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".

Paragraph: We describe an evidence-based approach to enhancing the resilience of healthcare workers in preparation for an influenza pandemic, based on evidence about the stress associated with working in healthcare during the SARS outbreak. SARS was associated with significant long-term stress in healthcare workers, but not with increased mental illness. Reducing pandemic-related stress may best be accomplished through interventions designed to enhance resilience in psychologically healthy people. Applicable models to improve adaptation in individuals include Folkman and Greer's framework for stress appraisal and coping along with psychological first aid. Resilience is supported at an organizational level by effective training and support, development of material and relational reserves, effective leadership, the effects of the characteristics of "magnet hospitals," and a culture of organizational justice. Evidence supports the goal of developing and maintaining an organizational culture of resilience in order to reduce the expected stress of an influenza pandemic on healthcare workers. This recommendation goes well beyond the provision of adequate training and counseling. Although the severity of a pandemic is unpredictable, this effort is not likely to be wasted because it will also support the health of both patients and staff in normal times. 
 Title: Applying the Lessons of SARS to Pandemic Influenza An Evidence-based Approach to Mitigating the Stress Experienced by Healthcare Workers
True

Paragraph: Objective: Increased hepatic expression of dipeptidyl peptidase 4 (DPP4) is associated with non-alcoholic fatty liver disease (NAFLD). Whether this is causative for the development of NAFLD is not yet clarified. Here we investigate the effect of hepatic DPP4 overexpression on the development of liver steatosis in a mouse model of diet-induced obesity. Methods: Plasma DPP4 activity of subjects with or without NAFLD was analyzed. Wild-type (WT) and liver-specific Dpp4 transgenic mice (Dpp4-Liv-Tg) were fed a high-fat diet and characterized for body weight, body composition, hepatic fat content and insulin sensitivity. In vitro experiments on HepG2 cells and primary mouse hepatocytes were conducted to validate cell autonomous effects of DPP4 on lipid storage and insulin sensitivity. Results: Subjects suffering from insulin resistance and NAFLD show an increased plasma DPP4 activity when compared to healthy controls. Analysis of Dpp4-Liv-Tg mice revealed elevated systemic DPP4 activity and diminished active GLP-1 levels. They furthermore show increased body weight, fat mass, adipose tissue inflammation, hepatic steatosis, liver damage and hypercholesterolemia. These effects were accompanied by increased expression of PPARg and CD36 as well as severe insulin resistance in the liver. In agreement, treatment of HepG2 cells and primary hepatocytes with physiological concentrations of DPP4 resulted in impaired insulin sensitivity independent of lipid content. Conclusions: Our results give evidence that elevated expression of DPP4 in the liver promotes NAFLD and insulin resistance. This is linked to reduced levels of active GLP-1, but also to auto-and paracrine effects of DPP4 on hepatic insulin signaling. (A. Schürmann). Abbreviations: Ad, adenovirus; Akt, Akt serineethreonine protein kinase; ALT, alanine aminotransferase; ApoB, apolipoprotein B; AST, aspartate aminotransferase; BAT, brown adipose tissue; CD36, fatty acid translocase; Cpt1a, carnitine palmitoyltransferase 1a; Dgat2, diacylglycerol O-acyltransferase 2; DPP4, dipeptidyl peptidase 4; Dpp4-Liv-Tg, transgenic mice with hepatocyte-specific Dpp4 overexpression; F4/80, adhesion G protein-coupled receptor E1; Gfp, green fluorescent protein; GGT, gammaglutamyl transpeptidase; GLP-1, glucagon-like peptide 1; gWAT, gonadal white adipose tissue; HFD, high-fat diet; HOMA-IR, homeostatic model assessment for insulin resistance; IL6, interleukin 6; MAPK, mitogen-activated protein kinase; MCP1, chemokine (C-C motif) ligand 2; MOGAT1, monoacylglycerol O-acyltransferase 1; NAFLD, nonalcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; NFkB, nuclear factor-kB; pAkt, phosphorylated Akt serineethreonine protein kinase; WT, wild-type; PPARg, peroxisome proliferator activated receptor gamma; rhDPP4, recombinant human dipeptidyl peptidase 4; rmDPP4, recombinant mouse dipeptidyl peptidase 4; SM, skeletal muscle; Srebf1, sterol regulatory element binding transcription factor 1; sWAT, subcutaneous white adipose tissue; TNFa, tumor necrosis factor a 
 Title: Elevated hepatic DPP4 activity promotes insulin resistance and non-alcoholic fatty liver disease
False

Paragraph: In herpes simplex virus 1 (HSV-1)-infected cells, G4s are massively present during viral replication. We here aimed at investigating the possibility to target the HSV-1 G4s by a core extended naphtalene diimide (c-exNDI) G4 ligand. Biophysical and biomolecular analysis proved that c-exNDI stabilized the HSV-1 G4s in a concentration dependent manner. In MS competition assays, c-exNDI preferentially recognized HSV-1 G4s over cellular telomeric G4s, the most represented G4s within cells; other less abundant cellular G4s were also recognized. Treatment of HSV-1 infected cells with c-exNDI at low nanomolar concentrations induced significant virus inhibition with no cytotoxicity. The mechanism of action was ascribed to G4-mediated inhibition of viral DNA replication, with consequent impairment of viral genes transcription. Our data suggest that the observed potent antiviral activity and low cytotoxicity mainly depend on a combination of c-exNDI affinity for HSV-1 G4s and their massive presence during infection. HSV-1 G4s may thus represent new effective antiviral targets: the fact that no current antiherpetic drug exploits them and their presence at the viral genome, responsible for both active and latent HSV infections, makes them particularly attracting. G-quadruplexes (G4s) are nucleic acids secondary structures that may form in single-stranded G-rich sequences under physiological conditions 1 . Four Gs bind via Hoogsteen-type hydrogen bonds base-pairing to yield G-quartets, which stack to form the G4. The presence of K + cations specifically supports G4 formation and stability 2 . Based on the strand orientation, G4s can adopt three main topologies: parallel, antiparallel, and hybrid-type structures. In eukaryotes, G4s have been shown to be involved in key regulatory roles, including transcriptional regulation of gene promoters and enhancers, translation, chromatin epigenetic regulation, DNA recombination 3-7 . Expansion of G-quadruplex-forming motifs has been associated with relevant human neurological disorders 4, 8, 9 . Formation of G4s in vivo has been consolidated by the discovery of cellular proteins that specifically recognize G4s 10, 11 and the development of G4 specific antibodies 12, 13 . Recently, the presence of G4s in viruses and their involvement in virus key steps has been provided 14 . G4s have been implicated in pathogenic mechanisms of the human immunodeficiency virus, where functionally significant G4s have been identified 5, 11, 15-17 and stabilized by G4 ligands with consequent antiviral effects 5, 18, 19 . G4s have been reported in the SARS coronavirus 20 , the human papilloma, Zika, Ebola and hepatitis C virus genome 21-24 . Among herpesviruses, RNA G4s have been implicated in the regulation of DNA replication and translation of the Epstein-Barr virus 25, 26 . We have shown that the herpes simplex virus 1 (HSV-1) possesses several repeats of important G4-forming sequences, which could be stabilized by a G4 ligand with inhibition of viral DNA replication 27 . In addition, HSV-1 G4s, visualized with the aid of a G4-specific antibody in infected cells 12 , were shown to form massively in the cell nucleus, peak during viral replication and localize according to the viral genome intracellular movements 28 . The involvement of G4 structures in several human diseases propelled the development of small molecules directed against G4s 7, 29 . However, only very few have been tested against viruses, i.e. Published: xx xx xxxx OPEN www.nature.com/scientificreports/ 2 Scientific RepoRts | 7: 2341 | 
 Title: A core extended naphtalene diimide G-quadruplex ligand potently inhibits herpes simplex virus 1 replication OPEN

True