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".

[Q]: Paragraph: Background: Detection of respiratory viruses by time-resolved fluoroimmunoassay based on monoclonal antibodies were developed in our laboratories in the late 1980s and they have been successfully used in daily diagnosis for more than seven years. Later, similar Biotin-EIAs were developed but the sensitivities were unsatisfactory. Objectives: Further optimization of monoclonal Biotin-EIAs and comparison of the optimized assays with TR-FIAs. Study design: Variations in test format, diluents, incubation times and temperatures, and different monoclonal antibodies were tested, and the final comparisons were made with TR-FIA using stored nasopharyngeal aspirates. Results: The improvements in Biotin-EIA featured four changes which increased sensitivity in the assay: (a) test diluent contained diethylenetriamino-pentaacetic acid; (b) antigen and biotinylated detector antibody were added simultaneously; (c) reaction time was extended from 1 h at 37°C to overnight at 4°C; (d) from the thirteen monoclonal antibodies used in TR-FIA, ten were optimal also in Biotin-EIA, but in the parainfluenza 1 and 2 assays other monoclonals proved more sensitive. Out of 257 originally positive specimens tested in the comparison studies, 192 (74.7%) were again positive and 54 (21.0%) were negative in both assays; nine were negative in TR-FIA but positive in Biotin-EIA, while two specimens were negative in Biotin-EIA but positive in TR-FIA. The overall agreement between the two assays was 95.7%. 
 Title: Clinical and Diagnostic Virology Comparison of monoclonal biotin-avidin enzyme immunoassay and monoclonal time-resolved fluoroimmunoassay in detection of respiratory virus antigens
[A]: False


[Q]: Paragraph: Background: Based on clinical representation of disease symptoms multiple sclerosis (MScl) patients can be divided into two major subtypes; relapsing remitting (RR) MScl (85-90%) and primary progressive (PP) MScl (10-15%). Proteomics analysis of cerebrospinal fluid (CSF) has detected a number of proteins that were elevated in MScl patients. Here we specifically aimed to differentiate between the PP and RR subtypes of MScl by comparing CSF proteins. Methodology/Principal Findings: CSF samples (n = 31) were handled according to the same protocol for quantitative mass spectrometry measurements we reported previously. In the comparison of PP MScl versus RR MScl we observed a number of differentially abundant proteins, such as protein jagged-1 and vitamin D-binding protein. Protein jagged-1 was over three times less abundant in PP MScl compared to RR MScl. Vitamin D-binding protein was only detected in the RR MScl samples. These two proteins were validated by independent techniques (western blot and ELISA) as differentially abundant in the comparison between both MScl types. 
 Title: Proteomics Comparison of Cerebrospinal Fluid of Relapsing Remitting and Primary Progressive Multiple Sclerosis
[A]: True


[Q]: Paragraph: Graphical Abstract Highlights d SARS-CoV causes a lethal respiratory infection in BALB/c mice d Robust SARS-CoV replication and delayed IFN-I signaling promote disease d IFN-I induces influx of pathogenic inflammatory monocytes and vascular leakage d Disease severity is ameliorated in the absence of IFN signaling SUMMARY Highly pathogenic human respiratory coronaviruses cause acute lethal disease characterized by exuberant inflammatory responses and lung damage. However, the factors leading to lung pathology are not well understood. Using mice infected with SARS (severe acute respiratory syndrome)-CoV, we show that robust virus replication accompanied by delayed type I interferon (IFN-I) signaling orchestrates inflammatory responses and lung immunopathology with diminished survival. IFN-I remains detectable until after virus titers peak, but early IFN-I administration ameliorates immunopathology. This delayed IFN-I signaling promotes the accumulation of pathogenic inflammatory monocytemacrophages (IMMs), resulting in elevated lung cytokine/chemokine levels, vascular leakage, and impaired virus-specific T cell responses. Genetic ablation of the IFN-ab receptor (IFNAR) or IMM depletion protects mice from lethal infection, without affecting viral load. These results demonstrate that IFN-I and IMM promote lethal SARS-CoV infection and identify IFN-I and IMMs as potential therapeutic targets in patients infected with pathogenic coronavirus and perhaps other respiratory viruses. 
 Title: Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice Article Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice
[A]:
True