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: Multiple sclerosis (MS) is a central nervous system (CNS) disease characterized by chronic neuroinflammation, demyelination, and axonal damage. Infiltration of activated lymphocytes and myeloid cells are thought to be primarily responsible for white matter damage and axonopathy. Over time, this neurologic damage manifests clinically as debilitating motor and cognitive symptoms. Existing MS therapies focus on symptom relief and delay of disease progression through reduction of neuroinflammation. However, long-term strategies to remyelinate, protect, or regenerate axons have remained elusive, posing a challenge to treating progressive forms of MS. Preclinical mouse models and techniques, such as immunohistochemistry, flow cytometry, and genomic and proteomic analysis have provided advances in our understanding of discrete time-points of pathology following disease induction. More recently, in vivo and in situ two-photon (2P) microscopy has made it possible to visualize continuous real-time cellular behavior and structural changes occurring within the CNS during neuropathology. Research utilizing 2P imaging to study axonopathy in neuroinflammatory demyelinating disease has focused on five areas: (1) axonal morphologic changes, (2) organelle transport and health, (3) relationship to inflammation, (4) neuronal excitotoxicity, and (5) regenerative therapies. 2P imaging may also be used to identify novel therapeutic targets via identification and clarification of dynamic cellular and molecular mechanisms of axonal regeneration and remyelination. Here, we review tools that have made 2P accessible for imaging neuropathologies and advances in our understanding of axonal degeneration and repair in preclinical models of demyelinating diseases. Abbreviations: 2d2, MOG peptide 35-55 TCR transgenic; APP, amyloid precursor protein; ATP, adenosine triphosphate; CerTN-L15, troponin C expressing Ca 2+ sensing transgenic animal; CFP, cyan fluorescent protein; EAE, experimental autoimmune/allergic encephalomyelitis; EB3, end-binding protein 3; FAD, focal axonal degeneration; FRET, Förster resonance energy transfer; GECI, genetically encoded Ca 2+ indicator; GFP, green fluorescent protein; JHMV, John Howard Mueller strain of murine hepatitis virus; LFB, Luxol fast blue; MHC, major histocompatibility complex; MOG, myelin oligodendrocyte glycoprotein; MRI, magnetic resonance imaging; MRS, magnetic resonance spectroscopy; MS, multiple sclerosis; NAWM, normal appearing white matter; NPC, neural precursor cell; OT-2, ovalbumin peptide 323-339 TCR transgenic-binding MHC Class II; PLP, proteolipid protein (promoter for mature oligodendrocytes); RAG, recombination activating-gene; RFP, red fluorescent protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; SMI31, Sternberger monoclonal incorporated monoclonal antibody 31; SMI32, Sternberger monoclonal incorporated monoclonal antibody 32; TCR, T-cell receptor; Thy1, thymocyte antigen 1 (promoter for neuron subset); TMEV, Theiler's murine encephalomyelitis virus; TN-XXL, troponin C expressing Ca 2+ sensing transgenic animal; XFP, "X" fluorescent protein (any spectral variant of GFP); YFP, yellow fluorescent protein. 
 Title: Article 189 1 Citation: Yandamuri SS and Lane TE (2016) Imaging Axonal Degeneration and Repair in Preclinical Animal Models of Multiple Sclerosis

Answer: False


Question: Paragraph: Immaturity of the neonatal immune system is causative for high morbidity in calves and colostrum intake is crucial for acquiring passive immunity. Pathogenesis is promoted by reactive oxygen species accumulating at birth if counter-regulation is inadequate. The flavonol quercetin exerts antioxidative and anti-inflammatory effects that may enhance neonatal health. The aim of this work was to study effects of quercetin feeding on metabolic, antioxidative and inflammatory parameters in neonatal calves to investigate whether quercetin could compensate for insufficient colostrum supply. Twenty-eight newborn calves were assigned to two dietary groups fed colostrum or milk-based formula on day 1 and 2 and milk replacer thereafter. From day 2 onwards, 7 calves per diet group were additionally fed quercetin aglycone (50 mg/(kg body weight × day)). Blood samples were taken repeatedly to measure plasma concentrations of flavonols, glucose, lactate, total protein, albumin, urea, non-esterified fatty acids, triglycerides, cholesterol, insulin, glucagon, cortisol, immunoglobulins, fibrinogen, haptoglobin and serum amyloid A. Trolox equivalent antioxidative capacity, ferric reducing ability of plasma, thiobarbituric acid reactive species and F2isoprostanes were analyzed to evaluate plasma antioxidative status. Expression of tumor necrosis factor, interleukin-1α, interleukin-1β, serum amyloid A, haptoglobin, fibrinogen, Creactive protein, catalase, glutathione peroxidase and superoxide dismutase mRNA were measured in liver tissue on day 8. Plasma flavonol concentrations were detectable only after quercetin-feeding without differences between colostrum and formula feeding. Plasma glucose, lactate, total protein, immunoglobulins, triglycerides, cholesterol, trolox equivalent antioxidative capacity and thiobarbituric acid reactive species were higher after colostrum feeding. Body temperature, fecal fluidity and plasma concentrations of cortisol and PLOS ONE | Competing Interests: The authors have declared that no competing interests exist. haptoglobin were higher in formula-than in colostrum-fed groups. Hepatic mRNA expression of tumor necrosis factor was higher after quercetin feeding and expression of C-reactive protein was higher after formula feeding. Data confirm that colostrum improves neonatal health and indicate that quercetin feeding cannot compensate for insufficient colostrum supply. Quercetin Supplementation in Neonatal Calves with Respect to Different Diet PLOS ONE | 
 Title: Quercetin Feeding in Newborn Dairy Calves Cannot Compensate Colostrum Deprivation: Study on Metabolic, Antioxidative and Inflammatory Traits

Answer: True


Question: Paragraph: Cardioviruses are members of the Picornaviridae family and infect a variety of mammals, from mice to humans. Replication of cardioviruses produces double stranded RNA that is detected by helicases in the RIG-I-like receptor family and leads to a signaling cascade to produce type I interferon. Like other viruses within Picornaviridae, however, cardioviruses have evolved several mechanisms to inhibit interferon production. In this review, we summarize recent findings that have uncovered several proteins enabling efficient detection of cardiovirus dsRNA and discuss which cell types may be most important for interferon production in vivo. Additionally, we describe how cardiovirus proteins L, 3C and L * disrupt interferon production and antagonize the antiviral activity of interferon effector molecules. 
 Title: Innate Immune Detection of Cardioviruses and Viral Disruption of Interferon Signaling

Answer:
False