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: Background: Chronic Hepatitis B (CHB) remains a major problem for global public health. Viral persistence and immune defects are the two major reasons for CHB, and it was hypothesized that based on a transient clearance of serum viral DNA and HBsAg "window stage", active immunization against hepatitis B virus (HBV) might initiate effective host immune responses versus HBV to achieve functional cure of CHB. Methods: Two experimental mouse models that mice hydrodynamic injected HBV DNA or infected with recombinant AAV/HBV were used. The "sandwich" therapeutic effect by using a potent human anti-HBsAg neutralizing monoclonal antibody (G12) in combination with antiviral drug tenofovir disoproxil fumarate (TDF), followed by active immunization with HBsAg-HBsAb (mYIC) was evaluated. Findings: A single G12 injection rapidly cleared serum HBsAg in HDI-HBV carrier mice, with a synergistic effect in decreasing viral DNA load when TDF was given orally. When both serum viral DNA and HBsAg load became low or undetectable, mYIC was administered. A more effective clearance of viral DNA and HBsAg was observed and serum HBsAb was developed only in these "sandwich"-treated mice. Efficient intrahepatic anti-HBV immune responses were also observed in these mice, including the formation of aggregates of myeloid cells with CD8 + T cells and increased TNF-α, granzyme B production. The "sandwich" combination therapy not only efficiently decreased HBsAg and HBV DNA levels but also induced effective cellular and humoral immunity, which may result in functional cure of CHB. Research in context section Persistence of HBV cccDNA and various host immune defects were shown as the two main obstacles for HBV clearance. Blocking a single target will not be sufficient to achieve functional cure of CHB. A very small percentage of CHB patients could attain "functional cure" by antiviral treatment fol- * Corresponding authors. .cn (Z. Yuan). lowed by interferon therapy. Therapeutic vaccination for CHB showed substantial efficacy. A humanized HBsAb G12 could efficiently block HBV infection and decrease HBsAg level in mice model. This research showed that when both serum viral DNA and HB-sAg load became low or undetectable by antiviral and HBsAb treatment, therapeutic vaccine (mYIC) add on induced effective, host humoral and intrahepatic cellular anti-HBV immune responses, with more rapid and efficient clearance of HBV and HBsAg. Based on optimized antiviral treatment with potent human HB-sAb to rapidly decrease serum HBsAg, followed by boosting host with active immunization provides a novel strategy for functional cure of CHB. 
 Title: Evaluation of antiviral -passive -active immunization ("sandwich") therapeutic strategy for functional cure of chronic hepatitis B in mice

Ex Output:
True


Ex Input:
Paragraph: We previously reported widespread differential expression of long non-protein-coding RNAs (ncRNAs) in response to virus infection. Here, we expanded the study through small RNA transcriptome sequencing analysis of the host response to both severe acute respiratory syndrome coronavirus (SARS-CoV) and influenza virus infections across four founder mouse strains of the Collaborative Cross, a recombinant inbred mouse resource for mapping complex traits. We observed differential expression of over 200 small The small RNAs identified also included many non-miRNA small RNAs, such as small nucleolar RNAs (snoRNAs), in addition to nonannotated small RNAs. An integrative sequencing analysis of both small RNAs and long transcripts from the same samples showed that the results revealing differential expression of miRNAs during infection were largely due to transcriptional regulation and that the predicted miRNA-mRNA IMPORTANCE Most studies examining the host transcriptional response to infection focus only on protein-coding genes. However, mammalian genomes transcribe many short and long non-protein-coding RNAs (ncRNAs). With the advent of deepsequencing technologies, systematic transcriptome analysis of the host response, including analysis of ncRNAs of different sizes, is now possible. Using this approach, we recently discovered widespread differential expression of host long (>200 nucleotide [nt]) ncRNAs in response to virus infection. Here, the samples described in the previous report were again used, but we sequenced another fraction of the transcriptome to study very short (about 20 to 30 nt) ncRNAs. We demonstrated that virus infection also altered expression of many short ncRNAs of diverse classes. Putting the results of the two studies together, we show that small RNAs may also play an important role in regulating the host response to virus infection. Citation Peng X, et al. 2011. Integrative deep sequencing of the mouse lung transcriptome reveals differential expression of diverse classes of small RNAs in response to respiratory virus infection. mBio 2(6):e00198-11. 
 Title: Integrative Deep Sequencing of the Mouse Lung Transcriptome Reveals Differential Expression of Diverse Classes of Small RNAs in Response to Respiratory Virus Infection

Ex Output:
True


Ex Input:
Paragraph: Precursor B acute lymphoblastic leukemias (pre-B ALLs) abnormally express a specific glycan structure, 9-O-acetylated sialic acid (9-O-Ac-Sia), on their cell surface, but glycoproteins that carry this modification have not been identified. Using three different lectins that specifically recognize this structure, we establish that nucleolin (NCL), a protein implicated in cancer, contains 9-O-Ac-Sia. Surprisingly, antibodies against the glycolipid 9-O-Ac-Sia GD3 also detected 9-O-Ac-Sia NCL. NCL is present on the surface of pre-B ALL cells as a sialoglycoprotein that is partly 9-O-acetylated and conversely, 9-O-Ac-Sia-containing structures other than NCL are present on these cells as well. Interestingly, NCL and the 9-O-Ac-Sia signal had less co-localization on normal pre-B cells. We also investigated regulation of NCL on the cell surface and found that sialidase treatment increased the percentage of cells positive for cell surface NCL, suggesting that sialylation of NCL promotes internalization. Treatment of pre-B ALL cells with the chemotherapy drug vincristine also increased the percentage of cells with surface NCL and correlated with increased 9-O-Ac-Sia expression. All tested leukemia cells including primary samples expressed NCL, suggesting it as a possible therapeutic target. We confirmed this by showing inhibition of cell proliferation in some pre-B ALLs by exposure to a NCLspecific aptamer AS1411. Precursor B-cell acute lymphoblastic leukemia (pre-B ALL) is the most prevalent malignancy of childhood 1 . Cell surface structures that selectively identify leukemia cells could be used for diagnosis or perhaps even treatment, and therefore previous studies reporting increased expression of a very specific glycan structure on pre-B ALL cells, consisting of sialic acid modified by 9-O-acetylation, are of significant interest in this context 2,3 . Sialic acids (Sias) belong to a family of 9-carbon carboxylated monosaccharides that most frequently are found as the terminal residues of glycoconjugates, which include glycoproteins and glycolipids. Sias are often highly expressed in cancer 4,5 , and, moreover, changes in sialylation promote cancer progression 6 . Sialic acids can carry further modifications, of which O-acetylation is the most common, and preferentially occurs at the hydroxyl group of carbon C9, yielding 9-O-Ac-Sia 7 . Sialic acids further modified by O-acetylation are expressed in a tissue and cell-specific manner on glycoproteins or glycolipids on normal cells, and those modified Sias can act as selective receptors for entry of some viruses 8 . However, abnormal expression of sialic acid-containing glycoconjugates and O-acetylated derivatives has also been noted to correlate with tumorigenesis. For example, the ganglioside GD2 is a tumor-specific marker for neuroblastoma, and antibodies against it are currently part of maintenance therapy for this pediatric malignancy 9 . Interestingly, the 9-O-acetylated form of GD2 may be a more specific treatment target than GD2 10 . The ganglioside GD3 and its 9-O-acetylated form (9-O-Ac-GD3, also called CD60b) are sialylated glycolipids expressed in glioblastomas 11 and melanomas 12 . In GD3 (Sia-α2,8-Sia-α2,3-Gal-β1,4-Glc-β1,1′-Cer), the terminal Sia is α2,8-linked and the O-acetylation only occurs on the terminal Sia residue. Published: xx xx xxxx OPEN www.nature.com/scientificreports/ 
 Title: Pre-B acute lymphoblastic leukemia expresses cell surface nucleolin as a 9-O-acetylated sialoglycoprotein OPEN

Ex Output:

False