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: This paper describes the molecular detection of respiratory viruses from nasopharyngeal flocked swabs (flocked swabs) and nasopharyngeal washes (washes) in a clinical setting. Washes and flocked swabs collected from children < 3 years old hospitalized with a lower respiratory tract infection were tested for parainfluenza virus 1-3, respiratory syncytial virus, influenza A and B and metapneumovirus (Group 1) and adenovirus, rhinovirus and coronavirus (Group 2) using realtime reverse transcriptase PCR (rRT-PCR). A consensuses standard was used to determine sensitivity and compare cycle thresholds (C T ) of washes and flocked swabs for each virus and group of viruses. Sensitivities ranged from 79 to 89% and 69 to 94% for flocked swabs and washes, respectively, excluding AdV which had a sensitivity of 35% for flocked swabs. When the flocked swabs and washes of Group 1 viruses were collected on the day of admission, the sensitivity of both sample types was 100%. Wash specimens had a lower C T value and higher sensitivity than flocked swabs; however there was no statistical difference in the sensitivity of a flocked swab (89%) versus wash (93%) for the detection of Group 1 viruses, particularly when samples were collected on the same day. Flocked swabs may be a useful alternative to washes for detection of respiratory viruses in clinical settings.
Title: Comparison of nasopharyngeal flocked swabs and nasopharyngeal wash collection methods for respiratory virus detection in hospitalized children using real-time polymerase chain reaction HHS Public Access
answer:
False

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Paragraph: Background: The purpose of this study is to determine the incidence and significance of hypouricemia in patients with severe acute respiratory syndrome (SARS). Pulmonary lesions in patients with SARS are thought to result from proinflammatory cytokine dysregulation. Acute renal failure has been reported in patients with SARS, but whether cytokines can injure renal tubules is unknown. Methods: Sixty patients diagnosed with SARS in Taiwan in April 2003 were studied. Patients were identified as hypouricemic when their serum uric acid (UA) level was less than 2.5 mg/dL (<149 mol/L) within 15 days after fever onset. Urine UA and creatinine levels were available for 43 patients; the serum cytokines interleukin-6 (IL-6), IL-8, and tumor necrosis factor- (TNF-) were measured in 16 patients. Results: Sixteen patients (26.7%) had hypouricemia (UA, 1.68 0.52 mg/dL [100 31 mol/L]). No differences in age, sex, symptoms, vital signs, hemogram, or other biochemistry data existed between the hypouricemic and normouricemic groups. Fractional excretion (FE) of UA (FE UA ) in 12 hypouricemic patients was 39.6% 23.4%, significantly greater than that of 31 normouricemic patients (16.4% 11.4%; P < 0.0001). After adjustments for age and sex, high FE UA was significantly associated with the lowest blood oxygenation (P 0.001; r 0.624). The number of catastrophic outcomes (endotracheal intubation and/or death) adjusted for older age and sex showed that hypouremic patients had an odds ratio of 10.57 (confidence interval, 2.33 to 47.98; P 0.002). Kaplan-Meier curves for catastrophic outcome-free results showed significant differences between patients with normouricemia or hypouricemia (P 0.01). Serum IL-8 levels correlated significantly with FE UA (P < 0.001; r 0.785) and inversely with serum UA level (P 0.044; r 0.509); neither IL-6 nor TNF- level showed such correlations. Conclusion: One fourth of patients with SARS developed hypouricemia, which might result from a defect in renal UA handling and was associated with a high serum IL-8 level. Renal hypouricemia is an ominous sign in patients with SARS. Am J Kidney Dis 45:88 -95.
Title: Renal Hypouricemia Is an Ominous Sign in Patients With Severe Acute Respiratory Syndrome
answer:
True

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, 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.
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