In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
One example: The severe acute respiratory syndrome (SARS) epidemic originating from China in 2002 was caused by a previously uncharacterized coronavirus that could be identified by specific RT-PCR amplification. Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients. A real-time fluorogenic RT-PCR assay based on the 3 -noncoding region (3 -NCR) of SARS-CoV genome was developed as a quantitative SARS diagnostic tool. The ideal amplification efficiency of a sensitive SARS-CoV RT-PCR assay should yield an E value (PCR product concentration increase per amplification cycle) equal to 2.0. It was demonstrated that the 3 -NCR SARS-CoV based RT-PCR reactions could be formulated to reach excellent E values of 1.81, or 91% amplification efficacy. The SARS-CoV cDNA preparations derived from viral RNA extract and the cloned recombinant plasmid both exhibit the identical amplification characteristics, i.e. amplification efficacy using the same PCR formulation developed in this study. The viral genomic copy (or genomic equivalences, GE) per infectious unit (GE/pfu) of SARS-CoV used in this study was also established to be approximate 1200-1600:1. The assay's detection sensitivity could reach 0.005 pfu or 6-8 GE per assay. It was preliminarily demonstrated that the assay could efficiently detect SARS-CoV from clinical specimens of SARS probable and suspected patients identified in Taiwan. The 3 -NCR based SARS-CoV assay demonstrated 100% diagnostic specificity testing samples of patients with acute respiratory disease from a non-SARS epidemic region.
Solution is here: Development and evaluation of an efficient 3 -noncoding region-based SARS coronavirus (SARS-CoV) RT-PCR assay for detection of SARS-CoV
Explanation: It's a correct title because the paragraph described the development of 3 -noncoding region of SARS-CoV genome and assay efficiently detecting SARS-CoV from clinical specimens.

Now, solve this: 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, Forster 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.
Solution:
Article 189 1 Citation: Yandamuri SS and Lane TE (2016) Imaging Axonal Degeneration and Repair in Preclinical Animal Models of Multiple Sclerosis