific N-terminal sequence. Our previous protocol for producing the protein from Escherichia coli involved several steps with low overall yield: expression as a fusion protein, denaturation and renaturation, oxidation of the cysteines, and cleavage by cyanogen bromide at an engineered methionine adjacent to the desired N-terminus. The new protocol described here, which is much faster and leads to a higher yield of native protein, involves the production of brazzein in E. coli as a fusion with SUMO. The isolated protein product contains the brazzein domain folded with correct disulfide bonds formed and is then cleaved with a specific SUMO protease to liberate native brazzein. This protocol represents an important advancement that will enable more efficient research into the interaction between brazzein and the receptor as well as investigations to test the potential of brazzein as a commercially viable natural low calorie sweetener. 
 Title: Efficient and rapid protein expression and purification of small high disulfide containing sweet protein brazzein in E. coli

Ex Output:
True


Ex Input:
Paragraph: Ageing individuals are immunologically characterized by loss of immunological protection and responsiveness, and autoimmunity occurs with increased incidence. Here we review studies on specific age-related changes in B cell generation, activation, and maintenance as well as characteristics of B cell responses and antibody levels during ageing in relation to other cells and factors that are interwoven with B cell biological processes. In the elderly, fewer new B cells are generated, B cell responsiveness to antigens is impaired, and smaller and fewer germinal centers are formed within an immune response with participation of less potent T cells and follicular dendritic cells, leading to the production of reduced, often insufficient plasma cell numbers. Recall responses in the elderly appear to be limited by the cells' proliferative capacity. Hence, vaccine responsiveness is often insufficient and autoantibody production emerges in the elderly. In total, B cells appear to be less affected by age as compared with T cells. Recently, new concepts have been developed to counteract immunosenescence beyond active vaccination, comprising the generation of specific monoclonal antibodies for passive vaccination, immune rejuvenation by immunoablation followed by autologous stem cell transplantation, and modulation of lifestyle. 
 Title: Characteristics of B Cells and B Cell Responses in Aged Individuals

Ex Output:
True


Ex Input:
Paragraph: To identify new host factors that modulate the replication of influenza A virus, we performed a yeast two-hybrid screen using the cytoplasmic tail of matrix protein 2 from the highly pathogenic H5N1 strain. The screen revealed a high-score interaction with cyclin D3, a key regulator of cell cycle early G 1 phase. Interestingly, the increase in virus production was due to cyclin D3 deficiency per se and not merely a consequence of cell cycle deregulation. A combined knockdown of Ccnd3 and Rb1, which rescued cell cycle progression into S phase, failed to normalize virus production. Infection by influenza A virus triggered redistribution of cyclin D3 from the nucleus to the cytoplasm, followed by its proteasomal degradation. When overexpressed in HEK 293T cells, cyclin D3 impaired binding of M2 with M1, which is essential for proper assembly of progeny virions, lending further support to its role as a putative restriction factor. Our study describes the identification and characterization of cyclin D3 as a novel interactor of influenza A virus M2 protein. We hypothesize that competitive inhibition of M1-M2 interaction by cyclin D3 impairs infectious virion formation and results in attenuated virus production. In addition, we provide mechanistic insights into the dynamic interplay of influenza virus with the host cell cycle machinery during infection. 
 Title: Cell Cycle-independent Role of Cyclin D3 in Host Restriction of Influenza Virus Infection

Ex Output:

True