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".

Input: Consider Input: Paragraph: Zika virus (ZIKV), a member of the Flaviviridae family, is the most recent emerging arbovirus with pandemic potential. During infection, viruses trigger the host cell stress response, leading to changes in RNA translation and the assembly of large aggregates of stalled translation preinitiation complexes, termed stress granules (SGs). Several reports demonstrate that flaviviruses modulate the assembly of stress granules (SG). As an emerging pathogen, little is known however about how ZIKV modulates the host cell stress response. In this work, we investigate how ZIKV modulates SG assembly. We demonstrate that ZIKV negatively impacts SG assembly under oxidative stress conditions induced by sodium arsenite (Ars), a treatment that leads to the phosphorylation of eIF2α. By contrast, no measurable difference in SG assembly was observed between mock and ZIKV-infected cells treated with sodium selenite (Se) or Pateamine A (PatA), compounds that trigger eIF2α-independent SG assembly. Interestingly, ZIKV infection markedly impaired the phosphorylation of eIF2α triggered in Ars-treated infected cells, and the abrogation of SG assembly in ZIKV-infected cells is, at least in part, dependent on eIF2α dephosphorylation. These data demonstrate that ZIKV elicits mechanisms to counteract host anti-viral stress responses to promote a cellular environment propitious for viral replication. Citation: Amorim R, Temzi A, Griffin BD, Mouland AJ (2017) Zika virus inhibits eIF2α-dependent stress granule assembly. PLoS Negl Trop Dis 11 (7): e0005775. https://doi.org/10.granules (SGs). We observed that ZIKV blocks SG assembly induced by sodium arsenite (Ars), but not by sodium selenite or Pateamine A. We demonstrate that this difference is related to the ability of ZIKV to modulate the dephosphorylation of eIF2α via its phosphatase. Our work demonstrates that ZIKV prevents a host stress response in order to maintain a cellular environment propitious for viral replication. Zika virus inhibits stress granule assembly PLOS Neglected Tropical Diseases | https://doi. 
 Title: Zika virus inhibits eIF2α-dependent stress granule assembly

Output: True


Input: Consider Input: Paragraph: Exaggerated complement activation is a key event in the pathogenesis of a range of autoimmune and inflammatory diseases. Complement Receptor 1 (CR1) has emerged as a molecule of immense interest in gaining insight to the susceptibility, pathophysiology, diagnosis, prognosis and therapy of such diseases. This review brings forth a composite view of the current understanding on the structure, functions, genetics, disease associations and therapeutic implications of CR1. 
 Title: Complement Receptor 1: Disease associations and therapeutic implications

Output: True


Input: Consider Input: 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


Output: False