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".

Example Input: Paragraph: Mice infected with neurotropic strains of coronavirus develop acute encephalomyelitis and eliminate infectious virus. However, control of acute infection is incomplete resulting in persistence of viral RNA in the central nervous system (CNS) associated with ongoing primary demyelination. A high prevalence of virus specific CD8 and CD4 T cells within the CNS correlates with ex vivo cytolytic activity and IFN-7 secretion, which are both required for virus reduction during the acute infection. Although most infected cell types are susceptible to perforin mediated clearance, IFNq' is required for controlling infection of oligodendrocytes. Furthermore, by enhancing class I expression and inducing class II expression within resident CNS cells IFN-7 optimizes T cell receptor dependent functions. In addition to its direct anti viral activity, these multifactorial effects make IFN-y more essential than perforin for viral control. CD4 T cells enhance CD8 T cell expansion, survival and effectiveness. Although both CD8 and CD4 T cells are retained within the CNS during persistence, they cannot control viral recrudescence in the absence of humoral immunity. Demyelination can be mediated by either CD8 or CD4 T cells; however, although a variety of effector molecules have been excluded, a dominant common denominator remains elusive. Thus concerted efforts to control infection coincide with a variety of potential mechanisms causing chronic demyelinating disease. 
 Title: Chapter C4 THE ROLE OF T CELLS IN CORONA-VIRUS- INDUCED DEMYELINATION
Example Output: False

Example 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
Example Output: False

Example Input: Paragraph: a summary of the evolution of infectiousness over time. When who-infects-whom is observed, the Nelson-Aalen estimator produces an unbiased estimate of the cumulative hazard function of the contact interval distribution. When who-infects-whom is not observed, we use an EM algorithm to average the Nelson-Aalen estimates from all possible combinations of who-infected-whom consistent with the observed data. This converges to a nonparametric maximum likelihood estimate of the cumulative hazard function that we call the marginal Nelson-Aalen estimate. We study the behavior of these methods in simulations and use them to analyze household surveillance data from the 2009 influenza A(H1N1) pandemic. 
 Title: Nonparametric survival analysis of infectious disease data Summary
Example Output:
True