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".

[EX Q]: Paragraph: In this second part of the chapter on underutilized spices, nine spices are discussed briefl y. They are mango ginger, fragrant pandan, pink pepper, rue, sumac, savory and wasabi. Morphology, chemical composition, medicinal and culinary uses are given briefl y in each of these spices. In addition short notes on 12 lesser known spices are provided; these are blue fenugreek, boldo leaves, chameleon plant, cicely, cresses, epazote, fi nger root, gale, lemon myrtle, Mexican pepper leaf, Tasmanian pepper and water pepper. 
 Title: Other herbs and spices: mango ginger to wasabi
[EX A]: False

[EX Q]: 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
[EX A]: False

[EX Q]: Paragraph: Interferons (IFNs) induce the expression of hundreds of genes as part of an elaborate antimicrobial programme designed to combat infection in all nucleated cells -a process termed cellautonomous immunity. As described in this Review, recent genomic and subgenomic analyses have begun to assign functional properties to novel IFN-inducible effector proteins that restrict bacteria, protozoa and viruses in different subcellular compartments and at different stages of the pathogen life cycle. Several newly described host defence factors also participate in canonical oxidative and autophagic pathways by spatially coordinating their activities to enhance microbial killing. Together, these IFN-induced effector networks help to confer vertebrate host resistance to a vast and complex microbial world. 
 Title: Interferon-inducible effector mechanisms in cell-autonomous immunity
[EX A]:
True