instruction:
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".
question:
Paragraph: Background: Adverse events are associated with significant morbidity, mortality and cost in hospitalized patients. Measuring adverse events is necessary for quality improvement, but current detection methods are inaccurate, untimely and expensive. The advent of electronic health records and the development of automated methods for encoding and classifying electronic narrative data, such as natural language processing, offer an opportunity to identify potentially better methods. The objective of this study is to determine the accuracy of using automated methods for detecting three highly prevalent adverse events: a) hospital-acquired pneumonia, b) catheter-associated bloodstream infections, and c) in-hospital falls. Methods/design: This validation study will be conducted at two large Canadian academic health centres: the McGill University Health Centre (MUHC) and The Ottawa Hospital (TOH). The study population consists of all medical, surgical and intensive care unit patients admitted to these centres between 2008 and 2014. An automated detection algorithm will be developed and validated for each of the three adverse events using electronic data extracted from multiple clinical databases. A random sample of MUHC patients will be used to develop the automated detection algorithms (cohort 1, development set). The accuracy of these algorithms will be assessed using chart review as the reference standard. Then, receiver operating characteristic curves will be used to identify optimal cut points for each of the data sources. Multivariate logistic regression and the areas under curve (AUC) will be used to identify the optimal combination of data sources that maximize the accuracy of adverse event detection. The most accurate algorithms will then be validated on a second random sample of MUHC patients (cohort 1, validation set), and accuracy will be measured using chart review as the reference standard. The most accurate algorithms validated at the MUHC will then be applied to TOH data (cohort 2), and their accuracy will be assessed using a reference standard assessment of the medical chart. Discussion: There is a need for more accurate, timely and efficient measures of adverse events in acute care hospitals. This is a critical requirement for evaluating the effectiveness of preventive interventions and for tracking progress in patient safety through time. 
 Title: Accuracy of using automated methods for detecting adverse events from electronic health record data: a research protocol
answer:
True


question:
Paragraph: Diseases caused by pathogenic microorganisms including bacteria and viruses can cause serious medical issues including death and result in huge economic losses. Despite the myriad of recent advances in the rapid and accurate detection of pathogens, large volume clinical samples with a low concentration of pathogens continue to present challenges for diagnosis and surveillance. We here report a simple and label-free approach via homobifunctional imidoesters (HIs) with a microfluidic platform (SLIM) to efficiently enrich and extract pathogens at low concentrations from clinical samples. The SLIM system consists of an assembled double microfluidic chip for streamlining large volume processing and HIs for capturing pathogens and isolating nucleic acids by both electrostatic and covalent interaction without a chaotropic detergent or bulky instruments. The SLIM system significantly increases the enrichment and extraction rate of pathogens (up to 80% at 10 CFU (colony forming unit) in a 1 mL volume within 50 min). We demonstrated its clinical utility in large sample volumes from 46 clinical specimens including environmental swabs, saliva, and blood plasma. The SLIM system showed higher sensitivity with these samples and could detect pathogens that were below the threshold of detection with other methods. Finally, by combining our SLIM approach with an isothermal optical sensor, pathogens could be detected at a very high sensitivity in blood plasma samples within 80 min via enrichment, extraction and detection steps. Our SLIM system thus provides a simple, reliable, cost-effective and ultrasensitive pathogen diagnosis platform for use with large volume clinical samples and would thus have significant utility for various infectious diseases. 
 Title: Simple and label-free pathogen enrichment via homobifunctional imidoesters using a microfluidic (SLIM) system for ultrasensitive pathogen detection in various clinical specimens
answer:
True


question:
Paragraph: In response to the endoplasmic reticulum (ER) stress induced by herpes simplex virus type 1 (HSV-1) infection, host cells activate the unfolded protein response (UPR) to reduce the protein-folding burden in the ER. The regulation of UPR upon HSV-1 infection is complex, and the downstream effectors can be detrimental to viral replication. Therefore, HSV-1 copes with the UPR to create a beneficial environment for its replication. UPR has three branches, including protein kinase RNA (PKR)-like ER kinase (PERK), inositol-requiring enzyme 1 (IRE1), and activated transcription factor 6 (ATF6). IRE1α is the most conserved branch of UPR which has both RNase and kinase activities. Previous studies have shown that IRE1α RNase activity was inactivated during HSV-1 infection. However, the effect of the two activities of IRE1α on HSV-1 replication remains unknown. Results in this study showed that IRE1α expression was up-regulated during HSV-1 infection. We found that in HEC-1-A cells, increasing RNase activity, or inhibiting kinase activity of IRE1α led to viral suppression, indicating that the kinase activity of IRE1α was beneficial, while the RNase activity was detrimental to viral replication. Further evidence showed that the kinase activity of IRE1α leads to the activation of the JNK (c-Jun N-terminal kinases) pathway, which enhances viral replication. Taken together, our evidence suggests that IRE1α is involved in HSV-1 replication, and its RNase and kinase activities play differential roles during viral infection. Keywords: endoplasmic reticulum (ER); herpes simplex virus 1 (HSV-1); inositol-requiring enzyme 1 (IRE1); unfolded protein response (UPR); X-box binding protein 1 (XBP1) Viruses 2017, 9, 235 9 of 17 3.3. The Effect of IRE1α Kinase Activity on HSV-1 Replication Next, we investigated the effect of kinase activity of IRE1α on viral replication. IRE1 phosphorylation is generally considered as a reliable indicator of IRE1α kinase activity [45, [49] [50] [51] . Kinase activity of IRE1α was induced at a later stage of viral infection, as indicated by the phosphorylation of IRE1α from 12 h p.i. (Figure 3A ). Viruses 2017, 9, 235 9 of 17 Next, we investigated the effect of kinase activity of IRE1α on viral replication. IRE1 phosphorylation is generally considered as a reliable indicator of IRE1α kinase activity [45, [49] [50] [51] . Kinase activity of IRE1α was induced at a later stage of viral infection, as indicated by the phosphorylation of IRE1α from 12 h p.i. (Figure 3A) . Figure 3. HSV-1 replication is regulated by kinase activity of IRE1α. (A) HSV-1 infection stimulated kinase activity of IRE1α in HEC-1-A cells. HEC-1-A cells were infected with HSV-1 (HF) (moi = 1). Cell lysates were prepared at the times indicated and subject to Western blot analysis using antibodies against total IRE1α, phosphorylated IRE1α, gD-1 and GAPDH; (B) XBP1 splicing induced by APY29 was attenuated by STF-083010 in a dose dependent manner. HEC-1-A cells were treated with both a serial concentration of STF-083010 and 3.125 μM of APY29, and then incubated for 24 h. Total RNA was prepared for measuring the expression of spliced and unspliced XBP1using reverse transcription-PCR analysis; (C,D) Viral replication was inhibited by APY29; (C) Confluent HEC-1-A cells cultured in a 96-well plate were pretreated with serial concentrations of APY29 and then infected with HSV-1 (HF) (moi = 1) for 24 h; (D) Before HEC-1-A cells were infected with HSV-1 (HF) (moi = 1), cells were incubated with both serial concentration of STF-083010 and 3.125 μM of APY29. gD-1 protein expression was determined via In-cell Western, and normalized by DRAQ5 fluorescence at 24 h p.i. Data are mean values ± SD of triplicate determinations (** p < 0.01). Representative results are shown; (E) Inhibition of IRE1α kinase activity had an inhibitory effect on HSV-1 replication in HEC-1-A cells. Cells were presence or absence of APY29 (3.125 μM) or STF-083010 (60 μM) or both of two drugs and then infected with HSV-1 (HF) at moi = 1. Total cellular cells lysates were prepared at 24 h p.i. and subject to Western blot analysis against antibodies to total IRE1α, phosphorylated IRE1α and gD-1; (F) Inactivation of IRE1α kinase activity suppressed HSV-1 replication in Hela cells. Hela cells were transfected with vehicle or IRE1 alpha KA-pcDNA3.EGFP or IRE1 alpha-pcDNA3.EGFP plasmid for 48 h and then infected or mock-infected with HSV-1 (moi = 1). The total and phosphorylated IRE1α, 
 Title: Opposite Roles of RNase and Kinase Activities of Inositol-Requiring Enzyme 1 (IRE1) on HSV-1 Replication
answer:

True