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".

Example Input: Paragraph: Introduction-HIV-1 uses a programmed -1 ribosomal frameshift to generate Gag-Pol, the precursor of its enzymes, when its full-length mRNA is translated by the ribosomes of the infected cells. This change in the reading frame occurs at a so-called slippery sequence that is followed by a specific secondary structure, the frameshift stimulatory signal. This signal controls the frameshift efficiency. The synthesis of HIV-1 enzymes is critical for the virus replication and therefore, the -1 ribosomal frameshift could be the target of novel antiviral drugs. Areas covered-This review examines various approaches used to select drugs interfering with the -1 frameshift of HIV-1. These include the selection and modification of chemical compounds that specifically bind to the frameshift stimulatory signal, the use of antisense oligonucleotides targeting this signal and the selection of compounds that modulate HIV-1 frameshift, by using bicistronic reporters where the expression of the second cistron depends upon HIV-1 frameshift. Expert opinion-The most promising approach is the selection and modification of compounds specifically targeting HIV-1 frameshift stimulatory signal. The use of antisense oligonucleotides binding to the frameshift stimulatory signal is still questionable. The use of bicistronic reporters preferentially selects compounds that modulate the frameshift by targeting the ribosomes, which is less promising.
Title: Targeting frameshifting in the human immunodeficiency virus
Example Output: True

Example Input: Paragraph: Gram-negative pathogen-induced nosocomial infections and resistance are a most serious menace to global public health. Qingfei Xiaoyan Wan (QF), a traditional Chinese medicine (TCM) formula, has been used clinically in China for the treatment of upper respiratory tract infections, acute or chronic bronchitis and pulmonary infection. In this study, the effects of QF on Pseudomonas aeruginosainduced acute pneumonia in mice were evaluated. The mechanisms by which four typical antiinflammatory ingredients from QF, arctigenin (ATG), cholic acid (CLA), chlorogenic acid (CGA) and sinapic acid (SPA), regulate anti-inflammatory signaling pathways and related targets were investigated using molecular biology and molecular docking techniques. The results showed that pretreatment with QF significantly inhibits the release of cytokines (TNF- and IL-6) and chemokines (IL-8 and RANTES), reduces leukocytes recruitment into inflamed tissues and ameliorates pulmonary edema and necrosis. In ;6(3):212-221 addition, ATG was identified as the primary anti-inflammatory agent with action on the PI3K/AKT and Ras/MAPK pathways. CLA and CGA enhanced the actions of ATG and exhibited synergistic NF-B inactivation effects possibly via the Ras/MAPK signaling pathway. Moreover, CLA is speculated to target FGFR and MEK firstly. Overall, QF regulated the PI3K/AKT and Ras/MAPK pathways to inhibit pathogenic bacterial infections effectively.
Title: Qingfei Xiaoyan Wan, a traditional Chinese medicine formula, ameliorates Pseudomonas aeruginosa-induced acute lung inflammation by regulation of PI3K/AKT and Ras/MAPK pathways-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)
Example Output: False

Example Input: Paragraph: An oligonucteotide containing multiple AP-1 binding sites was introduced into the regulatory sequence in the long terminal repeat (LTR) of feline immunodeficiency virus (FIV). Chloramphenicol acetyltransferase assay revealed that basal promoter activity of the mutated LTR was higher than that of the wildtype LTR in Crandell feline kidney (CRFK) cells. The mutated LTR was introduced into an infectious molecular clone of FIV and the clone was transfected into CRFK cells. The virus production of the mutant in the cells was as high as that of the wildtype when determined by the reverse transcriptase activity assay. The growth of the mutant virus obtained from the transfected CRFK cells was examined in feline T lymphoblastoid cell lines (MYA-1 and FeL-039 cells) and primary feline peripheral blood mononuclear cells (fPBMCs). The growth was delayed when compared with that of the wild-type virus in all the cells used. Upon examination by polymerase chain reaction, the length of the LTR of the mutant virus was shortened in both MYA-1 cells and fPBMCs. Sequence analysis revealed that the insertion was completely deleted 39 days after infection in the MYA-1 cells. T. Miyazawa et al. several putative binding sites for enhancer proteins such as AP-1, AP-4, C/EBP are present [13, 14, 26] . Previously we reported that by deletion of AP-1 and AP-4 related sequences in the LTR, promoter activity was reduced in Crandell feline kidney (CRFK) andfelis catus whole foetus-4 (fcwf-4) cells using the chloramphenicol acetyltransferase (CAT) assay [11, 19] . Recently, Thompson et al. [29] reported that protein(s) present in the nuclear extract from feline T cells (F422 cells) which are permissive for FIV replication bind to the putative AP-1 and AP-4 binding sites. These findings suggest that the AP-1 in feline cells can bind to the AP-1 binding site in the L T R and is critical for the basal promoter activity of the LTR. Conversely, a m u t a n t virus which lacks the AP-1 and AP-4 binding sites replicated in feline T lymphoblastoid cell lines (MYA-1 and FeL-039 cells) [19] and primary feline peripheral blood mononuclear cells (fPBMCs) [17] . These data indicate that the AP-1 and AP-4 binding sites are not necessary for the efficient replication of FIV in feline T lymphocytes. In this study, we introduced an oligonucleotide containing multiple AP-1 binding sites adjacent to the original AP-1 binding site in the U3 region of the L T R and examined the effects of the insertion on the promoter and growth activities of the mutant. Cell culture CRFK cells [3] and fcwf-4 [9] were maintained in Dulbecco's modified Eagle's medium supplemented with 10% heat-inactivated foetal calf serum (FCS). fPBMCs obtained from a specific pathogen-free cat were isolated as described previously [15, 16] . 21] and FeL-039 [30] cells, and fPBMCs were maintained in the RPMI 1640 growth medium supplemented with 10% FCS, antibiotics, 50 gM 2-merecaptoethanol, 2 g g/ml polybrene and 100 units/ml of recombinant human interleukin-2 at 37C in a humidified atmosphere of 5% CO 2 in air. DNA constructs
Title: Effects of insertion of multiple AP-1 binding sites into the U3 region of the long terminal repeat of feline immunodeficiency virus
Example Output:
True