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: Recent infectious outbreaks highlight the need for platform technologies that can be quickly deployed to develop therapeutics needed to contain the outbreak. We present a simple concept for rapid development of new antimicrobials. The goal was to produce in as little as one week thousands of doses of an intervention for a new pathogen. We tested the feasibility of a system based on antimicrobial synbodies. The system involves creating an array of 100 peptides that have been selected for broad capability to bind and/or kill viruses and bacteria. The peptides are pre-screened for low cell toxicity prior to large scale synthesis. Any pathogen is then assayed on the chip to find peptides that bind or kill it. Peptides are combined in pairs as synbodies and further screened for activity and toxicity. The lead synbody can be quickly produced in large scale, with completion of the entire process in one week.
Title: A Simple Platform for the Rapid Development of Antimicrobials

SOLUTION: True

PROBLEM: Paragraph: Accumulating evidence suggests that human T cells act as non-classical T cells and contribute to both innate and adaptive immune responses in infections. V2 V2 T (also termed V9 V2 T) cells exist only in primates, and in humans represent a dominant circulating T-cell subset. Primate V2 V2 T cells are the only T cell subset capable of recognizing microbial phosphoantigen. Since nonhuman primate V2 V2 T cells resemble their human counterparts, indepth studies have been undertaken in macaques to understand the biology and function of human V2 V2 T cells. This article reviews the recent progress for immune biology of V2 V2 T cells in infections.
Title: Immune biology of Ag-specific T cells in infections

SOLUTION: True

PROBLEM: Paragraph: The mitochondrial protein repertoire varies depending on the cellular state. Protein component modifications caused by mitochondrial DNA (mtDNA) depletion are related to a wide range of human diseases; however, little is known about how nuclear-encoded mitochondrial proteins (mt proteome) changes under such dysfunctional states. In this study, we investigated the systemic alterations of mtDNA-depleted (r 0 ) mitochondria by using network analysis of gene expression data. By modularizing the quantified proteomics data into protein functional networks, systemic properties of mitochondrial dysfunction were analyzed. We discovered that up-regulated and down-regulated proteins were organized into two predominant subnetworks that exhibited distinct biological processes. The down-regulated network modules are involved in typical mitochondrial functions, while up-regulated proteins are responsible for mtDNA repair and regulation of mt protein expression and transport. Furthermore, comparisons of proteome and transcriptome data revealed that r 0 cells attempted to compensate for mtDNA depletion by modulating the coordinated expression/transport of mt proteins. Our results demonstrate that mt protein composition changed to remodel the functional organization of mitochondrial protein networks in response to dysfunctional cellular states. Human mt protein functional networks provide a framework for understanding how cells respond to mitochondrial dysfunctions. Citation: Jeon J, Jeong JH,
Title: Network Clustering Revealed the Systemic Alterations of Mitochondrial Protein Expression

SOLUTION:
True