Part 1. Definition
In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
Part 2. Example
The severe acute respiratory syndrome (SARS) epidemic originating from China in 2002 was caused by a previously uncharacterized coronavirus that could be identified by specific RT-PCR amplification. Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients. A real-time fluorogenic RT-PCR assay based on the 3 -noncoding region (3 -NCR) of SARS-CoV genome was developed as a quantitative SARS diagnostic tool. The ideal amplification efficiency of a sensitive SARS-CoV RT-PCR assay should yield an E value (PCR product concentration increase per amplification cycle) equal to 2.0. It was demonstrated that the 3 -NCR SARS-CoV based RT-PCR reactions could be formulated to reach excellent E values of 1.81, or 91% amplification efficacy. The SARS-CoV cDNA preparations derived from viral RNA extract and the cloned recombinant plasmid both exhibit the identical amplification characteristics, i.e. amplification efficacy using the same PCR formulation developed in this study. The viral genomic copy (or genomic equivalences, GE) per infectious unit (GE/pfu) of SARS-CoV used in this study was also established to be approximate 1200-1600:1. The assay's detection sensitivity could reach 0.005 pfu or 6-8 GE per assay. It was preliminarily demonstrated that the assay could efficiently detect SARS-CoV from clinical specimens of SARS probable and suspected patients identified in Taiwan. The 3 -NCR based SARS-CoV assay demonstrated 100% diagnostic specificity testing samples of patients with acute respiratory disease from a non-SARS epidemic region.
Answer: Development and evaluation of an efficient 3 -noncoding region-based SARS coronavirus (SARS-CoV) RT-PCR assay for detection of SARS-CoV
Explanation: It's a correct title because the paragraph described the development of 3 -noncoding region of SARS-CoV genome and assay efficiently detecting SARS-CoV from clinical specimens.
Part 3. Exercise
Introduction: Type-I interferons (IFNs) have been used to treat several types of cancers including follicular lymphoma, hairy cell leukemia and chronic myeloid leukemia. Treatment with type-I IFNs is however associated with significant toxic side effects due to the ubiquitous expression of type-I IFN receptors. Type-III IFNs elicit similar cellular responses as type-I IFNs, but restricted expression of type-III receptors may limit potential side effects of treatment with type-III IFNs. A number of studies are now exploring the use of type-III IFNs, specifically IFN-k3, as anticancer agents. IFN-k4 is a newly discovered type-III IFN that is genetically regulated and produced in a subset of individuals. Previously, we showed that IFN-k4 inhibits proliferation in a hepatoma cell line, however its anticancer potential has not been explored in comparison to other type-III IFNs. Methods: We developed stable human hepatoma (HepG2) and B-cell lymphoma (Raji) cell lines, engineered to express either IFN-k4-GFP or IFN-k3-GFP upon induction by doxycycline. We compared antiproliferative activity of IFN-k3 and IFN-k4 by measuring BRDU incorporation before and after induction of IFN-k expression. We also compared cell viability, apoptosis, and changes in cell cycle between IFN-k3 and IFN-k4 expressing cell lines. RNAseq and pathway analysis were used to explore the antiproliferative effect induced by IFN-k4. We show that IFN-k4 has higher antiproliferative activity compared to IFN-k3 in Raji and HepG2 cell lines and this can be explained by inhibition of the cell cycle. IFN-k4 expressing cell lines showed increased apoptotic cell death compared to IFN-k3 expressing cell lines. We also show that antiproliferative activity of IFN-k4 may be a result of inhibition of the MAPK pathway. Conclusion: This study demonstrates that IFN-k4 has a more potent antiproliferative activity than IFN-k3 in hepatoma and B cell lymphoma cell lines and the anticancer potential of IFN-k4 should be further explored. Introduction: Interleukin-1b (IL-1b) is a potent proinflammatory cytokine that is implicated both in acute and chronic viral infection. Persistent hepatic inflammation is the hallmark of hepatitis C virus (HCV) infection wherein it serves as a platform for progressive liver injury and onset of liver cancer. We examined the role of IL-1b role in HCV-induced hepatic inflammation by first assessing the transcriptional profile of chronic HCV patient liver by next-gen sequencing (RNAseq) staged by inflammation and fibrosis score. (microenvironment) role of IRF5 in mammary tumor initiation and progression.
Answer:
P001 IFN-K4 HAS A POTENT ANTIPROLIFERATIVE ACTIVITY IN B-CELL LYMPHOMA AND HEPATOMA CELL LINES HCV CORE PROTEIN TRIGGERS IL-1B PRODUCTION VIA THE NLRP3 INFLAMMASOME P004 LOSS OF IRF5 INDUCES SPONTANEOUS MAMMARY TUMORIGEN- ESIS P005 PROTEOLYTIC ORIGIN OF THE SOLUBLE HUMAN IL-6R IN VIVO AND A DECISIVE ROLE OF N-GLYCOSYLATION DISTINCT ROLES FOR IRF5 IN MAMMARY EPITHELIAL CELLS AND HOST TUMOR IMMUNITY: LOSS OF IRF5 IN EITHER COMPART- MENT LEADS TO TUMORIGENESIS SEXUALLY DIMORPHIC ROLES OF STAT3 IN PEDIATRIC BRAIN CANCER P008 DISRUPTION OF PD-1/PD-L1 SIGNALING IN 2D VS. 3D COLORECTAL CANCER COCULTURE MODEL REVEALED BY RNAI HIGH THROUGH- PUT SCREEN