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 Input:
Paragraph: Nasopharyngeal carcinoma (NPC) is a unique malignancy derived from the epithelium of the nasopharynx. Despite great advances in the development of radiotherapy and chemotherapy, relapse and metastasis in NPC patients remain major causes of mortality. Evidence accumulated over recent years indicates that Epstein-Barr virus (EBV) lytic replication plays an important role in the pathogenesis of NPC and inhibition of EBV reactivation is now being considered as a goal for the therapy of EBV-associated cancers. With this in mind, a panel of dietary compounds was screened and emodin was found to have potential anti-EBV activity. Through Western blotting, immunofluorescence, and flow cytometric analysis, we show that emodin inhibits the expression of EBV lytic proteins and blocks virion production in EBV-positive epithelial cell lines. In investigating the underlying mechanism, reporter assays indicated that emodin represses Zta promoter (Zp) and Rta promoter (Rp) activities, triggered by various inducers. Mapping of the Zp construct reveals that the SP1 binding region is important for emodin-triggered repression and emodin is shown to be able to inhibit SP1 expression, suggesting that it likely inhibits EBV reactivation by suppression of SP1 expression. Moreover, we also show that emodin inhibits the tumorigenic properties induced by repeated EBV reactivation, including micronucleus formation, cell proliferation, migration, and matrigel invasiveness. Emodin administration also represses the tumor growth in mice which is induced by EBV activation. Taken together, our results provide a potential chemopreventive agent in restricting EBV reactivation and NPC recurrence. Genetic, environmental, and viral factors have been incriminated in the etiology of NPC and Epstein-Barr virus (EBV) is strongly associated with the occurrence of NPC. EBV is a member of the gamma herpesviruses, with a 172 kb double-stranded DNA genome. The life cycle of EBV includes latency and lytic replication. Eleven gene products, EBNAs 1~6, LMPs 1, 2A, and 2B, and small RNAs EBER 1 and 2, are expressed during latent infection [6] . Upon induction by chemicals or stress, EBV is activated and enters the lytic cycle, known as reactivation. Three subsets of lytic genes, immediate-early, early, and late genes, are expressed sequentially and, subsequently, viral particles are packaged and released [7, 8] . Through years of study, EBV latent infection has been considered to play an important role in NPC carcinogenesis. In recent years, accumulating evidence has suggested that EBV lytic infection also contributes to the tumorigenesis of NPC. Sero-epidemiological surveys indicate that patients with elevated antibody titers against EBV lytic proteins, such as viral capsid antigen (VCA), DNase, DNA polymerase, and early antigen (EA), have a high risk of NPC [9] [10] [11] [12] [13] [14] [15] . Several EBV lytic products have been detected in the NPC biopsies [16] [17] [18] . In addition, EBV lytic proteins, including BARF1, BHRF1, BRLF1, BALF3, BGLF4, and DNase, have been shown to have various tumorigenic functions [16, [19] [20] [21] [22] . In our previous study, we found that EBV reactivated by chemicals promotes cellular genome instability and tumor growth [23, 24] . Collectively, these reports suggest that inhibition of EBV reactivation might be useful for NPC prevention and therapy. Accordingly, for safety and convenience, we have screened several dietary compounds for anti-EBV activity. We reported that the flavonoids have activity against EBV reactivation and through the inhibition of EBV, NPC tumorigenesis has been repressed [25] [26] [27] . Here, we report that the phytochemical emodin has the potential ability to inhibit EBV reactivation. Emodin, a common traditional Chinese medicine, is an anthraquinone derivative present in the roots or rhizomes of rhubarb. Emodin has various medical applications, including anti-cancer, anti-oxidation, anti-inflammation or allergy, anti-diabetes, and anti-viral or bacterial activities [28] . For its anti-viral effect, emodin has the ability to inhibit the SARS coronavirus [29] , and block the replication of HBV [30], Coxsackievirus [31], zika virus [32], and influenza A virus [33] . Moreover, emodin has been suggested to inhibit the replication of herpesviruses [34] [35] [36] . However, the detailed mechanism is not well elucidated. In this study, based on our screening, we show that emodin inhibits EBV reactivation in epithelial cells, through the mechanism of repressing SP1 expression to inhibit the Zta and Rta promoter activities. Moreover, through its anti-EBV activity, NPC tumorigenesis could be relieved, suggesting emodin is a potential agent for therapy of EBV-associated cancer. Results Emodin (1,3,8-trihydroxy-6-methyl-anthraquinone, Figure 1a ) has been shown to be cytotoxic to human cell lines. Before investigating the anti-EBV effect of emodin, two EBV-positive NPC cell lines, NA and HA, and their parental cells TW01 and HONE-1, were assessed for susceptibility to the cytotoxicity of emodin. The cells were seeded into 96-well plates 24 h prior to treatment; then, emodin was added for 48 h to determine its cytotoxic effect on the NPC cell lines NA and HA. Emodin has significant toxicity to TW01 cells, while the derivative NA cells showed little resistance to the compound (Figure 1b) . A similar effect was seen on HONE-1 and HA cells (Figure 1b) . Furthermore, to evaluate these results more precisely, half maximum of cytotoxicity concentrations 50 (CC50) were calculated and are shown in the top panels of Figure 1b . The CC50 values of TW01 and the derivative NA cell lines were 31 and 79 M, while the values for HONE-1 and HA were 58 and 65 M, respectively (Figure 1b) , implying that the cells harboring EBV seemed to be more resistant to emodin (TW01 vs.
Title: Emodin Inhibits EBV Reactivation and Represses NPC Tumorigenesis

Ex Output:
False

Ex Input:
Paragraph: Spongiform degeneration is characterized by vacuolation in nervous tissue accompanied by neuronal death and gliosis. Although spongiform degeneration is a hallmark of prion diseases, this pathology is also present in the brains of patients suffering from Alzheimer's disease, diffuse Lewy body disease, human immunodeficiency virus (HIV) infection, and Canavan's spongiform leukodystrophy. The shared outcome of spongiform degeneration in these diverse diseases suggests that common cellular mechanisms must underlie the processes of spongiform change and neurodegeneration in the central nervous system. Immunohistochemical analysis of brain tissues reveals increased ubiquitin immunoreactivity in and around areas of spongiform change, suggesting the involvement of ubiquitin-proteasome system dysfunction in the pathogenesis of spongiform neurodegeneration. The link between aberrant ubiquitination and spongiform neurodegeneration has been strengthened by the discovery that a null mutation in the E3 ubiquitin-protein ligase mahogunin ring finger-1 (Mgrn1) causes an autosomal recessively inherited form of spongiform neurodegeneration in animals. Recent studies have begun to suggest that abnormal ubiquitination may alter intracellular signaling and cell functions via proteasome-dependent and proteasome-independent mechanisms, leading to spongiform degeneration and neuronal cell death. Further elucidation of the pathogenic pathways involved in spongiform neurodegeneration should facilitate the development of novel rational therapies for treating prion diseases, HIV infection, and other spongiform degenerative disorders. transmissible spongiform encephalopathy (TSE); retroviral infection; mahogunin ring finger-1 (Mgrn1); oxidative stress; autophagy; endocytic trafficking NIH Public Access
Title: The ubiquitin-proteasome system in spongiform degenerative disorders

Ex Output:
True

Ex Input:
Paragraph: Lower respiratory tract infections by respiratory syncytial virus (RSV) are the foremost cause of infant hospitalization and are implicated in lasting pulmonary impairment and the development of asthma. Neutrophils infiltrate the airways of pediatric patients with RSV-induced bronchiolitis in vast numbers: approximately 80% of infiltrated cells are neutrophils. However, why neutrophils are recruited to the site of viral respiratory tract infection is not clear. In this review we discuss the beneficial and pathologic contributions of neutrophils to the immune response against RSV infection. Neutrophils can limit viral replication and spread, as well as stimulate an effective antiviral adaptive immune response. However, low specificity of neutrophil antimicrobial armaments allows for collateral tissue damage. Neutrophilinduced injury to the airways during the delicate period of infant lung development has lasting adverse consequences for pulmonary architecture and might promote the onset of asthma in susceptible subjects. We suggest that pharmacologic modulation of neutrophils should be explored as a viable future therapy for severe RSV-induced bronchiolitis and thereby prevent the inception of subsequent asthma. The antiviral functions of neutrophils suggest that targeting of neutrophils in patients with RSV-induced bronchiolitis is best performed under the umbrella of antiviral treatment. (J Allergy Clin Immunol 2015;136:838-47.)
Title: Neutrophils in respiratory syncytial virus infection: A target for asthma prevention

Ex Output:
False