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: 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. Schurmann). 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
answer:
False

question:
Paragraph: Objective: Tumor-treating fields are currently used to successfully treat various cancers; however, the specific pathways associated with its efficacy remain unknown in the immune responses. Here, we evaluated tumor-treating fields-mediated initiation of the macrophage-specific immune response. Materials and Methods: We subjected RAW 264.7 mouse macrophages to clinically relevant levels of tumor-treating fields (0.9 V/cm, 150 kHz) and evaluated alterations in cytokine expression and release, as well as cell viability. Additionally, we investigated the status of immunomodulatory pathways to determine their roles in tumor-treating fields-mediated immune activation. Results and Discussion: Our results indicated that tumor-treating fields treatment at 0.9 V/cm decreased cell viability and increased cytokine messenger RNA/protein levels, as well as levels of nitric oxide and reactive oxygen species, relative to controls. The levels of tumor necrosis factor a, interleukin 1b, and interleukin 6 were markedly increased in tumor-treating fields-treated RAW 264.7 cells cocultured with 4T1 murine mammary carcinoma cells compared with those in 4T1 or RAW 264.7 cells with or without tumor-treating fields treatment. Moreover, the viability of 4T1 cells treated with the conditioned medium of tumor-treating fields-stimulated RAW 264.7 cells decreased, indicating that macrophage activation by tumor-treating fields effectively killed the tumor cells. Moreover, tumor-treating fields treatment activated the nuclear factor kB and mitogen-activated protein kinase pathways involved in immunomodulatory signaling. Conclusion: These results provide critical insights into the mechanisms through which tumor-treating fields affect macrophagespecific immune responses and the efficacy of this method for cancer treatment.
Title: Tumor-Treating Fields Induce RAW264.7 Macrophage Activation Via NK-kB/MAPK Signaling Pathways
answer:
True

question:
Paragraph: The new era in systems pharmacology has revolutionized the human biology. Its applicability, precise treatment, adequate response and safety measures fit into all the paradigm of medical/clinical practice. The importance of mathematical models in understanding the disease pathology and epideomology is now being realized. The advent of high-throughput technologies and the emergence of systems biology have resulted in the creation of systems pharmacogenomics and the focus is now on personalized medicine. However, there are some regulatory issues that need to be addresssed; are we ready for this universal adoption? This article details some of the infectious disease pharmacogenomics to the developments in this area.
Title: System pharmacogenomics application in infectious diseases
answer:
True